September 2011

EPA/600/R-10/076B

Integrated Science Assessment for Ozone 

and Related Photochemical Oxidants

National Center for Environmental Assessment-RTP Division

Office of Research and Development

U.S. Environmental Protection Agency

Research Triangle Park, NC
DISCLAIMER

This document is the second external review draft for review purposes only and does not 

constitute U.S. Environmental Protection Agency policy. Mention of trade names or 

commercial products does not constitute endorsement or recommendation for use.
Draft – Do Not Cite or Quote iii September 2011

TABLE OF CONTENTS

AUTHORS, CONTRIBUTORS, AND REVIEWERS __________________________________XXVII

CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE OZONE NAAQS REVIEW PANEL ____ XXXI

ACRONYMS AND ABBREVIATIONS ___________________________________________ XXXIII

PREAMBLE_________________________________________________________________ XLIX

Process of ISA Development _____________________________________________________________________ xlix

EPA Framework for Causal Determination____________________________________________________________ liii

Evaluating Evidence for Inferring Causation___________________________________________________________ liv

Consideration of evidence from scientific disciplines ________________________________________________ lv

Application of Framework for Causal Determination _______________________________________________ lix

Table I Aspects to aid in judging causality ______________________________________ lx

Determination of Causality ___________________________________________________________________ lxi

Table II Weight of evidence for causal determination _____________________________ lxii

Quantitative relationships: Effects on Human Populations_____________________________________lxiii

Quantitative relationships: Effects on Ecosystems or Public Welfare ____________________________ lxv

Concepts in Evaluating Adversity of Health Effects ________________________________________________ lxv

Concepts in Evaluating Adversity of Ecological Effects _____________________________________________lxvi

PREFACE _________________________________________________________________ LXVIII

Legislative Requirements for the NAAQS Review ________________________________________________lxviii

History of the NAAQS for Ozone ______________________________________________________________lxix

Table III Summary of primary and secondary NAAQS promulgated for ozone 

during the period 1971-2008 _________________________________________ lxx

References _____________________________________________________________________________lxxiii

1 EXECUTIVE SUMMARY ______________________________________________________1-1

1.1 Introduction______________________________________________________________________________ 1-1

1.2 Scope __________________________________________________________________________________ 1-1

1.3 Atmospheric Chemistry and Ambient Concentrations _____________________________________________ 1-2

Figure 1-1 Schematic overview of photochemical processes influencing stratospheric 

and tropospheric ozone._____________________________________________1-3

1.4 Human Exposure _________________________________________________________________________ 1-4

1.5 Dosimetry and Modes of Action ______________________________________________________________ 1-4

Table 1-1 Summary of ozone causal determinations by exposure duration and 

health outcome____________________________________________________1-5

1.6 Integration of Ozone Health Effects ___________________________________________________________ 1-6

1.6.1 Respiratory Effects ___________________________________________________________________1-6

Figure 1-2 The continuum of respiratory effects, noting increases in severity but 

decreases in the proportion of the population affected moving up the 

pyramid. _________________________________________________________1-7

1.6.2 Mortality Effects _____________________________________________________________________1-8

1.6.3 Emerging Evidence __________________________________________________________________1-8

1.6.4 Populations at Increased Risk __________________________________________________________1-9

1.6.5 Ozone Concentration-Response Relationship _____________________________________________1-10

1.7 Integration of Effects on Vegetation and Ecosystems ____________________________________________ 1-10

Table 1-2 Summary of ozone causal determination for welfare effects ________________1-11

1.7.1 Visible Foliar Injury __________________________________________________________________1-11

1.7.2 Growth, Productivity, Carbon Storage and Agriculture_______________________________________1-12

1.7.3 Water Cycling ______________________________________________________________________1-12
Draft – Do Not Cite or Quote iv September 2011

1.7.4 Below Ground Processes_____________________________________________________________1-13

1.7.5 Community Composition _____________________________________________________________1-13

1.7.6 Ozone Exposure-Response Relationships________________________________________________1-13

1.8 The Role of Tropospheric Ozone in Climate Change and UV-B Effects ______________________________ 1-14

Figure 1-3 Schematic illustrating the effects of tropospheric O3 on climate. _____________1-15

Table 1-3 Summary of ozone causal determination for climate change and UV-B 

effects__________________________________________________________1-16

1.9 Conclusion _____________________________________________________________________________ 1-16

2 INTEGRATIVE SUMMARY ____________________________________________________2-1

2.1 Policy-Relevant Questions for O3 NAAQS Review________________________________________________ 2-1

2.2 ISA Development and Scope ________________________________________________________________ 2-4

2.3 Atmospheric Chemistry and Ambient Concentrations _____________________________________________ 2-6

2.3.1 Physical and Chemical Processes _______________________________________________________2-6

Figure 2-1 Schematic overview of photochemical processes influencing stratospheric 

and tropospheric ozone._____________________________________________2-7

2.3.2 Atmospheric Modeling of Background Ozone Concentrations__________________________________2-8

2.3.3 Monitoring_________________________________________________________________________2-10

Figure 2-2 GEOS-Chem modeled U.S. policy relevant background seasonal-mean 

surface ozone concentrations in spring (left) and summer (right), 2006._______2-10

2.3.4 Ambient Concentrations ______________________________________________________________2-11

2.4 Human Exposure ________________________________________________________________________ 2-12

2.5 Dosimetry and Mode of Action ______________________________________________________________ 2-14

2.6 Integration of Ozone Health Effects __________________________________________________________ 2-17

Table 2-1 Summary of evidence from epidemiologic, controlled human exposure, 

and animal toxicological studies on the health effects associated with 

short- and long-term exposure to ozone _______________________________2-18

2.6.1 Respiratory Effects __________________________________________________________________2-20

Figure 2-3 Snapshot of evidence for the association of O3 with the continuum of 

respiratory effects, including sub-clinical effects (bottom level of the 

pyramid) and clinical effects, increasing in severity moving up the 

pyramid. ________________________________________________________2-23

2.6.2 Mortality Effects ____________________________________________________________________2-29

2.6.3 Cardiovascular Health Effects _________________________________________________________2-30

2.6.4 Central Nervous System Effects _______________________________________________________2-30

2.6.5 Reproductive and Developmental Effects ________________________________________________2-31

2.6.6 Cancer and Mutagenicity and Genotoxicity _______________________________________________2-31

2.6.7 Policy Relevant Considerations ________________________________________________________2-31

2.6.7.1 Populations at Increased Risk __________________________________________________2-31

2.6.7.2 Lag Structure in Epidemiologic Studies ___________________________________________2-33

2.6.7.3 Ozone Concentration-Response Relationship______________________________________2-34

2.7 Integration of Effects on Vegetation and Ecosystems ____________________________________________ 2-36

2.7.1 Visible Foliar Injury __________________________________________________________________2-37

Figure 2-4 An illustrative diagram of the major pathway through which O3 enters 

leaves and the major endpoints that O3 may affect in plants and 

ecosystems. _____________________________________________________2-37

Table 2-2 Summary of ozone causal determinations for vegetation and ecosystem 

effects__________________________________________________________2-38

2.7.2 Growth, Productivity, Carbon Storage and Agriculture_______________________________________2-39

2.7.2.1 Natural Ecosystems __________________________________________________________2-39

2.7.2.2 Agricultural Crops____________________________________________________________2-41

2.7.3 Water Cycling ______________________________________________________________________2-42

2.7.4 Below-Ground Processes_____________________________________________________________2-42

2.7.5 Community Composition _____________________________________________________________2-43

2.7.6 Policy Relevant Considerations ________________________________________________________2-44

2.7.6.1 Air Quality Indices ___________________________________________________________2-44

2.7.6.2 Exposure-Response__________________________________________________________2-45

2.8 The Role of Tropospheric Ozone in Climate Change and UV-B Effects ______________________________ 2-46
Draft – Do Not Cite or Quote v September 2011

2.8.1 Tropospheric Ozone as a Greenhouse Gas_______________________________________________2-47

Figure 2-5 Schematic illustrating the effects of tropospheric O3 on climate including 

the relationship between precursor emissions, tropospheric O3

abundance, radiative forcing, climate response, and climate impacts. ________2-48

2.8.2 Tropospheric Ozone and UV-B related effects_____________________________________________2-48

2.9 Summary of Causal Determinations for Health Effects and Welfare Effects ___________________________ 2-50

Table 2-3 Summary of ozone causal determinations by exposure duration and 

health outcome___________________________________________________2-50

Table 2-4 Summary of ozone causal determination for welfare effects ________________2-51

Table 2-5 Summary of ozone causal determination for climate change and UV-B 

effects__________________________________________________________2-51

2.10 References ____________________________________________________________________________ 2-52

3 ATMOSPHERIC CHEMISTRY AND AMBIENT CONCENTRATIONS___________________3-1

3.1 Introduction______________________________________________________________________________ 3-1

3.2 Physical and Chemical Processes ____________________________________________________________ 3-1

Figure 3-1 Schematic overview of photochemical processes influencing stratospheric 

and tropospheric ozone._____________________________________________3-2

3.2.1 Sources of Precursors Involved in Ozone Formation_________________________________________3-5

Figure 3-2 Estimated anthropogenic emissions of ozone precursors for 2005. ___________3-6

3.2.2 Gas Phase Reactions Leading to Ozone Formation _________________________________________3-9

3.2.3 Multiphase Processes _______________________________________________________________3-13

3.2.3.1 Indoor Air 3-15

3.2.4 Temperature and Chemical Precursor Relationships________________________________________3-15

Figure 3-3 Measured concentrations of O3 and NOZ_______________________________3-19

3.3 Atmospheric Modeling ____________________________________________________________________ 3-20

Figure 3-4 Sample CMAQ modeling domains. ___________________________________3-21

Figure 3-5 Main components of a comprehensive atmospheric chemistry modeling 

system, such as the U.S. EPA’s Community Model for Air Quality 

(CMAQ) System. _________________________________________________3-22

3.3.1 Global Scale CTMs__________________________________________________________________3-26

Figure 3-6 Comparison of global CTM predictions of maximum daily 8-h avg ozone 

concentrations and multi-model mean with monthly averaged CASTNET 

observations in the Intermountain West and Southeast regions of the U.S. ____3-27

3.4 Background Ozone Concentrations __________________________________________________________ 3-28

Figure 3-7 Schematic overview of contributions to North American background 

concentrations of ozone, i.e., ozone concentrations that would exist in the 

absence of anthropogenic emissions from the U.S., Canada, and Mexico. ____3-30

3.4.1 Contributions from Anthropogenic Emissions outside North America ___________________________3-30

Figure 3-8 Time series of daily maximum 8-h avg ozone concentrations (ppm) 

measured at Trinidad Head, CA, from April 18, 2002 through December 

31, 2009. _______________________________________________________3-33

3.4.2 Contributions from Natural Sources _____________________________________________________3-33

3.4.2.1 Contributions from the Stratosphere _____________________________________________3-33

3.4.2.2 Contributions from Other Natural Sources_________________________________________3-35

3.4.3 Estimating Background Concentrations __________________________________________________3-37

Figure 3-9 North American background ozone concentration in surface air for spring 

and summer 2006 (top). GEOS-Chem calculated concentrations for the 

base case, i.e., including all sources in surface air for the U.S., Canada 

and Mexico for spring and summer of 2006 (bottom). _____________________3-39

Figure 3-10 North American background ozone concentrations calculated when base 

case ozone is > 60 ppb. ____________________________________________3-41

Figure 3-11a Simulated vs. observed daily 8-h max ozone concentrations for spring 

(March-May) and summer (June-August) 2006 for the ensemble of 

CASTNET sites in the intermountain West. _____________________________3-42

Figure 3-11b Simulated vs. observed daily 8-h max ozone concentrations for spring 

(March-May) and summer (June-August) 2006 for the ensembles of 

CASTNET sites in the Northeast U.S., Great Lakes, and the Southeast 

U.S. ___________________________________________________________3-43
Draft – Do Not Cite or Quote vi September 2011

Figure 3-12 Frequency distributions of daily 8-h max ozone concentrations in MarchAugust 2006 for the ensemble of low-altitude (<1.5 km) and high-altitude 

CASTNET sites in the U.S. _________________________________________3-44

3.4.4 Summary of Background Results_______________________________________________________3-45

3.5 Monitoring______________________________________________________________________________ 3-46

3.5.1 Routine Monitoring Techniques ________________________________________________________3-46

3.5.2 Precision and Bias __________________________________________________________________3-49

Table 3-1 Summary of ozone monitors meeting 40 CFR Part 58, Appendix A 

Precision and Bias Goals___________________________________________3-50

Figure 3-13 Box plots of precision data by year (2005-2009) for all ozone monitors 

reporting single-point QC check data to AQS. ___________________________3-50

Figure 3-14 Box plots of percent-difference data by year (2005-2009) for all ozone 

monitors reporting single-point QC check data to AQS. ___________________3-51

3.5.2.1 Precision from Co-located UV Ozone Monitors in Missouri ____________________________3-51

Figure 3-15 Box plots of RPD data by year for the co-located ozone monitors at two 

sites in Missouri from 2006-2009. ____________________________________3-52

Figure 3-16 Box plots of RPD data by year for all U.S. ozone sites reporting singlepoint QC check data to AQS from 2005-2009.___________________________3-52

3.5.3 Performance Specifications ___________________________________________________________3-53

Table 3-2 Performance specifications for ozone based in 40 CFR Part 53 _____________3-53

3.5.4 Monitor Calibration __________________________________________________________________3-53

3.5.5 Other Monitoring Techniques __________________________________________________________3-55

3.5.5.1 Portable UV Ozone Monitors ___________________________________________________3-55

3.5.5.2 NO-based Chemiluminescence Monitors__________________________________________3-55

3.5.5.3 Passive Air Sampling Devices and Sensors _______________________________________3-56

3.5.5.4 Differential Optical Absorption Spectrometry _______________________________________3-57

3.5.5.5 Satellite Remote Sensing______________________________________________________3-58

3.5.6 Ambient Ozone Network Design _______________________________________________________3-59

3.5.6.1 Monitor Siting Requirements ___________________________________________________3-59

Figure 3-17 U.S. ozone sites reporting data to AQS in 2010. _________________________3-62

Figure 3-18 U.S. Rural NCore, CASTNET and NPS POMS ozone sites in 2010. _________3-63

3.5.6.2 Probe/Inlet Siting Requirements ________________________________________________3-63

3.6 Ambient Concentrations ___________________________________________________________________ 3-64

3.6.1 Measurement Units, Metrics, and Averaging Times_________________________________________3-65

Figure 3-19 Distribution in nation-wide year-round site-level correlations between daily 

ozone metrics including 24-h avg, 1-h daily max and 8-h daily max using 

AQS data, 2007-2009. _____________________________________________3-66

3.6.2 Spatial Variability ___________________________________________________________________3-67

3.6.2.1 Urban-Focused Variability _____________________________________________________3-67

Figure 3-20 Required ozone monitoring time periods (ozone season) identified by 

monitoring site.___________________________________________________3-68

Table 3-3 Summary of ozone data sets originating from AQS_______________________3-69

Figure 3-21 Location of the 457 ozone monitors meeting the year-round data set 

completeness criterion for all 3 years between 2007 and 2009. _____________3-70

Figure 3-22 Location of the 1,064 ozone monitors meeting the warm-season data set 

completeness criteria for all 3 years between 2007 and 2009. ______________3-70

Table 3-4 Nationwide distributions of ozone concentrations (ppb) from the yearround data set ___________________________________________________3-71

Table 3-5 Nationwide distributions of ozone concentrations (ppb) from the warmseason data set __________________________________________________3-72

Table 3-6 Seasonally stratified distributions of 8-h daily max ozone concentrations 

(ppb) from the year-round data set (2007-2009) _________________________3-73

Figure 3-23 Highest monitor (by county) 3-year avg (2007-2009) of the 8-h daily max 

ozone concentration based on the year-round data set (top map) with 

seasonal stratification (bottom 4 maps). _______________________________3-74

Figure 3-24 Highest monitor (by county) 3-year avg (2007-2009) of the 8-h daily max 

ozone concentration based on the warm-season data set (top map) with 

annual stratification (bottom 3 maps). _________________________________3-75

Table 3-7 Focus cities used in this and previous assessments ______________________3-78

Table 3-8 City-specific distributions of 8-h daily max ozone concentrations (ppb) 

from the warm-season data set (2007-2009)____________________________3-79
Draft – Do Not Cite or Quote vii September 2011

Figure 3-25 Map of the Atlanta CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. _______________________3-80

Figure 3-26 Map of the Boston CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. _______________________3-80

Figure 3-27 Map of the Los Angeles CSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. ______________3-81

Figure 3-28 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Atlanta CSA.__________________________________________________3-82

Figure 3-29 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Boston CSA.__________________________________________________3-82

Figure 3-30 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Los Angeles CSA. _____________________________________________3-84

Figure 3-31 Pair-wise monitor correlations expressed as a histogram (top), contour 

matrix (middle) and scatter plot versus distance between monitors 

(bottom) for the Atlanta CSA.________________________________________3-86

Figure 3-32 Pair-wise monitor correlations expressed as a histogram (top), contour 

matrix (middle) and scatter plot versus distance between monitors 

(bottom) for the Boston CSA.________________________________________3-87

Figure 3-33 Pair-wise monitor correlations expressed as a histogram (top), contour 

matrix (middle) and scatter plot versus distance between monitors 

(bottom) for the Los Angeles CSA. ___________________________________3-88

Figure 3-34 Pair-wise monitor COD expressed as a histogram (top), contour matrix 

(middle) and scatter plot versus distance between monitors (bottom) for 

the Atlanta CSA.__________________________________________________3-89

Figure 3-35 Pair-wise monitor COD expressed as a histogram (top), contour matrix 

(middle) and scatter plot versus distance between monitors (bottom) for 

the Boston CSA.__________________________________________________3-90

Figure 3-36 Pair-wise monitor COD expressed as a histogram (top), contour matrix 

(middle) and scatter plot versus distance between monitors (bottom) for 

the Los Angeles CSA. _____________________________________________3-91

Figure 3-37 Terrain map showing the location of two nearby AQS ozone monitoring 

sites (red dots) along the western edge of the Los Angeles CSA. Site AL 

is near shore, 3 m above sea level, while Site AK is in an agricultural 

valley surrounded by mountains, 262 m above sea level. __________________3-93

Figure 3-38 Terrain map showing the location of four AQS ozone monitoring sites (red 

dots) located in or near the city limits in the center of the Boston CSA. 

Site characteristics range from Site A near downtown at 6 m above sea 

level to Site D in a forested area on Blue Hill at 192 m above sea level._______3-94

3.6.2.2 Rural-Focused Variability and Ground-Level Vertical Gradients ________________________3-96

Table 3-9 Rural focus areas_________________________________________________3-97

Figure 3-39 Rural focus area site information, statistics and box plots for 8-h daily 

max ozone from AQS monitors meeting the warm-season data set 

inclusion criteria within the rural focus areas. ___________________________3-98

Figure 3-40 Terrain map showing the location of five AQS ozone monitoring sites 

(green/black stars) in Great Smoky Mountain National Park, NC-TN

(SMNP). ________________________________________________________3-99

Figure 3-41 Pair-wise monitor correlations (left) and coefficients of divergence (COD, 

right) expressed as a histogram (top), contour matrix (middle) and scatter 

plot vs. distance between monitors (bottom) for Great Smoky Mountain 

National Park, NC-TN (SMNP). _____________________________________3-100

Figure 3-42 Terrain map showing the location of the AQS ozone monitoring site in 

Rocky Mountain National Park, CO (black/green star) and the Denver 

CSA (red dots) along with ozone monitoring sites used in the Brodin et al. 

