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HomeMy WebLinkAboutAgenda Packet 04/03/20127avtessc, AGENDA is q PORTANGELES CITY COUNCIL MEETING 321 East 5th Street W .- w ASH[ M GTO N, U s. A, APRIL 3, 2012 REGULAR MEETING - 6:00 p.m. 4 AGENDA STEM ,• First Page., ,RECOMMENDATION Note The Mayor may determine the order of business for a particular City Council meeting The agenda should be arranged to best serve the needs and/or convenience of the Council and the public The items of business for regular Council meetings may inc hide the following A. CALL TO ORDER - REGULAR MEETING AT 6:00 p.m. B. ROLL CALL PLEDGE OF ALLEGIANCE CEREMONIAL MATTERS, PROCLAMATIONS & EMPLOYEE RECOGNITIONS C. PUBLIC COMMENT D. LATE ITEMS TO BE PLACED ON THIS OR FUTURE AGENDAS as determined by City Manager or Councilmember CONSENT AGENDA 1. City Council Meeting Minutes for March 20, 26, and 27, 2012. E-1 1. Accept Consent Agenda 2. Expenditure Approval List: 3/10/12 to 3/23/12 for $3,094,126.68. E-9 3. City of Burlington Interlocal Joint Purchasing Agreement E-39 4. Parks, Recreation & Beautification Commission Appointments E-44 5. Surplus Equipment for Disposal / Backhoe & Sweeper E-45 F. QUASI-JUDICIAL MATTERS — REQUIRING PUBLIC HEARINGS (6:30 P.M. or soon thereafter) G. PUBLIC HEARINGS — OTHER (6:30 P.M. or soon thereafter) 1. Medic 1 Ambulance Transport Rate Adjustments G-1 1. Open Public Hearing; 1' Reading; Continue to April 17, 2012 2. Proposed Electric Utility Time -of -Use Rate Ordinance G-6 2. Open Public Hearing; V Reading; Continue to April 17, 2012 H. ORDINANCES NOT REQUIRING PUBLIC HEARINGS 1. Fire Department Related Municipal Code Updates H-1 1. 2"d Reading / Adopt I. RESOLUTIONS NOT REQUIRING PUBLIC HEARINGS ---- NOTE: HEARING DEVICES AVAILABLE FOR THOSE NEEDING ASSISTANCE MAYOR TO DETERMINE TIME OF BREAK April 3, 2012 Port Angeles City Council Meeting Page - 1 W4 Z, 4( 4rb, First W ' GENDA,IfEM* RUCOMMENDA,11L N,�,,z-l_, J. OTHER CONSIDERATIONS 1. Chamber of Commerce / Semi -Annual Report ----- I Information Only Presentation by Russ Veenema, Executive Director 2. Equipment Purchase - Excavator J-1 2. Approve 3. Proposal for Public Forum — Biomass Facilities J-2 3. Consider K. FINANCE L. COUNCIL REPORTS - M. INFORMATION City Manager Reports: 1. Planning Commission Minutes M-1 2. Parks, Recreation & Beautification Commission Minutes M-4 3. Public Works / Construction Contract Status Report M-9 4. Public Works / Grants and Loans Status Report M-10 5. Waterfront Project - Bond Financing M-12 6. Professional Agreement / City Clerk, Police, Mechanical Remodel M-14 Project PD02-201 I N. EXECUTIVE SESSION - under the authority ofRCW 42 30 110(1)(t) to discuss potential litigation with legal council O. ADJOURNMENT - PUBLIC HEARINGS Public hearings are set by the City Council in order to meet legal requirements In addition, the City Council may set a public hearing in order to receive public input prior to making decisions, which impact the citizens Certain matters may be controversial, and the City Council may choose to seek public opinion through the public hearing process NOTE: HEARING DEVICES AVAILABLE FOR THOSE NEEDING ASSISTANCE MAYOR TO DETERMINE TIME OF BREAK April 3, 2012 Port Angeles City Council Meeting Page - 2 PUBLIC INTEREST SIGN-UP SHEET PORTANGELES WASHINGTON, U S A DATE OF MEETING: April 3, 2012 You are encouraged to sign below if: CITY COUNCIL REGULAR MEETING LOCATION: City Council Chambers 1. You are here to listen to the City Council discussion on a particular agenda item; 2. You want to speak during the Public Comment period of the agenda. If several members of the public are interested in a particular agenda item, the Mayor may move that item so it is discussed earlier in the meeting. Also, the Mayor may use the information provided to organize the Public Comment period. During the Public Comment portion of the meeting, the Mayor will invite citizens to talk with the Council about topics that are not scheduled for public testimony on the evening's agenda. Prior to the start of the "Public Comment" portion of the public hearing, all persons wishing to be heard are asked to sign in with the Clerk, giving their names and addresses, and topic. The Mayor may arrange the order of speakers so that testimony is heard in the most logical groupings. To allow time for the Council to complete its legislative agenda, comments should be limited to no more than 5 minutes per person and a total of 15 minutes for this comment period. At the discretion of the Mayor, these time periods may be lengthened or shortened. Following any public comment, the Mayor may allow time, limited to five minutes, for response from City Council members and/or City staff. No speaker may convey or donate his or her time for speaking to another speaker. If many people wish to speak to a particular issue, the Mayor may limit the total amount of time dedicated to that single issue. Written comments may be submitted into the record of a Council meeting by presenting the written document to the Clerk prior to the meeting, in which case a copy of the document will be provided to each Council Member, but the document will not be read aloud; or a document may be distributed to the City Council, with a copy to the Clerk, by a speaker while the speaker is addressing the Council. M 1 G�Q&kn Ild 40-17- `L `lewpI�OWIGcs 5 Y _� Y N / Y/ N I a K V q,1' 1w, cJ 1, U� t% UJ v �, d ,n Y / N G:\Group\Clerk\Forms\Council Attendance Roster.doc PUBLIC INTEREST SIGN-UP SHEET G:\Group\Clerk\Forms\Council Attendance Roster.doc 211 LZ,,s 4Q, -St C (3/N (l r4 Y A T Y/6 y, i Y Y/(9 TUS I� l 1 4 ru—, GY N fJ S(A l v ee-0 171 ec.c�zeaY ""'N SS Y / N Y SSU' •Z�i�n/ V6EG�lC-QUt d Y N —66(XeI76r-d mart, r�`T u��D �.�{Y /L Y / T } 1 c (e � 1 h, vee O / N I,,S% �C1�� (9iN �U"Lj� , /-)-, ,,, Y / I "_I JA, YN 61N C 'A'33 5J(C+aJ r �i l N YL CIJ o Y\ 600 W Y/ / -0/ N N Y /9 U < <�i U/N N G:\Group\Clerk\Forms\Council Attendance Roster.doc 1✓ a i PUBLIC INTEREST SIGN-UP SHEET G:\Group\Clerk\Forms\Council Attendance Roster.doc 7t�4&, 124 V&)VV(_ l N 1 yl( S �v� r �cp uC �S2 Y / N c 2C c� i � • n� Yom? i yr Y /,d i(� I c� �-, - Y / N nT L�l mbal is t771" W uS' Io m a ss ON N ��, /N Y/ �r rti z4 .s S Y i Y/N Y/N Y/N Y/N Y/N Y/N Y/N Y/N Y/N Y/N Y/N Y/N Y/N G:\Group\Clerk\Forms\Council Attendance Roster.doc (ar��C G (A XMI =404ADO Clallam County Economic Development Co unci! Resolution of Support for Nippon Paper Group's Port Angeles CHP Biomass Plant Whereas, Nippon Paper Group owns and operates a mechanical paper mill in Port Angeles that produces 155,000 tons per year of paper; Whereas, Nippon's Port Angeles mill has been operating for nearly 90 years and has about 240 employees with an annual payroll of $25,000,000 Whereas, the current mill relies upon an existing 1950's main boiler that warrants replacement; Whereas, Nippon Paper Group's Board of Directors approved a "Green Energy Project" at the Port Angeles mill in which Nippon will invest over $70 million dollars; Whereas, the Port Angeles Green Energy Project entails the replacement of the existing 1950s boiler with state of the art modern co -generation equipment and emission controls; Whereas, the project will meet all environmental and regulatory requirements of the City of Port Angeles, Olympic Regional Clean Air Agency, and other state and/or federal regulations; Whereas, the regulatory agencies responsible for environmental review and permitting have approved, or are in the process of approving permits for the project; Whereas, the finished project is expected to further reduce the Nippon USA mill's fossil fuel consumption, particulate omissions, and ash output; Whereas, the completed project will create approximately 25 - 30 new jobs and retain 240 jobs while reducing the Port Angeles mill's utilization of fossil fuels and generating 20MW of green, renewable power; Whereas, Nippon's Port Angeles project was selected as one of four pilot biomass utilization projects as part of the Forest Biomass Initiative authorized by the State Legislature and implemented by the Commissioner of Public Lands; Whereas, the Clallam EDC has identified renewable energy as one of its four focus areas and this project falls within those particular focus areas; Whereas, the Clallam County Economic Development Council has the ability to support and advocate for economic development efforts within the region; 905 W. 9th Street, Suite 137-139 P.O. Box 1085, Port Angeles WA 98362 360/457-7793 www.clallam.org NOW, therefore, be it resolved by the Board of Directors of the Clallam County Economic Development Council that: 1. The Council formally endorses and supports the Nippon Paper Group's Green Energy Initiative that will result in a modernized Port Angeles mill; 2. The Council further extends its appreciation and gratitude to the Nippon Paper Group's Board of Directors for its continual support and investment in its Port Angeles mill thereby ensuring the continued significant role that Nippon's Port Angeles operations provides in this region; 3. The Council also appreciates Nippon Paper Group's recent decision to make a substantial investment within the community associated with the corporation's Green Energy Project that will result in the modernization of the Port Angeles mill; 4. The Council's Board of Directors hereby authorizes its officers and staff to take reasonable efforts to advocate in support ofNippon's Port Angeles Green Energy Project; 5. The Council's Board of Directors understands, supports, and approves of its officers and staff articulating positions within public processes, permitting and/or regulatory in nature, that are reflective of and consistent with this resolution with the acknowledgement that all issues of interpretation regarding the authorization of this Resolution shall be vested within the Officers of the Board subject to the Council's by-laws. Approved by a vote of the Board of Directors of the Clallam County Economic Development Council on this 21" day of October 2010 during its regularly scheduled meeting. 905 W. 9"' Street, Suite 137-139 P.O. Box 1085, Port Angeles WA 98362 360/457-7793 www.clallam.or2 Dr. Christopher Penoyar 780 East Peacock Hill Lane Shelton, WA 98584 360-463-6951 Port of Shelton Commissioners Thomas M. "Tom" Wallitner, Jack Miles, Jay Hupp 21 W Sanderson Way Shelton, WA 98584 Dear Commissioners Wallitner, Miles, and Hupp: The active staff physicians of Mason County have worked together to discuss and research the current findings relative to the health effect of biomass incineration. After careful review of the current proposals and evaluating the growing body of medical evidence, especially in the last three years, a clear consensus was reached. We have released a no dissention supermajority opinion on August 2, 2010. The signed petition states the following. We are opposed to the currently proposed biomass power plants based on the grounds that these facilities pose unacceptable health risks. The attached petition has been signed by the active medical staff. Our concerns have been forwarded to the Mason County Commissioners as well as the Washington State Medical Ass. and the Washington Osteopathic Medical .' Association. This follows similar action taken b y the Massachusetts Society, the Florida Medical Society, and the Oregon State Medical Society. 'al Medical science is, of course, continuously being updated and new research has revealed that current regulations and permitting systems may not be adequate to protect the community health. Community members with a particular interest in the subject have been encouraged to review the American Heart Association article in Circulation June 2010: Particulate Matter Air Pollution and Cardiovascular Disease. We have encouraged community members and officials with questions to contact us for further information. They may do so by calling Dr. Christopher Penoyar at 360-463-6951 or Dr. Mark Schlauderaff at 360-426-2500 Sincerely, Dr. Christopher Penoyar • attch: Petition from Mason County Physicians • • • irculation JOURNAL OF THE AMERICAN HEART ASSOCIATION American Heart 000 Association® ro Learn and Live.. Particulate Matter Air Pollution and Cardiovascular Disease: An Update to the Scientific Statement From the American Heart Association Robert D. Brook, Sanjay Rajagopalan, C. Arden Pope, III, Jeffrey R. Brook, Aruni Bhatnagar, Ana V. Diez -Roux, Fernando Holguin, Yuling Hong, Russell V. Luepker, Murray A. Mittleman, Annette Peters, David Siscovick, Sidney C. Smith, Jr, Laurie Whitsel, Joel D. Kaufinan and on behalf of the American Heart Association Council on Epidemiology and Prevention, Council on the Kidney in Cardiovascular Disease, and Council on Nutrition, Physical Activity and Metabolism Circulation 2010;121;2331-2378; originally published online May 10, 2010; DOI: 10.1161 /CIR.Ob013e3 l 81 dbece 1 Circulation is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX 72514 Copyright © 2010 American Heart Association. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajoumals.org/cgi/content/full/121/21/2331 Subscriptions: Information about subscribing to Circulation is online at http://circ.ahajoumals.org/subscriptions/ Permissions: Permissions & Rights Desk, Lippincott Williams & Wilkins, a division of Wolters Kluwer Health, 351 West Camden Street, Baltimore, MD 21202-2436. Phone: 410-528-4050. Fax: 410-528-8550. E-mail: joumalpermissions@lww.com Reprints: Information about reprints can be found online at http://www.lww.com/reprints Particulate Matter Air Pollution and Cardiovascular Disease An Update to the Scientific Statement From the American Heart Association Robert D. Brook, MD, Chair; Sanjay Rajagopalan, MD; C. Arden Pope III, PhD; Jeffrey R. Brook, PhD; Aruni Bhatnagar, PhD, FAHA; Ana V. Diez -Roux, MD, PhD, MPH; Fernando Holguin, MD; Yuling Hong, MD, PhD, FAHA; Russell V. Luepker, MD, MS, FAHA; Murray A. Mittleman, MD, DrPH, FAHA; Annette Peters, PhD; David Siscovick, MD, MPH, FAHA; Sidney C. Smith, Jr, MD, FAHA; Laurie Whitsel, PhD; Joel D. Kaufman, MD, MPH; on behalf of the American Heart Association Council on Epidemiology and Prevention, Council on the Kidney in Cardiovascular Disease, and Council on Nutrition, Physical Activity and Metabolism Abstract—In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 pm in diameter (PM2.5) over a few hours to weeks can trigger cardiovascular disease–related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy >� within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM2 5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality. (Circulation. 2010;121:2331-2378.) Key Words: AHA Scientific Statements ■ atherosclerosis ■ epidemiology ■ prevention ■ air pollution ■ public policy n 2004, the American Heart Association (AHA) published researchers, healthcare providers, and regulatory agencies its fust scientific statement regarding air pollution and with a comprehensive review of the evidence linking air cardiovascular disease (CVD).' The rationale was to provide pollution exposure with cardiovascular morbidity and mor - The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may anse as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest. This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on February 22, 2010. A copy of the statement is available at http://www.americanheart.org/presenterjhtm]?identifier=3003999 by selecting either the "topic list" link or the "chronological list" link (No KB -0038). To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com. The American Heart Association requests that this document be cited as follows: Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR, Bhamagar A, Diez -Roux AV, Holguin F, Hong Y, Luepker RV, Mittleman MA, Peters A, Siscovick D, Smith SC Jr, Whitsel L, Kaufman JD; on behalf of the American Heart Association Council on Epidemiology and Prevention, Council on the Kidney in Cardiovascular Disease, and Council on Nutrition, Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation. 2010,121:2331-2378. Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development, visit http://www.ameiicanheart.org/presenter.jhtml?identifier=3023366 Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.americanheart.org/presenterjhtml? identifier =443 1. A link to the "Permission Request Form" appears on the right side of the page. © 2010 American Heart Association, Inc Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIR-Ob0136181ilbecel Downloaded from circ.ahajournals.org at Unive?s'iW of Michigan–Ann Arbor on December 6, 2010 2332 Circulation June 1, 2010 tality. There was also an explicit aim to educate clinicians about the importance of this issue, because the cardiovascular health consequences of air pollution generally equal or exceed those due to pulmonary diseases.' -4 Finally, a list of key remaining scientific questions and strategic avenues for investigation were provided to help foster and guide future research. The first AHA writing group concluded that short-term exposure to particulate matter (PM) air pollution contributes to acute cardiovascular morbidity and mortality' and that exposure to elevated PM levels over the long term can reduce life expectancy by a few years. Although some mechanistic details remained incompletely described, the existing science was deemed adequate to substantiate several plausible bio- logical pathways whereby PM could instigate acute cardio- vascular events and promote chronic disease. There is mounting evidence from a rapid growth of published data since the previous statement related to the harmful cardiovascular effects of air pollution .3.4 Most, but not all, epidemiological studies corroborate the elevated risk for cardiovascular events associated with exposure to fine PM <2.5 µm in aerodynamic diameter (PM,,). PMZ 5 generally has been associated with increased risks of myocardial infarction (MI), stroke, arrhythmia, and heart failure exacer- bation within hours to days of exposure in susceptible individuals. Several new studies have also demonstrated that residing in locations with higher long-term average PM levels elevates the risk for cardiovascular morbidity and mortality. Some recent evidence also implicates other size fractions, such as ultrafine particles (UFPs) <0.1 µm, gaseous copol- lutants (eg, ozone and nitrogen oxides [NO,]), and specific sources of pollution (eg, traffic). In addition, there have been many insights into the mechanisms whereby PM could prove capable of promoting CVDs.2-4 Air pollutants have been linked with endothelial dysfunction and vasoconstriction, increased blood pressure (BP), prothrombotic and coagulant changes, systemic inflammatory and oxidative stress re- sponses, autonomic imbalance and arrhythmias, and the progression of atherosclerosis. In the interim, the US Envi- ronmental Protection Agency (EPA) completed its updated "Air Quality Criteria for Particulate Matter"5 and afterward strengthened the National Ambient Air Quality Standards (NAAQS) for daily PM2 5 levels starting in 2006 (down from 65 to 35 µg/m).6 The most recent scientific review coordi- nated by the EPA, the final report of the Integrated Science Assessment for Particulate Matter (http://cfpub.epi.gov/ncea/ cfm/recordisplay.cfm?deid=216546), has also been made available publicly. These numerous changes and advances provide the rationale for the present updated AHA scientific statement on PM air pollution and CVD. This updated statement is similar in scope, content, and overall structure to the fust document; however, it provides many additional conclusions and recommendations that can now be made because of the expanded number and quality of studies. Objectives and Methods The primary objective of this scientific statement is to provide a comprehensive updated evaluation of the evidence linking PM exposure with CVDs. The focus of this review is explicitly on PM because the majority of air pollution studies have centered on its cardiovascular effects, and the strength of the evidence makes it possible to provide consensus opinions and recommendations. Except for in a few circum- stances, such as when copollutants have been shown to (or not to) modify the responses to PM exposure or to have independent cardiovascular effects in epidemiological studies of major importance, a detailed discussion of other air pollutants (eg, ozone and NO2) is beyond the scope of this document. Additional objectives are to provide expert con- sensus opinions on aspects related to the current state of science, to specifically highlight the health and clinical implications of the reviewed findings, and to provide prudent and practical recommendations for measures to reduce PM exposure that might thereby lower the associated cardiovas- cular risk. This updated scientific statement is structured to first provide a clinical perspective on the cardiovascular risks posed by PM exposure and then briefly review the compo- nents of air pollution. The following sections highlight the major findings from epidemiological studies, including mor- tality, morbidity, and surrogate outcome results. Next, the animal and human mechanistic studies are reviewed, ,and an overall framework whereby PM exposure could cause CVDs is outlined. Finally, updated consensus opinions and conclu- sions are provided, followed by suggestions for areas of future research and policy considerations. Members of the current writing group were selected from across a broad range of disciplines, including cardiovascular and environmental epidemiology and statistics, atmospheric sciences, cardiovascular and pulmonary medicine, basic sci- ence research, and public policy. The writing group identified studies published in the English language between January 1, 2004, and March 31, 2009, by a World Wide Web -based literature search using Medline, PubMed, and Google search engines. Key terms included air pollution or particulate matter plus any of the following: cardiovascular, myocardial, heart, cardiac, stroke, heart failure, arrhythmia, heart rate variability, autonomic, sympathetic, atherosclerosis, vascu- lar, blood pressure, hypertension, diabetes, metabolic, throm- bosis, and coagulation. Additional studies were identified within the references of these publications and by the per- sonal knowledge of the writing group members. A few studies published after March 31, 2009, were added (luring the review process. All of the identified epidemiological studies that provided mortality data or hard cardiovascular outcomes (eg, MIs) and controlled human exposure protocols were included. In a few circumstances, studies before 2004 were included briefly in the discussion or tables when it was believed that they provided contextual background and/or relevant findings from earlier analyses of ongoing studies (eg, Harvard Six Cities and American Cancer Society [ACS] cohorts) from which new results after 2004 have been published. It is a limitation of the present review that it was not possible to cite all surrogate outcome human studies because of the enormous number of publications. Some were not included, without intentional bias with regard to results, when multiple referenced studies demonstrated similar find- ings. In such a situation (eg, heart rate variability WV]), this Downloaded from eirc.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 is • r� �.J • • Brook et al limitation was noted within the specific section A main theme of the present statement is to provide clinical context and recommendations for healthcare providers, and thus, it was beyond the scope and not the intent of this document to include all animal, ex vivo, or toxicological studies. A number of these publications were also not included, without intentional bias with regard to results. The writing group included publications that were believed to have relevant implications for human cardiovascular health, those that formed the foundation of the mechanistic hypotheses, and studies that were deemed of major importance. Finally, the "evidence summary" statements and all points in the conclu- sions and recommendations represent consensus expert opin- ions agreed on by all members of the writing group during formal discussions. It is explicitly stated when no such agreement was reached. These statements and the points within Tables 6 and 7 do not represent the result of applying the standard AHA criteria (ie, level and class) to the sum findings of the present review, because those do not apply, but rather the qualitative consensus opinions agreed on by the writing group. The purpose is to provide expert opinions on the comparative relative ranking and the strength of the overall evidence regarding different areas within this field of science. Perspective on the Air Pollution— Cardiovascular Risk Association Traditional cardiovascular risk factors account for the major portion of the risk for ischemic cardiac events within a population .7 Individuals with optimal levels of all risk factors have been shown to have a low lifetime cardiovascular event rate." Thus, control of the traditional risk factors is recognized to be of paramount importance to prevent CVDs. In this context, there has been some debate about the overall clinical relevance and utility of adding novel risk factors to risk - prediction models to incrementally improve their overall predictive value, even when assessed by multiple methodol- ogies.9 On the other hand, the ability to predict future events by existing models remains imperfect. In addition to several mathematical and statistical explanations for this shortcom- ing,10.11 it is important to recognize that the development of vascular or atherosclerotic disease (the factor predicted by most statistical models) is usually a necessary but insufficient cause of future ischemic events in and of itself. Cardiovas- cular events must also be triggered by an additional factor at some unknowable future time, and therefore, they transpire as a stochastic process within a population.12 This is one of several reasons why PM air pollution is a uniquely important public health issue among the list of novel risk factors; PM inhalation is an established trigger of cardiovascular events that occur within hours to days after exposure. 12 Because of the ubiquitous and involuntary nature of PM exposure, it may continuously enhance acute cardiovascular risk among mil- lions of susceptible people worldwide in an often inconspic- uous manner. Moreover, beyond serving as a simple trigger, PM elicits numerous adverse biological responses (eg, sys- temic inflammation) that, in premise, may further augment Particulate Matter Air Pollution and CVD 2333 future cardiovascular risk over the long term after months to years of exposure. Effects of Short -Term Exposure Time -series studies estimate that a 10-1Lg/m3 increase in mean 24-hour PM2 5 concentration increases the relative risk (RR) for daily cardiovascular mortality by approximately 0.4% to 1.0%.3 Despite theoretical statistical risks ascribed to all individuals, this elevated risk from exposure is not equally distributed within a population. At present-day levels, PM2.1 likely poses an acute threat principally to susceptible people, even if seemingly healthy, such as the elderly and those with (unrecognized) existing coronary artery or structural heart disease. 13 Therefore, the absolute risk rather than the RR of exposure may more effectively convey the tangible health burden within a population. A 10-11g/m3 increase during the preceding day contributes on average to the premature death of approximately 1 susceptible person per day in a region of 5 million people (based on annual US death rates in 2005).3•14 Although the dangers to 1 individual at any single time point may be small, the public health burden derived from this ubiquitous risk is enormous. Short-term increases in PM2., levels lead to the early mortality of tens of thousands of individuals per year in the United States alone.1.3.5 Effects of Long -Term Exposure Cohort studies estimate that the RR associated with living in areas with higher PM levels over the long term is of greater magnitude than that observed from short-term exposure increases (RR between 1.06 and 1.76 per 10 gg/m3 PM2 5).3 In this context, the World Health Organization estimated that PM2.5 contributes to approximately 800 000 premature deaths per year, ranking it as the 13th leading cause of worldwide mortality. 15 Hence, PM air pollution appears to be an impor- tant modifiable factor that affects the public health on a global scale. Air Pollution The fust AHA statement on air pollution reviewed the size fractions, sources, and chemical constituents of PM and the main gaseous air pollutants: Nitrogen oxides (NO.; ie, NO+NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (03).1 Therefore, this section within the updated statement focuses on several other contemporary aspects of air pollution characterization and exposure assessment, par- ticularly in relation to their potential influences on cardiovas- cular health. In brief, PM is broadly categorized by aerody- namic diameter: All particles <10 gm (thoracic particles [PM1o1), all particles <2.5 gm (fine particles [PM251), all particles <0.1 gm (UFP), and particles between 2.5 and 10 gm (coarse particles [PM10-2.51)• Hence, PM10 contains within it the coarse and PM2.5 fractions, and PM2.5 includes UFP particles. The concentrations of PM10 and PM2.5 are typically measured in their mass per volume of air (gg/m), whereas UFPs are often measured by their number per cubic centimeter (Table 1). The major source of PM2.5 throughout Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 2334 Circulation June 1, 2010 Table 1. Ambient Air Pollutants Most Recent NAAQS for Criteria US Typical Pollutants Pollutant US Average Range Peak' (Averaging Time) Ost 0-125 ppb 200 ppb 75 ppb (8 h)$ NOZt 0 5-50 ppb 200 ppb 100 ppb (1 h)§ 5 ppm Formaidehydet 01-10 ppb 53 ppb (Annual Acetaldehydet 0.1-5 ppb 20 ppb mean) Not 0-100 ppb 200 ppb 2-20 ,,,,/m3 i,,,,/m3 SOZt 01-50 ppb 150 ppb 140 ppb (24 h)II 1,3 -Butadiene¶ 0.1-2 , N,, /m3 10 30 ppb (Annual 20-300 Ag/m3 1000 ,,,,/m3 parbcles¶ mean) Got 0.1-5 ppm 20 ppm 35 ppm (1 h)II Sulfate¶ 0 5-10 pWm3 30 Pg/m3 g ppm (8 h)11 PM"s 10-100 µg/m3 300 ,,,,/m3 FAgg/m3 150 µg/m3 (24 h)# PM2_51 ,,,,/ 5-50 m3 100 15 n)„„/m3 (Annual carbon¶ (Mean=13.4±5.6) mean) 35 ,,,,rm3 2-30 ng/m3 200 ng/m3 UFPt (24 h)— PM2_, lead$ 0.5-5 ng/m3 150 ng/m3 015 µg/m3 (Rolling 3 -month average)tt NH3t 0.1-20 ppb 100 ppb HNO3t 0-5 ppb 10 ppb Methanet 1-2 ppm 5 ppm Formaidehydet 01-10 ppb 40 ppb Acetaldehydet 0.1-5 ppb 20 ppb NMHC (VOC)¶ 20-100 µg/m3 250 F„„/m3 Propane$ 2-20 ,,,,/m3 i,,,,/m3 500 MWm3 Benzene$ 0.5-10 100 ,,,,/m3 FPgg/m3 1,3 -Butadiene¶ 0.1-2 , N,, /m3 10 Total suspended 20-300 Ag/m3 1000 ,,,,/m3 parbcles¶ PMI0-2511 5-50 F,,,,/m3 200 µg/m3 Sulfate¶ 0 5-10 pWm3 30 Pg/m3 Nitrate¶ 0.1-5 pVm3 20 µg/m3 Organic carbon¶ 1-20 ,,,,/m3 30 l,*m3 Elemental 0.1-3 ,,,J /m3 W 10 4M3 carbon¶ PAH¶ 2-30 ng/m3 200 ng/m3 UFPt 1000-20 000/cm3 100 000/cm3 ppb Indicates parts per billion, ppm, parts per million, and PAH, polycyclic aromatic hydrocarbon. "Generally not in concentrated plumes or locations of direct source emission impact tTypical hourly average concentrations reached in US cities $The 8 -hour standard is met when the 3 -year average of the 4th highest daily maximum 8 -hour average is less than or equal to the indicated number In January 2010, the EPA proposed a more stringent 8 -hour standard within the range of 60 to 70 ppb (httpJ/www epa.gov/air/ozonepollubon/actions htmq. §To attain this standard, the 3 -year average of the 90 percentile of the daily maximum 1 -hour average at each monrtor within an area must not exceed this value. Ijfhe level is not to be exceeded more than once per year. $Typical 24-hour average concentrations. #The level is not to be exceeded more than once per year on average over 3 years —The daily standard is met when the 3 -year average of the 98th percentile of 24-hour PM level is less than or equal to the indicated number ttAfthough the typical concentrations shown in the table are for PM25, the lead standard continues to be based on measurements in total suspended particulate. the world today is the human combustion of fossil fuels from a variety of activities (eg, industry, traffic, and power gener- ation). Biomass burning, heating, cooking, indoor activities, and nonhuman sources (eg, fires) may also be relevant sources, particularly in certain regions. Common air pollutants and those designated as EPA criteria pollutants (ie, specifically targeted in regulations through limits on emissions or government standards such as the NAAQS) are listed in Table 1. The World Health Organization also provides ambient guidelines (http://www. euro.who.int/Document/E90038.pdf). As a result, many pol- lutant concentrations are tracked in the United States by nationwide monitoring networks, with up to approximately 1200 sites for 03 and PM2 5. Data are archived by the EPA and are available to the public (http://www.epa.gov/ttn/airs/ airsags/). 03 levels exceed the national standard in many areas, and thus, daily information is provided to assist the public in reducing their exposure. A lower standard for ozone concen- trations was proposed recently, which will lead to more fi-equent occurrences of outdoor exposures deemed to be excessive (Table 1). The reporting of PM2.5 is also becoming common because of its impact on public health and frequent violations of standards. Current and forecast air quality indices and information on both PM2 5 and ozone are available (httpJ/aimow.gov/). At the end of 2008, 211 US counties (or portions of counties) were in nonattainment of the 2006 daily PM2.5 NAAQS (http://www. epa.gov/pmdesignations/2006standards/state.htm). On a positive note, the various regulations that have been established have led to substantial reductions in PM and other pollutant levels over the past 40 years in the United States and contributed toward similar improvements in other countries. However, reducing the levels of some pollutants, such as 03, remains a challenge because of the complex chemical processes that lead to their formation in the atmosphere.16 The population of many devel- oping nations (China, India, Middle Eastern countries) continues to be exposed to high levels, particularly of PM, which can routinely exceed 100 pg/m3 for prolonged periods (httpJ/ siteresources.worldbank.org/DATASTATISTICS/Rescources/ table 3_13.pdf). Air Pollution Mixtures, Chemistry, and Sources Detailed information regarding PM sizes, composition, chem- istry, sources, and atmospheric interactions is beyond the scope of this document but can be found in the 2004 US EPA Air Quality Cnteria for Particulate Matter final report (http:// cfpub.epa.gov/neea/cfm/recordisplay.cfm?deid=87903). The source for much of the information provided in this brief summary is this document, unless otherwise specifically referenced. The typical range of ambient concentrations for several air pollutants in the United States, including the latest US NAAQS for the criteria pollutants, is given in Table 1. Classification of air quality according to 1 single pollutant and by size or mass provides an incomplete picture, because ambient air pollution is a complex mixture of gases, particles, and liquids that are continually changing and interacting with each other and natural atmospheric gases. Although PM2 5 mass has rightfully attracted considerable attention as a target for regulation and epidemiological study, more than 913% of Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 C • • • • U Brook et al the air pollutant mass in the mixture we breathe in urban settings is from gases or vapor -phase compounds such as CO, nonmethane hydrocarbons or volatile organic carbons (VOCs), NO2, NO, 03, and SO2. Each of these can have independent and potentially synergistic or antagonistic effects with each other and with PM; however, at present, the cardiovascular health impact of exposure to combinations of air pollutants is not well understood. Most of the studies linking CVDs with PM exposures have focused on particle mass; thus, this association is evaluated and reported in the majority of epidemiological and toxico- logical studies reviewed. Although PM is regulated by mass concentration, the aspect of PM most harmful to cardiovas- cular health may not be best quantified by mass measurement alone. The sum effect of many features related to chemical composition and size/morphology (eg, oxidative stress poten- tial, solubility, charge, surface area, particle count, lung deposition, and stability within the atmosphere and biological tissues) is important to consider. With regard to specific "toxic" compounds within PM, several lines of existing evidence support the idea that transition metals, organic compounds, semiquinones, and endotoxin are likely relevant in relation to promoting CVDs. In addition, certain charac- teristics of UFPs (eg, high surface area, particle number, metal and organic carbon content) suggest that they may pose a particularly high cardiovascular risk after short-term expo- sure.17 Both the additional characterization of "criteria" pollutants and the measurement of several other pollutants (discussed below) are important to inform air quality man- agement practices that involve air quality modeling, as well as epidemiological studies and risk assessment, which ulti- mately aim to improve risk -reduction strategies. In addition to their mass concentration, pollutants can be characterized on the basis of their origin or chemical and physical properties. In terms of origin, nitrogen oxides (NO+NO2), CO, SO2, and PM2_5, as well as carbon dioxide (CO2), are mainly associated with combustion of fuel or other high-temperature industrial processes. Combustion PM is composed of many chemical compounds, including organic carbon species, elemental or black carbon, and trace metals (eg, lead and arsenic). They range in size from molecular clusters a few nanometers in diameter to light -scattering particles that peak on a mass contribution basis in the diameter range of 200 to 1000 nm (0.2 to 1 µm). UFP numbers are also strongly linked to fresh combustion and traffic -related pollution. Ammonia, methane, pesticides (per- sistent organic pollutants), reduced sulfur compounds, resus- pended dust, and natural coarse particles (PM10-2 5) are associated with noncombustion surface or fugitive releases that arise from a variety of human (eg, agriculture) and natural (eg, erosion) activities. Agricultural emissions and releases from a range of industrial processes and waste management are also important sources. Road and wind- blown dust from agricultural practices and from certain industrial facilities (eg, mineral industry) also contribute to these particles, which are typically in the coarse (PM,, -2 5) or even larger (>PM,o) range. In addition to pollutants formed directly by combustion, many others are produced primarily through chemical reac- Particulate Matter Air Pollution and CVD 2335 tions in the atmosphere among directly emitted pollutants. These are known as secondary pollutants. Sunlight, water vapor, and clouds are often involved in this atmospheric chemistry, which leads to greater oxidation of the pollutants. Examples include PM -associated sulfate, nitrate, and ammo- nium and many of the organic compounds within PM2.5- Besides 03, which is the most prevalent secondary gaseous oxidant, a number of inorganic and organic acids and VOCs form in the atmosphere. Examples are the hydroxyl radical, peroxyacetyl nitrate, nitric acid, formic and acetic acid, formaldehyde, and acrolein. VOCs and semivolatile organic compounds (SVOCs), the latter of which are found in both the gas and particle phase, are an additional large class of pollutants. They are associated with both combustion and fugitive emissions, as well as with second- ary formation. Key examples are benzene, toluene, xylene, 1,3 -butadiene, and polycyclic aromatic hydrocarbons. VOCs are among the 188 hazardous air pollutants listed by the EPA, and their main emission sources have been identified and are regulated (http://www.epa.gov/ttn/atw/mactfnlalph.html). VOCs can undergo reactions that convert toxic substances to less toxic products or vice versa. Many VOCs contribute to the formation of 03 and are oxidized in the atmosphere, becoming SVOCs, and subsequently partition within particles and contribute to the composition of PM2 5, as well as to its mass. A great deal of research has focused on PM2 5 in the past decade, which has led to advances in measurement technologiesl$ and greater understanding of its chemistry and atmospheric behavior.19 Nonetheless, understanding is in- complete, particularly with regard to formation of the sec- ondary organic fraction, the relative role of anthropogenic and biogenic emissions to organics, surface chemistry, oxi- dative potential,20 and gas -to -particle partitioning. An alternative to attempting to identify one by one which pollutant(s) or chemical compounds are most harmful is to focus on identifying the sources, which typically emit mix- tures of pollutants, of greatest concern. It may be the mixture of pollutants (along with the source from which it is derived, which determines its characteristics) that is most pertinent to human health outcomes. Such information may actually be more relevant for aiding the development of effective air quality policies. One important example reviewed in the epidemiology section is that the evidence continues to grow regarding the harmful cardiovascular effects of traffic -related pollution. Traffic is ubiquitous in modem society, with a sizeable proportion of the population, particularly persons disadvantaged by low socioeconomic status, living close enough (within 500 m) to a major road or a freeway to be chronically exposed to elevated concentrations. Additionally, daily behavior brings most people close to this source, with the average US citizen over 15 years of age spending 55 minutes each day traveling in motor vehicles.21 However, despite the consistent epidemiological findings, these studies have yet to elucidate which of the many pollutants or other associated risks (ie, noise) produced by traffic are responsible for the increase in risk for CVD. Until the most harmful agents are identified, the only practical manner to potentially reduce health consequences would be to reduce overall traffic and related emissions and to configure cities and lifestyles Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 2336 Circulation June 1, 2010 such that there is greater separation between the people and the source, so that we could spend less time in traffic (a major source of personal exposures in our society). There are also a myriad of other important pollutant sources of known toxic pollutants that have been implicated in health -effect studies (eg, power generation, industrial sources, steel mills, and wood smoke). A better understanding of the factors that influence population exposure to these sources, of how their emissions and mixtures of different sources affect health, and about the factors that make individuals more susceptible will aid in the development of more effective environmental health policies. Determinants of Air Pollution Exposure Many aspects of air pollution play a role in the characteristics of population- and individual -level exposures. Pollutants vary on multiple time scales, with emission rates, weather patterns, and diurnal/seasonal cycles in solar radiation and temperature having the greatest impact on concentrations. The temporal behavior of a pollutant is also governed by its formation rate and the length of time it remains in the atmosphere. As such, the concentrations of many air pollutants tend to co -vary. For example, NO., and CO are emitted during combustion, as are some particle constituents (eg, elemental carbon) and VOCs, and thus, their concentrations peak during rush hour. On the other hand, 03 and other photochemical oxidants, including secondary PM2 5 and secondary VOCs, peak in the afternoon, particularly given certain meteorologic conditions (eg, more sunshine). Among the common air pollutants, O_; and PM2.5 have the longest atmospheric lifetime and thus can build up over multiple days and spread, by the prevailing winds, over large geographic regions. This can lead to similarities in their temporal and spatial patterns over broad regions and to greater numbers of people being exposed to similar levels, thus lessening interindividual variability in exposure Periods of suppressed horizontal and vertical mixing in the lower atmosphere lead to the buildup of multiple pollutants. These situations are most common under slow-moving or stationary high-pressure systems, which bring light winds, a stable atmosphere, and more sunshine. The frequency and seasonality of these meteorologic conditions and how they affect concentrations vary geographically, which leads to differences in the characteristics of pollution episodes from the western to the eastern United States, as well as within these regions. The commonality of meteorology and emission sources leads to covariation in pollutant concentrations on multiple temporal and spatial scales, which makes it more challenging for epidemiological studies to identify the health effects of individual pollutants and the effects of copollutants or mix- tures. Studies that depend on daily counts of mortality or morbidity events have difficulties separating the effects of the different pollutants in the urban mix. Even prospective panel studies measuring specific end points on a subdaily time scale are hindered by pollutant covariation. Some of these chal- lenges could potentially be addressed by undertaking studies covering multiple geographic locations with differences in the structure of pollutant covariation due to different meteo- rology and source mixes. Indeed, this has been done, at least in part, by several existing multicity studies. Consistency in the findings in individual studies conducted in different cities also helps isolate the pollutants that may be more responsible for the health effects. The consistent positive findings with certain pollutants (eg, PM mass concentration) have helped strengthen the evidence regarding PM,o and PM25 effects, but regardless of location, there remains the strong underlying commonality of fossil fuel combustion for many pollutants. A final issue to consider is the cardiovascular health effects of exposures that occur at the personal level because of the different microenvironments or activities an individual expe- nences (eg, time in traffic, indoor sources, secondhand tobacco smoke, occupational exposure, and degree of indoor penetration of ambient PM into homes) versus the effects of exposures from less variable urban- to regional -scale ambient concentrations (ie, background pollution that most individu- als encounter more uniformly). Personal monitoring demon- strates substantial variations among individual pollution ex- posures or characteristics among those living within the same metropolitan area and even the same neighborhood.22.23 However, the differing additive, synergistic, and/or con- founding effects on cardiovascular health of these 2 contrast- ing components of a person's overall exposure have not been well described. For the most part, the magnitude of the findings reported by the major epidemiological studies (see next section) are indicative of the effects of the urban- to regional -scale ambient concentrations. Actual exposures to all pollutants also vary at the personal level. The cardiovas- cular health importance of these individual -level variations (above and beyond the effect of urban/regional levels) re- mains largely unknown, in part because it has been difficult to quantify. The degree to which measurement of personal expo- sures or more precise exposure assessment (eg, use of geo- graphic information systems, land -use regression models, spatial -temporal models, and adjustments for indoor penetration) can reduce the effects of exposure misclassification in epidemi- ological studies also remains to be fully elucidated.24-26 Epidemiological Studies of Air Pollution Epidemiological studies of air pollution have examined the health effects of exposures observed in real-world settings at ambient levels. Associations between relevant health end points and measures of air pollution are evaluated while attempting to control for effects of other pertinent factors (eg, patient and environmental characteristics). Despite substan- tial study and statistical improvements and the relative consistency of results, some potential for residual confound- ing of variables and publication bias '27 of positive studies are limitations to acknowledge. Probably the most relevant, well-defined, and extensively studied health end points in- clude mortality (all -cause and cause -specific), hospilaliza- tions, and clinical cardiovascular events. This section reviews the results of the epidemiological research with a focus on new studies since the fust AHA statement was published,] as well as on the cardiovascular health implications. In sum, numerous studies of varied design have been published in the interim that significantly add to the overall weight of evi- Downloaded from cire.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 C7 0 • �1 • Brook et al Particulate Matter Air Pollution and CVD 2337 Table 2. Comparison of Pooled Estimated of Percent Increase (and 95% Cl or Posterior Interval or t Value) in RR of Mortality Estimated Across Meta -Analyses and Multicity Studies of Daily Changes in Exposure CI indicates confidence interval or posterior interval "Cardiovascular and respiratory deaths combined tischemic heart disease deaths. tChronic obstructive pulmonary disease deaths §Includes general additive model -based analyses with potentially inadequate convergence IlResults for PM10-25 are from 47 cities ¶Results of 2 pollutant models controlling for alternate PM size in 47 cities dence that exposure to air pollutants at present-day levels contributes to cardiovascular morbidity and mortality. Mortality and Air Pollution Time -Series and Related Studies Time -series and case -crossover studies explore associations between short-term changes in air pollution and daily changes in death counts. The sum of current evidence supports the findings of an earlier review28 that demonstrated that short- term elevations in daily PM levels lead to a greater absolute risk for CVD -related mortality than for all other causes. Even if similar acute RR elevations (-1.01) are estimated between cardiovascular and pulmonary mortality, CVDs account for 69% of the increase in absolute mortality rates compared with 28% for pulmonary diseases attributable to short -tern PM exposure. Recently, more rigorous modeling techniques have been used in attempts to better estimate pollution -mortality associations while controlling for other time -dependent con- founding covariables.29,30 There have been well over 100 published daily time -series studies reporting small but statis- tically significant PM -mortality associations that have been the subject of quantitative reviews or meta-analyses.3,27,31-33 Table 2 summarizes recent multicity analyses and studies published since 2004. To address concerns about city selection bias, publication bias, and influences of copollutants, several large, multicity, daily time -series studies have been conducted worldwide. One of the largest was the National Morbidity, Mortality, and Air Pollution Study (NMMAPS). Published reports from this study included as few as 20 US cities '44,45 as many as 100 cities,46,47 and more recently, data for hundreds of counties (Table 2).48 The observed relation- ship between PM exposure and excess mortality remained independent of several gaseous copollutants (NO2, CO, or SO2). Recent analyses suggest that 03 may also indepen- dently contribute to cardiopulmonary mortality risk49,50; however, coexposures to secondary particle pollutants may be responsible in part for this latter association.51 Several studies have also been conducted outside the United States, including the Air Pollution and Health: A European Approach (APNEA and APHEA-2) projects, which examined daily PM -related mortality effects in multiple cities.36,52 PM air pollution was significantly associated with daily mortality counts for all -cause, car- diovascular, and respiratory mortality (Table 2). Further analyses of the European data suggest that CVD deaths are also associated with exposure to NO253and CO.54 A few new time -series studies have also confirmed similar in- creases in cardiovascular mortality related to short-term PM exposure in China55-57 and Bangkok, Thailand.42 Additional multicity studies have been conducted world- wide with analyses of CVD deaths (Table 2),38-42,58-60 Finally, in a recent analysis that included several Asian Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 Primary Source Exposure Increment Percent Increases in Mortality (95% CI) All -Cause Cardiovascular Respiratory Meta-esbmate with and without Anderson et a127 2005 20 µg/m3 PM10 1.0 (0.8-1.2) ... ... adjustment for publication bias 1 2 (1.0-1.4) Meta -estimates from COMEAP COMEAP37 2006 20 PVM3 PM10 ... 