### Draft

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## 1 EXECUTIVE SUMMARY

Introduction and Purpose

The purpose of this Integrated Science Assessment (ISA) is to provide a synthesis and 

### 1

evaluation of the most policy

- relevant science that forms the scientific foundation for the 

### 2

review of the primary (health

- based) and secondary (welfare

- based) national ambient air 

### 3

quality standard (NAAQS) for ozone (O 3 ) and related photochemical oxidants. The ISA 

### 4

is intended to inform the EPA Risk and Exposure Assessment and Policy Assessment and 

### 5

thereby support decisions by the EPA Administrator on the NAAQS for O 3 (See Figure I 

### 6

in Preamble). The current primary O 3 standard includes an 8

- hour average standard set in 

### 7

2008 at 75 parts per billion (ppb). The secondary standard for O 3 is equal to the primary 

### 8

standard. The current primary NAAQS protects against respiratory health effects incurred 

### 9

after short

- term exposure to O 3 , while the secondary NAAQS protects against damage to 

### 10

vegetation and ecosystems. 

### 11



## Scope and Methods

EPA has developed an extensive and robust process for evaluating the scientific evidence 

### 12

and drawing conclusions regarding air pollution

- rel ated health and welfare effects, which 

### 13

is applied to the health and welfare effects resulting from current ambient concentrations 

### 14

of O 3 . Building upon the findings of previous assessments, this review includes 

### 15

identification, selection, evaluation, and integration of the relevant results pertaining to 

### 16

the atmospheric science of O 3 ; short

- and long

- term exposure to ambient O 3 ; health 

### 17

effects due to relevant O 3 concentrations as characterized in epidemiologic, controlled 

### 18

human exposure, and toxicological studies; and ecological or welfare effects; as well as 

### 19

O 3 concentration

- response relationships, mode(s ) of action, and populations at increased 

### 20

risk for O 3 - related health effects. T he conclusions and key findings from previous 

### 21

reviews provide the foundation for the consideration of evidence from recent studies (i.e., 

### 22

studies published since the completion of the 2006 O 3 AQCD). Conclusions are drawn 

### 23

based on the synthesis of evidence across disciplines from recent studies and building 

### 24

upon the extensive evidence presented in previous reviews. 

### 25

EPA has developed a consistent and transparent approach to evalua te the causal nature of 

### 26

air pollution

- related health and environmental effects for use in developing ISAs; the 

### 27

framework for causal determinations is described in the Preamble to this document. 

### 28

Causality determinations are based on the evaluation and synth esis of evidence across 

### 29

scientific disciplines; however, the type of evidence that is most important for such 

### 30

determinations will vary by pollutant or assessment. EPA assesses the entire body of 

### 31

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- 2 June 2012 peer

- reviewed literature, building upon evidence available du ring the previous NAAQS 

### 1

reviews, to draw conclusions on the causal relationships between relevant pollutant 

### 2

concentrations and health or welfare effects. EPA also evaluates the quantitative evidence 

### 3

and draws scientific conclusions, to the extent possible, regarding the 

### 4

concentration

- response relationships and the loads to ecosystems, exposure doses or 

### 5

concentrations, duration and pattern of exposures at which effects are observed. 

### 6

A five

- level hierarchy is used to classify the weight of evidence for causat ion, not just 

### 7

association. This weight of evidence evaluation is based on various lines of evidence 

### 8

from across the health and environmental effects disciplines. These separate judgments 

### 9

are integrated into a qualitative statement about the overall weight of the evidence and 

### 10

causality. The causal determinations are: 

### 11

 Causal relationship 

### 12

 Likely to be a causal relationship 

### 13

 Suggestive of a causal relationship 

### 14

 Inadequate to infer a causal relationship 

### 15

 Not likely to be a causal relationship 

### 16



## Ambient Ozone Con centrations

Ozone is naturally present in the stratosphere, where it serves the beneficial role of 

### 17

blocking harmful ultraviolet radiation from the Sun

, and preventing the majority of this 

### 18

radiation from reaching the surface of the Earth. However, in the tr oposphere, O 3 acts as 

### 19

a powerful oxidant and can harm living organisms and materials. Tropospheric O 3 is 

### 20

present not only in polluted urban air, but throughout the globe. Ozone can be influenced 

### 21

by local meteorological conditions, circulation patterns, emi ssions, and topographic 

### 22

barriers, resulting in heterogeneous concentrations across an individual urban area. On a 

### 23

larger scale, O 3 persists in the atmosphere long enough that it can be transported from 

### 24

continent to continent. 