(2010) study (blue circles)._________________________________________3-101

Figure 3-43 Terrain map showing the location of two AQS ozone monitoring sites 

(black/green stars) in Sequoia National Park, CA._______________________3-102

3.6.3 Temporal Variability ________________________________________________________________3-103

3.6.3.1 Multiyear Trends____________________________________________________________3-103

Figure 3-44 National 8-h ozone trends, 2001-2008 (average of the annual fourth 

highest 8-h daily max concentrations in ppm).__________________________3-104

3.6.3.2 Hourly Variations ___________________________________________________________3-105
Draft – Do Not Cite or Quote viii September 2011

Figure 3-45 Diel patterns in 1-h avg ozone for Atlanta, Boston and Los Angeles 

between 2007 and 2009 using the year-round data set for the cold 

month/warm month comparison (left half) and the warm-season data set 

for the weekday/weekend comparison (right half). ______________________3-106

3.6.4 Associations with Co-pollutants _______________________________________________________3-109

Figure 3-47 Distribution of Pearson correlation coefficients for comparison of 8-h daily 

max ozone from the year-round data set with co-located 24-h avg CO, 

SO2, NO2, PM10 and PM2.5 from AQS, 2007-2009 _______________________3-110

Figure 3-48 Distribution of Pearson correlation coefficients for comparison of 8-h daily 

max ozone from the warm-season (May-Sept) data set with co-located 

24-h avg CO, SO2, NO2, PM10 and PM2.5 from AQS, 2007-2009. ___________3-111

3.7 Chapter Summary ______________________________________________________________________ 3-112

3.7.1 Physical and Chemical Processes _____________________________________________________3-112

3.7.2 Atmospheric Modeling ______________________________________________________________3-113

3.7.3 Background Concentrations __________________________________________________________3-115

3.7.4 Monitoring________________________________________________________________________3-116

3.7.5 Ambient Concentrations _____________________________________________________________3-117

3.8 Supplemental Ozone Model Predictions from the Literature ______________________________________ 3-120

3.8.1 Time Series of GEOS-Chem Model Predictions and Observations at Selected CASTNET Sites _____3-120

Figure 3-49 Comparison of time series of measurements of daily maximum 8-hour 

average ozone concentrations at four CASTNET sites in the Northeast 

with GEOS-Chem predictions for the base case and for the North 

American background case in 2006. _________________________________3-121

Figure 3-50 Comparison of time series of measurements of daily maximum 8-hour 

average ozone concentrations at four CASTNET sites in the Southeast 

with GEOS-Chem predictions for the base case and for the North 

American background case in 2006. _________________________________3-121

Figure 3-51 Comparison of time series of measurements of daily maximum 8-hour 

average ozone concentrations at four CASTNET sites in the Upper 

Midwest with GEOS-Chem predictions for the base case and for the 

North American background case in 2006. ____________________________3-122

Figure 3-52 Comparison of time series of measurements of daily maximum 8-hour 

average ozone concentrations at CASTNET sites in the Intermountain 

West with GEOS-Chem predictions for the base case and the North 

American background case in 2006. _________________________________3-122

Figure 3-53 Comparison of time series of measurements of daily maximum 8-hour 

average ozone concentrations at CASTNET sites in the Intermountain 

West with GEOS-Chem predictions for the base case and the North 

American background case in 2006. _________________________________3-123

Figure 3-54 Comparison of time series of measurements of daily maximum 8-hour 

average ozone concentrations at CASTNET sites in the West with GEOSChem predictions for the base case and the North American background 

case in 2006. ___________________________________________________3-123

Figure 3-55 Comparison of time series of measurements of daily maximum 8-hour 

average ozone concentrations at monitoring sites in Californiawith GEOSChem predictions for the base case and the North American background 

case in 2006. ___________________________________________________3-124

Figure 3-56 Comparison of daily maximum 8-h average ozone predicted using GEOSChem at 0.5°×0.67° and 2°×2.5° (left figure only) resolution with 

measurements at Mount Bachelor, OR (left) and Trinidad Head, CA 

(right) from March to August 2006. __________________________________3-124

Figure 3-57 Comparison of monthly mean ± 1 standard deviation ozone calculated 

GEOS-Chem (in red) with ozonesondes (in black) at Trinidad Head and 

Boulder, CO during April and August 2006.____________________________3-125

3.9 Supplemental Ozone Model Predictions Using the Latest Release of GEOS-Chem____________________ 3-125

3.9.1 Introduction_______________________________________________________________________3-125

3.9.2 GEOS-Chem Model Application_______________________________________________________3-126

3.9.3 Model Scenarios___________________________________________________________________3-127

Table 3-10 Summary of GEOS-Chem model scenarios ___________________________3-128

3.9.4 Model Performance Evaluation _______________________________________________________3-128

Figure 3-58 Frequency distributions of 8-hr daily max ozone concentration from March 

– August 2006 for low-elevation (<1.5 km; top panel) and high-elevation 

(>1.5 km; bottom panel) CASTNET sites. _____________________________3-130
Draft – Do Not Cite or Quote ix September 2011

3.9.5 Model Results_____________________________________________________________________3-131

Figure 3-59 Mean 8-hr daily max O3 concentration (ppb) for the Base Case (left panel) 

and North American Background scenario (right panel), based on the 

2006, 2007 and 2008 simulation period. ______________________________3-132

Figure 3-60 Mean 8-hr daily max O3 concentration (ppb) for the North American 

Background scenario during winter (Dec-Feb, upper right panel), spring 

(Mar-May, upper right panel), summer (Jun-Aug, lower left panel), and fall 

(Sep-Nov, lower right panel), based on the 2006, 2007 and 2008 

simulation period.________________________________________________3-133

3.9.6 Model Attributes and Limitations ______________________________________________________3-134

3.9.7 Summary of Modeling Results ________________________________________________________3-135

3.10 Supplemental Figures of Observed Ambient Ozone Concentrations________________________________ 3-136

3.10.1 Ozone Monitor Maps for the Urban Focus Cities __________________________________________3-136

Figure 3-61 Map of the Atlanta CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-137

Figure 3-62 Map of the Baltimore CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-137

Figure 3-63 Map of the Birmingham CSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. _____________3-138

Figure 3-64 Map of the Boston CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-138

Figure 3-65 Map of the Chicago CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-139

Figure 3-66 Map of the Dallas CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-139

Figure 3-67 Map of the Denver CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-140

Figure 3-68 Map of the Detroit CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-140

Figure 3-69 Map of the Houston CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-141

Figure 3-70 Map of the Los Angeles CSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. _____________3-141

Figure 3-71 Map of the Minneapolis CSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. _____________3-142

Figure 3-72 Map of the New York CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-142

Figure 3-73 Map of the Philadelphia CSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. _____________3-143

Figure 3-74 Map of the Phoenix CBSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-143

Figure 3-75 Map of the Pittsburgh CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-144

Figure 3-76 Map of the Salt Lake City CSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. _____________3-145

Figure 3-77 Map of the San Antonio CBSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. _____________3-145

Figure 3-78 Map of the San Francisco CSA including ozone monitor locations, 

population gravity centers, urban areas, and major roadways. _____________3-146

Figure 3-79 Map of the Seattle CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-146

Figure 3-80 Map of the St. Louis CSA including ozone monitor locations, population 

gravity centers, urban areas, and major roadways. ______________________3-147

3.10.2 Ozone Concentration Box Plots for the Urban Focus Cities _________________________________3-147

Figure 3-81 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Atlanta CSA._________________________________________________3-148

Figure 3-82 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Baltimore CSA._______________________________________________3-148

Figure 3-83 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Birmingham CSA._____________________________________________3-149
Draft – Do Not Cite or Quote x September 2011

Figure 3-84 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Boston CSA._________________________________________________3-149

Figure 3-85 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Chicago CSA.________________________________________________3-150

Figure 3-86 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Dallas CSA. _________________________________________________3-150

Figure 3-87 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Denver CSA. ________________________________________________3-151

Figure 3-88 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Detroit CSA. _________________________________________________3-151

Figure 3-89 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Houston CSA. _______________________________________________3-152

Figure 3-90 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Los Angeles CSA. ____________________________________________3-153

Figure 3-91 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Minneapolis CSA._____________________________________________3-154

Figure 3-92 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the New York CSA. ______________________________________________3-154

Figure 3-93 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Philadelphia CSA. ____________________________________________3-155

Figure 3-94 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Phoenix CBSA. ______________________________________________3-155

Figure 3-95 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Pittsburgh CSA. ______________________________________________3-156

Figure 3-96 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Salt Lake City CSA. ___________________________________________3-156

Figure 3-97 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the San Antonio CBSA. ___________________________________________3-157

Figure 3-98 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the San Francisco CSA.___________________________________________3-157

Figure 3-99 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the Seattle CSA._________________________________________________3-158

Figure 3-100 Site information, statistics and box plots for 8-h daily max ozone from 

AQS monitors meeting the warm-season data set inclusion criteria within 

the St. Louis CSA. _______________________________________________3-158

3.10.3 Ozone Concentration Relationships for the Urban Focus Cities ______________________________3-159

Figure 3-101 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Atlanta CSA. _______________________________3-159

Figure 3-102 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Baltimore CSA. _____________________________3-160

Figure 3-103 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Birmingham CSA. ___________________________3-161

Figure 3-104 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Boston CSA. _______________________________3-162
Draft – Do Not Cite or Quote xi September 2011

Figure 3-105 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Chicago CSA. ______________________________3-163

Figure 3-106 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Dallas CSA. ________________________________3-164

Figure 3-107 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Denver CSA. _______________________________3-165

Figure 3-108 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Detroit CSA.________________________________3-166

Figure 3-109 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Houston CSA. ______________________________3-167

Figure 3-110 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Los Angeles CSA. ___________________________3-168

Figure 3-111 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Minneapolis CSA. ___________________________3-169

Figure 3-112 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the New York CSA. _____________________________3-170

Figure 3-113 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Philadelphia CSA. ___________________________3-171

Figure 3-114 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Phoenix CBSA. _____________________________3-172

Figure 3-115 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Pittsburgh CSA. _____________________________3-173

Figure 3-116 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Salt Lake City CSA. __________________________3-174

Figure 3-117 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the San Antonio CBSA. __________________________3-175

Figure 3-118 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the San Francisco CSA. of R. _____________________3-176

Figure 3-119 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the Seattle CSA. _______________________________3-177

Figure 3-120 Pair-wise monitor correlation coefficients (R) expressed as a histogram 

(top), contour matrix (middle) and scatter plot versus distance between 

monitors (bottom) for the St. Louis CSA. ______________________________3-178

Figure 3-121 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Atlanta CSA. ________________________3-179

Figure 3-122 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Baltimore CSA. ______________________3-180

Figure 3-123 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Birmingham CSA. ____________________3-181

Figure 3-124 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Boston CSA. ________________________3-182

Figure 3-125 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Chicago CSA. _______________________3-183
Draft – Do Not Cite or Quote xii September 2011

Figure 3-126 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Dallas CSA._________________________3-184

Figure 3-127 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Denver CSA. ________________________3-185

Figure 3-128 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Detroit CSA. ________________________3-186

Figure 3-129 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Houston CSA. _______________________3-187

Figure 3-130 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Los Angeles CSA.____________________3-188

Figure 3-131 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Minneapolis CSA. ____________________3-189

Figure 3-132 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the New York CSA. ______________________3-190

Figure 3-133 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Philadelphia CSA. ____________________3-191

Figure 3-134 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Phoenix CBSA. ______________________3-192

Figure 3-135 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Pittsburgh CSA.______________________3-193

Figure 3-136 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Salt Lake City CSA.___________________3-194

Figure 3-137 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the San Antonio CBSA.___________________3-195

Figure 3-138 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the San Francisco CSA. __________________3-196

Figure 3-139 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the Seattle CSA. ________________________3-197

Figure 3-140 Pair-wise monitor coefficient of divergence (COD) expressed as a 

histogram (top), contour matrix (middle) and scatter plot versus distance 

between monitors (bottom) for the St. Louis CSA._______________________3-198

3.10.4 Hourly Variations in Ozone for the Urban Focus Cities _____________________________________3-199

Figure 3-141 Diel patterns in 1-h avg ozone for select CSAs between 2007 and 2009 

using the year-round data set for the cold month/warm month comparison 

(left half) and the warm-season data set for the weekday/weekend 

comparison (right half). ___________________________________________3-199

Figure 3-142 Diel patterns in 1-h avg ozone for select CSAs between 2007 and 2009 

using the year-round data set for the cold month/warm month comparison 

(left half) and the warm-season data set for the weekday/weekend 

comparison (right half). ___________________________________________3-200

Figure 3-143 Diel patterns in 1-h avg ozone for select CSAs between 2007 and 2009 

using the year-round data set for the cold month/warm month comparison 

(left half) and the warm-season data set for the weekday/weekend 

comparison (right half). ___________________________________________3-201

Figure 3-144 Diel patterns in 1-h avg ozone for select CSAs/CBSAs between 2007 and 

2009 using the year-round data set for the cold month/warm month 

comparison (left half) and the warm-season data set for the 

weekday/weekend comparison (right half). ____________________________3-202

Figure 3-145 Diel patterns in 1-h avg ozone for select CSAs/CBSAs between 2007 and 

2009 using the year-round data set for the cold month/warm month 

comparison (left half) and the warm-season data set for the 

weekday/weekend comparison (right half). ____________________________3-203
Draft – Do Not Cite or Quote xiii September 2011

3.11 References ___________________________________________________________________________ 3-204

4 EXPOSURE TO AMBIENT OZONE _____________________________________________4-1

4.1 Introduction______________________________________________________________________________ 4-1

4.2 General Exposure Concepts ________________________________________________________________ 4-1

4.3 Exposure Measurement ____________________________________________________________________ 4-4

4.3.1 Personal Monitoring Techniques ________________________________________________________4-4

4.3.2 Indoor-Outdoor Concentration Relationships _______________________________________________4-5

Table 4-1 Relationships of Indoor and Outdoor Ozone Concentration _________________4-6

4.3.3 Personal-Ambient Concentration Relationships_____________________________________________4-8

Figure 4-1 Variation in hourly personal and ambient concentrations of O3 and PM2.5

in various microenvironments during daytime hours._______________________4-9

Table 4-2 Correlations between Personal and Ambient Ozone Concentration __________4-11

Table 4-3 Ratios of Personal to Ambient Ozone Concentration _____________________4-13

4.3.4 Co-Exposure to Other Pollutants and Environmental Stressors _______________________________4-14

4.3.4.1 Personal Exposure to Ozone and Co-pollutants ____________________________________4-14

4.3.4.2 Near-Road Exposure to Ozone and Co-pollutants___________________________________4-15

Figure 4-2 Correlations between 1-week concentrations of O3 and copollutants 

measured near roadways. __________________________________________4-16

4.3.4.3 Indoor Exposure to Ozone and Co-pollutants ______________________________________4-16

4.4 Exposure-Related Metrics _________________________________________________________________ 4-17

4.4.1 Activity Patterns ____________________________________________________________________4-17

Figure 4-3 Distribution of time that NHAPS respondents spent in ten 

microenvironments based on smoothed 1-min diary data. _________________4-18

4.4.2 Ozone Averting Behavior _____________________________________________________________4-19

4.4.3 Population Proximity to Fixed-Site Ozone Monitors _________________________________________4-21

Table 4-4 Fraction of the 2009 population living within a specified distance of an 

ozone monitor in selected U.S. cities__________________________________4-23

4.5 Exposure Modeling_______________________________________________________________________ 4-24

Table 4-5 Characteristics of exposure modeling approaches _______________________4-24

4.5.1 Concentration Surface Modeling _______________________________________________________4-25

4.5.2 Residential Air Exchange Rate Modeling _________________________________________________4-27

4.5.3 Microenvironment-Based Models_______________________________________________________4-29

4.6 Implications for Epidemiologic Studies________________________________________________________ 4-32

4.6.1 Nonambient Ozone Exposure _________________________________________________________4-33

4.6.2 Spatiotemporal Variability_____________________________________________________________4-33

4.6.2.1 Spatial Variability ____________________________________________________________4-35

4.6.2.2 Seasonality 4-37

4.6.3 Exposure to Co-pollutants and Ozone Reaction Products____________________________________4-38

4.6.4 Averting Behavior ___________________________________________________________________4-38

Figure 4-4 Adjusted asthma hospital admissions by age on lagged ozone by alert 

status, ages 5-19._________________________________________________4-40

Figure 4-5 Adjusted asthma hospital admissions by age on lagged ozone by alert 

status, ages 20-64 ________________________________________________4-40

4.6.5 Exposure Estimation Methods in Epidemiologic Studies _____________________________________4-41

4.7 Summary and Conclusions_________________________________________________________________ 4-41

4.8 References ____________________________________________________________________________ 4-44

5 DOSIMETRY AND MODE OF ACTION___________________________________________5-1

5.1 Introduction______________________________________________________________________________ 5-1

Figure 5-1 Schematic of the O3 exposure and response pathway. _____________________5-2

5.2 Human and Animal Ozone Dosimetry _________________________________________________________ 5-2

5.2.1 Introduction_________________________________________________________________________5-2

Figure 5-2 Representation of respiratory tract regions in humans. _____________________5-3

Figure 5-3 Structure of lower airways with progression from the large airways to the 

alveolus._________________________________________________________5-4

5.2.2 Ozone Uptake_______________________________________________________________________5-5
Draft – Do Not Cite or Quote xiv September 2011

Table 5-1 Human respiratory tract uptake efficiency data ___________________________5-6

5.2.2.1 Gas Transport Principles _______________________________________________________5-6

5.2.2.2 Target Sites for Ozone Dose ____________________________________________________5-7

5.2.2.3 Upper Respiratory Tract Ozone Removal and Dose __________________________________5-8

5.2.2.4 Lower Respiratory Tract Ozone Uptake and Dose ___________________________________5-9

Figure 5-4 Total ozone uptake efficiency as a function of breathing frequency at a 

constant minute ventilation of 30 L/min.________________________________5-11

Figure 5-5 Ozone uptake fraction as a function of volumetric penetration (Vp) in a 

representative subject._____________________________________________5-12

5.2.2.5 Mode of Breathing ___________________________________________________________5-12

5.2.2.6 Interindividual Variability in Dose ________________________________________________5-13

5.2.2.7 Physical Activity _____________________________________________________________5-15

Figure 5-6 Modeled effect of exercise on tissue dose of the LRT. ____________________5-16

5.2.2.8 Summary 5-16

5.2.3 Ozone Reactions and Reaction Products ________________________________________________5-17

Figure 5-7 Schematic overview of ozone interaction with PUFA in ELF and lung 

cells.___________________________________________________________5-19

5.2.3.1 Summary 5-24

Figure 5-8 Details of the O3 interaction with the airway ELF to form secondary 

oxidation products.________________________________________________5-24

5.3 Possible Pathways/Modes of Action__________________________________________________________ 5-25

5.3.1 Introduction________________________________________________________________________5-25

5.3.2 Activation of Neural Reflexes __________________________________________________________5-26

5.3.3 Initiation of inflammation______________________________________________________________5-29

5.3.4 Alteration of epithelial barrier function ___________________________________________________5-34

5.3.5 Sensitization of bronchial smooth muscle ________________________________________________5-35

5.3.6 Modification of innate/adaptive immune system responses___________________________________5-39

5.3.7 Airways remodeling _________________________________________________________________5-43

5.3.8 Systemic inflammation and oxidative/nitrosative stress ______________________________________5-44

5.3.9 Impaired alveolar-arterial O2 transfer ____________________________________________________5-45

5.3.10 Summary _________________________________________________________________________5-46

Figure 5-9 The modes of action/possible pathways underlying the health effects 

resulting from inhalation exposure to O3. _______________________________5-46

5.4 Interindividual Variability in Response ________________________________________________________ 5-50

5.4.1 Dosimetric Considerations ____________________________________________________________5-50

5.4.2 Mechanistic Considerations ___________________________________________________________5-52

5.4.2.1 Gene-Environment Interactions _________________________________________________5-52

5.4.2.2 Pre-existing Diseases and Conditions ____________________________________________5-56

5.4.2.3 Nutritional Status ____________________________________________________________5-61

5.4.2.4 Lifestage 5-62

5.4.2.5 Attenuation of Responses _____________________________________________________5-64

5.4.2.6 Co-Exposures with Particulate Matter ____________________________________________5-66

5.4.2.7 Summary 5-67

Figure 5-10 Factors which contribute to the interindividual variability in responses 

resulting from inhalation exposure to ozone. ____________________________5-67

5.5 Species Homology and Interspecies Sensitivity_________________________________________________ 5-67

5.5.1 Dosimetry _________________________________________________________________________5-68

Figure 5-11 Species comparison of antioxidant / protein ratios of: (a) nasal lavage 

fluid and, (b) bronchoalveolar lavage fluid. _____________________________5-70

Figure 5-12 Humans and animals are similar in the regional pattern of O3 tissue dose 

distribution.______________________________________________________5-71

Figure 5-13 Oxygen-18 incorporation into different fractions of BALF from humans 

and rats exposed to 0.4 and 2.0 ppm 18O3. _____________________________5-72

5.5.2 Homology of Response ______________________________________________________________5-73

5.5.3 Summary _________________________________________________________________________5-75

5.6 Chapter Summary _______________________________________________________________________ 5-76

5.7 References ____________________________________________________________________________ 5-77
Draft – Do Not Cite or Quote xv September 2011

6 INTEGRATED HEALTH EFFECTS OF SHORT-TERM OZONE EXPOSURE_____________6-1

6.1 Introduction______________________________________________________________________________ 6-1

6.2 Respiratory Effects ________________________________________________________________________ 6-1

6.2.1 Lung Function_______________________________________________________________________6-3

6.2.1.1 Controlled Human Exposure ____________________________________________________6-3

Figure 6-1 Cross-study comparison of mean ozone-induced FEV1 decrements 

following 6.6 hours of exposure to ozone. _______________________________6-7

Figure 6-2 Frequency distributions of FEV1 decrements observed by Schelegle et al. 

