December 2012

EPA/600/R-12/056F



# Provisional Assessment of Recent

Studies on Health Effects of

Particulate Matter Exposure

National Center for Environmental Assessment RTP Division

Office of Research and Development

U.S. Environmental Protection Agency

Research Triangle Park, NC 27711i 

### DISCLAIMER

This document has been reviewed in accordance with U.S. Environmental Protection Agency

policy and approved for publication. Mention of trade names or commercial products does not

constitute endorsement or recommendation for use.ii 

# Table of Contents

Table of Contents

................................................................................................ .......................................... ii

List of Tables

................................................................................................ ............................................... iii

List of Figures

................................................................................................ .............................................. iv

Authors, Contributors, Reviewers

................................................................................................................. v

EXECUTIVE SUMMARY

........................................................................................................................ vii

1. INTRODUCTION AND METHODOLOGY

....................................................................................... 1

2. OVERVIEW OF RECENT HEALTH STUDIES RESULTS

.............................................................. 3

2.1. Epidemiologic Studies of Long

- Term Exposure

............................................................................... 3

2.1.1. Mortality

................................................................................................ .................................. 4

2.1.2. Morbidity

– Cardiovascular Effects

...................................................................................... 12

2.1.3. Morbidity

– Respiratory Effects

............................................................................................ 14

2.1.4. Morbidity

– Reproductive and Developmental Effects

......................................................... 16

2.2. Epidemiologic Studies of Short

- Term Exposure

............................................................................ 16

2.2.1. Mortality

................................................................................................ ................................ 17

2.2.2. Morbidity

............................................................................................................................... 21

2.2.2.1. Associations between Short

- Term Exposures to PM and Respiratory Morbidity

........ 21

2.2.2.2. Associations between Short

- Term Exposures to PM and Cardiovascular Morbidity

.. 26

2.3. Health Effects Related to Sources or Components of PM

.............................................................. 30

2.3.1. Epidemiologic Studies Using Source Apportionment

........................................................... 30

2.3.2. Epidemiologic Studies on Effects of Fine PM Components and Sources

............................. 31

2.3.3. Toxicology Studies

– So urce Apportionment and Fine PM Components

............................ 35

2.3.3.1. Toxicology Studies Comparing Ambient Fine PM Sources and Components

............. 35

2.3.3.2. Toxicology Studies Comparing Source

- Derived PM and Components

....................... 39

3. SUMMARY AND CONCLUSIONS

................................................................................................ . 41

Appendix A Studies Included in t he PM Provisional Science Assessment

........................................... 43

References

................................................................................................ ................................................... 59iii 

# List of Tables

Table 2

- 1 Causal Determinations for Short

- and Long

- term Exposure to PM 2.5

................................ ...... 3

Table 2

- 2 Association between Mortality Outcomes and PM 2.5 Components using a 30

- km Buffer

(n=43,220) (Adapted from Ostro et al. [ 2011])

................................ ................................ ............. 34

Table 2

- 3 Concentrated Ambient Particles (CAPs): Sources and Associated Endpoints

...................... 37

Table A

- 1 Characterization of studies of Long

- term Exposure to PM 2.5 and Mortality

......................... 43

Table A

- 2 Characterization of Studies of Long

- term Exposure to PM 10

- 2.5 and Mortality

..................... 45

Table A

- 3 Characterization of Studies of Long

- term Exposure to PM 2.5 and Cardiovascular Effects

... 45

Table A

- 4 Characterization of Studies of Long

- term Exposure to PM 2.5 and Respiratory Effects

......... 47

Table A

- 5 Characterization of Studies of Long

- term Exposure to PM 2.5 and Reproductive and

Developmental Effects

................................ ................................ ................................ ................... 49

Table A

- 6 Characterization of U.S. and Canadian Studies of Short

- term Exposure to PM 2.5 and

Mortality

................................ ................................ ................................ ................................ ........ 51

Table A

- 7 Characterization of U.S. and Canadian Studies of Short

- term Exposure to PM 2.5 and

Respiratory Hospital Admissions and Emergency Department Visits

................................ .......... 52

Table A

- 8 Characterization of U.S. and Canadian Studies of Short

- term Exposure to PM10

- 2.5 and

Respiratory Hospital Admissions and Emergency Department Visits

................................ .......... 55

Table A

- 9 Characterization of U.S. and Canadian Studies of Short

- term Exposure to PM 2.5 and

Cardiovascular Hospital Admissions and Emergency Department Visits

................................ ..... 55

Table A

- 10 Characterization of U.S. and Canadian Studie s of Short

- term Exposure to PM 2.5 and Out

of Hospital Cardiac Arrests

................................ ................................ ................................ ............ 58

Table A

- 11 Characterization of U.S. and Canadian Studies of Short

- term Exposure to PM 2.5 and Time

of Stroke Symptom Onset

................................ ................................ ................................ .............. 58iv 

# List of Figures

Figure 2.1 All

- cause mortality risk estimates, long

- term exposure to PM 2.5 in recent cohort studies. Red

text and triangles represent new studies published since the completion of the 2009 PM ISA.

...... 6

Figure 2.2. Cardiovascular mortality risk estimates, long

- term exposure to PM 2.5 in recent cohort

studies. Red text and triangles represent new studies published since the completion of the 2009

PM ISA.

................................................................................................ ........................................... 7

Figure 2.3

. Respiratory mortality risk estimates, long

- term exposure to PM 2.5 in recent cohort studies. Red

text and triangles represent new studies published since the completion of the 2009 PM ISA.

...... 8

Figure 2.4

. Percent increase in non

- accidental and cause

- specific mortality for a 10 μg/m 3 increase in 24

- h

average PM 2.5 concentrations in single

- pollutant models from U.S. and Canadian studies. Red text

and triangles represent recent studies published since the completion of the 2009 PM ISA.

........ 20

Figure 2.5 Percent increase in respiratory

- related hospital admissions and ED visits for a 10 μg /m 3

increase in 24

- h average PM 2.5 concentrations in single

- pollutant models from U.S. and Canadian

studies. Red text and triangles represent recent studies published since the completion of the 2009

PM ISA.

................................................................................................ ......................................... 25

Figure 2.6 Percent increase in cardiovascular

- related hospital admissions and ED visits for a 10 μg/m 3

increase in 24

- h average PM 2.5 concentrations in single

- pollutant models from U.S. and Canadian

studies. Red text and triangles represent recent studies published since the completion of the 2009

PM ISA.

................................................................................................ ......................................... 29v 

# Authors, Contributors, Reviewers

Executive Direction

Dr. John Vandenberg (Director)

– National Center for Environmental Assessment

- RTP Division,

U.S. Environmental Protection Agency, Research Triangle Park, NC

Ms. Debra Walsh (Deputy Director)

– National Center for Environmental Assessment

- RTP

Division, U.S. Environmental Protection Agency, Research Triangle Park, NC

Dr. Mary Ross (Branch Chief)

– National Center for Environmental Assessment, U.S.

Environmental Protection Agency, Research Triangle Park, NC

Principal Authors

Mr. Jason Sacks (Team Lead)

– National Center for Environmental Assessment, U.S.

Environmental Protection Agency, Research Triangle Park, NC

Dr. Ellen Kirrane

– National Center for Environmental Assessment, U.S. Environmental

Protection Agency, Research Triangle Park, NC

Dr. Thomas Luben

– National Center for Environmental Assessment, U.S. Environmental

Protection Agency, Research Triangle Park, NC

Dr. Elizabeth Oesterling Owens

– National Center for Environmental Assessment, U.S.

Environmental Protection Agency, Research Triangle Park, NC

Contributors

Ms. Laura Datko

- Williams

– Oak Ridge Institute for Science and Education Research Fellow,

National Center for Environmental Assessment, U.S. Environment al Protection Agency,

Research Triangle Park, NC

Reviewers

Dr. Dan Costa

, Air, Climate, and Energy Research Program, Office of Research and

Development, U.S. Environmental Protection Agency, Research Triangle Park, NC

Dr. Aimen Farraj

, National Health and Environmental Effects Research Laboratory, U.S.

Environmental Protection Agency, Research Triangle Park, NC

Dr. Ian Gilmour

, National Health and Environmental Effects Research Laboratory, U.S.

Environmental Protection Agency, Research Triangle Park, NCvi Ms. Beth Hassett

- Sipple, Office of Air Quality Planning and Standards, U.S. Environmental

Protection Agency, Research Triangle Park, NC.

Dr. Karen Martin, Office of Air Quality Planning and Standards, U.S. Environmental Protection

Agency, Research Triangle Park, NC.

Dr. Lucas Neas

, National Health and Environmental Effects Research Laboratory, U.S.

Environmental Protection Agency, Research Triangle Park, NC

Mr. Steven Silverman, Office of General Council, U.S. Environmental Protection Agency,

Washington, D.C.

Dr. Lindsay Wichers Stanek , National Exposure Research Laboratory, U.S. Environmental

Protection Agency, Research Triangle Park, NCvii 

# EXECUTIVE SUMMARY

In the proposed rule on the National Ambient Air Quality Standards for particulate matter

(PM), EPA committed to conduct a review and assessment of the numerous studies relevant to

assessing the health effects of PM that were published too recently to be included in the 2009

PM Integrated Science Assessment (ISA). This report presents the findings of EPA’s survey and

provisional assessment of such studies. EPA has screened and surveyed the recent literature and

developed a provisional assessment that places those studies of potentially greatest relevance to

the current PM NAAQS review in the context of the findings of the 2009 PM ISA. The focus is

on: (a) epidemiologic studies that used PM 2.5 (i.e., fine PM) or PM 10

- 2.5 (i.e., coarse PM) and were

conducted in the U.S. or Canada, and (b) toxicolog ical or epidemiologic studies that compared

effects of PM from different sources, PM components, or size fractions. T he provisional

assessment is not intended to critically review individual studies or integrate the scientific

findings to draw causal conclusions as is done for an ISA.

This survey and assessment finds that that the new studies expand the scientific

information and provide important insights on the relationships between PM exposure and health

effects of PM. H owever, the new information and findings do not materially change any of the

broad scientific conclusions regarding the health effects of PM exposure made in the 2009 PM

ISA. In brief, this report finds the following:

• Recent epidemiologic studies, most of which are extensions of earlier work, continue to

support the conclusions of the 2009 PM ISA for long

- term exposure to PM 2.5 and

mortality, cardiovascular effects, respiratory effects, and reproductive and

developmental effects

. Notably, updated findings from the Harvard Six Cities and

American Cancer Society cohorts continue to observe an association between long

- term

PM 2.5 exposure and mortality, which supports the findings from previous studies

conducted in these cohorts. Additionally, a new Canadian multicity study observed

associations with mortality at long

- term mean PM 2.5 concentrations below those reported

in the PM ISA. Recent cause

- specific mortality studies also provide more evidence for

cardiovascular mortality associations, especially in women, and additional evidence for

respiratory mortality including lung cancer. Studies of cardiovascular effects provide

evidence of myocardial infarction, hypertension, diabetes, and stroke, especially among

women, which is consistent with the conclusions of the 2009 PM ISA. Recent studies

continue to demonstrate associations with respiratory morbidity including respiratory

symptoms and hospital admissions, as well as incident asthma among children.

Reproductive and developmental effects studies continue to provide evidence for

associations between long

- term exposure to PM 2.5 and reduced birth weight.

• Recent epidemiologic studies have also continued to report associations between short

term exposure to PM 2.5 and mortality and morbidity health endpoints, which furtherviii support the causality determinations presented in the 2009 PM ISA. These include multi

and single- city analyses that demonstrate consistent positive associations across all

respiratory and cardiovascularhospital admissions and emergency department visits as

well as cause

- specific outcomes, particularly asthma. Although limited to single- city

studies, recent studies continue to demonstrate associations between short- term fine PM

exposures and nonaccidental and cardiovascular mortality. Additionally, new evidence

for stroke which focuses on assigning exposure from the time of stroke onset, instead of

entry to the hospital, provides new information regarding an uncertainty recognized in

the PM ISA.

• New toxicological and epidemiologic studies have continued to link health outcomes

with a range of PM 2.5 sources and components. Several new epidemiologic analyses

continue to demonstrate health effects attributed to multiple sources and PM components

including combustion activities (e.g., motor vehicle emissions, coal combustion, oil

burning, power plants, and wood smoke/vegetative burning), crustal sources, and

secondary sulfate . Toxicolog ical studies examined various source categories and found

that no source consistently showed the strongest association with cardiovascular health

effects. Additionally, an examination of a number of PM 2.5 components found

associations with various components and both cardiovascular and respiratory endpoints.

• Only a few recent epidemiologic studies have examined health effects of short- and

long- term exposures to coarse particles (PM 10

- 2.5 ) . A short- term exposure and

respiratory emergency department visits ( ED ) visits study found a positive and

significant association with pediatric asthma ED visits in Atlanta, GA. One long- term

exposure and mortality study did not find any evidence of an association with all

- cause

mortality though there was a positive but not statistically significant association with

coronary heart disease ( CHD ) mortality.1 

### 1. I NTRODUCTION AND M ETHODOLOGY

EPA is currently in the final stages of the review of the N ational A mbient A ir Q uality S tandards

(NAAQS) for particulate matter (PM). As described in more detail in the Federal Register Notice

of EPA’s proposed rule on the PM NAAQS (7 7 FR 38890 ), EPA has prepared the Integrated

Science Assessment for Particulate Matter (hereafter 200 9 PM ISA ) which reviewed,

summarized, and integrated the latest scientific knowledge useful in indicating the kind and

extent of all identifiable effects on public health or welfare that may be expected from the

presence of PM in the ambient air in varying quantities, as required by section 108 of the Clean

Air Act (CAA) ( U.S. EPA, 2009 )

. As noted in the PM proposal, 1 EPA is aware that numerous

studies potentially relevant to assessing the health effects of ambient PM have been published

recently that were not included in the 200 9 PM ISA ( U.S. EPA, 2009 )

. The p roposal notice also

indicates the Agency’s intent to conduct a review and assessment of these new studies before a

final decision is made on the PM NAAQS. The purpose of this report is to present the findings of

EPA’s survey and provisional assessment of potentially relevant recent studies on the health

effects of PM exposure. This provisional assessment will inform a decision by the EPA

Administrator to proceed with final rulemaking or to revise the ISA to include the new studies

.

T his provisional assessment is focused on those studies most important to the major conclusions

presented in the 2009 PM ISA and most relevant to the considerations of the current review of

the PM NAAQS

. EPA

, therefore, identified potentially relevant studies by applying the

following selection criteria to those studies published through August 2012 : ( 1 ) epidemiologic

studies that used PM 2.5 (i.e., fine PM) or PM 10

- 2.5 (i.e., coarse PM) and were conducted in the U.S.

or Canada

, and ( 2 ) toxicolog ical or epidemiologic studies that compared effects of PM from

different sources, PM components, or size fractions

. In addition, we considered studies identified

by public comments submitted to the docket of the proposed rule. Studies that met these criteria

were evaluated by EPA staff and their key findings were summarize d. T his preliminary

assessment was then developed to place those new studies of potentially greatest relevance in the

context of the findings of the 200 9 PM ISA including a judgment as to whether the new studies

materially change the major conclusions of the 2009 PM ISA

. T he provisional assessment

presented here does not attempt to critically review individual studies or to provide the kind of

full integration found in a typical ISA

.

1 As stated in the PM NAAQS proposal: “ The EPA is aware that a number of new sc ientific studies on the health

effects o f PM have been published since the mid

- 200 9 cutoff date for inclusion in the Int egrated Science

Assessment. As in the last PM NAAQS review, the EPA intends t o conduct a provisional review and ass essment of

any significant new studies pu blished since the cl ose of the Integrated Science Assessment, including studies that

may be submitted durin g the public comment period on this proposed rule in or der to ensure that, befor e making a

final decision, the Administr ator is fully aware of the new science that has d eveloped since 2009. In this p rovisional

assessment, the EPA will exam ine these new studies in light of the literature evaluated in the Integ rated Science

Assessment. This provis ional assessment and a summary of the key conclusions will be placed in the rulemaking

docket. ” (77 FR 38899)2 The literature search and submissions from public commenters found that more than 1,500

studies have been published since the ISA closed on the health effects of particulate matter.

Application of the selection criteria resulted in a list of over 100 studies that are summarized in

the main body of this report. Additional details of the air quality distributions observed in these

studies can be found in the annex to this report. The most significant studies are discussed in the

assessment, and where feasible, quantitative results are compared to those from the 200 9 PM

ISA

. A comprehensive list of s tudies identified as being potentially relevant through the survey

effort

, including those studies not discussed in detail in this report can be found here:

http://hero.epa.gov/pm

. S tudies not discussed in detail include controlled human exposure

studies, and toxicological studies that examined health effects attributed to specific PM size

fractions, as well as studies that focused on ultrafine particles

.

The overview in the main body of this report is organized into three main sections:

( 2. 1) E pidemiologic studies on effects associated with long

- term exposure to PM, focusing on

U.S. and Canadian studies with measurements of PM 2.5 or PM 10

- 2.5 ; ( 2. 2) E pidemiologic studies

on effects associated with short

- term PM exposure

, again focusing on U.S. and Canadian studies

with measurements of PM 2.5 or PM 10

- 2.5 ; and ( 2. 3) T oxicolog ical and epidemiologic studies that

have evaluated health effects with exposure to PM components and PM from different sources.

This last section includes results of studies that assessed the effects of a range of PM sources or

components

, including those using source apportionment methods or comparing effects for

numerous PM components, and not on studies of individual components

. Most studies have

focused on components or sources of PM 2.5 , but information related to sources of PM 10

- 2.5 was

also included to the extent available. Unless otherwise noted, the majority of new studies

included in this assessment did not examine the robustness of single

- pollutant results in

copollutants models.3 

### 2. OVERVIEW OF RECENT HEALTH STUDIES RESULTS

As stated in the 2009 PM ISA

, EPA integrated the scientific evidence from toxicological,

controlled human exposure, and epidemiologic studies in combination with evidence from

atmospheric chemistry and exposure assessment studies and developed causal determinations for

health outcomes categories (e.g., respiratory effects, card iovascular effects, mortality, etc.) for

different exposure durations (i.e., short

- or long

- term) and PM size fractions. Causal judgments

drawn for short

- and long

- term exposure to PM 2.5 and short

- term exposure to PM 10

- 2.5 are

included in Table 2.1.

Table 2

- 1 Causal Determinations for Short

- and Long

- t erm Exposure to PM 2.5

Long

- term Exposure to PM 2.5

Size Fraction Outcome Causality Determination

Cardiovascular Effects Causal

Respiratory Effects Likely to be causal

PM 2.5 Mortality Causal

Reproductive and Developmental Suggestive

Cancer, Mutagenicity, and Genotoxicity Suggestive

Short

- term Exposure to PM 2.5

Size Fraction Outcome Causality Determination

Cardiovascular Effects Causal

PM 2.5 Respiratory Effects Likely to be causal

Mortality Causal

Short

- term Exposure to PM 10

- 2.5

Size Fraction Outcome Causality Determination

Cardiovascular Effects Suggestive

PM 10

- 2.5 Respiratory Effects Suggestive

Mortality Suggestive

The following sections of this document summarize the scientific evidence published since the

completion of the 2009 PM ISA for each of the health outcome categorie s presented in Table 2.1

.