### 25

Ozone in the troposphere orig inates from both anthropogenic (i.e., man

- made) and 

### 26

natural source categories. Ozone attributed to anthropogenic sources is formed in the 

### 27

atmosphere by photochemical reactions involving sunlight and precursor pollutants 

### 28

including volatile organic compounds , nitrogen oxides, and carbon monoxide. Ozone 

### 29

attributed to natural sources is formed through the same photochemical reactions 

### 30

involving natural emissions of precursor pollutants from vegetation, microbes, animals, 

### 31

biomass burning, and lightning. Because O 3 is produced downwind of urban source areas 

### 32

and O 3 tends to persist longer in rural than in urban areas as a result of lower chemical 

### 33

### Draft

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- 3 June 2012 scavenge, resulting in concentrations in rural areas that are often higher than those in 

### 1

urban areas. 

### 2

In the context of a review of the NAAQS, it is useful to define background O3 

### 3

concentrations in a way that distinguishes between concentrations that result from 

### 4

precursor emissions that are relatively less controllable from those that are relatively 

### 5

more controllable through U.S. policies. North American (NA) background can be 

### 6

defined as those concentrations resulting from natural sources everywhere in the world 

### 7

and from anthropogenic sources outside the U.S., Canada and Mexico. Since NA 

### 8

background is a construct that cannot be measured, NA background O 3 concentrations are 

### 9

estimated using chemistry transport models. Seasonal mean daily maximum 8

- h average 

### 10

NA background O 3 concentrations are generally higher in spring than in summer across 

### 11

the U.S. The highest estimates are fo und in the Intermountain West during the spring and 

### 12

in the Southwest during the summer. The lowest estimates occur over the East in the 

### 13

spring and over the Northeast in the summer (See Section 3.4 ). 

### 14



## Human Exposure to Ozone

The widespread presence of O 3 in the environment results in exposure as people 

### 15

participate in normal daily activities. The relationship between personal exposure and 

### 16

ambient concentration measured at fixed

- site monitors can be described in terms of 

### 17

correlation, or how they covary in time, and ratio, which describes their relative 

### 18

mangnitude. Personal

- ambient O 3 correlation s are generally moderate (0.3

- 0.8), although 

### 19

low correlations have been observed with increased time spent indoors, low air exchange 

### 20

rate, and concentrations below the personal sampler detection limit (See Section 4.3 ). 

### 21

Ratios of 0.1

- 0.3 between personal exposure and ambient concentration have been 

### 22

observed for the general population, with ratios of up to 0.9 observed for outdoor 

### 23

workers. Evidence su ggests that some groups, particularly children, older adults, and 

### 24

those with respiratory problems, change their behavior on high

- O 3 days to reduce 

### 25

exposure (See Section 4.4.2 ). Such behavioral changes may result in reduced effect 

### 26

estimates in epidemiologic studies that do not account for averting behavior on high

- O 3 

### 27

days. Variation in O 3 concentrations occurs over multiple spatial and temporal scales, and 

### 28

this introduces exposure error into epidemiologic results (See Section 4.6.2 ). However, 

### 29

epidemiologic studies evaluating the influence of spat ial scale and monitor selection find 

### 30

little difference among effect estimates, and comparable risk estimates have been 

### 31

reported in studies using a variety of exposure assessment techniques expected to produce 

### 32

different levels of personal

- ambient associatio ns. This suggests that there is no clear 

### 33

indication that a particular method of exposure assessment produces stronger 

### 34

epidemiologic results. 

### 35

### Draft

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## Dosimetry and Modes of Action

When O 3 is inhaled, the amount of O 3 that is absorbed is affected by a number of fact ors 

### 1

including the shape and size of the respiratory tract, route of breathing (nose or mouth), 

### 2

as well as how quickly and deeply a person is breathing. The site of the greatest O 3 dose 

### 3

to the lung tissue is the junction of the conducting airway and the gas exchange region, in 

### 4

the deeper portion of the respiratory tract. Additionally, the primary site of O 3 uptake 

### 5

moves deeper into the respiratory tract during exercise when breathing becomes faster 

### 6

and the breathing route changes from the nose only to oronas al breathing (i.e., through 

### 7

the nose and mouth) (See Section 5.2 ). 

### 8

Once O 3 has been absorbed, there are several key events in the toxicity pathway of O 3 in 

### 9

the respiratory tract that lead to O 3 - induced health effects (See Section 5.3 ). These 

### 10

include formation of secondary oxidation products in the lung, activation of neural 

### 11

reflexes, initiation of inflammation, alterations of epithelial barrier function, sensitization 

### 12

of bronchial smooth muscle, modification of innate and adaptive immunity, and airway 

### 13

remodeling. Another key event, systemic inflammation and vascular oxidative/nitrosative 

### 14

stress, may be critical to the extrapulmonary effects of O 3

. 