(2009) in young healthy adults (16 F, 15 M) following 6.6-h exposures to 

ozone or filtered air. _______________________________________________6-13

6.2.1.2 Epidemiology6-23

Table 6-1 Mean and upper percentile concentrations of ozone in epidemiologic 

studies examining lung function in populations with increased outdoor 

exposures_______________________________________________________6-24

Figure 6-3 Changes in FEV1 (ml) or PEF (ml/sec) in association with ambient ozone 

exposure in studies of children attending summer camp. __________________6-26

Table 6-2 Additional characteristics and quantitative data for studies represented in 

Figure 6-3_______________________________________________________6-27

Figure 6-4 Percent change in FEV1 in association with ambient ozone exposures of 

adults exercising outdoors. _________________________________________6-28

Table 6-3 Additional characteristics and quantitative data for studies represented in 

Figure 6-4 and results from studies in children exercising outdoors __________6-29

Figure 6-5 Percent change in lung function in association with ambient ozone 

exposures among outdoor workers.___________________________________6-31

Table 6-4 Additional characteristics and quantitative data for studies represented in 

Figure 6-5_______________________________________________________6-31

Table 6-5 Associations between ambient ozone exposure and lung function 

decrements in different ranges of ambient ozone concentrations ____________6-32

Table 6-6 Mean and upper percentile concentrations of ozone in epidemiologic 

studies examining lung function in children with asthma ___________________6-34

Figure 6-6 Percent change in FEV1 in association with ambient ozone exposures 

among children with asthma. ________________________________________6-35

Table 6-7 Additional characteristics and quantitative data for studies represented in 

Figure 6-6_______________________________________________________6-36

Figure 6-7 Percent change in PEF or FEF25-75% in association with ambient ozone 

exposures among children with asthma. _______________________________6-37

Table 6-8 Additional characteristics and quantitative data for studies represented in 

Figure 6-7_______________________________________________________6-38

Table 6-9 Mean and upper percentile concentrations of ozone in epidemiologic 

studies examining lung function in adults with respiratory disease ___________6-44

Table 6-10 Mean and upper percentile concentrations of ozone in epidemiologic 

studies examining lung function in populations not restricted to individuals 

with asthma _____________________________________________________6-45

Figure 6-8 Percent change in lung function in association with ambient ozone 

exposures in studies not restricted to children with asthma. ________________6-46

Table 6-11 Additional characteristics and quantitative data for studies represented in 

Figure 6-8 and results from other studies in children______________________6-47

Table 6-12 Associations between ambient ozone exposure and changes in lung 

function in studies of adults _________________________________________6-49

Figure 6-9 Comparison of ozone-associated changes in lung function in single- and 

copollutant models. _______________________________________________6-52

Table 6-13 Additional characteristics and quantitative data for studies presented in 

Figure 6-9_______________________________________________________6-53

6.2.1.3 Toxicology 6-56

6.2.2 Airway Hyperresponsiveness __________________________________________________________6-57

6.2.2.1 Controlled Human Exposures __________________________________________________6-57

6.2.2.2 Toxicology 6-59

6.2.3 Pulmonary Inflammation, Injury and Oxidative Stress _______________________________________6-61

6.2.3.1 Controlled Human Exposures __________________________________________________6-61

6.2.3.2 Epidemiology6-66
Draft – Do Not Cite or Quote xvi September 2011

Table 6-14 Mean and upper percentile ozone concentrations in studies examining 

biological markers of pulmonary inflammation and oxidative stress __________6-67

Figure 6-10 Percent change in exhaled nitric oxide (eNO) per standardized increment 

in ambient ozone exposure in studies of individuals with and without 

asthma. ________________________________________________________6-68

Table 6-15 Additional characteristics and quantitative data for studies represented in 

Figure 6-10______________________________________________________6-69

Table 6-16 Associations between short-term ambient ozone exposure and biological 

markers of pulmonary inflammation and oxidative stress __________________6-69

6.2.3.3 Toxicology 6-79

Table 6-17 Morphometric observations in non-human primates after acute O3

exposure _______________________________________________________6-81

6.2.4 Respiratory Symptoms and Medication Use ______________________________________________6-84

6.2.4.1 Children with Asthma _________________________________________________________6-86

Table 6-18 Mean and upper percentile ozone concentrations in epidemiologic studies 

examining respiratory symptoms, medication use, and activity levels in 

children with asthma ______________________________________________6-87

Figure 6-11 Associations of ambient ozone exposure with respiratory symptoms in 

children with asthma. ______________________________________________6-88

Table 6-19 Additional characteristics and quantitative data for studies presented in 

Figure 6-11______________________________________________________6-89

Figure 6-12 Associations of ambient ozone exposure with asthma medication use. _______6-92

Table 6-20 Additional characteristics and quantitative data for studies presented in 

Figure 6-12______________________________________________________6-92

6.2.4.2 Adults with Respiratory Disease ________________________________________________6-93

Table 6-21 Mean and upper percentile ozone concentrations in epidemiologic studies 

examining respiratory symptoms and medication use in adults with 

respiratory disease________________________________________________6-94

6.2.4.3 Populations not Restricted to Individuals with Asthma________________________________6-95

Table 6-22 Mean and upper percentile ozone concentrations in epidemiologic studies 

examining respiratory symptoms in populations not restricted to 

individuals with asthma ____________________________________________6-95

Figure 6-13 Associations of ambient ozone exposure with respiratory symptoms in 

studies not restricted to children with asthma. ___________________________6-97

Table 6-23 Additional characteristics and quantitative data for studies presented in 

Figure 6-13______________________________________________________6-97

6.2.4.4 Confounding in Epidemiologic Studies of Respiratory Symptoms and Medication Use ______6-98

Table 6-24 Associations between short-term ozone exposure and respiratory 

symptoms in single- and copollutant models ____________________________6-99

6.2.4.5 Summary of Epidemiologic Studies of Respiratory Symptoms and Asthma Medication Use _6-100

6.2.5 Lung Host Defenses________________________________________________________________6-101

6.2.5.1 Mucociliary Clearance _______________________________________________________6-102

6.2.5.2 Alveolobronchiolar Transport Mechanism ________________________________________6-102

6.2.5.3 Alveolar Macrophages _______________________________________________________6-103

6.2.5.4 Infection and Adaptive Immunity _______________________________________________6-104

6.2.6 Allergic and Asthma-Related Responses________________________________________________6-108

6.2.7 Hospital Admissions, Emergency Department Visits, and Physicians Visits _____________________6-110

6.2.7.1 Summary of Findings from 2006 Ozone AQCD____________________________________6-110

Table 6-25 Mean and upper percentile concentrations of respiratory-related hospital 

admission and emergency department visit studies evaluated _____________6-112

6.2.7.2 Hospital Admission Studies ___________________________________________________6-113

Figure 6-14 Percent increase in respiratory hospital admissions from natural spline 

models for a 40 ppb increase in 1-h max ozone concentrations for each 

location of the APHENA study. _____________________________________6-116

Table 6-26 Corresponding effect estimates for Figure 6-14_________________________6-117

Figure 6-15 Estimated relative risks (RRs) of ozone-related asthma hospital 

admissions allowing for possible nonlinear relationships using natural 

splines.________________________________________________________6-123

6.2.7.3 Emergency Department Visit Studies ___________________________________________6-124

Figure 6-16 Risk ratio for respiratory ED visits and different ozone exposure metrics in 

Atlanta from 1993-2004.___________________________________________6-125
Draft – Do Not Cite or Quote xvii September 2011

Figure 6-17 Loess dose-response estimates and twice-standard error estimates from 

generalized additive models for associations between 3-day avg ozone 

concentrations and ED visits for pediatric asthma. ______________________6-128

Figure 6-18 Relative risk of asthma ED visits children and adults for a 30 ppb increase 

in max 8-h avg O3 concentrations in Seattle, WA, 1998-2002. _____________6-130

6.2.7.4 Outpatient and Physician Visit Studies __________________________________________6-131

6.2.7.5 Summary 6-132

Figure 6-19 Percent increase in respiratory-related hospital admission and ED visits in 

studies that presented all-year and/or seasonal results. __________________6-133

Table 6-27 Corresponding Effect Estimates for Figure 6-19 ________________________6-134

Figure 6-20 Percent increase in respiratory-related hospital admissions and ED visits 

for studies that presented single and copollutant model results. ____________6-135

Table 6-28 Corresponding effect estimates for Figure 6-20_________________________6-136

6.2.8 Respiratory Mortality________________________________________________________________6-136

6.2.9 Summary and Causal Determination ___________________________________________________6-137

6.3 Cardiovascular Effects ___________________________________________________________________ 6-143

6.3.1 Controlled Human Exposure _________________________________________________________6-143

6.3.2 Epidemiology _____________________________________________________________________6-144

6.3.2.1 Arrhythmia 6-145

Table 6-29 Characterization of ozone concentrations (in ppb) from studies of 

arrhythmias ____________________________________________________6-145

6.3.2.2 Heart Rate/Heart Rate Variability_______________________________________________6-147

Table 6-30 Characterization of ozone concentrations (in ppb) from studies of heart 

rate variability___________________________________________________6-148

6.3.2.3 Stroke 6-151

Figure 6-21 Odds ratio (95% confidence interval) for stroke by quintiles of ozone. _______6-153

6.3.2.4 Biomarkers 6-153

Table 6-31 Characterization of ozone concentrations (in ppb) from studies of 

biomarkers _____________________________________________________6-154

6.3.2.5 Myocardial Infarction (MI)_____________________________________________________6-159

6.3.2.6 Blood Pressure_____________________________________________________________6-160

Table 6-32 Characterization of ozone concentrations (in ppb) from studies of blood 

pressure _______________________________________________________6-160

6.3.2.7 Hospital Admissions and Emergency Department Visits _____________________________6-161

Table 6-33 Characterization of ozone concentrations (in ppb) from studies of HAs 

and ED visits ___________________________________________________6-162

Figure 6-22 Odds ratio (95% CI) per increment ppb increase in ozone for over all 

cardiovascular ED visits or HAs. ____________________________________6-166

Table 6-34 Odds ratio (95% CI) per increment ppb increase in ozone for overall 

cardiovascular ED visits or HAs in studies presented in Figure 6-22 ________6-167

Figure 6-23 Odds Ratio (95% CI) per increment ppb increase in ozone for congestive 

heart failure ED visits or HAs. ______________________________________6-168

Table 6-35 Odds Ratio (95% CI) per increment ppb increase in ozone for congestive 

heart failure ED visits or HAs for studies in Figure 6-23 __________________6-169

Figure 6-24 Odds Ratio (95% confidence interval) per increment ppb increase in 

ozone for ischemic heart disease, coronary heart disease, myocardial 

infarction, and angina pectoris ED visits or HAs. ________________________6-170

Table 6-36 Odds Ratio (95% CI) per increment ppb increase in ozone for ischemic 

heart disease, coronary heart disease, myocardial infarction, and angina 

pectoris ED visits or HAs for studies presented in Figure 6-24 _____________6-171

Figure 6-25 Odds Ratio (95% confidence interval) per increment ppb increase in 

ozone for stroke ED visits or HAs. ___________________________________6-172

Table 6-37 Odds Ratio (95% CI) per increment ppb increase in ozone for stroke ED 

visits or HAs for studies presented in Figure 6-25 _______________________6-173

Figure 6-26 Odds Ratio (95% confidence interval) per increment ppb* increase in 

ozone for arrhythmia and dysrhythmia ED visits or HAs.__________________6-173

Table 6-38 Odds Ratio (95% CI) per increment ppb* increase in ozone for arrhythmia 

and dysrhythmia ED visits or HAs for studies presented in Figure 6-26 ______6-174

6.3.2.8 Cardiovascular Mortality______________________________________________________6-174

6.3.2.9 Summary of Epidemiologic Studies _____________________________________________6-175

6.3.3 Toxicology _______________________________________________________________________6-175
Draft – Do Not Cite or Quote xviii September 2011

6.3.3.1 Summary of Findings from Previous Ozone AQCDs ________________________________6-175

6.3.3.2 Recent Cardiovascular Toxicology Studies _______________________________________6-177

Table 6-39 Characterization of study details for Section 6.3.3.2 _____________________6-182

6.3.4 Summary and Causal Determination ___________________________________________________6-183

6.4 Central Nervous System Effects____________________________________________________________ 6-184

Table 6-40 Central Nervous System and Behavioral Effects of Short-term O3

Exposure in Rats ________________________________________________6-189

6.4.1 Neuroendocrine Effects _____________________________________________________________6-190

6.4.2 Summary and Causal Determination ___________________________________________________6-191

6.5 Effects on Other Organ Systems ___________________________________________________________ 6-192

6.5.1 Effects on the Liver and Xenobiotic Metabolism __________________________________________6-192

6.5.2 Effects on Cutaneous and Ocular Tissues_______________________________________________6-193

6.6 Mortality ______________________________________________________________________________ 6-193

6.6.1 Summary of Findings from 2006 Ozone AQCD ___________________________________________6-193

6.6.2 Associations of Mortality and Short-Term Ozone Exposure__________________________________6-194

Figure 6-27 Summary of mortality risk estimates for short-term ozone exposure and 

all-cause (nonaccidental) mortality from all-year and summer season 

analyses. ______________________________________________________6-195

Table 6-41 Corresponding effect estimates for Figure 6-27_________________________6-196

Table 6-42 Range of mean and upper percentile ozone concentrations in previous 

and recent multicity studies ________________________________________6-197

6.6.2.1 Confounding 6-198

Table 6-43 Correlations between PM and ozone by season and region _______________6-199

Figure 6-28 Scatter plots of ozone mortality risk estimates with versus without 

adjustment for PM10 in NMMAPS cities._______________________________6-200

Figure 6-29 Community-specific ozone-mortality risk estimates for nonaccidental 

mortality per 10 ppb increase in same-day 24-h avg summertime ozone 

concentrations in single-pollutant models and copollutant models with 

sulfate. ________________________________________________________6-202

Figure 6-30 Percent increase in all-cause (nonaccidental) and cause-specific mortality 

from the APHENA study for single- and copollutant models._______________6-204

Table 6-44 Corresponding Effect Estimates for Figure 6-30 ________________________6-205

Table 6-45 Sensitivity of ozone risk estimates per 10 μg/m3 increase in 24-h avg 

ozone concentrations at lag 0-1 to alternative methods for adjustment of 

seasonal trend, for all-cause mortality using Berkey MLE and TLNSE 

Hierarchical Models ______________________________________________6-207

6.6.2.2 Effect Modification __________________________________________________________6-207

Table 6-46 Additional percent change in ozone-related mortality for individual-level 

susceptibility factors______________________________________________6-209

Figure 6-31 Ozone mortality risk estimates and community-specific characteristics, 

U.S., 1987-2000. ________________________________________________6-211

Table 6-47 Percent change in all-cause mortality, for all ages, associated with a 

40ppb increase in 1-h max ozone concentrations at Lag 0–1 at the 25th 

and 75th percentile of the center-specific distribution of selected effect 

modifiers_______________________________________________________6-212

Table 6-48 Percentage increase in daily mortality for a 10 ppb increase in 24-h avg 

ozone concentrations during the previous week by geographic region in 

the U.S., 1987-2000______________________________________________6-213

Figure 6-32 Community-specific Bayesian ozone-mortality risk estimates in 98 U.S. 

communities. ___________________________________________________6-214

Figure 6-33 Map of spatially dependent ozone-mortality coefficients for 8-h max 

ozone concentrations using summer data. ____________________________6-214

6.6.2.3 Interaction 6-215

6.6.2.4 Evaluation of the Ozone-Mortality C-R Relationship and Related Issues ________________6-216

Table 6-49 Estimated effect of a 10 ppb increase in 8-h max ozone concentrations on 

mortality during the summer months for single-day and distributed lag 

models ________________________________________________________6-218

Figure 6-34 Estimated combined smooth distributed lag for 48 U.S. cities during the 

summer months. ________________________________________________6-219
Draft – Do Not Cite or Quote xix September 2011

Table 6-50 Estimated percent increase in cause-specific mortality (and 95% CIs) for 

a 10-μg/m3 increase in maximum 8-h ozone during June-August, for the 

same day (lag 0), the average of the same and previous day (lag 0-1), the 

unconstrained distributed lag model for the sum of 0-20 days and the 

penalized distributed lag model (lag 0-20) _____________________________6-220

Figure 6-35 Estimated combined smooth distributed lag in 21 European cities during 

the summer (June-August) months.__________________________________6-222

Table 6-51 Percent excess all-cause mortality per 10 ppb increase in daily 8-h max 

ozone on the same day, by season, month, and age groups ______________6-223

Figure 6-36 Estimated combined C-R curve for ozone and nonaccidental mortality 

using the nonlinear (spline) model. __________________________________6-225

6.6.2.5 Associations of Cause-Specific Mortality and Short-term Ozone Exposure ______________6-227

Figure 6-37 Percent increase in cause-specific mortality.___________________________6-229

Table 6-52 Corresponding effect estimates for Figure 6-37_________________________6-230

