Appendix H 

Public Hearing Record 
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Public Hearing Record i 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Appendix H 

North Carolina Reasonable Further Progress Demonstration November 30, 2009 

Table of Contents 

Hearing Officer’s Report ................................................................................................................1 

Comment Letter: 10/15/2009, Kenneth Geathers, TAC Chair; Cabarrus Rowan Metropolitan 

Planning Organization .......................................................................................................10

Comment Letter: 11/13/2009, Eldewins M. Haynes, Air Quality Specialist for Charlotte DOT ..11 

Comment Letter: 11/13/2009, Richard A. Schutt, Chief of Air Planning Branch US 

Environmental Protection Agency Region 4 ....................................................................13 

Comment Letter: 11/19/2009, June Blotnick, Director of “Clean Air Carolina” submitted article 

“Long-Term Ozone Exposure and Mortality” (from www.nejm.org March 12, 2009) ....14 

Comment Letter: 11/19/2009, June Blotnick, Director of “Clean Air Carolina” submitted article 

“Is Healthy Air in Charlotte’s Future” ...............................................................................25 

Comment Letter: 11/13/2009, J. David Farren, Senior Attorney, Director of Regional Transport 

Initiative, with Thomas Gremillion, Associate Attorney Sothern Environmental Law 

Center .................................................................................................................................27 

Letter: 11//2009, B. Keith Overcash, Response to US Environmental Protection Agency Region 

4 11/13/2009 comment letter .............................................................................................48 

Letter: 11//2009, B. Keith Overcash, Response to Southern Environmental Law Center 

11/13/2009 comment letter ................................................................................................49 

The Charlotte Observer Affidavit ..................................................................................................51 
Public Hearing Record ii 

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North Carolina Reasonable Further Progress Demonstration November 30, 2009 

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Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc R. P. Fisher 

MEMORANDUM 

TO: Keith Overcash, Director, DAQ 

 

FROM: Robert P. Fisher, RAQS, Washington RO 

 

DATE: November 19, 2009 

SUBJECT: Hearing Officer’s Report and Recommendations 

The North Carolina 8-Hour Ozone Reasonable Further Progress (RFP) 

Demonstration for the Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

Nonattainment Area 

As requested in an October 9, 2009 email from Keith Overcash, I served as the public hearing 

officer for the draft North Carolina 8-Hour Ozone RFP Demonstration for the CharlotteGastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area. 

The hearing was held on November 13, 2009 at the Mecklenburg County Air Quality Office at 

700 N. Tryon Rd in Charlotte, NC. Two (2) people requested time to present oral comments out 

of approximately 6 people attending the hearing (not including NCDAQ or LUESA DAQ staff). 

I am recommending that this SIP be submitted to EPA with appropriate consideration of the 

hearing officer’s recommendations. 

Four (4) people submitted written comments during the public comment period. As announced 

at the hearing, the public comment period officially closed on November 13, 2009. All 

comments are included in the hearing record. These comments and the hearing registration 

forms have been emailed to Laura Boothe, acting Chief of the DAQ Planning Section. 

Attached is a copy of the hearing report for the RFP Demonstration. The report contains a 

summary of the comments received, responses to the comments, the hearing officer’s 

recommendations, the written comments received, and the public notice. 

I wish to thank DAQ staff members who assisted me in my search for information and who 

assisted in the hearing: Laura Boothe and George Bridgers; also Ron Slack of the Mooresville 

Regional Office. 

cc: Laura Boothe 

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

 1 

 Appendix H 

Novemeber 30, 2009
Hearing Officer's Report

North Carolina Division of Air Quality

Public Hearing on November 13, 2009

. For

The North Carolina 8-Hour Ozone Reasonable Further

Progress Demonstration for the Charlotte-Gastonia- Rock

Hill, NC-SC 8-Hour Ozone Nonattainment Area

November 19, 2009

Robert P. Fisher- Hearing Officer

Regional Air Quality Supervisor

Washington Regional Office

Washington, North Carolina

Robert P. Fisher

, ((/I~/~ 'f

Date

Metrolina RFP Demonstration Hearing Report November 19 2009.doc Page 2 of9

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

 2 

 Appendix H 

Novemeber 30, 2009
Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc R. P. Fisher 

Overview & Introduction 

On November 13, 2009 a public hearing was held for the draft North Carolina 8-Hour Ozone 

Reasonable Further Progress (RFP) Demonstration for the Charlotte-Gastonia-Rock Hill, NC-SC 

8-Hour Ozone Nonattainment Area (Cabarrus, Gaston, Lincoln, Mecklenburg, Rowan, Union 

Counties and Coddle Creek and Davidson Townships in Iredell County). The hearing was 

conducted in Auditorium 1 at the Mecklenburg County Services Center, 700 North Tryon Street, 

Charlotte, North Carolina. The purpose of the public hearing was to inform interested parties 

about the RFP Demonstration and solicit comments from the public. The public comment period 

closed on November 13, 2009. 

According to the public hearing registration forms, a total of six (6) people attended the hearing, 

not including North Carolina Division of Air Quality (NCDAQ) or Land Use and Environmental 

Services Agency (LUESA) Mecklenburg County Airy Quality (MCAQ) staff, and two (2) people 

requested time to present oral comments. Written comments were received from the Cabarrus 

Rowan Metropolitan Planning Organization (CRMPO), Charlotte Department of Transportation 

(CDOT), the United States Environmental Protection Agency (USEPA), Southern 

Environmental Law Center (SELC), and Clean Air Carolina. 

Kenneth Geathers, TAC Chair of CRMPO, submitted written comments received on October 15, 

2009. Eldewins M. Haynes, Air Quality Specialist with the CDOT submitted comments via 

email on November 13, 2009. Also on November 13, 2009, Richard A. Schutt, Chief of Air 

Planning Branch of USEPA, Region 4, submitted comments via email. June Blotnick, Director 

of “Clean Air Carolina” submitted two articles directly to the hearing officer at the hearing. J. 

David Farren, Seniour Attorney, Director of Regional Transportation Initiative, with Thomas 

Gremillion, Associate Attorney, both of the SELC, submitted written comments via email on 

November 13, 2009. 

Based on the information contained in this report, I recommend the following: 

I recommend that the “North Carolina 8-Hour Ozone Reasonable Further Progress 

Demonstration for the Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area 

(Cabarrus, Gaston, Lincoln, Mecklenburg, Rowan, Union Counties and Coddle Creek and 

Davidson Townships in Iredell County)” be approved for submittal to the USEPA after 

addressing the hearing officer’s recommendations as described in the body of this report. 

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

 3 

 Appendix H 

Novemeber 30, 2009
Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc Page 2 of 9 

Hearing Officer’s Report 

For 

 The North Carolina 8-Hour Ozone 

Reasonable Further Progress Demonstration for 

the Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area 

November 19, 2009 

Robert P. Fisher 

On November 13, 2009 a public hearing was held for the draft North Carolina 8-Hour Ozone 

Reasonable Further Progress (RFP) Demonstration for the Charlotte-Gastonia-Rock Hill, NC-SC 

8-Hour Ozone Nonattainment Area (Cabarrus, Gaston, Lincoln, Mecklenburg, Rowan, Union 

Counties and Coddle Creek and Davidson Townships in Iredell County). The hearing was 

conducted in Auditorium 1 at the Mecklenburg County Services Center, 700 North Tryon Street, 

Charlotte, North Carolina. The purpose of the public hearing was to inform interested parties 

about the RFP Demonstration and solicit comments from the public. The public comment period 

closed on November 13, 2009. 

Background (borrowed from the draft plan)

In July 1997, the United States Environmental Protection Agency (USEP A) promulgated a new 

8-hour ozone NAAQS, setting a standard at 0.08 parts per million (ppm) averaged over an 8-

hour period. Section 182(b)(1) of the Clean Air Act Amendments (CAAA) mandates a 15 

percent volatile organic compounds (VOC) emission reduction, accounting for growth, in the 

first six years after the baseline year (2002) for Moderate and above ozone nonattainment areas. 

Thus, for the Charlotte-Gastonia-Rock Hill, NC-SC 8-hour ozone nonattainment area (referred to 

as the Metrolina area), a RFP analysis between 2002 and 2008 is required. 

The methodology the North Carolina Division of Air Quality (NCDAQ) used to calculate the 

RFP target levels of VOC emissions is based on the method developed in the CAAA, while 

taking into account the restrictions on creditable emissions and the need to use the 2002 

inventory as a baseline. Since the actual 2008 VOC emissions were calculated to have been well 

below the target level, RFP is demonstrated for the Metrolina nonattainment area. 

The NCDAQ must also show continued progress from 2008 through the attainment date. To do 

so, the NCDAQ calculated the expected benefits from the fleet turnover for the on-road and offroad mobile sectors. Based on modeling emissions for 2009 and 2011, the NCDAQ expects 

approximately 14 tons per day of nitrogen oxides (NOx) emissions reductions from fleet 

turnover, demonstrating continued reasonable further progress toward attainment beyond 2008. 