2.1. Epidemiologic Studies of Long

- Term Exposure

The majority of the epidemiologic evidence evaluated in the 2009 PM ISA ( U.S. EPA, 2009 )

focus ed on health effects of PM 2.5 exposure, with very limited evidence for health effects of4 long

- term exposure to PM 10

- 2.5

. These studies demonstrated consistent positive associations

between long

- term PM 2.5 exposures and a variety of health effects (Chapter 7

, ( U.S. EPA, 2009 ) ).

Sections 2.1.1

- 2.1. 4 highlight results from epide miologic studies of mortality

, cardiovascular

effects, respiratory effects, and reproductive and developmental effects, respectively, published

since the completion of the 2009 PM ISA ( U.S. EPA, 2009 ) because these were the health

outcomes specifically taken into consideration in developing the proposed rule (77 FR 38890)

.

Tables A

. 1 through A

. 5 (Appendix A) summarize the recent epidemiologic studies that evaluated

relationships between health effects and long

- term exposure to PM 2.5 and PM 10

- 2.5

. The

discussions below emphasize results of studies conducted in the U.S. and Canada.

2.1.1. Mortality

Long

- term exposure to PM 2.5

**Summary of**  **2009 PM**  **ISA Conclusions** 

The 2009 PM ISA synthesized the epidemiologic literature characterizing the association

between long

- term exposure to PM 2.5 and increased risk of mortality and concluded that “ a

causal relationship exists between long

- term exposure to PM 2.5 and mortality ” (See Section 7.6

of the 2009 PM ISA)

. Long

- term m ean 2 PM 2.5 concentrations ranged from 13.2 to 32 .0 μg/m 3

during the study periods in the areas in which these studies

, comprising the entire body of

evidence reviewed in the 2009 ISA, were conducted. When evaluating cause

- specific mortality,

the strongest evidence contributing to this causal determination was observed for associations

between PM 2.5 and cardiovascular mortality

. Positive associations were also reported between

PM 2.5 and lung cancer mortality

. Both the Harvard Six Cities ( Laden et al., 2006 ; Dockery et al.,

1993 ) and the American Cancer S ociety (ACS) ( Krewski, 2009 ; Pope III et al., 2004 ; Pope et al.,

2002 ) studies continued to provide strong e vidence for the associations between long

- term

exposure to PM 2.5 and cardiopulmonary disease (CPD) and ischemic heart disease (IHD)

mortality

. Additional evidence from a study that used the Women’s Health Initiative ( WHI )

cohort ( Miller et al., 2007 ) found a particularly strong association between long

- term exposure to

PM 2.5 and cardiovascular disease (CVD) mortality in post

- menopausal women

.

**Recent Mortality**  **Studies**

Since the completion of the 2009 PM ISA ( U.S. EPA, 2009 )

, a number of studies have been

published that examine d the association between long

- term exposure to PM 2.5 and all

- cause

mortality (See Figure 2.1 ) and cause

- specific mortality (See Figure s 2.2 and 2.3 ), including

updated results for both the Harvard Six Cities an d ACS cohorts

. Lepeule et al. ( 2012 ) extended

the analysis of the Harvard Six Cities cohort using 11 additional years of follow

- up and PM 2.5

2 For long

- term exposure studies, the long

- term mean PM 2.5 concentration refers to the average PM 2.5 concentrations

reported across the entire study duration, which could equate to the monthly or annual PM 2.5 concentration averaged

over many years.5 monitoring data and explored a variety of issues that might affect the size and timing of the

mortality effect

. Generally, the authors observed results similar to those reported by Laden et al.

( 2006 ) for all

- cause and cardiov ascular mortality, though the central estimate was slightly

diminished and had slightly narrower confidence intervals ( all

- cause mortality: RR

= 1.14 [95%

CI: 1.07, 1.22] 3 for Lepeule et al. ( 2012 ) versus RR

= 1.16 [95% CI: 1.07, 1.26] for Laden et al.

( 2006 ) ; cardiovascular mortality: RR

= 1.26 [95% CI: 1.14, 1.40] for Lepeule et al. ( 2012 ) versus

RR

= 1.28 [95% CI: 1.13, 1.44] for Laden et al. ( 2006 )

. The authors applied both spline and linear

models to investigate the concentration

- response relationship, and observed that for all

- cause

mortality, the model fit was better without the spline, indicating a no threshold, linear

relationship with PM 2.5 down to the lowest observed concentration (i.e., 8 μg/m 3 )

. Jerrett et al.

( 2009a ) reanalyzed data from the ACS cohort, including data from 86 metropolita n statistical

areas (MSAs) across the U.S with monitoring data for PM 2.5

. The authors observed an

association between PM 2.5 and all

- cause mortality in single pollutant models (RR 1.048 [95% CI:

1.024, 1.071]) that increased in magnitude in a copollutant model adjusting for ozone ( O 3 )

concentration (RR 1.080 [95% CI: 1.048, 1.113])

. The associations were stronger when limited

to mortality due to cardiovascular disease (CPD mortality: RR 1.129 [95% CI: 1.094, 1.071];

CVD mortality: RR 1.150 [95% CI: 1.111, 1.191]; IHD mortality: RR 1.211 [95% CI: 1.156,

1.268]); these associations also became stronger in copollutant models adjusting for O 3

concentration

. No statistically significant association was observed between PM 2.5 and

respiratory mortality in this re

- analysis of the ACS cohort

. In another analysis among the AC S

cohort, McKean

- Cowdin et al. ( 2009 ) examined the association between long

- term exposure to

PM 2.5 and brain cancer mortality

. The authors observed no associations with brain cancer

mortality.

3 All effect estimates for associations between long

- term exposure to PM 2.5 and mortality are presented for a 10

μ g/m 3 increase in PM 2.5 concentration.6 Figure 2.1 All

- cause mortality risk estimates, long

- term exposure to PM 2.5 in recent cohort studies

. R ed text and triangles

represent new studies published since the completion of the 2009 PM ISA

.7 * Note: As discussed in Federal Register Notice of EPA’s proposed rule on the PM NAAQS (77 FR at 38929 and 38934 n. 82). CV = cardiovascular disease, CHD = coronary heart

disease, IHD = ischemic heart disease, CPD = cardiopulmonary disease.

Figure 2.2. Cardiovascular mortality risk estimates, long

- term exposure to PM 2.5 in recent cohort studies

. R ed text and triangles

represent new studies published since the completion of the 2009 PM IS A.8 Figure 2.3 Respiratory mortality risk estimates, long

- term exposure to PM 2.5 in recent cohort studies

. R ed text and triangles

represent new studies published since the completion of the 2009 PM ISA.9 In an update to a study by Janes et al. ( 2007 )

, Greven et al. ( 2011 ) used data from a nationwide

Medicare mortality cohort to develop a statistical approach for est imating the associations

between monthly mean PM 2.5 concentrations averaged over the preceding 12 months and

monthly mortality rates among subjects living within ZIP code s with a geographic centroid

within a six mile radius of one of 814 monitoring stations from 2000 to 2006

. The study authors

decomposed the association between PM 2.5 and mortality into two components: (1) the

association between the “national” trend in the monthly PM 2.5 concentrations averaged over the

previous 12 months and the national average trend in monthly mortality rates (purely temporal

association); and (2) the association between the “local” trend in the deviation in the

community

- specific trend from the national average trend of monthly averages of PM 2.5 and the

deviation of the community

- specific trends from the national average trend of mortality rates

(residual spatio

- temporal association). Th e authors posit that this second component provide s

evidence as to whether locations having steeper declines in PM 2.5 also have steeper declines in

mortality r elative to the national trend. The authors conclude that differences in effect estimates

at these two spatiotemporal scales raise concerns about confounding bias in these analyses, with

the association for the national trend more likely to be confounded tha n the as sociation for the

local trend. The authors observed no evidence for a “local” effect, but did observe evidence for a

“national” effect. Similar to the study by Janes et al. ( 2007 )

, Greven et al. ( 2011 ) eliminate all of

the spatial variation in air pollution and mortality in their data set when estimating the “national”

effect, focusing instead on sub

- chronic (monthly) temporal differences in the data. As noted by

the authors, this eliminates 90% of the variance in the data set used for these analyses that is

attributable to spatial variability ( Janes et al. ( 2007 )

, Table 1)

. Only 5% of the variance in the

data set used in these analyses is attributable to the space by time component, which was the

focus of the papers by Janes et al. ( 2007 ) and Greven et al. ( 2011 )

. Thus, while the results of the

papers themselves provide evidence for an association between exposure to PM 2.5 and mortality,

it is not possible to directly compare the results of these studies to the results of other cohort

studies investigating the relationship between long

- term exposure to PM 2.5 and mortality, which

make use of spatial variability in air pollution and mortality data. As noted by Pope and Burnett

( 2007 ) and highlighted in the 2009 PM ISA (Section 7.6.1, ( U.S. EPA, 2009 ) )

, the conclusions of

Janes et al. ( 2007 ) “ largely excludes the sources of variability that are exploited in those other

[cohort] studies.” These comments are also applicable to the study by Greven et al. ( 2011 )

.

Crouse et al. ( 2012 ) conducted a nationwide study of the relationship between long

- term

exposure and PM 2.5 in Canada and provide new evidence for a positive association at relatively

low concentrations of PM 2.5

. The authors investigated the association between long

- term

exposure to ambient PM 2.5 and non

- accidental mortality

. The level of ambient PM 2.5 to which the

study population was exposed was estimated from satellite observations and assigned to the

cohort of 2.1 million Canadian adults that completed detailed census data in 1991

. The study

included deaths between 1991 and 2001

. The authors observed a hazard ratio (HR) of 1.15 (95%

CI: 1.13, 1.16) for non

- accidental mortality

. Using spatial random

- effects models, the HR was

slightly diminished (1.10 [95% CI: 1.05, 1.15])

. The strongest association was observed for10 deaths due to ischemic heart disease (HR: 1.31 [95% CI: 1.27, 1.35])

. Using spatial random

effects models did not substantially change the association ( HR: 1.30 [95% CI: 1.18, 1.43])

. The

associations between PM 2.5 and deaths due to CVD and circulatory diseases were similar in

magnitude to that observed for non

- accidental mortality

. There was a weaker association with

mortality due to cerebrovascular disease (CBD) (HR: 1.04 [95%CI; 0.99, 1.10]). Sensitivity

analyses including 11 Canadian cities with ground

- based PM 2.5 measurements produced similar

associations to those observed in the full cohort that utilized satellite observations to estimate

PM 2.5 exposure (See Figure 2.1)

.

A number of studies have looked at the association between long

- term exposure to ambient

PM 2.5 and all

- cause mortality among different occu pational cohorts

. Hart et al. ( 2010 ) examined

the association between residential exposure to PM 2.5 and mortality among men in the U.S.

trucking industry

. The authors observed a 10% (95% CI: 2.5

, 18) increase in all

- cause mortality

.

This association was stronger when the cohort was restricted to truck drivers that maintained

local routes, and long haul drivers were excluded (15% increase [95% CI: 5.0, 26.6] for all

- cause

mortality; 59.7% increase [95% CI: 18.7, 114.9%] for respiratory mortality )

. The associations for

other causes of death (i.e., lung cancer, CVD, IHD, chronic obstructive pulmonary disease

[COPD]) were generally positive, but were not statistically significant. Puett et al. ( 2009 )

examined the relationship of long

- term PM 2.5 exposures with all

- cause mortality among women

from the Nurses’ Health Study

. The authors found an increased risk of all

- cause mortality (HR

1.26 [95% CI: 1.02

, 1.54]) and coronary heart disease ( CHD ) mortality (HR 2.02, 95% CI: 1.07

, 3.78) associated with long

- term exposure to PM 2.5

. More recently, Puett et al. ( 2011 ) used the

same spatiotemporal exposure estimati on models to characterize the association between long

term exposure to PM 2.5 and mortality among male subjects in the Health Professionals Follow

- up

Study

. In this cohort, long

- term exposure to PM 2.5 was not associated with all

- cause or CHD

mortality

. Ostro et al. ( 2010 ) examined the association between long

- term exposures to PM 2.5 and

all

- cause

, CPD, IHD and pulmonary disease mortality among the subjects from the California

Teachers Study

. No associations were observed between all

- cause mortality and PM 2.5

. There

was a positive association between long

- term exposure to PM 2.5 and CPD mortality (HR: 1.19

[95% CI: 1.05, 1.37]) and IHD mortality (HR: 1.56 [95% CI: 1.24, 1.94]). In a f ollow

- up study,

Lipsett et al. ( 2011 ) examined the associations between long

- term exposure to PM 2.5 and all

cause and cause

- specific mortality among the subjects in the California Teachers Study

. The

authors did not observe an association between long

- term exposure to PM 2.5 and all

- cause

mortality in this cohort

, but observed an association with IHD mortality (HR 1.20 [95% CI: 1.02,

1.41])

. They also observed positive associations for respiratory mortality and CBD mortality,

though these associations were not statistically significant.

In a single

- city study conducted in Toronto, Ontario, Canada, Jerrett et al ( 2009b ) examined the

association between long

- term exposure to PM 2.5 and all

- cause mortality among subjects from a

respiratory clinic

. The authors observed positive, though not statistically significant associations

with all

- cause, circulatory or respiratory mortality

. A limited number of deaths in the cohort and

low variability in PM 2.5 concentrations (limiting the exposure contrast) led the authors to11 conclude that “no definitive conclusions [could] be drawn about these associations with PM 2.5 ”

.

In a single

- city study conducted in Vancouver, British Columbia, Cana da, Gan et al. ( 2011 )

conducted a population

- based cohort study to evaluate the association between traffic

- related

pollutants and risk of mortality due to CHD

. Land

- use regression models were used to estimate

exposure over a 5 year period (1994

- 1998) and the cohort was followed up for 4 years (1999

-

2002). Exposure to PM 2.5 was weakly associated with CHD mortality.

Recent studies that examined the association between long

- term PM 2.5 exposure and mortality

further support the conclusions of the 2009 PM ISA. The strongest evidence for mortality was

from the Harvard Six Cities ( Laden et al., 2006 ; Dockery et al., 1993 ) and American Cancer

Society cohorts ( Krewski, 2009 ; Pope III et al., 2004 ; Po pe et al., 2002 )

, which was supported by

a number of other cohort studies. Updated results from the Harvard Six Cities ( Lepeule et al.,

2012 ) and American Cancer Society ( Jerrett et al., 2009a ) cohorts support the findings of the

2009 PM ISA, while a new Canadian multicity study ( Crouse et al., 2012 ) observed associations

below those reported in the PM ISA (i.e., < 10 μg/m 3 ). In the 2009 PM ISA, for cause

- specific

mortality, the strongest evidence was for cardiovascular

- related mortality, particularly among

post

- menopausal women ( Miller et al., 2007 )

. Respiratory

- related mortality was also observed,

particularly for lung cancer mortality ( Naess et al., 2007 )

. Recent studies provide more evidence

for strong associations with cardiovascular

- related mortality among women ( Lipsett et al., 2011 ;

Puett et al., 2009 ) and additional evidence for respiratory mortality including lung cancer

mortality ( Lepeule et al., 2012 )

.

Long

- term exposure to PM 10

- 2.

5

**Summary of**  **2009 PM**  **ISA Conclusions** 

The 2009 PM ISA synthesized the epidemiologic literature characterizing the association

between long

- term exposure to PM 10

- 2.5 and increased risk of mortality and concluded that the

evidence was too limited to adequately characterize the associations for PM 10

- 2.5

. The findings

from the AHSMOG ( Chen et al., 200 5 ) and Veterans ( Lipfert et al., 2006 ) cohort studies

provided limited evidence for associations between long

- term exposure to PM 10

- 2.5 and mortality

in areas with mean concentrations in the range of 16 to 25 μg/m 3

. Overall, the evidence was

determined to be inadequate to determine if a causal relationship exists between long

- term

exposure to PM 10

- 2.5 and mortality (See Section 7.6 of the 2009 PM ISA)

. Recent studies

published since the completion of the 2009 PM ISA are characterized in Table A

. 1

.

**Recent Mortality**  **Studies**

Since the completion of the 2009 PM ISA, Puett et al

. ( 2009 ) examined the relationship of long

term exposure to PM 10

- 2.5 with all

- cause and CHD mortality among women from the Nurses’

Health Study

. The authors did not find an association between PM 10

- 2.5 and the risk of all

- cause

m ortality (HR 1.03 [95% CI: 0.89, 1.18]). The association between PM 10

- 2.5 and CHD mortality

was positive, but not statistically significant (HR: 1.14 [95% CI: 0.73, 1.77] ). More recently,12 Puett et al. ( 2011 ) used the same spatiotemporal exposure estimation models to characterize the

association between PM 10

- 2.5 and mortality among male subjects in the Health Professionals

Follow

- up Study

. In this cohort, long

- term exposure to PM 10

- 2.5 was not associated with all

- cause

or CHD mortality.

In summary, two new studies ( Puett et al., 2011 ; Puett et al., 2009 ) evaluated the association

between long

- term exposure to PM 10

- 2.5 and mortality

. The long

- term mean PM 10

- 2.5

concentrations reported in these studies were lower than those reported in the 2009 PM ISA (7.7

and 10.1 μ g/m 3

, respectively). These studies do not provide any additional evidence for an

association between long

- term exposure to PM 10

- 2.5 and mortality that would be sufficient to

materially change conclusions made in the 2009 PM ISA

.

2.1.2. Morbidity

– Cardiovascular Effects

**Summary of**  **2009 PM**  **ISA Conclusions** 

The 2009 PM ISA concluded that “the evidence from epidemiologic and toxicological studies is

sufficient to conclude that a causal relationship exists between long

- term exposures to PM 2.5 and

cardiovascular effects.” The strongest evidence was provided by large, multicity, U.S.

- based

studies of cardiovascular mortality (See Section 7.2.10 of the 2009 PM ISA) with supporting

evidence from a U.S.

- based epidemiologic study (Miller et al. ( 2007 ) ) that reported associations

between PM 2.5 and incident stroke and myocardial infarction ( MI ) among post

- menopausal

women at mean PM 2.5 concentrations of 13.5 μg/m 3

. 4

**Recent Cardiovascular**  **Morbidity Studies** 

Several new studies of long

- term exposure to PM 2.5 and cardiovascular disease were conducted

since the completion of the 2009 PM ISA

. In a study of male subjects enrolled in the Health

Professionals Foll ow

- Up Study, Puett et al. ( 2011 ) used spatiotemporal models to estimate

exposure to PM 2.5 by combining data from available air monitoring networks with geographic

information system ( GIS ) derived variables such as distance to roadway and elevation. The

authors reported no association between long

- term PM 2.5 and total CVD or ischemic stroke;

however, in fully adjusted models (i.e. adjusted for covariates including body mass index ( BMI )

, hypertension, hypercholesterolemia, diabetes, family history of MI, smoking physical activity,

diet) elevated HRs for non

- fatal MI and hemorrhagic stroke were observed (HR: 1. 1 6 [ 95% CI:

0. 81

, 1. 64 ] and 1. 69 [ 95%CI: 0. 59

, 3

. 71 ] ) 5

. Associations of PM 2.5 with all

- cause mortality and

fatal CHD were not observed in this all male cohort. A cross

- sectional study of male and female

patients attending a pulmonary clinic after reporting respiratory complaints reported no

associations of long

- term PM 2.5 exposure with prevalent IHD, although an association with

4 Listed as 12.9 μg/m 3 for the reasons stated in Federal Register Notice of EPA’s proposed rule on the PM NAAQS

(77 FR 38 934 n. 82 ).