6.6.3 Summary and Causal Determination ___________________________________________________6-231

6.7 Overall Summary _______________________________________________________________________ 6-233

Table 6-53 Summary of causal determinations for short-term exposures to ozone_______6-233

6.8 References ___________________________________________________________________________ 6-234

7 INTEGRATED HEALTH EFFECTS OF LONG-TERM OZONE EXPOSURE______________7-1

7.1 Introduction______________________________________________________________________________ 7-1

7.2 Respiratory Effects ________________________________________________________________________ 7-1

7.2.1 New Onset Asthma___________________________________________________________________7-2

Figure 7-1 Interaction of gene presence and O3 level on the Hazard Ratio (HR) of 

new-onset asthma in the 12 Children’s Health Study communities. ___________7-5

Figure 7-2 Ozone modifies the effect of TNF G-308A genotype on bronchitic 

symptoms among children with asthma in the CHS. _______________________7-8

7.2.2 Asthma Hospital Admissions and ED Visits _______________________________________________7-11

Figure 7-3 Ozone-asthma concentration-response relationship using the mean 

concentration during the entire follow-up period. _________________________7-13

7.2.3 Pulmonary Structure and Function______________________________________________________7-14

7.2.3.1 Pulmonary Structure and Function: Evidence from Toxicological Studies_________________7-17

Table 7-1 Respiratory effects in nonhuman primates and rodents resulting from 

long-term O3 exposure _____________________________________________7-22

7.2.4 Pulmonary Inflammation, Injury, and Oxidative Stress_______________________________________7-23

7.2.5 Allergic Responses__________________________________________________________________7-25

7.2.6 Host Defense ______________________________________________________________________7-27

7.2.7 Respiratory Mortality_________________________________________________________________7-27

7.2.8 Summary and Causal Determination ____________________________________________________7-28

Table 7-2 Summary of selected key new studies examining annual ozone exposure 

and respiratory health effects________________________________________7-29

Table 7-3 Studies providing evidence concerning potential confounding by PM for 

available endpoints _______________________________________________7-31

7.3 Cardiovascular Effects ____________________________________________________________________ 7-33

7.3.1 Cardiovascular Disease ______________________________________________________________7-33

7.3.1.1 Cardiovascular Epidemiology___________________________________________________7-33

7.3.1.2 Cardiovascular Toxicology _____________________________________________________7-34

Table 7-4 Characterization of study details for Section 7.3.1.2 ______________________7-36

7.3.2 Cardiac Mortality____________________________________________________________________7-36

7.3.3 Summary and Causal Determination ____________________________________________________7-36

7.4 Reproductive and Developmental Effects _____________________________________________________ 7-37

7.4.1 Effects on Sperm ___________________________________________________________________7-38

7.4.2 Effects on Reproduction ______________________________________________________________7-39

7.4.3 Birth Weight _______________________________________________________________________7-41

Figure 7-4 Birthweight deficit by decile of 24-h avg O3 concentration averaged over 

the entire pregnancy compared with the decile group with the lowest O3

exposure. _______________________________________________________7-42

Table 7-5 Brief summary of epidemiologic studies of birth weight ____________________7-44

7.4.4 Preterm Birth ______________________________________________________________________7-45
Draft – Do Not Cite or Quote xx September 2011

Table 7-6 Brief summary of epidemiologic studies of PTB__________________________7-49

7.4.5 Fetal Growth_______________________________________________________________________7-50

Table 7-7 Brief summary of epidemiologic studies of fetal growth____________________7-53

7.4.6 Postnatal growth____________________________________________________________________7-53

7.4.7 Birth Defects_______________________________________________________________________7-54

Table 7-8 Brief summary of epidemiologic studies of birth defects ___________________7-56

7.4.8 Developmental Respiratory Effects _____________________________________________________7-57

7.4.9 Developmental Central Nervous System Effects ___________________________________________7-61

7.4.9.1 Laterality 7-61

7.4.9.2 Brain Morphology and Neurochemical Changes ____________________________________7-61

7.4.9.3 Neurobehavioral Outcomes ____________________________________________________7-62

7.4.9.4 Sleep Aberrations after Developmental Ozone Exposure _____________________________7-63

7.4.10 Early Life Mortality __________________________________________________________________7-63

7.4.10.1 Stillbirth 7-64

7.4.10.2 Infant Mortality, Less than 1 Year _______________________________________________7-64

7.4.10.3 Neonatal Mortality, Less than 1 Month____________________________________________7-65

7.4.10.4 Postneonatal Mortality, 1 Month to 1 Year_________________________________________7-65

7.4.10.5 Sudden Infant Death Syndrome_________________________________________________7-67

Table 7-9 Brief summary of infant mortality studies _______________________________7-68

Table 7-10 Summary of Key Reproductive and Developmental Toxicological Studies _____7-69

7.4.11 Summary and Causal Determination ____________________________________________________7-70

7.5 Central Nervous System Effects_____________________________________________________________ 7-71

7.5.1 Effects on the Brain and Behavior ______________________________________________________7-71

Table 7-11 Central nervous system effects of long-term O3 exposure in rats ____________7-73

7.5.2 Summary and Causal Determination ____________________________________________________7-74

7.6 Carcinogenic and Genotoxic Potential of Ozone ________________________________________________ 7-75

7.6.1 Introduction________________________________________________________________________7-75

7.6.2 Lung Cancer Incidence and Mortality____________________________________________________7-77

7.6.3 DNA Damage ______________________________________________________________________7-77

7.6.4 Summary and Causal Determination ____________________________________________________7-80

7.7 Mortality _______________________________________________________________________________ 7-80

Figure 7-5 Adjusted ozone-mortality relative risk estimates (95% CI) by time period 

of analysis per subject-weighted mean O3 concentration in the Cancer 

Prevention Study II by the American Cancer Society. _____________________7-81

Table 7-12 Relative risk (and 95% CI) of death attributable to a 10-ppb change in the 

ambient O3 concentration* __________________________________________7-84

7.7.1 Summary and Causal Determination ____________________________________________________7-85

7.8 Overall Summary ________________________________________________________________________ 7-85

Table 7-13 Summary of causal determinations for long-term exposures to ozone ________7-85

7.9 References ____________________________________________________________________________ 7-86

8 POPULATIONS POTENTIALLY AT INCREASED RISK FOR OZONE-RELATED HEALTH 

EFFECTS __________________________________________________________________8-1

8.1 Preexisting Disease/Conditions ______________________________________________________________ 8-3

Table 8-1 Prevalence of respiratory diseases, cardiovascular diseases, and 

diabetes among adults by age and region in the U.S. ______________________8-4

8.1.1 Influenza/Infections___________________________________________________________________8-4

8.1.2 Asthma 8-4

8.1.3 Chronic Obstructive Pulmonary Disease (COPD) ___________________________________________8-7

8.1.4 Cardiovascular Disease _______________________________________________________________8-8

8.1.5 Diabetes __________________________________________________________________________8-10

8.1.6 Hyperthyroidism ____________________________________________________________________8-10

8.2 Lifestage _______________________________________________________________________________ 8-10

8.2.1 Children 8-11

8.2.2 Older Adults _______________________________________________________________________8-14

8.3 Sex ___________________________________________________________________________________ 8-16

8.4 Genetics _______________________________________________________________________________ 8-18
Draft – Do Not Cite or Quote xxi September 2011

8.5 Diet ___________________________________________________________________________________ 8-23

8.6 Body Mass Index and Physical Conditioning ___________________________________________________ 8-25

8.7 Socioeconomic Status ____________________________________________________________________ 8-26

8.8 Race/Ethnicity___________________________________________________________________________ 8-28

8.9 Smoking _______________________________________________________________________________ 8-29

8.10 Heightened Exposure _____________________________________________________________________ 8-30

8.11 Healthy Responders ______________________________________________________________________ 8-32

8.12 Summary ______________________________________________________________________________ 8-32

8.13 References ____________________________________________________________________________ 8-34

9 ENVIRONMENTAL EFFECTS: OZONE EFFECTS ON VEGETATION AND ECOSYSTEMS 9-1

9.1 Introduction______________________________________________________________________________ 9-1

Figure 9-1 An illustrative diagram of the major pathway through which O3 enters 

plants and the major endpoints that O3 may affect in plants and 

ecosystems. ______________________________________________________9-3

9.2 Experimental Exposure Methodologies ________________________________________________________ 9-3

9.2.1 Introduction_________________________________________________________________________9-3

9.2.2 “Indoor,” Controlled Environment, and Greenhouse Chambers_________________________________9-4

9.2.3 Field Chambers _____________________________________________________________________9-4

9.2.4 Plume and FACE-Type Systems ________________________________________________________9-6

9.2.5 Ambient Gradients ___________________________________________________________________9-7

9.2.6 Comparative Studies _________________________________________________________________9-8

9.3 Mechanisms Governing Vegetation Response to Ozone__________________________________________ 9-10

9.3.1 Introduction________________________________________________________________________9-10

9.3.2 Ozone Uptake into the Leaf ___________________________________________________________9-12

9.3.2.1 Changes in Stomatal Function__________________________________________________9-13

Figure 9-2 The microarchitecture of a dicot leaf.__________________________________9-15

Figure 9-3 Possible reactions of ozone within water. ______________________________9-15

Figure 9-4 The Crigee mechanism of ozone attack of a double bond. _________________9-16

9.3.3 Cellular to Systemic Responses________________________________________________________9-17

9.3.3.1 Ozone Sensing and Signal Transduction__________________________________________9-17

9.3.3.2 Gene and Protein Expression Changes in Response to Ozone ________________________9-18

Figure 9-5 Composite diagram of major themes in the temporal evolution of the 

genetic response to ozone stress. ____________________________________9-23

9.3.3.3 Role of Phytohormones in Plant Response to Ozone ________________________________9-24

Figure 9-6 The oxidative cell death cycle. _______________________________________9-26

9.3.4 Detoxification ______________________________________________________________________9-26

9.3.4.1 Overview of Ozone-Induced Defense Mechanisms__________________________________9-26

9.3.4.2 Role of Antioxidants in Plant Defense Responses___________________________________9-27

9.3.5 Effects on Primary and Secondary Metabolism ____________________________________________9-30

9.3.5.1 Light and Dark Reactions of Photosynthesis _______________________________________9-30

9.3.5.2 Respiration and Dark Respiration _______________________________________________9-32

9.3.5.3 Secondary Metabolism________________________________________________________9-33

9.3.6 Summary _________________________________________________________________________9-36

9.4 Nature of Effects on Vegetation and Ecosystems _______________________________________________ 9-38

9.4.1 Introduction________________________________________________________________________9-38

9.4.1.1 Ecosystem Scale, Function, and Structure ________________________________________9-39

9.4.1.2 Ecosystem Services__________________________________________________________9-40

9.4.2 Visible Foliar Injury and Biomonitoring ___________________________________________________9-41

9.4.2.1 Biomonitoring9-42

9.4.2.2 Summary 9-44

9.4.3 Growth, productivity and carbon storage in natural ecosystems _______________________________9-45

9.4.3.1 Plant growth and biomass allocation _____________________________________________9-45

9.4.3.2 Summary 9-49

9.4.3.3 Reproduction 9-49
Draft – Do Not Cite or Quote xxii September 2011

Table 9-1 Ozone effects on plant reproductive processes (derived from Table AX9-

22 of the 2006 ozone AQCD)________________________________________9-51

9.4.3.4 Ecosystem Productivity and Carbon Sequestration__________________________________9-51

Table 9-2 Comparison of models used to simulate the ecological consequences of 

O3 exposure _____________________________________________________9-53

9.4.3.5 Summary 9-57

Table 9-3 Modeled effects of ozone on primary production, C exchange, and 

C sequestration __________________________________________________9-58

9.4.4 Crop yield and quality in agricultural systems _____________________________________________9-58

9.4.4.1 Yield 9-59

9.4.4.2 Crop Quality 9-64

9.4.4.3 Summary 9-64

Table 9-4 Summary of recent studies of ozone effects on crops (exclusive of growth 

and yield) _______________________________________________________9-66

Table 9-5 Modeled effects of ozone on crop yield loss at regional and global scales _____9-68

9.4.5 Water Cycling ______________________________________________________________________9-68

Figure 9-7 The potential effects of ozone exposure on watering cycling. _______________9-69

9.4.5.1 Summary 9-71

9.4.6 Below-Ground Processes_____________________________________________________________9-72

Figure 9-8 Conceptual diagram showing where ozone alters C, water and nutrient 

flow in a tree-soil system, including transfer between biotic and abiotic 

components below ground that influence soil physical and chemical 

properties. ______________________________________________________9-73

9.4.6.1 Litter Carbon Chemistry, Litter Nutrient and Their Ecosystem Budgets___________________9-73

Table 9-6 The effect of elevated ozone on leaf/litter nutrient concentrations____________9-75

9.4.6.2 Decomposer Metabolism and Litter Decomposition__________________________________9-75

9.4.6.3 Soil respiration and carbon formation ____________________________________________9-76

Table 9-7 The temporal variation of ecosystem responses to ozone exposure at 

Aspen FACE site _________________________________________________9-77

9.4.6.4 Nutrient cycling______________________________________________________________9-79

9.4.6.5 Dissolved Organic Carbon and Biogenic Trace Gases Emission _______________________9-80

9.4.6.6 Summary 9-81

9.4.7 Community composition ______________________________________________________________9-81

9.4.7.1 Forest 9-82

9.4.7.2 Grassland and Agricultural Land ________________________________________________9-83

9.4.7.3 Microbes 9-84

9.4.7.4 Summary 9-85

9.4.8 Factors that Modify Functional and Growth Response ______________________________________9-86

9.4.8.1 Genetics 9-87

9.4.8.2 Environmental Biological Factors________________________________________________9-87

9.4.8.3 Physical Factors_____________________________________________________________9-88

9.4.8.4 Interactions with other Pollutants ________________________________________________9-89

Table 9-8 Response of plants to the interactive effects of elevated ozone exposure 

and N enrichment_________________________________________________9-91

9.4.9 Insects and Other Wildlife ____________________________________________________________9-93

9.4.9.1 Insects 9-93

9.4.9.2 Wildlife 9-96

9.4.9.3 Indirect Effects on Wildlife _____________________________________________________9-97

9.4.9.4 Summary 9-100

9.5 Effects-Based Air Quality Exposure Indices and Dose Modeling___________________________________ 9-100

9.5.1 Introduction_______________________________________________________________________9-100

9.5.2 Description of Exposure Indices Available in the Literature __________________________________9-101

Figure 9-9 Diagrammatic representation of several exposure indices ________________9-102

9.5.3 Important Components of Exposure Indices _____________________________________________9-107

9.5.3.1 Role of Concentration _______________________________________________________9-107

Figure 9-10 Trends in May to September 12-h SUM06, peak 1-h ozone concentration 

and number of daily exceedances of 95 ppb ___________________________9-109

Figure 9-11 The number of hourly average concentrations between 50 and 89 ppb for 

the period 1980-2000 for the Crestline, San Bernardino County, CA, 

monitoring site.__________________________________________________9-110
Draft – Do Not Cite or Quote xxiii September 2011

9.5.3.2 Diurnal and Seasonal Exposure________________________________________________9-110

Figure 9-12 Mean diurnal. ___________________________________________________9-113

Figure 9-13 Maximum 3-month, 12-h W126 plotted against maximum 6-month, 12-h 

W126._________________________________________________________9-115

9.5.4 Ozone Uptake/Dose Modeling for Vegetation ____________________________________________9-116

9.5.5 Summary ________________________________________________________________________9-118

9.6 Ozone Exposure-Plant Response Relationships _______________________________________________ 9-120

9.6.1 Introduction_______________________________________________________________________9-120

9.6.2 Estimates of Crop Yield Loss and Tree Seedling Biomass Loss in the 1996 and 2006 Ozone AQCDs 9-123

Figure 9-14 Quantiles of predicted relative yield loss for 34 NCLAN crop experiments.____9-125

Figure 9-15 Quantiles of predicted relative yield loss for 4 crop species in NCLAN 

experiments.____________________________________________________9-126

Figure 9-16 Quantiles of predicted relative biomass loss for 49 tree species in 

NHEERL/WED experiments. _______________________________________9-127

Figure 9-17 Quantiles of predicted relative biomass loss for 4 tree species in 

NHEERL/WED experiments. _______________________________________9-128

Table 9-9 Ozone exposures at which 10 and 20% yield loss is predicted for 50 and 

75% of crop species______________________________________________9-129

Table 9-10 Ozone exposures at which 10 and 20% yield loss is predicted for 50 and 

75% of crop species under drought conditions and adequate moisture ______9-129

Table 9-11 Ozone exposures at which 10 and 20% biomass loss is predicted for 50 

and 75 %of tree species, based on composite functions for the 50th and 

75th percentiles of 49 Weibull curves for relative above-ground biomass 

loss data from 49 studies of 11 tree species grown under well-watered 

conditions for 1 or 2 year; curves were standardized to 90-day W126 _______9-130

9.6.3 Validation of 1996 and 2006 Ozone AQCD Models and Methodology Using the 90 day 12-h W126 and 

Current FACE Data ________________________________________________________________9-130

9.6.3.1 Comparison of NCLAN-Based Prediction and SoyFACE Data ________________________9-132

Table 9-12 Comparison between change in yield observed in the SoyFACE 

experiment between elevated and ambient ozone, and change predicted 

at the same values of ozone by the median composite function for 

NCLAN________________________________________________________9-133

Table 9-13 Comparison between yield observed in the SoyFACE experiment and 

yield predicted at the same values of ozone by the median composite 

function for NCLAN ______________________________________________9-133

Figure 9-18 Comparison of yield observed in SoyFACE experiment in a given year 

with yield predicted by the median composite function based on NCLAN. ____9-134

Figure 9-19 Comparison of composite functions for the quartiles of 7 curves for 7 

genotypes of soybean grown in the SoyFACE experiment, and for the 

quartiles of 11 curves for 5 genotypes of soybean grown in the NCLAN 

project. ________________________________________________________9-135

9.6.3.2 Comparison of NHEERL/WED-Based Prediction of Tree Biomass Response and Aspen FACE 

Data 9-136

Table 9-14 Comparison between change in above-ground biomass elevated and 

ambient ozone in Aspen FACE experiment in 6 year, and change 

predicted at the same values of ozone by the median composite function 

for NHEERL/WED (two-parameter relative biomass model) _______________9-137

Table 9-15 Comparison between above-ground biomass observed in Aspen FACE 

experiment in 6 year and biomass predicted by the median composite 

function based on NHEERL/WED (three-parameter absolute biomass 

model with intercept scaled to Aspen FACE data)_______________________9-137

Figure 9-20 Comparison between above-ground biomass observed in Aspen FACE 

experiment in 6 year and biomass predicted by the median composite 

function based on NHEERL/WED.___________________________________9-138

9.6.3.3 Exposure-Response in a Gradient Study_________________________________________9-139

Figure 9-21 Above-ground biomass for one genotype of cottonwood grown in seven 

locations for one season in 3 years.__________________________________9-140

9.6.3.4 Meta-analyses of growth and yield studies _______________________________________9-141

Table 9-16 Meta-analyses of growth or yield studies published since 2005 ____________9-141

9.6.3.5 Additional exposure-response data _____________________________________________9-142

9.6.4 Summary ________________________________________________________________________9-142

Table 9-17 Summary of studies of effects of ozone exposure on growth and yield of 

agricultural crops ________________________________________________9-144
Draft – Do Not Cite or Quote xxiv September 2011