1.8 (1.4-2.4) ... report to the UK Department of 10 µg/m3 PM,., 1.4 (0.7-2.2) Health on CVD and air pollution NMMAPS, 20 to 100 US cities Dominici et a134 2003 20 4m3 PM10 0 4 (0.2-0.8) 0.6 (0.3-1.0)* APHEA-2, 15 to 29 European cities Katsouyanni et a135 2003 20 µg/m3 PM10 1.2 (0.8-1.4) 1.5 (0 9-2.1) 1.2 (0.4-1.9) Analibs et a136 2006 US, 6 cities Klemm and Mason37 2003 10 µg/m3 PMIS 1.2 (0 8-1.6) 1.3 (0.3-2.4)t 0 6 (-2.9, 4.2)t US, 27 cities, case -crossover Franklin et a138 2007 10 4m3 PM2.5 1.2 (0.3-2.1) 0.9 (-.1, 2.0) 1 8(02,34) California, 9 cities Ostro et a139 2006 10 µg/m3 PM25 06(02-1.0) 0 6 (0 0,1.1) 2.2 (0.6, 3 9) France, 9 cities Le Tertre et a140 2002 20 µg/m3 BS 1.2 (0.5-1.8)§ 1.2 (0.2-2 2)§ 1.1 (-1.4, 3 2)§ Japan, 13 cities, age >65 y Omon et a141 2003 20 / ,,,,/m3 SPM 1.0 (0.8-1.3) 1 1 (0.7-1.5) 1.4 (0.9-2.1) Asia, 4 cities Wong et a142 2008 10 AWM3 PM,O 0 55 (0.26-0.85) 0.59 (0 22-0.93) 0.62 (0.16-1.04) US, 112 cities Zanobeth et a143 2009 10 MWm3 PM25 0 98 (0 75-1.22) 0 85 (0.46-1.24) 1.68 (1.04-2 33) 10 4m3 PM,a2511 0 46 (0.21-0.71) 0.32 (0 OD -0 64) 1.16 (0.43-1.89) 10 4m3 PM25¶ 0.77 (0.43-1.12) 0.61 (0.05-1.17) 1.63 (0.69-2.59) 10 µg/m3 PM'0_"l 0.47 (0.21-0 73) 0 29 (-0.04, 0.61) 1.14 (0 043-1.85) CI indicates confidence interval or posterior interval "Cardiovascular and respiratory deaths combined tischemic heart disease deaths. tChronic obstructive pulmonary disease deaths §Includes general additive model -based analyses with potentially inadequate convergence IlResults for PM10-25 are from 47 cities ¶Results of 2 pollutant models controlling for alternate PM size in 47 cities dence that exposure to air pollutants at present-day levels contributes to cardiovascular morbidity and mortality. Mortality and Air Pollution Time -Series and Related Studies Time -series and case -crossover studies explore associations between short-term changes in air pollution and daily changes in death counts. The sum of current evidence supports the findings of an earlier review28 that demonstrated that short- term elevations in daily PM levels lead to a greater absolute risk for CVD -related mortality than for all other causes. Even if similar acute RR elevations (-1.01) are estimated between cardiovascular and pulmonary mortality, CVDs account for 69% of the increase in absolute mortality rates compared with 28% for pulmonary diseases attributable to short -tern PM exposure. Recently, more rigorous modeling techniques have been used in attempts to better estimate pollution -mortality associations while controlling for other time -dependent con- founding covariables.29,30 There have been well over 100 published daily time -series studies reporting small but statis- tically significant PM -mortality associations that have been the subject of quantitative reviews or meta-analyses.3,27,31-33 Table 2 summarizes recent multicity analyses and studies published since 2004. To address concerns about city selection bias, publication bias, and influences of copollutants, several large, multicity, daily time -series studies have been conducted worldwide. One of the largest was the National Morbidity, Mortality, and Air Pollution Study (NMMAPS). Published reports from this study included as few as 20 US cities '44,45 as many as 100 cities,46,47 and more recently, data for hundreds of counties (Table 2).48 The observed relation- ship between PM exposure and excess mortality remained independent of several gaseous copollutants (NO2, CO, or SO2). Recent analyses suggest that 03 may also indepen- dently contribute to cardiopulmonary mortality risk49,50; however, coexposures to secondary particle pollutants may be responsible in part for this latter association.51 Several studies have also been conducted outside the United States, including the Air Pollution and Health: A European Approach (APNEA and APHEA-2) projects, which examined daily PM -related mortality effects in multiple cities.36,52 PM air pollution was significantly associated with daily mortality counts for all -cause, car- diovascular, and respiratory mortality (Table 2). Further analyses of the European data suggest that CVD deaths are also associated with exposure to NO253and CO.54 A few new time -series studies have also confirmed similar in- creases in cardiovascular mortality related to short-term PM exposure in China55-57 and Bangkok, Thailand.42 Additional multicity studies have been conducted world- wide with analyses of CVD deaths (Table 2),38-42,58-60 Finally, in a recent analysis that included several Asian Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2338 Circulation June 1, 2010 cities, SO2, N021 03, and PM10 were all associated with excess cardiovascular mortality.42 In an attempt to evaluate the coherence of multicity studies across continents, the Air Pollution and Health: A Combined European and North American Approach (APHENA) study analyzed data from the APNEA, NMMAPS, and Canadian studies.61 The combined effect on all -cause mortality ranged from 0.2% to 0.6% for a 10-µg/m3 elevation in daily ambient PM10, with the largest effects observed in Canada. Among individuals older than 75 years, the effects were greater for cardiovascular mortality than for overall and pulmonary mortality (0.47% to 1.30%). Older age (>75 years) and higher rates of unemployment were related to greater PM mortality risks in both continents Higher NO2 levels were associated with larger PM10 effects on mortality, particularly in Europe. Finally, there appeared to be no lower -limit threshold below which PM10 was not associated with excess mortality across all regions. Evidence Summary The overall evidence from time -series analyses conducted worldwide since publication of the first AHA statement' confirms the existence of a small, yet consistent association between increased mortality and short-term elevations in PM10 and PM25 approximately equal to a 0.4% to 1.0% increase in daily mortality (and cardiovascular death specif- ically) due to a 10-µg/m3 elevation in PM2_5 during the preceding 1 to 5 days (Table 2). Cohort and Related Studies Although short-term changes in PM concentrations have deleterious health effects, longer-term exposures may have a more pertinent clinical health effect on cardiovascular morbidity and mortality given that individuals are typically exposed to higher air pollution levels over extended periods of time. An additional source of exposure variabil- ity that has been exploited in epidemiological studies is spatial variability, which includes differences in average ambient concentrations over extended periods of time across metropolitan areas or across smaller communities within local areas. Recent emphasis has been on prospec- tive cohort studies that control for individual differences in multiple confounding variables and cardiovascular risk factors. A summary of these studies is presented in Table 3 and Figure 1. These cohort studies generally demonstrate larger overall mortality effects than the results of time - series analyses. Harvard Six Cities and ACS Studies Two landmark cohort -based mortality studies, the Harvard Six Cities62 and the ACS studies,66 were reported in the mid 1990s and were discussed previously.' In both, PM2.5 and sulfate particulate pollution were associated with increases in all -cause and cardiopulmonary disease (Table 3). In addition, intensive independent reanalyses63 Corrob- orated the original findings of both studies and resulted in innovative methodological contributions that demonstrated the robustness of the results to alternative modeling approaches. In both the Harvard Six Cities62.64 and the ACS67 studies, PM air pollution -related mortality was substantially higher for cardiovascular- than for pulmo- nary -related causes. Since 2004, there have been further analyses of both studies. Laden et a164 extended the mortality follow-up of the Harvard Six Cities cohort for an additional 8 years. PM2_5 associations, similar to those found in the original analysis, were observed for all -cause and CVD mortality (Table 3). Furthermore, reductions in PM2 5 concentrations for the extended follow-up period were associated with reduced mortality risk. Further analysis suggested that the health effects of changes in exposure were seen primarily within 2 years. 114 In addition to confirming the earlier mortality relationship, the recent observations suggest that the adverse health effects mediated by longer-term I'M air pollution exposure can be estimated reasonably accurately by the previous few years of particle levels. Extended analyses of the ACS cohort that emphasize efforts to control for the effects of other covariates and risk factors have corroborated the previously reported mortality associations with particulate and sulfur oxide pollution 68 Elevated mortality risks were most strongly associated with PM, 5. Coarse particles (PMIo-2.5) and gaseous pollutants, except for SO2, were generally not significantly related to mortality. In another extended analysis,67 the death certificate classifications of underlying causes of death due to PM25 exposures were observed to be principally ischemic heart disease, arrhythmias, heart failure, and cardiac arrest. Finally, recent additional analyses attempted to control for the fact that variations in exposure to air pollution across cities or within cities may correlate with socioeconomic or demo- graphic gradients that influence health and susceptibility to environmental exposures.85.116 When controlled for individual risk factor data, the mortality associations for intrametropoli- tan PM2 5 concentration differences within the Los Angeles, Calif, area were generally larger than those observed in the full cohort across metropolitan areas.69 However, the results were somewhat sensitive to the inclusion of zip code -level ecological variables, which suggests potential contextual neighborhood confounding. Krewski et x170 subsequently observed that full adjustments for multiple ecological covari- ates did not reduce the estimated PM2 5 -related mortality effect. The association for ischemic heart disease mortality in particular was highly robust across various study areas and modeling strategies and after controlling for both individual and ecological covariates. An additional recent analysis of the ACS cohort evaluated the health effects of ozone compared with PM2 5.87 The findings reconfirmed the independent cardiovascular mortal- ity increase related to fine -particle exposure. However, after adjustment for PM2 5, ozone was associated solely with an elevated risk of death due to respiratory causes; there was no independent risk of ozone exposure on CVD -related rnortal- ity. This suggests that the positive findings reported in NMMAPS50 regarding cardiopulmonary mortality and short- term ozone exposure could be explained at least in part by the enhanced risk of mortality due to lung disease categories. Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 • • • Brook et al Particulate Matter Air Pollution and CVD 2339 Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 Table 3. Summary of Cohort Study Results Percent Increases in Mortality (95% CI) Associated With 10 PVM3 PM25 (or Other When Indicated) Size of Cohort Follow -Up Covanates Ischemic Heart Study (000s) Period Controlled for All -Cause Cardiopulmonary Cardiovascular Disease Harvard Six Cities, original —8 1974-1991 Individual 13(42-23) 18(6.0-32) ... ... (Dockery et a162 1993) (smoking+others) Harvard Six -Cities, HEI —8 1974-1991 Individual 14(54-23) 19(6.5-33) reanalysis, Krewski et al63 (smoking+others) 2004 Harvard Six -Cities, extended, —8 1974-1998 Individual 16(7-26) ... 28(13-44) ... Laden et a164 2006 (smoking+others) Six-Crhes Medicare cohort, -340 2000-2002 Individual (age, 21 (15-27) ... ... ... Eftim et ai65 2008 sex) ACS, Original, Pope et al66 —500 1982-1989 Individual 6.6(35-98) 12(6.7-17) ... 1995 (smoking+others) ACS, HEI reanalysis, Krewski —500 1982-1989 Individual 7.0 (3.910) 12(7.4-17) 13(81-18) ... et a163 2004 (smoking+others) +ecological ACS, extended I, Pope et —500 1982-1998 Individual 6.2(16-11) 9.3 (3.3-16) 12(8-15) 18(14-23) a167.66 2002, 2004 (smoking+others) ACS, intrametro Los Angeles, —23 1982-2000 Individual 17(5-30) 12(-3-30) 39(12-73) Jerrett et a169 2005 (smoking+others) +ecological ACS, extended 11, Krewski —500 1982-2000 Individual 5.6(35-78) 13(9.5-16) 24(20-29) et aP° 2009 (smoking+others) +ecological ACS, Medicare cohort, 7333 2000-2002 Individual (age, 11(9-13) ... Efhm et a165 2008 sex)+ecological +COPD US Medicare cohort, 13 200 2000-2005 Individual (age, 6.8 (4 9-8 7),- ... ... ... easticentml/west, Zeger sex)+ecological 13(95-17) et a171 2008 +COPD —1.1 (-3 to 0.8) Women's Health Initiative, —66 1994-2002 Individual ... ... 76(25-147), ... Miller et a172 2007 (smoking+others) 24 (9-41)t Nurses' Health Study, —66 1992-2002 Individual 7.0 (-3 0 to 18)$ ... 30 (0-71)$ ... Puett et a173 2008 (smoking+others) ecological AHSMOG, males only, —4 1977-1992 Individual 8.5 (-2.3 to 21) 23 (-3 to 55) McDonnell et a174 2000 (smoking+others) AHSMOG, females only, —4 1977-2000 Individual ... 42(6-90) .._ Chen et a175 2005 (smoking+others) VA hypertensive male 1 —42 1989-1996 Individual 15 (5-26)§ ... ... study, Lipfert et al76 2006 (smoking+others) +ecological VA hypertensive male 11 —30 1997-2001 Individual 6 (-6 to 22) study, Lipfert et a177 2006 (smoking+others) +ecological 11 CA county, elderly, —36 1973-2002 Individual 4(1-7)11. ... Enstrom78 2005 (smoking+others) 1 (-0.6 to 2.6) +ecological French PAARC, Filleul —14 1974-2000 Individual 7 (3-10)$ 5 (-2 to 12)$ et a179 2005 (smoking+others) German women, Gehring —5 19808, Individual 12 (-8 to 38) 52(9-115) ... ... et a180 2006 1990s-2003 smoking and • socioeconomic status (Continued) Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 2340 Circulation Table 3. Continued June 1, 2010 Size of Cohort Follow -Up Covanates Study (000s) Period Controlled for Oslo, Norway, intrametro, —144 1992-1998 Individual age, Naess et a161 2007 occupational class, education Percent Increases in Mortality (95% CI) Associated With 10 iug/m' PM25 (or Other When Indicated) Ischemic Heart All -Cause Cardiopulmonary Cardiovascular Disease Dutch cohort, Beelen —121 1987-1996 Individual 6 (-3 to 16) et a182 2008 (smoking+others) +ecological 10(5-16),$ 14(6-21), 5(1-8), 3(0-5) 4(-10 to 21) Great Britain, Elliott —660 1966-1998 Socioeconomic 1.3 (1 0-1.6)$# 1.7 (1.3-2 2)$# 1.2 (0.7-1.7)$# et a183 2007 status HEI indicates Health Effects Institute; VA, Veterans Affairs, COPD, chronic obstructive pulmonary disease, and CA, California *Three estimates are for the East, Central, and West regions of the United States, respectively tAny cardiovascular event #Associated with 10 4m3 British Smoke (BS) or PM10 §Estimates from the single -pollutant model Effect estimates were smaller and statistically insignificant in analyses resincted to counties with nitrogen dioxide data County -level traffic density was a strong predictor of survival, and stronger than PM25 when included with PM25 in joint regressions. [Two estimates are for the follow-up penod 1973-1982 and the follow-up penod 1983-2002, respectively. ¶Four estimates are for men 51-70 y old, women 51-70 y old, men 71-90 y old, and women 71--90 y old, respectively #Using last 0- to 4 -year exposure window. Additional Cohort Studies Several additional cohort studies have been published in the past few years (Table 3). Eftim and colleagues65 studied 2 very large "cohorts" of US Medicare participants who lived in locations included in the Harvard Six Cities and ACS studies. Effects of PM2.5 exposure on mortality for the period 2000 to 2002 were estimated after controlling for multiple factors, although not at the individual patient level. For all -cause mortality, the PM2.57-mortality associations were larger than those observed in the Harvard Six Cities or ACS cohorts. In an additional analysis of 13.2 million US Medi- care participants for the time period 2000 to 2005,71 PM2 5 - mortality associations were shown to be similar to those observed in the Harvard Six Cities and ACS studies in the East and Central regions of the United States (and when the data were pooled for the entire United States). However, PM25 was not associated with mortality in the Western United States or for the oldest age group (>85 years old). These findings generally corroborate the earlier cohort stud- ies and add evidence that aspects of exposure (PM sources or composition) and patient susceptibility might play important roles in determining the health risks. In a cohort of postmenopausal women without prior CVD from the Women's Health Initiative Observational Study,72 an association between longer-term PM2.5 exposure (median follow-up of 6 years) and cardiovascular events (primary end point) was observed. After adjustment for age and other risk factors, an incremental difference of 10 µg/m3 PM2 5 was associated with a 24% (95% confidence interval [CI]9% to 41%) increase in all first cardiovascular events (fatal and nonfatal, with a total of 1816 cases). Notably, an incremental difference of 10 µg/m3 PM2 5 was also associated with a large 76% (95% CI 25% to 147%) increase in fatal cardiovascular events, based on 261 deaths. The risks for both coronary heart disease and strokes were found to be similarly elevated. Interestingly, within -city PM2 5 gradients appeared to have larger cardiovascular effects than those between cities, al- though this difference was not statistically significant. Fi- nally, overweight women (body mass index >24.8 Ig/M2) were at relatively greater cardiovascular risk due to particu- late air pollution than leaner women. Noteworthy aspects of this study were improved assessment of the end points by medical record review (rather than by death certificate) and long-term particle exposure estimation. The control for individual -level confounding variables was also superior to that of previous cohort studies In another cohort of women, a subset of the Nurses' Health Study from the northeastern United States,73 an increase of 10 11g/m3 modeled estimates of PM,o exposures was associated with an approximately 7% to 16% increased risk of all -cause mortality and a 30% to 40% increase in fatal coronary heart disease, depending on the level of adjustment for covariates. This study found that the strongest health risks for all -cause and cardiovascular mortality were seen in association with the average PMho exposure during the previous 24 months before death. Similar to the findings of the Women's Health Initiative, the cardiovascular mortality risk estimates were larger than those of previous cohort studies. In addition, obese women (body mass index >30 kg/m2) were at greater relative risk, and the increases in mortality (all -cause and cardiovascular) were larger than the effects on nonfatal events. The results were also in accordance with the latest Harvard Six Cities analyses64 that show that exposure over the most recent preceding 1 to 2 years can accurately estimate the majority of the health risks due to longer-term PM air pollution exposures. The pollution -mortality association has also been assessed in several other cohort studies in the United States and Europe (Table 3).76-83 In a recent analysis of the Adventist Health Study of Smog (AHSMOG) cohort with a much Downloaded from eirc.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 Ll • • • 90 85 80 75 70 3 65 60 w 55 >. 50 45- 0 40 - m 35 w ea 30 25 m 20 IL 15- 10- 5- 0- -5 - -10 - Brook et al Particulate Matter Air Pollution and CVD 2341 Figure 1. Risk estimates provided by several cohort studies per increment of 10 µg/m3 in PM2.5 or PM,(). CPD indicates cardiopulmo- nary disease; IHD, ischemic heart disease. longer follow-up than the original studies,74.88 fatal coronary heart disease was significantly associated with PM2, among females but not males.75 These observations along with the remarkably robust health effects in the Women's Health Initiative Observational Study and Nurses' Health Study suggest that women may be at special risk from PM exposure. The overall cohort study evidence demonstrates that a 10- µg/m3 increase in PM2., exposure is in general positively associated with excess mortality, largely driven by increases in cardiopulmonary or cardiovascular deaths (Figure 1). Independent results from the Women's Health Initiative Study,72 the US Medicare cohorts,71 the German women cohort,80 and the intracity Oslo (Norway) study81 contribute substantially to this evidence. Although the Dutch cohort, 8'- AHSMOG,74.75 French PAARC (Pollution Atmosph6rique et Affections Respiratoires Chroniques [air pollution and chronic respiratory diseases]),79 Veterans Affairs hypertensive male study,77 and 11 CA county78 studies observed increased mortality risks associated with higher PM2 5 exposure that were statistically significant in some analyses, the observed health risks were less robust. A finding that is somewhat consistent across the Veterans Affairs hypertensive male study,77 11 CA county,78 Oslo,81 and US Medicare cohorts71 is that the PM2.5- mortality effect estimates tend to decline with longer periods of follow up or in a substantially older cohort. These studies also often observed elevated mortality risks according to alternative indicators of air pollution exposure, especially metrics of traffic - related exposure. Evidence Summary The overall evidence from the cohort studies demonstrates on average an approximate 10% increase in all -cause mortality per 10-µg/m3 elevation in long-term average PM2.5 exposure. The mortality risk specifically related to CVD appears to be elevated to a similar (or perhaps even greater) extent, ranging from 3% to 76% (Table 3). This broader estimated range in risk compared with the short-term effects observed in time series is due to several recent cohort studies72.73 that demon- strated larger cardiovascular mortality risks (eg, >30%) than in earlier cohort observations. This may reflect superior aspects of these studies that allowed for a better character- ization of the cardiovascular risk of long-term exposure, the fact that these cohorts consisted of only women, or other unclear reasons. Compared with cardiovascular mortality, there is less existing evidence to support an increase in the risk for nonfatal cardiovascular events related to PM2 5 exposure among the existing cohort studies, because many of them did not specifically investigate nonfatal outcomes, and several of the more recent studies reported nonsignificant relationships.72,73 Natural Experiment and Intervention Studies Several studies have shown improvements in health outcomes in association with exposures using well-defined natural experiments or interventions, such as abrupt reductions in air pollution89-91 or changes over a longer period of time.64,92 Downloaded from clrc.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 All Cause CPD o $ CVD IHD N N Q (C 6 � O 0 0 CD 0 is m c °D 0 ACS aD N N N D > mN N N C N O N N 111 m N N •_ U N W N N N N OO LA p m N •C m 1) /Q "m O] m m d E N C N m m .L-. y N d N Evl m O w d ' m m N N m m 7 d m ° m W 75 y S= Z OZ O Ng GO 0 mm y .� m OS 1° � m ._ m in m� 2E m 0 m y m N m U 3 Q i- r- E o m m m _ m m c m C7 ami 3 d C7 °= U y U m Q 3 3 m m U U W m m g = o s Q c N x_ U ACS °' m m L Z l m ACS u v m 2 ¢ U li Z _ m v m Q 0 E E s o y w 7 U) N Q a y 0 0 cc Q : U m LL -------- *— l — — ---- — — — — — — — — — -- Figure 1. Risk estimates provided by several cohort studies per increment of 10 µg/m3 in PM2.5 or PM,(). CPD indicates cardiopulmo- nary disease; IHD, ischemic heart disease. longer follow-up than the original studies,74.88 fatal coronary heart disease was significantly associated with PM2, among females but not males.75 These observations along with the remarkably robust health effects in the Women's Health Initiative Observational Study and Nurses' Health Study suggest that women may be at special risk from PM exposure. The overall cohort study evidence demonstrates that a 10- µg/m3 increase in PM2., exposure is in general positively associated with excess mortality, largely driven by increases in cardiopulmonary or cardiovascular deaths (Figure 1). Independent results from the Women's Health Initiative Study,72 the US Medicare cohorts,71 the German women cohort,80 and the intracity Oslo (Norway) study81 contribute substantially to this evidence. Although the Dutch cohort, 8'- AHSMOG,74.75 French PAARC (Pollution Atmosph6rique et Affections Respiratoires Chroniques [air pollution and chronic respiratory diseases]),79 Veterans Affairs hypertensive male study,77 and 11 CA county78 studies observed increased mortality risks associated with higher PM2 5 exposure that were statistically significant in some analyses, the observed health risks were less robust. A finding that is somewhat consistent across the Veterans Affairs hypertensive male study,77 11 CA county,78 Oslo,81 and US Medicare cohorts71 is that the PM2.5- mortality effect estimates tend to decline with longer periods of follow up or in a substantially older cohort. These studies also often observed elevated mortality risks according to alternative indicators of air pollution exposure, especially metrics of traffic - related exposure. Evidence Summary The overall evidence from the cohort studies demonstrates on average an approximate 10% increase in all -cause mortality per 10-µg/m3 elevation in long-term average PM2.5 exposure. The mortality risk specifically related to CVD appears to be elevated to a similar (or perhaps even greater) extent, ranging from 3% to 76% (Table 3). This broader estimated range in risk compared with the short-term effects observed in time series is due to several recent cohort studies72.73 that demon- strated larger cardiovascular mortality risks (eg, >30%) than in earlier cohort observations. This may reflect superior aspects of these studies that allowed for a better character- ization of the cardiovascular risk of long-term exposure, the fact that these cohorts consisted of only women, or other unclear reasons. Compared with cardiovascular mortality, there is less existing evidence to support an increase in the risk for nonfatal cardiovascular events related to PM2 5 exposure among the existing cohort studies, because many of them did not specifically investigate nonfatal outcomes, and several of the more recent studies reported nonsignificant relationships.72,73 Natural Experiment and Intervention Studies Several studies have shown improvements in health outcomes in association with exposures using well-defined natural experiments or interventions, such as abrupt reductions in air pollution89-91 or changes over a longer period of time.64,92 Downloaded from clrc.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 2342 Circulation June 1, 2010 Table 4. Comparison of Pooled Estimated of Percent Increase in Risk of Hospital Admission for CVD Estimated Across Meta -Analyses and Multicity Studies of Daily Changes in Exposure Small but statistically significant drops in mortality were associated with an 81/2 -month copper smelter strike that resulted in sharp reductions in sulfate PM and related air pollutants across 4 Southwest states, even after controlling for other factors.93 Data from US Medicare enrollment files were used to estimate the association between changes in monthly mortality rates for US counties and average PM2 5 concentra- tions for the previous 12 months.94 PM25-mortality associa- tions were observed at the national scale but not the local scale, which raises concerns about possible staistical con- founding due to unmeasured individual and ecological vari- ables as a cause for any positive findings in this study. However, a recent large study found that reductions in PM air pollution exposure on a local scale (across US counties) over a 2 -decade period (1980s and 1990s) were associated with increased life expectancy even after controlling for changes in socioeconomic, demographic, and proxy smoking vari- ables.95 Indeed, a decrease of 10 µg/m3 in the long-term PM2.5 concentration was related to an increase in mean life expectancy of 0.61±0.20 years. Hospitalization Rates There are many daily time -series or case -crossover studies that have evaluated associations between cardiovascular hos- pitalizations and short-term changes in air pollution. Because of the great number of publications, all studies (particularly those focusing on nonparticulate air pollutants) cannot be discussed individually. Nevertheless, Table 4 presents a comparison of pooled estimates of percent increase in RR of hospital admission for general cardiac conditions across a previous meta-analysis of 51 published estimates (COMEAP [Committee on the Medical Effects of Air Pollutants]) and results from many selected multicity studies published after 2004. Several studies before 2004 are included in Table 4 only to demonstrate the consistency of effect. Because of its comparatively large size and importance, the results of a recent analysis of Medicare files in 204 US urban counties with 11.5 million individuals older than 65 years merit discussion. Daily changes in PM2_5 levels were associ- ated with a variety of cardiovascular hospital admission subtypes.103 A 10-1kg/m3 increase in PM2.5 exposure was related to increases in hospitalizations for cerebrovascular disease by 0.81% (95% Cl 0.3% to 1.32%), peripheral vascular disease by 0.86% (95% Cl -0.06% to 179%) , ischemic heart disease by 0.44% (95% Cl 0.02% to 0 86%), arrhythmias by 0.57% (95% CI -0.01% to 1.15%), and heart failure by 1.28 (95% CI 0.78% to 1.78%). The moss rapid effects, which occurred largely on the same day of PM2 5 elevation, were seen for cerebrovascular, arrhythmia, and heart failure admissions. Ischemic heart disease events tended to increase to a greater extent 2 days after exposures. A consistent finding was that the cardiovascular effects of pollution were much stronger in the Northeast than in other regions. In fact, there were few significant associations in Western US regions. It was speculated that these differences reflected variations in particle composition (eg, greater sul- fate in the East and nitrate components in the West) and pollution sources (eg, power generation in the East and transportation sources in the West). In a follow-up analysis by Peng et al,104 PM10_25 levels were not statistically associated with cardiovascular hospitalizations after adjustment for PM2.,. This suggests that the smaller particles (ie, PM2,) are principally responsible for the cardiovascular hospitalizations attributed in prior studies to the combination of both fine and coarse particles (ie, PM10). Given the differences between the size fractions, the results imply that particles and their components derived from combustion sources (ie, PM,, 5) are more harmful to the cardiovascular system than larger coarse particles. Finally, there is some evidence that gaseous pollut- ants may also instigate hospitalizations. Hospital admissions for cardiovascular causes, particularly ischemic heart disease, were found to rise in relation to the previous -day and same-day level of SO2, even after adjustment for PM10 levels.105 Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 C] • • Primary Source Exposure Increment % Increase (95% Cl) Cardiac admissions, meta-analysis of 51 estimates COMEAP31 2006 20 µg/m3 PMiO 1.8 (1.4-1.2) Cardiac admissions, 8 US cites Schwartz 1999 20 µg/m3 PM10 2.0 (1.5-2.5) Cardiac admissions, 10 US cities Zanobett et al 97 2000 20 "/m3 PM10 2.6(20-30) Cardiac admissions, 14 US cites Samet et a198 2000 20 4m3 PM10 2.0 (15-2.5) Schwartz et a199 2003 Cardiac admissions, 8 European cities Le Tertre et a140 2002 20 µg/m3 PM10 1.4 (0.8-2 0) Cardiovascular admissions, 14 Spanish cites Ballester et a1700 2006 20 µg/m3 PM10 1.8(7-3.0) Cardiovascular admission, 8 French cities Larrieu et al10' 2007 20 ,,,,/m3 PM70 lPgg/m3 1.6 (0.4-3.0) Cardiovascular admissions, 202 US counties Bell et a11112 2008 20 PM10 08(06-1.0) Medicare nabonal claims history files Dominici et a1103 2006 10 WJ ,,,,/m3 PMS Ischemic heart disease, 0 44 (0.02-0 86) Cerebrovascular disease 0.81 (0.30-1.32) Heart failure 1.28 (0 78-178) Heart rhythm 0.57 (-0.01 to 1.15) Small but statistically significant drops in mortality were associated with an 81/2 -month copper smelter strike that resulted in sharp reductions in sulfate PM and related air pollutants across 4 Southwest states, even after controlling for other factors.93 Data from US Medicare enrollment files were used to estimate the association between changes in monthly mortality rates for US counties and average PM2 5 concentra- tions for the previous 12 months.94 PM25-mortality associa- tions were observed at the national scale but not the local scale, which raises concerns about possible staistical con- founding due to unmeasured individual and ecological vari- ables as a cause for any positive findings in this study. However, a recent large study found that reductions in PM air pollution exposure on a local scale (across US counties) over a 2 -decade period (1980s and 1990s) were associated with increased life expectancy even after controlling for changes in socioeconomic, demographic, and proxy smoking vari- ables.95 Indeed, a decrease of 10 µg/m3 in the long-term PM2.5 concentration was related to an increase in mean life expectancy of 0.61±0.20 years. Hospitalization Rates There are many daily time -series or case -crossover studies that have evaluated associations between cardiovascular hos- pitalizations and short-term changes in air pollution. Because of the great number of publications, all studies (particularly those focusing on nonparticulate air pollutants) cannot be discussed individually. Nevertheless, Table 4 presents a comparison of pooled estimates of percent increase in RR of hospital admission for general cardiac conditions across a previous meta-analysis of 51 published estimates (COMEAP [Committee on the Medical Effects of Air Pollutants]) and results from many selected multicity studies published after 2004. Several studies before 2004 are included in Table 4 only to demonstrate the consistency of effect. Because of its comparatively large size and importance, the results of a recent analysis of Medicare files in 204 US urban counties with 11.5 million individuals older than 65 years merit discussion. Daily changes in PM2_5 levels were associ- ated with a variety of cardiovascular hospital admission subtypes.103 A 10-1kg/m3 increase in PM2.5 exposure was related to increases in hospitalizations for cerebrovascular disease by 0.81% (95% Cl 0.3% to 1.32%), peripheral vascular disease by 0.86% (95% Cl -0.06% to 179%) , ischemic heart disease by 0.44% (95% Cl 0.02% to 0 86%), arrhythmias by 0.57% (95% CI -0.01% to 1.15%), and heart failure by 1.28 (95% CI 0.78% to 1.78%). The moss rapid effects, which occurred largely on the same day of PM2 5 elevation, were seen for cerebrovascular, arrhythmia, and heart failure admissions. Ischemic heart disease events tended to increase to a greater extent 2 days after exposures. A consistent finding was that the cardiovascular effects of pollution were much stronger in the Northeast than in other regions. In fact, there were few significant associations in Western US regions. It was speculated that these differences reflected variations in particle composition (eg, greater sul- fate in the East and nitrate components in the West) and pollution sources (eg, power generation in the East and transportation sources in the West). In a follow-up analysis by Peng et al,104 PM10_25 levels were not statistically associated with cardiovascular hospitalizations after adjustment for PM2.,. This suggests that the smaller particles (ie, PM2,) are principally responsible for the cardiovascular hospitalizations attributed in prior studies to the combination of both fine and coarse particles (ie, PM10). Given the differences between the size fractions, the results imply that particles and their components derived from combustion sources (ie, PM,, 5) are more harmful to the cardiovascular system than larger coarse particles. Finally, there is some evidence that gaseous pollut- ants may also instigate hospitalizations. Hospital admissions for cardiovascular causes, particularly ischemic heart disease, were found to rise in relation to the previous -day and same-day level of SO2, even after adjustment for PM10 levels.105 Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 C] • • • • • Brook et al Particulate Matter Air Pollution and CVD 2343 Table 5. Comparisons of Estimated Percent Increase in Risk of Ischemic Heart Disease Events due to Concurrent or Recent Daily PM Exposure Event/Study Area Primary Source Exposure Increment % Increase (95% CI) MI events—Boston, Mass Peters et alto 2001 10 µg/m3 PM25 20(5.4-37) MI, 1st hospitalization—Rome, Italy D'ippolyd et a112 2003 30 PVm3 TSP 71 (1.2-13.1) MI, emergency hospitalizations -21 US cities Zanobetti and Schwartz13 2005 20 Ag/m3 PM,o 1.3 (0.2-2 4) Hospital readmissions for MI, angina, dysrhythmia, Von Mot et al14 2005 20 µg/m3 PM10 4.2 (0.8-8.0) or heart failure of MI survivors -5 European cities MI everts—Seattle, Wash Sullivan et a115 2005 10 µg/m3 PMIS 4.0 (-4.D-14 5) MI and unstable angina events—Wasatch Front, Utah Pope et a173 2006 10 µg/m3 PM25 4.8 (1.0-6 6) Tokyo metropolitan area Murakami et al'os 2006 TSP >300 µg/m3 for 1 h vs 40(0--97)' reference periods <99 AW Nonfatal MI, Augsburg, Germany Peters et all" 2004 Exposure to traffic 1 h before MI 292(222-383) (note. not PM but self-reported traffic exposure) Nonfatal MI, Augsburg, Germany Peters et al1e 2005 Ambient UFP, PM25, and PM,o No association with UFP or PM25 levels on same day. Positive associations with PM25 levels on 2 days prior TSP indicates total suspended particulate matter 'Adjusted rate ratio for MI deaths. Evidence Summary Excess cardiovascular mortality and increased rates of hos- pitalizations are similarly associated with day-to-day changes in PM air pollution (Tables 2 and 4). However, significant differences between geographic regions in the risk relation- ships have been observed, and more investigation is required to explain this heterogeneity. Specific Cardiovascular Events/Conditions Ischemic Heart Disease Among the cohort studies that provided relevant results, the ACS study found a relationship between increased risk for ischemic heart disease death and long-term exposure to elevated PM2.5 levels (Table 3).67•69.106 Indeed, ischemic cardiac events accounted for the largest relative (RR 1.18, 95% CI 1.14 to 1.23) and absolute risk for mortality per 10-µg/m3 elevation in PM2 5.67 A survival analysis of US Medicare data for 196 000 survivors of acute MI in 21 cities showed the risk of an adverse post -MI outcome (death, subsequent MI, or first admission for congestive heart failure) was increased with higher exposure to PM 10.107 Data from the Worcester Heart Attack study also found that long-term exposure to traffic -related air pollution was associated with significantly increased risk of acute MI.108 However, in the Women's Health Initiative72 and the Nurses' Health Study,73 only disease categories that included fatal coronary events, but not nonfatal MI alone, were statistically elevated in relation to PM2 5. The effect size for cardiovascular mortality was much larger and much more statistically robust than for nonfatal events such as MI in both studies. Various time -series and case -crossover studies have also reported increased ischemic heart disease hospital admissions associated with short-term elevated concentrations of inhal- able and/or fine PM air pollution.31•40,103 In the US Medicare study, a reduction of PM2.5 by 10 11g/m3 was estimated to reduce ischemic heart disease admissions in 204 counties by 1523 (95% posterior interval 69 to 2976) cases per year.103 Several studies have also found positive associations between elevated PM or traffic exposures over a period as brief as a few hours109-111 or a few days and an elevated risk for MI (Table 5).13,110.112-115 In general, acute increases in risk for ischemic heart disease events have been observed consis- tently, even as rapidly as 1 to 2 hours after exposure to elevated PM, in case -crossover analyses. 109-111 Other studies have reported an increased risk for MI shortly after exposure to traffic. Peters et allll reported in 691 subjects in Augsburg, Germany, a strong association (odds ratio 2.92, 95% Cl 2.22 to 3.83) between onset of MI and traffic exposure within the past hour, although whether this was a result of the air pollution or a combination of other factors (eg, noise and stress) is not certain. Additional analyses did not report an association between recent UFP exposures and MI onset; however, the levels of PM2 5 and several gaseous pollutants 2 days earlier were related to MI risk. 116 The lack of relation- ship between MI and UFPs may be due to the fact that the levels were measured regionally and remote from the local- ized source and may therefore reflect exposure misclassifica- tion. Finally, in the only study in which participating subjects had coronary angiograms performed previously, ischemic cardiac events were found to occur in relation to PM air pollution exposure solely among individuals with obstructive coronary atherosclerosis in at least 1 vesse1.13 This finding suggests the importance of patient susceptibility (eg, the presence of preexisting coronary artery disease) for PM to trigger an acute ischemic event within hours to days after exposure. Heart Failure In the ACS cohort study, it appeared that deaths due to arrhythmias, heart failure, and cardiac arrest (RR 1.13, 95% Cl 1.05 to 1.21 per 10 µg/ru) were also associated with Downloaded from crrc.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2344 Circulation June 1, 2010 prolonged exposure to PM2 5, although not as strongly as ischemic heart disease mortality,67 although potential mortal- ity misclassification on death certificates makes the actual cause of death not entirely certain in all circumstances. Heart failure rates or mortality associations were not reported in the other cohort studies. Daily hospitalizations for heart failure have also been associated with short-term changes in PM exposure.31 Heart failure associations with PM were observed in a large daily time -series analysis of PM2_5 and cardiovascular and re- spiratory hospitalizations by use of a national database constructed from US Medicare files.103 A 10-µg/m3 in- crease in concurrent -day PM2 5 was associated with a 1.28% (95% CI 0.78% to 1.78%) increase in heart failure admissions, the single largest cause for hospitalization in this cohort. A reduction of PM2_5 by 10 ,ug/m3 was estimated to reduce heart failure admissions in 204 coun- ties by 3156 (95% posterior interval 1923 to 4389) cases per year.103 Another analysis in Medicare recipients in 7 US cities found a 10-µg/m3 increase in concurrent -day PM10 was associated with a 0.72% (95% Cl 0.35% to 1.10%) increase in heart failure admissions.117 Traffic - related air pollution has also been shown to be signifi- cantly associated with increased mortality risk after acute heart failure.18 Finally, a study from Utah's Wasatch Front area explored longer lagged -exposure periods and found that a 14 -day lagged cumulative moving average of 10 µg/m3 PM25 was associated with a 13.1% (95% CI 1.3% to 26.2%) increase in heart failure admissions.719 Cerebrovascular Disease Among the cohort studies that provided pertinent results, the Women's Health Initiative reported significant increases in both nonfatal stroke (hazard ratio 1.28, 95% CI 1.02 to 1.61) and fatal cerebrovascular disease (hazard ratio 1.83, 95% CI 1.11 to 3.00) per 10-µg/m3 elevation in prolonged exposure to PM2 5.72 However, no significant association between stroke mortality and PM air pollution was found in the ACS study.67 Several studies have also reported small but statistically significant associations between short-term PM exposure and cerebrovascular disease. Daily time -series studies of stroke mortality in Seoul, Korea,120.121 observed that elevated air pollution (including measures of PM, NO2, CO, and 03) was associated with increases in stroke mortality. When analyzed separately by stroke type,121 the pollution association was associated with ischemic but not hemorrhagic stroke. Risk of stroke mortality was also associated with daily increases in PM10 and NO2 in Shanghai, China .56 A daily time -series study in Helsinki, Finland, 122 found that PM25 and CO were associated with stroke mortality in the warm but not the cold seasons. Several studies have also observed increased stroke or cerebrovascular hospital admissions associated with in- creased exposure to PM or related pollutants.31.38.40.46.123-125 For example, a study of hospital admissions for Medicare recipients in 9 US cities125 found that several measures of air pollution (PM10, CO, NO2, and SO2) 0 to 2 days before admission were associated with ischemic but not heamorrhagic stroke. Studies of ischemic stroke and transient ischemic attacks based on population -based surveillance have also been conducted in Dijon, France,126 where 03 exposure (but not PM 10) was associated with ischemic stroke, and in Corpus Christi, Tex,127 where both PM25 and 03 were associated with ischemic strokes and transient ischemic attacks. Peripheral Arterial and Venous Diseases There have been only a few studies that have explored a relationship between air pollution and peripheral vascular dis- eases. Studies using Medicare data for 204 US counties observed nearly statistically significant positive associations between daily changes in measures of PM pollution and hospitalizations for peripheral vascular diseases. 103,104 The ACS cohort foand no association between other atherosclerotic and aortic aneurysm deaths and long-term PM25 exposure.67 Recently, a case -control study from the Lombardy region of Italy found a 70% increase in risk of deep vein thrombosis per 10-µg/m3 elevation in long-term PM 10 level. 128 This is the fust observation that particulate air pollution can enhance coagulation and thrombosis risk in a manner that adversely affects the venous circulation in addition to the arterial cardiovascular system. Cardiac Arrhythmias and Arrest Several studies have observed associations between fine PM and related pollutants and cardiac arrhythmias, often based on data from implanted cardioverter-defibrillators.129-136 How- ever, no clear pollution -related associations were observed in studies from a relatively clean metropolitan area, Vancouver, British Columbia, Canada,137,138 or from a relatively large study in Atlanta, Ga.139 Similarly, pollution -related associa- tions have been observed with cardiac arrest in Rome, Italy,140 and Indianapolis, Ind,141 but not in Seattle, Wash.142,143 The mixed results may reflect different PM compositions due to different sources or variations among the methods used. Evidence Summary On the basis of the available epidemiological studies that have reported the associations between PM exposures with specific subsets of cardiovascular outcomes (morbidity, mor- tality, or hospitalizations), the existing level of overall evi- dence is strong for an effect of PM on ischemic heart disease, moderate (yet growing) for heart failure and ischemic stroke, and modest or mixed for peripheral vascular and cardiac arrhythmia/arrest (Table 6). Ambient Air Pollution and Subclinicall Pathophysiological Responses in Human Populations It is likely that many subclinical physiological changes occur in individuals in response to PM2.5 exposures that do not become overtly manifest as a cardiovascular event (eg, death or MI). The illustration of these more subtle responses bolsters the plausibility of the observable outcome associa- tions and provides insight into the pathways whereby air Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 • • • Brook et al Table 6. Overall Summary of Epidemiological Evidence of the Cardiovascular Effects of PM,_, Traffic -Related, or Combustion -Related Air Pollution Exposure at Ambient Levels Short -Term Longer -Term Exposure Exposure (Months to Health Outcomes (Days) Years) Clinical cardiovascular end points from epidemiological studies at ambient pollution concentrations Cardiovascular mortality T T T T T T Cardiovascular hospitalizations T T T T Ischemic heart disease* T T T T T T Heart failure* T T T Ischemic stroke* T T T Vascular diseases T T t Cardiac arrhythmia/cardiac arrest T T Subclinical cardiovascular end points and/or surrogate measures in human studies Surrogate markers of WA atherosclerosis Systemic inflammation T T Systemic oxidative stress T Endothelial cell activatlont T T blood coagulation Vascular/endothelial T T dysfunction BP T T Altered HRV T T T Cardiac ischemia T Arrhythmias T The arrows are not indicators of the relative size of the association but represent a qualitative assessment based on the consensus of the writing group of the strength of the epidemiological evidence based on the number and/or quality, as well as the consistency, of the relevant epidemiological studies. T T T Indicates strong overall epidemiological evidence T T Indicates moderate overall epidemiological evidence. T Indicates some but limited or weak available epidemiological evidence. Blank indicates lack of evidence WA indicates not applicable *Categones include fatal and nonfatal events tDeep venous thrombosis only pollutants mediate CVDs. The `Biological Mechanisms" section discusses the hypothesized global pathways and reviews the studies related to the fundamental cellular/ molecular mechanisms elucidated by controlled human and animal exposures and toxicological/basic science experi- ments. The following section reviews the recent evidence that ambient exposure to air pollution can mediate potentially harmful subclinical cardiovascular effects. In general, many positive associations are found (Table 6). Numerous complex interactions between variations in the characteristics, sources, and chemistry of the particles, coupled with diversity in time frames, mixtures of exposures, and degrees of individual Particulate Matter Air Pollution and CVD 2345 susceptibility, likely explain some of the disparity among findings. Systemic Inflammation There is evidence that under some circumstances, exposure to ambient PM can be associated with elevated circulating proinflammatory biomarkers that are indicative of a systemic response after PM air pollution inhalation that is not limited to the confines of the lung. Early reports found associations with day-to-day variation in acute-phase proteins, such as C-reactive protein (CRP), fibrinogen, or white blood cell counts,144-147 as reviewed previously.' Limited evidence on the association between cumulative PM exposures and fibrin- ogen levels and counts of platelets and white blood cells was also available. 148 A number of more recent studies have reported positive associations with short-term ambient PM exposure and day- to-day elevations in inflammatory markers. These include increases in CRP in an elderly population149 and individuals with coronary atherosclerosis 150; CRP and fibrinogen in young adults151 and elderly overweight individuals 152; and CRP, tumor necrosis factor -a (TNF -a), and interleukin (IL) -1/3 in children. 153 Recent evidence has also been found for an upregulation of circulating soluble adhesion molecules (eg, intercellular adhesion molecule -1) in 92 Boston, Mass— area individuals with diabetes 154 and 57 male subjects with coronary artery disease in Germany. 150 In a larger analysis of 1003 Ml survivors, also in Germany, CRP was not related to PM exposure; however, ambient particle number concentra- tion and PM10 were associated with increased IL-6 and fibrinogen, respectively. 155 Short-term levels of in -vehicle PM2.5 have also been linked to increases in CRP among healthy highway patrol troopers.756 In a follow-up analysis, elevations in certain particulate components of traffic pollu- tion (eg, chromium) were associated with increased white blood cell counts and increased IL-6 levels.157 Short-term changes in ambient PM levels have also been linked to acute (1 to 3 days later) alterations in biomarkers of inflammation, oxidative stress, and platelet activation among elderly adults with coronary artery disease living in retirement communities in Los Angeles, Calif. 158,159 Pollutants associated with pri- mary combustion (eg, elemental and black carbon, primary organic carbon) and UFPs rather than PM2_5 appeared to be strongly associated with adverse responses in this population. Regarding more long-term exposures,160 a positive associ- ation between white blood cell count and estimated long-term 1 -year exposure to PM10 was reported in the Third National Health and Nutrition Examination Survey. Among 4814 adults in Germany, small increases in annual mean PM2_5 (3.9 µg/ru) were associated with increases in high -sensitivity CRP by 23.9% and in fibrinogen by 3.9% among men only. Estimated long-term traffic exposure was not related to inflammatory changes in either sex.161 Several studies, including some with improved exposure assessment,162 some that included analyses of large popula- tion cohorts,163,164 and a recent evaluation of long-term annual PM10 levels in England, 165 have not found a relation- ship between particulate exposure and inflammation. It is Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2346 Circulation June 1, 2010 conceivable that differences in the magnitude or character of the inflammatory response will occur because of variations in the particulate chemistry and duration/intensity of' exposures. Certain individuals may also be more susceptible. The evi- dence suggests that subjects with underlying cardiovascular risk factors and the metabolic syndrome may exhibit stronger associations. 157,160.166 Conversely, antiinflammatory medica- tions such as statins may mitigate the actions of ambient particles. 152,155 All together, there is some evidence for a positive association between recent and long-term PM expo- sure and a systemic proinflammatory response; nevertheless, there is variation in the strength and consistency of changes among the variety of biomarkers and patient populations evaluated (Table 6). Systemic Oszdative Stress A state of oxidative stress refers to a condition in which levels of free radicals or reactive oxygen/nitrogen species (eg, 02-, H2O2, ONOO-) are higher than normal (eg, healthy individ- uals in whom they are countered by homeostatic; processes such as antioxidants) and thus are capable of exerting many adverse biological effects (eg, lipid/protein/deoxyribonucleic acid [DNA] oxidation, initiation of proinflammatory cas- cades). Although many biomarkers of differing systemic responses are available (eg, lipid or protein oxidation prod- ucts), oxidative stress may occur at the local cellular/tissue level and not be directly observable by circulating markers. In addition, oxidative stress is often induced by and elicits inflammatory processes. The 2 processes are biologically linked. Therefore, human studies investigating the effect of PM on oxidative stress per se are difficult to perform. Only a few studies have directly investigated the occurrence of systemic oxidative stress in humans in relation to ambient PM exposure. Three studies of young adults conducted in Den- mark demonstrated elevations in biomarkers of protein, lipid, or DNA oxidation in relation to PM exposure from traffic sources. 167-169 In a study of 76 young adults from Taipei, Taiwan,151 the investigators found evidence of increased levels of 8 -hydroxy -2' -deoxyguanosine adducts in DNA in relation to short-term elevations in ambient PM. Two studies have also demonstrated increases in plasma homocysteine, evidence that exposure to ambient PM can elevate this circulating mediator of oxidative stress.170,171 Finally, Romieu et a1172 found that dietary supplementation with omega-3 polyunsaturated fatty acids might be capable of altering the systemic oxidative stress response (reduction in copper/zinc superoxide dismutase and glutathione) induced by air pollutants among residents living to a nursing home in Mexico City, Mexico. Because of the relatively small number of studies, more investigation is required to make firm conclusions and to understand the nature of the systemic oxidative stress response potentially induced by ambient PM (Table 6). Thrombosis and Coagulation Early reports indicated that increased plasma viscosity'44 and elevated concentrations of fibrinogen146 are associated with short-term changes in ambient PM concentrations. More recent evidence was found for an upregulation of circulating von Willebrand factor in 57 male subjects with coronary artery disease in Germany150 and 92 Boston -area individuals with diabetes. 154 Riediker157 found that com- ponents of in -vehicle PM2 5 were also related to increased von Willebrand factor and decreased protein C among highway patrol troopers. In the Atherosclerosis Risk in Communities study, a 12.8-µg/m3 elevation in ambient PM70 was associated with a 3.9% higher von Willebrand factor level, 173 but only among those with diabetes. There was no linkage between PM10 exposure and fibrinogen or white blood cell levels. Alterations in other markers that indicate changes in thrombosis, fibrinolysis, and global coagulation have also been reported. An immediate elevation in soluble CD40- ligand concentration, possibly reflecting platelet activa- tion, recently was found to be related to ambient UFP and accumulation -mode particle (PMO,-, 0) levels in patients with coronary artery disease. 155 Ambient PM10levelshave also been associated with augmented platelet aggregation 24 to 96 hours after exposure among healthy adults.174 In this study, there were no concomitant observable changes in thrombin generation, CRP, or fibrinogen induced by PMI(). Increases in plasminogen activator inhibitor -1 and fibrinogen levels have been noted in healthy subjects,151 as well as elevated plasminogen activator inhibitor -1 in patients with coronary artery disease only, 175 in association with ambient PM levels in Taipei. Chronic indoor pollu- tion exposure to biomass cooking in rural India has also been associated with elevated circulating markers of plate- let activation.176 Recently, Baccarelli et a1128,177 demon- strated in healthy subjects and among individuals with deep venous thrombosis living in the Lombardy region of Italy that prothrombin time was shortened in relation to recent and long-term ambient PM10 concentrations. Nev- ertheless, some studies found no effects of ambient pollu- tion,178 nor have significant changes been reported among all the biomarkers or subgroups of individuals investigat- ed. 150, 154,170,173 Similar to the study on systemic inflarnma- tion, the results related to thrombosis/coagulation are quite variable given the differences in study designs, patients, biomarkers evaluated, and pollutants; however, these ad- verse effects appear somewhat more consistent among higher -risk individuals (Table 6). Systemic and Pulmonary Arterial BP Several studies have reported that higher daily PM levels are related to acute increases in systemic arterial BP (approximately a 1- to 4 -mm Hg increase per 10-µg/m3 elevation in PM).179-184 In a small study of patients with severe heart failure,185 pulmonary artery and right ventric- ular diastolic BP were found to increase slightly in relation to same-day levels of PM. Chronic exposure to elevated PM2 5 was associated with increased levels of circulating endothelin (ET) -1 and elevated mean pulmonary arterial pressure in children living in Mexico City. 186 These results may explain in part the risk for heart failure exacerbations due to PM Downloaded from circ.ahajournals.