5 All effect estimates for associations between long

- term exposure to PM 2.5 and cardiovascular morbidity are

presented for a 10 μ g/m 3 increase in PM 2.5 concentration.13 nitrogen dioxide ( NO 2 ) was reported ( Beckerman et al., 2012 )

. Interactions among exposures,

risk factors and potential confounders were tested and no statistically significant effect modifiers

were identified. A study using satellite derived aerosol optical depth (AOD) measurements to

predict PM 2.5 concentrations, reported a 3.12% (95% CI: 0.30

, 4.29) increase in cardiovascular

hospital admission among older adults for an increase in long

- term PM 2.5 exposure ( Kloog et al.,

2012a )

. A similar increase in risk was reported for stroke hospital admissions (3.49 [95% CI:

0.09

, 5.18]).

The stronger evidence linking long

- term PM 2.5 exposure with cardiovascular disease was

apparent in studies of women as originally demonstrated in the 2009 PM ISA

. In a study of

female teachers residing in C alifornia, Lipsett et al. ( 2011 ) used concentration data from 1999

-

2000 and applied inverse distance w eighted interpolation techniques to develop monthly PM 2.5

concentration surfaces from ambient monitor data. This study reported an increased risk for

incident stroke (HR: 1.15 95% CI 1.00

- 1.33), which was highest among post

- menopausal

women, but no association between PM 2.5 and incident MI (HR: 0.99 95% CI 0.84

- 1.15). This

study supports the findings of Miller et al. ( 2007 ) linking incident stroke to long

- term PM 2.5

exposure among post

- menopausal women ; however, they also reported an association with

incident MI. Coogan et al. ( 2012 ) followed African American women who ranged in age from 21

to 69 years at enrollment in the Black Women’s Health Study for 10 years to investigate incident

hypertension and diabetes in association with long

- term exposure to PM 2.5

. PM 2.5 concentrations

were spatially interpolated using monitoring data from state and local stations in the Los Angeles

basin for the year 2000. This study reported an increased risk of incident hypertension (IRR: 1.48

95%CI: 0.95

- 2.31)

. This risk was attenuated

, but remained positive in a copollutant model

containing NO 2 (IRR: 1.32 95%CI: 0.84

- 2.05).

Several studies have been published from the Multi

- Ethnic Study of Atherosclerosis (MESA)

that was designed to inform on mechanistic pathways by which PM 2.5 exposure may act on the

cardiovascular system

. L ong

- term PM 2.5 exposure was associated with increased prevalent QT

prolongation (OR: 1.6 95% CI: 1.2

- 2.2) and intraventricular conduction delay (OR: 1.7 95% C I

1.0

- 2.6) ( Van Hee et al., 2011 )

. In addition, both long

- and short

- term PM 2.5 exposure was

associated with a narrowing of retinal vessel diameter ( Adar et al., 2010 )

. R eductions in flow

mediated dilation have been observed in association with short

- term exposures to PM 2.5 (S ee

Section 6.2.4 of the PM ISA) ; however, O’Neill et al. ( 2011 ) found no association of long

- term

PM 2.5 exposure with chronic arterial stiffness

.

Generally, the results of recent studies are consistent with the evidence for an association

between long

- term exposure to PM 2.5 and cardiovascular morbidity characterized in the 2009 PM

ISA

. F indings on incident stroke reported by Miller et al ( 2007 ) in a cohort of post

- menopausal

women are supported by a new study of female teachers ( Lipsett et al., 2011 )

, while a recent

study of black women reports an association between PM 2.5 and incident hypertension ( Coogan

et al., 2012 ) at long

- term mean PM 2.5 concentrations ranging from 15.6

– 21.5 μg/m 3 ( Table

A .3)

.14 2.1.3. Morbidity

– Respiratory Effects

**Summary of**  **2009 PM**  **ISA Conclusions** 

The epidemiologic evidence reviewed in the 2009 PM ISA demonstrated associations between

long

- term exposure to PM 2.5 and decrements in lung function growth, increased respiratory

symptoms, and asthma development in study locations with mean PM 2.5 concentrations ranging

from 13.8 to 30 μg/m 3 during the study periods (See Sections 7.3.1.1 and 7.3.2.1 of the 2009 PM

ISA )

. These studies contributed to a body of evidence that was sufficient to conclude that “ a

causal relationship is likely to exist between long

- term exposures to PM 2.5 and respiratory

effects. ”

**Recent Respiratory**  **Morbi dity**  **Studies**

Since the completion of the 2009 PM ISA, a number of studies have been published that examine

the association between long

- term exposure to PM 2.5 and respiratory outcomes ( Table A

. 4 )

.

These recent studies are consistent with the associations observed for respiratory outcomes

reported in the 2009 PM ISA and provide additional evidence for associations between long

- term

exposure to PM 2.5 and respiratory symptoms and asthma development

. For example, in a recent

prospective community i ntervention study in Libby, MT ( Noonan et al., 2012 ) ambient PM 2.5

concentrations decreased by 26.7% over four winters following the replacement of over 1

, 100

wood stoves in the community with new lower emission wood stoves or other heating sources

.

This decrease in PM 2.5 concentrations was associated with decreases in reported wheeze and

respiratory infections (including colds, bronchitis, influenza and throat infection) among school

children

. These results suggest that beneficial health impacts are associated with decreases in

ambient PM 2.5 concentrations

.

A number of other studies evaluated the association between long

- term exposure to PM 2.5 and

respiratory symptoms

. Several nationwide U.S. studies that used data from the National Health

Interview Survey reported associations between long

- term exposure to PM 2.5 and respiratory

symptoms among children ( including respiratory allergy/hay fever ( Parker et al., 2009 )

, and

respirator y allergy and frequent ear infections ( Bhattach aryya and Shapiro, 2010 ) and adults

(including asthma among African

- Americans ( Nachman and Parker, 2012 ) ; sinusitis ( Nachman

and Parker, 2012 ; Bhattacharyya, 2009 ) ; and hay fever ( Bhattacharyya, 2009 )

. Meng et al.

( 2010 ) examined long

- term exposure to PM 2.5 in the San Joaquin Valley of California and

weekly asthma symptoms among participants with physician

- diagnosed asthma

. They observed

associations between annual average concentrations of PM 2.5 and frequent asthma symptoms

. In

a study conducted in New York City, Patel et al. ( 2009 ) examined long

- term exposure to PM 2.5

and respiratory symptoms in children through 24 months of age

. Long

- term exposure to PM 2.5

was not associated with wheeze or cough in this study, though several PM 2.5 constituents were

associated with wheeze and/or cough (see Section 2.4.2 for results on PM 2.5 constituents).15 A substantial body of evidence exists that has evaluated short

- term exposure to PM 2.5 and

emergency department visits and hospitalizations for respiratory causes (See Section 2.2.2.1)

.

Several recent studies have evaluated the association between long

- term exposure to PM 2.5 and

respiratory hospitalizations

. Karr et al. ( 2009a ; 2009b ) examined exposure to PM 2.5 averaged

over an infant’s lifetime ( 0

- 12 months ) and did not observe an association between PM 2.5 and

bronchiolitis hospitalizations in the Pu get Sound Region of Washington ( Karr et al., 2009a ) or in

the Georgia Air Bas in of British Columbia, Canada ( Karr et al., 2009b )

. Kloog et al. ( 2012a )

investigated hospital admi ssions for all respiratory causes among residents of New England 65

years of age and older

. The authors observed a 4.22% (95% CI 1.06, 4.75) 6 increase in

respiratory hospital admissions associated with long

- term PM 2.5 concentratio ns

. Similarly,

Neupane et al. ( 2010 ) restricted their analyses of pneumonia hospitalizations to those 65 years of

age and older and found that long

- term exposure to PM 2.5 was associated with hospitalization for

community

- acquired pneumonia (OR 13.64, 95% CI : 1.79, 101.01)

. Meng et al. ( 2010 )

examined long

- term exposure to PM 2.5 in the San Joaquin Valley of California and asthma

related emergency department visits or hospitalizations (analyzed together) among participants

with physician

- diagnosed asthma

. They observed associations between annual average

concentrations of PM 2.5 and emergency department visits and hospitalizations.

The 2009 PM ISA identified a number of prospective cohort studies that provided evidence of an

association between long

- term exposure to PM 2.5 and the development of asthma

. Recent studies

contribute to this weight of evidence, reporting results that are consistent with those summarized

in the 2009 PM ISA

. Akinbami et al. ( 2010 ) conducted a nationwide U.S. study with data on

children (ages 3

- 17 years) from the National Health Interview Survey and observed a positive

association between county

- wide annual average PM 2.5 concentration and current asthma (OR

1.43, 95% CI: 0.98, 2.10 comparing highest quartile of exposure to lowest) and/or a recent

asthma attack (OR 1.30, 95% CI: 0.89, 1.90 comparing highest quartile of exposure to lowest)

.

Two studies examining the relationship between long

- term exposure to PM 2.5 and incident

asthma were conducted in British Colu mbia, Canada

. Carlsten et al. ( 2011 ) evaluated birth year

exposure to PM 2.5 and physician

- diagnosed asthma at age 7 and observed an association with an

increased risk of incident as thma

. Similarly, Clark et al. ( 2010 ) assigned exposure b ased on

average PM 2.5 concentration during the first week of life and the association with incident asthma

between ages 3 and 4

. The authors did not observe an association between PM 2.5 and inc ident

asthma

. McConnell et al

. ( 2010 ) characterized the relationship between childhood incident

asthma and long

- term exposure to PM 2.5 among the Southern California Children’s Health Study

participants

. In this cohort, asthma

- free kindergarten and first

- grade children were followed up

for three years and the authors observed a positive association (HR 1.34, 95% CI: 0.95, 1.90),

though this association was diminished when the authors adjusted for traffic related pollution

concentrations measured near the child’s home and school.

6 All effect estimates for associations between long

- term exposure to PM 2.5 and respiratory morbidity are presented

for a 10 μ g/m 3 increase in PM 2.5 concentration.16 In summary, the results of recent studies generally continue to demonstrate an association

between long

- term exposure to PM 2.5 and respiratory morbidity. Recent e pidemiologic studies

reported associations with respiratory symptoms and respiratory hospitalizations. New f indings

on incident asthma among children are consistently positive, though not statistically significant.

These recent studies demonstrate associations at long

- term mean PM 2.5 concentrations ranging

from 9.7 to 27 μg/m 3 ( Table A. 4)

.

2.1.4. Morbidity

– Reproductive and Developmental Effects

**Summary of**  **2009 PM**  **ISA Conclusions** 

The 2009 PM ISA synthesized the epidemiologic literature characterizing the association

between long

- term exposure to PM 2.5 and increased risk of reproductive and developmental

effects and concluded that the evidence was suggestive of a causal relationship between long

term exposure to PM 2.5 and reproductive and developmental outcomes (See Section 7.4 of the

2009 PM ISA)

. The strongest evidence was for reduced birth weight and infant mortality,

especially due to respiratory causes during the post

- neonatal period

. The mean PM 2.5

concentrations during the study periods ranged from 5.3

– 27.4 μg/m 3

, with effects becoming

more precise and consistently positive in locations with mean PM 2.5 concentrations of 15 μg/m 3

and above

. The epidemiologic literature did not consistently report associations between long

term exposure to PM 2.5 and preterm birth, growth restriction, birth defects or decreased sperm

quality

.

**Recent Reproductive**  **and Developmental**  **Outcome Studies** 

Since the completion of the 2009 PM ISA, a number of studies have been published that examine

the association between long

- term exposure to PM 2.5 and reproductive and developmental

outcomes ( Table A. 5 )

. These recent studies are consistent with the associations observed for

reproductive and developmental outcomes reported in the 2009 PM ISA

, within similar

concentrations ( long

- term mean PM 2.5 concentrations ranging from 11.0

– 19.8 μg/m 3 ), and

provide additional evidence for associations between long

- term exposure to PM 2.5 and reduced

birth weight ( Ghosh et al., 2012 ; Kloog et al., 2012b ; Kumar, 2012 ; Darrow et al., 2011b ; Bell et

al., 2010 ; Morello

- Frosch et al., 2010 ; Salihu et al., In Press )

. Recent evidence remains

inconsistent for the association between exposure to PM 2.5 and preterm birth, with some studies

providi ng evidence for an association ( Chang et al., 2012b ; Wu et al., 2009 )

, while others did no t

( Rudra et al., 2011 ; Darrow et al., 2009 )

.

2.2. Epidemiologic Studies of Short

- Term Exposure

The 200 9 PM ISA included the results of many new epidemiologic studies reporting associations

between short

- term exposure to PM and a range of health outcomes. The epidemiologic evidence

evaluated in the ISA contributed to the determination that there is sufficient evidence to conclude

that “a causal relationship exists” between short

- term PM 2.5 exposure and cardiovascular effects17 and mortality, and a “likely to be causal relationship exists” between short

- term PM 2.5 exposure

and respiratory effects (Chapter 2, 2009 PM ISA )

. Additionally, the epidemiologic evidence

contributed to a “suggestive” causal determination for short

- term PM 10

- 2.5 exposure and

cardiovascular and respiratory effects, and mortality (Chapter 2, 2009 PM ISA).

Sections 2.2.1 and 2.2.2 highlight results from recent epidemiologic studies. Tables A. 6 through

A

. 11 (Appendix A) summarize results of recent epidemiologic studies that evaluated

relationships between health effects and short

- term exposure to PM 2.5 and PM 10

- 2.5

.

The 200 9 PM ISA included a particular focus on results of multicity studies due to their

evaluation of a wide range of PM exposures and large numbers of observations, which lead to

generally more precise effects estimates than most smaller scale studies of single cities. The

multicity studies also allowed investigation of homogeneity or heterogeneity of PM health

relationships, evaluation of confounding by co

- pollutants across communities with different air

pollution mixtures, and assessment of potential effect modifiers. Since the completion of the

2009 PM ISA, n umerous multicity analyses have been published that evaluate morbidity

outcomes

.

2.2.1. Mortality

**Summary of**  **2009 PM**  **ISA Conclusions** 

Overall, in the evaluation of m ulti

- and single

- city studies in the 2009 PM ISA and in the 2004

PM Air Quality Criteria Document ( AQCD ) ( U.S. EPA, 2004 ) consistent positive associations

were observed at mean 24

- h average 7 PM 2.5 concentrations above 12.8 μg/m 3

. This collective

evidence contributed to the conclusion that “a causal relationship exists between short

- term

PM 2.5 exposure and mortali t y.” Building on the evidence presented in the 2004 PM AQCD ( U.S.

EPA, 2004 )

, multi

- and single

- city studies evaluated in the 2009 PM ISA reported consistent

positive associations between short

- term PM 10

- 2.5 exposure and mortality (Section 6.5.2.3, 2009

PM ISA ).

**Recent Mortality**  **Studies**

Several recent studies evaluated the effects of short

- term exposure to PM 2.5 on mortality in single

city analyses

. No new multi

- city studies have been published. Additionally, n o new studies have

been published that examined associations between short

- term PM 10

- 2.5 exposure and mortality in

the U.S. or Canada.

N ew studies have continued to report associations between PM 2.5 and mortality that are

consistent with the conclusions of the 2009 PM ISA as shown in Figure 2.4. T wo of these studies

were conducted in New York City. Ito et al. ( 2011a ) examined the relationship between short

term exposure to PM 2.5 and PM components and cardiovascular disease (CVD) mortality for the

7 For short

- term exposure studies the mean 24

- h avg PM 2.5 concentration refers to the mean of all daily 24

- h avg

PM2.5 concentrations over the course of the study duration.18 population ≥ 40 years old in New York City for the years 2000

- 2006. PM 2.5 was associated with

CVD mortality at lag 1 in the all

- year and cold season (October

- March) analyses, but the

strongest association with CVD mortality was observed during the warm season (April

September) at lag 0 and 1

. Also in Ne w York City, Chang et al. ( 2012a ) used a novel approach to

examine the relationship between short

- term exposure to PM 2.5 concentrations and

cardiorespiratory mortality

. The authors used a spat io

- temporal deterministic model that was

bias

- corrected with monitoring data to predict daily PM 2.5 concentrations. The authors developed

a statistical model to consider personal exposure to PM 2.5 from outdoor sources to improve

exposure assessment. Using data from 2001

- 2005, positive associations were observed for those

greater than 65 years old

. The model that accounted for personal exposure found a higher risk of

mortality (2.32% [95% CI: 0.68, 3.94] at lag 1) 8 compared to a model that used only PM 2.5

concentrations (1.13% [95% CI: 0.27, 2.00]) suggesting that risk estimates derived using ambient

concentrations as a proxy for exposure are biased towards the null

.

Additional single

- city analyses were conducted in Seattle, Detroit, and Atlanta

. Zhou et al.

( 2011 ) conducted a study using daily PM 2.5 data collected in Seattle and Detroit to examine the

effect of short

- term PM 2.5 exposure on all

- cause, cardiovascular, and respiratory mortality for the

years 2002

- 2004. In a distributed lag model of 0

- 2 days, a strong association was observed

between PM 2.5 and all

- cause and cardiovascular mortality, with some evidence of an association

with respiratory mortality in Detroit during the warm season (April

- September) (quantitative

results not presented)

. There was no evidence of an association with PM 2.5 and any mortality

outcome in Seattle in the warm season. In the cold season (October

- March)

, the strongest

associations were for all

- cause and cardiovascular mortality in Seattle, while there was no

evidence of an association between PM 2.5 and any mortality outcome in Detroit. Interestingly the

magnitude of the cardiovascular mortality association in Seattle in the cold season is larger than

that in Detroit in the warm season even though mean PM 2.5 concentrations are lower, 11.4 μg/m 3

and 14.9 μg/m 3

, respectively. Klemm et al. ( 2011 ) conducted an extended analysis of two

previously published studies ( Klemm et al., 2004 ; Klemm and Mason, 2000 ) that examined the

effect of air pollution on mortality in Atlanta, GA. This analysis included an additional 7.5 years

of data and expanded the study location to include two additional counties. Focusing on deaths in

individuals 65 years of age and older, the authors found a positive association between short

term PM 2.5 exposure and nonaccidental (0.78% [95% CI:

- 0.43, 2.0]; lag 0

- 1 for a 10 μg/m 3

increase in 24

- h avg PM 2.5 concentrations) and cardiovascular mortality (0.83% [95% CI:

- 1.1,

2.8]), but no evidence of an association with respiratory mortality (

- 0.86% [95% CI:

- 4.4, 2.8]).