Table 9-18 Summary of studies of effects of ozone exposure on growth of natural 

vegetation______________________________________________________9-146

9.7 References ___________________________________________________________________________ 9-148

10 THE ROLE OF TROPOSPHERIC OZONE IN CLIMATE CHANGE AND UV-B EFFECTS__10-1

10.1 Introduction_____________________________________________________________________________ 10-1

10.2 Physics of the Earth’s Radiation Budget ______________________________________________________ 10-1

Figure 10-1 Diagram of the factors that determine human exposure to ultraviolet 

radiation. _______________________________________________________10-2

10.3 Effects of Tropospheric Ozone on Climate_____________________________________________________ 10-3

Background _____________________________________________________________________________10-3

10.3.1 Climate Change Evidence and the Influence of Tropospheric Ozone ___________________________10-4

10.3.1.1 Climate Change in the Recent Past ______________________________________________10-4

10.3.1.2 Projections of Future Climate Change ____________________________________________10-5

10.3.1.3 Metrics of Potential Climate Change _____________________________________________10-6

10.3.1.4 Tropospheric Ozone as a Greenhouse Gas _______________________________________10-7

Figure 10-2 Schematic illustrating the effects of tropospheric ozone on climate. __________10-8

Figure 10-3 Global average radiative forcing (RF) estimates and uncertainty ranges in 

2005 for anthropogenic CO2, CH4, ozone and other important agents and 

mechanisms. ____________________________________________________10-9

10.3.2 Factors that Influence the Effect of Tropospheric Ozone on Climate____________________________10-9

10.3.2.1 Trends in the Concentration of Tropospheric Ozone ________________________________10-10

10.3.2.2 The Effect of Surface Albedo on Ozone Radiative Forcing ___________________________10-13

10.3.2.3 The Effect of Vertical Distribution on Ozone Radiative Forcing ________________________10-13

10.3.2.4 Feedback Factors that Alter the Climate Response to Changes in Ozone Radiative Forcing_10-13

10.3.2.5 Indirect Effects of Tropospheric Ozone on the Carbon Cycle _________________________10-15

10.3.3 Competing Effects of Ozone Precursors on Climate _______________________________________10-15

10.3.4 Calculating Radiative Forcing and Climate Response to Past Trends in Tropospheric Ozone _______10-17

Figure 10-4 Ensemble average 1900-2000 surface temperature trends (oC per 

century) in response to tropospheric ozone changes. ____________________10-18

10.4 UV-B Related Effects and Tropospheric Ozone________________________________________________ 10-19

10.4.1 Background ______________________________________________________________________10-19

10.4.2 Human Exposure and Susceptibility to Ultraviolet Radiation _________________________________10-19

10.4.3 Human Health Effects due to UV-B Radiation ____________________________________________10-20

10.4.4 Ecosystem and Materials Damage Effects Due to UV-B Radiation ____________________________10-22

10.4.5 UV-B Related Effects Associated with Changes in Tropospheric Ozone Concentrations ___________10-24

10.5 Summary _____________________________________________________________________________ 10-27

10.5.1 Summary of the Effects of Tropospheric Ozone on Climate _________________________________10-27

10.5.2 Summary of UV-B Related Effects on Human Health, Ecosystems, and Materials Relating to Changes in 

Tropospheric Ozone Concentrations ___________________________________________________10-28

10.6 References ___________________________________________________________________________ 10-29

11 REFERENCES_____________________________________________________________11-1
Draft – Do Not Cite or Quote xxv September 2011

OZONE PROJECT TEAM 

Executive Direction

Dr. John Vandenberg (Director)—National Center for Environmental Assessment-RTP Division, 

Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle 

Park, NC

Ms. Debra Walsh (Deputy Director)—National Center for Environmental Assessment-RTP Division, 

Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle 

Park, NC

Dr. Mary Ross (Branch Chief)—National Center for Environmental Assessment, Office of Research 

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

Scientific Staff

Dr. James Brown (O3 Team Leader)—National Center for Environmental Assessment, Office of 

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

Dr. Christal Bowman—National Center for Environmental Assessment, Office of Research and 

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

Dr. Barbara Buckley—National Center for Environmental Assessment, Office of Research and 

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

Ms. Ye Cao—Oak Ridge Institute for Science and Education, National Center for Environmental 

Assessment, Office of Research and Development, U.S. Environmental Protection Agency, 

Research Triangle Park, NC

Mr. Allen Davis—National Center for Environmental Assessment, Office of Research and 

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

Dr. Jean-Jacques Dubois—National Center for Environmental Assessment, Office of Research and 

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

Dr. Steven J. Dutton—National Center for Environmental Assessment, Office of Research and 

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

Dr. Jeffrey Herrick—National Center for Environmental Assessment, Office of Research and 

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

Dr. Erin Hines—National Center for Environmental Assessment, Office of Research and 

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

Dr. Doug Johns—National Center for Environmental Assessment, Office of Research and 

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

Dr. Dennis Kotchmar—National Center for Environmental Assessment, Office of Research and 

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

Dr. Meredith Lassiter—National Center for Environmental Assessment, Office of Research and 

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

Dr. Lingli Liu— Oak Ridge Institute for Science and Education, National Center for Environmental 

Assessment, Office of Research and Development, U.S. Environmental Protection Agency, 

Research Triangle Park, NC

Dr. Thomas Long—National Center for Environmental Assessment, Office of Research and 

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

Dr. Thomas Luben—National Center for Environmental Assessment, Office of Research and 

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

Dr. Qingyu Meng— Oak Ridge Institute for Science and Education, National Center for 

Environmental Assessment, Office of Research and Development, U.S. Environmental Protection 

Agency, Research Triangle Park, NC
Draft – Do Not Cite or Quote xxvi September 2011

Dr. Kristopher Novak—National Center for Environmental Assessment, Office of Research and 

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

Dr. Elizabeth Oesterling Owens—National Center for Environmental Assessment, Office of 

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

Dr. Molini Patel—National Center for Environmental Assessment, Office of Research and 

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

Dr. Joseph P. Pinto—National Center for Environmental Assessment, Office of Research and 

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

Ms. Joann Rice—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Mr. Jason Sacks—National Center for Environmental Assessment, Office of Research and 

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

Dr. Lisa Vinikoor-Imler—National Center for Environmental Assessment, Office of Research and 

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

Technical Support Staff

Mr. Kenneth J. Breito–Senior Environmental Employment Program, National Center for 

Environmental Assessment, Office of Research and Development, U.S. Environmental Protection 

Agency, Research Triangle Park, NC 

Mr. Gerald Gurevich—National Center for Environmental Assessment, Office of Research and 

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

Mr. Ryan Jones—National Center for Environmental Assessment, Office of Research and 

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

Ms. Ellen Lorang—National Center for Environmental Assessment, Office of Research and 

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

Mr. J. Sawyer Lucy–Student Services Authority, National Center for Environmental Assessment, 

Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle 

Park, NC

Ms. Deborah Wales—National Center for Environmental Assessment, Office of Research and 

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

Mr. Richard N. Wilson–National Center for Environmental Assessment, Office of Research and 

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

Ms. Barbara Wright—Senior Environmental Employment Program, National Center for 

Environmental Assessment, Office of Research and Development, U.S. Environmental Protection 

Agency, Research Triangle Park, NC
Draft – Do Not Cite or Quote xxvii September 2011

AUTHORS, CONTRIBUTORS, AND REVIEWERS

Authors

Dr. James Brown (O3 Team Leader)—National Center for Environmental Assessment, Office of 

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

Dr. Christal Bowman—National Center for Environmental Assessment, Office of Research and 

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

Dr. Barbara Buckley—National Center for Environmental Assessment, Office of Research and 

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

Dr. Maggie Clark—Department of Environmental and Radiological Health Sciences, Colorado State 

University, Fort Collins, CO

Dr. Jean-Jacques Dubois—National Center for Environmental Assessment, Office of Research and 

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

Dr. Steven J. Dutton—National Center for Environmental Assessment, Office of Research and 

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

Dr. Kelly Gillespie— Donald Danforth Plant Science Center, St. Louis, MO

Dr. Terry Gordon—Department of Environmental Medicine, New York University School of 

Medicine, Tuxedo, NY

Dr. Jeffrey Herrick—National Center for Environmental Assessment, Office of Research and 

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

Dr. Erin Hines—National Center for Environmental Assessment, Office of Research and 

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

Dr. Kazuhiko Ito—Department of Environmental Medicine, New York University School of Medicine, 

Tuxedo, NY

Dr. Doug Johns—National Center for Environmental Assessment, Office of Research and 

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

Dr. Dennis Kotchmar—National Center for Environmental Assessment, Office of Research and 

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

Dr. Meredith Lassiter—National Center for Environmental Assessment, Office of Research and 

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

Dr. Lingli Liu— Oak Ridge Institute for Science and Education, Postdoctoral Research Fellow to 

National Center for Environmental Assessment, Office of Research and Development, 

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

Dr. Thomas Long—National Center for Environmental Assessment, Office of Research and 

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

Dr. Thomas Luben—National Center for Environmental Assessment, Office of Research and 

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

Dr. Loretta J. Mickley—School of Engineering & Applied Sciences, Harvard University, Cambridge, 

MA

Dr. Kristopher Novak—National Center for Environmental Assessment, Office of Research and 

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

Dr. Elizabeth Oesterling Owens—National Center for Environmental Assessment, Office of 

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

Dr. Molini Patel—National Center for Environmental Assessment, Office of Research and 

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

Dr. Jennifer Peel—Department of Environmental and Radiological Health Sciences, Colorado State 

University, Fort Collins, CO 
Draft – Do Not Cite or Quote xxviii September 2011

Dr. Joseph Pinto—National Center for Environmental Assessment, Office of Research and 

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

Ms. Joann Rice—on detail to the National Center for Environmental Assessment, Office of 

Research and Development, from the Office of Air Quality Planning and Standards, Office of Air 

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

Mr. Jason Sacks—National Center for Environmental Assessment, Office of Research and 

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

Dr. George Thurston—Department of Environmental Medicine, New York University School of 

Medicine, Tuxedo, NY

Dr. Lisa Vinikoor-Imler—National Center for Environmental Assessment, Office of Research and 

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

Dr. Cosima Wiese—Department of Biology, Misericordia University, Dallas, PA

Contributors

Mr. Brian Adams—Oak Ridge Institute for Science and Education, National Center for 

Environmental Assessment, Office of Research and Development, U.S. Environmental Protection 

Agency, Research Triangle Park, NC

Dr. Halil Cakir—Oak Ridge Institute for Science and Education, National Center for Environmental 

Assessment, Office of Research and Development, U.S. Environmental Protection Agency, 

Research Triangle Park, NC

Ms. Ye Cao—Oak Ridge Institute for Science and Education, National Center for Environmental 

Assessment, Office of Research and Development, U.S. Environmental Protection Agency, 

Research Triangle Park, NC

Mr. Allen Davis—National Center for Environmental Assessment, Office of Research and 

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

Mr. Mark Evangelista—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Mr. Jay Haney—ICF International, San Rafael, CA

Dr. E. Henry Lee—National Health and Environmental Effects Research Laboratory, U.S. 

Environmental Protection Agency, Corvallis, OR

Dr. Qingyu Meng—Oak Ridge Institute for Science and Education, Postdoctoral Research Fellow to 

National Center for Environmental Assessment, Office of Research and Development, U.S. 

Environmental Protection Agency, Research Triangle Park, NC

Mr. David Mintz—Office of Air Quality Planning and Standards, Office of Air and Radiation, U.S. 

Environmental Protection Agency, Research Triangle Park, NC

Mr. Tom Myers—ICF International, San Rafael, CA

Mr. Mark Schmidt—Office of Air Quality Planning and Standards, Office of Air and Radiation, U.S. 

Environmental Protection Agency, Research Triangle Park, NC

Dr. Huiquin Wang—School of Engineering and Applied Science, Harvard University, Cambridge, 

MA

Mr. Benjamin Wells—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. Lin Zhang—School of Engineering and Applied Science, Harvard University, Cambridge, MA

Reviewers

Dr. Christian Andersen—National Health and Environmental Effects Research Laboratory, U.S. 

Environmental Protection Agency, Corvallis, OR

Ms. Lea Anderson—Office of General Counsel, U.S. Environmental Protection Agency, 

Washington, D.C.
Draft – Do Not Cite or Quote xxix September 2011

Dr. Susan Anenberg—Office of Air Quality Planning and Standards, U.S. Environmental Protection 

Agency, Washington, D.C.

Dr. Robert Arnts—National Exposure Research Laboratory, Office of Research and Development, 

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

Dr. John Balmes— Department of Medicine, University of California, San Francisco and School of 

Public Health, University of California, Berkeley, CA

Dr. Lisa Baxter—National Exposure Research Laboratory, Office of Research and Development, 

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

Dr. Souad Benromdhane—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. Fitzgerald Booker—USDA-ARS Plant Science Research Unit, Raleigh, NC

Dr. Michael Breen—National Exposure Research Laboratory, Office of Research and Development, 

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

Dr. Philip Bromberg—School of Medicine, University of North Carolina, Chapel Hill, NC

Dr. Kent Burkey—USDA-ARS Plant Science Research Unit, Raleigh, NC

Dr. David DeMarini—National Health and Environmental Effects Research Laboratory, Office of 

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

Dr. Russ Dickerson—Department of Atmospheric and Oceanic Science, University of Maryland, 

College Park, MD

Mr. Patrick Dolwick—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. Aimen Farraj—National Health and Environmental Effects Research Laboratory, Office of 

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

Dr. Arlene Fiore—NOAA/Geophysical Dynamics Laboratory, Princeton, NJ

Dr. Ian Gilmour—National Health and Environmental Effects Research Laboratory, Office of 

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

Dr. Stephen Graham—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. Tara Greaver—National Center for Environmental Assessment, Office of Research and 

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

Dr. Gary Hatch—National Health and Environmental Effects Research Laboratory, Office of 

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

Dr. Bryan Hubbel—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. Kristin Isaacs—National Exposure Research Laboratory, Office of Research and Development, 

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

Dr. Scott Jenkins—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. Karl Jensen—National Health and Environmental Effects Research Laboratory, Office of 

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

Dr. Urmila Kodavanti—National Health and Environmental Effects Research Laboratory, Office of 

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

Dr. Petros Koutrakis—Department of Environmental Health, Harvard School of Public Health, 

Boston, MA

Mr. John Langstaff—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. Christopher Lau—National Health and Environmental Effects Research Laboratory, Office of 

Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC
Draft – Do Not Cite or Quote xxx September 2011

Mr. Gary Lear— Office of Administration and Policy, Office of Air and Radiation, U.S. Environmental 

Protection Agency, Washington, DC

Dr. Morton Lippmann—Nelson Institute of Environmental Medicine, New York University, Tuxedo, 

NY

Dr. Karen Martin—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Ms. Connie Meacham—National Center for Environmental Assessment, Office of Research and 

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

Mr. David Mintz—Office of Air Quality Planning and Standards, Office of Air and Radiation, U.S. 

Environmental Protection Agency, Research Triangle Park, NC

Dr. Pradeep Rajan—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. John Rogers—National Health and Environmental Effects Research Laboratory, Office of 

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

Ms. Vicki Sandiford—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Ms. Susan Stone—Office of Air Quality Planning and Standards, Office of Air and Radiation, 

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

Dr. John Vandenberg—National Center for Environmental Assessment, Office of Research and 

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

Dr. James G. Wagner—Department of Pathobiology and Diagnostic Investigation, Michigan State 

University, East Lansing, MI

Ms. Debra Walsh—National Center for Environmental Assessment, Office of Research and 

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

Dr. Jason West—Department of Environmental Sciences & Engineering, University of North 

Carolina, Chapel Hill, NC
Draft – Do Not Cite or Quote xxxi September 2011

CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE 

OZONE NAAQS REVIEW P ANEL

Chair of the Environmental Protection Agency’s Clean Air Scientific Advisory Committee

Dr. Jonathan M. Samet*, Department of Preventive Medicine at the Keck School of Medicine, and 

Director of the Institute for Global Health at the University of Southern California, Los Angeles, CA

Chair of the Ozone Review Panel

Dr. Jonathan M. Samet*, Department of Preventive Medicine at the Keck School of Medicine, and 

Director of the Institute for Global Health at the University of Southern California, Los Angeles, CA

Members

Dr. George A. Allen*, Northeast States for Coordinated Air Use Management (NESCAUM), Boston, 

MA

Professor Ed Avol, Department of Preventive Medicine, Keck School of Medicine, University of 

Southern California, Los Angeles, CA

Dr. John Bailar, The National Academies, Washington, D.C.

Dr. Michelle Bell, School of Forestry & Environmental Studies, Yale University, New Haven, CT

Dr. Joseph Brain*, Department of Environmental Health, Harvard School of Public Health, Harvard 

University, Boston, MA

Dr. David Chock, Independent Consultant, Bloomfield Hills, MI

Dr. William Michael Foster, Division of Pulmonary, Allergy, and Critical Care Medicine, Duke 

University Medical Center, Durham, NC

Dr. H. Christopher Frey*, Department of Civil, Construction and Environmental Engineering, 

College of Engineering, North Carolina State University, Raleigh, NC

Dr. Judith Graham, Independent Consultant, Pittsboro, NC

Dr. David Grantz, College of Natural and Agricultural Sciences, Air Pollution Research Center, 

University of California Riverside, Parlier, CA

Dr. Jack Harkema, Center for Integrated Toxicology, Michigan State University, East Lansing, MI

Dr. Daniel Jacob, Atmospheric Chemistry and Environmental Engineering, Harvard University, 

Cambridge, MA

Dr. Steven Kleeberger, National Institute of Environmental Health Sciences, National Institutes of 

Health, Research Triangle Park, NC

Dr. Frederick J. Miller, Independent Consultant, Cary, NC

Dr. Howard Neufeld, Department of Biology, Appalachian State University, Boone, NC

Dr. Armistead (Ted) Russell*, Department of Civil and Environmental Engineering, Georgia Institute 

of Technology, Atlanta, GA

Dr. Helen Suh MacIntosh*, Environmental Health, NORC at the University of Chicago, and the 

School of Public Health, Harvard University, Boston, MA

Dr. James Ultman, Department of Chemical Engineering, Pennsylvania State University, University 

Park, PA

Dr. Sverre Vedal, Department of Environmental and Occupational Health Sciences, School of 

Public Health and Community Medicine, University of Washington, Seattle, WA

Dr. Kathleen Weathers*, Cary Institute of Ecosystem Studies, Millbrook, NY
Draft – Do Not Cite or Quote xxxii September 2011

Dr. Peter Woodbury, Department of Crop and Soil Sciences, Cornell University, Ithaca, NY

* Members of the statutory Clean Air Scientific Advisory Committee (CASAC) appointed by the EPA 

Administrator 

Science Advisory Board Staff 

Dr. Holly Stallworth, Designated Federal Officer, U.S. Environmental Protection Agency, Mail Code 

1400R, 1300 Pennsylvania Avenue, NW, Washington, DC, 20004, Phone: 202-564-2073, Email: 

stallworth.holly@epa.gov
Draft – Do Not Cite or Quote xxxiii September 2011

ACRONYMS AND ABBREVIATIONS

129 mouse strain (129S1/SvlmJ)

α alpha, ambient exposure factor 

α-ATD alpha 1-antitrypsin deficiency

α-SMA alpha-smooth muscle actin

α-tocopherol alpha-tocopherol 

α-TOH alpha tocopherol 

a air exchange rate of the 

microenvironment 

A2 climate scenario in IPCC

AADT annual average daily traffic

A1B climate scenario in IPCC

ABA abscisic acid 

ABI abscisic acid insensitive 

A1c glycosylated hemoglobin blood 

test

Ach acetylcholine

ACM (Harvard University) Atmospheric 

Chemistry Modeling (Group)