-org at University of Michigan --Ann Arbor on December 6, 2010 is s r� L_J r� L_J Brook et al Particulate Matter Air Pollution and CVD 2347 exposure; however, not all studies of systemic arterial BP have been positive.187-189 Recently, Dvonch et a1190 demonstrated significant as- sociations between increases in systolic BP and daily elevations in PM2 5 across 347 adults living in 3 distinct communities within metropolitan Detroit, Mich. Much larger effects were observed 2 to 5 days after higher PM2.5 levels within a specific urban location of southwest Detroit (8.6 mm Hg systolic BP increase per 10-µg/m3 PM2 5) than throughout the entire region or cohort (3.2 mm Hg). This suggests that specific air pollution sources and components contribute significantly to the potential for PM exposure to raise BP. Interestingly, it was recently reported in a crossover study of 15 healthy individuals that systolic BP was significantly lower (114 versus 121 mm Hg) during a 2 -hour walk in Beijing, China, while the subjects were wearing a high -efficiency particulate -filter facemask than when they were not protected.191 Wearing the facemask was also associated with increased HRV, which suggests that the rapid BP -raising effects of particle inhalation may be mediated through the autonomic nervous system (ANS). In a similar fashion,192 reducing exposure to particulate pollution from cooking stoves was shown to be associated with lower systolic (3.7 mm Hg, 95% CI —8.1 to 0.6 mmHg) and diastolic (3.0 mmHg, 95% CI —5.7 to —0.4 mm Hg) BP among Guatemalan women than among control subjects after an average of 293 days. These findings demonstrate that indoor sources of PM (eg, cooking, biomass) may have important cardiovascular health consequences and that reductions in particulate exposure are capable of lowering BP, and they suggest that chronic exposure to PM air pollution may alter long-term basal BP levels. Even given the rapid variability of BP on a short-term basis and the numerous factors involved in determin- ing individual responses (eg, patient susceptibility, PM compo- sition, and time frames of exposure), overall, it appears that ambient PM can adversely affect systemic hemodynamics, at least under certain circumstances (Table 6). Vascular Function In the first ambient PM study related to changes in vascular function, O'Neill et a1193 reported that both endothelium -dependent and -independent vasodilation were blunted in relation to air pollution levels in Boston. The largest changes occurred in association with sulfate and black carbon, suggestive of coal -burning and traffic sources, respectively. Significant adverse responses were observed within 1 day yet were still present and slightly more robust up to 6 days after exposure. Moreover, the adverse responses occurred solely among diabetic individ- uals and not in patients at risk for diabetes mellitus. Two other studies'14.194 also demonstrated impaired vascular function due to short-term changes in ambient PM among diabetic patients. In the study by Schneider et a1,194 endothelium -dependent vasodilation was blunted during the first day, whereas small -artery compliance was im- paired 1 to 3 days after elevated ambient PM levels. Interestingly, higher concentrations of blood myeloperox- idase were related to a greater degree of endothelial dysfunction, which suggests that white blood cell sources of reactive oxygen species (ROS) may be involved. In healthy adults, very short-term exposure to elevated levels of ambient PM from traffic sources while exercising for 30 minutes near roadways195 and when resting by bus stops for 2 hours196 has been related to impaired endothe- lium -dependent vasodilation. Daily changes in ambient gaseous pollutants (SO2 and NO.) in Paris, France, have also been associated with impaired endothelium -dependent vasodilation among nonsmoking men. 197 Finally, indoor particulate air pollution may also be harmful to vascular function. Brauner and colleagues'98 recently reported that reductions in 48-hour PM2 5 levels due to filtering of air in subjects' homes resulted in improved microvascular vas- cular function among elderly subjects. Nevertheless, changes in short-term ambient PM levels have not been linked with impaired conduit197 or microvascular'78 endo- thelial function in all studies. Even when the few negative studies are considered, the overall evidence supports the concept that ambient PM is capable of impairing vascular function, particularly among higher -risk individuals (eg, those with diabetes) and after traffic -related exposure (Table 6). Atherosclerosis A few cross-sectional studies have reported an association between measures of atherosclerosis in humans and long- term exposures to ambient air pollution levels. The fust study to demonstrate this relationship was an analysis of data from 798 participants in 2 clinical trials conducted in the Los Angeles area. A cross-sectional contrast in exposure of 10 µg/m3 PM2 5 was associated with an adjusted nonsignificant 4.2% (95% CI —0.2% to 8.9%) increase in common carotid intima -media thickness'99; however, in certain subgroups of patients, such as women, the effect was much larger (13.8%, 95% CI 4.0% to 24.5%). In a population -based sample of 4494 subjects from Germany,200 it was found that residential proximity to major roadways was associated with increased coronary artery calcification. A reduction in distance from a major road by half was associated with a 7% (95% CI 0.1% to 14.4%) higher coronary artery calcium score. Proximity to traffic was also related to an increased risk for peripheral artery disease in women but not men.201 In an analysis of 3 measures of subclinical disease (carotid intima -media thick- ness, coronary calcium, and ankle -brachial index) among 5172 adults from the Multi -Ethnic Study of Atherosclerosis, only common carotid intima -media thickness was modestly (yet significantly) associated with 20 -year exposure to PM2 5.202 In a related study from the same cohort, abdominal aortic calcium was associated with long-term PM2 5 exposure, especially for residentially stable participants who resided near a PM2.5 monitor.203 Although it appears that long-term exposure to higher levels of ambient PM might accelerate the progression of atherosclerosis, more investigations are needed (Table 6). Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2348 Circulation June 1, 2010 Heart Rate Variability Numerous studies have continued to explore associations between daily changes in PM air pollution exposure and alterations (typically reductions) in HRV metrics, putative markers of cardiac autonomic balance. 129•149,156.204-242 Recent observations in the Nonnative Aging Study cohort have shown strong effect modification of the PM-HRV relation- ship by obesity and genes that modulate endogenous oxida- tive stress or xenobiotic metabolism, such as glutathione S -transferase M1, methylenetetrahydrofolate reductase, and the hemochromatosis gene. 207,243,244 Additional findings suggest protective effects of statins, dietary antioxidants, and B vitamins, as well as omega-3 polyunsaturated fatty acids. 205,207,215,243,244 These results suggest that pathways that reduce endogenous oxidative stress have a protective effect that mitigates reductions in HRV due to ambient PM exposure. However, the overall results are not entirely consistent. Some studies have reported increases in HRV mediated by PM, specifically among younger healthy people and patients with chronic obstructive lung disease.156,208,216 Nevertheless, the general pattern suggests that PM exposure is associated with increased heart rate and reductions in most indices of HRV among older or susceptible individuals, such as those with obesity and the metabolic syndrome. Typically, time - domain measures (eg, standard deviation of normal RR intervals) and total power are reduced within hours after exposure. Most, but not all, pertinent studies have also found that the largest reduction in power is within the high - frequency domain. In sum, these observations provide some evidence that ambient PM air pollution exposure rapidly reduces HRV, a surrogate marker for a worse cardiovascular prognosis (Table 6). Although studies corroborating changes in autonomic activity by other methods (eg, microneurogra- phy or norepinephrine kinetics) have not been performed, the HRV findings are perhaps reflective of the instigation of a generalized cardiovascular autonomic imbalance due to rela- tively greater parasympathetic than sympathetic nervous sys- tem withdrawal. Cardiac Ischemia and Repolarization Abnormalities There has been limited direct evidence for the actual induc- tion of cardiac ischemia or repolanzation abnormalities in the electrocardiogram (ECG) by exposure to ambient levels of PM.223,245 Recent follow-up analyses from the initial ULTRA study (Exposure and Risk Assessment for Fine and Ultrafine Particles in Ambient Air)245 suggested that traffic -related combustion pollutants were most strongly related to the promotion of ST -segment depression among elderly non- smokers during exercise stress testing.246 Moreover, even very acute PM2_5 exposure within the past 1 or 4 hours has been associated with cardiac ischemia during exercise.247 New findings support these associations in elderly subjects248 and in patients with coronary artery disease in Boston.249 In the latter study, traffic -related PM was most strongly related to the incidence of ST -segment depression during 24-hour Holter monitoring, and the risk for ischemia was greatest within the first month after a cardiac event among patients with diabetes. Overall, there is a modest level of evidence that PM exposure can promote cardiac ischemia in susceptible individuals (Table 6). Epigenetic Changes There have been relatively few studies examining gene—air pollution exposure interactions, and most have done so while investigating a small number of loci for genetic polymorphisms. Although some studies have suggested greater air pollution susceptibility with one or another genomic polymorphism,207,243,244 few have evaluated the potential for epigenetic changes after exposures. Reduced levels of DNA methylation have been linked to aging, oxidative stress, and CVD. Recently, Baccarelli et a1250 have shown among 718 elderly participants in the Norma- tive Aging Study that short-term exposures (over 1 to 7 days) to PM2 5 and black carbon are associated with decreased "global' DNA methylation in long interspersed nucleotide elements. It was posited that oxidative stress from air pollution exposure could have interfered with the capacity for methyltransferases to interact with DNA or altered the expression of genes involved in the methylation process. This observed effect of pollution exposure; was analogous to changes seen with 3.4 years of aging m the cohort. Additional findings among workers in a furnace steel plant support these observations.251 Nevertheless, the mechanisms involved and the cardiovascular implications of these preliminary, although provocative, epigenetic changes require more investigation. Traditional Cardiovascular Risk Factors In addition to the fact that individuals with traditional risk factors are likely to be at higher risk for cardiovascular events due to PM exposure, air pollutants may also promote the development of these risk factors over a prolonged period of time. Few published studies have investigated this possibility. A report from the Multi - Ethnic Study of Atherosclerosis has demonstrated that residential proximity to major roadways was associated with a higher left ventricular mass index as measured by cardiac magnetic resonance imaging.252 The degree of increase was analogous to a 5.6 -mm Hg increase in sys- tolic BP among the study participants. This suggests that traffic -related exposures may have increased left ventric- ular mass by chronically elevating systemic arterial BP, a common cause of left ventricular hypertrophy. However, other mechanisms cannot be excluded, such as systemic inflammation and oxidative stress, which could potentially activate neurohormonal pathways (eg, ANS imbalance, renin -angiotensin system) that could directly mediate such a finding. In addition, a recent study of adults older than 30 years of age (n=132224) participating in the National Health Interview Survey reported a significant association between self-reported hypertension and estimated annual PM2.5 exposure using US EPA monitoring data.253 A 10-µg/m3 elevation in PM2_, was associated with an Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 7 0 • I] • Brook et al adjusted odds ratio of 1.05 (CI 1.00 to 1.10) for the presence of hypertension. The increase in risk was found only among non -Hispanic whites. These studies provide some initial evidence that longer-term PM exposures may augment the risk for developing chronically elevated BP levels or even overt hypertension. Brook et a1254 have also demonstrated a novel relation- ship between a metric of long-term traffic exposure (NO2 level by residence) and the odds of having the diagnosis of diabetes mellitus among patients in 2 respiratory clinics in Ontario, Canada. In women only, the odds ratio of diabetes was 1.04 (95% CI 1.00 to 1.08) for each increase of 1 parts per billion (ppb) of NO2. Across the interquartile range (4 ppb NO2), exposures were associated with nearly a 17% increase in odds for diabetes mellitus. The first biological support for this finding comes from a study in Iran that demonstrated that the previous 7 -day -long exposure to PM10 was independently associated with worse metabolic insulin sensitivity among 374 children 10 to 18 years of age .255 These findings suggest that the systemic proinflam- matory and oxidative responses due to long-term PM air pollution exposure could potentially increase the risk for developing clinically important aspects of the metabolic syndrome, such as hypertension and diabetes mellitus. Further studies in this regard are warranted. Evidence Summary Table 6 provides a consensus qualitative synopsis based on the expert opinions of the writing group members of the overall level of existing support, linking each surrogate or intermediate cardiovascular outcome with exposures to PM at ambient concentrations, based solely on the database of observational studies. Additional Epidemiological Findings and Areas of Continued Research Responsible Sources and Pollution Constituents Although PM concentration (mass per cubic meter) has been associated with cardiovascular events in numerous studies, the specific particulate constituents and the sources responsible remain less clear. Despite the fact that it is a difficult undertaking, several epidemiological stud- ies have attempted to identify the culprit components within the PM mixtures With regard to PM -associated inorganic ions (nitrate and sulfate), it has been suggested that the overall toxicological data do not clearly implicate these compounds as responsible for mediating the cardio- vascular health effects of PM2 5.256 Nevertheless, sulfate particles have been associated with cardiopulmonary mor- tality in the ACS and Harvard Six Cities studies.62.68 A recent time -series analysis among 25 US cities found that cardiovascular risk was increased when PM mass con- tained a higher proportion of sulfate, as well as some metals (aluminum, arsenic, silicon, and nickel).257 It is possible that these positive findings represent sulfate serving as a marker for an effect mediated by a toxic PM mixture derived from commonly associated sources (eg, Particulate Matter Air Pollution and CVD 2349 coal combustion). Nevertheless, a direct role for particle sulfate in causing cardiovascular events cannot be ex- cluded entirely.256 In California, short-term exposures to several different PM constituents that likely reflect combustion -derived particu- lates, including organic and elemental carbon and nitrates, were most strongly associated with higher cardiovascular mortality.258 Certain metals (zinc, titanium, potassium, and iron) and sulfate levels in the winter months were also positively related. Similarly, ambient levels of organic and elemental carbon have been most strongly linked among PM constituents with hospitalizations for CVDs in multipollutant models in a study among 119 US cities.2259 Finally, PM1_5 composed of higher levels of elemental carbon, along with the metals nickel and vanadium,48 has also been linked with greater risks for cardiovascular hospitalizations. 260 These results support that the chemistry or composition of the PM2 5 (eg, organic/elemental carbon and certain metals) along with the responsible source from which these mixtures are derived (eg, fresh combustion, traffic) may play important roles in determining the risk for cardiovascular events. However, the extent to which these constituents mediate specific responses, alone or together, and their importance beyond the concentration of PM, 5 mass alone represent an area of active research that requires more investigation to reach firm conclusions. Many experiments have demonstrated the especially toxic properties and strong oxidizing potential of the smallest particle sizes (eg, UFP) and of the specific chemical species typically rich within this size fraction (eg, transition metals, organic compounds, and semiquinones).261 Although some epidemiological evidence suggests that exposure to ultrafine compounds17 may be associated with higher cardiovascular risk (eg, an elevation of UFP count by 9748/cm3 has been associated with an increase in cardiovascular mortality of approximately 3% within 4 days in Erfurt, Germany262) and adverse responses, 158,159 there have been few such studies because they are challenging to conduct, for numerous reasons. Moreover, there are few UFP monitors, and the levels measured at regional sites may not accurately reflect an individual person's exposure because of marked spatial heterogeneity, because the concentrations are dominated by local point sources of fresh combustion (eg, roadways). This could help explain some of the previously negative study findings. 116 Similarly, coarse particulates between 0.25 and 1.0 µm in diameter may affect the cardiovascular system, 221.264265 and although the available data related to hard events and cardiovascular mortality have suggested a relation- ship,265.266 recent findings have been less consistent.1O4 In the most recent time -series analysis of 112 US cities, coarse PM was independently associated with elevated all -cause, stroke, and pulmonary, but not cardiovascular, mortality after controlling for PM2.5.43 Coarse PM was also not associated with either fatal or nonfatal cardiovascular events after controlling for PM2 5 levels in the Nurses' Health Study267 or the Women's Health Initiative cohort analyses.72 Additional research is required to establish whether there are independent health effects of the other Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2350 Circulation June 1, 2010 particulate size fractions beyond those posed by fine particles. On the other hand, PM2 5 mass concentration is the metric most consistently associated with cardiovascu- lar morbidity and mortality. It remains to be determined whether this reflects limitations of available data, the long-lived and regionally homogenous atmospheric nature Of PM25, that few studies have investigated the indepen- dent effects of the other sizes, difficulties in performing epidemiology studies with adequate UFP exposure esti- mates, or that specific constituents within the fine PM fraction (or another unidentified agent correlated with that fraction) are actually responsible for causing cardiovascu- lar events. Although particles <0.1 µm (ie, UFPs) do make up a small fraction of PM2 5 mass, the correlation between UFP particle number and total PM2 5 mass concentration is often weak. Because of their minute size, UFPs make up only a small portion of the total PM2 5 mass, even though they represent the largest actual number of particles within fine PM. They also have the highest surface area and a differing surface chemistry. Therefore, changes in the underlying UFP concentration do not likely account for or explain the linkages between PM2 5 mass concentration and cardiovascular events observed in large: multicity studies. The overall epidemiological evidence thus indi- cates that fine PM poses an independent cardiovascular risk and that any putative effects of these other size fractions cannot fully explain the observed PM2 5—cardio- vascular morbidity/mortality relationship. On the other hand, there is mounting evidence for a distinctive role played by motor vehicle traffic—related expo- sures in elevating cardiovascular risk. 108,111,268,269 Lipfert et a176.77 interpreted the results of their analysis of the Veterans Affairs hypertensive male cohort as suggesting that traffic density was a more "significant and robust predictor of survival in this cohort" than PM2_5. Analyses of the Oslo,81 Dutch,82 AHSMOG,74.75,88 French PAARC,79 and German women cohorts80 and related studies from areas in the United Kingdom,270 Canada,271 Norway,272 and Rome 273 found that measures that often indicate traffic -related exposure (NO2, NO., traffic density, and living near major roads) were also associated with increased mortality. Long-term 5 -year aver- age traffic -generated air pollution exposure has been associ- ated with an increased risk of fatal MI (odds ratio 1.23, 95% CI 1.15 to 1.32 per 31-µg/m3 increase in NO2) but not nonfatal MI in Stockholm County, Sweden.274 The results mirror the results of several cohort studies72,73 that found that air pollution exposures appeared to be more strongly linked with cardiovascular mortality than nonfatal events. Recently, an analysis from a cohort in the Netherlands demonstrated that several metrics of traffic -related air pollution exposure remained significantly associated with increased risk for cardiovascular events even after adjustment for higher levels of traffic noise .275 The effect of long-term traffic -related exposure on inci- dence of fatal and nonfatal coronary heart disease was recently assessed after adjustment for background air pollut- ants and cardiovascular risk factors in 13 309 adults in the Atherosclerosis Risk in Communities study.276 Interestingly, background chronic ambient PM2,5 concentrations were not related to the interpolated traffic exposure levels or to heart disease outcomes, which supports the highly localized nature of traffic sources of exposure. After 13 years of follow-up in 4 US communities, individuals residing within the highest quartile of traffic density had a relative risk of 1.32 (95% CI 1.06 to 1.65) for fatal and nonfatal heart disease events. Despite multiple statistical adjustments, the investigators also acknowledged the possibility for residual confounding as a potential source of bias. The specific traffic -related pollution components, such as UFP or gaseous -phase chemicals (eg, SVOCs), that are responsible for the positive findings among these studies remain unknown. The close proximity to road- ways within these epidemiological studies (eg, 400 m) required to observe an association with elevated cardiovas- cular risk, however, matches the atmospheric fate of these shorter -lived pollutants. The findings may thus suggest the existence of cardiovascular health effects mediated by spe- cific air pollutants rather than PM2.5 per se. There is room for improvement in assessment of traffic exposures in epidemi- ological research, and better approaches are now being incorporated into research projects, such as accounting for associated factors (eg, noise or spatial autocoirelation with socioeconomic status).275.277 Geographic differences in cardiovascular risk due to PM have also been observed across US regions, with more consistent or stronger effects observed in Eastern versus Western states.77,703,257 Differences between North American and European cities have also been reported.b1 PM exposures are typically, but not always,258 associated with larger effects during warmer months (spring through fall) than in the winter.45.103.257 Variations in pollution characteristics (eg, sulfate), time spent outdoors, air conditioning usage and particle penetration indoors, ambient temperature and mete- orology, and mobile (eg, diesel) or stationary (eg, coal combustion) sources of exposure may help explain these differences. Finally, variations in the cardiovascular risk posed by PM may also occur because of heterogeneity in the metric of exposure, such as personal versus background regional,25 indoor versus outdoor sources, and differences in intracity versus intercity gradients.69 A better understanding of the responsible constituents and sources is important and could potentially lead to more targeted and effective regula- tions. On the other hand, finding continued evidence that the adverse cardiovascular health effects cannot be linked con- clusively to a particular or specific chemical species or source of pollution but rather that they occur in response to a variety of exposure types or mixtures would support the present-day policy of reducing exposure to overall fine particulate mass to achieve public health benefits. Time Course and Concentration -Response Relationships Many studies have demonstrated that PM air pollution expo- sure does not simply advance the mortality by a few days of critically ill individuals who would have otherwise died (eg, mortality displacement or "harvesting"). 278,279 There also appears to be a monotonic (eg, linear or log -linear) concentration -response relationship between PM2.5 and mor - Downloaded from eirc.ahajoumals.org at University ofMichigan--AnnArbor on December 6, 2010 0 • 2 17 16 15 14 13 12 11 10 10 US cities, / all cause / i 10 Euro cities, cardio Brook et al Particulate Matter Air Pollution and CVD Harvard Six Cities, all cause Southwest states .! vs NMMAPS, all cause / •' ACS vs NMMAPS, / cardiopul. / ACS vs NMMAPS, `l Dublin, cardio all cause Utah Valley, all cause Dublin, all cause 10 Euro cities, all cause 20 3040 183 365 (6 mo) (1 yr) Time (days) tality risk observed in cohort studies that extends below present-day regulations of 15 µg/m3 for mean annual levels, without a discernable "safe" threshold .67,70,84 Cardiovascular risk due to particle exposure was also shown to extend below 15 µg/m3 in the recent analysis of the Women's Health Initiative Observational Study.72 This monotonic association supports the idea that any reduction in particulate pollution will translate into health benefits within a population of people, each with their own individual level of susceptibility. It also suggests that a larger decrease in PM2 5 exposures will produce a greater reduction in mortality. Finally, a recent analysis of the literature provided important new insights into the nature of the PM exposure -response relationship.280 The risk for cardiovascular mortality was shown to increase in a linear fashion across a logarithmically increasing dosage of inhaled fine -particle levels that ranged from ambient PM air pollution (-0.2 mg/d), through secondhand smoke (xl mg/d), to active smoking (200 mg/d). This means that the exposure response is extremely steep at very low PM levels (ie, ambient air pollution) and flattens out at higher concen- trations (ie, active smoking). This may help explain the seemingly incongruent and comparatively very high degree of cardiovascular risk posed by the much lower levels of PM exposure from ambient pollution and secondhand smoke versus the much higher doses due to active smoking. Thus, the cardiovascular system may be extremely sensitive to very low levels of PM inhalation as encountered with ambient pollution. At present, the underlying nature and full scope of the temporal -risk relationship posed by longer-term PM expo - 3653 (10 Yrs) 2351 Figure 2. Comparison of estimates of percent change in mortality risk associ- ated with an Increment of 10 µg/m3 in PM25 or 20 µg/m3 of PM10 orBritish Smoke (BS) for different time scales of exposure (log scale of approximate num- ber of days, updated and adapted from Pope281a) Euro indicates European; car- dio, cardiovascular disease; and car- diopul, cardiopulmonary. sures remain uncertain.2281 The writing group members did concur that the available epidemiological studies demonstrate larger cardiovascular risks posed by more prolonged expo- sures to higher PM levels than observed over only a few days (Figure 2). Cohort studies using Cox regression survival analyses (over months to years) are capable of evaluating a more complete portion of the temporal -risk relationship than time -series analyses over only a few days that use Poisson regression. However, given the lack of complete information, no conclusions could be drawn on the full magnitude of the augmented risk posed by chronic exposures, the time window (a few months versus decades) required to exhibit this enhanced risk, the underlying biological causes, the extent to which statistical differences between study types explain the variations in risk, and whether clinically relevant chronic CVDs are precipitated by chronic exposures. Some writing group members believe it is important to differentiate as 2 distinct issues the potentially greater effect of long-term exposures on increasing the risk for acute events (eg, cardio- vascular mortality) compared with the putative effect on initiating or accelerating the development of chronic CVD processes per se (eg, coronary atherosclerosis). As such, it is possible that the greater risks observed in cohort studies could be capturing the fact that repetitive exposures over months or years augment the risk for sudden cardiovascular events in susceptible people, without actually worsening an underlying "chronic" disease process. On the one hand, the available studies demonstrate that the majority of the larger risk -effect sizes posed by longer-term versus short-term exposures appear to be manifested within Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2352 Circulation June 1, 2010 only 1 to 2 years of follow-up. Extending the duration of follow-up increases cardiovascular risk, but to a progressively smaller degree over time (Figure 2). The discrepancy in the effect sizes among study types (eg, cohort versus time -series studies) could also reflect differences in statistical methodol- ogies or population susceptibilities. 282--284 Recent attempts to investigate this matter64.84 suggest that the risk for acute events associated with chronic exposures may be reasonably well estimated by only the most proximal l to 2 years of PM levels. The most recent time frames of exposure also explain a substantial portion of the excess cardiovascular risk ob- served in several cohort studies. 70.72,73,83 These findings bolster the argument that relatively rapid and pliable (and potentially reversible) biological responses, such as the insti- gation of plaque instability or the enhanced thrombotic potential caused by PM -mediated inflammation or endothe- lial dysfunction (which can occur and abate over only a few weeks to months), could explain the biology responsible for this greater relative risk. On the other hand, cogent alternative arguments can be made to explain the differences in relative risk between the cohort and time -series studies. The likely high correlation of a recent year's exposure levels with exposures over many years, as well as the uniform rank ordering of exposure severity over time among cities, can explain why only a short period of PM exposure assessment is required to understand the risk of longer-term exposures. In addition, no studies have evaluated the potential risks of exposure over decades or a lifetime. PM augments the ability of traditional risk factors to accelerate the development of atherosclerosis in experimental settings. As such, it is also plausible that long-term exposures may enhance cardiovascular risk to an even greater extent by increasing an individual's susceptibility for future cardiovas- cular events or acute exposures. In addition, the full extent of this possibility may not be illustrated by the limited follow-up period (4 to 5 years) of the majority of cohort studies. The writing group thus agreed that this important issue requires more investigation. It is also possible that these 2 explanations are not mutually exclusive. Furthermore, it cannot be concluded from avail- able information that a long period of time is required for reductions in PM levels to translate into a decrease in cardiovascular risk. On the contrary, reductions in second- hand smoke 285 and PM air pollution levels 64.84.90,95 appear to produce fairly rapid decreases in cardiovascular event rates, within a few months to years .284 At present, the available data do not allow for firm conclusions regarding the underlying biology and the full extent of the potentially nonuniform PM exposure—to— cardiovascular risk temporal relationship. Susceptibility to Air Pollution Exposure Susceptibility refers to a heightened risk for a particular cardiovascular end point or event to occur compared with the general population at the same concentration of P1V1 exposure. Typically, this is indicative of an underlying medical condi- tion (eg, diabetes) or personal characteristic (eg, old age) that causes this enhanced risk. This is in contrast to the term "vulnerability," which refers to a population of individuals at greater risk for more frequent or high levels of exposures. Earlier studies reviewed in the first AHA scientific state- ment' suggested that susceptible populations include the elderly; individuals with diabetes; patients with preexisting coronary heart disease, chronic lung disease, or heart failure; and individuals with low education or socioeconomic status. In the ACS study, current and previous smokers appew-ed to be at the same or greater degree of risk.67 Among more recent studies, the Women's Health Initiative also reported positive findings among active smokers and an elevated risk for cardiovascular mortality induced by PM2 5.72 Conversely, current smokers were found to be at no increased risk for cardiovascular mortality in response to PM2 5 exposure in the Nurses' Health Study.73 Thus, the effect modification of smoking status requires more investigation. The APHENA study of European and North American cities recently con- firmed that elderly and unemployed individuals are at higher risk of short-term PM exposure.61 In a multicity time --series study in Asia, women, the elderly, and individuals with lower education and socioeconomic status were also shown to be at elevated risk.286 A few additional studies have reported some evidence of susceptibility to short-term PM exposures among older individuals, people with diabetes, and those with a lower level of education. 287-219 Finally, a recent study illus- trated that present-day levels of PM2 5 likely increase the risk for a cardiac event within a few days of exposure principally (or even solely) among individuals with preexisting signifi- cant coronary artery disease, even if they are seemingly healthy (eg, without anginal symptoms). Patients without obstructive lesions on heart catheterization were not at any risk for PM2 5 -induced myocardial events over the short term 13 This is not surprising, because most acute cardiovas- cular events occur among individuals with underlying vul- nerable substrate (eg, unstable plaques) and not in individuals with normal coronary arteries. Obesity has been newly recognized as a possible suscep- tibility factor. Two cohort studies have shown that a greater body mass index enhances the susceptibility for PM -induced cardiovascular mortality, at least among women.72,73 Al- though individuals with diabetes showed a trend toward greater risk in the Women's Health Initiative,72 hypertension, high cholesterol, smoking, elderly age, education, and income did not alter the risk association. Overall, there appears to be little effect modification by race, hypercholesterolemia, or BP among the studies. Finally, sex may also be a risk -effect modifier. The particularly robust risk estimates of the 2 cohort studies that included only women,72,73 the fact that PM increased cardiovascular risk in female but not male partici- pants of the AHSMOG study,75 and the multicity time -series findings in Asia 286 suggest that women may be at greater risk for cardiovascular mortality related to PM. Further studies are needed to clarify whether obese individuals and women are indeed susceptible populations. Biological Mechanisms There has been substantial improvement in our understanding of the biological mechanisms involved in PM -mediated Downloaded from cire.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 a s • r� • Brook et al Particulate Matter Air Pollution and CVD 2353 PM or constituents In the circulation UFP, soluble metals Organic compounds I VaSculature vasoconstriction Endothelial dysfundion PM=mediated ROS t t3P, ? ,Atherosclerosis Blood 7 t Platelet aggregation �'�rrru�p s. "Systemic Q_ • .. spill-over Systemic Oxidative Stress and Inflammation Cellular inflammatory response (t activated WBCs, platelets, MPO) I Cytokine expression/levels (t IL -1(3, IL-6, TNF -a) ? t ET, histamine, cell microparticles, oxidized lipids; 4 anti -oxidants 1 1 Acute phase response t Adipokines -I sp t Clotting factors (PAi-1. Resisbn) - Fibrinogen, CRP Ac Ovated or Activated or ki lamed let hdkarned hear Oi�ct acfiw+a V83Culature Endothelial oetl dysfunctiontvasoconstrlction, ,IROS Atha wcierosis progressiontpiaque,v aWityy t Thrombogerwm*'(e.g. tissue factor) Met bollsm Insulin resistance; dystipidernia, impaired HDL function Wood f Coagulation, thrombosis; i fit dn*sis (e.g. PAH) ANS imbalance iSNS ! J�PSNS Vasculature Vasoconstriction Endothelial dysfunction Neural-mediaRec! ROS t BP Blood t Platelet•aggregation Heart i HRV I Heart rate t Arrhythmia potential Figure 3. Biological pathways linking PM exposure with CVDs. The 3 generalized intermediary pathways and the subsequent specific biological responses that could be capable of instigating cardiovascular events are shown. MPO indicates myeloperoxidase; PAI, plas- minogen activator inhibitor; PSNS, parasympathetic nervous system; SNS, sympathetic nervous system; and WBCs, white blood cells. A question mark (?) indicates a pathway/mechanism with weak or mixed evidence or a mechanism of likely yet primarily theoretical existence based on the literature. cardiovascular effects. Studies before 2004 were reviewed previously,' and only some are again discussed here for contextual background. A number of new experiments have demonstrated very rapid effects of air pollution, such as vascular dysfunction, which argues for the existence of pathways that convey signals systemically within hours of PM inhalation. On the other hand, there is also support for chronic biological effects, such as the promotion of athero- sclerosis. At the molecular level, persuasive evidence sup- ports an integral role for ROS -dependent pathways at multi- ple stages, such as in the instigation of pulmonary oxidative stress, systemic proinflammatory responses, vascular dys- function, and atherosclerosis. In sum, new studies continue to support the idea that inhalation of PM can instigate extrapul- monary effects on the cardiovascular system by 3 general "intermediary" pathways. These include pathway 1, the release of proinflammatory mediators (eg, cytokines, acti- vated immune cells, or platelets) or vasculoactive molecules (eg, ET, possibly histamine, or microparticles) from lung - based cells; pathway 2, perturbation of systemic ANS balance or heart rhythm by particle interactions with lung receptors or nerves; and pathway 3, potentially the translocation of PM (ie, UFPs) or particle constituents (organic compounds, met- als) into the systemic circulation (Figure 3). Exposure Considerations Animal and human exposure studies are discussed separately and apart from the effect of ambient PM because their methodologies and clinical relevancies vary widely. Con- trolled exposure studies involve exposing a subject to various size fractions of PM within a chamber connected to ambient air (concentrated or nonconcentrated) or a source of aerosol- ized particles. Virtual impactor systems that deliver concen- trated ambient particles (CAPs) from "real-world" ambient air are a commonly used approach for mimicking exposures to higher levels of ambient particles without requiring inva- sive methods or the generation of artificial particles.' Both a strength and limitation, however, is that CAPs can vary considerably from day to day in composition. Additionally, only certain particle size ranges are typically concentrated (eg, PM from 0.1 to 2.5 jum in the fine -CAP system), whereas Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2354 Circulation June 1, 2010 ambient air contains a mixture of particle sizes, volatile organics, and gases that are not concentrated (and can be lowered). Potential interactions between PM and gaseous copollutants on health end points are therefore excluded, unless the latter are reintroduced in an artificial fashion. Other methods of controlled -inhalation exposures include diesel engine exhaust (diluted and aged mixtures of high numbers of fresh combustion UFPs with vapor -phase components), road- side aerosols, and wood -burning sources. Regarding animal exposures, intratracheal instillation methods may sometimes be required because of the limited availability of inhalation exposure systems. Unfortunately, particle size and surface characteristics—mostly retained in inhalation systems with fresh sources of pollution and which may be important in influencing biological effects—are likely significantly altered in instillation systems or by methods that use previously collected particulate. However, the use of carefully modeled exposures (eg, deposition calculation) and the recognition that areas of "hot spots" containing markedly higher PM levels within the lung may occur even during normal inhala- tion make the results of these experiments potentially rele- vant.2 Further detailed discussions of exposure considerations are reviewed elsewhere.290 The protocol details vary considerably among the studies. Many aspects of exposure, including the duration, concentra- tion, PM size ranges and composition, and gaseous copollut- ants, are important to consider. A wide variety of outcomes may be anticipated depending on the biological pathways evoked by differing exposures. Moreover, there are multiple determinants of the subsequent physiological responses, in- cluding the time frames of investigation, preexisting suscep- tibility, animal models, and the details of the; outcomes investigated. All of these factors may explain some of the heterogeneity in the reported study results and must be taken into consideration when interpreting the findings. Animal Exposure and Toxicological Studies Studies that investigate the effects of exposure on susceptible animals (eg, those with preexisting cardiovascular or meta- bolic abnormalities) may be preferable in many circum- stances because of the increasing recognition that the path- ways underlying the biological effects of PM overlap (ie, modify and/or enhance) those of conventional cardiovascular risk factors. Such factors (eg, hypertension or atherosclerosis) may also be necessary or at least responsible for the evocation of a more readily observable or robust response. For example, in the context of systemic oxidative stress or inflammation, the cellular machinery for the generation of excess ROS and proinflammatory responses (eg, adhesion molecule and cyto- kine expression) is already primed or operational in suscep- tible animals. Pulmonary Oxidative Stress and Inflammation The molecular events responsible for triggering pulmonary oxidative stress and inflammation, along with the interactions between lung and immune cells, the inhaled PM, and the protective secretions (eg, surfactant, proteins, and antioxi- dants), are highly complex 4-6 as reviewed in detail elsewhere.290a.290b,414 In brief, size, charge, solubility, aggre- gation, ROS -producing potential, and chemistry play roles in determining the responses. These include the particle fate (eg, lung clearance versus retention rates), the nature of the PM -cell interactions (eg, immune versus lung cell uptake, host cell responses, and intracellular sequestration/location), and the dose (likely typically a small percentage of inhaled PM) and pathways of potential systemic transmission of PM or its constituents, such as in the circulation [free, intracellu- lar within circulating cells, (lipo)protein-bound] or via lym- phatic spread .4,5,29oa 2906 Because of their nano -scale size, UFPs may directly enter multiple lung cell types via nonph- agocytic pathways and adversely affect organelles, such as mitochondria.6.290a,290b Larger unopsonized fine particles are more typically taken up by phagocytes through interactions with innate immunity receptors such as MARCO (macro- phage receptor with collagenous structure) or other scavenger receptors .5,290,.2901, This may in fact be a protective mecha- nism that sometimes prevents harmful lung inflammation. Certain particle compounds may directly generate ROS in vivo because of their surface chemistry (eg, metals, organic compounds, and semiquinones) or after bioactivation by cytochrome P450 systems (eg, polycyclic aromatic hydrocar- bon conversion to quinones).6.2902,290b A particle surface or anions present on otherwise more inert particles may disrupt iron homeostasis in the lung and thereby also generate; ROS via Fenton reactions.291 Other PM constituents may do so indirectly by the upregulation of endogenous cellular sources (eg, nicotinamide adenine dinucleotide phosphate [NADPH]) oxidase)292.293 or by perturbing organelle function (eg, mito- chondria) by taken -up PM components.261 Particle stimula- tion of irritant and afferent ANS fibers may also play a role in local and systemic oxidative stress formation .294 Given the rich antioxidant defenses in the lung fluid, secondarily generated oxidization products of endogenous molecules (eg, oxidized phospholipids, proteins) or a reduction in endoge- nous antioxidants per se may be responsible at least in part for the state of oxidative stress in the lungs (along with instigat- ing the subsequent cellular responses) rather than ROS derived directly from PM and its constituents. Subsequent to oxidative stress, antioxidant and phase II defenses may be activated (eg, inducible nitric oxide syn- thase, glutathione) via transcription factor Nrf2-dependent pathways.261 When inadequate, pathological oxidative stress can initiate a variety of pulmonary inflammatory responses. For example, ROS in the lungs has been shown to augment the signal transduction of membrane ligand (eg, epidermal growth factor by disrupting phosphatases) or pattern - recognition receptors (eg, toll -like receptors [TLR])295-299 and/or stimulate intracellular pathways (eg, mitogen -acti- vated protein kinases) that lead to the activation of proinflam- matory transcription factors (eg, nuclear factor -KR) that upregulate expression of a variety of cytokines and clhemo- kines.261 Alteration in lung cell redox status may itself stimulate nuclear factor -KR. Biological components within coarse PM could also directly trigger inflammation (eg, nuclear factor -KR pathways) by binding to T1R2 or TLR4 receptors or other innate immune pattem-recognition recep- tors.297 It is also possible that other components of metal -rich Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 • • C C] • • Brook et al PM could instigate inflammatory pathways via TLR activa- tion directly or via the oxidation of endogenous biological compounds that then serve as TLR ligands.300 Finally, there is some evidence that PM can activate inflammatory mitogen - activated protein kinase signaling by angiotensin 11 receptor - dependent pathways.295 These inflammatory responses can also exacerbate the initial oxidative stress [eg, via upregula- tion of cellular NAD(P)H oxidase] and thus initiate a positive -feedback cycle. Available studies support important contributions to pul- monary inflammation from innate immune cells such as neutrophils and macrophages (TNF -a, IL-6), as well as from the adaptive immune system, such as T cells (IL-1, IL-4, IL-6, and II. -10). Although the dominant source of cytokines likely represents the alveolar macrophages and lung epithelial cells, the role of other innate and adaptive immune cells cannot be ruled out.299,301,302 Recently, myeloperoxidase activity was shown to increase after PM exposure in the same time course of appearance of cellular inflammation (primarily neutro- phils) in the lung.303 Gaseous components such as ozone may also amplify the toxicity of PM.304 Systemic Inflammation In the context of examining the cardiovascular effects of air pollution, it is important to consider the inflammatory medi- ators that are released from lung cells after contact with PM, because some could conceivably spill over to the general circulation or increase liver production of acute-phase pro- teins (eg, CRP, fibrinogen). An increase in circulating proin- flammatory mediators (eg, activated immune cells, cytokines) could thus serve as a pathway to instigate adverse effects on the heart and vasculature. Numerous experiments have dem- onstrated increased cellular and inflammatory cytokine con- tent, such as IL-6, II., -1p, TNF -a, interferon -y, and IL-8, of bronchial fluid and sometimes in circulating blood after acute exposure to a variety of pollutants.292,305-311 Critical roles for the elevations in systemic and pulmonary levels of IL-6 and TNF -a have been observed after PM exposure, typically coincident with pulmonary inflamma- tion.292,302,306,309,311-314 There is at least some evidence that the degree of pulmonary inflammation and systemic inflam- mation (IL-6) correlates with the elevation of systemic cytokines and systemic vascular dysfunction.314 In a 4 -week inhalation exposure to freshly generated diesel exhaust, IL-6 knockout mice did not demonstrate increased cellular inflam- mation or TNF -a in bronchial fluid, which implies a role for IL -6.315 Consistent with these findings, acute intratracheal exposure to PM10 resulted in an increase in IL-6, TNF -a, and interferon -y in the bronchial fluid.316 However, in this study, II. -6-/- mice showed roughly the same levels of TNF -a in bronchial fluid as wild -type mice, although interferon --y was decreased to control values.316 The results also suggested that lung macrophages play an important role, because depletion of these cells abolished the increases in some of the cytokines and systemic cardiovascular responses. Although our under- standing of the source of IL-6 and TNF -a and their involve- ment in the systemic inflammatory response after PM expo- sure remains incomplete, these and other experiments appear Particulate Matter Air Pollution and CVD 2355 to suggest that at least with PM, particles, alveolar macro- phages play a dominant role. 309,314,316 Among remaining uncertainties, the upstream signaling pathway responsible for the recognition of PM components that in turn produce the systemic inflammation has not been fully elucidated317; however, there is some evidence with other particulates and experimental models of lung injury that ROS generated by NADPH oxidase or pattern -recognition receptors may modulate some of these responses. 292,299,318 NADPH -oxidase knockout mice demonstrated significantly lower IL-6 and macrophage inflammatory protein -2 re- sponses to collected PM than wild -type mice.292 Extrapulmo- nary sources may also be involved in promulgating the systemic inflammation. PM2_5 exposure in a model of diet - induced obesity in C57131/6 mice for a duration of 24 weeks resulted in elevations in TNF -a and IL-6. In addition, there were increases in circulating adipokines, such as resistin and plasminogen activator inhibitor -1.319 The elevation in cyto- kines, thought to be derived from adipose sources, in addition to findings of adipose inflammation in that study, raises the possibility of additional systemic nonpulmonary sources of such cytokines. Systemic Oxidative Stress Numerous in vitro studies have demonstrated activation of ROS -generating pathways by PM incubation, such as NADPH oxidases, mitochondrial sources, cytochrome P450 enzymes, and endothelial nitric oxide synthase in cultured cells or in pulmonary and vascular tissue. 