In summary, m ulti

- and single

- city studies evaluated in the 2009 PM ISA provided evidence of

consistent positive associations between short

- term PM 2.5 exposure and nonaccidental,

cardiovascular, and respiratory mortality. Relatively few mortality studies have been published

in the U.S. and Canada since the completion of the 2009 PM ISA and they are limited to single

-

8 All effect estimates for associations between short

- term exposure to PM 2.5 and mortality are presented for a 10

μ g/m 3 increase in PM 2.5 co ncentration.19 city studies. T hese studies continue to demonstrate evidence of positive associations between

short

- term PM 2.5 exposures and mortality in the same range of concentrations as those studies

included in the 2009 PM ISA (i.e., mean 24

- h avg concentrations of 12.8 μg/m 3 and above in the

multi

- city studies ).20 Note: Results presented from single

- pollutant models for purposes of comparing results across studies that included different mixes of copollutants

.

Figure 2.4 Percent i ncrease in non

- accidental and cause

- specific mortality for a 10 μg/m 3 increase in 24 -h average PM 2.5

concentrations in single

- pollutant models from U.S. and Canadian studies. R ed text and triangles represent recent

studies published since the completion of the 2009 PM ISA.21 2.2.2. Morbidity

2.2.2.1. Associations b etween Short

- Term Exposures to PM and Respiratory

Morbidity

**Summary of**  **2009 PM**  **ISA Conclusions** 

The association between short

- term PM 2.5 exposure and respiratory

- related emergency

department (ED) visits, hospital admissions, and physician visits was evaluated in Section 6.3.8

of the 2009 PM ISA ( U.S. EPA, 2009 )

. The numerous multi

- and single

- city studies evaluated

reported consistent positive associations with respiratory ED visits and hospital admissions for

COPD, asthma, and respiratory infection in study areas with mean 24

- h average PM 2.5

concentrations ranging from 6.1

– 22 μg/m 3

. However, associations for asthma were imprecise

and not consistently positive when limiting analyses to children. The evidence from respiratory

related emergency department (ED) visits, hospital admissions, and physician visits studies

contributed to the conclusion that a “causal relationship is likely to exist between short

- term

exposures to PM 2.5 and respiratory effects.”

Additional epidemiologic studies evaluated in the 2009 PM ISA examined associations between

short

- term PM 10

- 2.5 exposure and respiratory hospital admissions and ED visits. This limited

number of studies demonstrated consistent positive associations with respiratory

- related hospital

admissions and ED visits wit h the strongest evidence in children. The evidence from these

studies in combination with the evidence from toxicological and controlled human exposure

studies led to the conclusion that the collective evidence across disciplines “is suggestive of a

causal relationship between short

- term exposures to PM 10

- 2.5 and respiratory effects.”

**Recent Respiratory**  **Hospital Admission**  **Studies**

Within this section

, respiratory

- related hospital admissions and ED visit studies are discussed

separately. This is because ED visits for respiratory

- related outcomes often represent less

serious, but more common health effects. Additionally, only a small percentage of respiratory

related ED visits result in a hospi tal admission. Therefore

, it is important to discuss the evidence

for each respiratory

- related health outcome separately.

Respiratory

- r

elated Hospital Admissions

A number of studies published since the completion of the 2009 PM ISA conducted mu lti city or

multi

- location analyses to examine the association between short

- term PM 2.5 exposures and

respiratory hospital admissions. Figure 2.5 summarizes the evidence from single

- pollutant

models from studies evaluated in the 2009 PM ISA as well as recent studies published since its

completion. Bell et al. ( 2012 ) represented a consolidated and more de tailed account of a number

of previous publications, of which most were discussed in the 2009 PM ISA ( Bell et al., 2009a ;

Bell et al., 2009b ; Bell et al., 2008 ; Bell et al., 2007 )

. In an all

- year an alysis of 187 U.S. counties,22 short

- term exposure to PM 2.5 was positively associated with respiratory hospital admissions in

individuals 65 years of age and older across lags of 0 to 2 days, with the strongest association at

lag 2 (0.41% [95% CI: 0.09, 0.74]) 9

. In seasonal analyses, the association at lag 2 was

consistently positive across seasons, but the strongest association was at lag 0 (1.05% [95% CI:

0.29, 1.82]) in the winter season with the largest magnitude of an effect in the Northeast region.

Of note the Northeast region comprised 53% of all counties included in the analysis. In a n

additional analysis using this data ( Bell et al., 2009a )

, there was no evidence of a reduction in the

association between PM 2.5 and respiratory hospital admissions when accounting for air

conditioning use

. In a multi

- city study conducted in the New England region o f the U.S., Kloog

et al. ( 2012a ) examined associations between short

- term PM 2.5 exposure and respiratory hospital

admissions in individuals 65 years of age and older. To estimate exposure the authors developed

a novel prediction model that combined land use regression with physical measurements from

satellite aerosol optical depth. T he authors observed a 0.70% (95% CI: 0.35, 1.05) increase in

respiratory hospital admissions for lags days 0

- 1

. The results obtained using the novel approach

presented (i.e., 0.70% increase in respiratory hospital admissions) were consistent with the

percent increase in respiratory hospital admissions observed in a traditional time

- series analysis

(i.e., 1.51%).

In addition to the multicity studies presented above, a few single city studies were conducted in

the U.S. that examined asthma and acute bronchitis. Silverman and Ito ( 2010 ) conducted a study

to evaluate the effect of short

- term PM 2.5 and O 3 exposure on asthma hospital admissions, both

general and those that required a stay in the intensive care unit (ICU) in New York City.

Analyses focused on four age groups (i.e., <6, 6

- 18, 19

- 49, and 50+) and were limited to the

warm season (April

- August). Positive associations were observed for each age group and for all

ages combined when considering general asthma hospital admissions, with the strongest

association for the age group 6

- 18 (15.5% [95% CI: 9.1, 22.0] at lag 0

- 1). When limiting the

analysis to ICU asthma admissions, again the strongest association was for the age group 6

- 18

(21.1% [95% CI: 8.3, 35.5]). The observed associations remained robust in copollutant models

with O 3

. The authors also examined the shape of the concentration

- response ( C

- R ) relationship

using linear, smooth functions, which allowed for a possible nonlinear relationship. This analysis

found evidence that the linear fit is a reasonable approximation of the relationship between short

term PM 2.5 concentrations and asthma hospital admissions. Grineski et al. ( 2011 ) primarily

focused on examining the effect of dust and low wind events on asthma and acute bronchitis

hospital admissions in El Paso, TX; however, since daily PM 2.5 data were available the authors

also examined associations between short

- term PM 2.5 exposures and each respiratory health

effect. T he authors found that PM 2.5 was positively

, but weakly associated with asthma

(OR=1.02 [95% CI: 0.96, 1.09]) and acute bronchitis (OR=1.01 [95% CI: 0.92, 1.12]) hospital

admissions.

9 All effect estimates for associations between short

- term exposure to PM 2.5 and morbidity are presented for a 10

μ g/m 3 increase in PM 2.5 concentration.23 **Recent Respiratory** 

**- related**  **ED Visits**  **Studies**

Of the recent studies identified that focused on short

- term exposures to PM 2.5 and respiratory

related ED visits the majority consisted of single

- city studies. However, a couple large

, multi

city stud ies w ere conducted in the U.S

. and Canada

. Zanobetti et al. ( 2009 ) examined the

association between short

- term PM 2.5 exposure and respiratory ED visits in individuals 65 years

of age and older in 26 U.S. communities. In an all

- year analysis, PM 2.5 was strongly associated

with respiratory ED visits (2.1 [95% CI: 1.2, 3.0] at lag 0

- 1), while in seasonal analyses positive

associations were observed across seasons with the strongest association in the spring (4.3%

[95% CI: 2.2, 6.5]). Stieb at al. ( 2009 ) conducted a study in 7 Canadian cities to examine the

effect of air pollution on ED visits for multiple respiratory

- re lated health outcomes including

asthma, COPD, and respiratory infection. The authors found no evidence of an association

between short

- term PM 2.5 exposure and COPD ED visits at any of the single

- day lags examined.

In all

- year analyses, positive associations were observed for asthma with the magnitude of the

association decreas ing as lag day increased (i.e., the strongest association was observed at lag 0,

2.1% [95% CI:

- 3.0, 7.5]). However, in a warm season analysis (April

- September), the

magnitude of the association between PM 2.5 and asthma was nearly 4 times higher (9.3% [95%

CI: 6.3, 12.5]).

A couple of single city studies were also conducted that examined all respiratory

, multiple

respiratory effects, or asthma ED visits

. Darrow et al. ( 2011a ) examined the association between

short

- term air pollution exposure and respiratory ED visits in Atlanta using various exposure

metrics (i.e., 1

- h max, 24

- h avg, Commute (0700

- 1000, 1600

- 1900 hours), Day

- time (0800

- 1900

hours), and Night

- time (2400

- 0600 hours). PM 2.5 (lag 1) was positively associated with

respiratory ED visits across exposure metrics, with the magnitude ranging from 0.2% to 0.4%

.

Kim et al. ( 2011 ) ex amined the associations between short

- term PM 2.5 exposure and hospital

admissions in Denver, CO. The authors found no evidence of an association with all respiratory

(

- 0.44% [95% CI:

- 5.6, 5.4]), COPD or pneumonia hospital admissions (quantitative results only

presented for all respiratory). However, there was evidence of a delayed effect of PM 2.5 on

asthma hospital admissions with effects not occurring until approximately lag day 4.

A number of studies focused on ED visits and hospital admissions for asthma. Strickland et al.

( 2010 ) conducted an analysis in Atlanta using the same air quality data as Darrow et al. ( 2011a )

to examine the association between air pollution and pediatric (ages 5

- 17) asthma ED visits.

PM 2.5 was strongly associated with pediatric asthma ED visits in both all

- year (2.2% [95% CI:

0.2, 4.2] at lag 0

- 2) and warm season (4.7% [95% CI: 1.7, 7.6]) analyses. The magnitude of the

association was robust to the inclusion of O 3 in the model. An examination of the C

- R

relationship through a quintile analysis and a loess C

- R analysis using lag 0

- 2 day PM 2.5

concentrations found evidence of increased risk of pediatric asthma ED visits down to relatively

low ambient concentrations (i.e., mean 24

- h avg concentrations < 14 μg/m 3 )

. In Tacoma, WA,

Mar et al. ( 2010 ) also examine d the association between short

- term PM 2.5 exposure and asthma

ED visit s

. Individual lag days of 0 to 5 days were examined with the strongest association24 occurring at lag 2 (5.7% [95% CI : 1.4, 10.1])

. Li et al. ( 2011 ) examined the C

- R relationship

between short

- term PM 2.5 exposures and asthma ED visits in children 2 to 18 years of age in

Detroit. Associations were examined in both a time

- series and time

- stratified case

- crossover

study design assuming: (1) no deviation from linearity and (2) a change in linearity at 12 μg/m 3

.

In the analyses assuming linearity, similar effect estimates were observed in both models for a 0

-

4 day lag, (time series: RR=1.03 [95% CI: 1.00, 1.07]; case

- crossover: OR=1.04 [95% CI: 1.01,

1.07]). In the models assuming a deviation from linearity at 12 μg/m 3

, the authors reported

slightly larger effect estimates

, compared to the linear model, for asthma ED visits in the time

series (RR=1.07 [95% CI: 1.03, 1.11]; lag 0

- 4) and case

- crossover analyses (OR=1.06 [95% CI:

1.03, 1.09]; lag 0

- 4), respectively

. Glad et al. ( 2012 ) conducted a study in Pittsburgh, PA that

found PM 2.5 to be positively associated with asthma ED visits in analyses of all ages and ages 18

to 64 for single lag days and the average of 0

- 5 days (i.e., all ages: OR=1.04 [95% CI: 0.98, 1.10]

and 18 to 64: OR=1.053 [95% CI: 0.99, 1.12] at lag 0

- 5). Additionally, when stratifying by race

there was some evidence for larger effects in African Americans compared to Caucasian

Americans.25 * Note: ED visit studies. ** Median concentration.

Figure 2.5 Percent i ncrease in respiratory

- related hospital admissions and ED visits for a 10 μg/m 3 increase in 24 -h average PM 2.5

concentrations in single

- pollutant models from U.S. and Canadian studies. R ed text and triangles represent recent

studies published since the completion of the 2009 PM ISA.26 The 2009 PM I SA evaluated a number of multi

- and single

- city studies that found consistent

positive associations with all and cause

- specific respiratory hospital admissions and ED visits,

specifically COPD and respiratory infections in study areas with mean 24

- h PM 2.5 concentrations

ranging from 6.1

– 22.0 μg/m 3

. Additionally, there was evidence for asthma hospital admissions

and ED visits, but the effects were not consistent in children. Recent multi

- and single

- city

studies have continued to demonstrate consistent positive associations for all respiratory

- related

hospital admissions and ED visits, and provide additional evidence for increases in asthma

hospital admissions and ED visits. The associations observed in th e new studies occur in

locations with mean concentrations similar (i.e., mean 24

- h avg concentrations ranging from 6.7

– 16.4 μg/m 3 ) to those studies included in the 2009 PM ISA.

The 2009 PM ISA also found evidence that associations between short

- term PM 10

- 2.5 exposures

and respiratory

- related hospital admissions and ED visits were strongest among children. A

recent study by Strickland et al. ( 2010 ) that examined the association between short

- term PM 10

-

2.5 exposure and pediatric asthma ED visits in Atlanta, GA further supports this conclusion.

Positive associations were observed in both all

- year (5.8% [95% CI: 1.9, 9.9] at lag 0

- 2) and

seasonal analyses, with the strongest association in the cold season (7.0% [95% CI: 1.7, 12.7]).

An examination of the C

- R relationship in both quintile and smooth estimates of the

concentration

- response provided evidence of associations at relatively low ambient

concentrations for all pollutants, including PM 10

- 2.5 (i.e., mean 24

- h avg concentrations < ~12

μg/m 3 )..

2.2.2.2. Associations b etween Short

- Term Exposures to PM and

Cardiovascular Morbidity

**Summary of**  **2009 PM**  **ISA Conclusions** 

The associations between short

- term PM 2.5 exposure and cardiovascular

- related hospital

admissions and ED visits was evaluated in Section 6.2.10 of the 2009 PM ISA ( U.S. EPA, 2009 )

. Epidemiologic studies that examined the effect of PM 2.5 on cardiovascular ED visits and hospital

admissions reported consistent positive associations (predominantly for IHD and congestive

heart failure [CHF]) in study areas with mean 24

- h average concentrations ranging from 7.0

– 18

μg/m 3

. This evidence contributed to the conclusion that “a causal relationship exists between

short

- term PM 2.5 exposure and cardiovascular effects.”

Epidemiologic studies of the association of short

- term PM 10

- 2.5 exposure with cardiovascular

hospital admissions and ED visits were also evaluated in the 2009 PM ISA, and the evidence

from these studies contributed to the conclusion that the evidence “is suggestive of a causal

relationship between short

- term exposures to PM 10

- 2.5 and cardiovascular effects.

**Recent Cardiovascular** 

**- related**  **Hospital Admissions/ED**  **Visits Studies** 

Recent multi

- city and multi

- location studies, as well as single

- city studies, add to the collective

body of evidence that examined associations between short

- term PM 2.5 exposure and27 cardiovascular

- related hospital admissions and ED visits evaluated in the 2009 PM ISA. Figure

2.6 summarizes the results from single

- pollutant models from studies evaluated in the 2009 PM

ISA as well as recent studies published since its completion. No new studies have been published

that examined the association between short

- term PM 10

- 2.5 exposure and cardiovascular hospital

admissions or ED visits in the U.S. or Canada.

In a recent Health Effects Institute ( HEI ) report, Bell et al. ( 2012 ) compiled findings from

several multicity analyses of Medicare data (older adults, ≥ 65 years of age) for 204 counties

across the U.S. (some analyses included fewer counties)

. Although additional detail is provided

in the HEI report, these analyses were largely included in the 2009 PM ISA ( Bell et al., 2008 ;

Dominici et al., 2006 )

. In an analysis using the same da ta, Bell et al. ( Bell et al., 2009a ) found a

h igher prevalence of central air conditioning was associated with a decrease in the risk of PM 2.5

-

associated hospitalization for cardiovascular disease.

Recent studies are consistent with the evidence assessed in the 2009 PM ISA. In a time

- series

analysis of Medicare records for older adults ≥65 years of age in 26 US communities for 2 000

-

2003, Zanobetti et al. ( 2009 ) reported increases in hospital admissions for all CVD (1.89%

95%CI: 1.34 to 2.45), MI (2.25% 95%CI: 1.10 to 3.42) and CHF (1.85% 95%CI: 1.19 to 2.51;

lag 0

- 1)

. Although the largest excess risks were observed in the spring, statistically significant

excess risks were also observed in the winter

. In a time

- series analysis of hospital admissions in

seven Canadian cities, a 17% (95%CI: 0 to 37%) increase in hospital admissions for heart failure

was observed at lag 0 ( Stieb et al., 2009 )

. Weak, nons ignificant associations were observed

between PM 2.5 and d ysrhythmia and MI hospitalizations.

In a study of emergency hospitalizations among New York City residents ≥ 40 years of age, Ito

et al. ( 2011a ) reported an excess risk of 1.0% (95% CI: 0.40, 1.6

, lag 0). The excess risk was

stronger in the cold season (1.1% [95% CI 0.2 to 2.0]). These results were not sensitive to the

choice of method used to control temperature

. Using a subset of these emergency hospitaliz ation

data, Mathes et al. ( 2011 ) defined two cardiovascular syndromes from a database containing text

descriptions of the chief complaint reported by the patient upon admission to the hospital. This

study reported that PM 2.5 was associated with both cardiac and more general cardiovascular

syndromes. In case

- crossover analysis of cardiovascular disease admissions across New York

state from 2001 to 2005, Haley et al. ( 2009 ) found a 3.9% increase in heart failure admissions

per 10 μg/m 3 increase in PM 2.5 (lag 0

- 2)

. A case

- crossover study of atrial fibrillation

hospitalizations between 1993 and 2008 in Utah (Wasatch Front) reported consistent ly positive

,

but non

- significant, associations across all lags examined in the study (lag 0 through 21 day

moving average) (quantitative results not provided) ( Bunch et al., 2011 )

. Finally, a 1 .03% (95%

CI: 0.69, 1.34) increase in cardiovascular admissions was reported in a time

- series study of

hospitalizations across New England among older adults (65 years) with predicted PM2.5

concentrations using satellit e

- derived AOD measurements ( Kloog et al., 2012b )

.28 Acute Stroke

Wellenius et al. ( 2012 ) examined the association of PM 2.5 with neurologist

- confirmed ischemic

stroke in predominately white female patients admitted to the Beth Israel Deaconess Medical

Center (BIDMC) in Boston from 1999 to 2008. T ime of stroke symp tom onset (exact or

estimated) was available for most patients included in the study. The OR of stroke onset was

1.30 (95% CI: 1.08 to 1.58) per 10 μg/m 3 increase in PM 2.5 in the previous 24 hours. Authors

report a 34% (95% CI: 13 to 58) higher risk of ischemic stroke during the previous 24 hours in

an analysis comparing moderate PM 2.5 exposure (≥15 μg/m 3 ) to good (<15 μg/m 3 ) exposure, as

defined by EPA’s Air Quality Index (AQI)

. These results were confirmed in an additional

analysis conducted by Mostofsky et al. ( 2012 ) using a subset of the data (i.e., 2003

- 2008) used

by Wellenius et al. ( 2012 )

. Mostofsky et al. ( 2012 ) found a 22.7% (95% CI: 3.1, 47.0) increase in

ischemic strok e onset for an increase in PM 2.5 over the previous 24 hours.