ACS American Cancer Society 

ACS-CPSII ACS Cancer Prevention Study II 

ADC arginine decarboxylase 

ADSP Adirondack State Park, NY 

AER air exchange rate 

AH2 ascorbic acid; ascorbate 

AHR airway(s) hyperresponsiveness, 

airway(s) hyperreactivity 

AhR aryl hydrocarbon receptor 

AHSMOG (California Seventh Day) Adventist 

Heath and Smog (Study) 

AI alveolar interstitial 

AIC(s) Akaike’s information criterion

AIRS Aerometric Information Retrieval 

System; Atmospheric Infrared 

Sounder (instrument) 

A/J mouse strain

Ala-9Val genotype associated with 

Manganese superoxide dismutase 

(MnSOD) gene

AM alveolar macrophage(s) 

ANF atrial natriuretic factor 

AOT20 seasonal sum of the difference 

between an hourly concentration 

at the threshold value of 20 ppb, 

minus the threshold value of 20 

ppb 

AOT30 seasonal sum of the difference 

between an hourly concentration 

at the threshold value of 30 ppb, 

minus the threshold value of 30 

ppb 

AOT40 seasonal sum of the difference 

between an hourly concentration 

at the threshold value of 40 ppb, 

minus the threshold value of 40 

ppb 

AOT60 seasonal sum of the difference 

between an hourly concentration 

at the threshold value of 60 ppb, 

minus the threshold value of 60 

ppb 

AOTx family of cumulative, cutoff 

concentration-based exposure 

indices 

AP activated protein

A2p climate scenario in IPCC 

(preliminary version of A2)

APEX Air Pollutants Exposure (model) 

APHEA(2) Air Pollution on Health: a

European Approach (study) 

APHENA Air Pollution and Health: A 

European and North American 

Approach 

ApoB apolipoprotein B

ApoE apolipoprotein E

APX ascorbate peroxidase 

aq aqueous form: (aq)O3

AQCD Air Quality Criteria Document 

AQI Air Quality Index

AQS (U.S. EPA) Air Quality System 

(database) 

AR acoustic rhinometry

AR4 Fourth Assessment Report (AR4) 

from the IPCC 

AR5 Fifth Assessment Report (AR5) 

from the IPCC

ARG arginase variants (ex., ARG1, 

ARG2, ARG1h4) 

ARIC Atherosclerosis Risk in 

Communities 

ARIES (Atlanta) Aerosol Research and 

Inhalation Epidemiology Study

atm atmosphere

ATP adenosine triphosphate 

ATPase adenosine triphosphatase; 

adenosine triphosphate synthase 

ATS American Thoracic Society 

avg average

AVHRR advanced very high resolution 

radiometer

β beta, beta coefficient; regression 

coefficient; standardized 

coefficient; shape parameter; scale 

parameter 

B boron 

B1 climate scenario in IPCC

B6 mouse strain (C57BL/6J)

BAL bronchoalveolar lavage

BALB/c mouse strain

BALF bronchoalveolar lavage fluid 

bb bronchials 
Draft – Do Not Cite or Quote xxxiv September 2011

BB bronchial airways 

BC black carbon 

B cells bone-marrow-derived 

lymphocytes; B lymphocytes 

B6C3F1 mouse strain

BDNF brain-derived neurotrophic factor 

BEAS-2B human bronchial epithelial cell line 

BEIS Biogenic Emissions Inventory 

System 

BELD Biogenic Emissions Landcover 

Database

BIPM International Bureau of Weights 

and Measures 

BM basement membrane 

BMI body mass index 

BNP β -type natriuretic peptide 

BP blood pressure 

BPD biparietal diameter

bpm breaths per minute 

Br bromine

BRFSS Behavioral Risk Factor 

Surveillance System

BS black smoke 

BSA bovine serum albumin

Bsp, BSP black smoke particles

Bt, BT, bt Bacillus thuringiensis; bacterium 

proteins used in pesticides (or 

genetically engineered plants 

produce Bt toxin)

BTEX family of compounds (benzene, 

toluene, ethylbenzene, and xylene)

BW body weight 

C carbon; concentration; ([vitamin] C, 

ascorbate)

oC degrees Celsius 13C carbon-13 isotope

C3 mouse strain (C3H/HEJ)

C3 plants that use only the Calvin 

cycle for fixing the carbon dioxide 

from the air 

C4 plants that use the Hatch-Slack 

cycle for fixing the carbon dioxide 

from the air 

C16:0 palmitic acid (saturated fatty acid)

C18:1 unsaturated fatty acid 

Ca calcium

Ca ambient concentration 

[Ca] calcium concentration

Ca2+ calcium ion 

CA Canada (ICD-10-CA)

CAA Clean Air Act 

CALINE4 California line source dispersion 

model for predicting air pollutant 

concentrations near roadways

CAM plants that use crassulacean acid 

metabolism for fixing the carbon 

dioxide from the air 

CAMP Childhood Asthma Management 

Program

CAMx Comprehensive Air Quality Model, 

with extensions

CAN Canada

CAP(s) concentrated ambient particles 

CAR centriacinar region 

CASAC Clean Air Scientific Advisory 

Committee 

CASTNET Clean Air Status and Trends 

Network 

CAT catalase

CB carbon black; CMAQ mechanisms 

(ex., CB04, CB05, CB06)

C57BL/6 mouse strain

C57BL/6J mouse strain

CBSA core-based statistical area 

C/C carbon of total carbon

CCSP Clara cell secretory protein 

CD cluster of differentiation (various 

receptors on T-cells: CD8+, CD44, 

etc.); criteria document (see 

AQCD)

CD-1 mouse strain 

CDC Centers for Disease Control and 

Prevention 

CF charcoal-filtered; carbon filtered air

CF2 twice-filtered air (particulate filter 

and activated charcoal filter)

C-fibers afferent, slow, unmylenated nerves 

innervating the respiratory system

CFR Code of Federal Regulations

CGRP calcitonin gene-related peptide 

CH3 methyl group 

CH4 methane 

C2H2 acetylene 

C2H4 ethylene 

C3H mouse strain (C3H/HEJ or 

C3H/OuJ) 

C3H6 propylene 

CHAD Consolidated Human Activity 

Database 

CH3Br methyl bromide 

CH3-CHO acetaldehyde 

CH3Cl methyl chloride 

CH3-CO acetyl radical(s)

CHD coronary heart disease 

CHF congestive heart failure 

C2H5–H ethane

C3H/HeJ mouse strain

CH3I methyl iodide 

CHIP Effects of Elevated Carbon Dioxide 

and Ozone on Potato Tuber 

Quality in the European Multiple 

Site Experiment 

CH3O2

• methyl peroxy (radical) 

CH3OOH acetic acid; methyl hydroperoxide

CHS Child Health Study 

CI confidence interval(s)
Draft – Do Not Cite or Quote xxxv September 2011

Cj airborne O3 concentration at 

microenvironment j 

Cl chlorine

Cl− chlorine ion

Cl2 chlorine gas

CLE Current Legislation (climate 

scenario in IPCC) 

CLM chemiluminescence method 

ClNO2 nitryl chloride

cm centimeter(s)

cm2 square centimeters 

CM Clinical Modification (ICD-9-CM)

CMAQ Community Multi-scale Air Quality 

modeling system

CN constant atmospheric nitrogen 

deposition (in PnET-CN 

ecosystem model)

CNA continental North America

CNS central nervous system 

CO carbon monoxide; Cardiac output

CO2 carbon dioxide 

COD coefficient of divergence; 

coefficient of determination 

Col-0 (Arabidopsis ecotype) Columbia-0

COP Conference of Parties (to the 

UNFCCC)

COPD chronic obstructive pulmonary 

disease 

COX-2 cyclooxygenase 2 enzyme

C-R concentration-response 

CRA Centro di ricerca per la 

cerealicoltura (CRA) [The Centre 

for Cereal Research] – Unit 5: The

Research Unit for Cropping 

Systems in Dry Environments in 

Bari, Italy (water-stressed 

conditions)

CRP C-reactive protein 

CS corticosteroid 

CSA cross-sectional area; combined 

statistical area 

csb, Csb cockayne syndrome (cb) 

gene/protein group A

CSF colony-stimulating factor

CST central standard time 

CSTR continuous stirred tank reactor 

CSV comma-separated values (a 

spreadsheet format)

CT computer tomography

CTM(s) chemical transport model(s) 

cum avg cumulative average

CUOt The cumulative stomatal uptake of 

O3, using a constant O3 uptake 

rate threshold (t) of nmol/m2

/s 

CV, C.V. coefficient of variation 

cv, c.v. cultivar 

CVD cardiovascular disease 

CXC chemokine family of cytokines, 

with highly conserved motif:cysxxx-cys (CXC) amino acid group

CXCR2 CXC chemokine receptor 2 

(CXCR2)

CXR Chest (x-ray) radiograph(s)

CyS protein cysteines 

Cys-LT cysteinyl leukotrienes (LTC4, LTD4, 

LTE4)

cyt cytosolic-free

Δ, δ delta, difference; change 

ΔFEV1 change in FEV1

ΔVD change in dead space volume of 

the respiratory tract 

2-D two-dimensional

3-D three-dimensional

DAHPS 3-deoxy-D-arabino-heptulosonat7-phosphate synthase 

DBP diastolic blood pressure 

DC(s) dendritic cell(s)

DDM direct decoupled method

DEP(s) diesel exhaust particle(s)

df degrees of freedom 

DGGE denaturing gradient gel 

electrophoresis

DHA dehydroascorbate

DHAR dehydroascorbate reductase 

DHBA 2,3-dihydroxybenzoic acid 

DLEM Dynamic Land Ecosystem Model 

dm3 cubic decimeter(s)

DNA deoxyribonucleic acid 

DOAS differential optical absorption 

spectroscopy 

DOC dissolved organic carbon 

DR type of human leukocyte antigens

(HLA-DR)

dt Portion of time-period spent in 

microenvironment j

DTH delayed-type hypersensitivity

DU Dobson unit(s) 

DW dry weight

E embryonic day (ex., E15, E16, 

etc); [vitamin] E

Ea exposure to pollutant of ambient 

origin 

EBC exhaled breath condensate (fluid) 

EC elemental carbon 

ECE endothelin converting enzyme(s) 

[i.e., ECE-1]

ECG electrocardiogram 

ECOPHYS physiological process modeling to 

predict the response of aspen 

forest ecosystems (modeling 

growth and environmental stress in 

Populus)

ED emergency department; embryonic 

day (ex., ED5, ED20)
Draft – Do Not Cite or Quote xxxvi September 2011

EGEA (The) Epidemiology (study on) 

Genetics and Environment of 

Asthma, (adults and children with 

asthma)

EGEA2 follow-up study on EGEA (adults 

with asthma only)

EHC-93 ambient PM reference sample 

(urban dust [air particles] collected 

in Ottawa Canada)

ELF extracellular lining fluid

EMI (U.S. EPA) Exposure Model for 

Individuals

Ena exposure to pollutant of 

nonambient origin 

ENA-78 epithelial cell-derived neutrophilactivating peptide 78 

eNO exhaled nitric oxide 

eNOS endothelial nitric oxide synthase 

ENVISAT (EAS) Earth Observation satellite

EOTCP European Open Top Chamber 

Programme 

EP epithelial cells 

EPA U.S. Environmental Protection 

Agency 

EPIC European Prospective 

Investigation into Cancer and 

Nutrition

ER emergency room

ESA European Space Agency

ET extrathoracic; endothelin (i.e. ET1)

ET1 anterior nasal passages within the 

extrathoracic (ET) region 

ET2 oral airway and posterior nasal 

passages within the extrathoracic 

(ET) region 

ETS environmental tobacco smoke 

EU European Union

EUS eastern U.S. 

Ф Phi; calculated efficiency 

ФPSII-max maximum photochemical effective 

quantum yield of PSII 

f Fraction of the relevant time period

F female 

F344 Fischer 344 (rat strain)

F2a 8-isoprostane (major F2 

prostaglandin [8 iso-PGF2a])

FA filtered air

FACE free-air−CO2 enrichment (system) 

FACES Fresno Asthmatic Children’s 

Environment Study

fB frequency of breathing 

FC fibrocartilaginous coat 

FEF forced expiratory flow 

FEF25-75 forced expiratory flow between the 

times at which 25% and 75% of 

the vital capacity is reached 

FEFx forced expiratory flow after (x)% 

vital capacity (e.g., after 25, 50, or 

75% vital capacity) 

FEM Federal equivalent method 

FeNO exhaled nitric oxide fraction

FEV1 forced expiratory volume in 1 

second 

FHM (USDA Forest Service) Forest 

Health Monitoring Program

FIA (USDA Forest Service) Forest 

Inventory and Analysis Program 

Finf infiltration factor 

Finf,i infiltration factor for indoor 

environment (i)

FLAG Federal land managers’ air quality 

related values workgroup 

FLRT fractional uptake efficiency of the 

lower respiratory tract (LRT) 

Fnose fractional uptake efficiency via 

nasal absorption 

Fo fraction of time spent in outdoor 

microenvironments 

FPM Forest Pest Management 

FR Federal Register

FRAP ferric reducing ability of plasma 

FRC functional residual capacity 

FRM Federal reference method 

FRT fractional uptake efficiency of the 

respiratory tract (RT) 

Fst01 flux cut off threshold 

FURT fractional uptake efficiency of the 

upper respiratory tract (URT) 

FVC forced vital capacity 

Fv/Fm a ratio: a measure of the maximum 

efficiency of Photosystem II 

FVI fruits and vegetables index 

γ gamma

γ-TOH gamma-tocopherol 

g, mg, kg, μg, ng, pg gram(s), milligram(s), kilogram(s), 

microgram(s), nanogram(s), 

picogram(s) 

G granulocyte; guanosine

g gram(s); gaseous form: (g)O3

GAM generalized additive model(s) 

gbs conductance through boundary 

layer and stomata

GCLC (glutathione genetic variant) 

glutamate-cysteine ligase catalytic 

subunit

GCLM (glutathione genetic variant) 

glutamate-cysteine ligase modifier 

subunit

G-CSF granulocyte colony-stimulating 

factor (receptor)

GD gestational day

GEE generalized estimating equations 

GEOS (NASA) Goddard Earth Observing 

System model

GEOS5 GEOS version 5

GEOS-Chem GEOS-Chemistry (tropospheric 

model) 

GFAP glial fibrillary acidic protein 
Draft – Do Not Cite or Quote xxxvii September 2011

GH growth hormone

GHG greenhouse gas 

GLM(s) generalized linear model(s) 

GMAO (NASA) Global Modeling and 

Assimilation Office

GM-CSF granulocyte macrophage colonystimulating factor 

GOME (ESA) Global Ozone Monitoring 

Experiment (spectrometer)

GOMOS Global Ozone Monitoring by 

Occultation of Stars (ESA 

ENVISAT spectrometer measuring 

long-term trends in O3)

G6P glucose-6-phosphate 

G6PD glucose-6-phosphate 

dehydrogenase 

GPP gross primary production 

G-proteins GTPases

GPT gas phase titration 

GR glutathione reductase 

GSH glutathione; reduced glutathione 

GSO3

−

/GSO3

2− guanine sulfonates

GSR glutathione reductase

GSS glutathione synthetase

GSSG glutathione disulfide

GST glutathione S-transferase 

GSTM1 glutathione S-transferase 

polymorphism M1 genotypes 

(GSTM1-null, -GSTM1-sufficient)

GSTP1 glutathione S-transferase 

polymorphism P1 genotypes

GTP guanosine triphosphate

GTPases G-proteins/enzymes

GWP global warming potential 

GxE gene-environmental interaction

h hour(s) 

h/day hour(s) per day 

H; H+; H• atomic hydrogen, hydrogen ion; 

hydrogen radical 3

H radiolabeled hydrogen; tritium 

H2 molecular hydrogen 

ha hectare 

HA hyaluronic acid 

HA(s) hospital admission(s)

Hb hemoglobin

HbA1c glycosylated hemoglobin (blood 

test)

HC(s) hydrocarbon(s) 

HCFC(s) hydrochlorofluorocarbon(s) 

HCHO formaldehyde 

H2CO formaldehyde 

HCO• formyl (radical) 

HDM house dust mite 

2HDM second-highest daily maximum

HDMA house dust mite allergen 3

He non-radioactive isotope of helium

HeJ O3-resistant C3H mouse strain 

(C3H/HeJ) 

HEPA high efficiency particle air (filter) 

HERO Health and Environmental 

Research Online, NCEA Database 

System 

12-HETE 12-Hydroxyeicosatetraenoic acid 

HF (HRV signal) high-frequency 

power 

HFCs hydrofluorocarbons 

Hg mercury 

HHP-C9 1-hydroxy-1-hydroperoxynonane 

HIST histamine 

HLA human leukocyte antigen 

HLA-DR human leukocyte antigen receptor 

genes

HMOX Heme oxygenase 

HMOX-1 heme-oxygenase-1 

(polymorphism)

HNE 4-hydroxynonenal 

HNO2 nitrous acid 

HNO3 nitric acid 

HNO4 pernitric acid 

HO hydroxyl; heme oxygenase 

HO• hydroxyl radical 

HO-1 heme oxygenase 1 

HO2• hydroperoxyl; hydroperoxy radical; 

protonated superoxide 

HO3• protonated ozone radical 

H2O water 

H2O2 hydrogen peroxide 

H3O+ hydronium ion 

HOCH2OOH hydroxymethylhydroperoxide 

HONO nitrous acid 

HO2NO2 peroxynitric acid 

HOONO pernitrous acid 

HOX hydrogen radical(s) 

hPa hectopascal

HPLC high-pressure liquid 

chromatography 

HPOT 13-hydroperoxide linolenic acid 

HR heart rate, hazard ratio

HRmax maximum heart rate 

HRP horseradish peroxidase 

HRV heart rate variability 

HSC Houston Ship Channel (Texas)

hs-CRP high-sensitivity C-reactive protein 

H2SO4 sulfuric acid 

HSP high speed pellet (after centrifuge 

spin)

HSP70 heat shock protein 70 

HSS high speed supernatant (after 

centrifuge spin)

5-HT 5-hydroxytryptamine 

hv Energy per photon of 

electromagnetic energy at 

frequency v 
Draft – Do Not Cite or Quote xxxviii September 2011

HVAC heating, ventilation, and air 

conditioning 

Hz hertz 

I iodine 

IARC International Agency for Research 

on Cancer 

IAS interalveolar septum 

IBM individual-based model or 

modeling 

IC inspiratory capacity; intracloud 

(lightning flash) 

ICAM-1 intercellular adhesion molecule 1

ICARTT International Consortium for 

Atmospheric Research on 

Transport and Transformation

ICAS Inner City Asthma Study 

ICC intraclass correlation coefficient

ICD implantable cardioverter 

defibrillator(s); International 

Classification of Diseases 

ICD-9 International Classification of 

Disease 9th revision 

ICD-10 International Classification of 

Disease 10th revision 

ICEM Indoor Chemistry and Exposure 

Model 

ICNIRP International Commission on NonIonizing Radiation Protection 

ICP Forests International Cooperative 

Programme on Assessment of Air 

Pollution Effects on Forests 

ICU Intensive Care Unit

ICVE ischemic cerebrovascular events

IDW inverse-distance-weighted 

IFN interferon (e.g., IFN-()) 

IFN-γ interferon-gamma 

Ig immunoglobulin (e.g., IgE) 

IgA immunoglobulin A 

IgE immunoglobulin E 

IGF-1 insulin-like growth factor 1 

IgG immunoglobulin G 

IgM immunoglobulin M

IHD ischemic heart disease 

IL interleukin (e.g., IL-2, IL-4, IL-6, IL8, etc.)