293,311,320-329 Similar to inflammation, the oxidative stress after PM inhalation may not always stay confined within the lungs.330 The sources of excess ROS within cardiovascular tissue may include circu- lating immune cells or cytokines, depletion of defense mech- anisms (eg, impaired high-density lipoprotein function), ox- idation of lipoproteins or other plasma constituents, 331 activation of ANS pathways,294 or circulating PM constitu- ents (eg, soluble metals, organic compounds) reaching the vasculature.261 Activation of ROS -dependent pathways mod- ulates diverse responses with far-reaching consequences, including vascular inflammation/activation, atherosclerosis, impaired basal vasomotor balance, enhanced coagulation/ thrombosis, and platelet activation.290b Recent experiments have indeed confirmed the existence of footprints or markers of oxidative stress within the cardio- vascular system in the in vivo context. Acute -exposure studies332 have shown a relationship between the vascular dysfunction in spinotrapezius microvessels and the release of myeloperoxidase from leukocytes into the vasculature within only hours after the pulmonary instillation of PM.332 Inter- estingly, an insoluble particle (TiO2) induced very similar effects. More long-term studies333 have demonstrated that 10 weeks of exposure to PM2 5 increased superoxide production in response to angiotensin II and resulted in upregulation of NAD(P)H oxidase subunits and depletion of tetrahydrobiop- terin in the vasculature. These effects had functional conse- quences in terms of increases in systemic vascular resistance and BP. In another investigation that involved apolipoprotein E -deficient (ApoE-/-) fed a high-fat diet, chronic exposure Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2356 Circulation June 1, 2010 to PM2 5 exacerbated vascular oxidant stress and promoted atherosclerosis progression.334 The proatherogenic effects of ambient UFPS331 versus PM2 5 in genetically susceptible ApoE-1- mice in a mobile facility close to a Los Angeles freeway have also been compared. Exposure to UFPs resulted in an inhibition of the antiinflammatory capacity of plasma high-density lipoprotein and greater systemic oxidative stress, as evidenced by increased hepatic malondialdehyde and upregulation of Nrf2-regulated antioxidant genes.331 Other experiments294 have suggested that ANS imbalance may play an important role in PM -induced cardiac oxidative stress. Pharmacological inhibition of the ANS could signifi- cantly reduce chemiluminescence in the heart after expo- sure.303 More recently, an upstream modulator, the transient receptor potential vanilloid receptor -1, within the lung was identified as central to the inhaled CAP -mediated induction of cardiac chemiluminescence .335 In these studies, capsaz- epine was able to abrogate ECG alterations in rats during the 5 -hour exposure, which suggests that neural ANS pathways are crucial. Thrombosis and Coagulation Earlier studies using intratracheal instillation of high concen- trations of diesel exhaust particles demonstrated the induction of lung inflammation, platelet activation, and increased pe- ripheral vascular thrombosis in both arteries and veins after photochemical injury.336,337 Thrombosis susceptibility was ascribed to direct passage of the instilled UFPs in the blood, because large polystyrene particles unlikely to cross the lung -blood barrier did not increase peripheral thrombosis. In a subsequent study, a persistent increase in thrombosis susceptibility to diesel exhaust particles was shown after 24 hours, an effect that was mitigated by pretreatment with sodium cromoglycate, which indicates that this response was secondary to histamine release from basophil degranula- tion.338 These same effects, however, were mimicked by 400 -nm polystyrene particles with a low likelihood of trans- gressing the pulmonary barrier, which implicates pulmonary release of histamine as a mediator of thrombosis at the later time point. Because histamine was increased in the plasma at 6 and 24 hours after exposure, and diphenhydramine miti- gated diesel PM -induced thrombosis at later time points but not at 1 hour, it was hypothesized that additional direct effects of PM constituents reaching the circulation may be respon- sible for the earliest prothrombotic effects.339 No increase in circulating von Willebrand factor was observed after instil- lation of both particles. Finally, pulmonary instillation of carbon nanotubes produced neutrophil lung influx 24 hours later. Circulating platelet -leukocyte conjugates were elevated 6 hours after exposure, whereas procoagulant microvesicular tissue factor activity and peripheral thrombotic potential were increased 24 hours later. Inhibition of P-selectin abrogated these responses, which demonstrates that rapid activation of circulating platelets by the pulmonary deposition of PM plays a vital role.340 This series of studies suggests that release of lung cell -derived mediators (eg, histamine) after several hours along with the more rapid activation of circulating platelets by lung inflammation via P-selectin-dependent processes may mediate distant system prothrombotic effects without necessarily inducing systemic endothelial damage. In a study using C57BL/6J mice, intratracheal PMIo particles rich in transition metals decreased bleeding, pro- thrombin, and activated partial thromboplastin time's and enhanced the levels of several coagulation factors as well as thrombosis times in response to experimental FeCl3 injury.316 This prothrombotic effect was mitigated in IL-6-'-- and macrophage -depleted mice, which suggests that IL-6. lung macrophages, and pulmonary inflammation are necessary initial steps. It is possible, however, that coarse -particle components (eg, endotoxin) could have been important mech- anistically via TLR activation. The effect of fine PM or UFPs per se requires more investigation. Chronic ambient exposure to PM,, has also been shown to increase tissue factor expression in macrophages and smooth muscle cells in atherosclerotic lesions. Complementary in vitro studies with cultured human smooth muscle cells and monocytes demon- strate dose-dependent increases in tissue factor in response to collected ambient particles.341 Other findings also support potential procoagulant and thrombotic effects of PM 342.343 These collective studies suggest that both short- and long- term PM inhalation can enhance thrombotic and coagulation tendencies, potentially via increases in circulating histamine and inflammatory cytokines and/or activated white cells and platelets. The plausibility of these pathways is supported by the well-recognized cross talk between inflammation and thrombosis.344 Potential additional roles for UFPs or soluble constituents that reach the circulation and directly enhance platelet aggregation or systemic oxidative stress (thus acti- vating the endothelium and blunting platelet-derived nitric oxide) require more investigation. Systemic and Pulmonary Hypertension Early animal studies suggested small or inconsistent effects of PM on BP,34$-347 sometimes dependent on the season348 of exposures. A potential explanation may be variations in experimental protocols, including differences in the delivery, duration, and composition of exposure and the methods used to measure BP. Moreover, PM by itself may represent a relatively weak stimulus but may act more robustly in concert with other predisposing factors to affect BP. Sun et x1333 recently demonstrated a significant interactive effect of fine - CAP exposure with the vasoconstrictor angiotensin II in rats. Preexposure to PM2_5 for a 10 -week period resulted in enhancement of its prohypertensive response measured con- tinuously by intra-arterial radiotelemetry. The exaggerated BP elevation was accompanied by endothelial dysfunction, including blunted endothelium -dependent vasodilation and enhanced vasoconstrictor reactivity, along with upregulation of NAPDH oxidase and Rho -kinase -signaling pathways. In vitro exposure to UFPs and PM2.5 was also associated with an increase in Rho -kinase activity, phosphorylation of myosin light chain, and myosin phosphatase target subunit. Pretreat- ment with the nonspecific antioxidant N -acetylcysteine and Rho -kinase inhibitors prevented these responses, which sug- gests an ROS -mediated mechanism for particle -mediated effects on vascular smooth muscle constriction. Further Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 • • • • C� U Brook et al studies corroborated the role of exaggerated Rho -kinase pathway activity in potentiating the hypertensive response to angiotensin ll in mice exposed to PM2.5.349 Moreover, parti- cle exposure augmented angiotensin -mediated cardiac hyper- trophy and collagen deposition. Blockade of Rho -kinase abolished these effects. These responses suggest that chronic PM2.5 exposure disrupts normal vascular homeostasis and vasoactive mediator balance through ROS -dependent mech- anisms in a manner that sensitizes the vessel toward vaso- constrictors. Activation of RhoA/Rho-kinase signaling path- ways appears to play an important mechanistic role. In conscious canines with implanted BP catheters, systemic arterial BP increased and baroreceptor sensitivity was rapidly altered over a few hours during CAP exposure.350 Interest- ingly, a -adrenergic antagonism abrogated the responses. The findings support a mechanistic role for acute activation of the sympathetic nervous system by inhaled particles. In a study with Wistar -Kyoto male rats, CAP exposure for 4 days upregulated ET -A receptor expression in the heart. This alteration was also weakly correlated with an increase in BP, which suggests a role for enhance ET activity.351 PM has also been demonstrated to alter the release of ET -1 and ET -3 from the lungs.352 Elevation in pulmonary vascular resistance and pulmonary arterial pressure, which suggests constriction of the pulmonary vessels, has also been demonstrated in re- sponse to respirable carbon black particles.353 Recently, ultraf ne carbon particles were shown to increase BP in spontaneously hypertensive rats 1 to 3 days after a 24-hour exposure.354 This response occurred concomitant with in- creased ET -1 messenger ribonucleic acid levels in lung tissue and small elevations in plasma renin concentration and angiotensin I and H in the systemic circulation. These findings further support the idea that ET may play a role in cardiovascular responses to PM exposure and suggest that activation of the renin -angiotensin system may also be involved. It is not clear whether the elevated circulating ET levels reflect increased release from the lungs and whether this mediates a systemic vasoconstrictor response. Alterna- tively, the increase may be more indicative of enhanced vascular tissue activity of these systems. Longer-term expo- sures of carbon black for 4 weeks in Sprague -Dawley rats has also been shown to significantly increase systolic BP con- comitant with increases in serum levels of IL-6 and CRP.355 Finally, in vitro exposure to soluble and insoluble compo- nents of UFPs induces constriction in isolated pulmonary arterial rings and activates intracellular signaling pathways such as phosphorylation of extracellular signal—regulated kinase -1/2 and p38 mitogen -activated protein kinase in pul- monary endothelial cells. These effects were antagonized by losartan, and several metal components (copper and zinc) could replicate the responses.295 This suggests a possible role for activation of angiotensin II receptor pathways relevant for the maintenance of vasomotor tone and smooth muscle constriction after inhalation of metal constituents within PM. In sum, the studies demonstrate that long-term PM expo- sures over a period of weeks are capable of enhancing vasoconstrictive responsiveness of the vasculature (eg, in- creased Rho -kinase activity and reduced nitric oxide bioavail- ability) by inflammatory and ROS -dependent cell -signaling Particulate Matter Air Pollution and CVD 2357 pathways. Shorter -term exposures over several hours to days may lead to vasoconstriction and increased pulmonary and systemic BP by pathways dependent on enhanced ET or angiotensin II signaling. Lung cells may release ET into the systemic circulation and thus increase its systemic activity, or the vascular ET system may be relatively upregulated be- cause of increased ROS or reduced nitric oxide. Activation of the renin -angiotensin system may also occur because of systemic oxidative stress or inflammation or as a conse- quence of ANS imbalance. The very acute increase in BP that occurs concomitant with the inhalation of particles or within only minutes to hours after exposure appears to be mediated by autonomic imbalance that favors a relative activation of the sympathetic nervous system. No study has evaluated the effect of air pollution on renal sodium handling or long-term pressure natriuresis mechanisms, which are fundamental to the generation of chronic hypertension. Vascular Dysfunction and Atherosclerosis Many early experiments demonstrated the capacity of PM constituents to blunt nitric oxide—dependent dilation and enhance vasoconstrictor tone in ex vivo vascular studies because of excess ROS formation.' The first in vivo experi- ment demonstrated the proatherosclerotic actions of intratra- cheal PM10 instillation.356 More recently, the pulmonary instillation of several different PM types was shown to rapidly impair microvascular endothelium -dependent vasodi- lation within days, likely by proinflammatory or ROS - dependent mechanisms (eg, myeloperoxidase).332 Several animal studies have now demonstrated that long-term expo- sure to ambient PM2 5, by use of ambient -exposure facilities without direct pulmonary instillation, not only causes endo- thelial dysfunction but also accelerates the progression of atherosclerosis. Sun et a1334 demonstrated that exposure of atherosclerosis -prone ApoE-1— mice to environmentally rel- evant levels of CAP, derived from regional northeastern PM2.5, for 6 months in conjunction with a high-fat chow diet potentiated plaque development and heightened vascular inflammation (CD68+ macrophage infiltration and inducible nitric oxide synthase expression) and oxidant stress. The atherosclerotic plaque progression was also accompanied by alterations in vasomotor tone, including decreased endothe- lium -dependent vasodilation and heightened vasoconstriction to adrenergic stimuli. Importantly, the normalized average PM2 5 concentration over the entire period was 15.2 µg/m3, which approximates the annual NAAQS. Similar findings were reported in other chronic CAP exposures that involved an ApoE-1— model.357 However, exposures to a double - knockout model of ApoE-deficient and low-density lipopro- tein receptor—deficient mice increased plaque cellularity, reflective of inflammation, but did not enhance plaque burden. It is possible that the atherosclerotic severity of this phenotype precluded the observation of more subtle effects of CAP exposures. Intratracheal instillation of UFP can acutely impair aortic endothelium -dependent vasodilation.358 Moreover, repeated 10 -week-long endotracheal dispersion of UFP carbon black increased atherosclerosis in low-density lipoprotein receptor— Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2358 Circulation June 1, 2010 knockout mice.359 This occurred without evidence of sys- temic translocation of particles into the cardiovascular tis- sues. UFP inhalation by use of exposure facilities has also recently been shown to augment atherosclerosis, perhaps to a greater degree than PM25. When investigating the effects of different PM size fractions, Araujo et a1331 compared the proatherogenic potential of exposure over 40 days to ambient particles <0.18 µm versus PM2.5 in ApoE-1- mice. UFPs caused more adverse cardiovascular responses (eg, systemic oxidative stress, impaired high-density lipoprotein function) and greater potency in accelerating atherosclerotic lesion formation, although PM2 5 did demonstrate qualitatively sim- ilar effects. Recent studies have also demonstrated that PM exposure likely promulgates systemic atherosclerosis by mechanisms that overlap those of other conventional cardio- vascular risk factors.360 Intratracheal instillation of PM,o particles caused a rapid impairment in endothelium - dependent vasodilation, stimulation of bone marrow -derived cells, and increased migration of monocytes into atheroscle- rotic plaques.361,362 Systemic inflammation (IL-6) was also related to the degree of endothelial dysfunction.314 Finally, the most compelling evidence for rapid impairment in nitric oxide bioavailability being directly involved in the origin of PM -induced endothelial dysfunction was demonstrated re- cently. Both fine -PM and UFM inhalation for only a few hours in normal rats blunted agonist -stimulated nitric oxide production within the microvasculature, measured by direct electrochemical sensors, concomitant with an observed im- pairment in vasomotor relaxation. Inhibition of myeloperox- idase or NADP(H) oxidase partially restored normal nitric oxide bioavailability and endothelial function, which suggests a role of activation of these endogenous radical --generating enzymes in this biological response.363 Potentially relevant adverse vascular effects of nonparticu- late PM components should not be discounted. 'There may also exist some synergy between vapor phase, gas, and particle constituents in relation to instigation of cardiovascu- lar responses. Recently,364 it was demonstrated in apoE-1- mice that whole gasoline engine exhaust over 1 or 7 days increased vascular messenger ribonucleic acid expression of matrix metalloproteinase (MMP) -2 and MMP -9. Levels of ET -1 and ROS were similarly increased. The vascular ROS and MMP -2 elevations were attenuated by tempol. Endothe- lial receptor antagonism ameliorated the vascular expression of MMP -2, MMP -9, and ROS. In separate experiments, diesel exhaust exposure to rats for 5 hours augmented ET -induced vasoconstriction, potentially via a blunting of ET -B -induced nitric oxide release.365 The findings suggest that exposure to a fresh mixture of PM, gases, and vapors may play a role in rapidly triggering atherosclerotic plaque vul- nerability via ROS and ET -dependent upregulation of MMP levels. Some studies suggest that predisposed animals may be more susceptible to air pollution -mediated vascular dysfunc- tion. Diesel exhaust particles delivered by intraperitoneal injection impaired nitric oxide -dependent vasodilation only in apoE-1- mice with atherosclerosis and not in healthy control animals.366 Aortas from prediabetic rats were found to be more susceptible to repeated exposures to oil combustion particles in causing noradrenergic -mediated constriction and impaired endothelium -dependent vasodilation.367 Taken together, the available studies suggest that short - and long-term particle exposures (including PMro, PM2 5, and UFP) can impair conduit and resistance arterial endothelium - dependent vasodilation. Chronic exposures have been shown to be capable of promoting atherosclerosis progression and enhancing plaque vulnerability. The underlying mechanisms likely involve vascular sequelae of systemic inflammation (due to interactions with innate immune cells and cytokines) or exaggerated oxidative stress pathways. Excess vascular ROS and inflammation will impair endogenous vasodilator bioavailability (eg, nitric oxide), enhance vasoconstrictor tone (eg, ET), and chronically activate multiple intracellular pathways that promote atherosclerosis. 368-370 Heart Rate Variability Some of the earliest indications of systemic effects of PM came from ECG studies in rats.371 In general, reductions in several measures of HRV have been shown.372-376 Most of the recent research has focused on exploring the roles of suscep- tibility and exposure characteristics. Decreases in heart rate and HRV indices have been reported to be pronounced in senescent mute, which indicates that aging may be a suscep- tibility factor.353 Using an anesthetized model of postinfarc- tion myocardium sensitivity, Wellenius and colleagues=177 did not demonstrate an effect of 1 hour of CAP exposure on heart rate or spontaneous ventricular arrhythmias. In contrast, in a post -MI heart failure model in Sprague -Dawley rats, diesel exhaust emissions reduced HRV in both healthy and heart failure groups and increased the incidence of premature ventricular contractions. Studies in mice have also indicated a potential role for transition metals and nickel in HRV alterations376 and provide initial clues on the PM components that could influence autonomic tone 48 Some beginning insight into the neural pathways inNolved has been reported recently. PM -induced ECG changes in rats were shown to be prevented by inhibiting the transient receptor potential vanilloid receptor in the lungs. This sug- gests that the relevant neural mechanism that leads to alter- ations in HRV or heart rhythm may be induced by activation of receptor-mediated autonomic reflexes in the lung.335 Cir- culating particle constituents or inflammatory mediators in- teracting with myocardial ion channels or electrophysiology did not appear to be a pertinent mechanism, at least in these studies.335 However, it is unknown whether similar rnecha- nisms can account for the HRV changes observed in humans, and a more detailed understanding of the anatomic pathways involved is required. Finally, it remains unclear whether the changes in cardiac HRV are actually caused by or merely illustrate an underlying alteration in ANS balance. Experi- ments that clearly define the direct contribution of sinnpa- thetic and parasympathetic nervous system activities (eg, microneurography, norepinephrine spillover rates, or auto- nomic receptor or ganglionic blockade) are needed. MI and Arrhythmia PM exposure can increase experimental infarct size and potentiate myocardial ischemia and arrhythmias in experi- Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 11 • 0 • • • Brook et al mental MI models. Relatively high concentrations of intra- tracheal UFP instillation induced pulmonary inflammation and doubled MI size in mice."' Conscious dogs exposed to fine CAP for several days experienced greater ST -segment changes during transient coronary artery occlusion.378 These studies suggested that particulate -related changes in myocar- dial blood flow may be responsible, a hypothesis recently supported by experiments in chronically instrumented dogs exposed to fine CAP before transient occlusion of the left anterior descending artery. PM exposure was associated with a small but significant decrease in total myocardial flow, especially in the ischemic zone, and increases in coronary vascular resistance without an alteration in rate-pressure product .379 The abnormalities were inversely related to PM mass, particle number, and black carbon concentration. Exposure to residual oil fly ash increases arrhythmia frequency in rats with preexisting premature ventricular complexes, which suggests that PM sensitizes ischemic myocardium to abnormal automaticity372; however, CAP had no effect in rats .3110 Nevertheless, the data suggest that PM exposure may potentially be capable increasing the sensitivity of the myocardium to ischemia, likely by impairing myocar- dial blood flow and perfusion. In theory, this could play a role in enhancing the propensity for ventricular arrhythmias. Insulin Resistance Recently, Sun et a1319 exposed C5713L/6 mice fed high-fat chow to fine CAP or filtered air for 24 weeks. Mice exposed to PM2_5 exhibited marked worsening of whole-body insulin resistance, systemic inflammation (increased IL-6 and TNF - a), and higher levels of adipokines, such as resistin and plasminogen activator inhibitor -1. PM25 increased visceral adiposity and inflammation (F4/80+ cells), with stromal vascular cells expressing higher TNF -a and IL-6 and lower IL-10 levels. Exposure also induced insulin -signaling abnor- malities and reduced phosphorylation of Akt and endothelial nitric oxide synthase in aortic tissue, accompanied by abnor- malities in vascular relaxation to insulin. Additionally, there was evidence that PM2 5 exaggerated adhesion of monocytes in mesenteric microvessels, culminating in accumulation in visceral adipose. These intriguing findings suggest that longer-term exposure to PM air pollution may promote the chronic development of insulin resistance, obesity, and the metabolic syndrome. Controlled -Exposure Studies in Humans Several new human exposure studies have been published, a few of which have even included patients with CVD or risk factors. Similar to the animal studies, large variations among the exposure protocols, measured outcomes, and subject susceptibilities likely explain much of the differences among findings and must be considered when interpreting the results. Systemic Inflammation Controlled human exposure studies have measured the effects on circulating inflammatory markers such as CRP, IL-6, and TNF -a. In many of these single -episode short-term exposures, Particulate Matter Air Pollution and CVD 2359 no overt changes in plasma cytokine levels were observed after CAp381-383 or diesel exhaust.345,3114-386 Similarly, CRP levels have not consistently been found to increase in the time frame and context of most of these studies. 313,3&'-386 However, there have also been some positive findings. Increases in IL -6313 and TNF -a 24 hours after exposure to diesel exhaust in healthy adults have been reported. High levels of ambient particles can stimulate the bone marrow to enhance the release of neutrophils, band cells, and monocytes into the circulation, which causes a cellular inflammatory response.387.388 Some controlled -exposure studies corroborate the existence of a cellular proinflammatory response that manifests as increases in circulating white blood cell or immune cell counts. In 1 study, increased peripheral ba- sophils in healthy older adults were noted 4 hours after a 2 -hour exposure to fine CAP.389 In a similar study, increased white blood cell counts were observed in healthy young adults 12 hours after exposure.381 Recently, investigators observed an increased in total white blood cell and neutrophil levels immediately after a 2 -hour exposure to CAP in downtown Toronto, Ontario, Canada.390 Conversely, de- creases in blood monocytes, basophils, eosinophils, and CD54 and CD 18 adhesion molecule expression on monocytes after exposure to ultrafine carbon (10 to 50 ttg/m) among exercising asthmatic individuals and healthy adults have also been reported.391 The authors suggested in the latter study that these results may represent the sequestration of these cells in tissue compartments such as the lung or vasculature, where there may be selective expression of the corresponding receptors for these ligands.362 However, other recent human clinical studies have found no association between peripheral blood cell counts and exposure to fine PM or UFPs such as zinc oxide,392 ultrafine carbon,393 or diesel exhaust. 313.384,385 More subtle, yet physiologically relevant or functional proinflammatory changes may be overlooked by the measure- ment of circulating cytokines or cell counts alone in human studies. Peretz et a1394 recently evaluated gene expression using an expression array in monocytes after 2 hours of exposure to diesel exhaust. Although initially a small study, 10 genes involved in the inflammatory response were mod- ulated in response to exposure (8 upregulated, 2 downregu- lated). These findings will need to be reproduced in larger studies and raise the possibility that functional changes in inflammatory cells may occur without discernible changes in their levels in the peripheral circulation.394 In sum, the findings from controlled human exposures do not demonstrate a robust inflammatory response; however, they have been limited by the fact that they are, by necessity, of short duration and relatively low concentration. Addition- ally, the results do not preclude an effect of higher exposures, the presence of more subtle responses, or alterations in other cellular inflammatory pathways not measurable by circulat- ing markers. Systemic Oxidative Stress The demonstration of systemic oxidative stress is difficult in human studies. Nonetheless, a few studies have reported positive findings. These include an increase in urinary excre- Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2360 Circulation June 1, 2010 tion of free 8 -iso -prostaglandin -2a among healthy adults after a 4 -hour exposure to concentrated wood smoke 395 and an increase in plasma antioxidant capacity 24 hours after a 1 -hour exposure to diesel exhaust in a group of healthy volunteers.313 The investigators speculated that systemic ox- idative stress after exposure may have been responsible for this upregulation in antioxidant defense .313 Other investiga- torS394 have observed significant differences in expression of genes involved in oxidative stress pathways due to diesel exhaust exposure. Brauner et a1167 recently investigated the effect of ultrafine traffic particles on oxidative stress—induced damage to DNA in healthy young adults exposed to low concentrations of ambient urban particles (PM25 and PM 10-2s mass of 9.7 and 12.6 µg/m3, respectively) in an exposure chamber above a busy road with high traffic density. The authors observed increased levels of DNA strand breaks and formamidopynmidine-DNA glycosylase sites in monocytes after exposure to PM but no changes in the DNA repair enzyme 7,8-dihydro-8-oxoguanine-DNA glycosylase. Simi- lar to their previous findings with ambient levels, 168 the results suggest that short-term exposure to UFPs may result in damage to DNA. This may occur through oxidative stress pathways, although there was no increase in messenger ribonucleic acid levels in heme oxygenase -1, a gene known to be regulated by Nrf2, a transcription factor regulated by oxidative stress.396 Moreover, more recent observations by the same investigators failed to demonstrate significant bi- omarker signals for lipid or protein oxidative damage after similar near -roadway exposures.178 Although not entirely consistent, the available studies demonstrate that acute expo- sure to PM, perhaps even at ambient levels, may be capable of inducing acute systemic oxidative stress in human subjects under certain circumstances. The assays used to assess the footprint of systemic "oxidative stress" or damage may also play a significant role in the results. Thrombosis and Coagulation Several new studies of controlled human exposure have evaluated the effects of PM on hemostatic markers (eg, factor VII, fibrinogen, platelet count, D-dimer, and von Willebrand factor). Although some of these studies have not observed changes after acute exposures,392 others have reported in- creases in fibrinogen levels at 8 to 24 hours after exposure to CAP.311,397 Mills and colleagues384,385 recently demonstrated a significant effect of diesel exhaust on fibrinolytic function in response to intermittent exercise both in healthy men and in men with coronary heart disease. In both groups of volunteers, bradykinin -induced release of tissue plasminogen activator was observed to decrease compared with filtered air at 6 hours after exposure to diesel exhaust. These perturba- tions in tissue plasminogen activator release did not persist 24 hours after exposure.313 In a randomized, controlled crossover study involving "at -risk" metabolic syndrome patients, no changes in plasminogen activator inhibitor -1 were noted over a 24-hour duration; paradoxically, a decrease in von Wille- brand factor was noted in this study.398 In a similar experi- ment conducted in healthy adults, diesel exhaust had no effect on D-dimer, von Willebrand factor, CRP, or platelet counts compared with filtered air up to 22 hours after exposare.386 Other investigators 395 recently evaluated the effect of wood smoke on markers of coagulation, inflammation, and lipid peroxidation in young healthy subjects. Serum amyloid A and the ratio of factor VIII to von Willebrand factor, an indicator of an increased risk of venous thromboembolism, were increased at 4 hours after exposure.395 Samet et a1383 reported an association between various coagulation markers and exposure to ultrafine, fine, and thoracic coarse CAP among healthy young adults. Although exposure to coarse CAP did not result in significant changes in hemostatic variables, the overall trend suggested a prothrombotic effect. Exposure to UFPs increased D-dimer levels, whereas fine -CAP effects tended to increase fibrinogen, similar to previously reported findings.381 The measurement of blood levels of coagulation factors or biomarkers of thrombosis could potentially miss a relevant biological effect at the vascular wall. Recently, ex vivo thrombus formation was assessed by use of the Badimon chamber after controlled exposures to dilute diesel exhaust in healthy volunteers.399 This protocol measures thrombus for- mation in native (nonanticoagulated) whole blood triggered by exposure to a physiologically relevant substrate, under flow conditions that mimic those found in diseased coronary arteries. It may therefore provide a superior estimate of actual in vivo conditions related to thrombosis potential. Interest- ingly, dilute diesel exhaust exposure increased thrombus formation within 2 hours, in association with increased platelet activation (ie, increased circulating platelet -monocyte aggregates and soluble CD40 ligand). Taken together, these new studies have provided additional evidence that short- term exposure to PM at near -ambient levels may have small yet potentially significant effects on hemostasis in humans. Whether direct interactions of circulating PM constituents with platelets, activation of platelets due to lung inflammation or secondary to elevated systemic cytokine levels, or an increase in procoagulant factors (eg, fibrinogen) as an acute- phase response to inflammation (or a combination of these pathways) is responsible warrants attention in future studies. Arterial BP Although several studies have evaluated the BP response to acute exposures, many inconsistencies in results have been reported.400 This must be considered in the context that BP was not the primary outcome of interest in most studies, nor was it typically assessed with adequate sophistication. In one of the earliest studies, PM2 5 increased systolic BP in healthy subjects but decreased it in asthmatic ind ividuals.401 Three other controlled studies did not report changes among healthy adults .343,402.403 However, in a more detailed reanalysis of the changes in BP during the actual period of exposure to CAP plus ozone, Urch et a1404 found a significant increase in diastolic BP of 6 mm Hg. The magnitude of response was associated with the concentration of organic carbon within PM2.5.405 Recent follow-up studies redemonstrated an acute prohypertensive response during the inhalation of CAP in 2 separate cities .390 The PM2.5 mass during exposure and decreases in several HRV metrics were associated with the Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 0 L-] r� �J • 0 0 Brook et al magnitude of the short-lived diastolic BP elevation. This suggested that the most plausible mechanism for this acute response was CAP -induced ANS imbalance that favored sympathetic over parasympathetic cardiovascular tone. Whether this reaction occurred because of a generalized stress response, as a consequence of specific soluble PM constituents directly altering central nervous system activity, or via altered ANS reflex arcs due to the interaction of inhaled particles with lung receptors/nerve endings remains to be elucidated. The effect of inhaled particulates on BP has also been investigated in several other recent controlled human expo- sure studies. Two new studies assessed BP changes after a 1 -hour exposure to diesel exhaust. Mills et a1384 found a 6 -mmHg increase in diastolic BP 2 hours after exposure, which was of marginal statistical significance (P=0.08); however, this trend did not persist for 24 hours '384 nor was it found among patients with coronary artery disease.385 The available data to date suggest that short-term exposure to PMZ 5 or diesel exhaust is capable in certain circumstances of rapidly raising BP. The most consistent and largest effects were seen concomitant with the inhalation of particles. Thus far, the most likely mechanism for such rapid hemodynamic responses appears to be ANS imbalance. However, it is possible that reductions in nitric oxide bioavailability that modulate basal arterial tone toward vasoconstriction or increases in ET among other hemodynamically active molecules (eg, angiotensin II) also play a role in some circumstances. Vascular Dysfunction The first controlled human exposure study related to vascular function reported that CAP plus ozone exposure caused acute conduit arterial vasoconstriction in healthy adults.' Endothe- lium -dependent and -independent vasodilation remained in- tact. Recent follow-up experiments determined that PM,.,, not ozone, was responsible for the adverse vascular effects. However, in these subsequent and larger experiments, fine - CAP exposure did prove capable of diminishing conduit artery endothelium -dependent vasodilation 24 hours (but not immediately) after exposure.390 Postexposure PM2 5 mass and TNF -a level were both associated with the degree of endo- thelial dysfunction, which suggests that systemic inflamma- tion induced by higher levels of particles was likely respon- sible. Finally, the CAP -induced endothelial dysfunction occurred during exposures in Toronto, Canada, but not Ann Arbor, Mich, which suggests that the composition of the particles is probably an important determinant of the vascular responses. An acute alteration in vascular function/tone after short- term controlled PM air pollution exposure was corroborated recently.406 In 27 adults (10 healthy adults and 17 with the metabolic syndrome), a 2 -hour exposure to dilute diesel exhaust caused a dose-dependent constriction of the brachial artery and elevation in plasma ET level without impairing endothelium -dependent vasodilation. Contrary to the hypoth- esis that metabolic syndrome patients would show greater effects, vasoconstriction was greater in magnitude among the Particulate Matter Air Pollution and CVD 2361 healthy participants. In an additional study, 2 -hour exposure to UFPs composed of elemental carbon impaired peak fore- arm blood flow response to ischemia 3.5 hours later. There were no other vascular changes or alterations at other time points. BP was also not affected.407 Several recent studies have also shown that dilute diesel exhaust can impair peripheral resistance vessel responses to acetylcholine, bradykinin, and nitroprusside 6 hours after exposure .384 The blunted responses to acetylcholine persisted for 24 hours in healthy adults.373 In contrast, bradykinin and sodium nitroprusside—mediated vasodilation and bradykinin - induced acute plasma tissue plasminogen activator release were not altered 24 hours later. In subsequent studies, patients with stable coronary artery disease exposed to dilute diesel exhaust for 1 hour during intermittent exercise demonstrated reduced bradykinin -mediated tissue plasminogen activator release; however, microvascular endothelial function was not impaired.385 This may be related to some degree of preexist- ing endothelial dysfunction in these patients. However, exercise-induced ST -segment depression and ischemic bur- den were significantly greater during diesel compared with filtered air exposure. These important findings experimen- tally highlight that PM air pollution exposure can trigger, or augment existing, myocardial ischemia extremely rapidly (in fact, concomitant with exposure). Reduced coronary flow reserve (that was not observed or resolved at the time of the postexposure brachial artery studies) due to rapid alterations in coronary microvascular function may have contributed to the acute myocardial ischemia. Alternatively, acute ANS imbalance induced by diesel exhaust inhalation may have acutely altered coronary tone and impaired myocar- dial perfusion. In a study that exposed healthy young adults to 100 µg/m3 of diesel exhaust for 2 hours,$64 it was recently demonstrated that this air pollution mixture acutely raised plasma ET -1 and MMP -9 expression and activity within 30 minutes. These results corroborate the animal data that even short-term exposures can rapidly alter factors, such as MMP activity, that are mechanistically linked with causing atherosclerotic plaque disruption (and thus acute MI). The increase in ET levels also corroborates previous studies406 that showed that diesel exhaust can acutely affect important endogenous reg- ulators of vasomotor tone. Controlled air pollution exposures have not always been shown to impair endothelial function or vasomotor tone. Despite an increase in exhaled 8-isoprostane concentrations that suggested pulmonary oxidative stress, fine CAP did not affect brachial flow—mediated dilation or basal diameter in northern Scotland exposures .3112 However, the PM2,5 con- sisted of relatively inert ambient sea -salt particles and was extremely low in combustion -derived sources. This is in contrast to the particle chemistry in the investigators' previ- ous diesel exposure studies that showed positive find- ings.408•409 Moreover, 24-hour exposure to ambient pollution shunted into a chamber next to a busy street did not impair microvascular endothelial function in 29 healthy subjects, as assessed by digital tonometry.778 This exposure to near - roadway ambient air, which consisted of ambient UFP and PM2_5, did not alter biomarkers of inflammation, hemostasis, Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2362 Circulation June 1, 2010 or protein and lipid oxidation. The authors speculated that the relatively low concentrations of UFP numbers and PM mass or the young, healthy status of the subjects could explain the null findings. Taken together, these studies suggest that brief PM exposure can trigger conduit arterial vasoconstriction, possibly in relation to increased ET activity or augmented sympathetic ANS tone. Under certain circumstances, conduit and resistance arteriole endothelium -dependent vasodilation can also be impaired within a few hours. This abnormality is more likely due to reduced nitric oxide bioavailability as a consequence of systemic proinflammatory and oxidative responses; however, alternative mechanisms and endogenous vasoactive pathways have not been fully explored. It is also apparent that the composition, source, and concentration of pollution, along with the susceptibility of the human subjects, play important roles in determining the vascular effects of acute air pollution exposure. Heart Rate Variability The results of several new controlled human exposure studies provide limited evidence to suggest that acute exposure to near -ambient levels of PM may be associated with small changes in HRV. There are at least 4 studies to support this. In the first study, healthy elderly individuals experienced significant decreases in HRV immediately after exposure.233 Some of these changes persisted for at least 24 hours. Gong et a1410 studied healthy and asthmatic adults exposed to coarse CAPS with intermittent exercise. HRV was not affected immediately after the exposure but decreased in both groups at 4 and 22 hours after the end of the exposure; greater responses were observed in nonasthmatic individuals.410 In another study, healthy elderly subjects and patients with chronic obstructive pulmonary disease were exposed to ap- proximately 200 µg/m3 CAP and filtered air for 2 hours with intermittent mild exercise. HRV over multihour intervals was lower after CAP than after filtered air in healthy elderly subjects but not in subjects with lung disease. A significant negative effect of CAP on ectopic heartbeats during or after CAP exposure relative to filtered air was noted in the healthy subjects, whereas the group with pulmonary disease experi- enced an improvement during or after CAP relative to filtered x.389 Other investigators recently compared the; effects of 2 -hour exposures with intermittent exercise to ultrafine (av- erage concentration 47 µg/m), fine (average concentration 120 µg/m3), and coarse (average concentration 89 µg/rn) CAP among healthy subjects.383 In both the ultrafine and coarse studies, a crossover design was used in which each subject was exposed to both PM and filtered air. In the case of the fine -PM study, subjects did not serve as their own control but were exposed to either PM or filtered air. Thoracic coarse fraction CAP produced a statistically significant de- crease in the standard deviation of normal -to -normal heart rate 20 hours after exposure compared with filtered air. No statistically significant effects on HRV were observed after exposure to UFPs as measured during controlled 5 -minute intervals. However, the authors did observe a significant decrease in the standard deviation of normal -to -normal heart rate after exposure to UFPs based on an analysis of the Table 7. Summary of Level of Evidence Supporting Global Biological Pathways and Speck Mechanisms Whereby PM25, Traffic -Related, or Combustion -Related Air Pollution Exposure Can Affect the Cardiovascular System Animal Studies Human Studies General "intermediary" pathways whereby PM inhalation can instigate extrapulmonary effects on the cardiovascular system Pathway 1. Instigation of TTT T ,r T systemic promflammatory responses Pathway 2 Alterations in T T T systemic ANS balance/activity Pathway 3. PM and/or T r associated constituents directly reaching the systemic circulation Specific biological mechanisms directly responsible for triggering cardiovascular events Vascular dysfunction or T T T T T vasoconstriction Enhanced thrombosis or T T T T coagulation potential Elevated arterial BP T T T T Enhanced atherosclerosis T T P or plaque vulnerability Arrhythmias T ,� The arrows are not indicators of the relative size of the association but represent a qualitative assessment based on the consensus of the writing group of the strength of the mechanistic evidence based on the number and/or quality, as well as the consistency, of the relevant studies T T T Indicates strong overall mechanistic evidence T T Indicates moderate overall mechanistic evidence. T Indicates some but limited or weak available mechanistic evidence. Blank indicates lack of evidence 24-hour measurements. No differences were reported in HRV with fine -PM exposures. Although some controlled -exposure studies have reported either no acute changes390 or, on occasion, increases in HRV metrics in subsets of individu- als 208,393,401 these studies generally demonstrate that acute PM exposure is capable of reducing HRV. More consistent reductions have been found among older adults (compared with younger subjects or those with lung diseases, who show mixed responses) and perhaps with exposures to larger parti- cles.233,389 Whether pulmonary ANS reflex arcs are activated by the deposition of PM within the lung or whether other pathways are responsible for these physiological changes in human expo- sure studies requires more investigation. Evidence Summary and Contextual Framework for Biological Mechanisms 0 Table 7 provides an outline of the level of evidence support- ing the generalized intermediary pathways and specific mech- anisms whereby PM exposures can be capable of eliciting Downloaded from circ.ahajoumals org at University of Michigan --Ann Arbor on December 6, 2010 • 0 • Brook et al cardiovascular events. At the molecular level, oxidative stress as a critically important cause and consequence of PM - mediated cardiovascular effects has a sound experimental basis. 261,2906,294,319,333,334,345-349,351,361-364,411 At the integrated physiological level, the collective body of evidence continues to support the existence of 3 general pathways (Figure 3). Some of these responses, such as systemic inflammation (via pathway 1), likely require antecedent pulmonary oxidative stress or inflammation in order to be initiated Others, including ANS imbalance (via pathway 2) and PM or its constituents reaching the systemic circulation (via pathway 3), may not. Although PM -associated metals412 and certain UFps261.413-415 might be capable of translocating into the blood stream, some studies have been negative in this regard. 355,416 Many issues related to this pathway are contro- versial and require resolution .416 These include the relevance of the dosages delivered to cardiovascular organs, the conse- quences of particle constituent modifications after interac- tions with lung tissue/fluids and plasma components, the means of transport within the circulation (eg, protein bound or within cells)'417 and the time course and ultimate sites of PM sequestration. It is also possible that increases in some vasoactive mediators or molecules with adverse effects on cardiovascular tissue, such as ET -1,351-354 may occur in the lung and systemic circulation without the need for antecedent lung inflammation. Moreover, the 3 general pathways repre- sent a simplification of complicated biological processes. They may not be mutually exclusive, may overlap tempo- rally, and likely exhibit synergies in causing manifest cardio- vascular disease events. Many of the biological pathways are also known to exhibit mutual interactions (eg, inflammation with thrombosis/coagulation and with autonomic function). The pathways are also likely to be principally active at differing time points (eg, more rapid cardiovascular effects of autonomic imbalance than systemic inflammation) and likely vary in importance in relation to different durations of exposure and in causing different cardiovascular sequelae. The chemical characteristics and sizes of inhaled PM may also determine the pathways activated. As opposed to UFPs or some particulate components or chemicals, larger fine and coarse PM are not likely transported into the circulation to any large degree and therefore are more apt to require intermediary pathways to cause extrapulmonary effects. It may also be that surface -bound components may be delivered into the circulation, whereas larger particles themselves serve as a means to deliver the responsible constituent into the pulmonary tree. The hyperacute physiological responses that occur minutes to hours after PM inhalation are likely mediated principally via pathways 2 and 3. These include ANS -mediated changes (eg, elevated BP, arrhythmias, and vasoconstriction), along with direct effects of circulating PM constituents on platelets (eg, procoagulant and thrombotic changes) and the endothe- lium (eg, oxidative stress and vasoconstriction). These re- sponses are liable to be the dominant mechanisms responsible for the actual triggering of acute cardiovascular events. Clinically meaningful effects undoubtedly become manifest only in the context of a susceptible patient, typified by the individual with "vulnerable plaque" in the case of acute Particulate Matter Air Pollution and CVD 2363 coronary syndromes or strokes, "vulnerable myocardium" in the context of arrhythmias, or the "vulnerable circulation" in the context of a heart failure patient at risk for circulatory overload. On the other hand, the biological consequences of systemic inflammation, such as activated white cells and elevated cytokines (via pathway 1), typically require longer periods. Their penultimate effect is the induction of a chronic underlying vulnerable milieu that leads to atherosclerotic plaque vulnerability, enhanced coagulation/thrombotic and arrhythmia potential, and impaired basal vasomotor balance. These actions thereby predispose individuals for future car- diovascular events, particularly when they occur in conjunc- tion with traditional risk factors or prompt susceptibility to the acute biological actions (via pathways 2 and 3) of later air pollution exposures. This hypothetical segregation of the biological effects of PM exposure as acute or chronic and into the broad pathways is artificial. It is useful in the broad context of understanding potential pathways; however, there is no doubt a large degree of overlap among the mechanisms and the timing of physio- logical responses. This is most aptly conveyed as the influ- ence of "acute on chronic" actions of exposure. For example, the activation of circulating platelets by the pulmonary deposition of particles or lung inflammation (eg, by P- selectin—dependent pathways, histamine, or IL-6) could oc- cur within hours and more rapidly than typical of the other consequences of inflammation (eg, progression of atheroscle- rosis). In the presence of a vulnerable or eroded coronary plaque due to long-term air pollution exposure, this sudden prothrombotic tendency could instigate an acute ischemic event (alone or in conjunction with other effects of short-term PM exposure via pathways 2 and 3). Furthermore, the epidemiological cohort studies demonstrate a larger relative risk for increased cardiovascular -related mortality than for morbidity. 72,73,227,274 If this is a true biological response and not simply a statistical phenomenon or a shortcoming of the available data, it not only suggests that exposures are capable of triggering acute cardiovascular events but that PM air pollution may also exaggerate their severity even if they would have otherwise occurred for reasons unrelated to air pollution. Therefore, exposure to PM could also be respon- sible for promoting fatal over nonfatal events. Conclusions and Recommendations A wide array of new studies that range from epidemiology to molecular and toxicological experiments have provided ad- ditional persuasive evidence that present-day levels of air pollutants contribute to cardiovascular morbidity and mortal- ity. Although not unexpected given the numerous and hetero- geneous nature of the published studies, all findings related to every single cardiovascular end point have not been consis- tent. However, the overall weight of scientific evidence now supports several new conclusions since the 2004 statement. These consensus points are given below by the AHA writing group after considering the strength, consistency, and coher- ence of the epidemiological findings, as well as in the context of evaluating the extent of the studies that provided related mechanistic support. Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 2364 Circulation June 1, 2010 • The preponderance of findings indicate that short-term exposure to PM2 5 over a period of a few hours to weeks can trigger CVD -related mortality and nonfatal events, including myocardial ischemia and MIs, heart failure, arrhythmias, and strokes. • The increase in risk for acute PM2 5 -associated cardiovas- cular morbidity and mortality is principally among suscep- tible, but not necessarily critically ill, individuals. Several studies suggest that susceptible individuals at greater risk may include the elderly, patients with preexisting coronary artery disease, and perhaps those with diabetes. Recent data suggest that women and obese individuals might also be at higher risk. • Most studies support the idea that longer-term PM2 5 exposures increase the risk for cardiovascular mortality to an even greater extent than short-term exposures. Because most studies have focused on mortality data, the effect of long-term exposures on nonfatal cardiovascular events is less consistent and requires more investigation. • The PM21 concentration—cardiovascular risk relationships for both short- and long-term exposures appear to be monotonic, extending below 15 µg/m3 (the 2006 annual NAAQS level) without a discernable "safe" threshold. • Long-term exposure to elevated concentrations of ambient PM2_, at levels encountered in the present-day environment (ie, any increase by 10 µg/m3) reduces life expectancy within a population probably by several months to a few years. Given that PM2 5 is most strongly associated with cardiovascular deaths in the cohort studies, the reduced life expectancy is most likely predominantly due to excess cardiovascular mortality. • The available studies are suggestive that reductions in PM levels decrease cardiovascular mortality within a time frame as short as a few years. • Many potential biological mechanisms exist whereby PM exposure could exacerbate existing CVDs and trigger acute cardiovascular events (over the short term) and instigate or accelerate chronic CVDs (over the long run). Experimental support is increasingly strong for several mechanisms, which lends biological plausibility for the epidemiological findings. • The existing evidence suggests that PM air pollution is capable of augmenting the development and progression of atherosclerosis. There is some support for a potential effect on several other chronic CVDs, including hypertension, heart failure, and diabetes. • Most recent studies support the conclusion that the overall absolute risk for mortality due to PM exposure is greater for cardiovascular than pulmonary diseases after both short- and long-term exposures. There are several additional areas worthy of highlighting in which the study results are reasonably consistent but in which the writing group believed further research was required to formulate firm conclusions. • Although there is only limited epidemiological evidence directly linking UFPs with cardiovascular health prob- lems,262 the toxicological and experimental exposure evi- dence is suggestive that this size fraction may pose a particularly high risk to the cardiovascular system. The likelihood of health effects and the causal pathways medi- ated specifically by UFP exposure have been debated among experts recently.418 Future research may help to more fully elucidate whether particles within the ultrafine size range (0.001 to 0.1 pm) and/or their constituents are more harmful to the cardiovascular system or pose a relatively greater cardiovascular risk than particles between 0.1 and 2.5 µm in diameter. • Similarly, many studies have found a strong association between metrics of traffic -related air pollution exposure and elevated cardiovascular risk. Whether this represents the harmful effects of UFPs or diesel exhaust particulates, major components of the traffic mixture, or other pollution components is unclear. Diesel and UFPs possess toxic properties that instigate harmful biological responses in experimental models. However, the particle size fraction(s) and roles played by other copollutants (gases, VOCs, SVOCs) within the traffic -related mixture have not been fully elucidated. Nevertheless, traffic -related pollution as a whole appears to be a specific source associated with cardiovascular risk. It likely poses a major public health burden, regardless of a putative higher toxicity, because of the commonness of exposure in modern society (eg, ac- counting for —60% of daily UFP exposure; http:// www.catf.us/projects/diesel/). • The importance of other specific sources, regional differ- ences in pollution composition, and other specific constit- uents remains less clear. However, toxicological studies have identified several transition metals (eg, iron, vana- dium, nickel, copper, and zinc), organic carbon species, semiquinones, and endotoxin as specific PM -related com- ponents capable of prompting oxidative stress and inflam- mation and thus likely imparting biological harm. Some source -apportionment studies also demonstrate that atten- tion should be given to these compounds as being among the most likely mediators of clinical CVD. More studies are required in this regard to clarify this issue and to better define these and other potentially responsible constituents and sources. • Although the focus of the present statement is on PM, we recognize that other au pollutants may also pose cardio- vascular risk alone or in conjunction with fine -particle exposure. In this context, we believe additional research is necessary to make firm conclusions regarding the indepen- dent cardiovascular risks posed by several gaseous pollut- ants (eg, ozone and NO2). Although ozone has been linked to increased cardiopulmonary mortality,50 strokes,126 and MIS419 in some short-term studies, long-term exposure was not associated with cardiovascular mortality after account- ing for PM in a recent analysis. 17 The recent finding that small changes in low levels of ambient carbon monoxide concentrations are related to cardiovascular hospitaliza- tions also merits further exploration.420 • Several secondary aerosols (eg, nitrate and sulfate) are often associated with cardiovascular mortality; however, whether these compounds are directly harmful ar are surrogate markers of toxic sources of exposure requires Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 • �1 LJ J • • 0 Brook et al more investigation. Similarly, the current literature re- garding the independent cardiovascular risks posed by coarse particles is mixed, with most recent findings not supporting an association after accounting for the effects of PM2 5,a3,72,104 Several recent cohort studies and intermediate end-point experiments suggest that obese individuals (and/or those with the metabolic syndrome) may be a susceptible popu- lation at greater risk for cardiovascular events due to PM2 5 exposure. This is a tremendously important public health issue to corroborate because of the enormous and growing prevalence of obesity worldwide. This updated review by the AHA writing group corroborates and strengthens the conclusions of the initial scientific state- ment. In this context, we agree with the concept and continue to support measures based on scientific evidence, such as the US EPA NAAQS, that seek to control PM levels to protect the public health. Because the evidence reviewed supports that there is no safe threshold, it appears that public health benefits would accrue from lowering PM2 5 concentrations even below present-day annual (15 µg/m3) and 24-hour (35 µg/m3) NAAQS, if feasible, to optimally protect the most susceptible populations. Evaluations of the effectiveness of such efforts would be warranted as well. Within the frame- work of attempting to establish causality between associated variables in epidemiological studies, there are several gener- ally accepted "aspects" that have been evaluated (the follow- ing phrases in italics per the Bradford Hill criteria)421: With regard to cardiovascular mortality and PM2 5 exposure, there is a consistent association that satisfies both a temporal and exposure -response relationship. There is coherence of find- ings among several fields of science, including toxicology, human and animal exposures, and different types of epide- miological studies and time frames of exposure. Rigorous experiments demonstrate multiple plausible biological mech- anisms. Finally, natural experiments have confirmed that a change (ie, reduction) in exposure produces a change (ie, decrease) in cardiovascular mortality. In this case, specificity of outcomes and strength of the observation are less pertinent, because PM exposure could be capable of causing multiple different types of events (eg, MIs, arrhythmias, and heart failure exacerbations), and the overall cardiovascular mortal- ity relative risk posed for any single individual is expected to be small. Nevertheless, given the ubiquity of exposure, the overall public health consequences can be substantial and observable in population- or large cohort—based studies. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and has been strengthened substantially since publication of the fust AHA scientific statement.' At present, no credible alternative explanation exists. These conclusions of our independent review are broadly similar to those found in the EPA's Integrated Science Assessment for Particulate Matter final report (http:// cfpub.epa.gov/ncea/cfi-n/recordisplay.chn?deid=216546). In summary, the AHA writing group deems that PM2_5 exposure Particulate Matter Air Pollution and CVD 2365 is a "modifiable factor contributing to cardiovascular mor- bidity and mortality." Clinical Recommendations Several precautionary recommendations can be made for healthcare providers who interact with individuals who are at risk for CVDs. Although they have not been clinically tested or proven to reduce mortality, they are practical and feasible measures that may help to reduce exposures to air pollution and therefore potentially lower the associated cardiovascular risk. Moreover, a recent observational study found that patient awareness of air quality indices and media alerts along with health professional advice can significantly affect re- ported changes in outdoor activity to avoid exposure to air pollutlon.422 • Evidence -based appropriate treatment of the traditional cardiovascular risk factors should be emphasized. This may also lessen the susceptibility of patients to air pollution exposures. • All patients with CVD should be educated about the cardiovascular risks posed by air pollution. • Consideration should also be given to educating patients without CVD but who are at high risk (eg, the elderly, individuals with the metabolic syndrome or multiple risk factors, and those with diabetes). • Part of patient education should include the provision of information regarding the available sources (local and national newspapers [USA Today], EPA World Wide Web site [http://aimow.gov/], and The Weather Channel and its World Wide Web site [http://www.weather.com/1) that provide a daily EPA Air Quality Index. • On the basis of the forecast Au Quality Index, prudent recommendations for reducing exposure and limiting ac- tivity should be provided based on the patient's level of risk. A list of such recommendations is provided on the EPA World Wide Web site (http://aimow.gov/). For exam- ple, when the Air Quality Index for PM is "unhealthy" (151 to 200), then the recommendations are as follows: "People with heart or lung disease, older adults, and children should avoid prolonged or heavy exertion. Everyone else should reduce prolonged or heavy exertion." The action recom- mendations are as follows: "You can reduce your exposure to particles by 1) planning strenuous activity when particle levels are forecast to be lower, 2) reducing the amount of time spent at vigorous activity, or 3) choosing a less strenuous activity (eg, going for a walk instead of a jog). When particle levels are high outdoors, they also can be - high indoors. Certain filters and room air cleaners are available that can help reduce particles indoors." Practical recommendations to reduce air pollution expo- sure should be given to at -risk patients. Although unproven to reduce cardiovascular events, there are a number of prudent and feasible measures, including reducing optional or unnecessary exposures. Additional measures could include eliminating or reducing nonman- datory travel to highly polluted regions and avoiding exposures or outdoor activities (eg, exercising, commut- Downloaded from circ.ahajoumals.org at University of Michigan --Ann Arbor on December 6, 2010 2366 Circulation June 1, 2010 ing) during highly polluted times (eg, rush hours) or in proximity to major sources of pollution (eg, roadways, industrial sources). Choosing to exercise indoors with windows closed and using efficient air conditioning and filtering systems may be prudent for certain high-risk patients, particularly during peak pollution periods. Indeed, not only can central air conditioners reduce the indoor exposure level to PM from outdoor sources, there is some evidence that they might reduce the risk for cardiovascular hospitalizations associated with higher ambient pollution levels .423 If travel/commutes cannot be avoided, maintaining optimal car filter systems, driving with windows closed, and recycling inside ve- hicle air may help reduce PM exposures (http://www. catf.us/projects/diesel/).424,425 However, at present, no specific recommendations regarding the appropriateness of undertaking more aggressive mea- sures, even those shown to provide some benefits in a few studies (eg, wearing facemasks, installing PM filters in households), can be made based on the limited evidence. Similarly, although measures that decrease long-term PM exposures may produce even greater cardiovascular health benefits than the provided recommendations that focus on reducing short-term exposures, no specific recommendations (eg, moving to less polluted regions) can be prudently made at this time given the limited evidence. We acknowledge that occupational and indoor sources along with secondhand tobacco smoke are additional significant sources of personal PM exposures that should be avoided or reduced as much as possible. Finally, in developing nations, reducing exposure to indoor cooking sources of PM and air pollution from biomass combustion is a major issue of concem.426 Additional sug- gestions are available on the EPA World Wide Web site. Finally, although the existing evidence supports a causal relationship between PM2 5 and cardiovascular mortality, we acknowledge the importance of continued research in areas of controversy and uncertainty to further understand the full nature of this issue. Although numerous insights have greatly enhanced our understanding of the PM -cardiovascular rela- tionship since the first AHA statement was published,' the following list represents broad strategic avenues for future investigation: Mechanistic Studies • Better describe the physiological relevance in humans and the fundamental details of the mechanisms underlying the intermediate general mediating pathways (ie, PM or con- stituent transport into the circulation versus effects of inflammatory cytokines or activated immune cells versus ANS imbalance or other pathways) through which PM inhalation might mediate cardiovascular effects remote from the site of pulmonary deposition. • Understand the clinical significance and relative impor- tance of the observed biological responses (eg, vascular dysfunction, thrombosis, arrhythmia, ANS imbalance) in relation to the various causes of PM -mediated cardiovas- cular morbidity and mortality. • Examine the efficacy of preventive measures (eg, patient education) and treatment modalities (eg, statins, antioxi- dants, fish oil, treatment of traditional risk factors, and reducing exposures by engineering controls, including filtration, personal protection via facemasks, or behavior modification) on cardiovascular health outcomes. • Investigate the interaction between preexisting traditional cardiovascular risk factors (eg, diabetes, hypertension) and PM exposure, as well as the potential of air pollutants to exacerbate or worsen these risk factors. Determine the extent to which treatment of such factors (eg, with statins, aspirin, or angiotensin-converting enzyme inhibitors), es- pecially among patients with known CVD, may modify the risk associated with PM exposure. • Describe the biological effects of acute on top of chronic exposures (eg, synergistic effects versus reduced susceptibility to acute exposures due to augmented protective mechanisms). • Determine the ability of long-term exposure to precipitate the development of chronic diseases, including clinically relevant atherosclerosis, hypertension, diabetes, and other vascular, metabolic, renal, or neurological diseases. Epidemiological and Exposure Studies • Expand our knowledge related to the "responsible" PM pollution constituents (eg, metals, organic compounds, sermquinones, endotoxin, and VOC and SVOC compounds), size fractions (eg, UFPs), sources (eg, traffic, power genera- tion, and biomass combustion), and mixtures of pollutants. • Investigate the cardiovascular health implications and im- portance of regional and intracity differences in composi- tion and combinations of pollutants. • Better understand the effects of mixtures of ambient pollutants (ie, potential synergism between PM and gas- eous or vapor -phase pollutants such as ozone). • Investigate the feasibility and utility of quantifying; risk coefficients (concentration -response functions) according to PM source or relevant indices of pollutant mixtures, as a function of susceptibility (eg, age, preexisting disease), for reliable application in integrated, multipollutant risk assessments. • Investigate the relative importance of various time frames of exposure in relation to PM causing cardiovascular events, including the relevance of epochs not well described, such as ultra -acute peak PM excursions (eg, 1 to 2 hours) and exposures of intermediate duration (eg, 1 to 12 months). • Better document the time course and specific cardiovascu- lar health benefits induced by reductions in PM. • Better define susceptible individuals or vulnerable populations. • Determine whether any "safe" PM threshold concentration exists that eliminates both acute and chronic cardiovascular effects in healthy and susceptible individuals and at a population level. Acknowledgments We would like to thank Robert Bard Consulting for reviewing and editing the manuscript and Tom Dann from Environment Canada and Joseph Pinto from the US EPA for assistance in the preparation of Table 1. Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 :7 Brook et al Particulate Matter Air Pollution and CVD 2367 • Disclosures Writing Group Disclosures Writing Group Member Employment Research Grant Other Research Support Speakers' Bureau/ Honoraria Expert Witness Ownership Interest Consultant/ Advisory Board Other Robert D. University of Electric Power Research Instrtutet, None None None None None None Brook Michigan EPAt; Harvard University, School of None California None None None None Kaufman Washington Public Healtht, NIEHSt, Pfizert Air Arum University of PI on NIH study "Cardiovascular toxicity None None None None None None Bhatnagar Louisville of environmental aldehydes"t Board* Jeffrey R. University of None None None None None None None Brook Toronto, and CVDt; NIHt Murray A Environment PI on a component of an NIH/NIEHS None None None None None None Mittleman Canada program project grant evaluating the Ana V. Universrty of EPAt; 1st EPA STAR grant to study the None None None None None None Diez -Roux Michigan effects of long-term PM exposures on Annette Peters Helmholtz Zentrum subdinicai atherosclerosis and None None None None None None Munchen (German inflammatory markers in MESA; #2 is a Research Institute subcontract to the University of for Environmental Washington to participate in a Health) long-term study of air pollution and progression of atherosclerosis, also in MESA Fernando Centers for Disease American Lung Association*, NIH*; Emory None None None None None Holguin Control and Pan-American Health Organization in University* Prevention/Emory conjunction with EPA* University Yuling Hong American Heart None None None None None None None III Association# Joel D • University of Health Effects Institute*; NIH/NIEHS*; None California None None None None Kaufman Washington US EPA*; NIEHS Discovery Center Study Air David University of focused on air pollution and CVDt None Resources None None None None Siscovick Washington funded by EPAt; NIEHS Discovery Board* Russell V University of None None None None None None None Luepker Minnesota and CVDt; NIHt Murray A Beth Israel PI on a component of an NIH/NIEHS None None None None None None Mittleman Deaconess Medical program project grant evaluating the Laurie Whitsel Center/Harvard effects of ambient air pollution on None None None None None None University CVDt Annette Peters Helmholtz Zentrum Co -PI on the Rochester Particle Center None None None None None None Munchen (German funded through the EPAt, European Research Institute Uniont for Environmental Health) C. Arden Pope Brigham Young None None None None None None None III University Sanjay Ohio State None None Takeda* None None None None Rajagopalan University David University of MESA AIR (ancillary study to MESA) None None None None None None Siscovick Washington funded by EPAt; NIEHS Discovery Center Study focused on air pollution and CVDt; NIHt Sidney C. University of North None None None None None None None Smith, Jr Carolina Laurie Whitsel American Heart None None None None None None None Association This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all members of the writing group are required to complete and submit A relationship is considered to be "signifiranf' If (1) the person receives $10 000 or more during any 12 -month period, or 5% or more of the person's gross income; or (2) the person owns 5% or more of the voting stock or share of the entity, or owns $10 000 or more of the fair market value of the entity A relationship is considered to be "modest" if it is less than "significant" under the preceding definition *Modest tSign'dicant. tDr Hong is currently with the Centers for Disease Control and Prevention, Atlanta, Ga Downloaded from circ.ahajournals.org at University of Michigan --Ann Arbor on December 6, 2010 2368 Circulation Reviewer Disclosures June 1, 2010 Other Research Speakers' Ownership ConsultanUAdvisuy Reviewer Employment Research Grant Support Bureau/Honoraria Expert Witness Interest Board Other Michael Brauer Doug Dockery Mark Frampton University of British Columbia Harvard University University of Rochester Jonathan M. University of Southern Samet California Health Canadat; British Columbia Lung Association[ National Institute of Environmental Health Sciences[, Health Effects Instltutet National Institutes of Healtht, American Petroleum Institute[, US EPAt None None None None None None None None None None None None None None MESA -Air Study (US EPA, None University of Washington) External Scientific Advisory Committee*; British Columbia Lung Association, Air Quality and Health Steering Committee* None Science Advisory Board None to MESA Air Study, University of Washington* None None Health Effects Institute* None None None This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all reviewers are required to complete and submit A relationship is considered to be "significant" if (1) the person receives $10000 or more during any 12 -month period, or 5% or more of the person's gross income, or (2) the person owns 5% or more of the voting stock or share of the entity, or owns $10 000 or more of the fair market value of the entity. 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J Occup Health 2005,47.471-480. 374 Chang CC, Hwang IS, Chan CC, Cheng TJ Interaction effects of ultrafine carbon black with iron and nickel on heart rate variability in spontaneously hypertensive rats Environ Health Perspect. 2007;115: 1012-1017 375 Chen LC, Hwang IS Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice- 1V. Characterization of acute and chronic effects of ambient air fine particulate matter exposures on heart -rate variability Inhal Toxicol 2005;17.209-216. 376 Anselme F, Lonot S, Henry JP, Dionnet F, Napoleom JG, Thuillez C, Morin JP. Inhalation of diluted diesel engine emission impacts heart rate variability and arrhythrma occurrence in a rat model of chronic ischemic heart failure Arch Toxicol. 2007;81:299-307. 377. Wellemus GA, Coull BA, Batalha JR, Diaz EA, Lawrence J, Godleski JI. 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Ghio AJ, Hall A, Bassett MA, Cascio WE, Devlin RB Exposure to concentrated ambient air particles alters hematologic indices in humans. Inhal Toxicol 2003;15.1465-1478. 382. Mills NL, Robinson SD, Fokkens PH, Leseman DL, Miller MR, Anderson D, Freney EJ, Heal MR, Donovan RJ, Blomberg A, Sandstrbm T, MacNee W, Boon NA, Donaldson K, Newby DE, Cassee FR Exposure to concentrated ambient particles does not affect vascular function in patients with coronary heart disease. Environ Health Perspect. 2008;116 709-715. 383. Samet JM, Graff D, Bemtsen J, Ghio AJ, Huang YC, Devlin RB. A comparison of studies on the effects of controlled exposure to fine, coarse and ultrafine ambient particulate matter from a single location. Inhal Toxicol 2007;19(suppl)-29-32. 384. Mills NL, Tornqvist H, Robinson SD, Gonzalez M, Darnley K, MacNee W, Boon NA, Donaldson K, Blomberg A, Sandstrom T, Newby DE. Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis Circulation. 2005;112:3930-3936. 385. Mills NL, Tdrngvist H, Gonzalez MC, Vink E, Robinson SD, Soderberg S, Boon NA, Donaldson K, Sandstrom T, Blomberg A, Newby DE. Ischemic and thrombotic effects of dilute diesel -exhaust inhalation in men with coronary heart disease. N Engl J Med. 2007;357.1075-1082. 386. Carlsten C, Kaufman JD, Peretz A, Trenga CA, Sheppard L, Sullivan JH. Coagulation markers in healthy human subjects exposed to diesel exhaust. Thromb Res 2007;120:849-855- 387. Tan WC, Qm D, Liam BL, Ng TP, Lee S11, van Eeden SF, D'Yachkova Y, Hogg JC. The human bone marrow response to acute air pollution caused by forest fires. Am J Respir Cnt Care Med 2000;161.1213-1217 388 van Eeden SF, Yeung A, Quinlam K, Hogg JC Systemic response to ambient particulate matter, relevance to chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2005,2:61-67. 389. Gong H, Latin WS, Terrell SL, Anderson KR, Clark KW, Sioutas C, Cascio WE, Alexis N, Devlin RB. Exposures of elderly volunteers with and without chronic obstructive pulmonary disease (COPD) to concentrated ambient fine particulate pollution. Inhal Toxicol 2004;16:731-744. Downloaded from circ.ahajoumals.org at University ofMichigan--AnnArbor on December 6, 2010 2378 Circulation June 1, 2010 390 Brook RD, Urch B, Dvonch IT, Bard RL, Speck M, Keeler G, Monshita M, Marsik FJ, Kamal AS, Kacirou N, Harkema J, Corey 11, Silverman F, Gold DR, Wellenius G, Mittleman MA, Rajagopalan S, Brook JR. Insights into the mechanisms and mediators of the effects of air pollution exposure on blood pressure and vascular function in healthy humans. Hypertension. 2009;54:659-667. 391. Frampton MW, Stewart JC, Oberdorster G, Morrow PE, Chalupa D, hetmpaoh AP, Frasier LM, Speers DM, Cox C, Huang LS, Utell MJ Inha- lation of ultrafine particles alters blood leukocyte expression of adhesion molecules in humans. Environ Health Perspect. 2006,114:51-58. 392. Beckett WS, Chalupa DF, Pauly -Brown A, Speers DM, Stewart JC, Frampton MW, Utell MJ, Huang LS, Cox C, Zareba W, Oberdorster G. Comparing inhaled ultrafine versus fine zinc oxide particles in healthy adults- a human inhalation study. Am J Respu Cni Care Med. 2005; 171:1129-1135. 393 Routledge HC, Manney S, Hanson RM, Ayres JG, Townend IN. Effect of inhaled sulphur dioxide and carbon particles on heart rate variability and markers of inflammation and coagulation in human subjects. Heart 2006;92.220-227. 394 Peretz A, Peck EC, Bammler TK, Beyer RP, Sullivan JH, Trenga CA, Snnouanprachnah S, Farm FM, Kaufman JD. Diesel exhaust inhalation and assessment of peripheral blood mononuclear cell gene transcription effects an exploratory study of healthy human volunteers Inhal Toxicol. 2007;19.1107-1119. 395 Barregard L, Sallsten G, Gustafson P, Andersson L, Johansson L, Basu S, Stigendal L Experimental exposure to wood -smoke particles in healthy humans: effects on markers of inflammation, coagulation, and lipid peroxidation. Inhal Toxicol. 2006;18-845-853, 396 Rangasamy T, Cho CY, Thimmulappa RK, Zhen L, Srisuma SS, Kensler TW, Yamamoto M, Petrache I, Tuder RM, Biswal S. Genetic ablation of Nrf2 enhances susceptibility to cigarette smoke -induced emphysema in mice J Cltn Invest 2004;114:1248-1259. 397 Ghio AJ, Kim C, Devlin RB- Concentrated ambient air particles induce mild pulmonary inflammation in healthy human volunteers Am J Respir Cnt Care Med 2000;162.981-988 398 Carlsten C, Kaufman JD, Trenga CA, Allen J, Peretz A, Sullivan JH. Thrombotic markers in metabolic syndrome subjects exposed to diesel exhaust Inhal Toxicol 2008;20:917-921 399. Lucking AJ, Lundback M, Mills NL, Faratian D, Barath SL, Pouiazar J, Cassee FR, Donaldson K, Boon NA, Badimon JJ, Sandstrom T, Blomberg A, Newby DE Diesel exhaust inhalation increases thrombus formation in man Eur Heart J 2008;29 3043-3051. 400 Brook RD, Rajagopalan S Particulate matter, air pollution, and blood pressure. J Am Sac Hypenens. 2009,3 332-350. 401 Gong H Jr, Linn WS, Sioutas C, Terrell SL, Clark KW, Anderson KR, Terrell LL. Controlled exposures of healthy and asthmatic volunteers to concentrated ambient fine particles in Los Angeles. Inhal Toxicol. 2003, 15.305-325 402 Brook RD, Brook JR, Urch B, Vincent R, Rajagopalan S, Silverman F Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults. Circulation 2002;105.1534-1536 403. Frampton MW Systemic and cardiovascular effects of airway injury and inflammation: ultrafine particle exposure in humans. Environ Health Perspect 2001;109(suppl):529-532 404. Urch B, Silverman F, Corey P, Brook JR, Lukic KZ, Rajagopalan S, Brook RD. Acute blood pressure responses in healthy adults during controlled air pollution exposures Environ Health Perspect. 2005,113 1052-1055 405. Urch B, Brook JR, Wasserstein D, Brook RD, Rajagopalan S, Corey P, Silverman F. Relative contributions of PM2.5 chemical constituents to acute arterial vasoconstriction in humans. Inhal Toxicol. 2004,16:345-352. 406 Peretz A, Sullivan JH, Leotta DF, Trenga CA, Sands FN, Allen J, Carlsten C, Wilkinson CW, Gill EA, Kaufman JD Diesel exhaust inhalation elicits acute vasoconstriction in vivo. Environ Health Perspect- 2008;116.937-942 407 Shah AP, Pietropaoli AP, Frasier LM, Speers DM, Chalupa DC, Delehanty JM, Huang LS, Utell MJ, Frampton MW. Effect of inhaled carbon ultrafine particles on reactive hypererma in healthy human subjects Environ Health Perspect. 2008;116 375-380. 408 Duffin R, Tran L, Brown D, Stone V, Donaldson K Pioinflammogemc effects of low -toxicity and metal nanoparucles in vivo and in vitro: highlighting the role of particle surface area and surface reactivity Inhal Toxicol 2007,19:849-856. 409. Oberdorster G, Oberdbrster E, Oberdorster J. Nanotoxicology- an emerging discipline evolving from studies of ultrafine particles. Environ Health Perspect. 2005;113:823-839 410. Gong H Jr, Linn WS, Terrell SL, Clark KW, Geller MD, Anderson KR, Cascio WE, Sioutas C Altered heart -rate variability in asthmatic and healthy volunteers exposed to concentrated ambient coarse particles Inhal To=ol 2004,16:335-343. 411. Bartob CR, Wellenius GA, Diaz EA, Lawrence J, Coull BA, Akiyama I, Lee LM, Okabe K, Vemer RL, Godleski JJ. Mechanisms of inhaled fine particulate air pollution -induced arterial blood pressure changes Environ Health Perspect. 2009;117:361-366 412. Wallenbom JG, McGee JK, Schladweiler MC, Ledbetter AD, Kodavanti UP. Systemic translocation of particulate matter -associated metals fol- lowing a single intratracheal instillation in rats Toxtcol Sci. 7.007;98 231-239 413. Phalen RF, Oldham MJ, Nel AE- Tracheobronchial particle dose con- siderations for in vitro toxicology studies. Toxicol Sci. 2006;92: 126-132. 414. Kreyhng WG, Semmler-Behnke M, Mbller W Ultrafine parncle-lung interactions does size matter? JAerosol Med 2006;19:74-83 415. Peters A, Veronesi B, Calder6n-Garciduefias L, Gehr P, Chen LC, Geiser M, Reed W, Rothen-Rutishauser B, Schurch S, Schulz FL Trans- location and potential neurological effects of fine and ultrafine particles a critical update Patz Fibre Toxicol- 2006;3.13. 416 Mills NL, Amm N, Robinson SD, Anand A, Davies J, Patel D, de la Fuente JM, Cassee FR, Boon NA, Macnee W, Millar AM, Donaldson K, Newby DE Do inhaled carbon nanoparticles translocate directly into the circulation in humans) Am J Respu Cnt Care Med 2006;173:426-431 417 Fumyama A, Kanno S, Kobayashi T, Hirano S. Extrapulmonary translo- cation of intratracheally instilled fine and ultiafine particles via dmt and alveolar macrophage -associated routes. Arch Toxicol. 2009;83:429-437. 418. Knol AB, de Hartog JJ, Boogaard H, Slotge P, van der Sluljs JP, Lebret E, Cassee FR, Wardekker JA, Ayres JG, Borm PJ, Brunelcreef B, Donaldson K, Forastiere F, Holgate ST, Kreyling WG, Nernery B, Pekkanen J, Stone V, Wichmann HE, Hoek G Expert elicitation on ultrafine particles: likelihood of health effects and causal pathways Part Fibre Toxicol 2009,6:19. 419. Ruidavets JB, Cournot M, Cassadou S, Giroux M, Meybeck M, Ferribres J. Ozone air pollution is associated with acute myocardial infarction. Circulation. 2005,111:563-569. 420 Bell ML, Peng RD, Dominici F, Samet JM. Emergency hospital admissions for cardiovascular diseases and ambient levels of carbon monoxide results for 126 United States urban counties, 1999-2005 Circulation. 2009;120-949-955 421 Hill AB The environment and disease: association or causation? Proc R Sac Med 1965;58:295-300. 422. Wen XJ, Balluz L, Mokdad A. Association between media alerts of air quality index and change of outdoor activity among adult asthrna in six states, BRFSS, 2005. J Community Health 2009,34.40-46. 423. Bell ML, Ebisu K, Peng RD, Dommici F. Adverse health effects of par- ticulate air pollution: modification by air conditioning. Epidemiology. 2009, 20:682-686 424 Pui DY, Qi C, Stanley N, Oberddrster G, Maynard A. Recirculating air filtration significantly reduces exposure to airborne nanoparticles Environ Health Perspect. 2008;116.863-866. 425. Zhu Y, Eiguren-Fernandez A, Hinds WC, Miguel AH. In -cabin commuter exposure to ultrafine particles on Los Angeles freeways Environ Set Teehnol. 2007;41:2138-2145. 426, Fullerton DG, Bruce N, Gordon SB Indoor air pollution from biomass fuel smoke is a major health concern in the developing world. Trans R Soc Trop Med Hyg 2008;102-843-851 Downloaded from circ.ahajoulnals.org at University of Michigan --Ann Arbor on December 6, 2010 • • � '�' � ��^! r r rte,` `�?+• - ` .� � aY `i^i` � � s Y vio �" . >•*Jw .:x 4 - - _ ` ♦ An`'` �r �. ..� • "�► ��`,*`1 �' Y Y .�v.��'�.` � ,.tea �-��t 71— Zvi w 40 - _ w Ak _ �: 'Its � = xr � _ • z� ��',� Y{� �;t � �,� , zi r � •� - \ =t Ys � ;` � � -L ``- M ..: '�. `aJ,+:fir yi�t. '. . 31 IL 55 �r r r • s r _ •t$„ 4 SF �i w�lF` x • ..- - -'�. l .. _ � �� .e� �, � � Fes- ��, #�.,��`*:.� r - C \ F � � v� K r - Richard G. Kott 94 Sutter Road Port Angeles, WA 98362 Tel- 360-457-0933 Email. rkott@wavecable com April 3, 2012 Port Angeles City Council 321 East 5th Street Port Angeles, WA 98362 Dear Council Members: My Name is Richard Kott. I am a long time resident of the Port Angeles area residing at 94 Sutter Road and am the former Resident Manager of the mill under Crown Zellerbach ownership. I have a strong interest in preserving our environment and maintaining a strong local economy. With that objective I can fully support the Nippon cogeneration plant as a win for clean air and water as well as a win for our community. The project has been through a thorough environmental vetting by experts and has received all of the permits necessary from the City, ORCAA, and other regulatory agencies. Proponents, opponents and citizens at large have had ample opportunity to have their concerns considered. To suggest now that there should be a moratorium on the project and a City -sponsored open forum for review again is disingenuous. In fact in my opinion it is tantamount to bad faith by the City. As a council I urge you to reject this course of action and recognize that It Is an attempt by project opponents to use political pressure to achieve what they have failed to accomplish in the permitting and review process. The following paragraphs taken from my presentation at the 05/17/11 ORCAA hearing provide a review of some of the key points concerning the project going forward versus what we might expect if it were stopped. Outcomes if the plant is built. 1. It will consume a fraction of the biomass available from logging operations on the Peninsula. This will come from additional usage of hog fuel or biomass currently supplied to its boiler. Fuel truck deliveries to the mill will increase from about one truck per hour to 2 trucks per hour. 2. It will generate about 20 MW of power at about 70% overall efficiency. This green energy will reduce 20 MW of thermally produced power elsewhere on the Bonneville system. In all likelihood it will be from a coal fired stand- alone utility with a condensing turbine having an efficiency of 30%-40%. To confirm these numbers I checked the EPA Perrin Quarles * study of the 50 best performing coal fired plants in the United States. The average heat rate reported was 9854 Btu/kwh which equates to an efficiency of 34.6%. Using this number and medium grade coal having a heating value of 11,670 btu/Ib I calculated the CO2 production at 470 tons/day. Alternatively when there is a process use for the waste heat such as for drying paper the EPA studies* shows that energy efficiency can exceed 70%. At 70% an equivalent coal fired cogeneration plant would only produce 235 tons of CO2 /day or half the amount. Because the carbon to hydrogen ratio of biomass fuel is less than that of coal, the amount of CO2 produced in the Nippon plant would be even lower, less than 50%. Other combustion gases including NO, would also be proportionately less. 3. The particulate control devices planned for this project will be far more efficient than the existing system using older boiler technology. The mill's present system still meets current emission requirements but the projected particulate reduction is 68% with the new boiler and its advanced train of in-line dust collection equipment. 4. Burning of logging slash in the new boiler under controlled conditions rather than in the field or at the landings will further reduce air pollutants. Recent studies show that 38% of the PM2.5+ particulate In Clallom County Is from slash burning, wildfires and other uncontrolled fires. * 5. Fresh water consumption will be increased about 1.2mgd. This Is insignificant In terms of prior water usage. At times in the past the industrial water line was supplied 65mgd to the pulp and paper mills in Port Angeles. 1.2mgd calculates to 1.86 cu ft/sec flow in the Elwho River which is less than the hourly variation in river flow and inconsequent1ol when compared to the average river flow of about 1,500 cu ft/sec. 6. The mill is small by Industry standards. The cogeneration project will reduce costs for years to come and help the mill retain its competitive position. 7. The cogeneration plant will generate 25-30 new permanent jobs plus help ensure the future availability of existing family wage Jobs at the mill. In addition there will be the spinoff impact of related and supporting Jobs in Peninsula communities. S. The green power generated by this project will helpmeet our State's demand for renewable energy as mandated by State Initiative 1-937. Outcomes if the plant is not built: 1. The environment is the big loser with the amount of CO2 and related emissions being more than doubled from the source of the replacement energy. 2. The Nippon mill is small compared to other paper mills thus making survivability difficult Competitive mills can produce more tonnage on one paper machine than the Nippon mill can on its two machines. It still enjoys a small quality and technology advantage over its mayor competitors but this cannot be sustained without a major shift In cost factors which would result from the cogeneration plant. 3. 1 hesitate making this last point because of the severe implications. In my opinion the Nippon mill has a limited life if the cogeneration project is not successfully completed. As a side bar to this permit application please keep in mind that on June 1, 2011 the Elwha dams will stop producing power. Thus in 15 days there will bean immediate demand on the Bonneville system for replacement power of at least 20MW. As long as thermal plants are operating In our region increased production from one of them will be the source. This will come with the unwelcome addition of about 500 tons/day of CO2 and other exhaust gas emissions. It is interesting to note that this adverse carbon footprint was never reported in the various studies supporting the removal of the Elwha dams. In summary, yes the differences between building or not building the cogeneration plant are stark. The only conclusion I can reach is that the cogeneration plant is a win for the environment a win for the mill and a win for Peninsula communities. It will also provide partial mitigation of the increased carbon footprint resulting from removal of the Elwha dams. I encourage ORCAA to consider the local and regional impacts of this project and to issue the necessary air permit so construction can proceed without further delay. The 12/15/09 EPA study completed an intensive review of Particulate Matter ("PM"), and issues related to nanoparticles. The "Integrated Science Assessment for Particulate Matter" is EPA's latest evaluation of the scientific literature on the potential human health and effects associated with exposures to particulate matter. This study is the basis for EPA decisions related to the review of the current PM NAAQS. The result is EPA has continued using the best available science to regulate <PM25and <PM10 With this as a foundation there is no credible basis that the Nippon cogeneration plant will result in harmful emissions. I respectfully ask the Council Members to reject the idea of a biomass moratorium along with a divisive forum and continue directing their attention on the many significant issues facing our community. Sincerely, Richard G. Kott References: *Clallam County Emission Inventory, DOE 200-2004 *Clean Air Markets Division, U 5 Environmental Protection, Perrin Quarles Associates, April 17, 2001 *http://www epa.gov/chp Tickfe Oimavera 2012 A Tickfe6affCeCe6ration ofSpring... Funds raised benefit Shane Park Playground Play ANYTIMEor ALL THE TIME! Leave and come back - unlimited All ages. All skill levels Lessons available Teams or individual Choice of times Equipment provided/Tennis shoes required Adults: $10 Children: $5 Suggested Donation Ages 5-17 Under 12 must be accompanied by adult 10 am Sat. April 21 -10 am Sun. April 22 IPMO Ver Burton Community Center You Tube search 308 E. 4 I Street Contact peninsula picklers 360.457.1991 360.681.7502 Register @ Port Angeles Senior Center 328 E 7t" Street 457-7004 First 200 registered receive McDonalds Coupon Sponsored 6y ('ort Angeles Senior Center and ('.A. Ticklers Fact Sheet Nippon Paper Mill Port Angeles, Washington January, 2012 In 2011 Nippon paid the City about $16 million for utilities including electrical and water utilities. i- In purchasing these utilities, Nippon paid more than $900,000 in utility taxes for the City's General Fund. That value will likely increase in 2012 due to higher BPA rates. Nippon owns the power lines feeding the mill and pays 100% of the maintenance costs on those power lines. Nippon also pays 100% of the maintenance costs on the industrial water line. ➢ In 2010, Nippon paid $374,000 in property taxes which support the City's General Fund. In 2011, Nippon paid about $432,000 in building permit fees for the new $71MM CoGen project of which the City has dedicated that amount to its waterfront improvements. i About 210 full-time personnel are directly employed by Nippon who earn very good family wages and benefits that support the local economy. i There are many Clallam County Companies and personnel who are direct suppliers to Nippon and who also enjoy family wages and benefits. ➢ Nippon spent $65MM locally in 2011. Using the Washington input output model that represents a further $260 MM in economic value to the area. Teresa Pierce From: paul lamoureux [paulrl@olypen com] Sent: Tuesday, April 03, 2012 11 21 AM To: Teresa Pierce Subject: . PROPOSED ELECTRIC UTILITY "TOU" RATE ORDINANCE - QUESTION HI, -T. ... PLZ. FRWRD. TO APPROPRIATE UTILITY DEPT. & CITY COUNCIL MEMBERS... ...In referencing to Pgs. (G-7) & (G-9) in the City Council packet for April 3rd meeting....... ..Do I understand that the proposed TOU rate ordinance hours are - for (light) hours are: 10 PM - 6 Am (Monday thru FRIDAY), and, Saturday 10PM to Monday 6 AM; and all NAERC Holidays ? ...My public comment on the proposed "Seasonal Months" for energy rate charges might better serve the public users with: May thru September as the "Summer" Months, and October thru April as the "Winter" months. That makes it a 7 Winter to a 5 Summer months Season ratio, rather than the proposed 9 Winter to a 3 Summer months Season ratio. ...Thank You, Paul Lamoureux ... (paurl(cbolypencom)... • CITY COUNCIL MEETING Port Angeles, Washington March 20, 2012 CALL TO ORDER- Mayor Kidd called the regular meeting of the Port Angeles City Council to order at REGULAR MEETING: 6:00 p.m. ROLL CALL: Members Present Mayor Kidd, Deputy Mayor Collins, Councilmembers Bruch, Di Guilio, Downie, Mania, and Nelson. Members Absent None. Staff Present Acting Manager West, Attorney Bloor, Deputy Clerk Pierce, G. Cutler, B. Smith, D. McKeen, L. Kheriaty, L. Dunbar. PLEDGE OF Mayor Kidd led the Pledge of Allegiance to the Flag. ALLEGIANCE: PUBLIC COMMENT: Virginia Vadset, 503 Roberson Road, Sequim, spoke in opposition to the Nippon Biomass incinerator. Anami Cloud, 133 E. First Street, spoke regarding the quality of life, public input, • estuary park, Waterfront Project, jobs, lack of population growth, urged Council to listen to the public, stormwater, the Combined Sewer Overflow project, soil conditions, use of consultants, low impact development (LID), dangers of wood smoke, and air pollution. Rose Marschall, 162 S. Baar Road, spoke regarding an email she sent to Council, lack of response from Council to her concerns regarding diesel fumes, the widening of Lauridsen Boulevard Bridge, the Nippon Biomass project, and dioxins. Mayor Kidd referred Ms. Marschall to Acting Manager West for more information regarding the Lauridsen Boulevard Bridge project. Diana Sommerville, 2399 E. 3`d Avenue, spoke regarding comments she made to the Clallam County Board of Health regarding the expenses to deal with the problems of air pollution and requested Council to rethink the biomass project. Nelson Cone, Port Angeles, spoke regarding the use of tax money for the cost of cleaning up the Port Angeles harbor and use of grants and subsidies. Marilyn Harbaugh 312 W. 5th Street, thanked Council for support of community gardens including the one located across the street from City Hall and invited others to garden. Lynne Lohr, 781 N. Kendall Road, Sequim, spoke in opposition to fluoridation of the water, the Biomass project, and diesel trucks and fumes. • E-1 CITY COUNCIL MEETING March 20, 2012 • LATE ITEMS TO BE Councilmember Mania requested the topic of a moratorium on the Biomass be PLACED ON THIS OR placed on a future agenda. FUTURE AGENDAS: CONSENT AGENDA: It was moved by Mania and seconded by Downie to approve the Consent Agenda to include: 1. City Council Meeting Minutes for January 21, March 6, and March 13, 2012 2. Expenditure Approval List: 2/25/12 to 3/9/12 for $1,442,544.49 3. Proposed Medic 1 Ambulance Transport Rate Adjustments / Set Public Hearing 4. Proposed Electric Utility Time of Use Rate Ordinance / Set Public Hearing 5. City Pier Fire Suppression System, Project PK03-09 ti. Dry Creek Water Association / Special Service Agreement No. 2 7. Bonneville Power Administration Commercial & Industrial Demand Response Grant Amendment No. 1 Motion carried 7-0. ORDINANCES NOT 1. Telecommunications Utility and Electric Fund Ordinance Amendments REQUIRING PUBLIC HEARINGS: Deputy Police Chief Smith briefly summarized the process to date. The UA(: Committee forwarded a favorable recommendation. Changes requested from the March 6 meeting were included in the ordinance. . Attorney Terry Mundorf of the Western Public Agencies Group gave a presentation using Powerpoint slides to outline the purposes of the ordinances under consideration, pros and cons of establishing a telecommunications utility, and recommendation to adopt. Council discussion followed. Mayor Kidd conducted a second reading of the ordinances by title, entitled, ORDINANCE NO. 3448 AN ORDINANCE of the City of Port Angeles, Washington, relating to Telecommunications Utility, adding a new Chapter, 13.53, to Title 13 of the Port Angeles Municipal Code. It was moved by Nelson and seconded by Mania to adopt the ordinance as read by title. Motion carried 7-0. 2 E-2 CITY COUNCIL MEETING March 20, 2012 is ORDINANCES NOT ORDINANCE NO. 3449 REQUIRING PUBLIC HEARINGS: AN ORDINANCE of the City of Port Angeles, Washington, amending Chapter (Cont'd) 3.24 of the Port Angeles Municipal Code relating to Electric Fund. It was moved by Di Guilio and seconded by Downie to adopt the ordinance as read by title. Motion carried 7-0. CEREMONIAL 1. Proclamation / Austin Fahrenholtz MATTERS/ PROCLAMATIONS/ Mayor Kidd presented Port Angeles High School Diving Coach Rich Butler a & EMPLOYEE proclamation on behalf of Port Angeles High School student and champion diver, RECOGNITIONS: Austin Fahrenholtz. ORDINANCES NOT 1. Fire Department Related Municipal Code Updates REQUIRING PUBLIC HEARINGS: Fire Chief McKeen briefly explained the purpose of updating ordinance to coincide with international fire code changes. Chief McKeen and Fire Marshal Dubuc explained each of the proposed changes many of which eliminate out-of-date terminology. Council discussion followed. Mayor Kidd conducted the first reading of the ordinance by title, entitled, 0 ORDINANCE NO. AN ORDINANCE of the City of Port Angeles, Washington, relating to the Fire Department; making changes to Chapters 2.16, 5.32, 14.03, 14.21, and 14.23 of the Port Angeles Municipal Code. OTHER 1. United Way — 2012 Funding & 2011 Year End Report CONSIDERATIONS: Deputy Mayor Collins recused himself from discussion as he is employed by one of the agencies funded through United Way. He departed Council Chambers at 7:02 p.m. Jody Moss, Executive Director of United Way of Clallam County presented Council with the 2012 Funding Allocations and the 2011 Year End Report.Moss thanked Council for prior support. She then outlined the process for preparing the 2012 funding allocations and reviewed the 2011 Year End Report. Council discussion followed. It was moved by Downie and seconded by Mania to approve the allocations as requested; Motion carried 6-0. Deputy Mayor Collins reentered Council Chambers at 7:26 p.m. BREAK: Mayor Kidd recessed the meeting for a break at 7:27 p.m. The meeting reconvened • at 7:35 p.m. E-3 CITY COUNCIL MEETING March 20, 2012 OTHER 2. Intergovernmental Cooperation Agreement — Port of Port Angeles / ]FEMA CONSIDERATIONS: Lawsuit (Cont'd) Acting City Manager West explained the purpose of the agreement was for the Port to share one-half, but not to exceed $2,500.00, of the City's legal costs. Council discussion followed. It was moved by Downie and seconded by Nelson to approve an intergovernmental cooperation agreement with the Port of Port Angeles regarding the National Wildlife Federal v. Federal Emergency Management Agency Litigation where the Port agrees to pay to the City one-half, but not to exceed $2,500.00, of the expense the City will incur in opposing the lawsuit. Council discussion followed. Motion carried 6-1, with Mania voting in opposition. CITY COUNCIL Councilmember Nelson reported participating in the St. Patrick's Day run. REPORTS: Councilmember Mania reported on attending numerous meetings regarding the Fine Arts Center. Councilmember Downie reported attending the National League of Cities (NLC) Conference in Washington, DC with Deputy Mayor Collins, and their meetings with Congressional staff. He found the conference extremely worthwhile and of beneficial importance. Mayor Kidd reported attending the day of remembrance ceremony in Seattle for the Tsunami anniversary and visiting with the Spanish consulate representatives. Deputy Mayor Collins reported on the NLC Conference and the leadership training seminar including five powers of public leadership, a program called Gifts for the Community; the Community & Economic Development Policy Meeting Committee meeting as part of the NLC Conference and a forum coming up in May in Cali Fornia that Director West may consider attending; and another meeting in DC with representatives from NOAA. Councilmember Bruch reported attending the first Transition Port Angeles meeting. Councilmember Di Guilio had no report. • 4 E-4 • is • CITY COUNCIL MEETING March 20, 2012 INFORMATION: Acting City Manager West spoke regarding a reminder of the special Council meeting on March 26, 2012, at 9:30 a.m. as a joint meeting with the Port of Port Angeles Commissioners; and the first Council Work Session on March 27, 2012, at 5:00 p.m. in Council Chambers. Acting City Manager West bid a fond farewell to Peninsula Daily News reporter Tom Callis on his leaving to take a job in Hawaii. Deputy Mayor Collins stated he spoke with the Cronauers regarding the previous action taken on the Birdwell property and the possibility of documented easements and suggested reconsidering the issue. Attorney Bloor responded a motion would be necessary to bring it back for Council consideration. It was moved by Collins and seconded by Bruch for Council to reconsider the Birdwell street vacation. Council discussion followed. Collins amended his motion to include the provision for Mr. Cronauer to provide the necessary information or documentation by the end of this week. Council discussion followed. Motion failed 3-4 with Kidd, Nelson, Mania, and Downie voting in opposition. EXECUTIVE SESSION: None AD3OURNMENT: Mayor Kidd adjourned the meeting at 8:08 p.m. Cherie Kidd, Mayor Teresa Pierce, Deputy City Clerk 5 E-5 CITY COUNCIL SPECIAL MEETING Joint Meeting with Port of Port Angeles Commissioners North Olympic Peninsula Skills Center Port Angeles, Washington March 26, 2012 CALL TO ORDER- Mayor Kidd called the special meeting of the Port Angeles City Council to order at SPECIAL MEETING: 9:30 a.m. ROLL CALL: Members Present Mayor Kidd, Deputy Mayor Collins, Councilmembers Bruch, Di Guilio, Downie, and Mania. Members Absent Councilmember Nelson. City Council moved and passed unanimously to excuse Councilmember Nelson. City Staff Present Manager Myers, Attorney Bloor, Director West. Port Commissioners Present President Calhoun, Commissioners Hallett and McHugh Port Staff Present Executive Director Robb, Attorney Neupert PLEDGE OF The :Pledge of Allegiance was led by Mayor Kidd. ALLEGIANCE: DISCUSSION: Port of Port Angeles Executive Director Robb made a presentation using Powerpoint slides to guide discussion and exchange views on cooperation and opportunities between the City and the Port regarding the following agenda ilems: 1. Composite Manufacturing Campus 2. Lincoln Park Master Plan 3. Waterfront Development Projects 4. Harbor Clean Up 5. Economic Development - Roles of the Port and the City Council and Commissioner discussion followed. No action was taken. ADJOURNMENT: Mayor Kidd adjourned the meeting at 12:00 p.m. Cherie Kidd, Mayor Teresa Pierce, Deputy City Clerk E - h • • • 0 CITY COUNCIL SPECIAL MEETING CITY COUNCIL WORK SESSION 321 E. Fifth Street / Port Angeles, Washington March 27, 2012 CALL TO ORDER- Mayor Kidd called the special meeting of the Port Angeles City Council to order at SPECIAL MEETING: 5:00 p.m. ROLL CALL: Members Present Mayor Kidd, Deputy Mayor Collins, Councilmembers Bruch, Di Guilio, Downie, Mania, and Nelson. Members Absent None. Staff Present Manager Myers, Attorney Bloor, Deputy Clerk Pierce, G. Cutler, D. McKeen, N. West, L. Kheriaty, B. Coons, T. Nevaril, and approximately 25 Public Works & Utilities Department employees. PLEDGE OF Pledge of Allegiance was led by Councilmember Downie. ALLEGIANCE: WORK SESSION City Manager Myers led City Council through a work session to discuss the . DISCUSSION: following agenda items: 1. Department Reorganization Efforts City Manager Myers conducted a presentation using PowerPoint slides. Human Resources Manager Coons outlined a brief history of the organization of the Public Works & Utilities Department and other City departments and distributed a report showing comparisons to other cities with Public Works functions. 1�1 Council discussion followed. Manager Myers will direct staff to research costs and legal requirements. A report will be brought back to Council for consideration. Council discussion followed. 2. Recruitment Process — Finance Director Manager Myers conducted a presentation using PowerPoint slides to outline the process he intends to use to appoint an interim Finance Director and process and expected timeline to recruit a permanent Finance Director. Council discussion followed. Human Resources Manager Coons spoke on the pros and cons of using a professional recruiter, the overall process and estimated costs. Council discussion followed. Council concurs with the process outlined. E-7 CITY COUNCIL SPECIAL MEETING March 27, 2012 • 3. 2012 Community -Wide Visioning Process City Manager Myers conducted a presentation using Powerpoint slides regarding their choice of process for community visioning. Council discussion followed. Director West noted concerns about the timing with the 2015 Comprehensive Plan update, not starting too early in the process, and not meeting the expectations of the public in a timely fashion. Council consensus was to coordinate a visioning process later with the 2015 update of the Comprehensive Plan. Emphasis for now will be on informing the public on the City's current strategic goals. 4. Budgeting for Priorities Manager Myers conducted a presentation using Powerpoint slides regairding the status of the 2011 Budget and the Budgeting for Priorities. Actual revenues exceed actual expenses in 2011 by $119,411. Council discussion followed. Council consensus was to remain committed to the Budgeting for Priorities process, with scoring to be initially completed by staff, be prepared to make program reductions, and consider new or increased fees or taxes. No action was taken. • ADJOURNMENT: Mayor Kidd adjourned the meeting at 7:03 p.m. Cherie Kidd, Mayor Teresa Pierce, Deputy City Clerk 0 W. cca Date 3/28/2012 City of Port Angeles i�' ` City Council Expenditure Report • "r#°'• f* From: 3/10/2012 To: 3/2312012 Vendor Description Account Number Invoice Amount BEACON ATHLETICS SPORTING & ATHLETIC EQUIP 001-0000-237.00-00 -32.59 CLALLAM CNTY TREASURER CVCA TO CLALLAM CO TREAS 001-0000-229.40-00 36668 ELECSYS INT'L CORP RADIX MAINTENANCE 001-0000-237.00-00 -21.34 Ciallam County Demo CC CITY COUNCIL CHAMBE4R DEP 001-0000-239.10-00 50.00 Con Humphries CLUBHOUSE DEPOSIT REFUND 001-0000-239.10-00 50.00 Larry Bourm LOOMIS CLUBHOUSE DEPOSIT 001-0000-239.10-00 50.00 US BANK CORPORATE PAYMENT SYSTEICIty Credit Card Pmt 001-0000-213.10-95 -10,842.92 City Credit Card Pmt 001-0000-213 10-95 13,311.56 Binders -Dubuc 001-0000-237.00-00 -10.03 Service Awards -Gallagher 001-0000-237.00-00 -4.24 Online Newspaper Subscpt 001-0000-237.00-00 -3.53 Arms/Access-Roggenbuck 001-0000-237.00-00 -151.43 Grappler PU Tool -Wray 001-0000-237.00-00 -20.10 WASHINGTON STATE TREASURER FEB BUILDING SURCHARGE 001-0000-229.10-00 81.00 DIST CT REV TO ST TREAS 001-0000-229.30-00 13,824.74 Division Total: $16,647.80 Department Total. $16,647.80 PATRICK DOWNIE DOWN IE -M ILEAGE/PEN DEV DI 001-1160-511.43-10 97.13 OLYMPIC PRINTERS INC PORT ANGELES CITY TREASURER BUS CARDS / KIDD AND COL PADA Dinner -Kidd 001-1160-511.31-01 001-1160-511.31-01 117.07 17.00 EDC Annual Dinner -Kidd 001-1160-511.31-01 37.50 EDC Lunch -Kidd 001-1160-511.31-01 9.00 US BANK CORPORATE PAYMENT SYSTEI Council Refreshments -JH 001-1160-511.31-01 7048 Conf Regist-Kidd 001-1160-511.43-10 175.00 Legislative Mayor & Council Division Total: $523.18 Legislative Department Total: $523.18 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-1210-513.42-10 1.18 03-05 A/C 3604529882811B 001-1210-513.42-10 1.18 03-05 A/C 3604525834211 B 001-1210-513.42-10 1.38 03-05 A/C 3604525109623B 001-1210-513.42-10 1.18 03-05 A/C 3604523877817B 001-1210-513.42-10 1.18 03-05 A/C 3604523712585B 001-1210-513.42-10 1.95 NATIONAL LEAGUE OF CITIES MEMBERSHIP DUES 001-1210-513.49-01 1,489.00 PORT ANGELES CITY TREASURER Lunch/Myers-Bruch 001-1210-513.31-01 11.38 EDC Lunch -Myers 001-1210-513.31-01 900 US BANK CORPORATE PAYMENT SYSTEI Business Meals -Myers 001-1210-513 31-01 181.19 Disputed Chg Credit 001-1210-513.31-01 -54.19 Travel -Myers 001-1210-513.43-10 479.30 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-1210-513.42-10 149.63 WASHINGTON (DES), STATE OF City Manager Department RADIO & TELECOMMUNICATION City Manager Office 001-1210-513.42-10 Division Total. 0.22 $2,273.58 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-1220-516 42-10 0.24 E-9 Pagel �q '41F7 kv � Date 3/28/2012 City of Port Angeles Iftag ,m^ ff City Council Expenditure Report 'PRY From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604529882811 B 001-1220-516 42-10 0.24 03-05 A/C: 3604525834211 B 001-1220-516.42-10 0.27 03-05 A/C: 3604525109623B 001-1220-516.42-10 0.24 03-05 A/C: 3604523877817B 001-1220-516 42-10 0.24 03-05A/C 3604523712585B 001-1220-516.42-10 0.39 US BANK CORPORATE PAYMENT SYSTEITravel-Coons 001-1220-516.43-10 179.49 Gas purchase -Gates 001-1220-516.43-10 34.32 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-1220-516.42-10 57.99 WA STATE PATROL WATCH CHECKS 001-1220-516.41-50 20.00 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-1220-516.42-10 121.18 City Manager Department Human Resources Division Total: $305.60 CENTURYLINK-QWEST 03-05 A/C: 3604529887652B 001-1230-514.42-10 0.12 03-05 A/C: 3604529882811B 001-1230-514 42-10 0.12 03-05 A/C: 3604525834211B 001-1230-514 42-10 0.14 03-05 A/C 36045251096238 001-1230-514.42-10 0.12 03-05 A/C 3604523877817B 001-1230-514.42-10 0.12 03-05 A/C 36045237125856 001-1230-514 42-10 0.19 DATA BASE RECORDS DESTRUCTION - FEB 001-1230-514.41-50 220.20 SOUND PUBLISHING INC WASHINGTON (DES), STATE OF COMMUNICATIONS/MEDIA SERV RADIO & TELECOMMUNICATION 001-1230-514 44-10 001-1230-514.42-10 28.44 4.92 City Manager Department City Clerk Division Total: $254.37 City Manager Department Department Total: $2,833.55 CENTURYLINK-QWEST 03-05 A/C: 3604529887652B 001-2010-514 42-10 0.83 03-05 A/C: 3604529882811 B 001-2010-514.42-10 0.83 03-05 A/C: 3604525834211 B 001-2010-514.42-10 0.96 03-05 A/C: 3604525109623B 001-2010-514.42-10 0.83 03-05 A/C: 3604523877817B 001-2010-514.42-10 0.83 03-05 A/C 3604523712585B 001-2010-514 42-10 1.37 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-2010-514.42-10 57.97 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-2010-514.42-10 4.84 Finance Department Finance Administration Division Total: $68.46 CENTURYLINK-QWEST 03-05 A/C: 3604529887652B 001-2023-514.42-10 1.07 03-05 A/C: 3604529882811 B 001-2023-514.42-10 1.07 03-05 A/C: 3604525834211 B 001-2023-514.42-10 1.24 03-05 A/C: 3604525109623B 001-2023-514.42-10 1.07 03-05 A/C: 3604523877817B 001-2023-514.42-10 1.07 03-05 A/C: 3604523712585B 001-2023-514.42-10 1.76 OLYMPIC STATIONERS INC SUPPLIES 001-2023-514.31-01 17.27 OFFICE SUPPLIES 001-2023-514.31-01 25.06 SOUND PUBLISHING INC PAYROLL_ SPECIALIST AD 001-2023-514.44-10 343 87 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-2023-514 42-10 i'.12 • Finance Department Accounting Division Total: $400.60 E-10 Page 2 Date 3/28/2012 City of Port Angeles City Council Expenditure Report • 'r°_,}fh From: 311012012 To: 312312012 Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 36045298876528 001-2025-514.42-10 1.54 03-05 A/C 3604529882811 B 001-2025-514.42-10 1.54 03-05 A/C 3604525834211 B 001-2025-514.42-10 1.79 03-05 A/C 3604525109623B 001-2025-514.42-10 1.54 03-05 A/C 3604523877817B 001-2025-514.42-10 1.54 03-05 A/C 3604523712585B 001-2025-514.42-10 2.54 ELECSYS INT'L CORP RADIX MAINTENANCE 001-2025-514.48-10 275.34 GRAINGER FLAME RESISTANT SHIRTS FO 001-2025-514.31-11 186.01 FLAME RESISTANT SHIRTS FO 001-2025-514.31-11 279.02 FLAME RESISTANT SHIRTS FO 001-2025-514.31-11 93.01 LEXISNEXIS PERSON SEARCHES 001-2025-514.41-50 106.83 OLYMPIC STATIONERS INC SUPPLIES 001-2025-514.31-01 17.27 OFFICE SUPPLIES 001-2025-514.31-01 3.57 PACIFIC OFFICE EQUIPMENT INC RIBBON FOR RECIPT PRNTR & 001-2025-514 31-01 119.98 PORT ANGELES CITY TREASURER Key-Dryke 001-2025-514.31-01 2.03 SHARP ELECTRONICS CORP RENTAULEASE EQUIPMENT 001-2025-514.45-31 117.56 SWAIN'S GENERAL STORE INC CLOTHING ALLOWANCE -DERIC 001-2025-514.31-11 90.95 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-2025-514.42-10 18.34 Finance Department Customer Service Division Total: $1,320.40 DIGITAL IMAGING SOLUTIONS INC FEB COPY COSTS 001-2080-514.45-31 313.74 GREAT AMERICA LEASING CORP RENTAULEASE EQUIPMENT 001-2080-514 45-31 607.63 RENTAULEASE EQUIPMENT 001-2080-514.45-31 638.27 MORNINGSIDE COMMUNICATIONS/MEDIA SERV 001-2080-514.41-50 855.00 SHARP ELECTRONICS CORP RENTAULEASE EQUIPMENT 001-2080-514.45-31 142.70 RENTAULEASE EQUIPMENT 001-2080-514.45-31 272.02 UNITED PARCEL SERVICE Shipping Chgs 001-2080-514.42-10 20.00 Finance Department Reprographics Division Total: $2,849.36 Finance Department Department Total. $4,638.82 CENTURYLINK-QWEST 03-05 A/C 36045298876528 001-3010-515.42-10 0.71 03-05 A/C 3604529882811 B 001-3010-515.42-10 0.71 03-05 A/C 3604525834211 B 001-3010-515.42-10 0.82 03-05 A/C 3604525109623B 001-3010-515.42-10 0.71 03-05 A/C 3604523877817B 001-3010-515.42-10 0.71 03-05 A/C 3604523712585B 001-3010-515.42-10 1.17 DIGITAL IMAGING SOLUTIONS INC FEB COPY COSTS 001-3010-515.45-31 25.99 GREAT AMERICA LEASING CORP FEB 2012 COPIER LEASE 001-3010-515.45-31 163.47 PORT ANGELES CITY TREASURER Envelopes-DeFrang 001-3010-515.31-01 3.26 US BANK CORPORATE PAYMENT SYSTEIWSAMA-Bloor 001-3010-515.49-01 30.00 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-3010-515.42-10 111.06 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-3010-515.42-10 2,20 • WEST GROUP FEB WESTLAW RESEARCH 001-3010-515.31-01 405.82 Attorney Attorney Office Division Total: $746.63 E-11 Page 3 oFTA :/ '•.