Out of Hospital Cardiac Arrests

The small number of studies of out

- of

- hospital cardiac arrest included in the 2009 PM ISA

reported mixed results. A recent time series analysis of cardiac arrests in New York City reported

an increased risk of 1.06 (95%CI 1.02, 1.10, lag 0

- 1) per 10 μg/m3 increase in PM 2.5 ( Silverman

et al., 2010 )

. Case cross

- over analysis of the same data produced a result that was similar in

magnitude but did not reach statistical significance. The association with cardiac arrest was

stronger in the warm season (1.09 95% CI: 1.03

- 1.15) compared to the cold season (1.01 95% CI

0.95 to 1.07).

I n summary, the 2009 PM ISA found consistent positive associations between short

- term PM 2.5

exposures and all and cause

- specific cardiovascular hospital admissions and ED visits,

specifically IHD and CHF in study areas with mean 24

- h PM 2.5 concentrations ranging from 7.0

– 18 .0 μg/m 3

. New multi

- and single

- city studies further support associations with all

cardiovascular hospital admissions and ED visits at mean 24

- h PM 2.5 concentrations ranging

from 6.7

– 15.3 μg/m 3

. Additional support for associations between short

- term PM 2.5 exposures

and cardiovascular effects comes from a new study of stroke onset (Wellenius et al. ( 2012 ) )

.29 * Note: ED visit studies. ** Median concentration. a = study only presented mean age of participants

Figure 2.6 Percent increase in cardiovascular

- related hospital admissions and ED visits for a 10 μg/m 3 increase in 24 -h average

PM 2.5 concentrations in single

- pollutant models from U.S. and Canadian studies. R ed text and triangles represent

recent studies published since the completion of the 2009 PM ISA.30 2.3. Health Effects Related to Sources or Components of PM

**Summary of**  **2009 PM**  **ISA Conclusions** 

The 2009 PM ISA evaluated epidemiologic, toxicological, and controlled human exposure

studies that examined health effects associated with ambient PM components and sources. These

studies used a variety of quantitative methods and examined a broad set of PM component s

(Section 6.6)

, and found evidence of health effects from sources and components associated with

a number of combustion activities (e.g., motor vehicle emissions, coal combustion, oil burning,

power plants, and wood smoke/vegetative burning), crustal sources, and secondary sulfate. As a

result, the ISA concluded that “ the evidence is not yet sufficient to allow differentiation of those

component s or sources that are more closely related to specific health outcomes.” These

conclusions are consistent with those presented in the 2004 PM AQCD where the studies

evaluated found evidence of health effects attributed to a number of source types, including

motor vehicle emissions, coal combustion, oil burning, and vegetative burning.

**Recent Studies**  **of Health**  **Effects Related**  **to Sources**  **or Components**  **of PM** 

Recent studies have continued to examine whether specific PM component s or sources are more

closely related to specific health outcomes

. For the purposes of this provisional assessment of

new literature published since the release of the 2009 PM ISA, emphasis has been placed on

studies that investigated the health effects related to PM sources or comparisons of various PM

components. To highlight the scientific content of the recent literature while focusing on key PM

study categories, this section focuses on results of studies that evaluated the effects of a range of

sources or components. Thus, the discussion includes: (1) recent epidemiologic studies using

source apportionment; (2) epidemiologic evidence on effects with PM components; and (3)

results of new toxicolog ical studies using source apportionment with exposures to concentrated

ambient particles (CAPs) to provide insight into potential effects related to PM from different

sources, and comparative toxicology studies using fine PM c omponents

. In addition, numerous

epidemiologic and/or toxicology studies have reported effects of several ultrafine PM as

discussed in the 2009 PM ISA. Specific findings for ultrafine PM are not discussed in detail;

instead, the available new studies ar e included in the reference list : http://hero.epa.gov/pm

.

2.3.1. Epidemiologic Studies Using Source Apportionment

Lall et al. ( 2011 ) examined the association between source

- specific daily PM 2.5 mass and

component data and hospital admissions in New York City for the years 2001

- 2002. The use of

daily data allowed for the examination of both single

- day lags and a distributed lag. Source

categories identified through positive matrix factorization included long

- range transported

sulfates, traffic, residual oil, steel metal works dust, and soil

. In single

- day lag models, total

respiratory hospital admissions were positively associated with residual oil at lag 2, but the

strongest associations were with steel metal works dust at lag 0 and 3. For cardiovascular

hospital admissions the strongest association s w ere observed with traffic at lag 0 and residual oil31 at lag 3. When examining associations between cause

- specific cardiovascular and the traffic

source category, the strongest associations were observed at lag 0 for total cardiovascular, heart

failure, and stroke. For associations between cause

- specific respiratory hospital admissions and

the steel source category, pneumonia was associated with steel metal works dust at lag 3, while

asthma was observed to have the largest magnitude of an association across all lags. The

distributed lag model demonstrated a stronger association between traffic and cardiovascular

hospital admissions and steel metal works dust and respiratory hospital admissions than the

single

- day lag models, indicating that single

- day lags may underestimate the magnitude of

associations. Finally, a sensitivity analysis using key tracers of each source (i.e., elemental

carbon for traffic and manganese for steel metal works) found similar patterns of associations as

the source

- specific analyses.

2.3.2. Epidemiologic Studies on Effects of Fine PM Components and Sources

In addition to examining the association between short

- term PM 2.5 exposures and mortality or

hospital admissions and ED visits a number of studies also attempted to identify if an individual

PM component or group of PM components could explain the observed association. The

following section describes the results from these studies some of which have been

aforementioned

.

Short

- term exposure to PM 2.5 components and sources and m ortality

In addition to examining the association between short

- term exposure to PM 2.5 and mortality, a

few single

- city studies also examined the effect of individual PM 2.5 components on mortality. Ito

et al. ( 2011a ) focused on key PM components (i.e., elemental carbon [ EC ]

, organic carbon [ OC ]

,

sulfate [ SO 4 ]

, nickel [ Ni ]

, vanadium [ V ]

, zinc [ Zn ]

, silicon [ Si ]

, selenium [ Se ]

, sodium [ Na ]

, and

bromine [ Br ] ) identified in previous source apportionment studies conducted in NYC. In all

- year

analyses, the strongest associations were observed at lag 1 for EC, OC, SO 4 , Si, Se, and Br. In

the warm season, strong associations were observed for secondary aerosols including OC and

SO 4 , Se, which is associated with transported coal emissions, EC, and Br. In the cold season, the

components associated with residual oil burning, Ni, V, and Zn, all showed a similar pattern of

associations, with the strongest effects at lag 3. Overall, the components representing regional

transport showed a seasonal pattern of associations similar to those found with PM 2.5 mass, while

associations were found throughout the year with EC and NO 2

.

Zhou et al. ( 2011 ) examined the association between PM components with all

- cause,

cardiovascular, and respiratory mortality in seasonal analyses in Seattle and Detroit

. The

components selected for analysis represent the major emissions sources of the two cities: soil

( aluminium [ Al ] and Si), smelter effluents ( iron [ Fe ] and Zn), residual oil burning (Ni and V),

coal burning ( sulfur [ S ] ), traffic (EC), sea salt (Na), and wood burning ( potassium [ K ] ). Daily

component data was available in both cities, which allowed for the examination of a 0

- 2 day

distributed lag

. In Detroit, S was associated with all

- cause and cardiovascular mortality and S32 and Ni were moderately associated with respiratory mortality in the warm season. No

components were positively associated with any mortality outcome in the cold season in Detroit.

In Seattle, in the warm season no component was significantly associat ed with any mortality

outcome, but Fe, K, and EC were positively associated with respiratory mortality. In the cold

season, Al, K, Si, Zn, and EC were strongly associated with all

- cause mortality, with the same

components, minus Al, strongly associated with cardiovascular mortality. No components were

associated with respiratory mortality in Seattle in the cold season. Overall, in Detroit the

components associated with mortality are indicative of coal burning while in Seattle the

components associated with mortality represent cold

- season traffic and combustion sources, such

as residual oil and wood burning.

In the study conducted by Klemm et al. ( 2011 ) in Atlanta, daily concentrations of the PM

components EC, OC, nitrate [ NO 3 ]

, and SO 4 were also available for the entire study duration.

The authors found that EC, OC, and NO 3 were positively associated with nonaccidental mortality

at lag 0

- 1 in individuals 65 years of age and older, with the strongest association for NO 3

. In

analyses of cause

- specific mortality, a similar pattern of associations was observed for

cardiovascular and respiratory mortality. SO 4 was not found to be associated with any of the

mortality outcomes examined.

Respiratory

- related Hospital Admissions and ED Visits

Recent multicity studies were identified that examined the effect of PM components on the

relationship between short

- term PM exposure and respiratory

- related ED visits and hospital

admissions. Zanobetti et al. ( 2009 ) conducted a second

- stage analysis, using the same

methodology as Franklin et al. ( 2008 ) (2009 PM ISA; p. 6

- 193

- 195) and examined whether

season and community

- specific long

- term mean seasonal concentration ratios of PM components

to PM 2.5 total mass modified the association between short

- term PM 2.5 concentrations and

respiratory ED visits. Of the components examined only Na + and Ni were found to modify the

association between PM 2.5 and respiratory ED visits

. Using a different approac h

, Levy et al.

( 2012 ) attempted to identify if some PM components are more toxic than others by focusing on

the four components that dominate PM 2.5 mass and are highly correlated with PM 2.5 (i.e., EC,

OC, SO 4 , and NO 3 ). In a time

- series analysis using Medicare data from 119 U.S. counties the

authors examined the association between each component and respiratory hospital admissions

across the U.S. and regionally (i.e., East and West). Of the components examined, only EC and

OC were positively associated with respiratory hospital admissions.

A few single

- city studies were also identified that examined associations between respiratory

related ED visits and hospital admissions and individual PM components. Strickland et al. ( 2010 )

focused on the PM components SO 4 , EC, OC, and water

- soluble metals. For each component

positive associations were observed with pediatric asthma ED visits in all

- year analyses. The

strongest associations were observed in the warm season with the magnitude being similar across

components. In addition, analyses including copollutant adjustment were conducted using warm33 season data. Risk estimates for PM 2.5 , EC, and SO 4 were attenuated, but remained positive when

including O 3 in the model. In LOESS C

- R analyses, there was evidence of a positive C

- R

relationship for each component. Kim et al. ( 2011 ) examined the lag structure of associations

between the PM components EC, OC, SO 4 , and NO 3 and respiratory hospital admissions. The

authors focused on these components because they comprise the majority of PM 2.5 mass in

Denver. Consistent with the PM 2.5 results, there was no evidence of an association with COPD or

pneumonia and any of the components. For both all respiratory and asthma hospital admissions

there was evidence of greater effects with EC and OC compared to SO 4 and NO 3 , and additional

evidence for delayed effects occurring 2 to 5 days after exposure.

Cardiovascular

- related Hospital Admissions and ED Visits

The 2009 PM ISA included multicity analyses of the effect of PM 2.5 components on

cardiovascular hospital admissions that reported associations between oil combustion and traffic

related PM 2.5 and CVD hospitalizations

.

Two recent studies investigated the association of PM 2.5 components with cardiovascular

hospital admissions. Using Medicare data from 26 US communities, Zanobetti et al. ( 2009 )

examined the modification of the associations of PM 2.5 with CVD, MI and CHF hospital

admissions by season

- and community

- specific PM 2.5 composition. Authors estimated the

relative contribution of specific components (EC, OC, SO 4 , NO 3 , Na, Ni, V, Zn, Si, Se, Br) by

computing concentration ratios (i.e. component species as a proportion of PM 2.5 mass). In the

second stage of a hierarchical model, season

- and community

- specific estimates of the

association between PM 2.5 and CVD hospitalizations were regressed on the concentration ratios.

The association of PM 2.5 with all CVD hospitalizations was significantly modified when the

proportion of Br, Na +

, Ni, V and Al in PM 2.5 was high. The association of PM 2.5 with all MI

hospitalizations was significantly modified when the proportion of arsenic [ As ]

, chromium [ Cr ]

,

manganese [ Mn ]

, OC, Ni, K and Na + was high. Additional increases in CVD hospitalizations per

interquartile range (IQR) increase in the proportion of the component ranged from 0.53% to

0.9% (larger, less precise increases were reported for MI)

. None of the components significantly

modified the association of PM 2.5 with CHF admissions (i. e. p

- value > 0.05). Ito et al. ( 2011b )

conducted a time series analysis of the lag structure and seasonal patterns in the association

between emergency hospitalization for CVD and PM 2.5 chemical components. Same day

concentration of most components examined was associated with CVD hospitalizations (EC,

OC, SO 4 , NO 3 , Na, Ni, V, Zn, Se, and Br)

. The association and lag structure of EC with CVD

hospitalization was constant across season; associations of OC, SO 4 , Ni, Zn, Si, Se and Br with

CVD hospitalizations were strongest in the cold season

.

An additional study ( Mostofsky et al., 2012 ) examined different approaches to modeling the

association between PM components and health outcomes using ischemic stroke onset as an

example. The authors used three different models that included parameters for the following: (1)

component concentration, (2) component concentration adjusted for total PM 2.5 mass, which34 accounts for total PM 2.5 mass, and (3) component residuals, which eliminates confounding by

total PM 2.5 mass. In model 1

, positive associations were observed for a number of components

including Al, cal cium [Ca], Br, lead [Pb], Se, titanium [Ti]

, and Fe with the strongest

associations for V, S, Ni, and black carbon [ BC ]

. Models 2 and 3 resulted in relatively few

components with positive associations, but the pattern of associations across pollutants was

consistent between the two models with the strongest associations for V, Ni, and BC.

Long

- term exposure to PM 2.5 components and mortality

Ostro et al. ( 2010 ) also examined the association between long

- term exposures to PM 2.5

components (i.e., EC, OC, SO 4 , NO 3 , Fe, K, Si, Zn) and all

- cause mortality among the subjects

from the California Teachers Study

. No associations were observed between all

- cause mortality

and any PM 2.5 component. In analyses of cause

- sp ecific mortality, Ostro et al. ( 2010 ) observed

an association between long

- term exposure to several PM 2.5 components and mortality from

CPD, IHD and pulmonary disease

. The authors observed positive associations of CPD and IHD

mortality with each of the measured components, and between pulmonary mortality and SO 4 and

NO 3

. Of the components analyzed, there were positive associations with nitrate, sulfate and

silicon for CPD mortality and all of the components were associated with mortality from IHD

(See Table 2.2 )

.

Table 2

- 2 Association between M ortality O utcomes and PM 2.5 C omponents using a 30

- km B uffer

(n=43,220) (A dapted from Ostro et al. [ 2011 ] )

Component (IQR, μg/m 3 ) All

- Cause* CPD* IHD* Pulmonary*

EC (0.65) 1.02 (0.93, 1.12) 1.07 (0.94, 1.22) 1.46 (1.17, 1.83) 0.88 (0.68, 1.15)

OC (0.84) 1.00 (0.95, 1.04) 1.04 (0.98, 1.11) 1.13 (1.01, 1.25) 0.95 (0.84, 1.06)

SO 4 (2.2) 1.06 (0.97, 1.16) 1.14 (1.01, 1.29) 1.48 (1.20, 1.82) 1.04 (0.82, 1.31)

NO 3 (3.2) 1.03 (0.98, 1.09) 1.11 (1.03, 1.19) 1.27 (1.12, 1.43) 1.04 (0.90, 1.20)

Fe (0.13) 1.01 (0.93, 1.11) 1.05 (0.93, 1.19) 1.39 (1.13, 1.72) 0.88 (0.69, 1.13)

K (0.07) 1.01 (0.94, 1.08) 1.06 (0.97, 1.17) 1.27 (1.07, 1.49) 0.90 (0.74, 1.09)

Si (0.03) 1.02 (0.99, 1.06) 1.05 (1.00, 1.10) 1.11 (1.02, 1.20) 0.98 (0.89, 1.08)

Zn (0.01) 1.03 (0.96, 1.11) 1.09 (0.98, 1.20) 1.33 (1.12, 1.58) 0.97 (0.79, 1.18)

*Hazard ratio and 95% confidence interval for an increase in PM 2.5 components equal to the interquartile range (IQR)

Source: A dapted from Ostro et al. ( 2011 )

Long

- term exposure to PM 2.5 components and sources and morbidity

In a study conducted in New York City, Patel et al. ( 2009 ) examined long

- term exposure to

PM 2.5 components (Ni, V, Zn, EC) and respiratory symptoms in children through 24 months of

age

. Positive associations were observed between Ni and wheeze, but not cough

. No other35 associations were observed between the other metals or EC and either wheeze or cough

. PM 2.5

mass w as not associated with wheeze and/or cough (see Section 2.1.3 for results on PM 2.5 mass ).

Several recent studies have examined the association between exposure to PM 2.5 components and

sources and birth outcomes, including birth weight and preterm birth

. Studies examining birth

weight and PM 2.5 components and sources found the strongest associati ons with metals/oil

combustion ( Bell et al., 2012 ; Darrow et al., 2011b ; Bell et al., 2010 ) and elemental

carbon/motor vehicles ( Wilhelm et al., 2012 ; Darrow et al., 2011b ; Bell et al., 2010 )

. Similarly,

when evaluating PM 2.5 components and preterm birth, the associations with metals, EC

, OC and

ammon ium nitrate were strongest ( Wilhelm et al., 2011 ; Darrow et al., 2009 )

. Several PM 2.5

sources were associated with preterm birth, including biom ass burning and diesel traffic

( Wilhelm et al., 2011 )

.

2.3.3. Toxicology Studies

– Source Apportionment and Fine PM Components

The 2009 PM ISA examined health effects associated with exposure to ambient PM components

and sources in animals. In vivo and in vitro studies reported a variety of sources and components

were linked with cardiopulmonary effects; however, there was insufficient evidence overall to

determine which sources or components were most closely related to the observed effects. Since

the completion of the 2009 PM ISA, a small number of animal toxicology studies have continued

to assess the role of PM sources and components on effects observed after exposure to PM 2.5

.