Another requirement of the RFP demonstration is that VOC motor vehicle emission budgets 

(MVEBs), for transportation conformity purposes, need to be set for the RFP milestone year 

2008. This means that the level of emissions estimated by the North Carolina Department of 

Transportation or the metropolitan planning organizations for the Transportation Improvement 

Program and Long Range Transportation Plan must not exceed the MVEBs as defined in this 

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

 4 

 Appendix H 

Novemeber 30, 2009
Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc Page 3 of 9 

RFP demonstration. The NCDAQ is setting MVEB, for transportation conformity purposes, as 

county budgets within the Metrolina nonattainment area. For purposes of SIP strengthening, the 

NCDAQ has additionally established NOx MVEBs for 2008. 

Summary of Public Hearing and Comment Period

According to the public hearing registration forms, a total of six (6) people attended the hearing, 

not including NCDAQ or Land Use and Environmental Services Agency (LUESA) Mecklenburg 

County Airy Quality (MCAQ) staff, and two (2) people requested time to present oral comments. 

Written comments were received from the Cabarrus-Rowan Metropolitan Planning Organization 

(CRMPO), the Charlotte Department of Transportation (CDOT), the USEPA, Southern 

Environmental Law Center (SELC), and Clean Air Carolina (formerly Carolinas Clean Air 

Coalition). It is my opinion that the concerns raised by the interested parties can be adequately 

addressed by the NCDAQ. 

The public comment period was open until 11:59PM on November 13, 2009. Two people spoke 

at the public hearing: June Blotnick, Director of Clean Air Carolina; and Thomas Gremillion, 

Associate Attorney for the SELC. During the public comment period the Hearing officer did not 

receive any phone calls commenting on the public notice. 

Kenneth Geathers, TAC Chair CRMPO, submitted written comments received on October 15, 

2009. Thomas Gremillion, Associate Attorney for the SELC submitted via email a written 

version of the oral comments he presented on November 13, 2009. June Blotnick, Director of 

Clean Air Carolina, at the hearing submitted to the Hearing Officer two articles: one about public 

health effects of long-term ozone exposure; and the other about air pollution levels in the 

Charlotte area. Eldewins M. Haynes, Air Quality Specialist with the CDOT submitted comments 

via email on November 13, 2009. Also on November 13, 2009, Richard A. Schutt, Chief of Air 

Planning Branch of US EPA Region 4 submitted comments via email. 

The following is a summary of the pertinent comments, with regard to NCDAQ’s jurisdiction, 

raised by all parties involved in the public hearing process along with the Hearing Officer’s

opinions and recommendations. Some comments received were very extensive and touched on a 

number of somewhat related issues. This report does not attempt to address comments that are 

not applicable to the RFP demonstration SIP. 

Clean Air Carolina (CAC): June Blotnick, Director of Clean Air Carolina, provided oral 

comments at the public hearing. Ms. Blotnick stated that CAC had signed on to the Southern 

Environmental Law Center’s written comments, which are discussed below. The issues raised in 

the CAC comments were the health issues surrounding ozone and the increase in adult onset 

asthma. Ms. Blotnick stated that the NCDAQ needed to be much more proactive and that the 

revised RFP SIP did not establish any new programs. Ms. Blotnick stated that the State needed 

to do something because what has been done is not working and she provided to articles relating 

to health issues and ozone. These articles are attached to this report. 

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

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 Appendix H 

Novemeber 30, 2009
Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc Page 4 of 9 

Hearing Officer’s Response: The CAC were more directed at health issues relating to ozone. 

The NCDAQ disagrees with Ms. Blotnick’s statement that the programs that have been 

established are not working. North Carolina has continued to see improvements in the air 

quality due to programs that have been established. When designations were made for the 1997 

8-hour ozone standards, the majority of the monitors across the State were violating the 

standard. Today, only one monitor in the State is slightly above the 1997 standard, and this 

monitor observed clean data in 2009. Her one comment relevant to the RFP SIP was that the 

revised RFP SIP did not establish any new programs. This revision was not to address new 

programs but rather address an issue that the USEPA recently raised with the original RFP SIP. 

The hearing officer does not believe any action, regarding the RFP SIP, is needed to address the 

CAC comments.

CDOT: CDOT submitted written comments received on November 13, 2009 that in general 

supports the RFP SIP. CDOT believes that regional motor vehicle emission budgets (MVEBs) 

would be more appropriate; however they conceded that they can work with the MVEBs 

recommended in the RFP SIP. 

Hearing Officer’s Response: No further action is required by the NCDAQ. 

CRMPO: CRMPO submitted written comments received on October 15, 2009, which endorsed 

the RFP SIP and corresponding county level MVEBs for Cabarrus and Rowan Counties.

Hearing Officer’s Response: No further action is required by the NCDAQ. 

USEPA: The USEPA submitted written comments received on November 13, 2009. The first 

comment requested that the NCDAQ provide the source of data used to develop the population 

estimates for Coddle Creek and Davidson townships used to adjust the partial county estimates 

for Iredell County. The second comment requested that the NCDAQ indicate the list of specific 

Maximum Achievable Control Technology standards that were used to develop the 2008 

inventory for the nonattainment area. 

Hearing Officer’s Response: The USEPA comments do not highlight anything controversial 

that cannot be addressed by the NCDAQ prior to the final submittal. The hearing officer 

recommends that the NCDAQ address the comments prior to the final submittal. 

SELC: SELC submitted written comments received on November 13, 2009 and also spoke at 

the public hearing reiterating their written comments. Since there were numerous comments 

from SELC, the comments will be generally grouped and addressed separately by the hearing 

officer. The first comment incorporated by reference the comments SELC sent to South 

Carolina officials on their portion of the attainment demonstration. 

Hearing Officer’s Response: These comments all deal with an attainment demonstration for the 

area and are not applicable to the RFP SIP. Therefore, these comments will not be addressed in 

this hearing officer’s report. 

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

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 Appendix H 

Novemeber 30, 2009
Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc Page 5 of 9 

SELC: SELC stated that the NCDAQ should voluntarily reclassify the Metrolina region to 

“Serious” nonattainment since the area has effectively failed to meet the applicable attainment 

date for the 1997 8-hour ozone standard. 

Hearing Officer’s Response: This comment is not applicable to the RFP SIP; however, the 

NCDAQ disagrees that the region should be reclassified to Serious. Although the region’s 3-

year design value is slightly over the 1997 8-hour ozone standard, the region has clean data for 

2009 and the NCDAQ believes that the area meets the requirements necessary request a 1-year 

extension of the attainment date. The hearing officer does not believe any action, regarding the 

RFP SIP, is needed to address this comment. 

SELC: The proposed RFP SIP retroactively establishes MVEBs for the year 2008. SELC 

recommends refocusing air quality resources on prospective strategies to improve air quality and 

meet future attainment challenges instead of a retrospective analysis that falls outside the 

regulatory scheme contemplated by the Clean Air Act (CAA). 

Hearing Officer’s Response: The CAA requires that volatile organic compounds (VOC) MVEBs 

be set for the RFP milestone year, which, for a moderate nonattainment area, is 2008. In the 

original RFP SIP submitted to the USEPA on 6/15/07, the NCDAQ had not set MVEBs since we 

believed that the mobile source VOC emissions were insignificant to ozone formation. In 

September 2009, the USEPA informed the NCDAQ that they would not approve the 

insignificance finding for the Metrolina nonattainment area. Therefore, in order to meet the 

CAA requirements, the NCDAQ had to revise the RFP SIP to include MVEBs for 2008. The 

hearing officer does not believe any action, regarding the RFP SIP, is needed to address this 

comment. 

SELC: SELC states “The “purpose of ‘reasonable further progress’ is to ensure attainment by 

the applicable attainment date. ... ... But the Metrolina area has now conclusively failed to meet 

the applicable attainment date for the 1997 effective ozone air quality standard of 84 parts per 

billion (ppb). Consequently, the proposed RFP-SIP is of questionable relevance to solving the 

Metrolina area’s ozone problem. ... ... ... Submission of the proposed RFP-SIP would not only 

fail to advance the Metrolina area’s progress in meeting existing legal requirements, it would 

also delay efforts to attain even stronger anticipated standards, which will be a major challenge 

for the region.” 

Hearing Officer’s Response: The purpose of the RFP SIP is to demonstrate that the region is 

making progress in reducing ozone precursors and making progress towards attaining the 

standard. The CAA requires the first RFP SIP to reduce VOC emissions by 15% within six years 

of the base year. The RFP SIP clearly demonstrates this reduction. The RFP SIP was submitted 

to the USEPA on time and this revision is to address an issue with the RFP SIP that the USEPA 

recently informed the NCDAQ about. It is unclear how addressing the USEPA’s concern with 

the original RFP SIP would fail to advance the Metrolina area’s progress in meeting the 

standard or delay efforts to attain any future standard. The hearing officer does not believe any 

action, regarding the RFP SIP, is needed to address this comment. 

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

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 Appendix H 

Novemeber 30, 2009
Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc Page 6 of 9 

SELC: The proposed RFP-SIP will not help the state to qualify for an extension of the 

attainment deadline because it is untimely. 

Hearing Officer’s Response: The original RFP SIP was submitted to the USEPA on time and 

has been waiting for action by the USEPA. The intension of the proposed revisions to the RFP 

SIP are to address issues recently raised by the USEPA on the original submission and not to 

help the State qualify for an extension of the attainment deadline. The hearing officer does not 

believe any action, regarding the RFP SIP, is needed to address this comment. 

SELC: South Carolina officials’ failure to collaborate on the proposed RFP SIP underscores the 

inappropriateness of the plan as well. 