� City of Port Angeles City Council Expenditure Report From: 3/10/2012 To: 3/23/2012 Date' 3/28/2012 • Vendor Description Account Number Invoice Amount CLALLAM CNTY SHERIFF'S DEPT JAN 2012 JAIL BILL 001-3012-598.51-23 49,612.41 FRIENDSHIP DIVERSION SERVICES PCR #S 18399 & 15319 001-3012-598.51-23 765.00 Attorney .tail Contributions Division Total: $50,377.41 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-3021-515 42-10 0.47 03-05 A/C 3604529882811 B 001-3021-515.42-10 0.47 03-05 A/C 3604525834211 B 001-3021-515 42-10 0.55 03-05 A/C 3604525109623B 001-3021-515.42-10 C.47 03-05 A/C 36045238778178 001-3021-515.42-10 0.47 03-05 A/C 3604523712585B 001-3021-515 42-10 0.78 CLALLAM CNTY DIST 1 COURT FEB.D.CT FILING FEES 001-3021-515.50-90 10,069.36 DIGITAL IMAGING SOLUTIONS INC FEB COPY COSTS 001-3021-515.45-31 25.99 GREAT AMERICA LEASING CORP FEB 2012 COPIER LEASE 001-3021-515.45-31 163.47 OLYMPIC PRINTERS INC COWGILL BUSINESS CARDS 001-3021-515.31-01 58.54 US BANK CORPORATE PAYMENT SYSTEIWSAMA-FiG/COwglll 001-3021-515.49-01 20.00 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-3021-515.42-10 111.06 WA ASSN PROSECUTING ATTRNYS H.MCKEEN TO WAPA TRAIN 001-3021-515.43-10 100.00 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-3021-515.42-10 9.10 WEST GROUP FEB.WESTLAW RESEARCH 001-3021-515.31-01 405.83 Attorney Prosecution Division Total: $10,9615.56 Attorney Department Total. $62,090.60 CENTURYLINK-QWEST 03-05 A/C 36045298876528 001-4010-558.42-10 0.89 03-05 A/C 3604529882811 B 001-4010-558.42-10 0.89 03-05 A/C 3604525834211 B 001-4010-558.42-10 1.03 03-05 A/C 36045251096238 001-4010-558.42-10 0.89 03-05 A/C 3604523877817B 001-4010-558.42-10 0.89 03-05 A/C 36045237125858 001-4010-558.42-10 1.46 SOUND PUBLISHING INC COMMUNICATIONS/MEDIA SERV 001-4010-558.44-10 450.39 US BANK CORPORATE PAYMENT SYSTEI Online Newspaper Subscpt 001-4010-558.49-01 4553 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-4010-558.42-10 28.98 WASHINGTON (DES), STATE OF RADIO &'TELECOMMUNICATION 001-4010-558.42-10 25.80 Community Development Planning Division Total: $556.75 CENTURYLINK-QWEST 03-05 A/C 36045298876528 001-4020-524.42-10 0.31 03-05 A/C 3604529882811 B 001-4020-524.42-10 031 03-05 A/C 3604525834211 B 001-4020-524.42-10 0.36 03-05 A/C 3604525109623B 001-4020-524.42-10 031 03-05 A/C 3604523877817B 001-4020-524.42-10 0.31 03-05 A/C 36045237125858 001-4020-524.42-10 051 OLYMPIC STATIONERS INC OFFICE SUPPLIES, GENERAL 001-4020-524.31-01 5356 SHARP ELECTRONICS CORP RENTAULEASE EQUIPMENT 001-4020-524.45-31 117.56 UNGER ENGINEERING INC, GENE ENGINEER REVIEW NIPPON 001-4020-524.41-50 2,831 00 NIPPON ENGINEERING REVIEW 001-4020-524.41-50 1,672,00 • Community Development Building Division Total: $4,676.23 E - 1;2 Page 4 x,.431 1 , City of Port Angeles Date 3/28/2012 City Council Expenditure Report From: 3/10/2012 To: 3/23/2012 Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-4030-559.42-10 0.05 03-05 A/C 3604529882811 B 001-4030-559.42-10 0.05 03-05 A/C 3604525834211 B 001-4030-559.42-10 0.05 03-05 A/C 3604525109623B 001-4030-559.42-10 0.05 03-05 A/C 3604523877817B 001-4030-559.42-10 0.05 03-05 A/C 3604523712585B 001-4030-559.42-10 0.08 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-4030-559.42-10 5.58 Community Development Code Compliance Division Total: $5.91 Community Development Department Total: $5,238.89 CAPACITY PROVISIONING INC Network Services 001-5010-521.42-12 66.65 Network Services 001-5010-521 42-12 201.08 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-5010-521 42-10 1.89 03-05 A/C 3604529882811B 001-5010-521.42-10 1.89 03-05 A/C 3604525834211B 001-5010-521.42-10 2.20 03-05 A/C 3604525109623B 001-5010-521.42-10 1.89 03-05 A/C 3604523877817B 001-5010-521.42-10 1.89 03-05 A/C 3604523712585B 001-5010-521.42-10 3.12 LANGUAGE LINE SERVICES FEB OVER THE PHONE INTERP 001-5010-521.42-10 65.78 Marilyn Walsh NWPAC LUNCH PROVIDED TO STAFF A 2012 ANNUAL DUES,TG 001-5010-521.31-01 001-5010-521.49-01 56.37 100.00 PORT ANGELES POLICE DEPARTMENT Key Fob Battery 001-5010-521.43-10 3.68 US BANK CORPORATE PAYMENT SYSTEI Gas purchase -Gallagher 001-5010-521 43-10 51.05 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-5010-521.42-10 120.50 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-5010-521 42-10 65.82 Police Department Police Administration Division Total. $743.81 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-5021-521 42-10 1.18 03-05 A/C 3604529882811 B 001-5021-521.42-10 1.18 03-05 A/C 36045258342116 001-5021-521.42-10 1.37 03-05 A/C 3604525109623B 001-5021-521.42-10 1.18 03-05 A/C 3604523877817B 001-5021-521.42-10 1.18 03-05 A/C 3604523712585B 001-5021-521 42-10 1.95 LEXISNEXIS PERSON SEARCHES 001-5021-521.31-01 54.20 US BANK CORPORATE PAYMENT SYSTEI Crime Scene BOX -TP 001-5021-521.31-80 75.98 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-5021-521.42-10 346.50 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-5021-521.42-10 11.81 Police Department Investigation Division Total. $496.53 A WORKSAFE SERVICE, INC DRUG TEST FOR FERNIE 001-5022-521 49-90 52.00 AIRPORT GARDEN CENTER POLICE EQUIPMENT & SUPPLY 001-5022-521.49-80 65.03 BAXTER AUTO PARTS #15 10 30 MIN FLARES,PATROL 001-5022-521.31-01 27.64 BLUMENTHAL UNIFORMS & EQUIP CLOTHING & APPAREL 001-5022-521.20-80 801.95 CENTURYLINK-QWEST 03-05 A/C 36045298876528 001-5022-521.42-10 3.31 03-05 A/C 36045298828116 001-5022-521.42-10 3.31 E-13 Page 5 Date 3/28/2012 City of Port Angeles City Council Expenditure Report r m From: 3110/2012 To: 3/23/2012 Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604525834211 B 001-5022-521.42-10 385 03-05 A/C 36045251096238 001-5022-521.42-10 3.31 03-05 A/C 3604523877817B 001-5022-521 42-10 3.31 03-05 A/C 3604523712585B 001-5022-521.42-10 5.47 EVERGREEN TOWING 2011 Tow Charges 001-5022-521.49-90 277.23 HEALTHFORCE OCCMED BILLING DEPT DRUG TEST FOR NEISINGER 001-5022-521.49-90 44.00 MICROFLEX LATEX GLOVES,PATROL 001-5022-521.31-01 838.48 OLYMPIC MEDICAL CENTER LAB EQUIP,BIO,CHEM,ENVIR 001-5022-521.49-90 100.00 PORT ANGELES POLICE DEPARTMENT Bridge Toll -Prisoner Tran 001-5022-521.43-10 4.00 RICHMOND 2 -WAY RADIO RADIO & TELECOMMUNICATION 001-5022-521.31-14 390.24 SWAIN'S GENERAL STORE INC POLICE EQUIPMENT & SUPPLY 001-5022-521.31-01 41 38 UNITED PARCEL SERVICE Shipping Chgs 001-5022-521.42-10 8.31 US BANK CORPORATE PAYMENT SYSTEIArms/Access-Roggenbuck 001-5022-521.20-80 1,954.20 Arms/Access-Roggen buck 001-5022-521.20-80 617.88 Shipping Program Mbership 001-5022-521.31-80 85.64 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-5022-521.42-10 2,010.97 WA STATE CRIMINAL JUSTICE BLEA 0100-9-Fernie 001-5022-521.43-10 3,283.33 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-5022-521.42-10 24.58 Police Department Patrol Division Total: $10,649.42 PORT ANGELES POLICE DEPARTMENT AARP Dr Safety Prog 001-5026-521.43-10 14.00 PRORIDER INC BIKE HELMETS FOR BIKE FAI 001-5026-521.44-30 446.34 US BANK CORPORATE PAYMENT SYSTEI Service Awards -Gallagher 001-5026-521.31-01 54.74 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-5026-521.42-10 3713 Police Department Reserves & Volunteers Division Total: $552.21 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-5029-521 42-10 1.18 03-05 A/C 3604529882811 B 001-5029-521.42-10 1.18 03-05 A/C 3604525834211B 001-5029-521.42-10 1.37 03-05 A/C 3604525109623B 001-5029-521.42-10 1.18 03-05 A/C 36045238778178 001-5029-521.42-10 1.18 03-05 A/C 3604523712585B 001-5029-521.42-10 1.95 PACIFIC OFFICE EQUIPMENT INC OFFICE SUPPLIES, GENERAL 001-5029-521.45-31 79.87 OFFICE SUPPLIES, GENERAL 001-5029-521.45-31 140.84 US BANK CORPORATE PAYMENT SYSTEI Box Sealing Tape -TG 001-5029-521.31-01 85.37 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-5029-521.42-10 72.27 WAPRO WAPRO TRAINING REGISTRATI 001-5029-521.43-10 125.00 WAPRO TRAINING REGISTRATI 001-5029-521.43-10 125.00 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-5029-521 42-10 15.91 Police Department Records Division Total: $652.30 Police Department Department Total: $13,0941.27 CAPACITY PROVISIONING INC Network Services 001-6010-522.42-12 333.22 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-6010-522.42-10 1.66 03-05 A/C 36045298828116 001-6010-522.42-10 1.66 E - 14 Page 6 • • • rr""'•t City of Port Angeles City Council Expenditure Report From: 3110/2012 To: 3/2312012 Date 3/28/2012 Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604525834211B 001-6010-522.42-10 1.92 03-05 A/C 3604525109623B 001-6010-522.42-10 1.66 03-05 A/C 3604523877817B 001-6010-522.42-10 1.66 03-05 A/C 3604523712585B 001-6010-522.42-10 2.73 03-05 A/C 3604529887652B 001-6010-522.42-11 0.47 03-05 A/C 3604529882811 B 001-6010-522.42-11 047 03-05 A/C 3604525834211B 001-6010-522.42-11 0.55 03-05 A/C 3604525109623B 001-6010-522.42-11 0.47 03-05 A/C 3604523877817B 001-6010-522.42-11 0.47 03-05 A/C 3604523712585B 001-6010-522.42-11 0.78 PACIFIC OFFICE EQUIPMENT INC TONER CARTRIDGE 001-6010-522.31-01 64.14 PORT ANGELES CITY TREASURER PSAB Mtg-Wheeler 001-6010-522.31-01 12.47 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-6010-522.42-10 59.61 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-6010-522.42-10 4.62 RADIO & TELECOMMUNICATION 001-6010-522.42-11 2.79 WHEELER, CORAL REFRESHMENTS PSAB MEETING 001-6010-522.31-01 35.97 POSTAGE 001-6010-522.42-10 10.25 Fire Department Fire Administration Division Total. $537.57 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-6020-522.42-10 1.54 03-05 A/C 3604529882811 B 001-6020-522.42-10 1.54 03-05 A/C 3604525834211B 001-6020-522.42-10 1.79 03-05 A/C 3604525109623B 001-6020-522.42-10 1.54 03-05 A/C 3604523877817B 001-6020-522.42-10 1.54 03-05 A/C 3604523712585B 001-6020-522.42-10 2.54 Chris Piper INSTRUCTOR I CLASS 2/24/1 001-6020-522.43-10 93300 PACIFIC OFFICE EQUIPMENT INC COMPUTERS,DP & WORD PROC. 001-6020-522.31-02 216.97 SWAIN'S GENERAL STORE INC BOATS,MOTORS,& MARINE SUP 001-6020-522.31-02 6.36 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-6020-522.42-10 1.03 WHEELER, CORAL WATER 001-6020-522.31-02 3.68 BATTERIES 001-6020-522.31-02 26.04 Fire Department Fire Supression Division Total. $1,197.57 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-6021-522.42-10 0.12 03-05 A/C 3604529882811 B 001-6021-522.42-10 0.12 03-05 A/C 3604525834211 B 001-6021-522.42-10 0.14 03-05 A/C 3604525109623B 001-6021-522.42-10 0.12 03-05 A/C 3604523877817B 001-6021-522.42-10 0.12 03-05 A/C 3604523712585B 001-6021-522.42-10 0.19 Fire Department Fire Volunteers Division Total. $0.81 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-6030-522.42-10 0.24 03-05 A/C 36045298828116 001-6030-522.42-10 0.24 • 03-05 A/C 3604525834211 B 001-6030-522.42-10 0.27 03-05 A/C 36045251096238 001-6030-522.42-10 0.24 E-15 Page 7 Page 8 Date 3/28/2012 City of Port Angeles City Council Expenditure Report F„'r°°•.• From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604523877817B 001-6030-522.42-10 0.24 03-05 A/C 3604523712585B 001-6030-522.42-10 039 KNOX COMPANY LOCK CORE 001-6030-522.31-01 85.63 US BANK CORPORATE PAYMENT SYSTEIBinders-Dubuc 001-6030-522.31-01 129.40 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 001-6030-522.42-10 58.84 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-6030-522.42-10 3.96 Fire Department Fire Prevention Division Total: $279.45 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-6040-522.42-10 024 03-05 A/C 3604529882811B 001-6040-522.42-10 0.24 03-05 A/C 36045258342116 001-6040-522.42-10 027 03-05 A/C 3604525109623B 001-6040-522.42-10 0,24 03-05 A/C 3604523877817B 001-6040-522.42-10 024 03-05 A/C 3604523712585B 001-6040-522.42-10 0,39 US BANK CORPORATE PAYMENT SYSTEITraining Room Projector 001-6040-522.31-01 564.41 Training Room Projector 001-6040-522.43-10 56441 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-6040-522.42-10 5.21 Fire Department Fire Training Division Total: $1,135.65 MRS CLEAN MONTHLY CLEANING 001-6050-522.41-50 395.00 WHEELER, CORAL SUPPLIES 001-6050-522.31-20 16.17 Fire Department Facilities Maintenance Division Total: $411.17 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-6060-525.42-10 1.07 03-05 A/C 3604529882811 B 001-6060-525.42-10 1 07 03-05 A/C 3604525834211B 001-6060-525.42-10 1.24 03-05 A/C 3604525109623B 001-6060-525.42-10 1.07 03-05 A/C 3604523877817B 001-6060-525.42-10 1.07 03-05 A/C 3604523712585B 001-6060-525.42-10 1.76 Fire Department Emergency Management Division Total: $7.28 Fire Department Department Total: $3,569.50 CAPACITY PROVISIONING INC Network Services 001-7010-532 42-12 10840 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-7010-532.42-10 3.65 03-05 A/C 3604529882811 B 001-7010-532 42-10 365 03-05 A/C 36045258342116 001-7010-532.42-10 4.27 03-05 A/C 36045251096236 001-7010-532.42-10 3.65 03-05 A/C 3604523877817B 001-7010-532.42-10 3.65 03-05 A/C 3604523712585B 001-7010-532.42-10 6.05 FEDERAL EXPRESS CORP Shipping Chgs 001-7010-532.42-10 5.61 INSIGHT PUBLIC SECTOR RENTAL/LEASE EQUIPMENT 001-7010-532.31-01 289.42 Randall Brackett MILEAGE REIMBURSEMENT 001-7010-532.31-01 42.73 SONDYA WRAY Mileage reimb-2011 001-7010-532 42-10 23.84 PSMJ RESOURCES, INC. JAMES BURKE CLASS REGISTR 001-7010-532.43-10 99500 ERIC WALRATH CLASS REGIST 001-7010-532.43-10 995.00 . OFFICE DEPOT SUPPLIES 001-7010-532.31-01 77.20 E - 113 Page 8 Date 3/28/2012 City of Port Angeles City Council Expenditure Report • Y}r'°'•r"� From: 3110/2012 To: 312312012 Vendor Description Account Number Invoice Amount OFFICE DEPOT SUPPLIES 001-7010-532.31-01 15.39 SUPPLIES 001-7010-532.31-01 721.15 SUPPLIES 001-7010-532.31-01 29.65 SUPPLIES 001-7010-532.31-01 61.76 SUPPLIES 001-7010-532.31-01 101.36 OLYMPIC STATIONERS INC SUPPLIES 001-7010-532.31-01 28.41 PACIFIC OFFICE EQUIPMENT INC COMPUTER ACCESSORIES&SUPF001-7010-532.31-01 80.75 OFFICE MACHINES & ACCESS 001-7010-532.45-31 478.47 PORT ANGELES CITY TREASURER Chamber Lunch-Cutler 001-7010-532.31-01 13.00 SHARP ELECTRONICS CORP MX260ON COPIER-MARCH 2012 001-7010-532.45-31 142.87 SOUND PUBLISHING INC ASST CIVIL ENGINEER AD 001-7010-532.44-10 692.70 US BANK CORPORATE PAYMENT SYSTEI Reception Chairs-Wray 001-7010-532.31-01 184.27 VERIZON WIRELESS 02-22 a/c 571136182-00001 001-7010-532.42-10 86.84 COMMUNICATIONS/MEDIA SERV 001-7010-532 42-10 58.39 02-28 a/c 271138138-00002 001-7010-532.42-10 40.10 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-7010-532.42-10 124.79 Public Works -Gen Fnd Pub Wks Administration Division Total: $5,422.02 Public Works -Gen Fnd Department Total: $5,422.02 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 03-05 A/C 3604529882811 B 001-8010-574.42-10 001-8010-574.42-10 0.35 0.35 03-05 A/C 3604525834211 B 001-8010-574.42-10 0.41 03-05 A/C 3604525109623B 001-8010-574.42-10 0.35 03-05 A/C 3604523877817B 001-8010-574.42-10 0.35 03-05 A/C 3604523712585B 001-8010-574.42-10 0.59 DIGITAL IMAGING SOLUTIONS INC FEB COPY COSTS 001-8010-574.45-31 33.76 OLYMPIC PRINTERS INC PRINTING,SILK SCR,TYPSET 001-8010-574.31-01 29.27 OLYMPIC STATIONERS INC OFFICE SUPPLIES, GENERAL 001-8010-574.31-01 177.95 PORT ANGELES CITY TREASURER Sponges/Soap-VBCC 001-8010-574.31-01 5.62 US BANK CORPORATE PAYMENT SYSTEI Office Supplies-Mozingo 001-8010-574.31-01 194.20 VERIZON WIRELESS 02-22 a/c 571136182-00005 001-8010-574.42-10 47.90 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-8010-574.42-10 5.87 Parks Dept Parks Administration Division Total: $496.97 CENTURYLINK-QWEST 03-02 a/c 3604171942413B 001-8012-555 42-10 53.23 02-20 a/c 206T217227465B 001-8012-555.42-10 57.46 03-05 A/C 36045298876528 001-8012-555.42-10 0.35 03-05 A/C 3604529882811 B 001-8012-555.42-10 0.35 03-05 A/C 3604525834211 B 001-8012-555.42-10 0.41 03-05 A/C 3604525109623B 001-8012-555.42-10 0.35 03-05 A/C 3604523877817B 001-8012-555.42-10 0.35 03-05 A/C 3604523712585B 001-8012-555 42-10 0.59 DIGITAL IMAGING SOLUTIONS INC FEB COPY COSTS 001-8012-555.45-31 31.16 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-8012-555.42-10 1.39 E-17 Page 9 Date3/28/2012 City of Port Angeles City Council Expenditure Report `}'' •+�" From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount Parks Dept Senior Center Division Total: $145.64 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-8050-536.42-10 0.24 03-05 A/C 3604529882811B 001-8050-536.42-10 0.24 03-05 A/C 3604525834211 B 001-8050-536.42-10 0.27 03-05 A/C 3604525109623B 001-8050-536.42-10 0.24 03-05 A/C 3604523877817B 001-8050-536.42-10 0.24 03-05 A/C 3604523712585B 001-8050-536.42-10 0.39 CLINICARE OF PORT ANGELES INC DOT PHYSICAL - MORSE 001-8050-536.49-90 70.00 Chester Conlin SELL BACK MOTHER'S BURIAL 001-8050-343.60-12 163.00 David S Conlin SELL MOTHES BURIAL SPACE 001-8050-343.60-12 163.00 DeAnn Conlin SELL BACK BURIAL SPACE TO 001-8050-343.60-12 163.00 OLYMPIC PRINTERS INC PRINTING,SILK SCR,TYPSET 001-8050-536.31-01 29.27 PACIFIC OFFICE EQUIPMENT INC COMPUTER ACCESSORIES&SUPF001 -8050-536.31 -01 282.91 PENINSULA AWARDS &TROPHIES BADGES & OTHER ID EQUIP. 001-8050-536.31-01 3692 BADGES & OTHER ID EQUIP 001-8050-536.34-01 22.05 QUIRING MONUMENTS INC CEMETERY MARKERS 001-8050-536.34-01 758.00 SOUND PUBLISHING INC COMMUNICATIONS/MEDIA SERV 001-8050-536.44-10 26500 SUNSET DO -IT BEST HARDWARE RENTAL/LEASE EQUIPMENT 001-8050-536 45-30 14.09 RENTAULEASE EQUIPMENT 001-8050-536.45-30 14.09 VERIZON WIRELESS 02-28 a/c :271138138-00001 001-8050-536.42-10 82.48 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-8050-536 42-10 0.15 Parks Dept Ocean View Cemetery Division Total: $2,065.58 AMSAN PAPER & PLASTIC-DISPOSABL 001-8080-576.31-01 3,62500 PLASTICS 001-8080-576.31-01 3,08398 JANITORIAL SUPPLIES 001-8080-576.31-01 1,275.15 JANITORIAL SUPPLIES 001-8080-576.31-01 139.40 ANGELES MILLWORK & LUMBER CO JANITORIAL SUPPLIES 001-8080-576.31-01 9.75 LUMBER& RELATED PRODUCTS 001-8080-576.31-20 8893 BAILEY SIGNS & GRAPHICS MARKERS, PLAQUES,SIGNS 001-8080-576.31-20 162.60 BEACON ATHLETICS SPORTING & ATHLETIC EQUIP 001-8080-576.31-20 420.55 CAPACITY PROVISIONING INC Network Services 001-8080-576.42-12 201.08 Network Services 001-8080-576.42-12 103„41 CED/CONSOLIDATED ELEC DIST INC ELECTRICAL EQUIP & SUPPLY 001-8080-576.31-20 85.86 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-8080-576.42-10 1,18 03-05 A/C 3604529882811 B 001-8080-576.42-10 1.18 03-05 A/C 3604525834211B 001-8080-576.42-10 1,.37 03-05 A/C 3604525109623B 001-8080-576.42-10 1.18 03-05 A/C 3604523877817B 001-8080-576.42-10 1.18 03-05 A/C 3604523712585B 001-8080-576.42-10 1,95 CLINICARE OF PORT ANGELES INC DOT PHYSICAL - MORSE 001-8080-576.49-90 35.00 LAWN EQUIPMENT SUPPLY LAWN MAINTENANCE EQUIP 001-8080-576.31-01 97.81 TOM MORSE CDL LICENSE RENEWAL FOR T 001-8080-576.49-90 61.00 E-18 Page 10 • • • CJ a.gorq„ ' City of Port Angeles Date 3/28/2012 City Council Expenditure Report ,,fy"•*" From: 3/10/2012 To: 3123/2012 Vendor Description Account Number Invoice Amount OFFICE DEPOT SUPPLIES 001-8080-576.31-01 64.54 PACIFIC OFFICE EQUIPMENT INC COMPUTER ACCESSORIES&SUPF001-8080-576.31-01 343.85 SANDERSON SAFETY SUPPLY CO FIRST AID & SAFETY EQUIP. 001-8080-576.31-01 156.73 SEARS COMMERCIAL ONE HOSES, ALL KINDS 001-8080-576.31-01 86.24 SKAGIT GARDENS INC NURSERY STOCK & SUPPLIES 001-8080-576.31-40 7,785.13 SOUND PUBLISHING INC SEASONAL LABORER AD 001-8080-576.44-10 270.25 SUNSET DO -IT BEST HARDWARE ELECTRICAL EQUIP & SUPPLY 001-8080-576.31-01 31.35 LAWN MAINTENANCE EQUIP 001-8080-576.31-20 27.78 RENTAULEASE EQUIPMENT 001-8080-576 45-30 21.14 RENTAULEASE EQUIPMENT 001-8080-576 45-30 21 14 SWAIN'S GENERAL STORE INC HARDWARE,AND ALLIED ITEMS 001-8080-576.31-01 19.25 FIRST AID & SAFETY EQUIP. 001-8080-576.31-01 36.57 THURMAN SUPPLY FASTENERS, FASTENING DEVS 001-8080-576.31-01 23.02 US BANK CORPORATE PAYMENT SYSTEI Grappler PU Tool -Wray 001-8080-576.35-01 259.38 Conf Reg-JB/JH/BK 001-8080-576 43-10 200.00 VERIZON WIRELESS 02-22 a/c 571136182-00003 001-8080-576.42-10 145.79 02-28 a/c 271138138-00004 001-8080-576 42-10 8006 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-8080-576.42-10 4.11 Parks Dept Park Facilities Division Total: $18,973.89 Parks Dept Department Total: $21,682.08 CED/CONSOLIDATED ELEC DIST INC ELECTRICAL EQUIP & SUPPLY 001-8112-555.31-20 10732 CENTURYLINK-QWEST 03-02 a/c 3604170786905B 001-8112-555.42-10 32.35 FASTENAL INDUSTRIAL HARDWARE,AND ALLIED ITEMS 001-8112-555.31-20 42.23 ORKIN EXTERMINATING COMPANY INC EXTERNAL LABOR SERVICES 001-8112-555.48-10 59.62 Facilities Maintenance Senior Center Facilities Division Total. $241.52 AMSAN JANITORIAL SUPPLIES 001-8130-518.31-01 24.33 JANITORIAL SUPPLIES 001-8130-518.31-01 17.04 CED/CONSOLIDATED ELEC DIST INC ELECTRICAL EQUIP & SUPPLY 001-8130-518.31-01 30.64 CENTURYLINK-QWEST 03-05 A/C 36045298876528 001-8130-518.42-10 0.12 03-05 A/C 3604529882811 B 001-8130-518.42-10 0.12 03-05 A/C 3604525834211 B 001-8130-518.42-10 0.14 03-05 A/C 3604525109623B 001-8130-518.42-10 0.12 03-05 A/C 3604523877817B 001-8130-518.42-10 0.12 03-05 A/C 3604523712585B 001-8130-518 42-10 0.19 VERIZON WIRELESS 02-22 a/c 571136182-00005 001-8130-518.42-10 19.14 Facilities Maintenance Custodial/Janitorial Svcs Division Total: $91.96 CED/CONSOLIDATED ELEC DIST INC ELECTRICAL EQUIP & SUPPLY 001-8131-518.31-20 269.92 ELECTRICAL EQUIP & SUPPLY 001-8131-518.31-20 66.76 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-8131-518 42-10 012 03-05 A/C 3604529882811 B 001-8131-518.42-10 0.12 03-05 A/C 3604525834211 B 001-8131-518.42-10 0.14 03-05 A/C 3604525109623B 001-8131-518 42-10 0.12 E-19 Page 11 Date 3/28/2012 City of Port Angeles ..n City Council Expenditure Report From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604523877817B 001-8131-518.42-10 0.12 03-05 A/C 3604523712585B 001-8131-518 42-10 0.20 ORKIN EXTERMINATING COMPANY INC EXTERNAL LABOR SERVICES 001-8131-518.48-10 78.46 THURMAN SUPPLY HOSES, ALL KINDS 001-8131-518.31-20 33.26 THYSSENKRUPP ELEVATOR CORP BUILDING MAINT&REPAIR SER 001-8131-518.48-10 857.33 Facilities Maintenance Central Svcs Facilities Division Total: $1,306.55 Facilities Maintenance Department Total: $1,640.03 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-8221-574.42-10 0.12 03-05 A/C 3604529882811 B 001-8221-574.42-10 0.12 03-05 A/C 3604525834211 B 001-8221-574.42-10 0.14 03-05 A/C 3604525109623B 001-8221-574 42-10 012 03-05 A/C 3604523877817B 001-8221-574.42-10 0.12 03-05 A/C 3604523712585B 001-8221-574.42-10 0.19 DIGITAL IMAGING SOLUTIONS INC FEB COPY COSTS 001-8221-574 45-31 59.72 DOBYNS, THERESA REFEREE PAYMENT 001-8221-574.41-50 29000 KONOPASKI, MARCUS SCOREKEEPER PAYMENT 001-8221-574.41-50 5000 PIMENTEL, HENRY REFEREE PAYMENT 001-8221-574.41-50 220.00 RAMSEY, SCOTT REFEREE PAYMENT 001-8221-574 41-50 440.00 ROONEY, RANDY L REFEREE PAYMENT 001-8221-574 41-50 308,00 THAYER, JEFFREY REFEREE PAYMENT 001-8221-574.41-50 374.00 THOMAS, GREGORY REFEREE PAYMENT 001-8221-574.41-50 8800 WARDELL, ADAM REFEREE PAYMENT 001-8221-574 41-50 484.00 Recreation Activities Sports Programs Division Total: $2,314.53 ANDERSEN, BRIAN L REFEREE PAYMENT 001-8222-574.41-50 220,00 AT&T MOBILITY Dan Estes Cell Phone 001-8222-574.42-10 21.56 BAKER, LARRY REFEREE PAYMENT 001-8222-574.41-50 17600 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-8222-574.42-10 0.12 03-05 A/C 3604529882811 B 001-8222-574.42-10 0,12 03-05 A/C 3604525834211 B 001-8222-574.42-10 0 14 03-05 A/C 3604525109623B 001-8222-574.42-10 012 03-05 A/C 3604523877817B 001-8222-574.42-10 012 03-05 A/C 3604523712585B 001-8222-574.42-10 019 DIGITAL IMAGING SOLUTIONS INC FEB COP`( COSTS 001-8222-574.45-31 5972 FRAZIER, BRIAN D REFEREE PAYMENT 001-8222-574.41-50 132.00 GUERRA, JOE REFEREE PAYMENT 001-8222-574.41-50 24200 GUNDERSON, HAYDEN SCOREKEEPER PAYMENT 001-8222-574.41-50 50.00 HANSEN'S TROPHY MARKERS, PLAQUES,SIGNS 001-8222-574.31-01 34688 MARKERS, PLAQUES,SIGNS 001-8222-574.31-01 693.76 HENSEN, JAMES C REFEREE PAYMENT 001-8222-574.41-50 220.00 JEFFERS, KYLEE B SCOREKEEPER PAYMENT 001-8222-574.41-50 10000 JEFFERS, TAYLYN NICOLE SCOREKEEPER PAYMENT 001-8222-574.41-50 110.00 • JONES, BAILEE C SCOREKEEPER PAYMENT 001-8222-574.41-50 50.00 E-213 Page 12 6&, BF74 . Date 3/28/2012 City of Port Angeles City Council Expenditure Report `�•=rf" � From: 3110/2012 To: 3/23/2012 Vendor Description Account Number Invoice Amount JONES, SKYLAR M SCOREKEEPER PAYMENT 001-8222-574.41-50 110.00 Wendolyn Windham REF.ENTRY FEE TO TEAM W/O 001-8222-347.60-21 25000 PARKER, PAUL RAMON REFEREE PAYMENT 001-8222-574.41-50 110.00 PIMENTEL, HENRY REFEREE PAYMENT 001-8222-574.41-50 220.00 RAMSEY, SCOTT REFEREE PAYMENT 001-8222-574.41-50 330.00 SADDLER, CHARLES M REFEREE PAYMENT 001-8222-574.41-50 220.00 THAYER, JEFFREY REFEREE PAYMENT 001-8222-574.41-50 154.00 ULIN, BRADLEY V REFEREE PAYMENT 001-8222-574.41-50 242.00 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-8222-574.42-10 6.16 Recreation Activities Special Events Division Total. $4,064.89 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 001-8224-574.42-10 0.12 03-05 A/C 3604529882811 B 001-8224-574.42-10 0.12 03-05 A/C 3604525834211 B 001-8224-574.42-10 0.14 03-05 A/C 3604525109623B 001-8224-574.42-10 0.12 03-05 A/C 3604523877817B 001-8224-574.42-10 0.12 03-05 A/C 3604523712585B 001-8224-574.42-10 0.19 DIGITAL IMAGING SOLUTIONS INC FEB COPY COSTS 001-8224-574.45-31 59.72 PORT ANGELES CITY TREASURER After School Movie Day 001-8224-574.31-01 500 US BANK CORPORATE PAYMENT SYSTEI Food Handler Card -AM 001-8224-574 31-01 10.00 • VERIZON WIRELESS 02-22 a/c 571136182-00005 001-8224-574.42-10 38.28 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 001-8224-574.42-10 0.29 Recreation Activities Youth/Family Programs Division Total: $114.10 Recreation Activities Department Total: $6,493.52 General Fund Fund Total: $143,874.26 PORT ANGELES CHAMBER OF COMM 2012 MEDIAIMKTG CAMPAIGN 101-1430-557.50-83 30,946.27 Lodging Excise Tax Lodging Excise Tax Division Total: $30,946.27 Lodging Excise Tax Department Total: $30,946.27 Lodging Excise Tax Fund Fund Total: $30,946.27 GRAPHIC PRODUCTS COMPUTER HARDWARE&PERIPHI102-0000-237.00-00 -79.83 Division Total. -$79.83 Department Total: -$79.83 AMSAN PAPER & PLASTIC-DISPOSABL 102-7230-542.31-01 57.24 ANGELES CONCRETE PRODUCTS ROAD/HWY MAT NONASPHALTIC 102-7230-542.31-05 2,755.67 ROAD/HWY MAT NONASPHALTIC 102-7230-542.31-20 133.92 ANGELES MILLWORK & LUMBER CO LUMBER& RELATED PRODUCTS 102-7230-542.31-20 284.05 LUMBER& RELATED PRODUCTS 102-7230-542.31-20 212.82 LUMBER& RELATED PRODUCTS 102-7230-542.31-20 46.31 FASTENERS, FASTENING DEVS 102-7230-542.31-20 33.25 FASTENERS, FASTENING DEVS 102-7230-542.31-20 17.32 • BAXTER AUTO PARTS #15 BELTS AND BELTING BELTS 102-7230-542.31-01 8.50 AND BELTING 102-7230-542.31-01 0.08 CAPACITY PROVISIONING INC Network Services 102-7230-542.42-12 116.63 E-21 Page 13 � Date 3/28/2012 City of Port Angeles City Council Expenditure Report From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604529887652B 102-7230-542.42-10 0.59 03-05 A/C 3604529882811 B 102-7230-542 42-10 0.59 03-05 A/C 3604525834211 B 102-7230-542.42-10 0.69 03-05 A/C 3604525109623B 102-7230-542.42-10 0.59 03-05 A/C 3604523877817B 102-7230-542.42-10 0.59 03-05 A/C 36045237125858 102-7230-542.42-10 098 GRAPHIC PRODUCTS COMPUTER HARDWARE&PERIPH1102-7230-542.31-25 1,030.13 HARTNAGEL BUILDING SUPPLY INC EPDXY BASED FORMULAS 102-7230-542.31-20 48.99 HOLCOMB & COMPANY, D ROAD/HWY MAT NONASPHALTIC 102-7230-542.31-20 382.70 LAKESIDE INDUSTRIES INC ROAD/HWY MATERIALS ASPHLT 102-7230-542.31-20 1,204.33 ROAD/HWY MATERIALS ASPHLT 102-7230-542.31-20 716.34 MOTOROLA SOLUTIONS, INC RADIO & TELECOMMUNICATION 102-7230-542.48-10 9,279.04 NAPA AUTO PARTS SUPPLIES 102-7230-542.31-01 12.99 OFFICE DEPOT SUPPLIES 102-7230-542.31-01 64.55 PACIFIC OFFICE EQUIPMENT INC COMPUTER ACCESSORIES&SUPE 102-7230-542.31-01 150.00 PUD #1 OF CLALLAM COUNTY Lauridsen Bvld/L St 102-7230-542.47-10 1341 RADIOSHACK ELECTRICAL EQUIP & SUPPLY 102-7230-542.35-01 43.35 SNAP-ON TOOLS - CHUGGER DEANE LAWN MAINTENANCE EQUIP 102-7230-542.35-01 95.39 SUNSET DO -IT BEST HARDWARE JANITORIAL SUPPLIES 102-7230-542.31-01 18.99 SUPPLIES 102-7230-542.31-01 58.60 • SUPPLIES 102-7230-542.31-01 -9.52 JANITORIAL SUPPLIES 102-7230-542.31-20 14.62 HARDWARE,AND ALLIED ITEMS 102-7230-542.31-20 7 10 PLUMBING EQUIP FIXT,SUPP 102-7230-542.31-20 11.21 FASTENERS, FASTENING DEVS 102-7230-542.31-20 5.56 MARKERS, PLAQUES,SIGNS 102-7230-542.31-25 17.50 HARDWARE,AND ALLIED ITEMS 102-7230-542.35-01 79.75 SWAIN'S GENERAL STORE INC HARDWARE,AND ALLIED ITEMS 102-7230-542.31-20 23.99 PAINTS,COATINGS,WALLPAPER 102-7230-542.31-25 1577 THURMAN SUPPLY PIPE AND TUBING 102-7230-542.31-20 9.14 TRAFFIC SAFETY SUPPLY CO MARKERS, PLAQUES,SIGNS 102-7230-542.31-25 606.71 US BANK CORPORATE PAYMENT SYSTEIConf Reg-JB/JH/BK 102-7230-542.43-10 100.00 USA BLUEBOOK SPRAYING EQUIPMENT 102-7230-542.31-20 298.20 VERIZON WIRELESS 02-22 a/c 571136182-00003 102-7230-542.42-10 119.51 02-28 a/c 271138138-00004 102-7230-542.42-10 7142 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 102-7230-542.42-10 2.57 WASHINGTON (DOT), STATE OF CONSTRUCTION SERVICES,GEN 102-7230-542.48-10 7,29440 Public Works -Street Street Division Total: $25,456.56 Public Works -Street Department Total: $25,456.56 Street Fund Fund Total: $25,376.73 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 103-1511-558.42-10 0.06 • 03-05 A/C 3604529882811 B 103-1511-558.42-10 006 E-22 Page 14 Date 3/28/2012 City of Port Angeles City Council Expenditure Report • "` •� `" From: 3110/2012 To: 3/2312012 Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C 3604525834211B 103-1511-558.42-10 0.07 03-05 A/C 3604525109623B 103-1511-558 42-10 0.06 03-05 A/C 3604523877817B 103-1511-558.42-10 0.06 03-05 A/C 3604523712585B 103-1511-558.42-10 010 KENYON DISEND, PLLC FEMA LAWSUIT 103-1511-558 41-50 1,057.35 PORT ANGELES CITY TREASURER PABA /Chamber -West 103-1511-558.31-01 2408 RADIO PACIFIC INC (KONP) KONP HOME SHOW CHOOSE LOC 103-1511-558.41-50 75.00 SOUND PUBLISHING INC COMMUNICATIONS/MEDIA SERV 103-1511-55844-10 50.56 US BANK CORPORATE PAYMENT SYSTEI Seminar Reg -West 103-1511-558.43-10 3000 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 103-1511-558.42-10 28.98 Economic Development Economic Development Division Total: $1,266.38 Economic Development Department Total. $1,266.38 Economic Development Fund Total. $1,266.38 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 106-1512-558.42-10 0.12 03-05 A/C 3604529882811 B 106-1512-558.42-10 0.12 03-05 A/C 3604525834211 B 106-1512-558.42-10 0.14 03-05 A/C 3604525109623B 106-1512-558.42-10 0.12 03-05 A/C 3604523877817B 106-1512-558.42-10 0.12 • WASHINGTON (DES), STATE OF 03-05 A/C 3604523712585B RADIO & TELECOMMUNICATION 106-1512-558.42-10 106-1512-558.42-10 0.20 0.22 Economic Development Archaeologist Division Total: $1.04 Economic Development Department Total: $1.04 Cultural Resources Fund Total: $1.04 CAPACITY PROVISIONING INC Network Services 107-5160-528.42-12 201.08 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 107-5160-528 42-10 3.20 03-05 A/C 3604529882811 B 107-5160-528.42-10 3.20 03-05 A/C 3604525834211 B 107-5160-528.42-10 371 03-05 A/C 3604525109623B 107-5160-528.42-10 3.20 03-05 A/C 3604523877817B 107-5160-528.42-10 3.20 03-05 A/C 3604523712585B 107-5160-528.42-10 5.27 03-02 a/c 360220380301 B 107-5160-528.42-11 1,036.43 Todd VanSickie AIRFARE -NWS CONFERENCE - 107-5160-528.43-11 261.60 NEW WORLD SYSTEMS DATA PROC SERV &SOFTWARE 107-5160-528 48-10 560.00 QUILL CORPORATION ENVELOPES, PLAIN, PRINTED 107-5160-528 31-01 123.13 SOUND PUBLISHING INC COMMUNICATIONS/MEDIA SERV 107-5160-528.41-50 283.28 COMMUNICATIONS/MEDIA SERV 107-5160-528.41-50 80.50 US BANK CORPORATE PAYMENT SYSTEITravel Accom Deposit -SR 107-5160-528.43-10 159.12 VERIZON WIRELESS COMMUNICATIONS/MEDIA SERV 107-5160-528.42-10 174.50 WAPRO SECURITY,FIRE,SAFETY SERV 107-5160-528.43-10 125.00 WASHINGTON (DES), STATE OF • Pencom RADIO & TELECOMMUNICATION Pencom 107-5160-528.42-10 Division Total: 76.04 $3,102.46 Pencom Department Total: $3,102.46 E-23 Page 15 Page 16 Date 3/28/2012 City of Port Angeles City Council Expenditure Report From: 3110/2012 To: 312312012 • Vendor Description Account Number Invoice Amount Pencom Fund Fund Total: $3,102.46 SARGENT ENGINEERING, INC STRUCTURAL ANALYSIS 310-7930-595.41-50 4,864.20 STUDIO CASCADE, INC WTIP 310-7930-595 41-50 2,964.49 WTIP 310-7930-595.41-50 3,811.49 WTIP 310-7930-595.41-50 847.00 WTIP 310-7930-595.41-50 847.00 Capital Projects -Pub Wks GF -Street Projects Division Total: $13,334.18 STUDIO CASCADE, INC WTIP 310-7961-595.41-50 97,997.98 Capital Projects -Pub Wks ST -Sidewalk Improvement Division Total: $97,997.98 Capital Projects -Pub Wks Department Total: $111,332.16 VIKING AUTOMATIC SPRINKLER COMPAt EQUIP MAINT & REPAIR SERV 310-8985-594.65-10 28,482'.86 EQUIP MAINT & REPAIR SERV 310-8985-594.65-10 8,597.96 EQUIP MAINT & REPAIR SERV 310-8985-594.65-10 64,671.66 Capital Proj-Parks & Rec Misc Parks Projects Division Total: $101,752.48 Capital PropParks & Rec Department Total: $101,752.48 Capital Improvement Fund Total: $213,084.64 ASPLUNDH TREE EXPERT CO Release Retainage 401-0000-223.40-00 4,432.97 BPA -POWER WIRES February Power Wire -EFT 401-0000-213.10-00 238,485.00 February Power Wire -EFT 401-0000-213.10-00 2,113,089.00 BLAGDON, JESSICA L FINAL BILL REFUND 401-0000-122.10-99 104.86 • BREITHAUPT, JEFF MANUAL CHECK 401-0000-122.10-99 148.09 BURR, JANET ELLEN MANUAL CHECK 401-0000-122.10-99 46.01 CAMPBELL, THOMAS P FINAL BILL REFUND 401-0000-122 10-99 53.10 DAVENPORT, DANIELLE W MANUAL CHECK 401-0000-122.10-99 0.78 ELDER, TREVOR C FINAL BILL REFUND 401-0000-122.10-99 2.21 FELDMAN, JOSHUA G FINAL BILL REFUND 401-0000-122.10-99 42.36 FLEMING, JOHN A FINAL BILL REFUND 401-0000-122.10-99 82.95 HAMRICK, JORDAN A FINAL BILL REFUND 401-0000-122.10-99 11.88 HONICKER, JUDY L FINAL BILL REFUND 401-0000-122 10-99 165.09 JOAQUIN, KELLY FINAL BILL REFUND 401-0000-122.10-99 190.11 JOHNSON, JEDEDIAH FINAL BILL REFUND 401-0000-122.10-99 39.58 JOHNSON, MARIAN FINAL BILL REFUND 401-0000-122.10-99 59.69 LUNDERVILLE, COLLEEN K FINAL BILL REFUND 401-0000-122.10-99 69.74 MARTINEZ, DINA UTILITY DEPOSIT REFUND 401-0000-122.10-99 125.00 MOHAMED, ALA ELDIN AHMED FINAL BILL REFUND 401-0000-122.10-99 20.25 REED, CHERILYN R FINAL BILL REFUND 401-0000-122.10-99 102.51 SOMERVILLE, DIANA E FINAL BILL REFUND 401-0000-122.10-99 0.06 SULLIVAN, DAVID L FINAL BILL REFUND 401-0000-122.10-99 1810 WILKINSON, GRAYSON FINAL BILL REFUND 401-0000-122.10-99 37.87 US BANK CORPORATE PAYMENT SYSTEI Safety Gloves-Hairell 401-0000-237.00-00 -26.49 US LIGHTING TECH ELECTRICAL EQUIP & SUPPLY 401-0000-141.40-00 10,320.85 • ELECTRICAL EQUIP & SUPPLY 401-0000-237.00-00 -799.77 E-2.4 Page 16 City of Port Angeles Date 3/28/2012 City Council Expenditure Report • �,' ,•x. ¢" From: 3/1012012 To: 3123/2012 Vendor Description Account Number Invoice Amount Division Total: $2,366,821.80 Department Total: $2,366,821.80 CAPACITY PROVISIONING INC Network Services 401-7111-533.42-12 99.97 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 401-7111-533 42-10 0.35 03-05 A/C 3604529882811 B 401-7111-533 42-10 0.35 03-05 A/C 3604525834211 B 401-7111-533.42-10 0.41 03-05 A/C 3604525109623B 401-7111-533.42-10 0.35 03-05 A/C 36045238778176 401-7111-533 42-10 0.35 03-05 A/C 3604523712585B 401-7111-533 42-10 0.59 BRIAN ANDERS TRAVEL REIMBURSEMENT FOR 401-7111-533.43-10 239.40 VERIZON WIRELESS 02-22 a/c 571136182-00001 401-7111-533.42-10 28.42 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 401-7111-533.42-10 2.42 Public Works -Electric Engineering -Electric Division Total: $372.61 CAPACITY PROVISIONING INC Network Services 401-7120-533.42-12 99.97 CENTURYLINK-QWEST 03-05 A/C 36045298876528 401-7120-533.42-10 0.35 03-05 A/C 3604529882811 B 401-7120-533.42-10 0.35 03-05 A/C 3604525834211 B 401-7120-533.42-10 0.41 03-05 A/C 3604525109623B 401-7120-533.42-10 0.35 03-05 A/C 36045238778178 03-05 A/C 3604523712585B 401-7120-533.42-10 401-7120-533.42-10 0.35 0.59 FEDERAL EXPRESS CORP Shipping Chgs 401-7120-533.42-10 870 MARSH MUNDORF PRATT SULLIVAN CONSULT-WPAG 401-7120-533.49-01 1,805.39 PORT ANGELES CITY TREASURER Chamber Lunch -Dunbar 401-7120-533.31-01 13.00 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 401-7120-533.42-10 33.97 Public Works -Electric Power Systems Division Total: $1,963.43 ADVANCED TRAFFIC PRODUCTS, INC ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 1,42986 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 88.35 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 39342 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 39342 CANON USA, INC RENTAL OR LEASE SERVICES 401-7180-533.45-31 176.61 CAPACITY PROVISIONING INC Network Services 401-7180-533.42-12 2,381.11 Network Services 401-7180-533.42-12 216.80 CED/CONSOLIDATED ELEC DIST INC ELECTRICAL EQUIP & SUPPLY 401-7180-533.31-20 20.87 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 21.68 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 17.18 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 -10840 ELECTRICAL, EQUIP & SUPPLY 401-7180-533.34-02 373.37 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 288.46 ELECTRICAL EQUIP & SUPPLY 401-7180-533.35-01 122.25 CENTURYLINK-QWEST 03-05 a/c 3604526236776B 401-7180-533.42-10 43.82 • 03-05 a/c 3604529541353B 401-7180-533.42-10 41.30 03-02 a/c 3604170786905B 401-7180-533.42-10 4456 E-25 Page 17 Page 18 Date: 3/28/2012 of Port Angeles lawCity City Council Expenditure Report e`Y From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-02 a/c 206Z020411942B 401-7180-533 42-10 96.69 03-05 A/C 3604529887652B 401-7180-533.42-10 2.84 03-05 A/C 3604529882811 B 401-7180-533.42-10 284 03-05 A/C 3604525834211 B 401-7180-533.42-10 330 03-05 A/C 3604525109623B 401-7180-533.42-10 2.84 03-05 A/C 3604523877817B 401-7180-533.42-10 2.84 03-05 A/C 36045237125858 401-7180-533.42-10 4.69 GENERAL PACIFIC INC ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 491,48 HUGHES UTILITIES LTD ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 36943 INVARION, INC MEMBERSHIPS 401-7180-533.48-02 97018 LINCOLN INDUSTRIAL CORP Refund-Rept Transformer 401-7180-379.00-00 570,19 MASON COUNTY PUD #3 EDUCATIONAL SERVICES 401-7180-533.41-50 3,162,04 EDUCATIONAL SERVICES 401-7180-533.41-50 3,686,16 MOTOROLA SOLUTIONS, INC RADIO &TELECOMMUNICATION 401-7180-533.48-10 9,547,87 OLYMPIC LAUNDRY & DRY CLEANERS LAUNDRY/DRY CLEANING SERV 401-7180-533 41-50 70.79 LAUNDRY/DRY CLEANING SERV 401-7180-533.41-50 74.76 OLYMPIC STATIONERS INC OFFICE SUPPLIES, GENERAL 401-7180-533.31-01 8,14 PACIFIC OFFICE EQUIPMENT INC RENTAL OR LEASE SERVICES 401-7180-533.45-31 25.80 PORT ANGELES POWER EQUIPMENT HAND TOOLS ,POW&NON POWER 401-7180-533.35-01 17.82 HAND TOOLS ,POW&NON POWER 401-7180-533.35-01 31 38 • QUILL CORPORATION OFFICE SUPPLIES, GENERAL 401-7180-533.31-01 59.73 OFFICE SUPPLIES, GENERAL 401-7180-533.31-01 10.82 ROHLINGER ENTERPRISES INC TESTING&CALIBRATION SERVI 401-7180-533.48-10 195.42 TESTI NG&CALI B RATION SERVI 401-7180-533.48-10 194.14 SANDERSON SAFETY SUPPLY CO FIRE PROTECTION EQUIP/SUP 401-7180-533.31-01 529.43 FIRE PROTECTION EQUIP/SUP 401-7180-533.34-02 105.80 SECURITY SERVICE NW, INC COMMUNICATIONS/MEDIA SERV 401-7180-533.41-50 650.00 SOUND PUBLISHING INC COMMUNICATIONS/MEDIA SERV 401-7180-533.44-10 33.18 SUNSET DO-IT BEST HARDWARE ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 32.52 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 662 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 60.38 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 3.37 SWAIN'S GENERAL STORE INC CLEANING COMPOSITION/SOLV 401-7180-533.34-02 16.54 THURMAN SUPPLY ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 3.51 US BANK CORPORATE PAYMENT SYSTEIBottled Water-Light ops 401-7180-533.31-01 28.00 Safety Gloves-Hairell 401-7180-533.31-01 341.80 Pizza/Drinks-Safety Mtg 401-7180-533.31-01 99.20 Hotel Reg-Hairell 401-7180-533.43-10 209.68 Trng Reg-Wahto/Rowley 401-7180-533.43-10 300.00 Training Accom-Eisele 401-7180-533 43-10 335.64 VERIZON WIRELESS 02-28 a/c 271138138-00003 401-7180-533.42-10 6989 • 02-22 a/c 1571136182-00002 401-7180-533.42-10 17462 E-2i) Page 18 Electric Utility Fund Date 3/28/2012 $2,399,726.36 City of Port Angeles SUPPLIES ter, City Council Expenditure Report FOWLER COMPANY, H D rx' ..x. From: 3/10/2012 To: 3/23/2012 1,910.46 Vendor Description Account Number Invoice Amount WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 401-7180-533.42-10 6.60 WESCO DISTRIBUTION INC ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 1,512.65 ELECTRICAL EQUIP & SUPPLY 401-7180-533.34-02 4618 WOODS LOGGING SUPPLY, INC MATERIAL HNDLING&STOR EQP 401-7180-533.35-01 146.06 WSU-SPS HUMAN SERVICES 401-7180-533 43-10 310.00 Public Works -Electric Electric Operations Division Total. $30,568.52 ROAD/HWY MAT NONASPHALTIC Public Works -Electric Department Total: $32,904.56 Electric Utility Fund Fund Total. $2,399,726.36 APWA SUPPLIES 402-0000-237.00-00 -2.69 FOWLER COMPANY, H D PIPE FITTINGS 402-0000-141.40-00 1,910.46 PLUMBING EQUIP FIXT,SUPP 402-0000-141.40-00 1,748.30 INVARION, INC MEMBERSHIPS 402-0000-237.00-00 -150.36 Division Total. $3,505.71 Department Total. $3,505.71 AMSAN PAPER & PLASTIC-DISPOSABL 402-7380-534.31-01 57.24 ANGELES CONCRETE PRODUCTS ROAD/HWY MAT NONASPHALTIC 402-7380-534.31-20 76.83 APWA SUPPLIES 402-7380-534.31-01 26.69 SHIPPING AND HANDLING 402-7380-534.31-01 8.00 CAPACITY PROVISIONING INC Network Services 402-7380-534.42-12 1,074.93 • Network Services 402-7380-534.42-12 379.40 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 402-7380-534.42-10 1.07 03-05 A/C 3604529882811 B 402-7380-534.42-10 1.07 03-05 A/C 3604525834211 B 402-7380-534.42-10 1.24 03-05 A/C 3604525109623B 402-7380-534.42-10 1.07 03-05 A/C 3604523877817B 402-7380-534.42-10 1.07 03-05 A/C 3604523712585B 402-7380-534.42-10 1.76 03-05 a/c 3604525230978B 402-7380-534.42-10 186.53 CLALLAM CNTY DEPT OF HEALTH TESTING&CALIBRATION SERVI 402-7380-534.41-50 276.00 HOLCOMB & COMPANY, D ROAD/HWY MAT NONASPHALTIC 402-7380-534.31-20 571.05 INVARION, INC MEMBERSHIPS 402-7380-534.48-02 970.18 MOTOROLA SOLUTIONS, INC RADIO & TELECOMMUNICATION 402-7380-534.48-10 3,516.50 OFFICE DEPOT COMPUTER ACCESSORIES&SUPF402-7380-534.31-01 571.08 SUPPLIES 402-7380-534.31-01 64.55 PORS ATTY AT LAW, THOMAS M PUD WATER CONTRACT 402-7380-534.41-50 466.00 PORT ANGELES POWER EQUIPMENT AUTO & TRUCK MAINT ITEMS 402-7380-534.35-01 32.41 SUNSET DO -IT BEST HARDWARE ELECTRICAL EQUIP & SUPPLY 402-7380-534.31-20 32.72 FASTENERS, FASTENING DEVS 402-7380-534.31-20 26.08 FUEL,OIL,GREASE, & LUBES 402-7380-534.31-20 28.28 SWAIN'S GENERAL STORE INC FOODS. PERISHABLE 402-7380-534.31-20 8.35 • THURMAN SUPPLY ELECTRICAL EQUIP & SUPPLY PIPE AND TUBING 402-7380-534.31-20 402-7380-534.31-20 97.04 37.66 TWISS ANALYTICAL LABORATORIES TEST[ NG&CALIBRATION SERVI 402-7380-534.41-50 215.00 E - 27 Page 19 �i,CFT4 . �. ' Date 3/28/2012 City of Port Angeles lam City Council Expenditure Report rr.°•= From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount TWISS ANALYTICAL LABORATORIES TESTI NG&CALI B RATION SERVI 402-7380-534.41-50 173.00 VERIZON WIRELESS 02-28 a/c 271138138-00005 402-7380-534.42-10 125.39 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 402-7380-534.42-10 0.51 Public Works -Water Water Division Total: $9,0213.70 Public Works -Water Department Total: $9,028.70 Water Fund Fund Total: $12,534.41 CAPACITY PROVISIONING INC Network Services 403-7480-535.42-12 1,126.63 CENTURYLINK-QWEST 03-05 A/C 36045298876528 403-7480-535.42-10 0.95 03-05 A/C 3604529882811 B 403-7480-535 42-10 0.95 03-05 A/C 3604525834211B 403-7480-535.42-10 1.10 03-05 A/C 3604525109623B 403-7480-535.42-10 0.95 03-05 A/C 3604523877817B 403-7480-535.42-10 0.95 03-05 A/C 3604523712585B 403-7480-535 42-10 1.56 03-05 a/c 3604529911834B 403-7480-535.42-10 82.59 03-02 a/c :3604170591196B 403-7480-535.42-10 41.30 03-02 a/c 36041701900808 403-7480-535.42-10 41 30 CONSTRUCTION SPECIALTIES, INC AIR CONDITIONING & HEATNG 403-7480-535.48-10 1,126.28 EDGE ANALYTICAL TESTING&CALIBRATION SERVI 403-7480-535.41-50 4,136.00 FASTENAL INDUSTRIAL HAND TOOLS ,POW&NON POWER 403-7480-535.35-01 9818 FEDERAL EXPRESS CORP Shipping C:hgs 403-7480-535.42-10 51.57 • FERRELLGAS INC GASES CONT.EQUIP.LAB,WELD 403-7480-535.32-10 1,501,91 Cyl Rental 403-7480-535.32-10 13.01 FOWLER COMPANY, H D EQUIP MAINT & REPAIR SERV 403-7480-535.31-20 17333 HACH COMPANY CHEMICAL LAB EQUIP & SUPP 403-7480-535.31-01 906.60 HARRINGTON INDUSTRIAL PLASTICS PLUMBING EQUIP FIXT,SUPP 403-7480-535.31-20 32010 JULIAN & SON INC, JOHN PUMPS & ACCESSORIES 403-7480-535.31-20 2,54525 Randy Raymond DOT PHYSICAL REIMBURSEMNT 403-7480-535.49-90 105.00 NEWFIELDS, LLC TESTING&CALIBRATION SERVI 403-7480-535.41-50 3,550.00 OLYMPIC PRINTERS INC BUSINESS CARDS 403-7480-535.31-01 117.07 OLYMPIC STATIONERS INC SUPPLIES 403-7480-535.31-01 98.68 SUPPLIES 403-7480-535.31-01 254.50 SUPPLIES 403-7480-535.31-01 22.98 Hanging folders 403-7480-535.31-01 -75.78 PACIFIC OFFICE EQUIPMENT INC OFFICE MACHINES & ACCESS 403-7480-535.45-31 6.97 PETTIT OIL COMPANY FUEL, OIL, GREASE, & LUBES 403-7480-535.31-01 111.86 PORT ANGELES CITY TREASURER File Cabinet -Freed 403-7480-535.31-01 43.36 Postage -Young 403-7480-535.42-10 26.95 Phone Card -Freed 403-7480-535.42-10 32.52 Postage -Young 403-7480-535.42-10 8.15 CDL Reimb-Williams 403-7480-535.49-90 10.00 PUD #1 OF CLALLAM COUNTY Masters Rd 403-7480-535.47-10 404.12 • SUNSET DO -IT BEST HARDWARE HARDWARE,AND ALLIED ITEMS 403-7480-535 31-20 16.37 E-213 Page 20 K"FT C", Date 3/28/2012 City of Port Angeles City Council Expenditure Report From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number Invoice Amount SUNSET DO -IT BEST HARDWARE PIPE FITTINGS 403-7480-535.31-20 33.40 HAND TOOLS ,POW&NON POWER 403-7480-535.31-20 55.77 SWAIN'S GENERAL STORE INC PAINTING EQUIPMENT & ACC 403-7480-535.31-01 64.21 HARDWARE,AND ALLIED ITEMS 403-7480-535.31-01 13.70 CHEMICAL LAB EQUIP & SUPP 403-7480-535.31-01 39.93 JANITORIAL SUPPLIES 403-7480-535.31-01 88.82 MARKERS, PLAQUES,SIGNS 403-7480-535.31-01 4586 EPDXY BASED FORMULAS 403-7480-535.31-20 15.56 THURMAN SUPPLY PIPE FITTINGS 403-7480-535.31-20 69.76 PIPE FITTINGS 403-7480-535.31-20 34.09 HAND TOOLS ,POW&NON POWER 403-7480-535.31-20 28.98 TRIANGLE PUMP AND EQUIPMNT INC EQUIP MAINT & REPAIR SERV 403-7480-535.48-10 991.70 VERIZON WIRELESS 02-28 a/c 271138138-00006 403-7480-535.42-10 93.74 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 403-7480-535.42-10 10.78 Public Works-WW/Stormw Wastewater Division Total: $18,489.56 Public Works-WW/Stormwtr Department Total. $18,489.56 Wastewater Fund Fund Total: $18,489.56 AMSAN PAPER & PLASTIC-DISPOSABL 404-7580-537.31-01 57.23 CAPACITY PROVISIONING INC CENTURYLINK-QWEST Network Services 404-7580-537.42-12 116.63 03-05 A/C 3604529887652B 404-7580-537.42-10 0.47 03-05 A/C 3604529882811 B 404-7580-537 42-10 0.47 03-05 A/C 3604525834211B 404-7580-537.42-10 0.55 03-05 A/C 3604525109623B 404-7580-537 42-10 047 03-05 A/C 3604523877817B 404-7580-537.42-10 0.47 03-05 A/C 3604523712585B 404-7580-537.42-10 0.78 OFFICE DEPOT SUPPLIES 404-7580-537.31-01 117.01 OLYMPIC PRINTERS INC BUSINESS CARDS 404-7580-537.31-01 117.07 OLYMPIC STATIONERS INC OFFICE SUPPLIES, GENERAL 404-7580-537.31-01 19.17 PACIFIC OFFICE EQUIPMENT INC COMPUTER ACCESSORIES&SUPF404-7580-537.31-01 150.00 PORT ANGELES CITY TREASURER Raffle Prize -Home Show 404-7580-537.44-10 47.95 Inflated Balloon -HF 404-7580-537.44-10 7.58 RADIO PACIFIC INC (KONP) COMMUNICATIONS/MEDIA SERV 404-7580-537.44-10 500.00 REHRIG PACIFIC COMPANY, INC HARDWARE,AND ALLIED ITEMS 404-7580-537.35-01 6,994.55 SWAIN'S GENERAL STORE INC SUPPLIES 404-7580-537.31-01 71.71 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 404-7580-537 42-10 1.61 Public Works -Solid Waste Solid Waste -Collections Division Total: $8,203.72 Public Works -Solid Waste Department Total: $8,203.72 Solid Waste -Collections Fund Total: $8,203.72 LOWER ELWHA SOCIAL SERV (ICW) LOWER ELWHA SOCIAL SERV ( 405-0000-213.10-90 1,000.00 LABORATORIES INC TESTING&CALIBRATION SERVI 405-0000-237.00-00 -18.06 •MIDWEST NORTHERN TOOL & EQUIPMENT CO AIR COMPRESSORS & ACCESS 405-0000-237.00-00 -100.80 Division Total: $881.14 E-29 Page 21 a,, •crq �Date 3/28/2012 City of Port Angeles City Council Expenditure Report � ` •* � From: 3/1012012 To: 3/23/2012 Vendor Description Account Number Invoice Amount 0.24 03-05 A/C 3604529882811 B Department Total: $881.14 BACKFLOW APPARATUS & VALVE CO PLUMBING EQUIP FIXT,SUPP 405-7538-537.31-20 246.61 CAPACITY PROVISIONING INC Network Services 405-7538-537.42-12 201.08 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 405-7538-537.42-10 0.47 PUGET SAFETY EQUIPMENT INC HAND TOOLS ,POW&NON POWER 406-7412-538.35-01 03-05 A/C: 3604529882811 B 405-7538-537.42-10 0.47 E-31) 03-05 A/C 3604525834211 B 405-7538-537.42-10 0.55 03-05 A/C 3604525109623B 405-7538-537.42-10 0.47 03-05 A/C 36045238778178 405-7538-537.42-10 0.47 03-05 A/C 3604523712585B 405-7538-537.42-10 0.78 CLALLAM CNTY ROAD DEPT BLDG CONSTRUC SERVICES- 405-7538-537.49-90 11,731.12 FEDERAL EXPRESS CORP Shipping Chgs 405-7538-537.41-50 17.95 Shipping Chgs 405-7538-537.42-10 15.79 INSIGHT PUBLIC SECTOR COMPUTER HARDWARE&PERIPHI 405-7538-537.41-51 65.02 LINCOLN INDUSTRIAL CORP METALS, BARS, PLATES, RODS 405-7538-537.31-20 691.38 MIDWEST LABORATORIES INC TESTING&CALIBRATION SERVI 405-7538-537.41-50 233.06 Michelle Hale MILEAGE REIMBURSEMENT 405-7538-537.31-01 11.10 OFFICE DEPOT SUPPLIES 405-7538-537.31-01 148.28 PORT ANGELES CITY TREASURER Postage -Hale 405-7538-537.42-10 2.35 SOUND PUBLISHING INC SCALE ATTENDANT AD 405-7538-537.44-10 218.65 US BANK CORPORATE PAYMENT SYSTEI Class Regist-Paynter 405-7538-537.43-10 100.00 US COMPOSTING COUNCIL MEMBERSHIPS 405-7538-537.49-01 500.00 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 405-7538-537.42-10 2.13 Public Works -Solid Waste SW •• Transfer Station Division Total: $14,187.73 ASPECT CONSULTING, LLC LANDFILL POST CLOSURE 405-7585-537.41-50 4,675.25 LANDFILL POST CLOSURE 405-7585-537.41-50 3,032.50 EDGE ANALYTICAL TESTI NG&CALI B RATION SERVI 405-7585-537 41-50 24.00 TESTING&CALIBRATION SERVI 405-7585-537 41-50 24.00 NORTHERN TOOL & EQUIPMENT CO AIR COMPRESSORS & ACCESS 405-7585-537.35-01 1,300.79 Public Works -Solid Waste Solid Waste -Landfill Division Total: $9,056.54 Public Works -Solid Waste Department Total: $23,244.27 Solid Waste-LF/Trf Stn Fund Total: $24,125.41 ADAPT CONSULTING INC COMMUNICATIONS/MEDIA SERV 406-0000-237 00-00 -28.68 Division Total: -$28.68 Department Total. -$213.68 • • ADAPT CONSULTING INC COMMUNICATIONS/MEDIA SERV 406-7412-538.41-50 370.05 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 406-7412-538.42-10 0.24 03-05 A/C 3604529882811 B 406-7412-538.42-10 0.24 03-05 A/C 3604525834211B 406-7412-538.42-10 0.27 03-05 A/C 3604525109623B 406-7412-538.42-10 0.24 03-05 A/C 3604523877817B 406-7412-538.42-10 0.24 03-05 A/C 3604523712585B 406-7412-538.42-10 0.39 • PUGET SAFETY EQUIPMENT INC HAND TOOLS ,POW&NON POWER 406-7412-538.35-01 1,609.75 E-31) Page 22 • 4 4Af'City Date 3/28/2012 421-7121-533.49-86 of Port Angeles am City Council Expenditure Report WIf"•*tel 03-05 A/C 3604525109623B CAPACITY PROVISIONING INC From: 311012012 To: 3/23/2012 Vendor SWAIN'S GENERAL STORE INC VERIZON WIRELESS WASHINGTON (DES), STATE OF Public Works-WW/Stormw Description HARDWARE,AND ALLIED ITEMS 02-22 a/c 571136182-00001 RADIO & TELECOMMUNICATION Stormwater Public Works-WW/Stormwtr PROGRESSIVE MEDICAL INTERNATIONAI SUPPLIES SUPPLIES Stormwater Fund CENTURYLINK-QWEST 03-05 A/C 36045298876528 421-7121-533.49-86 03-05 A/C 36045298828116 C & F INSULATION 03-05 A/C 3604525834211B 421-7121-533.49-86 03-05 A/C 3604525109623B CAPACITY PROVISIONING INC 03-05 A/C 3604523877817B 421-7121-533 42-12 03-05 A/C 3604523712585B CLALLAM CNTY FIRE DISTRICT 3 48 HOUR REFRESHER COURSE MOROZ, JAMES FIRST AID CLASS WESTPORT OLYMPIC OXYGEN PEN PRINT INC STEAM & HOT WATER BOILERS EMT REPORTS PROGRESSIVE MEDICAL INTERNATIONAISUPPLIES 0.24 SUPPLIES Fire Department Medic I Fire Department Medic I Utility Account Number 406-7412-538.35-01 406-7412-538 42-10 406-7412-538.42-10 Division Total: Department Total Fund Total: 409-0000-237.00-00 409-0000-237.00-00 Division Total. Department Total. 409-6025-526.42-10 409-6025-526.42-10 409-6025-526.42-10 409-6025-526.42-10 409-6025-526.42-10 409-6025-526.42-10 409-6025-526.43-10 409-6025-526.31-08 409-6025-526.31-13 409-6025-526.31-02 409-6025-526.31-02 409-6025-526.31-02 Division Total. Department Total. Invoice Amount 22.62 19.92 3.45 $2,027.41 $2,027.41 $1,998.73 -40.10 -25.94 -$66.04 -$66.04 1.42 1.42 1.65 1.42 1.42 2.34 295.00 200.00 20.53 406.50 334.68 517.49 $1,783.87 $1,783.87 Fund Total: $1,717.83 AIR FLO HEATING COMPANY INC CITY REBATE 421-7121-533.49-86 1,50000 C & F INSULATION CITY REBATE 421-7121-533.49-86 747.60 CAPACITY PROVISIONING INC Network Services 421-7121-533 42-12 430.00 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 421-7121-533 42-10 0.24 03-05 A/C 3604529882811 B 421-7121-533.42-10 0.24 03-05 A/C 3604525834211 B 421-7121-533.42-10 0.27 03-05 A/C 3604525109623B 421-7121-533.42-10 0.24 03-05 A/C 36045238778178 421-7121-533.42-10 0.24 03-05 A/C 36045237125856 421-7121-533.42-10 0.39 E -STAR NORTHWEST, LLC CITY REBATE 421-7121-533.49-86 400.00 CITY REBATE 421-7121-533.49-86 500.00 FLUID MARKET STRATEGIES CITY REBATE 421-7121-533.49-86 2,070.60 CITY REBATE 421-7121-533 49-86 5,257.75 Curtis G Johnson and WEATHERIZATION LN SETTLEM 421-7121-533.49-86 4,500.00 Design Lab LIGHTING DESIGN SEMINAR 421-7121-533.43-10 60.00 •Lighting PA DOWNTOWN ASSN CITY REBATE 421-7121-533.49-86 1,253.57 TRACY'S INSULATION CITY REBATE 421-7121-533.49-86 510.00 E-31 Page 23 Date 3/28/2012 City of Port Angeles fftai City Council Expenditure Report ` t•.*� From: 3/10/2012 To: 3/23/2012 • Vendor Description Account Number WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION 421-7121-533.42-10 Public Works -Electric Conservation Division Total: Public Works -Electric Department Total: Conservation Fund Total: CTS NORTHWEST, INC PW CONSTRUCTION & RELATED 451-0000-223.40-00 Division Total: Department Total: CTS NORTHWEST, INC PW CONSTRUCTION & RELATED 451-7188-594.65-10 PW CONSTRUCTION & RELATED 451-7188-594.65-10 PUD #1 OF CLALLAM COUNTY ELECTRICAL EQUIP & SUPPLY 451-7188-594.65-10 SUNSET DO -IT BEST HARDWARE ELECTRICAL EQUIP & SUPPLY 451-7188-594.65-10 WA STATE PATROL-WASIS FOUR BACKGROUND CHECKS 451-7188-594.65-10 Public Works -Electric Electric Projects Division Total: Public Works -Electric Department Total: Electric Utility CIP Fund Total: FOWLER COMPANY, H D ELECTRICAL EQUIP & SUPPLY 452-7387-594.65-10 PIPE FITTINGS 452-7387-594.65-10 Public Works -Water Admin -Water Utility CIP Division Total: SOUND PUBLISHING INC COMMUNICATIONS/MEDIA SERV 452-7388-594 44-10 Public Works -Water Water Projects Division Total: Public Works -Water Department Total: Water Utility CIP Fund Total: FARALLON CONSULTING, LLC ENGINEERING SVC -CSO 453-7488-594.41-50 OFFICE DEPOT SUPPLIES 453-7488-594.31-01 SARGENT ENGINEERING, INC STRUCTURAL ANALYSIS 453-7488-594.41-50 SOUND PUBLISHING INC COMMUNICATIONS/MEDIA SERV 453-7488-594.44-10 Public Works-WW/Stormw Wastewater Projects Division Total: Public Works-WW/Stormwtr Department Total: WasteWater Utility CIP Fund Total: BAXTER AUTO PARTS #15 AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 FIRESTONE COMPLETE AUTO CARE AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 Invoice Amount 34.65 $17,265.79 $17,265.79 $17,265.79 13,845.36 $13,845.36 $13,84:5.36 300,167.49 -300,16749 5,326.41 17.00 40.00 $5,383.41 $5,383.41 $19,228.77 580.74 2,887.52 $3,4611.26 12640 $126.40 $3,594.66 $3,594.66 2,841.00 55.89 2,745.00 148.52 $5,790.41 $5,790.41 $5,790.41 1480 407.,48 -49.57 49,57 1307 22,76 6.10 71.10 121,50 704 7.04 1,70285 E-32 Page 24 • • 6;•'Cc 4. Date 3/28/2012 City of Port Angeles ..