2.3.3.1. Toxicology Studies Comparing Ambient Fine PM Sources and

Components

Toxicology studies employing CAPs offer a relevant surrogate for atmospheric PM. Table 2.3

shows the endpoints that were associated with various source categories from rodents exposed to

CAPs from four locations. These three studies compare electrocardiogram ( ECG ) responses

during CAPs inhalation to PM 2.5 components associated with source factors ( Kamal et al., 2011 ;

Rohr et al., 2011 ; Chen et al., 2010 )

.

Chen et al. ( 2010 ) compared subchronic CAPs inhalation exposures from two locations in New

York, Sterling Forest (SF; undeveloped woodland park) and Manhattan in male hyperlipidemic

mice

. Using Manhattan CAPs ( mean CAPs concentration

, 122.9 ± 81.1 μg/m 3 )

, heart rate ( HR )

decreased with increased current day CAPs mass at all lags and several measures of heart rate

variability ( HRV ) increased with increased CAPs mass (i.e., standard deviation of the normal

- to

normal intervals, SDNN; root mean square of the standard deviation of the normal

- to

- normal

intervals

, r MSSD; and frequency domain indices, high

- frequency

, HF, low

- frequency

, LF, and

LF/HF ratio)

. Using SF CAPs ( mean CAPs concentration

, 133.3 ± 110.5 μg/m 3 )

, CAPs mass was

positively associated with HR, whereas HRV decreased with increased CAPs

. Using Manhattan

CAPs

, ECG changes were associated with components related to residual oil combustion > long

range transport > traffic > iron/steel > incineration > soil. Using SF CAPs

, ECG changes were

associated with long

- range transport > Ni refinery > soil > residual oil combustion/traffic. Chen

et al. ( 2010 ) also performed single

- element analysis and note that EC did not account for the36 acute ECG changes associated with PM 2.5 and that Ni may have an effect in Manhattan but not

SF.

Rohr et al. ( 2011 ) reported altered ECG responses in spontaneously hypertensive rats following

CAPs inhalation exposures from Detroit, Michigan over 13 consecutive days in both the summer

and winter. Source factors were identified using positive matrix factorization. In summer ( time

weighted average CAPs concentration

, 518 μg/m 3 )

, decreased HRV (SDNN) was associated with

cement/lime, iron/steel, and gasoline/diesel factors, and less so with sludge incineration. In

winter ( time weighted average CAPs concentration

, 357 μg/m 3 ) ; decreased HR was associated

with sludge incineration, cement/lime, and coal/secondary sulfate factors.

Kamal et al. ( 2011 ) also identified source factors (via positive matrix factorization) associated

with ECG alterations in hypertensive rats exposed for 13 days to CAPs (from Steubenville, OH ;

mean CAPs concentration 406 ± 266 μg/m 3 ). S tatistically s ignificant associations were found

between acute cardiac responses and PM components linked with incineration, metal processing,

mobile sources, and iron/steel production. The strength of the association with each source was

dependent upon wind direction; however, incineration was consistently found to be associated

with changes in HR and HRV. Several individual CAPs components were also associated with

cardiovascular responses, S, SO 2 , Pb, and oxides of nitrogen ( NO

x )

.37 Table 2

- 3 Concentrated A mbient P articles ( CAPs ): Sources and A ssociated E ndpoints

Source Category Elemental

Loading Endpoint

Affected Location Exposure

Duration References

Metal processing V, Cr, Ti, Mo,

La, Ce ↑ HR

↓ SDNN Steubenville, OH 13 days (s) Kamal et al. ( 2011 )

Incineration

(including sludge) Zn, Cd ↓ HR

↓ SDNN Steubenville, OH 13 days (s) Kamal et al. ( 2011 )

Zn, Ba, Mn,

Sr, Sb ↓ HR (w)

↓ SDNN (s) Detroit, MI 13 days (s & w) Rohr et al. ( 2011 )

Zn, Pb, Cu,

Fe ECG alterations Manhattan, NY 6 months Chen et al. ( 2010 )

Pb Pb, Cu ↓ HR Detroit, MI 13 days (s & w) Rohr et al. ( 2011 )

Iron/Steel

manufacturing Fe, Mn, Cu,

EC, Pb ↓ HR

↑ rMSSD Steubenville, OH 13 days (s) Kamal et al. ( 2011 )

Mn, Fe ECG alterations Manhattan, NY 6 months Chen et al. ( 2010 )

Fe, Mn, Cu ↑ rMSSD (w)

↓ SDNN (s) Detroit, MI 13 days (s & w) Rohr et al. ( 2011 )

Mobile/Traffic Fe, Sb, As, K,

CO ↓ SDNN

↑ rMSSD Steubenville, OH 13 days (s) Kamal et al. ( 2011 )

Fe, Ti, Zn ↓ SDNN (s)

↑ rMSSD (w) Detroit, MI 13 days (s & w) Rohr et al. ( 2011 )

EC, NO 2 , Si,

Fe, Cu ECG alterations Manhattan, NY 6 months Chen et al. ( 2010 )

Coal and Secondary

Sulfate S, Se, Al, V, P ↓ HR

↑ rMSSD Steubenville, OH 13 days (s) Kamal et al. ( 2011 )

S, Se ↓ HR (w)

↑ rMSSD (w) Detroit, MI 13 days (s & w) Rohr et al. ( 2011 )

Oil refinery La, Ce ↑ HR (w) Detroit, MI 13 days (s & w) Rohr et al. ( 2011 )

Cement/lime

processing Ca, Sr, Mg ↓ HR (w)

↓ SDNN (s) Detroit, MI 13 days (s & w) Rohr et al. ( 2011 )

Residual oil

combustion V, Ni, EC, Fe ECG alterations Manhattan, NY 6 months Che n et al. ( 2010 )

Ni

- refinery Cr, Ni ECG alterations Sterling Forest, NY 6 months Chen et al. ( 2010 )

Soil Al, Si, Ca, Fe ECG alterations Sterling Forest, NY

Manhattan, NY 6 months Chen et al. ( 2010 )

Long range transport S, Se, Br ECG alterations Sterling Forest, NY

Manhattan, NY 6 months Chen et al. ( 2010 )

(w) winter season, (s) summer season, HR: heart rate, SDNN: standard deviation of the normal

- to

- normal intervals, rMSSD: root

mean square of the standard deviation of the normal

- to

- normal intervals, Mo: molybdenum, La: lanthanum, Ce: cerium, Cd:

cadmium, Ba: barium, Sr: strontium, Sb: antimony, Cu: copper, CO: carbon monoxide, P: phosphorus38 Other studies have used regression and correlation approaches to estimate the relationship

between various PM components and sources with health effects. Happo et al. ( 2010b )

intratracheally instilled mice (10 mg/kg) with size

- segregated ambient PM samples collected in

six European cities over various seasons: Duisberg autumn, Prague winter, Amsterdam winter,

Helsinki spring, Barcelona spring, Athens summer. PM exposure (PM 10

- 2.5 and PM 2.5

- 0.2 )

increased bronc h oalveolar lavage fluid ( BALF ) total cell number and BALF protein

concentration. No formal source apportionment was conducted, but o xidized organic compounds

(e.g., dicarboxylic acids)

, transition metals (e.g., Fe and Cr), and source tracers for fuel oil

combustion ( i.e., Ni and V) were the most strongly correlated components of PM 2.5

- 0.2

contributing to the inflammatory response (i.e., BALF total cell number)

. These studies

measured response to PM 10

- 2.5 and PM 2.5

- 0.2 PM samples, and generally report stronger

inflammatory responses (e.g., BALF cytokines, cell number, and total protein) after exposure to

coarse PM compared to fine. Source tracers for soil (K +

, magnesium [ Mg 2+ ], Cu, manganese

[ Mn ]

, Fe) and sea spray (Na +

, chlorine [ Cl

- ], and NO 3 - ) found in PM 10

- 2.5 were the most strongly

correlated with inflammatory response.

A few studies discuss how seasonal variation in PM components may affect PM

- induced health

effects. Happo et al. ( 2010a ) intratracheally instilled mice (10 mg/kg) with size

- fractionated

ambient PM collected in Helsinki in the winter, spring, summer, and autumn. PM collected in the

spring produced the highest relative inflammatory activity (i.e., total cell number, total protein,

tissue necrosis factor alpha [ TNF

- α ]

, interleukin

- 6 [ IL

- 6 ]

, and keratinocyte

- derived chemokine in

BALF) when dose was adjusted to the PM per cubic meter of urban air, whereas the PM

collected in the autumn produced the highest inflammation per equal mass do s e

. This difference

was influenced by a greater PM mass concentration in urban air in the springtime. The overall

inflammatory activity of PM decreased with particle size, such that PM 10

- 2.5 and PM 2.5

- 1 had a

higher potency than PM 1

- 0.2 and PM 0.2

. Components of road dust (Ca 2+

, Fe, Mn, and Al) and

trace metals (presumed to be the result of non

- exhaust PM from traffic; Cu, Chromium [ Cr ]

,

cobalt [ Co ] ) were consistently correlated with BALF inflammatory response in PM 2.5

- 1

. Resuspension of road dust was also strongly correlated with inflammatory responses to PM 10

- 2.5

.

Farina et al. ( 2011 ) t reated mice (100 μg, intratracheal aerosolization) with size

- fractionated

ambient PM collected from Milano, Italy in summer and winter. A stronger inflammatory

activity was generally observed after administration of summer PM 10 and PM 2.5 than winter PM

.

PM 10 exposure resulted in a higher TNF

- α concentration (in BALF) compared to PM 2.5 , and this

was attributed to the greater endotoxin concentration and bacteria content of PM 10

.

Additional studies assess ed the differential responses of PM collected at different distances from

a highway. Cho et al. ( 2009 ) found similar composition in size

- fractionated ambient PM

collected near (20 m) and far (275 m) from a road in Raleigh, NC ; however, PM collected near

road was enriched with metals and a greater concentration of endotoxin

. Coarse PM samples

, but

not fine PM samples, produced pulmonary inflammation (i.e., BALF

, macrophage inflammatory

protein 2 [ MIP

- 2 ]

, TNF

- α, IL

- 6) in exposed mice (25 and 100 μg) irrespective of distance

collected from the road. Zhang et al. ( 2011 ) reported greater increase s in protein and lactate39 dehydrogenase [ LDH ] in BALF after instillation (7.5 mg/kg) of PM 2.5 collected near traffic

compared to far from traffic in Beijing, China. Chemical analysis of the near

- traffic PM revealed

higher concentrations of polycyclic aromatic hydrocarbons [ PAHs ] and heavy metal elements

( arsenic [ As ]

, Cd, Zn, S)

, but no statistical correlations were computed between these

components and the health effects observed

.

A number of studies have attempted to disentangle the role of PM and gaseous components in

the health effects associated with ambient air pollution exposure by removing PM from the

mixture using a high efficiency particle filter

. A few recent studies report cardiovascular,

respiratory, and reproductive effects after exposure to unfiltered (the whole mixture)

, but not

filtered Sao Paulo urban air (20 m from road) ( Pires et al., 2011 ; Matsumoto et al., 2010 ;

Akinaga et al., 2009 )

. These studies suggest that PM but not the gase ous components of the

urban air play a role in these responses.

2.3.3.2. Toxicology Studies Comparing Source

- Derived PM and Components

A number of studies attempt ed to characterize effects from ambient PM sources by exposing

animals in the laboratory to PM derived from potential ambient sources (e.g., coal combustion

,

diesel )

.

A series of studies evaluated the health effects resulting from various coal

- fired power plant

emissions scenarios ( Diaz et al., 2011 ; Godleski et al., 2011a ; Godleski et al., 2011c ; Godleski et

al., 2011b ; Lemos et al., 2011 ; Wellenius et al., 2011 )

. Stack emissions were collected from three

coal

- fired power plants and various atmospheric transformations (e.g., oxidation, reaction with α

pinene, neutralization) were simulated to investigate the toxicity of primary and photochemically

aged ( secondary ) particles. Particle mass concentrations varied from 43.8 to 257.1 μg/m 3 ( Kang

et al., 2011 )

. Rats were exposed to these simulated emissions scenarios for 6 hours and

demonstrated ( 1) increased BAL F total cells, macrophages, and neutrophils ( Godleski et al.,

2011a ) ; ( 2 ) moderately i ncreased heart and lung reactive oxygen species (measured by in vivo

chemilumi n escence) ( Lemos et al., 2011 )

, 3 ) i ncreased premature ventricular beat frequency

, but

no change in heart rate, HRV, or ECG intervals ( Wellenius et al., 2011 ) ; and 4 ) breathing pattern

changes ( Diaz et al., 2011 )

. Overall, specific PM components did not predict respiratory or

cardiovascular effects observed after PM exposure as well as simulated atmospheric

transformation scenarios.

Additionally, a few studies assessed respiratory, cardiovascular, and systemic effects following

exposure to filtered and unfiltered simulated downwind coal combustion emissions ( Barrett et

al., 2011 ; Mauderly et al., 2011 )

. Barrett et al. ( 2011 ) reported different respiratory effects after

exposure to fil tered and unfiltered emissions. Mauderly et al. ( 2011 ) found 17 out of 270 species

gender

- time

- outcome comparisons were affected by whole emissions and that PM participated in

only 3 responses (liver weight, serum K +

, and MIP

- 2). The authors concluded that PM

contributed to a few of the effects but that the pollutants responsible for the effects observed

were not able to be identified.40 Studies have also evaluated the role of PM in engine emissions on the progression of health

effects

. Tzamkiozis et al. ( 2010 ) instilled mice with PM collected from a gasoline Euro 3 car, a

diesel Euro 2 car, and a diesel Euro 4 car (with a diesel particle filter). Significant pulmonary

inflammation (i.e., BALF polymorphonuclear leukocytes ( PMN ) number) and injury (i.e., BALF

protein concentration) occurred 24 hours after treatment. The strongest associations with these

effects were observed for the PM components, P, Mn, Fe, Pb, reactive oxygen species ( ROS )

, benz( a )anthracene, chrysene, and medium and heavy PAHs. A strong association was also

observed between pulmonary injury and S.

A number of studies evaluated the impact of inhaled diesel exhaust on the cardiovascular system

with and without filtration ( Gordon et al., 2012 ; Lamb et al., 2012 ; Seilkop et al., 2012 ; Campen

et al., 2010 )

. Different cardiovascular effects were report ed after filtration of diesel exhaust by

Gordon et al. ( 2012 ) and Lamb et al. ( 2012 )

. Campen et al. ( 2010 ) found that filtration of PM

from diesel exhaust did not alter the vascular responses observed. Seilkop et al. ( 2012 ) ranked

components of diesel or gasoline exhaust, wood smoke, or simulated “downwind” coal emissions

by their ability to induce pro

- atherosclerotic responses in the aorta of mice that inhaled these

pollutant mixtures 6 hours/day for 50 days. Filtration of PM did not have a large effect on the

responses measured. Gases (i.e., SO 2 , ammonia ( NH 3 ), NO 2 , CO) ) were found to be most highly

predictive of the response indicators. These studies using filtration of PM from whole mixtures did not

consistently identify whether PM or gases from whole air pollution mixtures led to the cardiovascular,

respiratory, or reproductive effects observed.

Summary

The few epidemiologic studies that have been conducted since the completion of the 2009 PM

ISA continue to report health effects with a number of sources and components. Toxicological

studies have attempted to identify whether particular sources or components are responsible for

the health effects observed by comparing the health effects, primarily cardiopulmonary effects,

observed in response to exposures to ambient fine PM sources and components and source

derived PM and components. However, the toxicology studies did not find consistent evidence

that one source or component is most closely related to a specific health effect. Collectively these

studies continue to report that a variety of sources and components are linked with

cardiopulmonary effects and mortality; however, there is still insufficient evidence to determine

which sources or components are most closely related to the observed effects.41 

### 3. SUMMARY AND CONCLUSIONS

The new studies published since the completion of the 2009 PM ISA provide additional evidence

indicating a relationship between exposure to ambient PM and health effects. The new studies

provide important insights on the health effects of PM exposure, with the results continuing to

support a relationship between PM exposure and health effects at ambient concentrations similar

or lower than those observed in previous studies. Overall : (a) the new studies generally

strengthen the evidence that acute and chronic exposures to fine PM ; (b) although limited in

number, coarse PM studies provide evidence of an association with short

- exposures and pediatric

asthma ED visits, but no association between long

- term exposure and mortality ; ( c ) some of the

new epidemiologic studies report effects in areas with long

- term mean or mean 24

- h avg PM 2.5

concentrations lower than that reported in the 2009 PM ISA ; and ( d ) new toxicology and

epidemiologic studies continue to link various health outcomes with a range of fine PM sources

and components. In conclusion, the results of the new studies identified and described in this

provisional assessment does not materially change any of the broad scientific conclusions

regarding the health effects of PM exposure made in the 2009 PM ISA

.

In summary, this provisional assessment found:

Long

- term PM Exposure

• Mortality : Generally, the results of recent studies are consistent with the evidence for an

association between long

- term exposure to PM 2.5 and mortality (i.e., all

- cause and

cardiovascular) within the range of long

- term mean PM 2.5 concentrations characterized in the

2009 PM ISA (i.e., 13.2

– 32.0 μg/m 3 )

, with one new Canadian multi

- city study showing

associations at concentrations below 10 μg/m 3

. New studies provide additional evidence for

respiratory mortality, including lung cancer. T wo recent studies that examined associations

between long

- term PM 10

- 2.5 exposure and mortality do not observe an association in either

men or women.

• Cardiovascular morbidity: Recent studies continue to demonstrate the strongest

cardiovascular effects in women, specifically for stroke, incident MI, and incident

hypertension at long

- term mean PM 2.5 concentrations ranging from 9.7

– 21.5 μg/m 3

.

• Respiratory morbidity: R ecent studies provide additional evidence for respiratory

symptoms and incident asthma, as well as respiratory hospitalizations at long

- term mean

PM 2.5 concentrations ranging from 9.7

– 27.0 μg/m 3

, which is consistent with the conclusions

of the 2009 PM ISA.

• Reproductive and Developmental Outcomes: Recent studies continue to provide evidence

for developmental outcomes, specifically reductions in birth weight

, at long

- term mean PM 2.542 concentrations ranging from 11.0 – 19.8 μg/m 3

, which further support the conclusions of the

2009 PM ISA

.

Short

- Term PM Exposure

• Mortality: The limited numberof mortality studies conducted in the U.S. and Canada

further support the conclusions of the 2009 PM ISA and continue to demonstrate associations

between short

- term PM 2.5 exposure and mortality at mean 24-h average concentrations

greater than 12.8 μg/m 3

. Since the completion of the 2009 PM ISA no new studies have been

conducted that examined associations between short- term exposure to PM 10

- 2.5 and mortality.

• Respiratory hospital admissions/ED visits : New m ulti

- city and single- city studies

demonstrate consistent positive associations for all respiratory

- related hospital

admi ssions/ ED visits, and provide additional evidence for increase s in asthma hospital

admissions/ ED visits in areas with mean 24-h average PM 2.5 concentrations ranging from6.7

– 22.0 μg/m 3

, which further supports the conclusions of the 2009 PM ISA . One new study

was identified that examined the association between short- term PM 10

- 2.5 exposure and

respiratory

- related ED visits , and provided evidence of increases in pediatric asthma ED

visits.