Hearing Officer’s Response: The RFP SIP must be submitted by each state for their portion of 

the nonattainment area. The NCDAQ has decided to move forward with addressing the USEPA 

concerns with the North Carolina RFP SIP and it will be up to South Carolina to address any 

comments from the USEPA regarding their RFP SIP. The hearing officer does not believe any 

action, regarding the RFP SIP, is needed to address this comment. 

SELC: The proposed RFP SIP is a distraction from the challenge of cleaning up the Metrolina 

area’s unhealthy air – now the worst smog in the South. North Carolina officials should prepare 

a new SIP revision consistent with the Metrolina area’s legally required bump-up to “Serious” 

status and the State should focus efforts on actually achieving the tough new standards on the 

horizon. 

Hearing Officer’s Response: Although SELC believes the proposed revisions to the RFP SIP is 

a distraction from the challenge of improving air quality, this revision is required by the USEPA 

in order for the RFP SIP to be approved. The USEPA is reconsidering what the ozone standard 

should be set at and it will be 2010 before a new standard is promulgated. However, the 

NCDAQ is not waiting until a new standard is established before starting the SIP process. The 

NCDAQ has already started modeling analysis efforts to determine what additional controls will 

be needed to meet whatever level the standard is established at. Additionally, the NCDAQ has 

been working to reduce the mobile sector of emissions by developing an idle reduction rule for 

heavy duty vehicles and applying for and being awarded competitive diesel emission reduction 

grants from the USEPA. These diesel emission reduction grant funds will be used to reduce the 

on-road as well as off-road mobile source sector emissions. The hearing officer does not believe 

any action, regarding the RFP SIP, is needed to address this comment. 

Recommendation:

Based on the information contained in this report, I recommend approval of the draft North 

Carolina 8-Hour Ozone Reasonable Further Progress Demonstration for the Charlotte-GastoniaRock Hill, NC-SC 8-Hour Ozone Nonattainment Area (Cabarrus, Gaston, Lincoln, Mecklenburg, 

Rowan, Union Counties and Coddle Creek and Davidson Townships in Iredell County).

Public Hearing Record 

The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone 

North Carolina Reasonable Further Progress SIP 

 8 

 Appendix H 

Novemeber 30, 2009
Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc Page 7 of 9 

Attachments to Report:

(1) Kenneth Geathers, TAC Chair, CRMPO written comments dated October 15, 2009. 

(2) Eldewins M. Haynes, Air Quality Specialist for the CDOT written comments dated 

November 13, 2009. 

(3) Richard A. Schutt, Chief of Air Planning Branch of USEPA, Region 4, written comments 

dated November 13, 2009. 

(4) June Blotnick, Director of “Clean Air Carolina” submitted two articles directly to the 

hearing officer at the hearing: 

a. “Long-Term Ozone Exposure and Mortality” (Downloaded from www.nejm.org 

March 12, 2009) 

b. “Is Healthy Air in Charlotte's Future?” 

(5) J. David Farren, Seniour Attorney, Director of Regional Transportation Initiative, with 

Thomas Gremillion, Associate Attorney, both of the SELC written comments dated 

November 13, 2009. 

lab/rpf 

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Novemeber 30, 2009
l' heN EWE N G LAN 0 J 0 URN A L of M E 0 I C I N E

II

ORIGINAL ARTICLE

Long-Term Ozone Exposure and Mortality

MichaelJerrett, Ph.D., Richard T. Burnett, Ph.D., C. Arden Pope III, Ph.D.,

I<azuhiko Ita, Ph.D., George Thurston, Sc.D., Daniell<rewski, Ph.D.,

Yuan Ii Shl, M.D., Eugenia Calle, Ph.D., and Michael Thun, M.D.

ABSTRACT

BACKGROUND

Although many studies have linked elevations in tropospheric ozone to adverse

health outcomes, the effect oflong-term exposure to ozone on air pollution-related

mortality remains uncertain. We examined the potential contribution of exposure

to ozone to the risk of death from cardiopulmonary causes and specifically to death

from respiratory causes.

METHODS

Data from the study cohon of the American Cancer Society Cancer Prevention Study

II were correlated with air-pollution data from 96 metropolitan statistical areas in

the United States. Data were analyzed from 448,S50 subjects, with l1S,777 deaths

in an IS-year follow-up period. Data on daily maximum ozone concentrations were

obtained from April 1 to September 30 for the years 1977 through 2000. Data on

concentrations of fine particulate matter (particles that are ~.5 JLmin aerodynamic

diameter [PM2.J) were obtained for the years 1999 and 2000. Associations between

ozone concentrations and the risk of death were evaluated with the use of standard

and multilevel Cox regression models.

RESULTS

In single-pollutant models, increased concentrations of either PM2.5or ozone were

significantly associated with an increased risk of death from cardiopulmonary

causes. In two-pollutant models, PM2.5was associated with the risk of death from'

cardiovascular causes, whereas ozone was associated with the risk of death from

respiratory causes. The estimated relative risk of death from respiratory causes that

was associated with an increment in ozone concentration ofl0 ppb was 1.040 (95%

confidence interval, 1.010 to 1.067). The association of ozone with the risk of death

from respiratory causes was insensitive to adjustment for confounders and to the

type of statistical model used.

CONCLUSIONS

In this large study, we were not able to detect an effect of ozone on the risk of death

from cardiovascular causes when the concentration ofPM2.5was taken into account.

We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.

N ENGLJ MED 360;11 NEJM.ORG MARCH 12,2009

Downloaded from _.nejm.org by on March 12, 2009 .

Copyright e 2009 Massachusetts Medical Society. ADrights reserved.

II

From the University of California, Berkeley (MJ.); Health Canada, Ottawa (R.T.B.);

Brigham Young University, Provo, UT

(C.A.P.); New York University School of

Medicine, New York (K.I., G.T.); the University of Ottawa, Ottawa (D.K., Y.S.);

and the American Cancer Society, Atlanta

(E.C., M.T.). Address reprint requests to

Dr. Jerrett at the Division of Environmental Health Sciences, School of Public

Health, University of California, 710 University Hall, Berkeley, CA 94720, or at

jerrett@berkeley.edu.

N EnglJ Med 2009;360:1085-95.

~ 0 2009A_~ Medit:oISociety.

1085

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North Carolina Reasonable Further Progress SIP 

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 Appendix H 

Novemeber 30, 2009
rhe NEW ENGLAND JOURNAL o(MEDICINE

TUDIES CONDUCTED OVER THE PAST 15

years have provided substantial evidence

that long-term exposure to air pollution is

a risk factor for cardiopulmonary disease and

death.1-5Recent reviews of this literature suggest

that rrne particulate matter (particles that are

~2.5 #Lmin aerodynamic diameter [PM2.J) has a

primary role in these adverse health effects.6,7

The particulate-matter component of air pollution includes complex mixtures of metals, black

carbon, sulfates, nitIates, and other direct and

indirect byproducts of incomplete combustion

and high-temperature industrial processes.

Owne is a single, well~efined pollutant, yet

the effect of exposure to owne on air pollutionrelated mortality remains inconclusive. Several

studies have evaluated this issue, but they have

been short-term studies,8-10have fuiled to show

a .

statistically significant effect, 1,3 or have been

based on limited mortalitydata.11 Recentreviews

by the Environmental Protection Agency (EPA)12

and the National Research CouncilB have questioned the overall consistency of the available

data correlating exposure to ozone and mortality. Similar conclusions about the evidence base

for the long-term effects of owne on mortality

were drawn by a panel of experts in the United

Kingdom.14

Nonetheless, previous studies have suggested

that a measurable efrect of owne may exist, particularly with respect to the risk of death from

cardiopulmonary causes. In one of the larger

studies, owne was significantly associated with

death from cardiopulmonary causes15 but not

with death from ischemic heart disease. However, the estimated effect of ozone on the risk of

death from cardiopulmonary causes in this study

was attenuated when PM2.5was added to the

analysis in copoQutant models. On the basis of

suggested effects of ozone on the risk of death

from cardiopulmonary causes (which includes

.death from respiratory causes) but an absence of

evidence fur effects of ozone on the risk of death

from ischemic heart disease, we hypothesized

that ozone might have a primary effect on the

risk of death from respiratory causes.

METHODS

HEALTH, MORTALITY, AND CONFOUNDING DATA

Our study used data from the American Cancer

Society Cancer Prevention Study n (CPS II) cohort.16 The CPS n cohort consists of more than

1086

1.2 million participants who were enrolled by

American Cancer Society volunteers between September 1982 and February 1983 in all 50 states,

the District of Columbia, and Puerto Rico. Enrollment was restricted to persons who were at least

30 years of age living in households with at least

one person 45 years of age or older. After providing written informed consent, the participants

completed a confidential questionnaire that included questions on demographic characteristics,

smoking history, alcohol use, diet, and educatiOn.17Deaths were ascertained until August 1988

by personal inquiries of family members by the

volunteers and thereafter by linkage with the National Death Index. Through 1995, death certificates were obtained and coded fur cause of death.

Beginning in 1996, codes for cause of death were

provided by the National Death Index.18

The study population fur our analysis included only those participants in CPS n who resided

in U.S. metropolitan statistical areas within the

48 contiguous states or the District of Columbia

(according to their address at the time of enrollment) and fur whom data were available from at

least one pollution monitor within their metr0-

politan area. The study was approved by the 0ttawa Hospital Research Ethics Board, Canada.