IL-1β interleukin-1β 

Ile isoleucine 

i.m. intramuscular (route) 

IMPACT Interactive Modeling Project for 

Atmospheric Chemistry and 

Transport 

IMPROVE Interagency Monitoring of 

Protected Visual Environment 

IN intranasal

INF interferon 

inh inhalation 

iNKT invariant (type I) natural killer Tcell 

iNOS inducible nitric oxide synthase 

INRA National agronomical research 

institute (INRA) in ThivervalGrignon. France (adequatelywatered conditions)

INTRASTAND a stand-level model designed for 

hourly, daily and annual integration 

of forest carbon and water cycle 

fluxes 

I/O indoor-outdoor ratio 

IOM Institute of Medicine 

i.p. intraperitoneal (route) 

IPCC Intergovernmental Panel on 

Climate Change 

IPCC-A2 Intergovernmental Panel on 

Climate Change 2nd Assessment 

Report 

IPCC-AR4 Intergovernmental Panel on 

Climate Change 4th Assessment 

Report 

IPCC-AR5 Intergovernmental Panel on 

Climate Change 5th Assessment 

Report 

IPCC-TAR Intergovernmental Panel on 

Climate Change Third Assessment 

Report 

IPMMI International Photolysis Frequency 

Measurement and Modeling Intercomparison 

IQR interquartile range 

IR infrared 

I/R ischemia-reperfusion

IRIS Integrated Risk Information 

System 

IRP Integrated Review Plan for the 

Ozone National Ambient Air 

Quality Standards

ISA Integrated Science Assessment 

ISCCP International Satellite Cloud 

Climatology Project 

ISO International Standards 

Organization 

8-iso-PGF 8-isoprostane 

IT intratracheal

IU International Units 

IUGR intrauterine growth restriction 

i.v. intravenous (route) 

IVF in vitro fertilization 

j Microenvironment 

JA jasmonic acid 

Jmax maximum rate of electron transport 

(for regeneration of RuBP) 

JNK jun N-terminal kinase 

JPL Jet Propulsion Laboratory 

κ kappa

κB kappa B 

k dissociation rate; root:shoot 

allometric coefficient; rate of O3

loss in the microenvironment 

K potassium

K+ potassium ion 
Draft – Do Not Cite or Quote xxxix September 2011

Ka intrinsic mass transfer 

coefficient/parameter 

KC keratinocyte-derived chemokine

kg kilogram

Kg mass transfer coefficient for gas 

phase 

kHz kilohertz 

kJ kilojoules 

Kl mass transfer coefficient for liquid 

phase 

km kilometer 

KM particle optical reflectance 

KML keyhole markup language 

KMZ zipped KML computer language

KO knockout 

Kr reaction rate constant 

KROFEX Krauzberg Ozone Fumigation 

Experiment 

L, dL, mL, μL Liter, deciLiter, milliLiter, microLiter 

L0 Lag (e.x., Lag 0, Lag 1, etc.) 

LAI leaf area index 

LBL Lawrence Berkeley Laboratory 

LBLX Lawrence Berkeley Laboratory 

model including airflow from 

natural ventilation

Lb(s) pound(s) 

LBW low birth weight 

LC50 median lethal concentration 

LCL lower 95th% confidence limit 

LDH lactate dehydrogenase

LDL low-density lipoprotein ; lower 

detectable level

LF (HRV signal) low-frequency power 

LFHFR low frequency/high frequency 

(ratio) 

LFT lower free troposphere 

LI labeling index 

LIDAR Light Detection and Ranging 

(remote sensing system) 

LIF laser-induced fluorescence 

LINKAGES individual-based model of forest 

succession 

LIS lateral intercellular space 

LLJ low-level jet 

L/min liters per minute

Ln Natural logarithm 

LnRMSSD natural log of RMSSD; measure of 

HRV 

lnSDNN natural log of the standard 

deviation of NN intervals in an 

EKG 

LOAEL lowest observed adverse effect 

level 

LOD limit of detection 

LOEL lowest-observed-effect level 

LOESS locally weighted scatterplot 

smoothing 

LOP lipid ozonation products 

LOSU level of scientific understanding 

LOWESS locally weighted scatter plot 

smoother 

LOX-1 Lipoxygenase; lectin-like oxidized 

low density lipoprotein receptor-1 

LPS lipopolysaccharide 

LRS lower respiratory symptoms 

LRT lower respiratory tract; lower 

airways; Long range transport 

LST local standard time 

LT leukotriene (e.g., LTB4 , LTC 4, 

LTD4 , LTE4); local time 

LT-α lymphotoxin-α 

LTA lymphotoxin-alpha 

LUR land use regression 

LVEDD left ventricular chamber 

dimensions at end diastole 

LVEDP left ventricular end diastolic 

pressure

LWC liquid water content 

μ mu, micro 

μeq microequivalent 

μg microgram 

μg/m3 micrograms per cubic meter 

μm micrometer, micron 

m, cm, μm, nm meter(s), centimeter(s), 

micrometer/[micron](s), 

nanometer(s) 

M male

M, mM, μM, nM, pM Molar, milliMolar, microMolar, 

nanoMolar, picoMolar 

m2 square meters

m3 cubic meters 

M# Month (M1 Month1; M2 Month2; 

M3 Month3; M4 Month4)

M2 type of muscarinic receptor

M7 7-hour seasonal mean 

M12 12-hour seasonal mean of O3

ma moving average 

mAOT modified accumulated exposure 

over threshold 

MAP mitogen-activated protein; mean 

arterial pressure 

MAPK mitogen-activated protein 

kinase(s), MAP kinase 

MAQSIP Multiscale Air Quality Simulation 

Platform (model) 

MARAT Mid-Atlantic Regional Assessment 

Team 

MARCO Macrophage receptor with 

collagenous structure 

max maximum 

MBL marine boundary layer 

MCA minimum cross-sectional area

MCCP Mountain Cloud Chemistry 

Program 

Mch; MCh methacholine 

MCM master chemical mechanism 
Draft – Do Not Cite or Quote xl September 2011

MCP-1 monocyte chemotactic protein 1 

MDA malondialdehyde 

MDAR monodehydroascorbate reductase 

MDI Mediterranean diet index 

MDL minimum detection level 

MED minimal erythema dose 

MEF50% maximal midexpiratory flow at 50% 

of forced vital capacity 

MEGAN model of emissions of gases and 

aerosols from nature

MeJA methyl jasmonate 

MENTOR Modeling Environment for Total 

Risk Studies 

METs metabolic equivalent unit(s) [of 

work] 

MFR Maximum Feasible Reduction 

Mg magnesium 

MGDG monogalactosyldiacylglycerol 

mg/m3 milligrams per cubic meter

MHC major histocompatibility complex 

mi mile(s) 

MI myocardial infarction, “heart 

attack”

MIESR matrix isolation electron spin 

resonance (spectroscopy) 

min minute; minimum 

MIP macrophage inflammatory protein 

MIP-2 macrophage inflammatory protein2

mL milliliter 

mL/min milliliter(s) per minute 

MLN mediastinal lymph node 

Mm megameter 

mm millimeter(s)

MM Mt. Mt. Mitchell site 

MM5 National Center for Atmospheric 

Research/Penn State Mesoscale 

Model (version 5)

MMAD mass median aerodynamic 

diameter; mass median 

aerodynamic density 

MMEF maximal midexpiratory flow 

mmHg millimeters of mercury 

MMMD mean maximum mixing height 

depth 

MMP-2 matrix metalloproteinase-2

MMP-3 matrix metalloproteinase-3

MMP-9 metalloproteinase-9

MMSP Mount Mitchell State Park, NC 

Mn manganese 

M/N pooled data from mouth and nasal 

exposure 

MnSOD Manganese superoxide dismutase 

mo month(s) 

MOA(s) mode(s) of Action 

MOBILE (U.S. EPA) mobile vehicle 

emission factor model (on-road 

vehicles)

MOBILE6 vehicle emissions modeling 

software version 6; replaced by 

MOVES

MODNR Missouri Department of Natural 

Resources 

MONICA Monitoring of Trends and 

Determinants in Cardiovascular 

Disease 

MoOx molybdenum oxides 

MOSES Met Office Surface Exchange 

Scheme 

MOVES Motor Vehicle Emission Simulator 

(replaced MOBILE6; for estimating 

emissions from cars, trucks, and 

motorcycles

MOZAIC Measurement of Ozone and Water 

Vapor by Airbus In-Service Aircraft 

MOZART Model for Ozone and Related 

chemical Tracers

MPAN peroxymethacryloyl nitrate; 

peroxy-methacrylic nitric anhydride 

MPO myeloperoxidase 

MQL Minimum quantification limit 

MRI magnetic resonance imaging; 

Midwest Research Institute; 

Meteorological Research Institute 

mRNA messenger RNA 

ms millisecond(s) 

MS mass spectrometry; Mt. 

Moosilauke site 

MSA Metropolitan Statistical Area; 

methane sulfonic acid 

MSL mean sea level 

MS/MS tandem mass spectrometry 

MT million ton(s); metric ton(s) 

MT, Mt metallothionein

MT1 mitochondria 

MTBE methyl-tertiary-butyl ether 

mtDNA mitochondrial DNA

Mtn mountain 

MV minute volume 

MW molecular weight 

MyD88 myeloid differentiation primary 

response gene 88 

n, N number; number of observations 

N nitrogen; North; nasal exposure by 

natural breathing 15N nitrogen-15, stable isotope of 

nitrogen 

N2 molecular nitrogen; nonreactive 

nitrogen 

Na sodium 

NA noradrenaline; North American 

NA; N/A not available; not applicable

Na+ sodium ion 

NAAQS National Ambient Air Quality 

Standards 

NAD nicotinamide adenine nucleotide 
Draft – Do Not Cite or Quote xli September 2011

NADH reduced nicotinamide adenine 

dinucleotide; nicotinamide adenine 

dinucleotide dehydrogenase 

NADP National Atmospheric Deposition 

Program 

NADPH reduced nicotinamide adenine 

dinucleotide phosphate 

NADPH-CR reduced nicotinamide adenine 

dinucleotide phosphate -

cytochrome c reductase 

NaE sodium erythorbate 

NAG N-acetyl-glucosaminidase

Na-K-ATPase sodium-potassium-dependent 

adenosine triphosphatase 

NAMS National Ambient Monitoring 

Stations 

NAPAP National Acid Precipitation 

Assessment Program 

NAPBN National Air Pollution Background 

Network 

NARE North Atlantic Regional 

Experiment 

NARSTO North American Regional Strategy 

for Tropospheric Ozone 

NAS National Academy of Sciences; 

Normative Aging Study 

NASA National Aeronautics and Space 

Administration 

NBS National Bureau of Standards 

NBTH 3-methyl-2-benzothiazolinone 

acetone azine 

NCEA National Center for Environmental 

Assessment 

NCEA-RTP NCEA Division in Research 

Triangle Park, NC 

NCHS National Center for Health 

Statistics 

NCICAS National Cooperative Inner-City 

Asthma Study 

NCLAN National Crop Loss Assessment 

Network 

NCore National Core multi-pollutant 

monitoring network 

NC-R resistant clones of white clover 

NC-S sensitive clones of white clover 

ND; n.d. not detectable; not detected; no 

data 

2ndHDM second-highest daily maximum 

NDF neutral detergent fiber 

NEE net ecosystem CO2 exchange 

NEI National Emissions Inventory 

NEM National Ambient Air Quality 

Standards Exposure Model 

NEP Net Ecosystem Production 

NERL National Exposure Research 

Laboratory 

NESCAUM Northeast States for Coordinated 

Air Use Management 

NF National Forest; non-filtered air 

NF-κB nuclear factor kappa B 

ng nanogram(s)

NGF nerve growth factor

NH northern hemisphere

NH3 ammonia 

NH4

+ ammonium ion 

NH4HSO4 ammonium bisulfate 

(NH4)2HSO4 ammonium sulfate 

NHANES National Health and Nutrition 

Examination Survey 

NHANES III National Health and Nutrition 

Examination Survey III 

NHAPS National Human Activity Pattern 

Survey 

NHEERL (U.S. EPA) National Health and 

Environmental Effects Research 

Laboratory

NHIS National Health Interview Survey 

(NH4)2SO4 ammonium sulfate 

NIH National Institutes of Health 

NIST National Institute of Standards and 

Technology 

NK natural killer cells; neurokinin 

NKT natural killer T cells 

NL nasal lavage 

NLF nasal lavage fluid 

NM National Monument

NMHC(s) nonmethane hydrocarbon(s) 

NMMAPS National Morbidity, Mortality, and 

Air Pollution Study 

NMOC(s) nonmethane organic compound(s) 

NMVOCs nonmethane volatile organic 

compounds 

NN normal-to-normal (NN or RR) time 

interval between each QRS 

complex in the EKG 

NNK 4-(N-nitrosomethylamino)-1-(3-

pyridyl)-1-butanone 

nNOS neuronal nitric oxide synthase 

(NOS) 

NO nitric oxide 

·NO nitric oxide concentration 

(interpunct NO) 

NO2 nitrogen dioxide 

NO3; NO3• nitrate, nitrate radical 

NO3

− nitrate, nitrate ion 

N2O nitrous oxide 

N2O5 dinitrogen pentoxide 

NOAA National Oceanic and Atmospheric 

Administration 

NOAEL no observed adverse effect level 

NOS nitric oxide synthase (types, NOS1, NOS-2, NOS-3)

NOX nitrogen oxides, oxides of nitrogen 

(NO + NO2) 

NOY sum of NOX and NOZ; odd 

nitrogen species; total oxidized 

nitrogen 
Draft – Do Not Cite or Quote xlii September 2011

NOZ sum of all inorganic and organic 

reaction products of NOX (HONO, 

HNO3, HNO4, organic nitrates, 

particulate nitrate, nitro-PAHs, 

etc.) 

NP National Park 

NPP net primary production 

NPS National Park Service, U.S. 

Department of the Interior 

NQO1 NAD(P)H-quinone oxidoreductase 

(genotype) 

NQO1wt NAD(P)H-quinone oxidoreductase 

wild type (genotype) 

NR not reported 

Nr reactive nitrogen 

NRC National Research Council 

Nrf-2 nuclear factor erythroid 2-related 

factor 2 

Nrf2-ARE NF-E2-related factor 2-antioxidant 

response element 

NS; n.s. nonsignificant; non-smoker; 

national seashore; natural spline 

NSAID non-steroidal anti-inflammatory 

agent 

NSBR nonspecific bronchial 

responsiveness 

NSF National Science Foundation 

NTE nasal turbinate epithelial (cells) 

NTN National Trends Network 

NTP National Toxicology Program 

NTRMs NIST Traceable Reference 

Materials 

NTS nucleus of the solitary tract (in 

brainstem) 

NWR national wildlife refuge 

NWS National Weather Service 

NZW New Zealand white (rabbit) 

O oxygen; horizon forest floor 18O oxygen-18, stable isotope of 

oxygen 

O2 molecular oxygen 

O2

− superoxide 

O2• superoxide radical 

1

O2 singlet oxygen 

O3 ozone 

18O3 (oxygen-18 labeled) ozone 

O3* electronically excited ozone 

OAQPS Office of Air Quality Planning and 

Standards 

OAR Office of Air and Radiation 

OBMs observationally based methods 

OC organic carbon 

OD outer diameter; optical density 

O(1

D) electronically excited oxygen atom 

OH, OH• hydroxyl group, hydroxyl radical 

8-OHdG 8-hydroxy-2 ́-deoxyguanosine 

OLS ordinary least squares 

OMI Ozone Monitoring Instrument 

ON Ontario

ONOO− peroxynitrate ion

O(3

P) ground-state oxygen atom 

OPE ozone production efficiency 

OPECs Outdoor Plant Environment 

Chambers 

OR odds ratio 

ORD Office of Research and 

Development 

OSHA Occupational Safety and Health 

Administration 

OTC open-top chamber 

OuJ O3-sensitive C3H mouse strain 

(C3H/OuJ)

OVA ovalbumin 

OX odd oxygen species; total oxidants 

OxComp oxidative capacity of the 

atmosphere 

oz ounce(s) 

P pressure in atmospheres; plants 

grown in pots; phosphorus; 

penetration fraction of O3 into the 

microenvironment; pulmonary 

region 

p probability value 

P450 cytochrome P450 

p53 cell cycle protein gene

P90 90th percentile of the absolute 

difference in concentrations 

PACF partial autocorrelation function of 

the model residuals 

PAD peripheral arterial disease; 

pollutant-applied dose 

PAF platelet-activating factor; 

paroxysmal atrial fibrillation 

PAH(s) polycyclic aromatic hydrocarbon(s) 

PAI-1 plasminogen activator fibrinogen 

inhibitor-1

PAL phenylalanine ammonia lyase 

PAMS Photochemical Assessment 

Monitoring Stations network 

PAN peroxyacetyl nitrate

PaO2 arterial oxygen pressure 

PAPA Public Health and Air Pollution in 

Asia

PAR photosynthetically active radiation; 

proximal alveolar region 

Patm Pressure in atmospheres 

p-ATP para-acetamidophenol 

Pb Lead 

PBL planetary boundary layer; 

peripheral blood lymphocytes 

PBM population-based model or 

modeling 

PBN C-phenyl N-tert-butyl nitrone 

PBPK physiologically based 

pharmacokinetic (model) 

PBS phosphate buffered saline 

PC phosphatidylchloline 
Draft – Do Not Cite or Quote xliii September 2011

PC20 provocative concentration that 

produces a 20% decrease in 

forced expiratory volume in 1 

second 

PC20FEV1 provovative concentration that 

produces a 20% decrease in FEV1

PC50 provocative concentration that 

produces a 50% decrease in 

forced expiratory volume in 1 

second 

PCA principal component analysis 

PC-ALF 1-palmitoyl-2-(9-oxonononoyl)-snglycero-3-phosphocholine 

PCD programmed cell death 

PCl picryl chloride 

pCNEM Canadian version of National 

Ambient Air Quality Standards 

Exposure Model 

PCO2 Average partial pressure of O2 in 

lung capillaries 

pCO2 partial pressure of carbon dioxide 

PCR polymerase chain reaction 

PCR-DGGE PCR–denaturing gradient gel 

electrophoresis 

PD pregnancy day

PD20 provocative dose that produces a 

20% decrease in FEV1

PD20FEV1 provocative dose that produces a 

20% decrease in FEV1

PD100 provocative dose that produces a 

100% increase in sRAW 

PD100SRaw provocative dose that produces a 

100% increase in SRaw

PDI pain on deep inspiration

PE post exposure, 

phosphatidylethanolamine 

PEF peak expiratory flow 

PEF0.75 peak expiratory flow in 0.75 

second 

PEFR peak expiratory flow rate 

PEFT time to peak flow 

PEG-CAT polyethylene glycol-catalase 

PEG-SOD polyethylene glycol-superoxide 

dismutase 

PEM(s) personal exposure monitor(s) 

Penh enhanced pause 

PEPc phosphoenolpyruvate carboxylase 

PFD photosynthetic flux density 

PFT pulmonary function test 

pg picogram(s)

PG prostaglandin (e.g., PGE2 ,PGF2); 

phosphatidylglycerol 

6PGD 6-phosphogluconate 

dehydrogenase 

PGE2 prostaglandin E2

PGF2α prostaglandin F2-alpha

PGHS-2 prostaglandin endoperoxide G/H 

synthase 2 

PGP protein gene product (e.g., 

PGP9.5) 

PGSM Plant Growth Stress Model 

pH relative acidity; Log of the 

reciprocal of the hydrogen ion 

concentration 

PHA phytohemagglutinin A 

PI phosphatidylinositol; probability 

interval; posterior interval 

PIF peak inspiratory flow 

PiZZ respiratory phenotype 

PK pharmacokinetics 

pKa dissociation constant 

PLFA phospholipid fatty acid 

PM particulate matter

PMX Particulate matter of a specific size 

range not defined for regulatory 

use. Usually X refers to the 50% 

cut point, the aerodynamic 

diameter at which the sampler 

collects 50% of the particles and 

rejects 50% of the particles. The 

collection efficiency, given by a 

penetration curve, increases for 

particles with smaller diameters 

and decreases for particles with 

larger diameters. The definition of 

PMX is sometimes abbreviated as 

“particles with a nominal 

aerodynamic diameter less than or 

equal to X μm” although X is 

usually a 50% cut point.