• C ardio vascular hospital admissions/ED visits: New studies focusing primarily on all

cardiovascular hospital admissions/ED visits continue to demonstrate consistent positive

associations in areas with mean 24-h average PM 2.5 concentrations ranging from 6.7 – 15.3

μg/m 3 . Additionally, there is new evidence forpotential associations with hypertension ED

visits, and a new study demonstrating an association with stroke onset.

Health Effects Related to Sources or Components of PM

• Consistent with those studies evaluated in the 2009 PM ISA, new studies continue to

demonstrate cardiovascularand mortality effects with sources and components related to a

number of combustion activities (e.g., motor vehicle emissions, coal combustion, oil burning,

power plants, and wood smoke/vegetative burning), crustal sources, and secondary sulfate

.

Additional new studies also add to the limited number of studies that have examined

associations between sources and components and respiratory and birth outcome effects, as

well as, long- term exposure and mortality. Overall, new studies support the conclusions of

the 2009 PM ISA that many PM components can be linked with differing health effects and

the evidence is not yet sufficient to allow differentiation of those components or sources that

are more closely related to specific health outcomes.43 

### Appendix A Studies Included in the PM Provisional Science Assessment

Ta b l e A

- 1 C h ar act e r i zat i o n of s t u di e s of L ong

- t e r m E xp o su r e to PM 2. 5 an d M or t a li t y

A u t h o r Y ear s

o f

Stu d y L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r act i o

n L o n g

- t e rm

M ean

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

C r ous e

et al

. ( 201 2 ) 199 1

-

200 1 C an ada

( nat i o n

w i de) A ll

- C a us e,

CV D, I HD

M or t al i t y N on

- i m m i gr a nt

C an adi an a dul t s PM 2 .5 8. 7 M ax : 1 9. 2

G an

et al

. ( 201 1 ) A Q:

199 4

-

199 8;

D eat hs :

199 9

-

200 2 V anc o uv er

, BC

C an ada CHD

M or t al i t y Ad ul t s ( 45

- 85)

w i t ho ut k no w n

C H D at bas el i n e PM 2 .5 4. 08 M ax : 1 0. 24

G r ev en

et al

. ( 201 1 ) 200 0

-

200 6 U .S

. ( nat i o n

w i de) A ll

- C a us e M edi c ar e

r ec i pi ent s

(6 5 + y rs) PM 2 .5 13. 0 75t h: 14. 7

H ar t et

al

. ( 201 0 ) A Q:

200 0

D eat hs :

198 5

-

200 0 U .S

. ( nat i o n

w i de) A ll

- C a us e,

Lun g C a nc er

, CV D

D i s eas e,

I HD,

R es pi r at or y

D i s eas e,

CO P D

M or t al i t y A dul t m al es f r om

4 U

. S. t ru cki n g

c om pa ni es

PM 2 .5 14. 1 NR

J er r et t et

al

. ( 200 9b ) 199 2

-

200 2 T or ont o,

C an ada A ll

- C a us e,

C i r c ul at or y

M or t al i t y Ad u l t s f ro m

r es pi r at or y c l i n i c PM 2 .5 8. 71 75t h: 8. 83

J er r et t et

al

. ( 200 9a ) A Q:

199 9

-

200 0

D eat hs :

198 2

-

200 0 U .S

. ( nat i o n

w i de;

86 MSAs) A ll

- C a us e,

C ar di o

pul m onar y

, CV D, I HD,

R es pi r at or y A dul t s

PM 2 .5 14. 3 NR

Lep eul e

et al

. ( 201 2 ) 197 4

-

200 9 U

. S (6 c it ie s

i n E as t and

Mi d w e st ) A ll Ca u s e

, C V D an d

Lun g C a nc er

M or t al i t y A dul t s

PM 2 .5 15. 9

(si x ci t i e s

c om bi ned) ;

m eans f or

i ndi v i d ual

c i t i es r an ged

f ro m

11. 4

- 2 3. 6 NR44 A u t h o r Y ear s

o f

Stu d y L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r act i o

n L o n g

- t e rm

M ean

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

Li ps et t et

al

. ( 201 1 ) A Q:

199 9

-

200 5;

D eat hs :

199 5

-

200 5 C al i f or ni a A ll

- C a us e,

CV D,

R es pi r at or y

, Lun g C a nc er

, I HD, CB D A dul t s

( F em al e

t eac her s ) PM 2 .5 15. 64 M ax : 2 8. 35

McKe a n

C o w d en

et al

. ( 200 9 ) AQ :

197 9

-

198 3;

199 9

-

200 0;

D eat hs :

198 2

-

200 0 U .S

. ( nat i o n

w i de) B r ai n C anc er

M or t al i t y A dul t s

PM 2 .5 197 9

- 19 83:

21. 1

199 9

- 20 00:

14. 0

Avg :

17. 7 M a x:

197 9

- 19 83:

30. 0

199 9

- 20 00:

22. 2

Avg :

23. 6

O st ro

et al

. ( 201 0 ) A Q:

200 2

-

200 7 C al i f or ni a A ll

- C a us e,

CP D, I HD

M or t al i t y A dul t s

( F em al e

t eac her s ) PM 2 .5

and

c om po n

ent s

(EC

, OC

, SO 4 , NO 3 , Fe , K

, S i

, Z n) 17. 0 M ax : 3 4. 7

P uet t

et al

. ( 200 9 ) 199 2

-

200 2 U

. S. (Ea st

and

Mi d w e st ) A ll Ca u s e

and C H D

M or t al i t y A dul t s

(F e ma l e N u rse s) PM 2 .5 13. 9 75t h : 15. 6

M ax : 2 7. 6

P uet t

et al

. ( 201 1 ) 198 6

-

200 2 U

. S. (Ea st

and

Mi d w e st ) A ll Ca u s e

and C H D

M or t al i t y A dul t s

( M al e H e al t h

Pro f e ssi o n a l s) PM 2 .5 17. 8

( at bas el i ne) NR

CV D: Car di ov as c ul ar Di s eas e, CH D: Cor o nar y Hea r t Di s eas e; IHD: I s c hem i c Hear t Di s eas e; CO P D: C hr oni c O bs tr uc ti v e P ul m onar y

Di s eas e; CB D: C er ebr ov as c ul ar D i s eas e; NR: Not r epor ted45 Ta b l e A

- 2 C h ar act e r i zat i o n of St ud i e s of L ong

- t e r m Ex pos u r e to PM 10

- 2. 5 an d M o r ta l i ty

A u t h o r Y ear s

o f

Stu d y L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r act i o n L o n g

- t er m M e an

C o n c e n t r a t i o n

( μg / m 3 ) U p p er P er c en t i l e

C o n c e n t r a t i o n s

( μg / m 3 )

P uet t et

al

. ( 200 9 ) 199 2

-

200 2 U

. S. (Ea st

and

Mi d w e st ) A ll

- C a us e

and C HD

M or t al i t y A dul t s

( F em al e

N u rse s) PM 10

- 2 .5 7. 7 75t h : 9. 2

M ax : 2 6. 9

P uet t et

al

. ( 201 1 ) 198 6

-

200 2 U

. S. (Ea st

and

Mi d w e st ) A ll

- C a us e

and C H D

M or t al i t y A dul t s

(Ma l e H e al t h

Pro f e ssi o n a l s) PM 10

- 2 .5 10. 1 ( at bas el i ne) NR

CHD: Co r ona r y Hear t Di s eas e; N R: Not r e por ted

Ta b l e A

- 3 C h ar act e r i zat i o n of St ud i e s of L ong

- t e r m Ex pos u r e to PM 2. 5 an d C a r d i o vascu l ar E f fe c ts

A u t h o r Stu d y

Y ear s L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r act i o n L o n g

- t e rm

M ean

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

P uet t et al

. ( 201 1 ) 198 9

-

200 3 N or t h

- e as t

and

Mi d w e st

, U .S .* A ll

- c aus e

M or t al i t y

,

N o n fa ta l M I,

F a t a l CHD,

and

H e mo rrh a g i c

and I s c hem i c

St ro ke H eal t h

Pro f e ssi o n a l s

F o llo w

- U p

S t ud y

M en, 40

- 7 5 yr s

of age PM 2 .5 , PM 10

- 2 .5 P r edi c t e d

PM 2 .5 =

17. 8 ± 3. 4

P r edi c t e d

PM 10

- 2 .5 =

10. 1 ± 3. 3 I nt er

- quar t i l e

r ang e ( I Q R ) :

PM 2 .5 :

4. 3

PM 10

- 2 .5 :

4. 3

Li ps et t et al

. ( 201 1 ) 199 5

-

200 0 C al i f or ni a A ll Ca u s e

M or t al i t y

,

CV D M o r t a lit y

,

I HD M o r t a lit y

,

C er e br o

va scu l a r

D i s eas e

M or t al i t y

,

M I I nc i denc e,

St ro ke

I nc i de nc e C al i f or ni a

T eac her s

S t ud y

N

= 124, 6 14

W om en,

20

- > 80 y r s 15. 64 M ax : 2 8. 35

C oo gan

et al

. ( 2012 ) 199 5

-

200 5 Los

A nge l es

, CA H y per t e ns i o n

and D i ab et es

M e llit u s

( i nc i d enc e) Bl a ck W o me n ’ s

H eal t h S t ud y

N

= 420 4

( H y per

- t en s i on)

N

- 32 36

( D i ab et es )

D i s eas e f r ee

at bas el i n e PM 2 .5 20. 7 75 th : 21. 646 A u t h o r Stu d y

Y ear s L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r act i o n L o n g

- t e rm

M ean

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

Be cke rma n

et al

. ( 2012 ) 199 2

-

199 9 T or ont o,

O nt ar i o I HD

( pr ev al enc e) N

= 236 0

P ul m o nar y

C l i n i c pat i ent s PM 2 .5 50t h

per c e nt i l e:

8. 71 75t h: 8. 83

A dar et al

. ( 201 0 ) 200 2

-

200 3 6 U S

Cit ie s * * Re t in a l

Mi cro

v as c ul at ur e MESA,

N

= 4, 607

46

- 8 7 y ear s

,

No c lin ic a l

c ar di o -va scu l a r

di s e as e at

bas e l i n e

PM 2 .5 16 ( ± 3) 75t h:

17. 2

P er s on al

PM

pr ed i c t i on:

17. 2;

N ear es t

mo n i t o r PM:

17. 3

M a x:

P er s on al

PM

pr ed i c t i on:

26. 3;

N ear es t

mo n i t o r PM:

25. 4

O ' Ne ill e t al

. ( 201 1 ) 200 0

-

200 2 6 U S

Cit e s ** Art e ri a l

S ti ffn e s s MESA

N

= 3, 996

M en an d

W om en, 44

- 84

yr s PM 2 .5 I m put ed

20 y r av g:

21. 47

± 5. 00

16. 80

± 3. 90

( 200 5)

V an H e e et

al

. ( 201 1 ) Ju l y

200 0

-

A ug

200 2 6 U S

Cit e s ** Ve n t ri cu l a r

C on duc t i o n

and

R ep ol ar i z at i o n

A bnor m al i t i es MESA

N

= 4, 783

45 t o 84 y r s PM 2 .5

K l oo g et al

. ( 201 2a ) 200 0

-

200 6 N e w

E ngl and H os pi t al

Ad mi ssi o n s ≥ 65 y e ar s PM 2 .5 (p re

di c t ed) 9. 65 17. 7947 Ta b l e A

- 4 C h ar act e r i zat i o n of St ud i e s of L ong

- t e r m Ex pos u r e to PM 2. 5 an d R esp i r at o r y E f f ect s

A u t h o r Y ear s

o f

Stu d y L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r ac

ti o n L o n g

t e rm

M ean

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

N oo nan et al

. ( 201 2 ) 200 3

-

200 9 L i bby

, M T R es pi r at or y

i nf ec t i o ns

( i nc l u di ng

br onc hi t i s ) PM 2 .5 19. 0

-

27. 0 NR

B hat t ac har y y a

( 200 9 ) 199 7

-

200 6 US ( Na t io n

w i de) H a y F ev er an d

S in u s it is N at i o nal H eal t h

I nt er v i e w

Su rve y

r es po nde nt s PM 2 .5 13. 4

-

11. 6 NR

B hat t ac har y y a

and S h ap i r o

( 201 0 ) 199 7

-

200 6 US ( Na t io n

w i de) E ar I nf ec t i ons N at i o nal H eal t h

I nt er v i e w

Su rve y

r es po nde nt s PM 2 .5 13. 4

-

11. 6 NR

P at el et al

. ( 200 9 ) 199 8

-

200 6 NY C, NY W heez e a nd

C ou gh P ar t i c i p ant s i n

C ol um bi a

C ent er f or

C hi l dr e n’ s

E nv i r o nm ent a l

H eal t h bi r t h

c ohor t PM 2 .5 13. 0 M ax : 3 8. 4

P ar k er et al

. ( 200 9 ) 199 9

-

200 5 US ( Na t io n

w i de) R es pi r at or y

A lle r g ie s C hi l dr e n ( ages

3

- 17) i n

N at i o nal H eal t h

I nt er v i e w

Su rve y PM 2 .5 13. 1 75 th : 15. 2

N ac hm an an d

Pa rke r ( 20 12 ) 200 2

-

200 5 US ( Na t io n

w i de) Ast h ma

, si n u si t i s,

c hr on i c br onc hi t i s N at i o nal H eal t h

I nt er v i e w

Su rve y

r es po nde nt s PM 2 .5 12. 1 75 th : 14. 4

M ax : 2 7. 5

K ar r et al

. ( 200 9a ) 199 7

-

200 3 P uget

S oun d

R egi on, W A Bro n ch i o l i t i s

hos p i t al

adm i s s i on W as hi n gt on

S t at e B i r t h

Eve n t s R e g i st ry

D at ab as e PM 2 .5 12. 0 75t h: 14. 0

M ax : 3 6. 9

K ar r et al

. ( 200 9b ) 199 9

-

200 3 G eor gi a A i r

B as i n of

B C,

C an ada I npat i e nt or

out pat i ent

br onc hi o l i t i s I nf ant s bor n

bet w e en 1 999

-

200 2 PM 2 .5 5. 8 M ax : 1 2. 0

K l oo g et al

. ( 201 2a ) 200 0

-

200 6 N e w

E ngl and R es pi r at or y

hos p i t al

adm i s s i on R es i d ent s

≥ 65 ye a r s PM 2 .5 9. 7 75t h: 10. 1

M ax : 1 7. 848 A u t h o r Y ear s

o f

Stu d y L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r ac

ti o n L o n g

t e rm

M ean

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

N eu pan e et al

. ( 201 0 ) 200 3

-

200 5 Ha m ilt o n

, ON

, C an ada P neum oni a

hos p i t al

adm i s s i ons R es i d ent s

≥ 65 ye a r s PM 2 .5 10. 7 75t h: 11 3

95t h: 12. 4

M ax : 1 3. 0

M eng et al

. ( 201 0 ) 200 0

-

200 1 S an

J oaq ui n

V a ll e y

, CA Ast h ma

S y mp t o ms;

Ast h ma ED vi si t s

or

H os pi t al i z at i on s S an J oa qu i n

V al l e y r es i d ent s

par t i c i pat i n g i n

200 1 C al i f or n i a

H eal t h

I nt er v i e w

Su rve y ) PM 2 .5 21. 4 75t h: 23. 5

A k i nb am i et al

. ( 201 0 ) 200 1

-

200 4 US ( Na t io n

w i de) Ast h ma

pr ev a l enc e C hi l dr e n ( ages

3

- 17) i n

N at i o nal H eal t h

I nt er v i e w

Su rve y PM 2 .5 13. 3 75t h: 15. 7

C ar l s t e n et al

. ( 201 1 ) 199 5

-

200 3 V anc o uv er

, B C,

C an ada I nc i de nt A s t hm a B i r t h c ohor t

bor n i n 19 95 PM 2 .5 5. 6 NR

C l ar k et al

. ( 201 0 ) 199 9

-

200 4 S out h

w e s t er n

B C,

C an ada I nc i de nt Ast h ma C hi l dr e n bor n i n

199 9 an d 20 00

and f ol l o w e d u p

t o 3

- 4 yr s PM 2 .5 5. 6 75t h: 6. 1

M c C on nel l et al

. ( 201 0 ) 200 2

-

200 6 S out her n

C al i f or ni a I nc i de nt A s t hm a K i nd er gar t e n

and F i r s t gr ad e

c hi l dr en i n

S out her n

C al i f or ni a

C hi l dr e n’ s

H eal t h S t ud y PM 2 .5 13. 9 M ax : 1 7. 449 Ta b l e A

- 5 C h ar act e r i zat i o n of St ud i e s of L ong

- t e r m Ex pos u r e to PM 2. 5 a nd R ep r o d u ct i ve a nd

D evel o p men t a l E f fe c ts

A u t h o r Y ear s

o f

Stu d y L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r ac

ti o n L o n g

- t e rm

M ean C o n cen

tr a ti o n (μ g / m 3 ) Up p e r

P er c en t i l e

C o n cen

- t r at i o n s

( μg / m 3 )

Lee et al

. ( 201 1 ) 199 7

-

200 1 PA C

- r eac t i v e

pr ot ei n H eal t h y

w om en PM 2 .5 16. 4 75t h: 18. 7

95t h: 26. 2

100t h: 4 0. 8

Legr o

et al

. ( 201 0 ) 200 0

-

200 7 N or t h

eas t er n

U. S

. I n V i t r o

F e r t iliz a t io n

(I VF )

su cce ss W om en

und er go i n g

I VF PM 2 .5 14. 0

- 1 4. 5 NR

V i ni k oor

I ml e r

et al

. ( 201 2 ) 200 0

-

200 3 NC G es t at i ona l

H y per

t ens i o n A l l bi r t hs i n

NC PM 2 .5 14. 5 75t h: 15. 7

Ric h

et al

. ( 200 9 ) 199 9

-

200 3 NJ F et al G r o w t h A l l bi r t hs i n

NJ PM 2 .5 13. 8 NR

C ha ng

et al

. ( 201 2b ) 200 1

-

200 5 NC Pre -t e rm

b i rt h (PT B) A l l bi r t hs i n

NC PM 2 .5 13. 0

- 1 5. 3 NR

D a rro w

et al

. ( 200 9 ) 199 4

-

200 4 A t l ant a,

GA PT B A ll b ir t h s i n

A t l ant a

(5 c ount i es ) PM 2 .5 16. 5 M ax : 3 4. 1

R udr a

et al

. ( 201 1 ) 199 6

-

200 6 W es t er n

WA PT B H eal t h y

W om en PM 2 .5 10. 0 75t h: 12. 7

100t h: 1 7. 2

W ilh e lm

et al

. ( 201 1 ) 200 4

-

200 6 Los

A nge l es

, CA PT B A l l bi r t hs i n

LA c ount y PM 2 .5 18. 0 NR

M ar s hal l

et al

. ( 201 0 ) 199 8

-

200 3 NJ Bi rt h D e f e ct s

(O ra l Cle f t s ) A l l bi r t hs i n

NJ PM 2 .5 13. 4 NR

B el l et al

. ( 201 2 ) 200 0

-

200 4 C T and

MA Bi rt h w e i ght

(BW ) Al l b i rt h s f ro m

5 c ount i es PM 2 .5 14. 0 75t h: 16. 0

B el l et al

. ( 201 0 ) 200 0

-

200 4 C T and

MA BW Al l b i rt h s f ro m

5 c ount i es PM 2 .5 14. 0 NR

D a rro w

et al

. ( 201 1b ) 199 4

-

200 4 A t l ant a,

GA BW A l l bi r t hs i n

A t l ant a

(5 c ount i es ) PM 2 .5 16. 5 NR50 A u t h o r Y ear s

o f

Stu d y L o c a t i o n O u t c o m e P o p u l a t i o n Si ze

F r ac

ti o n L o n g

- t e rm

M ean C o n cen

tr a ti o n (μ g / m 3 ) Up p e r

P er c en t i l e

C o n cen

- t r at i o n s

( μg / m 3 )