Data on "ecologic" risk factors at the level of

the metropolitan area representing social variables (educational level, percentage ofhomes with

air conditioning, percentage of the population

who were nonwhite), economic variables (household income, unemployment, income disparity),

access to medical care (number of physicians and

hospital beds per capita), and meteorologic variables were obtained from the 1980 U.S. Census

and other secondary sources (see the Supplementary Appendix, available with the full text of this

article at NE}M.org). These ecologic risk factors,

as well as the individual risk factors collected

in the CPS n questionnaire, were assessed as p0-

tential confuunders of the effects of owne.3,5,19,20

ESTIMATES OF EXPOSURE TO AIR POLLUTION

Ozone data were obtained from 1977 (5 years

befure the identification of the CPS n cohort)

through 2000 fur all air-pollution monitors in

the study metropolitan areas from the EPA'sAerometric .Information Retrieval System. Ozone data

at each monitoring site were collected on an hourly basis, and the daily maximum value fur the site

was determined. All available daily maximum

values fur the monitoring site were averaged over

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Novemeber 30, 2009
OZONE AND AIR POLLUTION-RELATED MORTALITY

each quarter year. The quarterly average values

were reported for each monitor only when at least

75% of daily observations for that quarter were

available.

The averages of the second (April through

June) and third Guly through September) quarters were calculated for each monitor if both

quarterly averages were available. The period

from April through September was selected because ozone concentrations tend to be elevated

during the warmer seasons and because £ewer

data were available for the cooler seasons.

The average of the second and third quarterly

averages for each year was then computed for all

the monitors within each metropolitan area to

form a single annual time series of air-pollution

measurements fur each metropOlitan area fur the

period from 1977 to 2000. In addition, a summary measure of long-term exposure to ambient

warm-season ozone was dermed as the average

of annual time-series measurements during the

entire period from 1977 to 2000. Individual measures of exposure to ozone were then dermed by

assigning the average for the metropolitan area

to each cohort member residing in that area.

Data on exposure to PM:z..swere also obtained

from the Aerometric Information Retrieval System database for the 2-year period from 1999 to

2000 (data on PM2.s were not available before

1999 for most metropolitan areas).s The average

concentrations of PM:z..swere included in our

analyses to distinguish the effect of particulates

from that of ozone on outcomes.

STATISTICAL ANALYSIS

Standard and multilevel random-effects Cox proportional-hazard models were used to assess the

risk of death in relation to exposures to pollution. The subjects were matched according to age

(in years), sex, and race. A total of 20 variables

with 44 terms were used to control for individual

characteristics that might confound or modify

the association between air pollution and death.

These variables, which were considered to be of

potential importance on the basis of previous

studies, included individual risk.fuctors for which

data had been collected in the CPS n questionnaire. Seven ecologic covariates obtained from

the 1980 U.S. Census (median household income,

the proportion of persons living in households

with an income below 125% of the poverty line,

the percentage of persons over the age of16 years

who were unemployed, the percentage of adults

with less than a high-school [12th-grade] education, the percentage of homes with air conditioning, the Gini coefficient of income inequality

[ranging from 0 to I, with 0 indicating an equal

distribution of income and 1 indicating that one

person has all the income and everyone else has

no income2o:J,and the percentage of persons who

were white) were also included. These variables

were included at two levels: as the average for the

metropolitan statistical area and as the clifrerence

between the average for the ZIP Code of residence and the average for the metropolitan statistical area. Additional sensitivity analyses were

undertaken for ecologic variables that were available for only a subgroup of the 96 metropolitan

statistical areas (see the Supplementary Appendix). Models were estimated for either ozone or

PM2.s.In addition, models with both PM:z..sand

QZOnewere estimated.

In additional analyses, our basic Cox models

were modified by incorporating an adjustment fur

community-level random effects, which allowed

us to take into account residual variation in mortality among communities.21 The baseline hazard

function was modulated by a community-specific

random variable representing the residual risk of

death for subjects in that community after individual and ecologic risk fuctors had been controlled for (see the Supplementary Appendix).

A formal analysis was conducted to assess

whether a threshold existed for the association

between exposure to ozone and the risk of death

(see the Supplementary Appendix). A standard

threshold model was postulated in which there

was no association between exposure to ozone

and the risk of death below a specified threshold

co~ntration~aMearassocia~~nthe

logarithmic scale of the proportional-hazards

model) above the threshold.

The question of whether specific time windows

were associated with the health effects was investigated by subdividing the follow-up interval into

four periods (1982 to 1988, 1989 to 1992, 1993 to

1996, and 1997 to 2000). Exposures were matched

for each of these periods and also tested for a

lQ-year average on the basis of the 5-year followup period and the 5 years befure the follow-up

period (see the Supplementary Appendix).

RESULTS

The analytic cohort included 448,850 subjects residing in 96 metropolitan statistical areas (Fig. 1).

N ENGLJ MED 360;11 NEJM.ORG MARCH 12,2009

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Novemeber 30, 2009
The NEW ENGLAND JOURNAL of MEDICINE

fJ

o Colorado Springs

GPortlani.:.t

rProvidence

~

LasVeg<1ls " .

..

Angeles-longBeach

.hoen;,

~

EIPaso . . .h,evepon.

.

cb:<illcksonvillC!:

Ozone (ppb)

.

.

Houst~n N"'<

~

.

o 33.3-53.1

~

sanAnt~"'o .~ ,,"

. 53.2-57.4

tJc

7

Ch . FO~ lauderdalt>-Hollywood orpus flstl i

. 57.5-62.4

. 62.5-104.0

,...

Wichita

o

. .

Figure 1. Ozone Concentrations in the 96 Metropolitan Statistical Areas in Which Members ofthe American Cancer Society Cohort

Resided in 1982.

The average exposures were estimated from 1 to 57 monitoring sites within each metropolitan area from April 1 to September 30

for the years 1977 through 2000.

1088

In 1980, the populations of these 96 areas ranged

from 94,436 to 8,295,900. Data were available on

the concentration of ambient ozone from all 96

areas and on the concentration of PM2.s from 86

areas. The average number of air-pollution monitors per metropolitan area was 11 (range, 1 to 57),

and more than 80% of the areas had 6 or more

monitors.

The average ozone concentration for each

metropolitan area during the interval trom 1977 to

2000 ranged trom 33.3 ppb to 104.0 ppb (Fig. 1).

The highest regional concentrations were in

Southern California and the lowest in the Pacific

Northwest and parts ofthe Great Plains. Moderately elevated concentrations were present in

many areas of the East, Midwest, South, and

Southwest.

The baseline characteristics of the study population, overall and as a function of exposure to

ozone, are presented in Table 1. The mean age

of the cohort was 56.6 years, 43.4% were men,

93.7% were white, 22.4% were current smokers,

and 30.5% were former smokers. On the basis of

estimates from 1980 Census data, 62.3% of

homes had air conditioning at the time of initial

data collection.

During the 18-year follow-up period (from

initial CPS II data collection in 1982 through the

end of follow-up in 2000), there were 118,777

deaths in the study cohort (Table 2). Of these,

58,775 were trom cardiopulmonary causes, including 48,884 from cardiovascular causes (of which

27,642 were due to ischemic heart disease) and

9891 £fom respiratory causes.

In the single-pollutant models, exposure to

ozone was not associated with the overall risk of

.

death (relative risk, 1.001; 95% confidence interval [CI],0.996 to 1.007) (Table 3). However, it was

significantly correlated with an increase in the

risk of death from cardiopulmonary causes. A

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 Appendix H 

Novemeber 30, 2009
Table 1. Baseline Characteristics of the Study Population in the Entire Cohort and According to Exposure to Ozone.'"

Entire Cohort

Variable (N=448,850) Concentration of Ozone

33.3-53.1 ppb 53.2-57.4 ppb 57.5---62.4 ppb 62.5-104.0 ppb

(N

=

126,206) (N =95,740) (N

=

106,545) (N=120,359)

No.ofMSAs 96 24 24 24 24

No. ofMSAs with data on PM2.s 86 21 20 23 22

Concentration ofPM2.s (j.Ig/m3) 11.9x2.5 13.h2.9 14.h2.1 15.4x3.2

Individual risk factors

Age (yr) 56.6xlO.5 56.hlO.4 56.4xlO.7 56.h10.4 56.9x10.5

Male sex (%) 43.4 43.5 43.1 43.5 43.2

White race (%) 93.7 94.3 95.1 93.9 91.8

Education (%)

Less than high school 12.1 11.5 13.6 12.1 11.6

High school 30.6 30.2 33.6 32.1 27.4

Beyond high school 57.3 58.3 52.8 55.8 61.0

Smoking status

Current smokers

Percentage of subjects 22.4 22.0 23.5 22.2 21.9

No. of cigarettes/day 22.0x12.4 22.0x12.3 22.0x12.5 22.2x12.5 21.9x12.4

Duration of smoking (yr) 33.5Il1.0 33.4xlO.8 33.4x11.1 33.4x11.0 33.9x11.2

Started smoking <18 yr of age (%) 9.6 9.3 10.5 9.4 9.3

Started smoking ;,18 yr of age (%) 13.2 13.3 13.4 13.3 13.0

Former smokers

Percentage of subjects 30.5 31.2 30.8. 29.5 30.4

No. of cigarettes/day 21.6x14.7 2L6x14.6 22.2x15.1 21.6x14.6 21.h14.6

.Duration of smoking (yr) 22.2x12.6 22.h12.5 22.6x12.6 22.0x12.5 22.401012.7

Started smoking <18 yr of age (%) 11.9 11.8 12.7 11.5 11.8

Started smoking ;,18 yr of age (%) 18.5 19.3 17.9 17.9 18.5

Exposure to smoking (hr/day) 3.h4.4 3.2x4.4 3.4x4.5 3.4x4.5 3.h4.4

Pipe or cigar smoker only (%) 4.1 4.0. 4.2 4.3 3.8

Marital status (%)

Married 83.5 84.2. 83.0 83.7 83.1

Single 3.6 3.4 4.0 3.8 3.2

Separated, divorced, or widowed 12.9 12.4 13.0 12.5 13.7

OZONE AND AIR POLLUTION-RELATED MORTALITY

10-ppb increment in exposure to ozone elevated

the relative risk of death from the following

causes: cardiopulmonary causes (relative risk,

1.014; 95% CI, 1.007 to 1.022), cardiovascular

causes (relative risk, 1.011; 95% CI, 1.003 to

1.023), ischemic heart disease (relative risk, 1.015;

95% CI, 1.003 to 1.026), and respiratory causes

(relative risk, 1.029; 95% CI, 1.010 to 1.048).