� City Council Expenditure Report • rr ';r..x. From: 3110/2012 To: 3/23/2012 Vendor Description Account Number Invoice Amount LINCOLN INDUSTRIAL CORP AUTO & TRUCK MAINT. ITEMS 501-0000-141 40-00 21.01 MCMASTER-CARR SUPPLY CO AUTO & TRUCK MAINT ITEMS 501-0000-237.00-00 -12.13 MOTOR TRUCKS INC AUTO & TRUCK ACCESSORIES 501-0000-141.40-00 132.39 AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 74.17 NAPA AUTO PARTS AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 44.98 AUTO & TRUCK MAINT. ITEMS 501-0000-141.40-00 21.85 O'REILLY AUTO PARTS AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 101.16 HOSES, ALL KINDS 501-0000-141.40-00 21.92 HOSES, ALL KINDS 501-0000-141.40-00 21.92 PETTIT OIL COMPANY FUEL,OIL,GREASE, & LUBES 501-0000-141.20-00 550.63 FUEL,OIL,GREASE, & LUBES 501-0000-141.20-00 8,713.74 FUEL,OIL,GREASE, & LUBES 501-0000-141.20-00 7,359.34 AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 1,840.32 AUTO & TRUCK MAINT ITEMS 501-0000-141 40-00 1,362.80 SEATTLE AUTOMOTIVE DISTRIBUTING AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 417.99 US BANK CORPORATE PAYMENT SYSTEI Power Saw -McBride 501-0000-237.00-00 -11.34 Automotive Parts/Etc-DM 501-0000-237.00-00 -7.83 Key Cabinet -McBride 501-0000-237.00-00 -66.52 ORmgs/Minor Supplies -DM 501-0000-237.00-00 -10.56 • Dry Chemical Powder -DM 501-0000-237 00-00 -13.44 VALLEY FREIGHTLINER INC AUTO & TRUCK MAINT ITEMS 501-0000-141.40-00 87.41 Division Total: $23,023.55 Department Total: $23,023.55 ARAMARK LAUNDRY/DRY CLEANING SERV 501-7630-548.49-90 36.36 LAUNDRY/DRY CLEANING SERV 501-7630-548.49-90 2230 LAUNDRY/DRY CLEANING SERV 501-7630-548.49-90 214.72 BAXTER AUTO PARTS #15 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 293 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 3.26 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 3.99 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 1788 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 44.61 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 14.51 BELTS AND BELTING 501-7630-548.34-02 17.93 BRAUN NORTHWEST AUTO & TRUCK MAINT ITEMS 501-7630-548 34-02 99.18 SHIPPING AND HANDLING 501-7630-548.34-02 7.70 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 350.29 SHIPPING AND HANDLING 501-7630-548.34-02 8.29 CAPACITY PROVISIONING INC Network Services 501-7630-548.42-12 33.32 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 501-7630-548.42-10 0.83 03-05 A/C 3604529882811 B 03-05 A/C 3604525834211 B 501-7630-548.42-10 501-7630-548.42-10 0.83 0.96 03-05 A/C 3604525109623B 501-7630-548.42-10 0.83 E-33 Page 25 Dade- 3/28/2012 City of Port Angeles City Council Expenditure Report r> 3/10/2012 To: 3/23/2012 •From: Vendor Description Account Number Invoice Amount CENTURYLINK-QWEST 03-05 A/C, 3604523877817B 501-7630-548.42-10 0.83 03-05 A/C 3604523712585B 501-7630-548.42-10 '1.37 FAR -WEST MACHINE & HYDRAULICS AUTO & 1•RUCK MAINT ITEMS 501-7630-548.34-02 21.41 HEARTLINE AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 99.67 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 175.50 JENNINGS EQUIPMENT INC AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 79.15 SHIPPING AND HANDLING 501-7630-548 34-02 10.30 LES SCHWAB TIRE CENTER EXTERNAL LABOR SERVICES 501-7630-548.34-02 60.38 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 166.51 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 1,587.25 EXTERNAL LABOR SERVICES 501-7630-548.34-02 80.22 MCMASTER-CARR SUPPLY CO AUTO & TRUCK MAINT. ITEMS 501-7630-548.31-01 14£I 09 SHIPPING AND HANDLING 501-7630-548.31-01 7.43 MITCHELL 1 RENTAULEASE EQUIPMENT 501-7630-548.48-02 172'.36 NAPA AUTO PARTS AUTO & TRUCK MAINT ITEMS 501-7630-548.31-01 1.60 PACIFIC OFFICE EQUIPMENT INC OFFICE SUPPLIES, GENERAL 501-7630-548.31-01 7.82 PENINSULA LUBRICANTS AUTO & TRUCK MAINT ITEMS 501-7630-548.31-01 42.28 PETTIT OIL COMPANY FUEL,OIL,GREASE, & LUBES 501-7630-548.32-13 243.49 FUEL,OIL,GREASE, & LUBES 501-7630-548.32-13 287.80 FUEL,OIL,GREASE, & LUBES 501-7630-548.32-13 50.61 • PORT ANGELES FORD LINCOLN EXTERNAL LABOR SERVICES 501-7630-548.34-02 112.74 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 134.58 EXTERNAL LABOR SERVICES 501-7630-548.34-02 338.21 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 202.47 EXTERNAL LABOR SERVICES 501-7630-548.34-02 328.64 AUTO & TRUCK MAINT ITEMS 501-7630-548 34-02 291.25 EXTERNAL LABOR SERVICES 501-7630-548.34-02 716.60 PORT ANGELES TIRE FACTORY EXTERNAL LABOR SERVICES 501-7630-548.34-02 25778 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 6.50 EXTERNAL LABOR SERVICES 501-7630-548.34-02 10.84 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 26.43 EXTERNAL LABOR SERVICES 501-7630-548.34-02 37.89 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 13.23 EXTERNAL LABOR SERVICES 501-7630-548.34-02 35.72 EXTERNAL LABOR SERVICES 501-7630-548.34-02 15.12 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 2.17 EXTERNAL LABOR SERVICES 501-7630-548.34-02 46.07 BELTS AND BELTING 501-7630-548.34-02 5375 QUALITY 4X4 TRUCK SUPPLY AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 3324 EXTERNAL LABOR SERVICES AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 501-7630-548.34-02 81,30 234.11 • EXTERNAL LABOR SERVICES 501-7630-548.34-02 14228 E-3-4 Page 26 41.6{a:Plq Date 3/28/2012 City of Port Angeles City Council Expenditure Report • r'''"..x. From: 3/10/2012 To: 3/23/2012 Vendor Description Account Number Invoice Amount QUALITY 4X4 TRUCK SUPPLY BELTS AND BELTING 501-7630-548.34-02 30.34 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 75.22 EXTERNAL LABOR SERVICES 501-7630-548.34-02 121 95 RICHMOND 2 -WAY RADIO EXTERNAL LABOR SERVICES 501-7630-548.34-02 33.06 RUDDELL AUTO MALL EXTERNAL LABOR SERVICES 501-7630-548.34-02 41 40 AUTO & TRUCK MAINT. ITEMS 501-7630-548 34-02 165.45 EXTERNAL LABOR SERVICES 501-7630-548.34-02 225.17 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 78.83 EXTERNAL LABOR SERVICES 501-7630-548.34-02 77.81 RUDY'S AUTOMOTIVE AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 274.50 EXTERNAL LABOR SERVICES 501-7630-548.34-02 333.82 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 29.60 EXTERNAL LABOR SERVICES 501-7630-548.34-02 10.41 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 30.08 EXTERNAL LABOR SERVICES 501-7630-548.34-02 10.41 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 13.77 EXTERNAL LABOR SERVICES 501-7630-548.34-02 151.71 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 46.61 • EXTERNAL LABOR SERVICES AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 501-7630-548.34-02 70.41 163.10 EXTERNAL LABOR SERVICES 501-7630-548.34-02 291.38 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 16.69 EXTERNAL LABOR SERVICES 501-7630-548.34-02 151.71 SUNSET DO -IT BEST HARDWARE AUTO & TRUCK MAINT. ITEMS 501-7630-548.31-01 7.91 AUTO & TRUCK MAINT ITEMS 501-7630-548.31-01 -25.63 AUTO & TRUCK MAINT. ITEMS 501-7630-548 31-01 2.32 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 5.59 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 27.28 SYSTEMS FOR PUBLIC SAFETY, INC AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 38.48 EXTERNAL LABOR SERVICES 501-7630-548.34-02 86.72 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 424.25 EXTERNAL LABOR SERVICES 501-7630-548 34-02 257.45 AUTO & TRUCK MAINT. ITEMS 501-7630-548.34-02 424.25 EXTERNAL LABOR SERVICES 501-7630-548.34-02 257.45 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 38.48 EXTERNAL LABOR SERVICES 501-7630-548.34-02 86.72 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 516.39 EXTERNAL LABOR SERVICES 501-7630-548.34-02 346.88 AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 73.71 EXTERNAL LABOR SERVICES 501-7630-548 34-02 10840 • AUTO & TRUCK MAINT ITEMS 501-7630-548.34-02 38.48 EXTERNAL LABOR SERVICES 501-7630-548.34-02 86.72 E-35 Page 27 City of Port Angeles M 9 �=R' City Council Expenditure Report From: 3/1012012 Vendor Description SYSTEMS FOR PUBLIC SAFETY, INC AUTO & TRUCK MAINT ITEMS Fiber Opti; Trncvrs-JH EXTERNAL LABOR SERVICES Web Site Tracking Susbc AUTO & TRUCK MAINT. ITEMS EXTERNAL LABOR SERVICES AUTO & TRUCK MAINT. ITEMS EXTERNAL LABOR SERVICES AUTO & TRUCK MAINT. ITEMS EXTERNAL LABOR SERVICES AUTO & TRUCK ACCESSORIES AUTO & TRUCK MAINT ITEMS EXTERNAL LABOR SERVICES BELTS AND BELTING FUEL,OIL,GREASE, & LUBES TRANCO TRANSMISSIONS INC AUTO & TRUCK MAINT ITEMS EXTERNAL LABOR SERVICES AUTO & TRUCK MAINT. ITEMS EXTERNAL LABOR SERVICES US BANK CORPORATE PAYMENT SYSTEI Light Fixtures -McBride Good To Go Passes Automotive Parts/Etc-DM Key Cabinet -McBride ORmgs/Minor Supplies -DM Dry Chemical Powder -DM Power Saw -McBride Restocking Fee -McBride VERIZON WIRELESS 02-22 a/c 571136182-00003 WASHINGTON (DES), STATE OF RADIO & TELECOMMUNICATION WCIA (WA CITIES INS AUTHORITY) INSURANCE, ALL TYPES Public Works -Equip Svcs Equipment Services Public Works -Equip Svcs To: 312312012 Account Number 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.34-02 501-7630-548.31-01 501-7630-548.31-01 501-7630-548.31-01 501-7630-548.31-01 501-7630-548.31-01 501-7630-548.31-01 501-7630-548.35-01 501-7630-548.35-01 501-7630-548 42-10 501-7630-548.42-10 501-7630-548.49-90 Division Total: Department Total: Equipment Services Fund Total. IT XCHANGE CORP COMPUTER HARDWARE&PERIPH1502-0000-237.00-00 US BANK CORPORATE PAYMENT SYSTEI Blockout Dvcs-Harper 502-0000-237.00-00 SMTP Mail Svs-EFT 502-0000-237.00-00 Fiber Opti; Trncvrs-JH 502-0000-237.00-00 Web Site Tracking Susbc 502-0000-237.00-00 Division Total: Department Total. Invoice Amount 59.54 8672 397.15 346.88 351.16 130.08 38.48 86.72 937.80 686.08 1,989.65 27.90 27.33 60.42 57.89 114.66 5789 43.11 60.00 101.02 858.44 136.24 173.44 146.33 19.62 25.37 5.50 1,165.46 $20,68;2.87 $20,682.87 $43,706.42 -35.28 -6.48 -2.52 -11295 -23.18 -$180.41 -$180.41 is ANGELES COMMUNICATIONS INC LABOR 502-2081-518 41-50 82.00 AVAYA 2554 CORDED WALL PH 502-2081-518.41-50 6641 • WALL JACK PLATE 502-2081-518.41-50 11 29 TAX 502-2081-518.41-50 1341 E - 316 Page 28 Date 3/28/2012 City of Port Angeles a p City Council Expenditure Report • ��'°•} " i From: 3/10/2012 To: 3123/2012 Vendor Description Account Number ANGELES COMMUNICATIONS INC WWTP OPX 4890 & 4841 TROU 502-2081-518.41-50 AVAYA, INC RADIO & TELECOMMUNICATION 502-2081-518.48-02 CAPACITY PROVISIONING INC Network Services 502-2081-518.42-12 CDW GOVERNMENT INC COMPUTER ACCESSORIES&SUPF502-2081-518.31-60 CENTURYLINK-QWEST 03-05 A/C 3604529887652B 502-2081-518.42-10 03-05 A/C 3604529882811 B 502-2081-518.42-10 03-05 A/C 3604525834211 B 502-2081-518.42-10 03-05 A/C 3604525109623B 502-2081-518.42-10 03-05 A/C 3604523877817B 502-2081-518 42-10 03-05 A/C 3604523712585B 502-2081-518.42-10 CROSS TELECOM/SHARED SOLUTIONS EQUIP MAINT & REPAIR SERV 502-2081-518.48-02 1 T. XCHANGE CORP COMPUTER HARDWARE&PERIPH1502-2081-518.48-10 MICROSOFT CORPORATION COMPUTERS,DP & WORD PROC 502-2081-518.48-02 US BANK CORPORATE PAYMENT SYSTEIBlockout Dvcs-Harper 502-2081-518.35-01 Shipping -Hard Drive -JM 502-2081-518.42-10 SMTP Mad Svs-EFT 502-2081-518.48-02 Web Site Tracking Susbc 502-2081-518.48-02 Fiber Optic Trncvrs-JH 502-2081-518 48-10 WASHINGTON (DES), STATE OF WASHINGTON (DOP), STATE OF RADIO & TELECOMMUNICATION Powershell Scripting 502-2081-518,42-10 502-2081-518.43-10 Finance Department Information Technologies Division Total: Finance Department Department Total: TODD GERMAN Self Insurance PA DOWNTOWN ASSN CENTURYLINK-QWEST DIGITAL IMAGING SOLUTIONS INC Esther Webster/Fine Arts Information Technology Medical Reimb Other Insurance Programs Self Insurance Self -Insurance Fund FEB 2012 DECAL SALES FEB 2012 CDBIAA RECEIPTS FEB 2011 DUPAR RECEIPTS Off Street Parking Fund 03-05 A/C 3604529887652B 03-05 A/C 3604529882811 B 03-05 A/C 3604525834211B 03-05 A/C 3604525109623B 03-05 A/C 3604523877817B 03-05 A/C 3604523712585B FEB COPY COSTS Esther Webster/Fine Arts Fund Total: 503-1631-517.46-30 Division Total: Department Total: Fund Total: 650-0000-231.91-00 650-0000-231.92-00 650-0000-231.93-00 Division Total: Department Total: Fund Total 652-8630-575.42-10 652-8630-575.42-10 652-8630-575.42-10 652-8630-575.42-10 652-8630-575 42-10 652-8630-575.42-10 652-8630-575 45-31 Division Total. Invoice Amount 88.89 1,395.03 145.00 3,586.91 1 07 1.07 1.24 1.07 1.07 1.76 12,710.71 455.28 1,129.71 83.60 6.92 32.52 299.18 1,457.65 6.52 730.00 $22,308.31 $22,308.31 $22,127.90 313.37 $313.37 $313.37 $313.37 388.89 1,994.26 3,972.00 $6,355.15 $6,355.15 $6,355.15 0.35 0.35 041 0.35 0.35 0.59 1558 $17.98 E-37 Page 29 0�, ��C.F?4 , .. Date 3/28/2012 City of Port Angeles City Council Expenditure Report f� r. From: 3/10/2012 To: 3/23/2012 Vendor Description Account Number Invoice Amount Esther Webster/Fine Arts Department Total: $17.98 Esther Webster Fund Fund Total. $17.98 OLYMPIC COMMUNITY ACTION PRGMS PASS THE: BUCK DISTRIBUTIO 657-0000-239.91-00 2,861 63 Division Total: $2,8611.63 Department Total. $2,861.63 Util Vol Contrib Program Fund Total: $2,861.63 AFSCME LOCAL 1619 P/R Deductions pe 03-04 920-0000-231.54-40 9300 P/R Deductions pe 03-04 920-0000-231.54-40 186.00 CLALLAM CNTY SUPERIOR COURT P/R Deductions pe 03-04 920-0000-231.56-30 188.90 DIMARTINO/WSCFF DISABILITY P/R Deductions pe 03-04 920-0000-231.53-40 1,316.82 FIREFIGHTER'S LOCAL 656 P/R Deductions pe 03-04 920-0000-231.54-30 1,701,00 GUARANTEED EDUCATION TUITION P/R Deductions pe 03-04 920-0000-231.56-95 527.00 IBEW LOCAL 997 P/R Deductions pe 03-04 920-0000-231.54-20 1,02761 LEOFF P/R Deductions pe 03-04 920-0000-231.51-21 24,488.82 OFFICE OF SUPPORT ENFORCEMENT P/R Deductions pe 03-04 920-0000-231.56-20 71259 P/R Deductions pe 03-04 920-0000-231.56-20 169.85 PERS P/R Deductions pe 03-04 920-0000-231.51-10 1,67463 P/R Deductions pe 03-04 920-0000-231.51-11 9,71473 P/R Deductions pe 03-04 920-0000-231.51-12 41,461.75 POLICE ASSOCIATION P/R Deductions pe 03-04 920-0000-231.55-10 253.00 UNITED WAY (PAYROLL) P/R Deductions pe 03-04 920-0000-231.56-10 53563 WSCCCE AFSCME AFL-CIO P/R Deductions pe 03-04 920-0000-231.54-40 4,365.47 Division Total: $88,416.80 Department Total: $88,416.80 Payroll Clearing Fund Total: $88,416.80 Totals for check period From: 3/10/2012 To: 3/23/2012 $3,094,126.68 E-38 Page 30 • 1�1 • • • .70RT DATE: April 3, 2012 TO: CITY COUNCIL VGELES FROM: Glenn A. Cutler, P. E., Director of Public Works & Utilities SUBJECT: City of Burlington Interlocal Joint Purchasing Agreement Summary: The City of Burlington has requested that the City enter into a Joint Purchasing Agreement enabling them to purchase a new Hydro -Excavating Vacuum (HEV) Truck using our previous bid. Recommendation: Approve and authorize the City Manager to sign a Joint Purchasing Agreement with the City of Burlington, and to make minor modifications to the Agreement, if necessary. Background/Analysis: The City of Burlington has requested the City enter into a Joint Purchasing Agreement. An agreement of this nature saves time and money by negating the need for the bidding process in certain instances. The City of Burlington is interested in purchasing a Hydro - Excavating Vacuum Truck, also known as a Catchbasin Cleaning Jetter Truck, like the one we bid last year. The purchasing of equipment and materials by bid requires a good deal of time and money to develop the specifications and then advertise for bids. By utilizing the contract from another agency, these expenses are eliminated while still ensuring the best buy. The City has similar agreements with the City of Tacoma and such entities as Clallam County, PUD No. 1 of Clallam County, City of Seattle, and King County. It is recommended that Council approve and authorize the City Manager to sign a Joint Purchasing Agreement with the City of Burlington, and to make minor modifications to the Agreement, if necessary. Attachment: Interlocal Joint Purchasing Agreement N:\CCOUNCILTINAL\City of Burlington Interlocal Joint Purchasing Agreement.doex E-39 CITY OF PORT ANGELES - CITY OF BURLINGTON • INTERLOCAL AGREEMENT FOR PURCHASE OF GOODS AND MATERIALS THIS INTERLOCAL AGREEMENT made and entered into, pursuant to the Interlocal Cooperation Act, Chapter 39.34 of the Revised Code of Washington, on the day of April, 2012, by and between the CITY OF PORT ANGELES, a municipal corporation of the State of Washington (hereinafter referred to as "Port Angeles"), and the CITY OF BURLINGTON, a municipal corporation of the State of Washington (hereinafter referred to as "Burlington"), WITNESSETH: WHEREAS, the parties hereto desire to establish a procedure to make joint purchases so that each party may acquire goods and/or services upon favorable terms and conditions, and without needlessly duplicating efforts; and WHEREAS, Port Angeles has previously requested bids for certain goods and/or materials described herein. Further, Port Angeles advertised its solicitation for bids by either (i) posting the bid or solicitation notice on a web site established and maintained by a public agency, purchasing cooperative, or similar service provider, for purposes of posting public notice of bid or proposal • solicitations, or (ii) provided an access link on the state's web portal to the notice; and WHEREAS, Port Angeles' request for bids notified vendors the contract could be used by more than one government entity. NOW THEREFORE in consideration of their mutual covenants, conditions and promises, THE PARTIES HERETO DO HEREBY AGREE as follows: 1. SERVICES Port Angeles requested bids for a Catchbasin Cleaning Jetter Truck through a bid process accomplished in August 2011. This bid process included posting the solicitation notice on Port Angeles' web site, and the solicitation also notified vendors the contract could be used by more than one government entity. Burlington wishes to utilize this bid for purchase of a similar vehicle. 2. PERFORMANCE Neither party shall be responsible to the other party for the performance, non- performance, or flawed performance of contracts by vendors. 3. TERM OF AGREEMENT FOR SERVICES The term of this agreement shall be from the date hereof, and shall extend until terminated. This agreement may be terminated by either party by giving ten (10) • Page 1 E -40 • days written notice to the other party, provided that termination shall not affect or impair any joint purchases of the parties that are agreed to on or before the termination. 4. INDEMNIFICATION If such claims are caused by or result from the concurrent negligence of Port Angeles, or its agents, employees, and/or officers, and Burlington, or its agents, employees, and/or officers, then these indemnity provisions shall be valid and enforceable only to the extent of the negligence of the indemnifying party; provided that nothing herein shall require either party to hold harmless or defend the other party or the other party's agents, employees and/or officers from any claims arising from the sole negligence of the other party, or its agents, employees, and/or officers. By virtue of this provision, the parties shall not be deemed to have waived their immunity pursuant to Title 51 RCW, and nothing contained in this agreement shall be construed so as to operate as a waiver. 5. COMPLIANCE WITH REGULATIONS AND LAWS The parties shall comply with all applicable rules and regulations pertaining to them in connection with the matters covered herein. It shall be the obligation placing an order for goods or services to be certain that all legal requirements applicable to that party have been met. • 6. OTHER SOURCES Each party shall have the right to contract independently for the purchase of any goods or services, and to publish bid specifications that exclude the other party from purchasing goods under any contract awarded pursuant to such bid specifications, provided that this provision shall not be construed so as to impair existing or pending joint purchases by the parties. 7. ASSIGNMENT The parties shall not assign this Agreement or any interest, obligation or duty therein without the express written consent of the other party. 8. ATTORNEYS' FEES If either party shall be required to bring any action to enforce any provision of this Agreement, or shall be required to defend any action brought by the other party with respect to this Agreement, and in the further event that one party shall substantially prevail in such action, the losing party shall, in addition to all other payments required therein, pay all of the prevailing party's reasonable costs in connection with such action, including such sums as the court or courts may adjudge reasonable as attorney's fees in the trial court and in any appellate courts. Page 2 E - 41 9. NOTICES • All notices and payments hereunder may be delivered or mailed. If mailed, they shall be sent to the following respective addresses: To Port AnVes To Burlington 321 E 5 Street 833 S. Spruce Street PO Box 158 Burlington, WA 98233 Port Angeles, WA 98362 Attn: City Attorney Attn: Lucy Hanley or to such other respective addresses as either party hereto may hereafter from time to time designate in writing. All notices and payments mailed by regular post (including first class) shall be deemed to have been given on the second business day following the date of mailing, if properly mailed and addressed. Notices and payments sent by certified or registered mail shall be deemed to have been given on the day next following the date of mailing, if properly mailed and addressed. For all types of mail, the postmark affixed by the United States Postal Service shall be conclusive evidence of the date of mailing. 10. NONDISCRIMINATION Each of the parties, for itself, its heirs, personal representatives, successors in interest, and assigns, as a part of the consideration hereof, does hereby • covenant and agree that it will comply with pertinent statutes, Executive Orders and such rules as are promulgated to assure that no person shall, on the grounds of race, creed, color, national origin, sex, age, or the presence of any sensory, mental or physical handicap be discriminated against or receive discriminatory treatment by reason thereof. 11. MISCELLANEOUS A. All of the covenants, conditions and agreements in this Agreement shall extend to and bind the legal successors and assigns of the parties hereto. B. This Agreement shall be deemed to be made and construed in accordance with the laws of the State of Washington jurisdiction and venue for any action arising out of this Agreement shall be in Clallam County, Washington. C. The captions in this Agreement are for convenience only and do not in any way limit or amplify the provisions of this Agreement. D. Unless otherwise specifically provided herein, no separate legal entity is created hereby, as each of the parties is contracting in its capacity as a municipal corporation of the State of Washington. The identity of the parties hereto are as set forth hereinabove. E. The purpose of this Agreement is to accomplish the objectives of this Agreement. • Page 3 E-42 • F. The performances of the duties of the parties provided hereby shall be done in accordance with standard operating procedures and customary practices of the parties. G. No joint oversight and administration board is created hereby. H. This Agreement constitutes the entire agreement between the parties. There are no terms, obligations, covenants or conditions other than those contained herein. No modifications or amendments of this Agreement shall be valid or effective unless evidenced by an agreement in writing signed by both parties. I. Copies of this Agreement shall be filed with the Skagit County Auditor's Office, the Clallam County Auditor's Office, and with the respective City Clerks of the parties hereto. • • IN WITNESS WHEREOF the parties hereto have executed this Agreement as of the day and year first above written. CITY OF PORT ANGELES By: _ City Manager Approved as to form: City Attorney City Clerk CITY OF BURLINGTON By: L"Ie, (n / ;Lev-, LIdzrxj Edie Edmundson, Mayor Pro Tem Approved as to form: Scott G. thErmas, City Attorney Greg er, Finance Director Page 4 E -43 NGELES WASH ING TO N, CITY COUNCIL MEMO DATE: APRIL 3, 2012 To: CITY COUNCIL FROM: RICHARD BONINE, RECREATION SERVICES MANAGER SUBJECT: APPOINTMENT TO PARKS, RECREATION & BEAUTIFICATION COMMISSION Summary: There are currently two vacancies on the Parks, Recreation & Beautification Commission. It is necessary to appoint new members. • Recommendation: Appoint Kristi Knowles and Fowler Stratton to fill the vacant positions on the Parks, Recreation & Beautification Commission for four-year terms, March 1, 2012 -February 28, 2016. • Background/Analysis: Currently there are two vacant positions on the Parks, Recreation & Beautification Commission due to the term expirations of Eleanor Tschimperle and Fowler Stratton. It is the responsibility of the Commission to interview and recommend to the City Council candidates to fill vacant positions. The Commission conducted interviews of three potential candidates at its March 15, 2012, meeting and chose to recommend Kristi Knowles be appointed and Fowler Stratton be re -appointed to fill the vacant positions. Staff recommends that Kristi Knowles and Fowler Stratton be appointed to the Parks, Recreation and Beautification Commission from March 15, 2012 -February 28, 2016. E - 44 • • NGELES DATE: April 3, 2012 TO: CITY COUNCIL FROM: Glenn A. Cutler, P.E., Director of Public Works & Utilities SUBJECT: Surplus Equipment for Disposal Summary: The equipment listed below is not economically repairable and has been depreciated and/or replaced. Recommendation: Declare the equipment listed below as surplus and authorize the Director of Public Works and Utilities to dispose of it in the most efficient manner. Background/Analysis: The Fleet Manager has evaluated the equipment listed below and is recommending it be surplussed and disposed. SURPLUS LIST Vehicle # Dept/ Div Year Description Reason for Disposal Miles/Hours Status Johnson ST4500/4499 Streets/Stormwater 2004 Street Economically Due for 6,967 hrs. To be replaced Sweeper & Replacement by new sweeper r)onv motor DW1757 Water 1990 Case Economically Due for 5,754 hrs. Eliminate from Backhoe oe Replacement Fleet As outlined in the Dec 12, 2011 council memo seeking authorization to purchase a new sweeper, the Streets/Stormwater Sweeper is at the end of its useful life and needs to be replaced. The Drinking Water Division backhoe (DW 1757) is also at the end of its useful life. An excavator is proposed for purchase which will eliminate the need to replace DWI 757. The excavator will be assigned to the Equipment Services Pool for use by all divisions. At the same time, an existing Street/Stormwater Division backhoe (ST 1570) will also be moved to pool status with Equipment Services. Appropriate fund transfers will be made by Finance to reflect the equipment reassignments. These actions will result in more efficient use of equipment and both a backhoe and excavator will be available to all divisions. It is recommended that City Council declare the equipment listed as surplus and authorize the Director of Public Works and Utilities to dispose of it in the most efficient manner. NACCOUNCIL\FINAL\Surplus Equipment.docx E - 45 • • • 30RT DATE: APRIL 3, 2012 TO: CITY COUNCIL NGELES FROM: DAN MCKEEN, FIRE CHIEF SUBJECT: PROPOSED MEDIC 1 AMBULANCE TRANSPORT RATE ADJUSTMENTS Summary: Based on an audit of our current ambulance transport rates — comparing our rates against Medicare allowables and against the areas prevailing transport rates — the Fire Department proposes to adjust its Medic I transport charges by the following: -Basic life support (BLS) from $450 to $500 -Advanced life support (ALS -1) from $600 to $650 -Advanced life support (ALS -2) from $650 to $725 -Paramedic intercept service charge from $600 to $650 -Advanced life support, no transport from $600 to $650 -Mileage from $13 to $14 per mile The proposed fee adjustments will not affect City residents or an employee of a business within the City, as they are not billed beyond their private insurance coverage. Recommendation: (1) Hear presentation from staff, (2) Open public hearing, (3) Conduct first reading of Ordinance, (4) Continue to the April 17 Council meeting. Background/Analysis: As part of the 2012 budget process, the Fire Department requested Systems Design Northwest, LLC, conduct an audit of our current ambulance transport rates. Specifically, the Fire Department wanted our current ambulance transport rates compared against Medicare allowables and against the areas prevailing transport rates. Based upon the audit, Systems Design Northwest recommended the City increase its BLS ambulance transport rate from $450 to $500, its ALS -1 transport rate from $600 to $650, its ALS -2 transport rate from $650 to $725, its paramedic service charge from $600 to $650, its ALS no transport charge from $600 to $650, and its mileage rate from $13 to $14. The Fire Department concurs with System Design Northwest's recommendation and proposes to adjust the transport rates starting April 23, 2012. G-1 Proposed Medic 1 Ambulance Transport Rate Adjustments April 3, 2012 Page 2 Because the majority of the ambulance transport bills are paid based upon a fee schedule, raising our rates will not necessarily provide a corresponding increase in revenue. Medicare — our primary payer — will pay based upon their allowables, regardless of our rates. The comparative rate information for local area ambulance transport rates is provided in the table below. Agency Basic Life Support (BLS) Advanced Life Support (ALS -1) Advanced Life Support (ALS -2) Per Mile Charge Bremerton $425 $550 $550 $10 Central Kitsap $550 $700 $800 $15 Jefferson Co. #5 $500 $700 $700 $15 Joyce $450 $805 $805 $10 Port Ludlow $460 $600 $785 $14 Port Townsend $500 $600 $700 $15 Poulsbo $450 $600 $650 $11 Olympic Ambulance $650 $900 $900 $22 Quilcene $600 $700 $800 $15 AVERAGE $509 $684 $743 $14 Port Angeles current $450 $600 $650 $13 Port Angeles proposed $500 $650 $725 $14 The recommended rate adjustments will not affect City residents or employees of a business within the City as they are not billed beyond their governmental or private insurance coverage. In addition, protection against financial hardship for non-residents is provided. Non-resident charges may be waived or reduced in accordance with an income -based discount chart that is based upon federal poverty guidelines for Washington State. The public hearing will be continued to April 17, 2012, at which time the public hearing will be closed and staff will recommend that the proposed charges be adopted. Attachment: Proposed Ordinance Changes G-2 • • • • Legal Draft 03.05.12 • ORDINANCE NO. AN ORDINANCE of the City of Port Angeles, Washington, revising Chapter 3.70 of the Port Angeles Municipal Code relating to Medic I Charges. THE CITY COUNCIL OF THE CITY OF PORT ANGELES DO HEREBY ORDAIN AS FOLLOWS: Section 1. Ordinance 3143, as amended, and Chapter 3.70 of the Port Angeles Municipal Code are hereby amended by amending Section 3.70.095 PAMC to read as follows: 3.70.095 Fire Department Fees - Medic I. The following rates are established for ambulance services performed by the City's Medic I Program: A. Medic I transports that involve advanced life support (ALS) services requiring either the administration of at least three different medications or the provision of a least one ALS procedure as identified as ALS -2 in Medicare's current ambulance fee schedule. 1. Base charge.....$650.00 725.00 2. Disposable equipment charge $33.00 3. Mileage, per mile 14.00 B. Medic I transports that involve advanced life support services not covered by section A. above: 1. Base charge .....$608:08 650.00 2. Disposable equipment charge $33.00 3. Mileage, per mile 14.00 -1- G-3 C. Medic I transports that involve only basic life support services: • 1. Base charge .....$45&99 500.00 2. Disposable equipment charge $33.00 3. Mileage, per mile .....$914.00 D. Paramedic intercept service charge ..... $600.00 650.00 E. Advanced life support services, no transport.....$600.00 650.00 Section 2 -Severability. If any provisions of this Ordinance or its applications to any person or circumstances is held to be invalid, the remainder of the Ordinance or application of the provisions of the Ordinance to other persons or circumstances is not affected. Section 3 - Corrections. The City Clerk and the codifiers of this ordinance are authorized to make necessary corrections to this ordinance including, but not limited to, the correction of the scrivener's/clerical errors, references, ordinance numbering, section • subsection numbers and any references thereto. Section 4 - Effective Date. This ordinance, being an exercise of a power specifically delegated to the City legislative body, is not subject to referendum. This ordinance shall take effect five days after its publication by summary. PASSED by the City Council of the City of Port Angeles at a regular meeting of said Council held on the _ day of , 2012. Cherie, Kidd, Mayor -2- G - .4 • • ATTEST: Janessa Hurd, City Clerk APPROVED AS TO FORM: William E. Bloor, City Attorney PUBLISHED: By Summary G \LEGAL\a ORDINANCES&RESOLUTIONS\ORDINANCES 2012\08 - Medic 1 rates 03 05 12 rtf • G-5 JQRT Date: April 3, 2012 To: CITY COUNCIL NGELES From: Glenn A. Cutler, P.E., Director of Public Works & Utilities Subject: Proposed Electric Utility Time of Use Rate Ordinance — Presentation and Public Hearing Summary: On January 17, 2007, City Council approved a voluntary time of use rate. On December 14, 2010, City Council approved the Advanced Metering Infrastructure System Agreement with Mueller Systems, which incorporated a time of use rate in accordance with the Retail Tiered Rate Methodology Study. On November 1, 2011, City Council directed staff to develop time of use rates as soon as it is technically feasible to do so. Recommendation: Following a presentation, proceed with a public hearing on the proposed Electric Utility time of use rate ordinance. Continue the public hearing to April 17, 2012. Background/Analysis: On January 17, 2007, City Council approved a voluntary Time of Use (TOU) rate for the Electric Utility, which was required in accordance with Section 1252 of the Energy Policy Act of 2005. The Act required all electric utilities in the United States to offer smart metering and time -based rates to their customers no later than February 8, 2007. In anticipation of the Bonneville Power Administration wholesale power Tiered Rate Methodology (TRM), on April 20, 2010 City Council approved a consulting services agreement with EES Consulting to complete a retail TRM study. The retail TRM study was an ideal time to independently assess and evaluate retail rate design options for each Electric Utility customer rate class. At the completion of the retail TRM study, the City Council selected the TOU rate option for all customer rate classes. The City Council decision to proceed with TOU rates was incorporated into the Advanced Metering Infrastructure (AMI) System Agreement that was approved by City Council on December 22, 2010. TOU rates align the relationship between wholesale power rates and retail rates, and provide customers the price signals that reflect the cost of power and energy at the time it is consumed. The AMI System and TOU rates also give customers the opportunity to manage their electric power costs, and an incentive to conserve electric energy use by shifting use to lower priced periods. The proposed TOU rates were designed to generate the same amount of revenues in 2012 as the current uniform rates. There is no anticipated impact for the average customer by adopting the proposed TOU rates. - NACCOUNCIL\FINAL\Proposed Electric Utility Time of Use Rate Ordinance - Public Hearing.doc G E3 • • • Proposed Electric Utility Time of Use Rate Ordinance April 3, 2012 • Page 2 On November 1, 2011, at the conclusion of last year's Electric Utility rate study, City Council stated that it intended to discontinue the current uniform rates and establish TOU rates as soon as staff determined it was technically feasible to do so. The staff has determined that implementation of TOU rates will be technically feasible upon completion of the AMI System, which is anticipated by the end of this year. Staff plans to implement a customer education program on TOU rates prior to the completion of the AMI System. • C A summary of the proposed residential TOU energy rates is below for the winter and summer seasons. The proposed TOU periods include: "heavy" from 6:00:00 AM to 1:59:59 PM Monday through Saturday, "medium" from 2:00:00 PM to 9:59:59 PM Monday through Saturday; and "light" for all other hours and North American Electric Reliability Corporation holidays. A demand response monthly credit of $10.00 is also proposed if customers choose to participate in the voluntary peak power project. There are no proposed changes to the current $15.75 monthly base charge. Description Winter Time of Use Periods & Rates Heavy I Medium I Light Current Uniform Rate $0.06050 per kWh regardless of when consumed Proposed TOU Winter Rate $0.06700 per kWh $0.05800 per kWh $0.05000 per kWh Percent Difference from current Uniform to proposed TOU 10.7% -4.1% -17.4% Percent Difference from Heavy TOU period N/A -13.4% -25.4% Description Summer Time of Use Periods & Rates Heavy I Medium I Light Current Uniform Rate $0.06050 per kWh regardless of when consumed Proposed TOU Summer Rate $0.06930 per kWh $0.05990 per kWh $0.04520 per kWh Percent Difference from current Uniform to proposed TOU 14.6% -1.0% -25.3% Percent Difference from Heavy TOU period N/A -13.6% -34.8% This evening staff will provide a presentation on the proposed TOU rates followed by a public hearing to allow public input to the process after the presentation. The public hearing would be continued to April 17, 2012 at which time the public hearing will be closed. On April 10, 2012, the Utility Advisory Committee will be asked to forward its recommendations on the proposed ordinance to City Council. On April 17, 2012, City Council will be asked to continue the public hearing and consider adoption of the proposed ordinance. Attachment: Proposed Time of Use Rate Ordinance G-7 ORDINANCE NO. AN ORDINANCE of the City of Port Angeles, Washington, relating to electricity services and charges making changes to Chapter 13.12 of Title 13 of the Port Angeles Municipal Code. THE CITY COUNCIL OF THE CITY OF PORT ANGELES DO HEREBY ORDAIN AS FOLLOWS: Section 1. Ordinances 2054 as amended, and Title 13 of the Port Angeles Municipal Code Chapter 13.12 is amended to read as follows: CHAPTER 13.12 - ELECTRICITY—SERVICES AND CHARGES 13.12.010 - General provisions applicable to all services. 13.12.015 - Time of use electric rate • 13.12.020 - Uniform electric rate. 13.12.021 - Point of delivery. 13.12.025 - Rate Class assignment. 13.12.030 - Schedule R• -03 -Residential service. 13.12.031 - Schedule R--03- Residential service time of use rate. 13.12.040 - Schedule GS -03 -General service. 13.12.0401. Schedule GS -03 -General service time of use rate. 13.12.041 - Schedule GD -03 -General service demand. 13.12,0411.Schedule GD -03 -General service demand time of use rate. 13.12.042 - Schedule NP -03 -Nonprofit tax-deductible. 13.12.042 1Schedule NP -03 -Nonprofit tax-deductible time of use rate. 13.12.043 - Schedule GD -04 -General service demand -primary metered. 13.12.044 - Schedule GD -04 -General service demand -primary metered time of use rate. 13.12.060 - Schedule P 5-03-Primaryservice. 13.12.061 - Schedule PS -03 -Primary service time of use rate. 13.12.071 - Schedule IT -03 -Industrial transmission. 13.12.072 - Schedule L -•03 -Lighting 13.12.073 - Schedule MW -03 -Municipal water pumping. 13.12.074 - New or expanded loads. 13.12.075 - Schedule W -03 -Municipal water pumping time of use rate. -1- G-8 • • 13.12.080 - Contract sales and purchases. 13.12.100 - Electrical work permits and fees. 13.12.110 - Contract and administration charge. 13.12.015 — Time of use electric rate After City Council formally accents the Advanced Metering Infrastructure System, the monthly rate for electricity consumed shall be in accordance with Sections 13.12.031, 13 12 0401 13.12.0411., 13.12.0421..1 .12.044. 13.12.061. and 13.12.075.The monthly rate includes all applicable taxes. 13.12.020 - Uniform €electric rate. Before the City Council formally accents the Advanced Metering infrastructure System T -the monthly rate for electricity consumed shall be in accordance with sections 13.12.0303 13.12.040, 13.12.041 13 12.042. 13.12.043. 13.12.060 lifeugh 13.12.073, and the demand response credits in accordance with Sections 13.12-031,D, 13.12.0401.E, and 13 12 0421 D. The monthly rate includes all applicable taxes. • 13 12 031 — Schedule R-0 -Re idential service time of u e rate • A. Applicability. This schedule applies throughout the City for domestic uses in single family residences individual apartments or farms. Separately metered services incidental to single family residential and farm service may be served under this schedule B. Character of Service. Sixty cycle, alternating current. 120/240 volts nominal single phase service will be furnished under this schedule, supplied through a single meter and one point of delivery. C. Time of Use Rate: 1. Base charge $15.75 per month 2 Monthly energy charge between September 1 and May 31 $0.06700 per kWh during heavy load hours. $0.05800 per kWh during medium load hours and $0.05000 per kWh during light load hours. Monthly energy charge between June 1 and August 31 $0,06930 per kWh during heavy ad hours. $0.0599 per kWh during medium load hours,and $0.04520 per kWh__ d__u_ring light load hours. -2- XWO 4. Thermal storage system $10.00 credit per month. 13.12.0401. Schedule GS -03 - General service time of use rate. A Applicability. This schedule applies to all accounts not covered by 4 Heavy load hours are all hours from 6:00:00 a.m. to 1,59:59 p.m. Monday throuizh• Saturday. Medium load hours are all hours from 2:00:00 p.m. to 9:59:59 p.m. I ndav through Saturday. Light load hours are all other hours Monday through Saturday. gill day Sunday, and all day on North American Electric Reliability Corporation specified holidays. Pacific Prevailing Time Ijpplies (Pacific Standard Time or Pacific Daylight Tirne—as applicablel. B. Character of Service. Sixty cycle, alternating currentat such phase and voltage as the City may have available will be furnished under this schedule, D. Demand Response Credits. meter and one point of deliverv. Devices controlled byAh-e--City during demand events, providing the customer has not di as bled the controls or opted out of participation, shall receive a credit as follows: a. Single phase $21.50 per month 1. Water heater load control switch $10.00 credit per month. b. Three phase $53.75 pernth 2. Smart thermostat or home area network $10.00 credit per month. 3. Water heater load control switch and smart thermostat _$14.40 credit per month. e Municipal emergency management system $27.20 per month 4. Thermal storage system $10.00 credit per month. 13.12.0401. Schedule GS -03 - General service time of use rate. A Applicability. This schedule applies to all accounts not covered by other rate schedules with • the following types of service: 1 120/208 or 120/240 volts, single or three phase, service panel of 400 amps or smaller. 2. 240/480 or 277/480 volts, three phase, service panel of 200 amps or smaller. 3. Municipal traffic signal and street lights. 4. Municipal emergency management systems. 5 Cable television system and other communications systems, singlehp ase power supeLiesjn accordance with Section 10.2 of Ordinance no. 3116. B. Character of Service. Sixty cycle, alternating currentat such phase and voltage as the City may have available will be furnished under this schedule, applied through aisinngle meter and one point of deliverv. C. Time of Us-e--Rate- seRate:1. 1.Base Charge a. Single phase $21.50 per month b. Three phase $53.75 pernth c. Municipal traffic signal -11 l 79.00 per month d. Municipal street light $128.90 per month e Municipal emergency management system $27.20 per month 2. Monthly Energy Charge between September 1 and May 31 $0.06800 kWh during heav v load hours. $0.05800 per kWh during medium load hours. and $0.05000 per kWh during liiit load • hours. 3. Monthly Energy Charge between June -I and August 31 $0.07040 ner kWh during heavy load hours, $0.0599 per kWh during medium load hours. and $0.04520 per kWh during light load hours. 4. Heavy load hours are all hours from 6.00.00 A.M. to 1.59.59 P.M,, Monday through Saturday, Medium load hours are all hours from 2:00:00 P.M. to 9.59.59 P.M., Monday through Saturday. Light load hours are all other hours Monday through Saturday, all day unday, and all day on North American Electric Reliability Corporation specified holiday Pacific Prevailing Time applies (Pacific Standard Time or Pacific Davlight Time. as anplicablel. 5 The base charges for municipal traffic signals and street ljghts includes maintenance o existing luminaries and controls by the Public Works and Utilities Department 6 The municipal emergency management system base charge shall apply tosystems with a normal operating load of 150 watts or less which shall not be required to be metered D Municipal Streets Lights The electric utility rates for municinal street lighting shall recover the cost of providing service In different areas of the City, the Department shall meter representative 150 and 200 watt street lights, Each light so metered shall be charged a base charge. The monthly energy charge shall be determined by multiplying the number of street light fixtures, times the monthly consumption determined by the metered lights . E Demand Response redits, Devices controlled by the City during demand events providing the customer has not disabled the controls or opted out of participation shall receive a credit as follows: 1 Water heater load control switch $10.00 credit per month 2 Smart thermostat or home area network $10.00 credit per month 3. Water heater load control switch and smart thermostat $10.00 credit per month 4 Thermal storage system $10.00 credit per month. 13.12.0411. Schedule GD -03 - General service demand time of use rate A. Applicability. This schedule applies to all not covered by other rate schedules with the following types of service: 1. 120/208 or 120/240 volts single or three phase service panel larger than 400 amps, 2. 240/480 or 277/480 volts three phase service panel larger than 200 amrn_ B. Character of Service. Sixty cycle alternating current at such phase and voltage as the Citv may have available will be furnished under this schedule applied through a single meter and one point of delivery. C. Time of Use Rate- -4- G-11 1 Bae Char e: • a. Single phase $42.95 per month b. Three phase $107.40 per month 2. Monthly Energy Charge between September 1 and May 31 $0.04660 per kWh during heayy load hours. $0.04660 perk h during medium load hours. and $0.03750 per kWh durina 1 iaht load hours. 3. Monthly Energy Charge between June l and August 31 $0.04820 per kWh during heavy load hours. $0.04820 per kWh during medium load hours, and $0.03390 per kWh during]ght load hours. 4. Heavy load hours are all hours from 6:00:00 A.M. to 1:59:59 P.M., Monday through Saturday. Medium load hours are all hours from 2:00:00 P.M. to 9:59:59 P.M.. Monday through Saturday. Light load hoursare all other hours Monday through Saturday, all day Sunday, and all day on North American Electric Reliability Cornoration specified holidays. Pacific Prevailing Time applies (Pacific Standard Time or Pacific Daylight Timms applicable). 5. Billing Demand: a Billing demand for each month shall be based on the maximum hour of KVA (apparent power) during Heavy Load Hours. b Monthly Demand Charge between September 1 and May 31 _ $3.50 per KVA for 95% of 1-11 KVA and $9.80 per KVA for 5% of all KVA. • c. Monthly Demand Charge between June 1 and August 31 $3.50 per KVA for 95% of all KVA and $9.06 per KVA for 5% of all KVA. 13,12,042 1Schedule NP -03 - Nonprofit tax-deductible – time of use rate A. Applicability. This schedule applies to all nonprofit tax-deductible organizations. B Character of Service Sixty cycle alternating current at such phase and voltage as the City may have available will be furnished under this schedule applied through a single metf;r and one point of delivery. C. Time of Use Rate: 1. Base Charge aSingle phase $21.50 per month b. Three phase $53.75 per month 2. Monthly Energy Charge between September 1 and May 31 $0.07110 per kWh during heavy load hours. $0.05770 per kWh during medium load hours, and $0.04970 per kWh durins� 1, ight load h ur . 3. Monthly Energy Charge between June 1 and August 31 $0.07360 kWh during heavy load hours. $0.05960 per kWh during medium load hours. and $0.04490 per kWh during light load -5- • G-12 • hours 4. Heavy load hours are all hours from 6.00:00 A.M. to 1:59:59 P.M.. Monday through Saturday. Medium load hours are all hours from 2:00:00 P.M. to 9.59:59 P.M., Monday through Saturday. Light load hours are all other hours Monday through Saturday, all day undav, and all day on North American Electric Reliability Corporation specified holiday Pacific Prevailing Time applies (Pacific Standard Time or Pacific Daylight Time as applicablel. thermostat or home area network $10.00 credit per month D. Demand Response Credits Devices controlled by the City during demand events providing the customer has not disabled the controls or opted out of participation shall receive a credit as follows: 1 Water heater load control switch $10.00 credit per month 2. Smart thermostat or home area network $10.00 credit per month 3. Water heater load control switch and smart thermostat $10.00 credit per month 4. Thermal storage system $10.00 credit per month. 13.12.044 Schedule GD -04 - General service demand — primary metered — time of use rate A. Applicability. This schedule applies to all accounts not covered by other rate schedules with the following types of service: •1. 20/208 or 120/240 volts, single or three phase, service panel larger than 400 amps 2. 240/480 or 277/480 volts three phase service panel larger than 200 amps 3 When electric current is measured at primary voltage and delivery to the customer is at secondary voltage. B. Character of Service Sixty cycle alternating current at such phase and voltage as the City may have available will be furnished under this schedule applied through a single meter and one point of delivery. C. Time of Use Rate: 1. Base Charge: Single phase $42.95 per month b Three phase $107.40 per month 2. Monthly Energy Charge between September 1 and May 31 $0.04590 per kWh during heavy load hours. $0.04590 per kWh during medium load hours_ and $0.03690 per kwh durinv light load hours. 3. Monthly Energy Charge between June -I and August 31 $0.04740 per kWh during heavy load hours. $0.04740 per kWh during medium load hours, and $0.03330 per kWh during light load hours. 4 Heavy load hours are all hours from 6:00:00 A.M. to 1:59.59 P.M., Monday through Saturday. Medium load hours are all hours from 2:00:00 P.M. to 9.59.59 P.M., Monday through Saturday. Light load hours are all other hours Monday through Saturday, all day . -6- G-13 Sunday, nd all day on North American Electric Reliability Corporation s ecified holida s. • Pacific Prevailing Time applies (Pacific Standard Time or Pacific Daylight Tirne. as ap licable). 5. Billing Demand: a. Billing demand for each month shall be based on the maximum hour of KVA (apparent power) during Heavy Load Hours. b. Monthly Demand Charge between September 1 and May 31 $3.45 per KVA for 950X, of all KVA and $9.80 per KVA for 5% of all KVA. c, Monthly Demand Charge between June 1 and August 31 $3.45 per KVA for 95% of all KVA and $9.06 per KVA for 5% of all KVA. 13.12.061 Schedule PS -03 -Primary service — time of use rate. A. Applicability. This schedule applies to all accounts which own and operate a primary v 1� distribution system with a connected load greater than 1.000 KVA. B. Character of Service. Service to be furnished under this schedule is unregulated three phase sixty cycle, alternating current at primary voltage. 12.5 KV nominal. Service under this schedule shall be provided and metered at the point(s) of interconnection of the distribution facilities of the customer and the Citv. • C. Time of Use Rate: 1 Base Charge: $28 er month 2 Monthly Energy Charge between September 1 and May 31 $0.04100 per kWh during heeate load hours. $0.04100 per kWh during medium load hours, and $0.03300 per kWh durinf7 l load hours. 3. Monthly Energy Charge between June l and August 31 $0.04240 per kWh during heavylad hours. $0.04240 per kWh during medium load hours. and $0.02980 per kWh during light load hours. 4. Heavy load hours are all hours from 6:00:00 A.M. to 1:59:59 P.M.. Monday through Saturday. Medium load hours are all hours from 2:00:00 P.M. to 9:59:59 P.M.. Mo iDda through Saturday. Light load hours are all other hours Monday through Saturday. all day Sunday, and all day on North American Electric Reliability Corporation specified holidays. Pacific Prevailing Time applies (Pacific Standard Time or Pacific Daylight.—Time.--as applicable). 5. Billing Demand: a Billing demand for each month shall be based on the maximum hour of KVA (ap)arent power) during Heavy Load Hours, b. Monthly Demand Charge between September 1 and May 31 $4.30 per KVA for 95% of all KVA and $9.80 per KVA for 5% of all KVA. -7_ 0 G - 14 • c Monthly Demand Char e between June l and August 1 $4.30 per KVA ° r for 95 /. of all KVA and $9.06 per KVA for 5% of all KVA. 13 12 075 Schedule MW -03 - Municipal water Pumping —time of use rate A. Applicability. This schedule applies to municipal water pumping facilities where the connected load is greater than 500 KVA. B. Restrictions. Timers approved by the Public Works and Utilities Department shall be installed to prevent pumping during restricted hours as determined by the Public Works and Utilities Department. C. Character of Service. Service to be furnished under this schedule is three phase sixty cycle alternating current at such phase and voltage as the City may have available will he furnished under this schedule, applied throughgle meter and one point of delivery. D. Time of Use Rate. 1. Basic Charge: $286.35 per month 2 Monthly Energy Charge between SenLember 1 and May 31 $0.06440 Per kWh during heavy load hours. $0.06440 per kWh during medium load hours. and $0.03210 per kWh during light load hours. 3 Monthly Energy Charge between June 1 and August 31 $0 06650 per kWh during heavy load hours. $0.06650 per kWh during medium load hours. and $0.02900 per kWh during light load hours. 4. Heavy load hours are all hours from 6:00:00 A.M. to 1:59:59 P.M.,Monday through Saturday. Medium load hours _are _all _ hours from 2:00:00 P.M.to 9:59.59 P.M., Monday through Saturday. Light load hours are all other hours Monday through Saturday, all day Sunday, and all day on North American Electric Reliability Corooration specified holiday Pacific Prevailing Time applies (Pacific Standard Time or Pacific Daylight Time, as applicable). 5. Billing Demand: a. Billing demand for each month _shall be based on the maximum hour of KVA (apparent power) during Heavy Load Hours. b. Monthly Demand Charge between September 1 and May 31 $3.65 per KVA for 95% of all KVA and $9.80 per kW for 5% of all KVA c. Monthly Demand Charge between June 1 and August 31 $3.65 per KVA for 95% of all KVA and $9.06 per KVA for 5% of all KV G-15 Section 2 - Corrections. The City Clerk and the codifiers of this ordinance are • authorized to make necessary corrections to this ordinance including, but not limited to, the correction of the scrivener's/clerical errors, references, ordinance numbering, section/subsection numbers and any references thereto. Section 3 - Severability. If any provisions of this Ordinance, or its application to any person or circumstances, are held invalid, the remainder of the Ordinance, or application of the provisions of the Ordinance to other persons or circumstances, is not affected. Section 4 - Effective Date. This Ordinance, being an exercise of a power specifically delegated to the City legislative body, is not subject to referendum. This ordinance shall take effect five (5) days after passage and publication of an approved summary thereof consisting of the title. PASSED by the City Council of the City of Port Angeles at a regular meeting of said • Council held on the - day of April, 2012. ATTEST: Janessa Hurd, City Clerk PUBLISHED: 2012 By Summary MAYOR, CHERIE KIDD APPROVED AS TO FORM: William E. Bloor, City Attorney G \LEGAL\a ORDINANCES&RESOLUTIONS\ORDINANCES 2012\05 - Electric-TlmeotUse Chapter 3 12 02 22 12docx docx • G-16 CITYOF 0,R, -T,- NGELES • 1 WASHING -TON, U.S. A. 0 CITY COUNCIL MEMO DATE: APRIL 3, 2012 TO: CITY COUNCIL FROM: DAN MCKEEN, FIRE CHIEF SUBJECT: FIRE DEPARTMENT RELATED MUNICIPAL CODE UPDATES Summary: After a recent review of the Port Angeles Municipal Code, it was determined that several minor updates and corrections related to Fire Department items were required. Most of the corrections are due to numbering changes that are a result of regular International Fire Code updates. One notable update is the deletion of the requirement that some Institutional Occupancies have their fire alarm systems monitored by PenCom. This is an outdated requirement that places PenCom, a government agency, in direct competition with private alarm monitoring companies that provide the same service. In addition, the PenCom alarm monitoring equipment is aging, prone to false alarms and becoming increasingly difficult to maintain. Recommendation: Conduct second reading of ordinance and consider adoption. Background/Analysis: The Fire Department conducts regular reviews of the Port Angeles Municipal Code (PAMC) in order to ensure that the applicable sections are current and correct. After the most recent review, it was determined that several sections of the PAMC require minor updates and corrections. Most of the corrections are due to numbering changes in the International Fire Code. The International Codes are revised on a regular three-year schedule and it is not uncommon for these revisions to result in numbering changes. One notable update is a change in the fire alarm monitoring requirement for some Institutional Occupancies. Currently, the PAMC requires that Institutional Occupancies (such as nursing homes and hospitals) have their fire alarm systems monitored by PenCom. This section of the PAMC was written decades ago when fire alarm monitoring by PenCom was cutting edge technology. In the subsequent years, commercial fire alarm monitoring system technology has greatly surpassed the equipment in place at PenCom. The PenCom system is outdated and it is becoming increasingly difficult to maintain. The system is prone to false alarms and other system faults. In addition, alarm monitoring by PenCom, a service that has been provided for free, is in direct competition with commercial alarm monitoring companies that provide the same service. Once this PAMC change is approved, we can continue to move forward with weaning commercial accounts off of PenCom monitoring. H-1 City Council _ _ • Page 2 April 3, 2012 On March 20, 2012, the City Council received a presentation on the proposed updates and corrections to the Port Angeles Municipal Code. The discussion on this item was continued to April 3, 2012, at which time the Council can again review the proposed changes. Staff is recommending that the proposed changes be adopted at the April 3 meeting. These proposed ordinance changes have been approved by the City Attorney. Attachment — Proposed Ordinance Changes H-2 • • ORDINANCE NO. AN ORDINANCE of the City of Port Angeles, Washington, relating to the Fire Department; making changes to Chapters 2.16, 5.32, 14.03, 14.21, and 14.23 of the Port Angeles Municipal Code. THE CITY COUNCIL OF THE CITY OF PORT ANGELES DO HEREBY ORDAIN AS FOLLOWS: Section 1. Ordinance 1092 and Chapter 2.16 of the Port Angeles Municipal Code relating to Fire Department personnel are hereby amended by amending Section 2.16.010 to read as follows: 2.16.010 - Established—Composition. The City Fire Department is established and consists of officers and employees as follows: A Chief of Fire Department, Assistant Chiefs of Fire Department, F.. rite„ ...,eeh ,+:,., • s„ ,,.irAendei 4 ,.f..adie mid fife ..l,,f t..uek a.: ,: e emd sue Captains. Lieutenants, Firefighter/EMT's. Firefighter/Paramedics and other officers and employees as may be ata necessary for the proper conduct and administration of the Department. • Section 2. Ordinance 2050 as amended and Chapter 5.32 of the Port Angeles Municipal Code relating to Fireworks are hereby amended by amending Sections 5.32.050 C and 5.32.080 to read as follows: 5.32.050 - Permit—Application requirements and required information. C. A public liability and property damage insurance policy from an insurance company licensed to do business in this State, in the sum of at least $500,000.00 1 00 for bodily injury or death suffered by one or more persons in any accident or occurrence, and at least $100,000.00 for property damage. The insurance policies must name the City as an additional insured, to indemnify the City from damage or injury caused by the operation of retail fireworks stands; 1 H-3 5.32.080 - Dates when use permitted. No person, firm or corporation shall use or explode any fireworks within the City except from 9:00 a.m. to 11:00 p.m. on the Fourth day of July of any year; provided, that this prohibition shall not apply to duly authorized public displays, where the same are authorizedpursuant to the laws of the State_; E „def n n MG -5 32 020 fna.,, beusedf Section 3. Ordinance 2552 as amended and Chapter 14.03 of the Port Angeles Municipal Code relating to Amendments to International Codes are hereby amended by amending Section 14.03.020 to read as follows: 14.03.020 - Amendments to International Codes. Pursuant to RCW 19.27.040, RCW 19.27.060(3) and (4), and PANIC 14.04.3.020, the following amendments to the Inlernational Building Code, International Residential Code, International Fire Code, and Uniform Sign Code are adopted: • A. International Building Codes, Chapter 5, Table 503 is amended by adding the . following footnote: (9cg) Type V -B construction prohibited in CBD - Central Business District. B. International Building Code, Section 903.2.10 is amended by adding the following: 903.2.x -. 