G hos h

et al

. ( 201 2 ) 199 5

-

200 6 Los

A nge l es

, CA BW A l l bi r t hs i n

LA c ount y PM 2 .5 19. 8 NR

K l oo g

et al

. ( 201 2b ) 200 0

-

200 8 MA B W

, PT B A l l bi r t hs i n

MA PM 2 .5 9. 6 75t h: 11. 6

Ku ma r

( 201 2 ) 200 0

-

200 4 C hi c a go,

IL BW Al l b i rt h s f ro m

C hi c a go

MSA PM 2 .5 18. 0 NR

M or el l o

F ro sch

et al

. ( 201 0 ) 199 6

-

200 6 CA BW A l l bi r t hs i n

CA PM 2 .5 16. 7 75t h: 21. 0

S al i hu

et al

. ( I n

Pre ss ) 200 0

-

200 7 T am pa,

F L B W

, PT B W om en

par t i c i pat i n g

i n H e al t h

St a rt Pro j e ct PM 2 .5 11. 0 M ax : 2 3. 2

W ilh e lm

et al

. ( 201 2 ) 200 4

-

200 6 Los

A nge l es

, CA BW A l l bi r t hs i n

LA c ount y PM 2 .5 17. 9 NR

F ai z

et al

. ( 201 2 ) 199 8

-

200 4 NJ S t illb ir t h A l l bi r t hs i n

NJ PM 2 .5 14. 0 NR51 Ta b l e A

- 6 C h ar act e r i zat i o n o f U

. S

. a nd C a na dia n St ud ie s of Sh or t -t e r m Ex p os u r e t o PM 2. 5 a nd

M o rta l i ty

A u t h o r Y ear s L o c a t i o n Mo r ta l i ty P o p u l a t i o n Si ze

F r act i o n M ean

24 -h a vg

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

Ito e t a l

. ( 201 1a ) 200 0

-

200 6 N e w Yo rk,

NY C ar di o

v as c ul ar ≥ 40 PM 2 .5 ,

PM

c om po nent s

( E C , OC

, SO 4 , N i , V

, Zn , S i , S e

, N a

, Br,

NO 3 ) PM 2 .5

A ll -Ye a r:

14. 4

W a rm

(Ap ri l

- S ept ) :

14. 8

C ol d

(O ct -Ma r):

14. 1 NR

Z hou

et al

. ( 201 1 ) 200 0

-

200 4 D e tr o i t, M I

S eat t l e,

WA N on

ac c i d ent al

,

C ar di o

va scu l a r,

R es pi r at or

y A ll PM 2 .5 ,

PM

c om po nent s

(Al

, F e

, K,

Na

, Ni, S

, Si

, V, Z n

, E C) D et r oi t

A ll -Ye a r

( M edi a n) :

13. 2

W a rm

(Ap ri l

S ept em b er )

( M ean) :

15. 3

C ol d

(O ct o b er

Ma rch )

( M ean) :

14. 9

S eat t l e

A ll -Ye a r

( M edi a n) :

7. 9

W a rm

(Ap ri l

S ept em b er )

( M ean) :

8. 0

C ol d

( O c t ober

Ma rch )

( M ean) :

11. 4 D et r oi t

M ax : 6 5. 8

S eat t l e

M ax : 4 1. 352 A u t h o r Y ear s L o c a t i o n Mo r ta l i ty P o p u l a t i o n Si ze

F r act i o n M ean

24 -h a vg

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

C ha ng et

al

. ( 201 2a ) 200 1

-

200 5 N e w Yo rk,

NY C ar di o

v as c ul ar

,

R es pi r at or y ≥ 65 PM 2 .5 S pr i n g

(Ma rch

M a y ) : 14. 3

Su mme r

( J une

- A ug) :

17. 5

F al l ( S ept

N ov ) : 13. 3

W i nt er

( D ec

- F eb) :

15. 4 NR

Kl e mm e t

al

. ( 201 1 ) 19 98

-

200 7 A t l ant a,

G A (4

c ount i es ) N on

ac c i d ent al

,

C ar di o

va scu l a r,

R es pi r at or y ≥ 65 PM 2 .5 , PM

c om po nent s

( E C , OC

, NO 3 , SO 4 ) 17. 0 75t h: 21. 6

M ax : 7 2. 9

Ta b l e A

- 7 C h ar act e r i zat i o n o f U

. S

. an d C a n ad i a n S t u d i es o f Sh or t -t e r m Ex p os u r e t o PM 2. 5 a nd

R esp i r a t o r y H o sp i t a l A d mi ss i o n s an d E mer g en cy D ep a r t men t V i si t s

A u t h o r Y ear s L o c a t i o n H o sp i t al

A d m is s ion /E D

V is it P o p u l

at i o n Si ze

F r act i o n M ean

24 -h a vg

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

B el l et al

. ( 201 2 ) 200 0

-

200 5 187 U

. S

.

c ount i es H os pi t al

adm i s s i ons :

A l l r es pi r at or y ≥ 65 PM 2 .5 , PM

c om po nent s A ll -Ye a r:

14. 0

Su mme r:

16. 2

W i nt er : 13. 9 M a x:

Al l Ye a r:

26. 0

Su mme r:

28. 5

W i nt er : 32. 8

Z anob et t i

et al

. ( 200 9 ) 200 0

-

200 3 26 U .S

.

c om m uni t i es ED Vi si t s:

A l l r es pi r at or y ≥ 65 PM 2 .5 , PM

c om po nent s

(As, Al

, Br,

C r , Fe , P b

, M n , N i , K , S i

, V , Zn , N O3

, S O4 , N H 4

, Na + , E C , OC ) 15. 3 PM 2 .5 M ax

S pr i n g:

24

(R i ve rsi d e

, CA )

PM 2 .5 M a x

W i nt er :

29. 9

( F r es no,

CA )53 A u t h o r Y ear s L o c a t i o n H o sp i t al

A d m is s ion /E D

V is it P o p u l

at i o n Si ze

F r act i o n M ean

24 -h a vg

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

S t i eb et al

. ( 200 9 ) 199 2

-

200 3 7 C an adi an

c it ie s ED Vi si t s:

Ast h ma

CO P D

R es pi r at or y

I nf ec t i on A ll PM 2 .5 M ont r ea l

( 1/ 97

- 12/ 02) : 8. 6

Otta w a

( 4/ 92

- 12/ 00) : 6. 7

E dm ont o n

( 4/ 92

- 3/ 0 2) :

8. 5

Ha lif a x ( 1/ 99

- 12/ 02) : 9. 8

T or ont o

( 4/ 99

- 6/ 0 3) :

9. 1

V anc o uv er

( 1/ 99

- 2/ 0 3) :

6. 8 75t h:

M ont r ea l :

10. 9

Otta w a :

8. 7

E dm ont o n:

10. 9

Ha lif a x : 1 1

. 3

T or ont o:

11. 9

V anc o uv er :

8. 5

Lev y et al

. ( 201 2 ) 200 0

-

200 8 119 U

. S

.

c ount i es H os pi t al

Ad mi ssi o n s:

A l l r es pi r at or y ≥ 65 PM

c om po nent s

( E C , OC

, S O4 , N O3 ) --- ---

D a rro w

et al

. ( 201 1a ) 199 3

-

200 4

(PM 2 .5

c ol l ec t ed

f ro m

8/ 1/ 98

- 12/ 31/ 0 4) A tl a n ta , GA ED Vi si t s:

A l l r es pi r at or y A ll PM 2 .5 1

- h m a x : 29

24

- h av g:

16

C om m ut e:

17

Da y

- ti m e :

15

N i ght

- ti m e :

17 1

- h m a x:

75t h: 36

M ax : 1 88

24

- h av g:

75t h: 21

M a x: 7 2

C om m ut e:

75t h: 21

M a x: 7 6

Da y

- t i m e:

75t h: 19

M ax : 7 1

N i ght

- t i m e:

75t h: 14

M a x: 8 854 A u t h o r Y ear s L o c a t i o n H o sp i t al

A d m is s ion /E D

V is it P o p u l

at i o n Si ze

F r act i o n M ean

24 -h a vg

C o n cen

tr a ti o n

( μg / m 3 ) Up p e r

P er c en t i l e

C o n cen

t r at i o n s

( μg / m 3 )

St ri ckl a n d

et al

. ( 201 0 ) 199 3

-

200 4

(PM 2 .5

c ol l ec t ed

f ro m

8/ 1/ 98

- 12/ 31/ 0 4) A tl a n ta , GA ED Vi si t s:

Ast h ma 5

- 17 PM 2 .5 , PM

c om po nent s

(SO 4 , E C

, OC , w a te r

s ol u bl e

m et al s ) PM 2 .5

A ll -Ye a r:

16. 4

W ar m

(Ma y -O ct ):

18. 4

C ol d

( N ov -Ap r):

14. 3

PM 10

- 2 .5

A ll -Ye a r:

9. 0

W ar m : 9. 7

C ol d: 8. 3 NR

Ki m e t al

. ( 201 1 ) 200 3

-

200 7 D env er

, C O H os pi t al

Ad mi ssi o n s:

A l l r es pi r at or y

CO P D

Ast h ma

P neum oni a A ll PM 2 .5 , PM

c om po nent s

( E C , OC

, SO 4 , NO 3 ) 8. 0 59. 4

M ar et al

. ( 201 0 ) 199 8

-

200 2 T ac om a, W A ED Vi si t s:

Ast h ma A ll PM 2 .5 12. 3 NR

K l oo g

et al

. ( 201 2a ) 200 0

-

200 6 N e w E n gl a nd H os pi t al

Ad mi ssi o n s:

A l l r es pi r at or y ≥ 65

PM 2 .5 9. 6 M ax : 7 2. 6

Li et al

. ( 201 1 ) 200 4

-

200 6 D e tr o i t, M I ED Vi si t s:

Ast h ma 2

- 18

PM 2 .5 15. 0 75t h: 18. 5

M ax : 6 9. 0

G l ad et al

. ( 201 2 ) 200 2

-

200 5 P i t t s bur gh,

PA ED Vi si t s:

Ast h ma A ll

PM 2 .5 13. 3 M ax : 5 5. 0

G ri n e ski

et al

. ( 201 1 ) 200 0

-

200 3 El Pa so

, T X H os pi t al

Ad mi ssi o n s:

Ast h ma

A c ut e br onc hi t i s ≥ 1

PM 2 .5 12. 8 75t h: 15. 6

95t h: 26. 6

M ax : 1 19. 155 Ta b l e A

- 8 C h ar act e r i zat i o n o f U

. S

. an d C a n ad i a n S t u d i es o f Sh or t -t er m E xp o su r e t o P M 10

- 2. 5 an d R esp i r at o r y H o sp i t al A d m i ssi o n s an d

E me r g en cy D ep a r t men t V i s i t s

A u t h o r Y ear s L o c a t i o n H o sp i t al

A d m i s si o n s

/ ED V is it s P o p u l a t i o n S i z e F r act i o n M ean 24

- h a v g

C o n c e n t r a t i o n

( μg / m 3 ) U p p er P er c en t i l e

C o n c e n t r a t i o n s

( μg / m 3 )

S t r i c k l an d et al

. ( 201 0 ) 199 3

- 20 04

(PM 2. 5 c ol l ec t ed

f r om 8/ 1/ 98

- 12/ 31/ 0 4) A tl a n ta , GA E D V is it s :

Ast h ma 5

- 17 PM 10

- 2 .5 PM 10

- 2 .5

A ll

- Y e ar : 9. 0

W ar m : 9. 7

C ol d: 8. 3 NR

Ta b l e A

- 9 C h ar act e r i zat i o n o f U

. S

. an d C a n ad i a n S t u d i es o f Sh or t -t e r m Ex p os u r e t o PM 2. 5 an d C ar d i o vascu l a r H o sp i t a l A d mi ss i o n s an d

E me r g en cy D ep a r t men t V i s i t s

A u t h o r Stu d y Ye a r s L o c a t i o n O u t c o m e P o p u l a t i o n S i z e F r act i o n M ean 24

- h a v g

C o n c e n t r a t i o n ( μ g / m 3 ) U p p er P er c en t i l e

C o n c e n t r a t i o n s ( μ g / m 3 )

Z anob et t i et al

. ( 200 9 ) 200 0

- 20 03 U .S

. ( 26

c om m uni t i es ) ED Vi si t s:

M I

, CHF O l der ad ul t s

≥ 65 y r s PM 2 .5

PM 2. 5

c om po nent s :

As, Al

, Br, C r,

F e, P b, M n, N i

, K, Si

, V, Z n

, NO 3 , SO 4 , NH4

, Na + , E C , OC 15. 3 PM 2. 5 M ax S pr i ng:

24

(R i ve rsi d e

, C A)

PM 2 .5 M ax W i nt er :

29. 9

(F re sn o

, C A)

S t i eb et al

. ( 200 9 ) 199 0’ s

ear l y 2 000s

( dep end i n g

on c i t y ) C an ada

( 7 Cit ie s ) ED Vi si t s:

A ngi na/ M I

,

H ear t F ai l ur e,

D ys r h yt h m i a PM 2 .5 Cit y

- s pec i f i c m eans

( r ang e) :

6. 7

- 9. 8 Cit y S p e c if ic

75t h P er c e nt i l e s :

8. 5

- 11. 956 A u t h o r Stu d y Ye a r s L o c a t i o n O u t c o m e P o p u l a t i o n S i z e F r act i o n M ean 24

- h a v g

C o n c e n t r a t i o n ( μ g / m 3 ) U p p er P er c en t i l e

C o n c e n t r a t i o n s ( μ g / m 3 )

Ito e t a l

. ( 201 1a ) 200 0

- 20 06 N e w Yo rk, N Y ED Vi si t s:

CV D ≥ 40 y r s PM 2 .5

PM 2. 5

c om po nent s :

E C , OC , S O 4 , NO 3 , N a + , N i

, V

, Z n

, Si

, Se

, Br A l l y ear / W ar m / C ol d:

14. 44 / 14. 7 9 / 14

. 09

1. 13 / 1. 03 / 1. 24

4. 3 / 4. 51 / 4. 08

4. 14 / 4. 81 / 3. 42

2. 12 / 1. 52 / 2. 78

0. 14 / 0. 14 / 0. 15

0. 017 1 / 0. 011 1 / 0. 0236

0. 006 6 / 0. 005 4 / 0. 0080

0. 030 0 / 0. 021 6 / 0. 0389

0. 076 9 / 0. 088 6 / 0. 0643

0. 001 3 / 0. 001 1 / 0. 0015

0. 003 6 / 0. 003 1 / 0. 0040 N ot pr es e nt ed

( N ot e: S D pr ov i de d s o w e

c oul d c om put e )

M at hes et al

. ( 201 1 ) 200 0

- 20 02 N e w Yo rk, N Y ED Vi si t s:

CV D ≥ 40 y r s

PM 2 .5 --- ---

Sz y szko w i cz

et al

. ( 2012 ) A pr 199 2

-

M ar 200 2 C an ada

( E dm ont o n) ED Vi si t s:

H y per t e ns i o n N

= 5, 365

PM 2 .5 8. 5 75 th per c e nt i l e: 10. 9

M ax : 1. 3. 1

H al e y et al

. ( 200 9 ) 200 1

- 20 05 N e w Yo rk

S ta te E D V is it s D i s c har ges

f r om al l

N YS

hos p i t al s PM 2 .5 NR NR

B unc h et al

. ( 201 1 ) 199 3

- 19 98 W as at c h

F r ont

, U t ah H os pi t al

Ad mi ssi o n s A ll

PM 2 .5 C i t y s p ec i f i c m eans

( r ang e) : 9. 3

- 11

. 1 Cit y s p e c if ic

M ax : 9. 3

- 11. 1

K l oo g et al

. ( 201 2a ) N e w E n gl a nd H os pi t al

Ad mi ssi o n s ≥ 65 PM 2. 5 ( pr edi c t ed) 9. 6 72. 5957 A u t h o r Stu d y Ye a r s L o c a t i o n O u t c o m e P o p u l a t i o n S i z e F r act i o n M ean 24

- h a v g

C o n c e n t r a t i o n ( μ g / m 3 ) U p p er P er c en t i l e

C o n c e n t r a t i o n s ( μ g / m 3 )

K i m et al

. ( 201 1 ) 200 3

- 20 07 D env er H os pi t al

Ad mi ssi o n s A ll PM 2 .5

EC

OC

S ul f at e

Nit r a t e 7. 98

0. 47

3. 09

1. 08

1. 03 59. 41

3. 02

10. 28

14. 32

19. 7258 Table A

- 10 Characterization of U.S. and Canadian Studies of S hort -t erm Exposure to PM 2.5 and Out

of Hospital Cardiac Arrests

Author Study

Years Location Outcome Population Size

Fraction Mean

24 -h avg

Concentration

(μg/m 3 ) Upper Percentile

Concentrations

(μg/m 3 )

Silverman

et al.

( 2010 ) 2002

-

2006 USA

(New

York

City) Out

- of

hospital

cardiac

arrests N=8,216

<40 to ≥ 70

yrs PM 2.5 Median:

A ll year = 12

Apr

- Sept = 12

Oct- Mar = 12 Upper (95%):

A ll year = 30

Apr

- Sept = 31

Oct- Mar = 28

Table A

- 11 Characterization of U.S. and Canadian Studies of Short -t erm Exposure to PM 2.5 and Time

of Stroke Symptom Onset

Author Study

Years Location Outcome Population Size

Fraction Mean

24 -h avg

Concentration

(μg/m 3 ) Upper Percentile

Concentrations

(μg/m 3 )

Wellenius

et al.

( 2012 ) 1999

-

2008 Boston,

MA Time of

Symptom

Onset

(Ischemic

Stroke) Patients

admitted to

BIDMC PM 2.5 NR NR

BIDMC= Beth Israel Deaconess Medical Center59 

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