Inclusion of the concentration of PM2.5 measured in 1999 and 2000 as a copoIIutant (Table 3)

attenuated the association with exposure to ozone

for all the end points except death from respiratory causes, for which a significant correlation

persisted (relative risk, 1.040; 95% CI, 1.013 to

1.067). The concentrations of ozone and PM2.5

were positively correlated (r=O.64 at the subject

level and r=0.56 at the metropolitan-area level),

resulting in unstable risk estimates for both pollutants. The concentration of PM2.5 remained

significantly associated with death from cardioN ENGlJ MEO 360;11 NEJM.ORG MARCH 12, 2009 1089

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 Appendix H 

Novemeber 30, 2009
The NEW ENGLAND JOURNAL of MEDICINE

Table 1. (Continued.)

Entire Cohort

Variable (N=448,850) Concentration of Ozone

33.3-53.1 ppb 53.2-57.4 ppb 57.5-62.4 ppb 62.5-104.0 ppb

(N

=

126,206) (N =95,740) (N

=

106,545) (N

=

120,359)

Body.mass index"! 25.h4.1 25.h4.1 25.h4.2 25.h4.1 24.8z4.0

level of occupational exposure to particulate matter (%):j:

0 50.7 50.9 50.0 50.8 51.0

13.3 13.4 13.1 13.3 13.3

2 11.4 11.5 10.8 11.4 11.9

3 4.6 4.7 4.8 4.6 4.5

4 6.1 6.2 6.2 6.1 6.0

5 4.2 4.2 4.3 4.1 4.1

6 1.1 1.0 9.5 1.4 8.4

Not able to ascertai n 8.6 8.2 1.2 8.4 0.9

Self. reported exposure to dust or fumes (%) 19.5 19.5 19.8 19.7 19.1

level of dietary.fat consumption (%)~

0 14.5 13.7 14.9 14.1 15.3

1 15;9 15.8 16.5 15.6 15.9

2 17.4 17.6 17.7 17.2 17.1

3 21.2 21.8 21.1 21.3 20.8

4 30.9 31.1 29.8 31.9 30.9

level of dietary.fiber consumption (%)~

0 16.6 16.0 17.5 16.7 16.6

19.9 19.4 20.5 20.1 19.7

2 18.8 18.6 19.2 19.1 18.5

3 22.8 23.0 22.4 22.8 22.7

4 21.9 23.0 20.4 21.3 22.5

Alcohol consumption (%)

Beer

Drinks beer 22.9 24.3 23.2 22.9 21.4

Does not drink beer 9.7 9.5 9.3 9.5 10.2

No data 67.4 66.2 67.5 67.6 68.4

liq uor

Drinks liquor 28.0 30.4 27.9 25.4 27.9

Does not drink liquor 8.8 8.4 8.5 10.1 9.2

No data 63.2 61.2 63.6 65.5 62.9

Wine

Drinks wine 23.5 25.4 22.5 21.1 24.3

Does not drink wine 8.9 8.7 8.8 9.3 9.1

No data 67.6 65.9 68.7 69.6 66.6

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 Appendix H 

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Table 1. (Continued.)

Entire Cohort

Variable (N =448,850) Concentration of Ozone

33.3-53.1 ppb 53.2-57.4 ppb 57.5-62.4 ppb 62.5-104.0 ppb

(N

=

126,206) (N=95,740) (N

=

106,545) (N

=

120,359)

Ecologic risk factors II

Nonwhite race (%) 11.601016.8 10.501016.4 9.301015.5 10.201016.0 15.901018.3

Home with air conditioning (%) 62.301027.0 55.401031.2 59.401024.0 65.301024.8 69.h24.3

High-school education or greater (%) 51.70108.2 53.50107.9 52.40107.5 50.80107.2 50.00109.5

Unemployment rate (%) 11.70103.1 12.h3.4 11.30102.6 11.30102.9 11.80103.4

Gini coefficient ofincome inequality** 0.3 70100.04 0.370100.05 0.3 70100.04 0.370100.04 0.380100.04

Proportion of population with income 0.120100.08 0.lhO.08 0.12po0O.08 0.110100.07 0.130100.09

<125% of poverty line

Annual household income (thousands 20.70106.6 21.90107.1 19.80106.0 21.20106.7 19.70106.3

ofdollars)H

OZONE AND AIR POLLUTION-RELATED MORTALITY

*

MSA denotes metropolitan statistical area, and PM,.. fine particulate matter consisting of particles that are 2.5 /-1m or less in aerodynamic

diameter. Plus-minus values are means otSD. Because of rounding, percentages may not total 100. All baseline characteristics included in

the survival model are listed (age, sex, and race were includes as stratification factors). The model also includes squared terms for the

number of cigarettes smoked per day and the number of years of smoking for both current and former smokers and a squared term for

body-mass index.

t The body-mass index is the weight in.kilograms divided by the square of the height in meters.

:j: Occupational exposure to particulate matter increases with increasing index number. The index was calculated by assigning a relative level

of exposure to 'PM,.. associated with a cohort member's job and industry. These assignments were performed by industrial hygienists on

the basis of their knowledge of typical exposure patterns for each occupation and specific job."

§ Dietary-fat consumption increases with increasing index number. Dietary information from cohort members was used to define the level

of fat consumption according to five ordered categories.'o

~ Dietary-fiber consumption increases with increasing index number. Dietary information from cohort members was used to define the level

of fiber consumption according to five ordered categories."

II For the ecologic variables, the model included terms for influences at the level of the average for the metropolitan statistical area and at

the level of the difference between the value for the ZIP Code of residence and the average for the metropolitan statistical area to represent between- and within-metropolitan area confounding influence. Some values for ecologic variables and individual variables differ, although they appear to measure the same risk factor. For example, for the entire cohort, the percentage of whites as listed under individual

variables is 93.7, whereas the percentage of nonwhites as listed under ecologic variables is 11.601016.8. This apparent contradiction is explained by the fact that the former is an exact figure based on the individual reports of the study participants in the CPS II questionnaire,

whereas the latter is a mean (otSD) for the population based on Census estimates for each metropolitan statistical area.

** The Gini coefficient is a statistical dispersion measure used to calculate income inequality. The coefficient ranges from 0 to I, with 0 indicating an equal distribution of income and 1 indicating that one person has all the income and everyone else has no income.20 A coefficient of 0.37 indicates that on average there is a measurable inequality in the distribution of income among the different income groups

within the MSAs.

tt Average household incomes for the cohort and for each quartile of ozone concentration were calcu.lated from the median household income for the metropolitan statistical area.

pulmonary causes, cardiovascular causes, ami

ischemic heart disease when ozone was included

in the modeL The association of ozone concentrations with death from respiratory causes remained significant after adjustment for PM2.5'

Risk estimates for ozone-related death from

respiratory causes were insensitive to the use of

a random-effects survival model allowing for

spatial clustering within the metropolitan area

and state of residence (Table lS in the Supplementary Appendix). The association between increased ozone concentrations and increased risk

of death from respiratory causes was also insensitive to adjustment for several ecologic variables

considered individually (Table 2S in the Supplementary Appendix).

Subgroup analyses showed that environmental temperature and region of the country, but

not sex, age at enrollment, body-mass index, education, or concentration of PM2.5' significantly

modified the effects of ozone on the risk of

death from respiratory causes (Table 4).

Figure 2 illustrates the shape of the relation

between exposure to ozone and death from reN ENGLJ MED 360;11 NE)M.ORG MARCH 12,2009 1091

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 Appendix H 

Novemeber 30, 2009
Concentration of Ozone

33.3-53.1 ppb 53.2-57.4 ppb 57.5-62.4 ppb 62.5-104.0 ppb

(N

=

126,206) (N=95,740) (N

=

106,545) (N

=

120,359)

number of deafhs

32,957 25,642 27,782 32,396

16,328 12,621 13,544 16,282

13,605 10,657 11,280 13,342

7,714 6,384 6,276 7,268

2,723 1,964 2,264 2,940

The NEW ENGLAND JOURNAL oJ MEDICINE

Table 2. Number of'Deaths in the Entire Cohort and According to Exposure to Ozone.