PM2.5 In general terms, particulate matter 

with an aerodynamic diameter less 

than or equal to a nominal 2.5 μm; 

a measurement of fine particles in 

regulatory terms, particles with an 

upper 50% cut-point of 2.5 μm 

aerodynamic diameter (the 50% 

cut point diameter is the diameter 

at which the sampler collects 50% 

of the particles and rejects 50% of 

the particles) and a penetration 

curve as measured by a reference 

method based on Appendix L of 40 

CFR Part 50 and designated in 

accordance with 40 CFR Part 53, 

by an equivalent method 

designated in accordance with 40 

CFR Part 53, or by an approved 

regional method designated in 

accordance with Appendix C of 40 

CFR Part 58.
Draft – Do Not Cite or Quote xliv September 2011

PM10 In general terms, particulate matter 

with an aerodynamic diameter less 

than or equal to a nominal 10 μm; 

a measurement of thoracic 

particles (i.e., that subset of 

inhalable particles thought small 

enough to penetrate beyond the 

larynx into the thoracic region of 

the respiratory tract) in regulatory 

terms, particles with an upper 50% 

cut-point of 10± 0.5 μm 

aerodynamic diameter (the 50% 

cut point diameter is the diameter 

at which the sampler collects 50% 

of the particles and rejects 50% of 

the particles) and a penetration 

curve as measured by a reference 

method based on Appendix J of 40 

CFR Part 50 and designated in 

accordance with 40 CFR Part 53 

or by an equivalent method 

designated in accordance with 40 

CFR Part 53.

PM10-2.5 In general terms, particulate matter 

with an aerodynamic diameter less 

than or equal to a nominal 10 μm 

and greater than a nominal 2.5 

μm; a measurement of thoracic 

coarse particulate matter or the 

coarse fraction of PM10 in 

regulatory terms, particles with an 

upper 50% cut-point of 10 μm 

aerodynamic diameter and a lower 

50% cut-point of 2.5 μm 

aerodynamic diameter (the 50% 

cut point diameter is the diameter 

at which the sampler collects 50% 

of the particles and rejects 50% of 

the particles) as measured by a 

reference method based on 

Appendix O of 40 CFR Part 50 and 

designated in accordance with 40 

CFR Part 53 or by an equivalent 

method designated in accordance 

with 40 CFR Part 53.

PM10C The PM10-2.5 concentration of PM10-

2.5 measured by the 40 CFR Part 

50 Appendix O reference method 

which consists of currently 

operated, co-located low-volume 

(16.7 Lpm) PM10 and PM2.5

reference method samplers.

p38MAPK p38 mitogen-activated protein 

kinase(s)

PM-CAMx Comprehensive Air Quality Model 

with extensions and with 

particulate matter chemistry 

PMN(s) polymorphonuclear leukocyte(s) 

PMT photomultiplier tube 

PND post natal day 

pNEM probabilistic National Exposure 

Model 

PnET Photosynthetic EvapoTranspiration 

model 

PNN proportion of interval differences of 

successive normal-beat intervals 

in EKG 

PNN50 proportion of interval differences of 

successive normal-beat intervals 

greater than 50 ms in EKG 

PO2 partial pressure of oxygen

POC particulate organic carbon 

POD peroxidase 

polyADPR poly(adenosinediphosphateribose) 

POMS Portable Ozone Monitoring 

Systems 

ppb parts per billion 

ppb-h parts per billion per hour 

ppbv parts per billion by volume 

pphm parts per hundred million 

ppm parts per million 

ppm-h parts per million hours; weighted 

concentration values based on 

hourly concentrations: usually 

summed over a certain number of 

hours, day(s), months, and/or 

season. 

ppmv parts per million by volume 

PPN peroxypropionyl nitrate; 

peroxypropionic nitric anhydride 

PPPs power plant plumes 

ppt parts per trillion 

pptv parts per trillion by volume 

PQH2 plastoquinone 

PR pathogenesis-related (protein) 

PR-1 promoter region 1 

PRB policy-relevant background 

preproET-1 pre-protein form of ET-1 mRNA

PRYL predicted relative yield (biomass) 

loss 

PS penalized spline 

PS paradoxical sleep 

PS II Photosystem II: enzyme that uses 

light to obtain electrons from water 

(for photosynthesis). 

PSA picryl sulfonic acid 

PSC polar stratospheric clouds 

PTB preterm birth 

PTR-MS proton-transfer-reaction mass 

spectroscopy 

PU, PUL pulmonary 

PUFA(s) polyunsaturated fatty acid(s) 

PV potential vorticity 

PVCD peripheral vascular and 

cerebrovascular disease 

PVD peripheral vascular disease 

PVOCs photochemical volatile organic 

compounds 

PWM pokeweed mitogen 

PWTES (left ventricular) posterior wall 

thickness at end systole

Pxase peroxidase 

QA Quality Assurance 

QC quality control 
Draft – Do Not Cite or Quote xlv September 2011

QCE quasi continuous exercise 

qNP non-photochemical quenching 

qNP non-photochemical quenching 

qP photochemical quenching 

QRS A complex of three distinct 

electrocardiogram waves which 

represent the beginning of 

ventricular contraction 

QT interval measure of the time 

interval between the start of the Q 

wave and the end of the T wave in 

the heart’s electrical cycle 

QTc corrected QT interval

r Pearson correlation coefficient 

R, r correlation coefficient 

r

2 correlation coefficient 

R2 multiple regression correlation 

coefficient 

R2

, r2 coefficient of determination 

RACM Regional Atmospheric Chemistry 

Mechanism 

RADM Regional Acid Deposition Model 

rALP recombinant antileukoprotease 

RAMS Regional Atmospheric Modeling 

System 

RANTES regulated upon activation, normal 

T cell expressed and secreted 

(cells) 

Raw airway resistance 

RB respiratory bronchiole 

RBC(s) red blood cell(s); erythrocyte(s) 

rbcL Rubisco large subunit 

rbcS Rubisco small subunit 

R′CO acyl acyl carrier protein

R’C(O)–O2 acyl peroxy 

rcd1 Arabidopsis mutant radical 

induced cell death 

RCD3 rod-cone dysplasia 3 

RCP Representative Concentration 

Pathways 

RDBMS Relational Database Management 

Systems 

Re Reynolds number

REHEX Regional Human Exposure Model 

RER rough endoplasmic reticulum; 

Respiratory exchange ratio 

RF radiative forcing 

RGR relative growth rate 

RH relative humidity 

RIOPA Relationship of Indoor, Outdoor, 

and Personal Air (study) 

RL total pulmonary resistance 

RLKs receptor-like/Pelle kinase group 

RMNP Rocky Mountain National Park, 

Colorado 

RMR resting metabolic rate 

rMSSD root mean squared differences 

between adjacent normal-tonormal heartbeat intervals 

Rn nasal resistance 

RNA ribonucleic acid 

RO2 organic peroxyl; organic peroxy 

ROG reactive organic gases 

ROI reactive oxygen 

intermediate/superoxide anion 

RONO2 organic nitrate 

ROOH organic peroxides 

ROONO2, RO2NO2 peroxy nitrate 

ROS reactive oxygen species 

RPD relative percent difference 

RR normal-to-normal (NN or RR) time 

interval between each QRS 

complex in the EKG; risk ratio; 

relative risk; respiratory rate 

RRMS relatively remote monitoring sites 

RT respiratory tract 

RT transepithelial resistance 

RTLF respiratory tract lining fluid 

RuBisCO; Rubisco ribulose-1,5-bisphosphate 

carboxylase/oxygenase 

RuBP ribulose bisphosphate 

σ sigma, standard deviation 

σg sigma-g; (geometric standard 

deviation) 

s second 

S Short; smoker; sulfur; South 

s.c. subcutaneous (route) 

SA salicylic acid

SAB Science Advisory Board 

SAC Staphylococcus aureus Cowan 1 

strain 

SAG21 senescence 

SAI Systems Applications International 

S-allele short-allele 

SAMD S-adenosyl methionine 

decarboxylase 

SaO2 oxygen saturation of arterial blood 

SAPALDIA Study of Air Pollution and Lung 

Diseases in Adults 

SAPRC Stratospheric Processes and their 

Role in Climate; Statewide Air 

Pollution Research Center, 

University of California, Riverside

SAR systemic acquired resistance 

SAROAD Storage and Retrieval of 

Aerometric Data (U.S. EPA 

centralized database; superseded 

by Aerometric Information 

Retrieval System [AIRS]) 

SAWgrp small airway function group 

SBNF San Bernardino National Forest, 

California 

SBP systolic blood pressure 

SBUV Solar Backscatter Ultraviolet

Spectrometer 

SC stratum corneum 

Sc scandium 
Draft – Do Not Cite or Quote xlvi September 2011

SCAQS Southern California Air Quality 

Study 

SCE(s) sister chromatid exchange(s) 

SD standard deviation; SpragueDawley rat 

SDNN standard deviation normal-tonormal (NN or RR) time interval 

between each QRS complex in the 

EKG 

SE standard error 

SEBAS Social Environment and 

Biomarkers of Aging Study 

sec second

Sess. session

SEM simultaneously extracted metal; 

standard error of the mean; 

scanning electron microscopy 

SENP Sequoia National Park, California 

SES socioeconomic status 

SF San Francisco Bay Area 

SF6 sulfur hexafluoride (tracer gas) 

SGA small for gestational age 

sRaw specific airway conductance 

SH Shenandoah National Park site 

SHEDS Stochastic Human Exposure and 

Dose Simulation 

SHEN Shenandoah National Park 

sICAM-1 soluble intercellular adhesion 

molecule 

SIDS sudden infant death syndrome 

SIGMOID sigmoid weighted summed 

concentration 

SINIC Simple Nitrogen Cycle model 

SIP State Implementation Plan 

SIPK salicylic acid (SA) induced protein 

kinase 

SK shikimate kinase 

SLA specific leaf area 

SLAC1 (protein) slow anion channel 

associated 1 

SLAMS State and Local Air Monitoring 

Stations 

SM smooth muscle 

SMD soil moisture deficit 

SME soybean oil methyl ester 

SMNP Great Smoky Mountain National 

Park (North Carolina and 

Tennessee) 

SMOKE Spare-Matrix Operator Kernel 

Emissions 

SN normalized slope of the alveolar 

plateau

SNAAQS Secondary National Ambient Air 

Quality Standards 

SNP(s) single-nucleotide polymorphism 

SO2 sulfur dioxide 

SO4

2− sulfate 

SOA secondary organic aerosol 

SOC soil organic carbon 

SOD superoxide dismutase 

SOS Southern Oxidant Study 

SOX sulfur oxides 

SoyFACE Soybean Free Air gas 

Concentration Enrichment 

(Facility) 

SP surfactant protein (e.g., SPA, 

SPD); substance P 

SP-A surfactant protein-A 

SPF specific pathogen free 

SPMs special purpose monitors 

SP-NK substance P – neurokinin receptor 

complex

sRaw, specific airway resistance 

SRBC sheep red blood cell 

SRES Special Report on Emissions 

Scenarios 

SRM standard reference method 

SRP standard reference photometers 

SSCP single-strand conformation 

polymorphism 

129S1/SvlmJ mouse strain

STE stratosphere-troposphere 

exchange 

STEP Stratospheric-TroposphericExchange Project 

STN speciation trends network 

sTNFR1 soluble tumor necrosis factor 

receptor 1

STP standard temperature and 

pressure 

STPD standard temperature and 

pressure, dry 

STRF Spatio-Temporal Random Field 

(theory) 

subscript i Index of indoor microenvironments 

subscript o Index of outdoor 

microenvironments 

subscript o,i Index of outdoor 

microenvironments adjacent to a 

given indoor microenvironment i

SUM00 sum of all hourly average 

concentrations 

SUM06 seasonal sum of all hourly average 

concentrations ≥ 0.06 ppm 

SUM07 seasonal sum of all hourly average 

concentrations ≥ 0.07 ppm 

SUM08 seasonal sum of all hourly average 

concentrations ≥ 0.08 ppm 

SURE Sulfate Regional Experiment 

Program 

SVE supraventricular ectopy

S-W square-wave 

SWS slow wave sleep

SZA solar zenith angle 

τ tau, photochemical lifetime; 

atmospheric lifetime 

t t-test statistical value; t statistic 

T time; duration of exposure 
Draft – Do Not Cite or Quote xlvii September 2011

T cell(s) T lymphocyte(s), thymusdependent lymphocytes 

T1 first trimester 

T2 second trimester 

T3 triiodothyronine 

T3 third trimester 

T4 thyroxine 

TAR IPCC Third Assessment Report 

TAR WGI IPCC Third Assessment Report of 

Working Group I 

TB tracheobronchial; terminal 

bronchioles; tuberculosis 

TBA thiobarbituric acid 

TBARS thiobarbituric acid reactive 

substances 

TC total carbon 99mTc Technetium-99m 

T-cells T-lymphocytes, Thymus-derived 

lymphocytes 99mTc-DTPA 99mTcdiethylenetriaminepentaacetic acid 

Tco core temperature 

TDLAS Tunable Diode Laser Absorption 

Spectrometer 

Te expiratory time 

TEM transmission electron microscopy; 

Terrestrial Ecosystem Model 

TES Tropospheric Emission 

Spectrometer 

TexAQS Texas Air Quality Field Study 

Tg teragram(s) 

TGF transforming growth factor 

TGF β transforming growth factor beta 

Th T helper cell type 

Th2 T helper cell type 2 

THC Total hydrocarbon content

tHcy total homocysteine 

Ti inspiratory time 

Ti titanium 

TIA transient ischemic attack 

TIMP-2 tissue inhibitor of matrix 

metalloprotease-2

TiO2 titanium dioxide 

TLC total lung capacity 

TLNISE two-level normal independent 

sampling estimation 

Tlr toll-like receptor gene

TLR Toll-like receptor protein (ex., 

TLR2, TLR4)

TMPO tetramethylphrrolise 1-oxide 

TNC total nonstructural carbohydrate 

TNF tumor necrosis factor (e.g., TNF-α) 

TNF-308 tumor necrosis factor genotype 

TNF-α tumor necrosis factor alpha 

TNFR tumor necrosis factor receptor 

TOMS Total Ozone Mapping/Monitoring 

Satellite; total ozone mapping 

spectrometer 

TOPSE Tropospheric Ozone Production 

About the Spring Equinox 

tPA tissue plasminogen activator

TPLIF two-photon laser-induced 

fluorescence 

TRAMP TexAQS-II Radical and Aerosol 

Measurement Project 

TREGRO Tree Growth Model 

TRIFFID Top-down Representation of 

Interactive Foliage and Flora 

Including Dynamics 

TRIM Total Risk Integrated Methodology 

(model) 

TRIM.Expo Total Risk Integrated Methodology 

Exposure Event (model) 

TRP transient receptor potential (ion 

channel[s], ex., TRP-A1, TRP-V1, 

TRP-M8)

TSH thyroid stimulating hormone 

TSP total suspended particles 

TTFMS two-tone frequency-modulated 

spectroscopy 

TWA time-weighted average 

TX thromboxane (e.g., TXB2) 

TXB2 thromboxane B2 

UA uric acid; Urate 

UAM Urban Airshed Model 

UCL upper 95th% confidence limit 

UDGT UDP -galactose-1,2,-diacylglycerol 

galactosyltransferase 

UDP uridine diphosphate 

U.K. United Kingdom 

UNECE United Nations Economic 

Commission for Europe 

UNEP United Nations Environmental 

Programme 

UNFCCC United Nations Framework 

Convention on Climate Change 

U-O epioxides formed from uric acid

U-O2

− peroxides formed from uric acid

U-O3

− ozonides formed from uric acid

URI upper respiratory infection 

URS upper respiratory symptoms 

URT upper respiratory tract; upper 

airways 

U.S. United States (of America) 

USC; U.S.C. U.S. Code 

USDA U.S. Department of Agriculture 

USFS U.S. Forest Service 

USGCRP U.S. Global Change Research 

Program 

USGS U.S. Geological Survey 

UV ultraviolet radiation 

UV-A ultraviolet radiation at wavelengths 

of 320 to 400 nm 
Draft – Do Not Cite or Quote xlviii September 2011

UV-B ultraviolet radiation at wavelengths 

of 280 to 320 nm 

UV-C ultraviolet radiation at wavelengths 

of 200 to 280 nm 

UV-DIAL Ultraviolet Differential Absorption 

Lidar 

V vanadium 

V, mV, μV volt, millivolt, microvolt 

VA alveolar ventilation

Val valine 

VC vital capacity 

VCAM vascular cell adhesion molecule 

Vd deposition rate, deposition velocity 

(cm/s) 

VD volume of the anatomic or 

physiological dead space 

VE ventilation rate; minute ventilation; 

ventilatory volume

VEGF vascular endothelial growth factor 

VEmax maximum minute ventilation 

Vmax maximum velocity 

Vmax25% maximum expiratory flow at 25% 

of the vital capacity 

Vmax50% maximum expiratory flow at 50% 

of the vital capacity 

Vmax75% maximum expiratory flow at 75% 

of the vital capacity 

VMD volume median diameter 

Vn nasal volume 

VO2 oxygen consumption 

VO2max maximum volume per time, of 

oxygen (maximal oxygen 

consumption, maximal oxygen 

uptake or aerobic capacity) 

VOC(s) volatile organic compound(s) 

VP volumetric penetration 

VP50% volume at which 50% of an inhaled 

bolus is absorbed 

VPD vapor pressure deficit; Vehicles 

per day; Ventricular premature 

depolarization 

VT tidal volume 

VTB terminal bronchiole region volume 

VTmax maximum tidal volume 

VUA volume of the upper airways 

vWF von Willebrand factor 

W width; wilderness; week(s) 

W126 cumulative integrated exposure 

index with a sigmoidal weighting 

function 

W95 cumulative integrated exposure 

index with a sigmoidal weighting 

function 

WBC white blood cell 

WBGT wet bulb globe temperature 

wc sigmoidal weighting of hourly O3

concentration 

WCB warm conveyor belt 

WED (U.S. EPA NHEERL) Western 

Ecology Division 

WF, WFM White Face Mountain site 

WHI Women’s Health Initiative 

WHO World Health Organization 

wk(s) week(s) 

W/m2

, W m-2 watts per square meter 

WMO World Meteorological Organization 

WMO/UNEP World Meteorological 

Organization/United Nations 

Environment Program 

WRF Weather Research and 

Forecasting model 

Ws Wassilewskija Arabidopsis ecotype 

WS wood smoke 

WT wild type; White Top Mountain site 

wt % percent by weight 

WUS western U.S.

w/v weight per volume 

Y three parameter Weibull model 

yr year 

Z Airway generation 

ZAPS Zonal Air Pollution System 

ZELIG a forest succession simulation 

model 

Zn zinc