3 Automatic sprinklers shall be provided: (a) In all buildings where the floor area exceeds 6,250 square feet on all floors; (b) In any adult family home, boarding home, or group care facility that islicensed by the Washington State Department of Social and Health Services formore than five persons; However, the height and area increases specified in Section 504 and 506 (for sprinklers) shall be permitted. For the purpose of the subsection, portions of buildings separated from the rest of the building, in aeeefdance MSeetien Inc, ..:+i. epenings aW aetiva+ed by- smoke dete .+ien ,-leyiee installed ,t both sides e f said - 2 aid- • 2 H-4 • .in accordance with the International Building Code may be considered as separate buildings. Section 4. Ordinance 2552 as amended and Chapter 14.21 of the Port Angeles Municipal Code relating to Adoption of International Fire Code, appendices and storage are hereby amended by amending Section 14.21.010, 14.21.030, 14.21.040, and 14.21.050 to read as follows: 14.21.010 - Adoption of International Fire Code, appendices. There is adopted by the City Council for the purpose of prescribing regulations governing conditions hazardous to life and property from fire or explosion, that certain Code known as the International Fire Code, including Appendices ^rte,r—,4-Z and G, published by the International Code Conference as amended by the Washington State Building Code Council. In the case of any conflict between the Appendices adopted by this section and any other ordinance that addresses a specific requirement covered by the appendices, the other . specific ordinance shall control. 14.21.030 - Aboveground storage of flammable liquids. A. The limits referred to in Mien 7902.2.2.4 Chapter 34 of the International Fire Code, in which storage of flammable or combustible liquids in outside aboveground tanks is prohibited are established in all residential zones, and in all other zones when the total capacity exceeds 24,000 gallons, but not in the IH zone where there is no limitation. B. new bulk plants faf flafn+nable ef eetftbustible liquids afe pfehibited, afe established as fel-lews.- In a4 zone elassifieatieasNew bulk plants as described in International Fire Code Section -3406.4 are prohibited in all zone classifications except that part of the IH zone which lies west of Cedar Street as prescribed in Ordinance 1709 and subsequent ordinances amending the same. 14.21.040 - Bulk storage of liquefied petroleum. A. The limits referred to in Section 8204.2 3804 of the International Fire Code, in which bulk storage of liquefied petroleum gas is restricted, are established as follows: In all 3 H-5 zone classifications except that part of the IH zone which lies west of Cedar Street as • prescribed in Ordinance 1709 and subsequent ordinances amending the same. B. The liquefied petroleum gas container requirements referred to in A14iele 8 Chapter 38 of the International Fire Code shall include the requirement that containers be protected from damage that might result from earthquakes, the manner and extent of which protection shall be in accordance with the determination of the Wire eChie£ 14.21.050 - Storage of explosives. The limits referred to in £eetiei "�z Chanter 33 of the International Fire Code, in which storage of explosives and blasting agents is prohibited, are established as follows: In all zone classifications except that part of the IH zone which lies west of Cedar Street as prescribed in Ordinance 1709 and subsequent ordinances amending the same. Section 5. Ordinance 3124 as amended and Chapters 14.23.050, 14.23.15 0,14.23.160, 14.23.170, and 14.23.180 of the Port Angeles Municipal Code are hereby amended to read as follows: CHAIPTER 14.23 - FIRE ALARMS 14.23.010 - Purpose. 14.23.020 - Definitions 14.23.030 - Permits. 14.23.040 - General requirements. 14.23.050 - Occupancy specific requirements. 14.23.060 - Manual fire alarm system pull stations. 14.23.070 - Notification devices. 14.23.080 - Fire -extinguishing systems. 14.23.090 - Acceptance tests. 14.23. 100 - Instructions and zone maps. 14.23.110 - Remote annunciators. 14.23.120 - Inspection, testing, and maintenance. 14.23.130 -Lock boxes. 14.23.140 - Signage. 14.23.150 - Existing buildings_ i n 23 i tin Resi efit ,1 . ,,.+tiffs. 14.23.17860 - Repeated failure of equipment. 14.23.15870 - Violations. 14.23.050 - Occupancy specific requirements. • The occupancy types regulated in this section shall be defined as in the current edition of the International Building Code. • 4 H - Ei A. All Group "A" occupancies with an occupant load of 300 or more shall have a manual fire alarm system installed. B. All Group "B" and 'B" occupancies which are used for educational purposes shall be protected throughout by an approved addressable automatic fire detection system. C. All Group "F" occupancies that are two or more stories in height shall have a manual fire alarm system installed. D. All Group "H" 9occupancies shall have a manual fire alarm system installed. E. All Group "I" 9occupancies shall be protected throughout by an approved automatic addressable atAeffiatie fire detection system connected to the PaA Angeles C=easelida4ed Diss tee Cei4e an approved fire alarm receiving center. F. All Group "RI" occupancies shall be protected throughout by an approved addressable automatic fire detection system. G. All duplexes, two or more stories in height, shall be protected throughout by an approved automatic fire detection system. 14.23.150 - Existing buildings. Existing buildings shall not be made to conform to the provisions of this chapter; provided that if the Fire Department determines that structural deficiencies affecting life safety are involved and that the continued use of the building or structure without a fire alarm • system would be hazardous to the safety of the occupants, or, if an existing building undergoes a change in use or occupancy that results in a condition determined to be potentially hazardous to the safety of the occupants, the Fire Department may require compliance with the terms of this Chapter. • 14.23.17960 - Repeated failure of equipment. The Fire Department, due to repeated failure of equipment or circuitry, multiple fire alarms or failure to comply with all of the provisions of this chapter, may at any time order the discontinuance of any fire alarm system within the City. Such notice of discontinuance shall bemade in writing to both the agency supplying the alarm and to the persons, firms and/ orcorporations affected, at least 48 hours prior to the discontinuation of the fire alarm circuit. In the event of temporary failure of fire alarm equipment or circuitry, equipment malfunction, or multiple false alarms, the Fire Department, after notification of the occupants of the structure, may order all emergency response actions discontinued until repairs can be made by alarm agency personnel. Such notice shall be made in writing to the persons, firms, and/or corporations affected as soon as possible. 5 H-7 14.23.18870 - Violations. 0 Any willful violation of the terms of this chapter by any person or agency shall be deemed a misdemeanor and shall be punishable by a fine of up to $500.00 per day for each day that the violation continues. Section 6 - Corrections. The City Clerk and the codifiers of this ordinance are authorized to make necessary corrections to this ordinance including, but not limited to, the correction of the scrivener's/clerical errors, references, ordinance numbering, section/subsection numbers and any references thereto. Section 7 - Severability. If any provisions of this Ordinance, or its application to any person or circumstances, are held invalid, the remainder of the Ordinance, or application of the provisions of the Ordinance to other persons or circumstances, is not affected. Section 8 - Effective Date. This Ordinance, being an exercise of a power specifically delegated to the City legislative body, is not subject to referendum. This ordinance shall take effect April , 2012. APPROVED AS TO FORM: William E. Bloor, City Attorney ATTEST: Janessa Hurd, City Clerk PUBLISHED: , 2012 By Summary Ordinances 2012\06 — FrceDeptCodeAmendmenis 02 08 12 CHERIE KIDD, Mayor 6 H-8 • • • LJ NGELES DATE: April 3, 2012 TO: CITY COUNCIL FROM: Glenn A. Cutler, P.E., Director of Public Works & Utilities SUBJECT: Equipment Purchase — Excavator Summary: Funds were included in the 2012 budget to purchase an 18,000 lb. class excavator with attachments and trailer. The Fleet Manager researched pricing and sales options for the excavator and determined the most favorable pricing to the City through HGACBuy, an interlocal purchasing cooperative. The cost of the excavator increased higher than anticipated making it necessary to amend the budget to purchase a trailer. Recommendation: 1) Award and authorize the City Manager to sign a contract to purchase a John Deere 85D excavator from Pape Machinery, Inc. through HGACBuy Purchasing Cooperative Contract 11-2930 for an amount not to exceed $113,000.00, including sales tax, and to make minor modifications to the purchase contract, if necessary, and 2) Amend the 2012 budget to increase the Equipment Services Fund by $5,000.00 for purchase of a tandem axle tilt -bed trailer. Background/Analysis: The purchase of a small excavator is proposed as a means of adding versatility and productivity to excavation operations. For example, compared to a backhoe, an excavator can efficiently operate in a narrower worksite and reduce construction traffic congestion. The excavator will be assigned to the Equipment Services Pool and shared across divisions. Funds amounting to $115,000.00 were included in the Streets portion of the 2012 Equipment Services replacement budget to purchase an excavator and a used trailer large enough to transport the excavator along with a selection of digging attachments. The Fleet Manager identified the best purchasing option for an excavator through the City's membership in HGACBuy, an interlocal purchasing cooperative. A John Deere model 85D excavator was selected based on performance, durability, service support and price, and configured to City specifications. The excavator purchase is with a regional John Deere dealer, Pape Machinery, Inc., and includes 24 -inch, 36 -inch and 60 -inch buckets, for $103,900.00, plus tax totaling $112,627.60. This replaces vehicle 1570 which will be moved to the Equipment Services pool. Because of equipment cost escalation, an additional $5,000.00 is necessary to obtain a used trailer in good condition. That purchase will be executed through the City Manager's purchasing authority. It is recommended that City Council: 1) Award and authorize the City Manager to sign a contract to purchase a John Deere 85D excavator from Pape Machinery, Inc. through HGACBuy Purchasing Cooperative Contract 11-2930 for an amount not to exceed 113,000.00, and to make minor • modifications to the purchase contract, if necessary, and 2) Amend the 2012 budget to increase the Equipment Services Fund by $5,000.00 for purchase of a tandem axle tilt -bed trailer. J-1 NACCOUNCIL\FINAL\Equipment Purchase-Excavatondocx NGELE WASH ING TO N, CITY COUNCIL MEMO DATE: APRIL 3, 2012 TO: CITY COUNCIL FROM: KENT MYERS, CITY MANAGER SUBJECT: PROPOSAL FOR PUBLIC FORUM - BIOMASS FACILITIES Summary: During and following the March 20, 2012, City Council meeting, several citizens stated concerns about the current development of a biomass facility at Nippon. It was suggested the City Council might want to consider a moratorium on biomass facilities in the City Limits. Recommendation: City Council consider a proposal to sponsor a public forum on the pros and cons of biomass facilities. Background/Analysis: Following the March 20, 2012, City Council meeting, I met with Mayor Kidd, Councilmember Mania, and Attorney Bloor to discuss recent citizen concerns regarding biomass facilities. Since Nippon has secured all of the state and local permits for their biomass facility, it was agreed a moratorium would have very little impact. Therefore, the suggestion was offered for the City to consider sponsoring a public forum to present the pros and cons of biomass facilities. Council discussion and approval is needed prior to organizing such a forum. Do you want the City to be involved in organizing this type of forum? If so, what type of structure do you want to set for such a forum in terms of speakers, public comment, etc.? • • • Port Angeles Regional Chamber of Commerce Board Members 2012 Member 1 Hallett & Associates 2 Key Bank 3 Individual member 4 Windermere 5 Olympic Cellars Winery 6 Port Angeles Farmers Market 7 Coldwell Banker Reality 8 Individual member 9 Columbia Bank PO Box 3050 1633 E Front St 203 Shade Tree Lane 711 E Front St 255410 Hwy 101 PO Box 336 1115E Front St 139 E Ahlvers Rd PO FOX 891 Seawm ZIP 98362 Jim Hallett 98362 Julie Hatch 98362 Howard Fisher 98362 Alan Barnard 98362 Kathy Charlton 98362 Cynthia Warne 98362 Jim Wahlsten 98362 George Bergner 98382 Brian Kuh 98362 Shenna Straling 98362 Todd Ortloff 98362 Sharon Stevenson 98362 Ed Bedford 98362 Jim Jones 98362 Edna Petersen 98362 Jeff Robb 98362 Noelle Fuller 98362 Cherie Kidd 10 Sterling Savings Bank 1033 E First Street Clallam County 233 E 4th St 11 KONP-Radio Pacific PO Box 1450 Port of Port Angeles PO Box 1350 12 Olympic Medical Center 939 Caroline Street City of Port Angeles Council Member PO Box 1150 -13 Individual member 236 E Front St #15 14 Clallam County 233 E 4th St 15 Port Angeles Business Assn (CPI) 217 N Laurel St 16 Port of Port Angeles PO Box 1350 17 Port Angeles Downtown Association 108 E First St 18 City of Port Angeles Council Member PO Box 1150 d(&-olypen com Dec -12 filling term of M Rainey Ex Officio olympiccellars com Dec -12 elesfarmersmarket(cDg_m_ all comDec-12 City of Port Angeles City Manager PO Box 1150 Olympic National Park 600 East Park Ave 983621 Kent Myers 98362 Todd Seuss Title: Phone Past Pres 360 457 6000 360 452 4554 360 477 4758 360 457 0456 360 452 0160 360 460 0361 Treasurer 360 417 2792 360 797 4752 President 360 457 3601 360 477 9731 360 457 1450 360 417 7293 Vice Pres 360 808 5498 360-417-2233 360-457-6400 360 457 8527 360 417 8978 360 417 4500 Ex Officao 360-417-4804 Ex Officio 360 565 3002 Staff Chamber Staff 121 E Railroad 98362 Russ Veenema Exec Dir 360-452-2363 x13 Lindsey Veenema Vist Ctr 360 452 2363 x15 Address Ends Ilettadvlsors us Dec -08 stay on 2012 as Past President tcha)kevbank com Dec -12 1hotmall com Dec -12 d(&-olypen com Dec -12 filling term of M Rainey olympiccellars com Dec -12 elesfarmersmarket(cDg_m_ all comDec-12 filling term of,1 Eades llypen com Dec -13 Filling Donya Alward term rge4food_n_et Dec -13 :olumblabank com Dec -13 filling Chris McKinney term strahng(aD-sterlingsavingsbank com Dec -14 onp coal --- -- Dec -14 son(cDolymplcmedlcal org Dec -14 )rd wavecable com Dec -13 >,co dallam wa us Dec -12 appointed by county 2@olypen com Dec -12 appointed by PABA Lrtofpa com Dec -12 appointed by port 'uller85 yahoo com Dec -12 appointed by PADA cl�a_us Dec -12 appointed by Cdv A - BC D E F G H I J K L M N O 1 JAN FEB I MARCH I APRIL MAY JUNE JULY AUG SEPT OCT 1 NOV I DEC Totals 2 Income from City Room Tax 3 Updated March 5 2012 4 Total Income 5 s Expenses 7Internet Marketing s Web contracts s Web mamt & mise web work 10 OLYPEN for e-mail access 11 KIRO SEM/SEO 12 FaceBook ads 13 1a Total web related 21 22 Newspapers 23 NW Destinations by City Livl 24 WNPA (tion Planner er print 15K (down from 30K used ge for PA Vist Guide ast & Comcast.net ive of 30 second spot ast Online TV $350 $350 $350 $350 1 $350 1 $350 I 5350 I 5350 1 $350 1 $350 1 $350 1 $350 $250 $250 $250 $250 $250 $250 $250 $250 $250 $250 $250 $250 $20 $20 $20 $20 $20 $20 $20 $20 $20 $20 $20 $20 42 $2,500 $2,500 $2,500 $2,500 $500 1 $500 $500 1 $500 $500 $740 1 1 $740 1 $740 1 $740 $7,485 $3,100 $3,100 $6,200 $300 $300 5300 $500 $750 $2,000 $650 $500 $500 $300 $300 $6,400 $12,600 $500 1 $500 1 $500 1 $500 H4o 41 Vancouver Island Ferry Advertising on COHO TV 30 sec $300 $300 $300 $300 $300 $300 $300 $300 $300 $300 $300 $300 53,600 42 Cohn Terminal Victoria $100 $100 $100 $100 $100 $100 $100 $100 $100 $100 $100 $100 $1,200 43 5 Recreation Centers 30 sec $600 $600 $600 $600 $600 $600 $600 $600 $600 $600 $600 $600 $7,200 44 Tourism Victoria Visitor Center Big Screen $450 $450 $450 $450 $450 $450 $450 $450 $450 $450 $450 $450 $5,400 45 Brochure Distribution at Airport charge/was $792) $0 $0 $0 $0 $0 $0 $0 $0 $0 $0 $0 $0 $0 4s -no 47 Total Vancouver Island $17,400 49 19 so Washington State Ferry System Rack Card design and print 30K (down from 40K) $1,500 $1,500 21 Rack Cards via Certified full system $356 $356 $356 $356 $356 $356 $356 $356 $356 $3,204 52 Seattle Terminal/Pier52 BR $25 $25 $25 $25 $25 $25 $25 $25 $25 $225 53 Certified Edmonds/Kingston BR $110 $110 $220 54 Certified Seattle Bainbridge BR $135 $135 $270 55 Certified Edmonds/Kingston 9second digital $25 $25 $25 $25 $25 $25 $25 $25 $25 $25 $250 56 Certified Mukiliteo/Clinton & PT/Coupville 9 sec digital $25 $25 $25 $25 $25 $25 $25 $25 $25 $225 57 Certified Seattle Baingndge 9 second digital $25 $25 $25 $25 $25 $25 $25 S25 $25 $25 $250 ss Certified Seattle Terminal 9 second digital $25 $25 $25 $25 $25 $25 $25 $25 $25 $225 59 lCertified Vtips Olympic/Kitsap Peninsula $50 $50 $50 $50 $50 $50 $50 $50 $50 $50 $500 so IWA State Ferry Bainbridge Digital on board screens $258 $258 $258 $258 $258 $258 $258 $1,806 61 WA State Ferry Edmonds/Brambridge on board murals $851 $851 $851 $851 $851 $851 $851 $5,957 62 63 Total WA State Ferry System $14,632 64 ss Adm Support and contract management $4,167 $4,167 $4,167 $4,167 $4,167 $4,167 $4,167 $4,167 $4,167 $4,167 $4,167 $4,163 $50,000 ss OPTC $1,500 $1,500 $1,500 $1,500 $1,500 $1,500 $1,500 $1,500 $1,500 $1,500 $15,000 67 Sports/Event Grants $5,716 $5,714 $5.714 $6.714 $5.714 $6.714 $5.714 542.000 $416 1 $416 1 $416 for other ormects and adm 73 1 Sub -total $203,517 74 1 Contingency $5,983 7s 76 IMonthly totals $10,298 $13,434 $8,984 1 $16,009 1 $21,997 $20,288 j $26,900 $21,247 1 $26,242 1 $16,807 1 $14,562 1 $12,732 1 $209,500 res 2012 Special Event/Project Grant Requests Total Funds Available $42,000 Funding requests from room tax grant fund: For 2012 Event Date Request Approved NW Cup 4/6-4/8 $833 $833 NW Cup 4/26-4/29 $833 $833 _NW Cup 5/11-5/13 $833 $833 Juan De Fuca Festival 5/24-5/28 $11,000 $79000 North Olympic Discovery Marathon _ 6/2-6/3 $15,000 $79000 Arts In Action & Sand Sculpture 7/27 $51000 $29500 Ride The Hurricane 8/5 $2,000 $29000 Sprint Boat Race @ ESP 8/11 $1,666 $19666 Olympic Peninsula Senior Games 8/24 $39800 $2,000 Sprint Boat Race @ ESP 9/18 $1,666 $19666 Challenge Run @ ESP 9/29 $1,666 $19666 Blues Festival 9/14 $39000 $2,500 Dungeness Crab & Seafood Festival 10/12-10/14 $10,000 $99000 Story Telling Festival 10/19-10/21 $31000 $19500 PAFAC Art Park on going $1,200 $1,200 MINUTES • PLANNING COMMISSION Port Angeles, Washington 98362 March 14, 2012 6:00 p.m. Members Present: Doc Reiss, Amanda Anderson, David Miller, John Matthews, Tim Boyle, Duane Morris, Scott Headrick Members Excused: None Staff Present: Scott Johns, Nathan West, Sue Roberds Public Present: None PLEDGE OF ALLEGIANCE Chair Reiss opened the regular meeting at 6:00 p.m and led the Pledge of Allegiance. APPROVAL OF MINUTES Commissioner Miller moved to approve the February 22, 2012, regular meeting minutes. Commissioner Anderson seconded the motion which passed 5 — 0 with Commissioners • Morris and Headrick abstaining due to lack of attendance at the meeting. WORK SESSION: SHORELINE MASTER PLAN: Presentation of new draft shoreline master plan. Associate Planner Scott Johns reviewed the steps taken to formulate a new draft shoreline master plan as required by the State Department of Ecology and noted that the Department of Ecology requires a revision of shoreline master plans every 7 years. He explained that the main difference between the original plan and the new plan is a reorganization of specific element sections and he noted that the revised plan includes expanded environmental designations and an administration section. Public outreach events were reviewed that included a public survey to determine desired uses and important issues to the public and was taken early on in the planning process in order to develop the revised plan. Mr. Johns explained the intent of each section and noted that an administrative chapter was not included in the original plan. Mr. Johns responded to a question from Commissioner Reiss that existing uses and activities that are active will be allowed to continue under the revised plan as with any other enactment of law. Mr. West responded that he doesn't anticipate any more stringent development regulations for shoreline areas than currently exist; the revised plan will simply define environmental areas and procedures for use more completely. • M-1 Planning Commission Anutes March 14, 2012 Page 2 COMMUNICATIONS FROM THE PUBLIC • None STAFF REPORTS WATERFRONT TRANSPORTATION IMPROVEMENT PLAN (WTIP) Director Nathan West provided the Commission with a detailed description of actual on -the - ground planning for the City's Waterfront Transportation Improvement Plan (WTIP). Commission members asked questions as to the amenities that have been worked into the Plan that include an esplanade, new beach area, viewing points, and a short bridge over Peabody Creek. The City Council stressed that they want to see a good deal of citizen participation in the development of this project. Mr. West stated that over 23 meetings and outreach events have taken place up to this point. A Facebook page has been established, the City's web site is utilized, display boards have been set up in the lobby of City Hall, staff have taken the plan to various community groups who are all very excited about the project. Such an upgrade to the waterfront area has been in the concept stage for many years. The project is broken into 11 different phases so work can begin when funds becomes available. A west end beach park is planned that will include beach restoration, a fountain feature, • sculptures, art plaza, play area, restrooms, and an office pavilion. Total project costs from Hollywood Beach to the Valley Creek Estuary are $17M; the west end park is approximately $4.2M. It is hoped to begin the project in July, 2012, continuing through early months of 2013. Work will be coordinated with the municipal Combined Sewer Overflow project that will result in economic efficiencies. Personnel are working to minimize impacts to local businesses that may result from construction activities. Many local firms have been involved in development of the plan thus far and that coordination and input is something that is very important to City staff and City officials. Commissioner Morris suggested that, given the cool environment of the area, bright, warm colors are used rather than the cooler pallets. Mr. West responded to questions and described some of the private improvement projects that are also being planned along the waterfront area in conjunction with the upgrade construction. He hopes that the waterfront improvements will stimulate additional business investment to improve and expand their businesses as a result of the updates. Planning Manager Sue Roberds introduced new Planning Commission members Scott Headrick and Duane Morris. Commissioners Headrick and Morris provided brief bios and noted their interest in serving the community. • M-2 L_ • 0 Planning Commission Minutes :March 14, 2012 Page 3 REPORTS OF COMMISSION MEMBERS None ADJOURNMENT The meeting adjourned at 7:30 p.m. r� r Sue Roberds, ecretary PREPARED BY, S. Roberds ---"Doe Reiss, Chair M-3 City of Port Angeles Parks, Recreation & Beautification Comniission Special Meeting Port Angeles, Washington L' February 15, 2012 CALL TO ORDER- Chairperson Stratton called the special meeting of (lie Port Angeles Parks. SPECIAL MEETING: Recreation & Beautification Commission to order at 6:00 p.m, in the Cit" Council Chambers. ROLL CALL: {Members Present Chairperson Stratton, Vice Chairperson Pittis, Commissioners Rarnsey, Merritt, SharoZ'el, Student Representatives Wise, and Nelson Afenibers,lbsent: Commissioner Hordyk, Sta Manager Myers, NT. West, R Bourne, D. &Alanictite, S Jones, R. Korcz, Secretary, Kochanek, APPROVAL OF THE None. MINUTES: LINCOLN PARK MASTER Juliet 'Yong, president of Hough Beck & Baird Landscape Architecture PLAN CONSULTANT conducted a PowerPoint presentation on the Lincoln Park Master Plan process. REPORT- open house presentation, concepts, and gave a summary covering the next steps of the protect. Chairperson Stratton informed the commissioners that the meeting was now • open for public comment and that the commission would hold their questions and comments until the end of the meeting PUBLIC COMMENT: Devon Graywolf, 438 Lopez, spoke in opposition to removing the trees at Lincoln Park because of atmospheric annihilation due to frenzied massive global clear cutting and provided a written appeal for the City Council to preserve the Lincoln Park trees forever. William Hunt. 438 Lopez, spoke in opposition of the four concepts calling them null and void because no public comment was allowed at the first open house. Geri Thompson. 60771 Hxvy 112, spoke in opposition of moving tile BMX track as it would be detrimental to the program. Kim Weimer, 103 West 13"' Street, spoke in opposition to the removal of the trees at Lincoln Park as the trees provide a noise and wind buffer to the liciollbors. Gene Riniov. 1437 Dan Kell} Road, spoke in favor of removing the trees at Lincoln Park and opening tip the park to more bike trails. Mel Rudin. 1002 Strait View Drive. spoke in favor of a park plan that provides a full service community airport that can be used by all people. Dennis Toepke, 1818 West Lauridsen ff 11, spoke in support of a safe airport for all the public and pilots and felt the airport should not be treated any differently than a park that has safety issues. 0 M-4 0 PUBLIC COMMENT: Lois Danks, 1621 South 1'. Street, spoke in opposition of the removal of the (Cont'd) trees at Lincoln Park that provide a noise and wind buffer for neighbors W Brian Kuh, 121 East Railroad Avenue. spoke in favor of the airport and the importance of its economic vitality to the City of Port Angeles and that thinks the trees need to be removed. Andrew Mai, 483 Westridge Road. spoke of the unique opportunity, because of the trees at Lincoln Park, to come togethet and to work together making a park worthy of what we as citizens deserve Scan Coleman. 1.50 Olympian Way. spoke against movint, the BMX track as it would cripple the program. Dick Pilling, 72 Mount Pleasant Heigglits Lane, spoke against the few vocal L, C, minorities who want to keep the trees at Lincoln Park and in favor of the removal of the trees at Lincoln Park for the good of the community Scott Johns. 1034 West 5"' Street, spoke about the diseased trees at Lincoln Park and doing something that includes the redevelopment of Lincoln Park, with a horticultural element such as a botanical display, Marion Umbarger, 1211 West 18"` Street, spoke against removing the trees at Lincoln Park and messing tip the park-, Marilyn llarbaulgh, 312 12 West 5"' Street. spoke against removing all the trees at Lincoln Park and the concepts presented tonight. Carol Johnson. 123 1 letiry Boyd Road, spoke in favor of a safe, thriving,. and productive airport that is a significant economic driver to our community and would like to see the campground put back in Lincoln Park. Jim Lunt, 221 Lopez, spoke in opposition to losing any parking at Lincoln Park and hopes that everyone will work toward funding the project before any alterations are made because, once the Port of Port Angeles takes the trees down at Lincoln Paik, they will not care what happens to the park after that. Jon Didrickson, 731 East I Ph Street, spoke about the historical aspect of Lincoln Park and that Lincoln Park was there before airplanes were invented and there is a legal g principal that first in sight it is first in right, Randall McCoy, 112 East 11"' Street, spoke in favor of bike traits and rising the trees for stream restoration for salmon. Bonnie Baumgardner, 503 East 0 Street, spoke against removing the trees at Lincoln Park. Susan Lynch, 1511 West 16"' Street, spoke in favor of the concepts that provide a wet land and improvement to the trails. Lilly Thompson, 1228 West 19t" Street, spoke in i egards to her concerns about the funding for the project in these bard economic times, Khat the environmental impact would be to Lincoln Park, and felt moving the BMIX track would add unnecessary cost. M-5 PUBLIC COMMENT- George Titterness. 1717 West 5"' Street, spoke in regards to having an (Cont'd) environmental impact statement that would also include a noise studs, and what will the maintenance be once the Port of Port Angeles %valks awa),. LINCOLN PARK MASTER Chairperson Stratton invited the public to the Parks. Recreation & Beautification PLAN: Commission meeting February 16. 2011 at 6:00 p.m., to be held in Vern Burton (Cont'd) meeting room 0. Commissioner Ramsey asked about the number of parking spaces that may be lost. Chairperson Stratton spoke in favor of placing a community orchard at Lincoln Park. Julic Yong commented that the goal of the protect would be to add pat -king spaces not lose them and stated that an orchard is a possibility, but cautioned that a volunteer group would be needed to maintain the orchard. ADJOURNMENT: Chairperson Stratton adjourned the meeting at 7:29 p.m. Next Meeting February 16, 2012 Vern Burton ConiftlUnIty Center Meeting Room 43 6.00 p.m. FoMer Stratton, Chairperson Cindy Rg hhnek, Secretary M - (1) • r- I L___j Motion carried 6-0. ITEMS FROM AUDIENCE Bonnie Baumgardner, 503 East 4"' Street, spoke in opposition to removing, the NOT ON THE AGENDA- trees at Lincoln Park and voiced concerns about the maintenance cost to the four • concepts that were presented at the last park board meeting. Chairperson Stratton moved item number eleven on the agenda to item number five. 0 LATE Superintendent of Parks Delikat conducted a PowerPoint presentation on the ADD ITIONSiRECREATION Shane Park Playground replacement project. He addressed current and past SERVICES MANAGER finidraising events. Shane Park Committee goals, desig i, cost, and purchasing REPORT: Delikat asked the Parks, Recreation & Beatification Commission for approval to use surplus funds in the Park Improvement Account in the amount of $21,000 to assist the Committee with the purchase of playground tiles that will help complete Phase I of the project. It was moved by Hordyk and seconded by Pittis to: Recommend that City Council move $21,000 from the Park, Improvement Account to assist the Shane Park Committee with the purchase of playground tiles that will help complete Phase I of the project. Motion carried 6-0. The commission complimented Delikat on the wonderful job he has done on the project Commission discussion followed. LINCOLN PARK MASTER Recreation Services Manager Bonine asked the Commission if they had any PLAN DISCUSSION: concerns or thoughts about the Park. Recreation & Beautification meeting that was held in the City Council Chambers November 15, 2012. Commission discussion followed. M-7 City of Port Angeles • Parks, Recreation & Beautification Commission Port Angeles, Washington Februan,16,2012 CALL TO ORDER- Chairperson Stratton called the regular ineetingof the Port Ali,, ies Parks. C, --e REGULAR MEE.TING: Recreation & Beautification Commission to order at 6:00 p.rn. in the Vern Burton Meetinot, Room ;H3.3. ROLL, CALL: Alembers Present- Chairperson Stratton, Vice Chairperson Pittis, Commissioners, Merritt, I-lordyk, Shargel, Ramsey, and Student Representative Wise. itfeinbers Absent- Student Representative Nelson S1qfJ' Present- T. Galla -her. D. McKeem R, Bonine, C. Delikat. and Secretary Kochanek. APPROVAL OF THE It was moved by Pittis and seconded by Shargel to: MINUTES: Approve the minutes of the December S. 2011 meeting. Motion carried 6-0. ITEMS FROM AUDIENCE Bonnie Baumgardner, 503 East 4"' Street, spoke in opposition to removing, the NOT ON THE AGENDA- trees at Lincoln Park and voiced concerns about the maintenance cost to the four • concepts that were presented at the last park board meeting. Chairperson Stratton moved item number eleven on the agenda to item number five. 0 LATE Superintendent of Parks Delikat conducted a PowerPoint presentation on the ADD ITIONSiRECREATION Shane Park Playground replacement project. He addressed current and past SERVICES MANAGER finidraising events. Shane Park Committee goals, desig i, cost, and purchasing REPORT: Delikat asked the Parks, Recreation & Beatification Commission for approval to use surplus funds in the Park Improvement Account in the amount of $21,000 to assist the Committee with the purchase of playground tiles that will help complete Phase I of the project. It was moved by Hordyk and seconded by Pittis to: Recommend that City Council move $21,000 from the Park, Improvement Account to assist the Shane Park Committee with the purchase of playground tiles that will help complete Phase I of the project. Motion carried 6-0. The commission complimented Delikat on the wonderful job he has done on the project Commission discussion followed. LINCOLN PARK MASTER Recreation Services Manager Bonine asked the Commission if they had any PLAN DISCUSSION: concerns or thoughts about the Park. Recreation & Beautification meeting that was held in the City Council Chambers November 15, 2012. Commission discussion followed. M-7 PARK FACILITY Fire Marshal McKeen presented the Commission with a proposal to rename the, RENAMING PROCESS: Lincoln Park Loomis Buildint, to The Leonard and Tea Beil Community Log Cabin stating that Leonard and Tea Beil (rave selflessly to countless organizations, individuals, and businesses throughout their lives and Nkere key figures it) the relocation of the Loomis Building to Lincoln Park Greg Birch. 11 I Columbia Street, spoke in favor of ienanfing the Loomis Building, Chuck Hatten, 91 North Ridgeview Drive, spoke in I'm or of renaming the Loomis Building and presented the Commission with a letter of support from Flealtbv Families of Clallam Countv. Police Chief Gallagher spoke in favor of renaming the Loomis Building. Vice Chairperson Pittis spoke in opposition to the renaming of the Loomis Building. Commission discussion followed. It was moved by Hordyk and seconded by Shargel to: Send a memo six months from today recommending that the City Council approve renaming the Lincoln Park Loomis Building to The Leonard and Tea Beil Community Log Cabin Z� Motion carried 5-0 with Pittis abstaining. SEASONAL ICE RINK Recreation Services Manager Bonine stated that he would present the INFORMATION: information about the seasonal ice rink information at the next meeting. CHAIRPERSON REPORT: Moved to next meeting, ROUNDTABLE Chairperson Stratton asked the Commissioners for a motion to send a memo DISCUSHON: urging the City Council to place the Civic Field Improwment Bond issue on the August 7, 2012 ballot It was moved by Hordyk and seconded by Merritt to: Send a memo to the City Council strongly urging them to place the Civic Field Improvement Bond issue on the August 7. 2012 ballot. Motion carried 5-0. STUDENT MEMBER None INTERESTRE-PORT: ADJOURNMENT: Chairperson Stratton adjourned the meeting at 7:13 p.m. Next Meeting March 15, 2012 Vern Burton CommunitN Center Meeting Roam 43 6:00 p.m. jf 0 ALL/ -t-- i7oX—Nller Stratton, Chairp'crson Cindy K�#(nek, Secretar} I", 0 ZAW PUBLIC WORKS CONTRACT STATUS REPORT January 2012 / March 2012 (COSTS SHOWN INCLUDE APPLICABLE TAXES) ACTIVE CONSTRUCTION CONTRACTS AWARDED BY CITY COUNCIL PURCHASE ORDER CONTRACTS $7,500 - $25,000 AND LIMITED PUBLIC WORKS PROCESS OR SMALL WORKS ROSTER CONTRACTS UNDER $25,000 AWARDED IN LAST 30 DAYS (QUOTATIONS AVAILABLE FOR INSPECTION AT CORP YARD CONTRACTS OFFICE) CONTRACTOR OR VENDOR BUDGET ORIGINAL PRIOR FEB -MAR REVISED PROJECT TITLE 300 gallon garbage containers CONTRACT CHANGE CHANGE CONTRACT Shane Park Playground Equipment (Construction) AMOUNT ORDERS ORDERS AMOUNT Power Pole $1,734.40 Replacements, $900,000 $849,174.00 $0.00 $0.00 $849,174.00 (CL05-2010) Street Lighting Upgrades, CL05-2009 $1,200,000 $1,067,190.00 ($98,418.12) $229,907.60 $1,198,679.89 City Pier Fire Suppression System, $140,000 $137,589.95 $0.00 $38,957.02 $176,546.97 PK03-2009 Oak Street Sidewalk & Paving, CH -12-007 $53,293.50 $53,293.50 $0.00 $0.00 $53,293.50 PURCHASE ORDER CONTRACTS $7,500 - $25,000 AND LIMITED PUBLIC WORKS PROCESS OR SMALL WORKS ROSTER CONTRACTS UNDER $25,000 AWARDED IN LAST 30 DAYS (QUOTATIONS AVAILABLE FOR INSPECTION AT CORP YARD CONTRACTS OFFICE) CONTRACTOR OR VENDOR CONTRACT/ PO # DESCRIPTION DATE AWARDED AMOUNT Rotonics Manufacturing, Inc PO#022793 300 gallon garbage containers 2/28/2012 $14,947.28 Krauss Craft, Inc State Contract #03110 PO#022568 Shane Park Playground Equipment 2/27/2012 $94,896.92 *Blue Mountain Tree Services PO#22556 Waterfront Trail Tree Cutting 2/28/2012 $1,734.40 Smatu worxs Roster contract UPCOMING PUBLIC WORKS CONTRACTS (NEXT 60 DAYS; ESTIMATED DATES SHOWN) PROJECT ADVERTISE START END TITLE FOR BIDS BID OPENING CONSTRUCTION CONSTRUCTION None • bwe N \CCOUNCIL\FINAL\Feb 2012 - Mar 2012 Contract Status Report doc PUBLIC WORKS GRANT & LOAN STATUS REPORT February 2012 — March 2012 PROJECT PROJECT GRANT/LOAN GRANTMATCH AWARD DESCRIPTION COST SOURCE & COST OR LOAN DATA LISTING S STATUS P-,ower'Systems 3 F' 3 »33C: b'I�a qT Energy Conservation Bonneville Power December Agreement Incentive $1,541,000 Administration $1,541,000 BPA 2010 Completed Funding Bonneville $16,661 BEF October Solar4Schools $35,400 Environmental $18,739 City 2010 Completed Foundation Commercial and Bonneville Power $458,120 BPA September Industrial Demand $670,725 Administration $152,605 City 2010 Underway Response Pilot Project $60,000 Private Residential/Light Bonneville Power August Commercial Wind $157,000 Administration $157,000 BPA 2010 Underway Integration Pilot Project Shared Resource $70,000 Washington Department of $43,750 grant March Underway Conservation Manager Commerce $26,250 City 2010 Residential Demand Bonneville Power $362,750 BPA March Response Pilot Project $660,000 Administration $297,250 City 2010 Underway Broadband Technology National Telecommunication $2,600,000 BPA January Detailed design Opportunities Program $3,700,000 Infrastructure $1,100,000 City 2010 nearing complletion via NOANet Administration Energy Efficiency Washington $135,000 grant August Community Block $420,418 Department of $ 37,300 BPA 2009 Completed Grant Commerce $248,118 City Stormwater � � . >w _ _ . X42 Phase II Municipal $75,000 DOE Water No match October Nearly Stormwater Grants Quality Program required 2006 complete - Program - (funds Grant must file final permit compliance report for grant only) close out City of Port $121,229 DOE Local No match October Angeles Municipal Toxics Control required 2010 Underway Stormwater Account Capacity Grant City of Port $50,000 DOE Local No match February Angeles Municipal Toxics Control required 2012 Received offer — Stormwater Account To be executed Capacity Grant Extension M-10 • • • • PROJECT PROJECT GRANT/LOAN GRANT MATCH AWARD Department of Ecology DESCRIPTION COST SOURCE & COST OR LISTING STATUS PASD Port Angeles School District PSP LOAN DATA PWB: Public Works Board, administers the PWTF Program ,,Engineering Public Works Trust Fund RCO: Recreation and Conservation Office SRF: Salmon Recovery Funding Valley Creek Phase 3 Design $157,000 RCO Grant $139,000 grant $18,000 City Dec. 2009 ClosingGrant CSO Phase 1 Projects, DOE SRF Loan @ 2.5% int.; Notified by Construction $18,000,000 Construction Loan use PWTF loans as Jan. 2011 Ecology of 1 " place $10,000,000 match in ranking for loan $361,708.00 grant $50,000 PTC grant D Creek Bridge for Dry g $50,000 PTC in Bridge in place, additional trail Olympic Discovery $725,000 RCO Grant kind $160000 Lodging ogng Spring 2009 g Fork by Peninsula Trail , Tax Trails Coalition $110,000 National through early 2012 Park Service Lauridsen Blvd Bridge $4,644,600 BRAC Grant $3,715,680 grant Nov 2010 Begin design Replacement $928,920 City March 2012 ;Solid Waste. .°: a 2012-2013 Waste Reduction, Recycling, 214,000 DOE Coordinated 160,500 grant Feb 2012 Ongoing Moderate Risk Waste Prevention Grant 53,500 City Disposal • List of Acronyms BRAC: Bridge Replacement Advisory Committee BPA: Bonneville Power Administration DOE: Department of Ecology DWSRF or SRF Drinking Water State Revolving Fund or State Revolving Fund NOANet Northwest Open Access Network NOSC North Olympic Salmon Coalition PASD Port Angeles School District PSP Puget Sound Partnership PWB: Public Works Board, administers the PWTF Program PWTF: Public Works Trust Fund RCO: Recreation and Conservation Office SRF: Salmon Recovery Funding TIB, AIP or PSMP: Transportation Improvement Board, Arterial Improvement Program or Pedestrian Safety and Mobility Program WSDOT: Washington State Department of Transportation C� M-11 Waterfront and Transportation Improvement Plan (WTIP) Stakeholder Meeting February 29, 2012 Attendees: • Charles Smith (PADA), Barbara Frederick (PADA), John Ford (PA Citizen), Kaj Ahlburg (PABA, PA Forward), George Bergner (Chamber), Nathan West (City), Tom Sanford (Feiro), Kent Myers (City), Levon Mathews (First Federal), Jeff Robb (Port), Brad Collins (City), Randall McCoy (Lower Elwha Klallam Tribe, ATAPA), Betsy Wharton (Feiro, FMPA), George Galasso (NOAA), Brian Kuh (Chamber, Columbia Bank), Roberta Korcz (City) Meeting Purpose The meeting was held to discuss interest in supporting a $5-6 million bond measure to fund future phases of the WTIP project. The bond, along with a separate proposed $4 million bond to improve Civic Field, would replace existing expiring bonds, resulting in no new taxes. In order to move forward with the possible WTIP bond measure in 2012, there needs to be a strong commitment for advocacy from the project stakeholders. The initiative would have to be approved by City Council on May 11 in order for it to go to public vote in August. Status of the WTIP and possible bond -funded phases City Staff provided an overview of the entire Waterfront Project including the phase breakdown. Staff also provided details in support of the proposed project order. Phase 1 of the project, including the esplanade and Oak Street portions of the project, is fully funded and construction is intended to begin this summer. A possible bond measure would fund future phases of the project. Phase 2 of the project includes the West End Park portion located between Oak Street and the Valley Creek Estuary, which is anticipated to start in 2013 and could be fully funded if the bond measure is passed this fall. Another possibility is waiting to move forward with the bond measure to fund the eastern portions Railroad Avenue, Lincoln Street, Hollywood Beach, and City Pier which will be constructed between 2014 and 2017. The City intends to move forward with phase 2 regardless of a bond being passed. There is optimism that more grant funding will become available to the project as it becomes a higher priority on the State Transportation Improvement Plan. Recommendations and Concerns • If the bond is all the future local funds that will be available, we might lose ammunition for future grants by no longer having monetary matches. • Concern that if the bond goes to public vote and does not pass, it will kill the momentum and future of the project. • It was suggested that Bond funding could be allocated to cover a portion of each phase rather than all expended on one phase of the project. • Bond funding would be better allocated to project phases with lesser likelihoods of gaining grant funding. • Public web -survey to assess community support for the initiative. • Proactive outreach to adjacent property owners to get their commitment to invest in their properties prior to moving forward with a bond measure. • Concern about funding and staff availability to move forward with remaining phases. • There needs to be an advisory committee to take -on the initiative if it moves forward. • Continue to work closely with Feiro/NOAA on their feasibility study to make sure the plan accommodates their future facility needs. Next Steps Project stakeholders will go to their boards and memberships to get opinions, assess interest, willingness and commitment to support a WTIP bond. This group will reconvene on March 21, 2012 at 4 pm in the Pittis Conference • Room. M-1:? Waterfront and Transportation Improvement Plan (WTIP) Stakeholder Group Meeting • March 21, 2012 Attendees: Dan Gase, Betsy Wharton, Brad Collins, Carol Bernthal, George Bergner, Jeff Robb, John Ford, Kaj Ahlburg, Kent Myers, Charlie Smith, Barb Frederick, Nathan West, Randall McCoy, Tom Sanford, Mike Edwards, Roberta Korcz, Brian Kuh (not present). As a follow-up to a meeting held February 29, 2012, various stakeholders of the Waterfront and Transportation Improvement Plan (WTIP) were tasked with assessing whether there is support for proceeding with a bond measure to fund future portions of the project. As representatives of various community groups and public agencies, stakeholders reported on overall commitment and opinions on how to proceed. Feedback indicated uniform support of the project, but suggested holding off pursuing a bond initiative this August. Comments heard included: • Port Angeles Business Association: Wide support of the project, but "soft support" of a 2012 bond and no one individual committed to spearheading a campaign. Comments were also made about emphasis on security measures and other economic draws to ensure the future development brings people to the community. The PABA also supports the Civic Field bond measure. • City Council: Council supports the WTIP as the top City project, but need insurance there is a good shot of it passing if it goes to the voters in August. Waiting until November or 2013 would likely be a better possibility. • Chamber of Commerce: The Chamber is willing to take a lead in a campaign for a WTIP bond measure, but not this year. • • Port Angeles Downtown Association: A general feeling that a 2012 bond for the WTIP would lose in competition to a Civic Field bond measure, so holding off would be beneficial. It was also felt that waiting until phase 1 of the WTIP is completed would foster wider community support for the initiative. • • Feiro Marine Life Center: Concern was raised about a possible measure going to the voters this August during construction of phase 1 as it could be the height of negative opinions about the project. Waiting until next year when NOAA/Feiro have more concrete plans about future facility needs might be beneficial as well. • Alternative Transportation Advocacy of Port Angeles: A web survey indicated wide support of the Project indicated voter support for both a 2012 Civic Field and WTIP bond measure. • Port of Port Angeles: The Port will be discussing the Project and funding options as an upcoming joint Council meeting. One commissioner indicated that pursuing both a Civic Field and WTIP bond measure would be too much right now, and the WTIP should hold off. • Citizens at Large: With the economic times, it would not be a good idea to proceed right now, but waiting until something is successfully implemented would help with public support. The risk of losing momentum is a big concern, so moving forward regardless of a 2012 bond measure was emphasized. General consensus on the issue: The group is excited about the project and committed to supporting it, but adding it as a 2012 bond project is premature. The group recommends moving forward with a bond measure for the WTIP next year. The group will reconvene in a few months and generally organize themselves over the next six months to be ready to move forward with a 2013 campaign. City staff committed to providing the group with consistent Project updates including grant opportunities. M-13 NGELES Date: April 3, 2012 To: CITY COUNCIL From: Glenn A. Cutler, P.E., Director of Public Works and Utilities Subject: Professional Agreement for City Clerk, Police Department, and Mechanical Remodel — Project No. PD02-2011 Summary: Lindberg & Smith Architects, Inc. has been selected to provide professional architectural services for the remodel and renovation of the Police Department, City Clerk records storage, and to provide increased air conditioning and fire protection for IT requirements in City Hall and the Police Department. The final negotiated cost for phases 1 and 2 of the design project is a not -to -exceed amount of $25,000. There are 4 additional phases that may be awarded in the future by City Council. Recommendation: For information only; no action required. Background/Analysis: Gentry Architecture Collaborative had previously been selected to provide professional architectural services for this project. However, they have contacted city staff advising that they will not be able to take on this project at this time due to the increased amount of work they have recently taken on. Accordingly, Lindberg & Smith Architects, Inc. has been selected to prop ide professional architectural services for this project. The existing storage area for City records above the Police Department is inadequate to effectively and efficiently administer the increasing public records request requirements for the City. It is extremely difficult to work in due to the confines of its access and storage area. The area provides minimal security and fire protection and has no temperature controls. It is proposed that this function be relocated into the area of the weight room and vacant restroom in the northwest part of the Vern Burton facility. This would occur after that space is remodeled for this purpose, including proper ventilation, humidity and temperature control, and fire protection suitable for records storage. For the Police Department, 21 officers currently work in a hallway -like area. There is a critical need for storage space, interview rooms, and an improved prisoner holding area. This function could be served by the 2nd floor area currently occupied by the City Clerk records storage, as well as some upgrades to the first floor area. The final element of this remodel project would be to increase the capacity of air conditioning and fire protection for the IT system server rooms that serve both City Hall and the Police Department. The current air conditioning units are undersized and do not allow for adequate and sustained cooling of the computer servers in the Data Center. N:\CCOUNCIL\FINAL\Professional Agreement - Clerk, PD, Mechanical Remodel, Project PD02-201 Ldoc M - 1,4 • • • April 3, 2012, City Council Re: Professional Agreement — Clerk, PD, Mechanical Remodel, Project PD02-2011 • Page 2 The fire suppression system in the PenCom equipment room also needs to be replaced. The existing halon system is obsolete and is no longer supported due to ozone regulations for this gas. The current system is inoperable due to the inability to replace this prohibited gas. In addition, the PenCom equipment room, as well as the City Hall IT room, have wet sprinkle systems within them or above them which are incompatible for protecting electronic and communications equipment. If ever released, they would destroy all of the critical 911 and IT equipment in the room. It is imperative that the fire suppression systems and physical characteristics for protecting these rooms from the wet sprinkler systems be addressed expeditiously. • The project work will be planned and performed for five distinct tasks: Task 1 City Hall Information Technology (IT) Data Center Renovation Task 2 Police Department — IT Area Upgrades Task 3 City Clerk Storage Remodel Task 4 Additional Offices for Police Department Task 5 Police Department — 1 st Floor Renovation The services to be performed have been divided into six (6) phases. The phases are: 1. Review and summary report of all ADA and fire access requirements for all spaces 2. Programmatic phase for schematic design and estimate of all five tasks 3. 50% design phase submittal including estimate 4. 90% design phase submittal including estimate 5. Final design phase submittal including estimate 6. Post -award construction services Initial award of this Agreement will only be for phases 1 & 2. Phase 1 shall be completed prior to the approval of proceeding to Phase 2. In addition to the schematic design submittal, the Phase 2 deliverable of the estimate shall include both the estimated construction cost for each individual task and the budget estimate for the professional consultant services to accomplish each of the subsequent phases. Upon successful completion of Phase 2, subsequent phases may be awarded for any of the tasks based on a mutually agreed cost for consultant services. The choice of tasks to proceed to any subsequent phase will be at the sole discretion of the City. A notice to proceed will be issued at each phase of the project after City Council authorizes award and funding for those phases. In the 2012 budget, the City has authorized $250,000 for project PD02-2011. The final negotiated cost for phases 1 and 2 is a not -to -exceed amount of $25,000. The phase 2 programmatic budget estimate that will be produced by Lindberg & Smith Architects, Inc. will be used to correctly project the cost of the work for these improvements. The cost projection will be used in this year's Capital Facilities Program to adjust the final funding requirement needed for the entire scope of work. The initial award is expected to be signed on April 9, 2012 under the City Manager's authority of $25,000. This memorandum is being provided for informational purposes since any subsequent phases awarded under this professional services agreement will require City Council authorization. M-15 N:\CCOiJNCIL\FINAL\Professional Agreement -Clerk, PD, Mechanical Remodel, Project PD02-2011.doc