Cause of Death

Entire Cohort

(N =448,850)

Ischemic heart disease

Respiratory

118,777

58,775

48,884

27,642

9,891

Any cause

Cardiopulmonary

Cardiovascular

Table 3. Relative Risk of Death Attributable to a lO-ppb Change in the Ambient Ozone Concentration, '4'

Any cause

Cardiopulmonary

Respiratory

Cardiovascular

Ischemic heart disease

1.00l (0.996-1.007)

1.014 (1.007-1.022)

1.029 (1.010-1.048)

1.011 (1.003-1.023)

1.015 (1.003-1.026)

1.001 (0.996-1.007)

1.016 (1.008-1.024)

1.027 (1.007-1.046)

1.014 (1.005-1.023)

1.017 (1.~1.029)

PM2.5 (86 MSAs)

re/afill6 risk (95% 0)

1.048 (1.024-1.071)

1.129 (1.094-1.071)

1.031 (0.955-1.113)

1.150 (1.111-1.191)

1.211 (1.15~1.268)

Two-Pollutant Model:!:

Ozone (86 MSAs) PMz.s (86 MSAs)

Cause of Death Single-Pollutant Modelt

Ozone (96 MSAs) Ozone (86 MSAs)

0.989 (0.981~.996)

0.992 (0.982-1.003)

1.040 (1.013-1.067)

0.983 (0.971~.994)

0.973 (0.95~.988)

1.080 (1.048-1.113)

1.153 (1.104-1.204)

0.927 (0.83~1.029)

1.206 (1.150-1.264)

1.306 (1.22~1.390)

* MSA denotes metropolitan statistical area, and PM2.5 fine particulate matter consisting of particles that are 2.5 jlm or less in aerodynamic

diameter. Ozone concentrations were measured from April to September during the years from 1977 to 2000, with follow-up from 1982 to

2000; changes in the concentration of PM2.5 of 10 jig per cubic meter were recorded for members of the cohort in 1999 and 2000. These

models are adjusted for all the individual and ecologic risk factors listed in Table 1. For the ecologic variables, the model included terms for

influences at the level of the average for the metropolitan statistical area and at the level of the difference between the value for the ZIP

Code of residence and the average for the metropolitan statistical area to represent between- and within-metropolitan area confounding influence. The risk of death was stratified according to age (in years), sex, and race.

t The single-pollutant models were based on 96 metropolitan statistical areas for which information on ozone was available and 86 metropolitan statistical areas for which information on both ozone and fine particulate matter was available.

:j:The two-poliutant models were based on 86 metropolitan statistical areas for which information on both ozone and fine particulate matter

was available.

spiratory causes. There was limited evidence that

a threshold model specification improved model

fit as compared with a nonthreshold linear model

(P=O.06) <Table 3S in the Supplementary Appendix).

Because air-pollution data from 1977 to 2000

were averaged, exposure values for persons who

died during this period are based partly on data

that were obtained after death had occurred.

Further investigation by dividing this interval into

specific time windows of exposure revealed no

significant difference between the effects of earlier and later time windows within the period of

follow-up. Allowing for a 10-year period of exp0-

sure to ozone (5 years of follow-up and 5 years

before the follow-up period) did not appreciably

alter the risk estimates <Table4S in the Supplementary Appendix). Thus, when exposure values

were matched more closely to the follow-up period and when exposure values Were based on

data obtained before the deaths, there was little

change in the results.

DISCUSSION

Our principal rmding is that ozone and PM2..S

contributed independently to increased annual

mortality rates in this large, U.S. cohort study in

analyses that controlled for many individual and

ecologic risk factors. In two-poUutant models that

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 Appendix H 

Novemeber 30, 2009
Table 4. Relative Risk of Death from Respiratory Causes Attributable

to a 1O-ppb Change in the Ambient Ozone Concentration, Stratified

According to Selected Risk Factors.1\'

%of P Value

Subjects Relative Risk of Effect

Stratification Variable in Stratum (95% CI) Modification

Sex 0.11

Male 43 1.01 (0.99-1.04)

Female 57 1.04 (1.03-1.07)

Age at enrollment (yr) 0.74

<50 26 1.00 (0.90-1.11)

50-65 54 1.03 (1.01-1.06)

>65 20 1.02 (1.00-1.05)

Education 0.48

High school or less 43 1.02 (1.00-1.05)

Beyond high school 57 1.03 (1.01-1.06)

Body-mass indext 0.96

. <25.0 53 1.03 (1.01-1.06)

25.0-29.9 36 1.03 (0.99-1.06)

«30.0 11 1.03 (0.96-1.10)

PM2.5 CIIg/m'):t: 0.38

<14.3 44 1.05 (1.01-1.09)

>14.3 56 1.03 (1.00-1.05)

Region' 0.05

Northeast 24.8 0.99 (0.92-1.07)

Industrial Midwest 29.7 1.00 (0.91-1.09)

Southeast 21.0 1.12 (1.05-1.19)

Upper Midwest 5.2 1.14 (0.68--1.90)

Northwest 7.7 1.06 (1.00-1.13)

Southwest 3.9 1.21 (1.04-1.40)

Southern California 7.8 1.01 (0.96-1.07)

External temperature rq:t:' 0.01

<23.3 24 0.96 (0.90-1.01)

>23.3 to <25.4 29 0.97 (0.87-1.08)

>25.4 to <28.7 22 1.04 (0.92-1.16)

>28.7 25 1.05 (1.03-1.08)

OZONE AND AIR POLLUTION-RELATED MORTALITY

included ozone and PM2.5'ozone was significantly associated only with death from respiratory

causes.

For every lO-ppb increase in exposure to

ozone, we observed an increase in the risk of

death from respiratory causes of about 2.9% in

single-pollutant models and 4% in two-pollutant

models. Although this increase may appear moderate, the risk of dying from a respiratory cause

is more than three times as great in the metropolitan areas witJI the highest ozone concentrations as in those with the lowest ozone concentrations. The effects of ozone on the risk of

death from respiratOry causes were insensitive to

adjustment for individual, neighborhood, and

metropolitan-area confounders or to differences

in multilevel-model specifications.

There is biologic plausibility for a respiratory

effect of ozone. In laboratory studies, ozone can

increase airway inflammation24 and can worsen

pulmonary function and gas exchange.25 In addition, exposure to elevated concentrations of

tropospheric ozone has been associated with

numerous adverse health effects, including the

induction26 and exacerbation27,28of asthma, pulmonary dysfunction,29,30and hospitalization for

respiratory causes.31

Despite these observations, previous studies

linking long-term exposure to ozone with death

have been inconclusive. One cohort study conducted in the Midwest and eastern United States

reported an inverse but nonsignificant association between ozone concentrations and mortality.1Subsequent reanalyses of this study replicated

these findings but also suggested a positive association with exposure to ozone during warm

seasons.3 A study of approximately 6000 nonsmoking Seventh-Day Adventists living in Southern California showed elevated risks among men

after long-term exposure to ozone,11 but this

finding was based on limited mortality data.

Previous studies using the CPS II cohort have

also produced mixed results for ozone. An earlier examination based on a large sample of more

than 500,000 people fiom 117 metropolitan areas

and 8 years of follow-up indicated nonsignificant results for the relation between ozone and

death from any cause and a significant inverse

association between ozone and death fiom lung

cancer. A positive association between death fiom

cardiopulmonary causes and summertime exp0-

sure to ozone was observed in single-pollutant

* PM2.5 denotes fine particulate matter consisting of particles that are 2.5 /-1m

or less in aerodynamic diameter. Ozone exposures for the cohort were mea.

sured from April to September during the years from 1977 to 2000, with followup from 1982 to 2000, with adjustment for individual risk factors, and with

baseline hazard function stratified according to age (single-year groupings),

sex, and race. These analyses are based on the single-pollutant mOdel for ozone

shown in Table 3. Because of rounding, percentages may not total 100.

t The body-mass index is the weight in kilograms divided by the square of the

height in meters.

:t:Stratum cutoff is based on the median of the distribution at the metropolitanarea level, not at the subject level.

,Definitions of regions are those used by the Environmental Protection Agency.'

,External temperature is calculated as the average daily maximum temperature

recorded between April and September from 1977 to 2000.

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The NEW ENGLAND JOURNAL o{MEDICINE

0.2

...

..

ii!

.. 0.1 ::J ."li

'"

.

'

.

'

.

,

.

.' .

,

.. - .. -- ..

.--

-

.

~; -

0.0 ,;" - - ---

-.-.-.---.-....--.-.-.---

-,-,-,-'-'-

-

40 60 80 100

Daily I.Hr Maximum Ozone Level(ppb). 1977-2000

Figure 2. Exposure-Response Curve for the Relation between Exposure

to Ozone and the Risk or Death &om Respiratory Causes.

The curve is based on a natural spline with 2 df estimated from the residual

relative risk of death within a metropolitan statistical area (MSA) acco~ing

to a random-effects survival model. The dashed lines indicate the 95% confidence interval of fit, and the hash marks indicate the ozone levels of each

ofthe 96 MSAs.

models. but the association with ozone was nonsignificant in two-pollutant models.3 Further

analyses based on 16 years of fullow-up in 134

cities produced similarly elevated but nonsignificant associations that were suggestive of e£-

fects of summertime auf)' to September) exposure to ozone on death from cardiopulmonary

causes.5

The increase in deaths from' respiratory causes

with increasing exposure to ozone may represent

a combination of short-term effects of ozone on

susceptible subjects who have influenza or pneumonia and long-term effects on the respiratory

system caused by airway inflammation,24 with

subsequent loss of lung function in childhood,32

young adulthood,33,34and possibly later life.35If

exposure to ozone accelerates the natural loss of

adult lung function with age, those exposed to

higher concennations of ozone would be at ~

er risk of dying from a respiratory-related syndrome.

In our two-poIIutant models, the adjusted estimates of relative risk fur the effect of ozone on

the risk of death from caldiovascuIar causes were

significantly less than 1.0, seemingly suggesting

a protective effect. Such a beneficial influence of

ozone, however, is unlikely from a biologic standpoint. The association of ozone with cardiovascular end points was sensitive to adjustment fur

exposure to PM2.5'making it difficult to deter1094

mine precisely the independent contributions of

these copollutants to the risk of death. There

was notable collinearity between the concentrations of Ozone and PM2.5"

Furthermore, measurement at central monitors probably represents population exposure to

PM2.5more accurately than it represents exposure to ozone. OzOne concennation tends to vary

spatially within cities more than does PM2.5concennation, because of scavenging of ozone by

nitrogen oxide near roadways.36In the presence of

a high density of local naffic, the measurement

error is probably higher for exposure to ozone

than fur exposure to PM2.5'The effects of ozone

could therefore be confuunded by the presence of

PM2.5because of collinearity between the measurements of the two pollutants and the higher

precisionof measurements of PM2.5.37

Measurements of PM2.5were available only

for the end of the study fullow-up period (1999

and 2000). Widespread collection of these data

began only after the EPAadopted regulatory limits on such particulates in 1997. Since particulate air pollution has probably decreased .in most

metropolitan areas during the follow-up interval

of our study, it is likely that we have underestimated the effect of PM2.5in our analysis.

A limitation of our study is that we were not

able to account for the geographic mobility of

the population during the fullow-up period. We

had infurmation on home addresses fur the CPS

n cohort only at the time of initial enrollment in

1982 and 1983. Census data indicate that during

the interval between 1982 and 2000, approximately 2 to 3% of the population moved from

one state to another annually (with the highest

rates in an age group younger than that of our

study population). 38 However, any bias due to a

failure to account fur geographic mobility is 1ikely to have attenuated, rather than exaggerated,

the effects of ozone on monaIity.

In summary, we investigated the effect of tr0-

pospheric ozone on the risk of death from any

cause and cause-specific death in a large cohon,

using data from 96 metropolitan statistical areas

across the United States and controlling fur the

effect of particulate air poIIutants. We were unable to detect a significant effect of exposure to

ozone on the risk of death from cardiovascular

.

causes when particulates were taken into. account, but we did demonstrate a significant e£-

feet of exposure to ozone on the risk of death

from respiratory causes.

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OZONE AND AIR POLLUTION-RELATED MORTALITY

Supported by the Health Effects Institute.

Dr. Krewski reports receiving grant support from the Natural

Sciences and Engineering Research Council of Canada as holder

of the Industrial Research Chair in Risk Science. This chair is

funded by a peer-reviewed university-industry partnership program. No other potential conflict of interest relevant to this article was reported.

We thank the National Institute of Environmental Health Sciences for providing grant support (ES0026O) to the New York

University School of Medicine.

This article is dedicated to the memory of our coauthor and

friend, Dr. Jeanne Calle, who died unexpectedly on February 17,

2009.

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1. Dockery OW, Pope AC, Xu X, et al. An tion. Washington, DC: National Acade- posed to ozone: a cohort study. Lancet

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1993;329:1753-9. of Air Pollutants. The efrects on health of 27. Delfino R], Quintana PJ, Floro J, et al.

2. Jerrett M, Burnett RT, Ma R], et at. long-term exposure to ozone. London: De- Association of FEVI in asthmatic children

Spatial analysis of air pollution and mor- paftment of Health, 2007. (Accessed Fehru- with personal and microenvironmental

tality in Los Angeles. Epidemiology 2005; ary 17, 2009, at http-.//wwW.advisorybodies. exposure to airborne particuJate matter.

16:727-36. doh.gov.uk/comeap/statementsreports/ Environ Health Perspect 2004;112-932-41.

3. Krewski 0, Burnett RT, Goldberg MS, chptlongtermexpoozone.pdf.) 21. Thurston GO, Lippmann M, Scott MB,

et al. Reanalysis of the Harvard Six Cities 15. Krewski 0, Jerrett M, Burnett RT, et Fine JM. Summertime haze air pollution

Study and the American Cancer Society at. Extended fullow-up and spatial analy- and children with asthma. Am J Respir

Study of Particulate Air Pollution and Mar- sis of the American Cancer Society study Crit Care Med 1997;155:654-60.

tality: a special report of the institute's linking particulate air pollution and mar- 29. Spektor OM, Lippmann M, Lioy PJ, et

Particle Epidemiology Reanalysis Project. tality. Bostun: Health Etreets Institute (in al. Etreets of ambient ozone on respiraPart II. Sensitivity analyses. Cambridge, press). tory function in active, normal children.

MA: Health Etreets Institute, 2000. 16. American Cancer Society. Cancer pre- Am Rev Respir Dis 1988;137:313-20.

4. Miller KA, Siscovick OS, Sheppard L, vention study overviews. '(Accessed Febru- 30. Tager lB, Balmes J, Lurmann F, Ngo

et at. Long-term exposure to air pollution ary 17, 2009, at http://www.cancer.org/L.AlcornS.Kiinzli N. Chronic exposure

and incidence of cardiovascular events in docroot/RES/contenrJRES_6_2_Srudy_ to ambient ozone and lung function in

women. N Engl J Med 2007;356:#7-58. Overviews.asp?) young adults. Epidemiology 2005;16:751-9.

5. Pope CA ill, Burnett RT, Thun MJ, et al. 17. Thun MJ, Calle BE, Namboodiri MM, 31. Yang Q, Chen Y, Shi Y, Burnett RT,

Lung cancer, cardiopulmonary mortality, et at. Risk factors fur fatal colon cancer in McGrail KM, Krewski D. Association beand long-term exposure to fine particuJate a large prospective study. J NatI Cancer tween ozone and respiratory admissions.

air pollution. JAMA 2002;287:1132-41. Inst 1992;84:1491-500. among childten and the elderly in Van6. Brook RD, Franklin B, Cascio W, etal. J.I.. Calle BE, Terrell DO. Urility of the Na- couver, Canada. Inhal Toxicol 2003;15:

Air pollution and cardiovascular disease: tional Death Index for ascertainment of 1297-308.

a statement fur healthcare professionals mortality among Cancer Prevention Study 32. Rojas-Martinez R. Perez-Padilla R.

from the Expert Panel on Population and II participants. Am J Epidemioll993;137: OIaiz-Femandez G, et al. Lung function

Prevention Science of the American Heart 235-41. growth in children with long-term expoAssociation. Circulation 2004;109-.2655-71. 19. 1errett M, Burnett RT, Willis A, et al. sure to air pollutants in Mexico City. Am J

7. Pope CA III, Dockery OW. Health ef.. Spatial analysis of the air pollution-mar- Respir Crit Care Med 2007;176:377-84.

fects of fine particulate air pollution: lines tality relationship in the context of eco- 33. Galizia A, Kinney PI.. Long-term resithat connect. J Air Waste Manag AsSOC logic confuunders. J Toxicol Environ dence in areas ofhigh ozone: associarions

2006;56:709-42. Health A 2003;66:1735-77. with respiratory health in a nationwide

8. Bell ML, Dominici F, Samet1M. A meta- 20. Willis A, Krewski 0, Jerrett M, Gold- sample of nonsmoking young adults. Enanalysis of time-serles studies of ozone berg MS, Burnett RT. Selection of ecologic viron Health Perspect 1999;107:675-9.

and mortality with comparison to the Na- covariates in the American Cancer Society 34.. Chen C, Arjomandi M, Balmes J, Tagtional Morbidity, Mortality, and Air Pollu- study. J Toxicol Environ Health A 2003; er lB, Holland N. Efrects of chronic and

tion Srudy. Epidemiology 2005;16:436-45. 66:1563-89. acute ozone .exposure on lipid peroxida9. Ito K, De Leon SF, Lippmann M. Asso- n. Ma R. Krewski 0, Burnett RT. Ran- tion and antioxidant capacity in healthy

ciations between ozone and daily mortal- dam efrects Cox models: a Poisson model- young adults. Environ Health Perspect

ity: analysis and meta-analysis. Epidemi- ling approach. Biometrika 2003;90:157-69. 2007;115:1732-7.

ology 2005;16:446-57. 22. Siemiatyclri J, Krewski 0, Shi Y, Gold- 35. Ackermann-Liebrich U, Leuenberger

10. Levy ]I, Chemerynsld SM, Sarnat]A. berg MS, Nadon L, Lakhani 1. ConrroI- P, Scbwartz J, et at. Lung function and

Ozone exposure and mortality: an empiric ling fur potential confuunding by ~-

long term exposure to air pollutants in

Bayes metaregression analysis. Epidemi- tional exposures. J Toxicol Environ Health Switzerland. Am J Respir Crit Care Med

ology 2005;16:458-68. A 2003;66:1591-603. 1997;155:122-9.

11. Abbey DE, Nishino N, McDonnell WF, 23. Chao A, Thun MJ, Jacobs EJ, Henley 36. McConnell R. Berhane K, Yao L, Luret al. Long-term inhaJable particles and SJ, Rodriguez C, Calle BE. Cigarette smok- mann FW, Awl E, Perm; 1M. Predicting

other air pollutants related to mortality in ing and colorectal cancer mortality in the residential ozone deficits from nearby

nonsmokers. Am J Respir Crit Care Med Cancer Prevention Srudy IL J NatI Cancer traffic. Sci Total Environ 2006;363:166-74.

1999;159:373-82 Inst 2000;92:1888-96. 37. Zidek]V, Wong H, Le NO, Burnett 1.

12. Review of the national ambient air . 24. Mudway IS, KclIyFJ. An investigation of. Causality: measurement error and multiquality standards fur ozone: poIicy assess- inhaled ozone dose and the magnitude of collinearity in epidemiology. Environmetment of scientific and technical infurma- airway infI2mmJlt1()1'1in healthy adults. Am rics 1996;7:441-51.

tion. Research Triangle Park, NC: Envi- J Respir Crit Care Med 2004;169:1089-95. 38. Schachter J. Geographical mobility:

ronmental ProtectionAgency, 2007. (Report 25. Brown JS, Bateson TF, McDonnell WF. population characteristics. March 1999 to

no. EPA-452/R-07-OO7.) Effects of exposure to 0.06 ppm ozone on March 2000. Current population reports

13. Committee on Estimating Mortality FEYI in humans: a secondary analysis of PPL-l#. Washington, DC: Census Bureau,

Risk Reduction Benef'tts from Decreasing existing data. Environ Health Perspect May 2001. (Accessed February 17, 2009, at

Tropospheric Ozone Exposure. Estimat- 2008;116:1023-6. http://wwW.census.gm/prodI2OO1pubsi

ing mortality risk reduction and economic 26. McConnell R. Berhane K, Gilliland F, p20-538.pdf.)

benefits from conrrolling ozone air pollu- et al. Asthma in exercising children ex- ~ 0 2Of19ft_"'- M8Ii<oI.-".

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OCTOBER 2009 I Vol. 39, No.9

Mecklenburg Medicine

A Publication of the Mecklenburg County Medical Society I www.meckmed.org

,.

...

I

\

\

/J\~ Mecklenburg County Medical Society. Mecklenburg Medical Alliance and Endowment

Founders of: Bioethics Resource Group, Ltd., Hospitality House of Charlotte, Teen Health Connection, MedAssist of Mecklenburg, Physicians Reach Qut Mecklenburg County

Medical Society

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Novemeber 30, 2009
Is Healthy Air in Charlotte's Future?

By Stephen R. Keener, MD, MPH, and Maeve E. O'Connor, MD

D.

oes it seem like you are seeing more

patients with respiratory problems today

. than you were 10 years ago? That's not

just your imagination. There has been a noticeable

increase in asthma and cardiovascular disease in the

Charlotte region in the last few years. according to

the American Lung Association (ALA). The poor

state of Charlotte's air is partly to blame. Health

professionals are wise to be informed of the current

trends in regional air quality and how they may be

impacting patient health.

In the American Lung Association's 2009

State of the Air report, the Charlotte metro

region's air ranked eighth worst in terms of

ozone pollution when compared to the nation's

dirtiest cities, up from last year's 13th spot

According to the 2009 report, there was a 5

percent increase in the number of pediatric

asthma cases and a 21 percent increase in adult

asthma cases over the 2008 numbers. The ALA

report also gives Charlotte a failing grade for its

high levels of particle pollution. Fine particles are

of special concern to those with cardiovascular

problems. The number of cases of cardiovascular

disease noted in the 2009 report increased 13

percent from the 2008 report.

Since the early 199Os, the Charlotte region has

been in violation of the EPA's health-based standard

for ozone and, while our region's air quality has

improved somewhat, it's far from healthy. The

Clean Air Act requires the EPA to consider ouly

medical findings, not the cost of compliance, in

setting federal air pollution standards. Medical

research continues to show stronger correlations

between dirty air and poor health, and standards are

beginning to get more stringent

Regional air quality doesn't meet the 1m

standard of .080 parts per million (ppm), nor does it

meet the current standard of .075 ppm set last year

by the EPA. It's expected the EPA will adjust the

standard again within the coming year. Clearly, our

region has a long way to go before our air quality

can be considered healthy during ozone season.

Research shows physicians have a right to be

concerned about Charlotte's high ozone numbers.

New research from Princeton University reveals

exposure to ozone levels currently considered safe

e.075 ppm) has been shown to significantly impair

lung function in healthy individuals. Researchers

also found inhalation of .070 ppm ozone for

6.6 hours, well under the current EPA standard,

can induce significant reduction in FEY I - the

volume of air a person can forcibly eXhale in the

first second

-

according to a report in the Aug. 1

issue of the American Journal of Respiratory and

Critical Care Medicine. "The acute inhalation of

ambient concentrations of ozone induces several

health effect~, including airway irritation and

inflammation, decrements in pulmonary function,

and symptoms of respiratory discomfort," Edward

S. Schelegle, PhD, of the University of California

Davis, and colleagues assert. The researchers

found statistically significant decrements in

FEY I and increases in total subjective symptoms

scores (P«J.05) after exposure to mean ozone

concentrations of .070, .080 and .087 ppm.

Another concern for an ozone hotspot like

Charlotte is long-term exposure to high ozone

levels. An article entitled "Long-term Ozone

Exposure and Mortality" published in the March

2009 issue of the New Engl<md Journal of

Medicine, reports on a'study which analyzed

448,850 subjects over an 18-year period.

Researchers concluded that prolonged exposure

to ozone and/or particulate matter is linked to

increased mortality rates. Every .010 ppm of

additional ozone raises the death rate due to

respiratory disease by 4 percent In high ozone

cities like. Charlotte, researchers found citizens

have as much as a 30 percent higher chance of

dying from respiratory illness. The risk for other

nonfatal respiratory diseases also is elevated.

This study adds to the literature that already

documents the increase of asthma and heart

attacks when ozone levels peak.

Ozone is not the only danger lurking in

Charlotte's air. Fine particulate matter, which

is smaller than 10 microns, or one-tenth the

diameter of a human hair, is especially harmful.

These microscopic substances are too small to

be filtered by the nose and mouth and can enter

directly into the bloodstream. The burning

of fossil fuels in power plants and vehicles,

especially diesef engines, is a major contributor

to fine particle pollution. The link between fine

particles and cardiopulmonary disease has been

established for two decades.

In June, the Health Effects Institute (HEI)

published an extended analysis of the American

Cancer Society's study linking particulate air

pollution and mortality. This new appraisal of

.

existing studies shows mortality rates among

people exposed to the particles are twice as

high as previously thought The analysjs was

conducted by a team of resear«hers from the

University of Ottawa, led by Dr. Daniel Krewski.

The current EPA maximum annual average

standard for fine particles is 15.0 micrograms

per cubic meter. California has set a more

stringent annual average standard of 12.0.

Mecklenburg County fine particulate matter

levels are 14.9 micrograms per cubic meter.

Our entire community needs to come

together if we are to solve this major public

health problem. Physicians have an important

role to play. Your voice is stronger than you

might think! Public officials value and respect

the testimony of physicians who know the

serious impact air pollution has on patient health.

Clean Air Carolina (formerly Carolinas Clean

Air Coalition), a local nonprofit organization

working to improve air quality, has started a new

initiative, Medical Advocates for Healthy Air,

to provide health professionals an avenue for

getting involved in the quest for clean air.

Simple actions

-

like adding your name

to a medical sign-on letter supporting stronger

regulation of air toxies, or submitting a joint

letter to the editor or Op-ed column on the

dangers diesel pollution from old school

buses has on children's health - can make a

difference in raising awareness. Educating your

patients, colleagues and family members about

the link between air pollution and illness also

is an extremely important public service you

can provide. More than 75 health professionals

statewide have gotten involved in this effort

and many more are needed if we are to have an

impact Lawrence W. Raymond, MD, Carolinas

Medical Center, Maeve E. O'Connor, MD,

Carolina Asthma and Allergy, and Stephen

R. Keener, MD, Mecklenburg County Health

Department are three of the leaders of this

new initiative. We invite you to join us as we

work together to help restore healthy air for the

residents of the Charlotte region.

.1. State of the Air: 2009. American Lung

Association. April 29, 2009. www.stateoftheair.

org/2009/stateslnorth-caro1ina.

State of the Air:" 2008. American Lung

Association, May 2, 2008. www.stateoftheair/2008/

stateslnorth-carolina.

2. Scheiegle E, et al "6.6-hour inhalation

of ozone concentrations from 60 to 87 parts per

billion in healthy humans" American Journal of

Respiratory and Critical Care Medicine, 2009;

180: 265-72

3. Jerrett M. "Long-Term Ozone Exposure

and Mortality", New England Journal of Medicine, -

360;11. March 12,2009.

4. Barringer, Felicity. "Analysis finds

Elevated Risk from Soot Particles in tbe Air". The

New York Tunes. June 3, 2009.

Mecklenburg Medicine. October 2009 I 15

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