### 15

Overall, biological respo nses to O 3 exposure are common across many species (See 

### 16

Section 5.5 ). Thus, animal studies are used to add to the understanding of the full range 

### 17

o f potential O 3 - mediated health effects. 

### 18



## Integration of Ozone Health Effects

The body of evidence from short

- term (i.e., hours, days, weeks) or long

- term 

### 19

(i.e., months to years) exposure studies is evaluated and integrated across scientific 

### 20

disciplines (i.e

., controlled human exposure studies, toxicology, and epidemiology) and 

### 21

interpreted for the health effects evidence that spans all lifestages, and which vary in 

### 22

severity from minor subclinical effects to death. The results from the health studies, 

### 23

supporte d by the evidence from atmospheric chemistry and exposure assessment studies, 

### 24

contribute to the causal determinations made for the health outcomes

. The conclusions 

### 25

from the previous NAAQS review and the causality determinations from this review are 

### 26

summari zed in Table 1

- 1 . Additional details are provided here for respiratory health 

### 27

effects and mortality, for which there is the strongest evidence of an e ffect from O 3 ; 

### 28

details for a wider range of health effects are provided subsequent chapters

. 

### 29

### Draft

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- 5 June 2012 Table 1

- 1 Summary of ozone causal determinations by exposure duration

and health outcome

Health Outcome Conclusions from Previous Review Conclusions from

2012 3rd Draft ISA

Short

- Term Exposure to O 3

Respiratory effects The overall evidence supports a causal relationship between acute ambient O 3 exposures and increased respiratory morbidity outcomes. Causal Relationship

Cardiovascular effects The limited evidence is highly suggestive that O 3 directly and/or indirectly contributes to

cardiovascular

- related morbidity, but much remains to be done to more fully

substantiate the association. Suggestive of a Causa l Relationship

Central nervous system

effects Toxicological studies report that acute exposures to O 3 are associated with alterations in neurotransmitters, motor activity, short and long term memory, sleep patterns, and histological signs of neurodegeneration. Suggestive of a Causal Relationship

Total Mortality The evidence is highly suggestive that O 3 d irectly or indirectly contributes to non

accidental and cardiopulmonary

- related mortality. Likely to be a Causal Relationship

Long

- term Exposure to O 3

Respiratory effects The current evidence is suggestive but inconclusive for respiratory health effects from long

- term O 3 exposure. Likely to be a Causal Relationship

Cardiovascular effects No studies from previous review. Suggestive of a Causal Relationship

Reproductive and developmental effects Limited evidence for a relationship between air pollution and birth

- related health outcomes, including mortality, premature births, low birth weights, and birth defects, with little evidence being found for O 3 effects. Suggestive of a Causal Relationship

Central nervous system

effects Evidence regarding chronic exposure and neurobehavioral effects was not available. Suggestive of a Causal Relationship

Cancer Little evidence for a relationship between chronic O 3 exposure and increased risk of lung cancer. Inadequate to infer a Causal Relationship

Total Mortality There is little evidence to suggest a causal relationship between chronic O 3 exposure and increased risk for mortality in humans. Suggestive of a Causal Relationship



### Respiratory Effects

The clearest evidence for health effects associated with exposure to O 3 is provided by 

### 1

studies of respiratory effects. Collectively, a very large amount of evidence spanning 

### 2

several decades supports a relationship between exposure to O 3 and a broad range of 

### 3

respiratory effects (See Section 6.2.9 and Section 7.2.8 ). The majority of this evidence is 

### 4

derived from studies investigating short

- term exposure (i.e., hours to weeks) to O 3 , 

### 5

although animal toxicological studies and recent epidemiologic evidence demonstrate 

### 6

that long

- term exposure (i.e., months to years) may also be detriment al to the respiratory 

### 7

system. 

### 8

The last review concluded that there was clear, consistent evidence of a causal 

### 9

relationship between short

- term exposure to O 3 and respiratory health effe cts. This causal 

### 10

association is substantiated by the coherence of effect s observed across recent controlled 

### 11

human exposure, epidemiologic, and toxicological studies indicating associations of 

### 12

### Draft

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- term O 3 exposures with a range of respiratory health endpoints from respiratory 

### 1

tract inflammation to respiratory

- related emergenc y department (ED) visits and hospital 

### 2

admissions. Across disciplines, short

- term O 3 exposures induced or were associated with 

### 3

statistically significa nt declines in lung function. An equally strong body of evidence 

### 4

from controlled human exposure and toxicol ogical studies demonstrated O 3 - induced 

### 5

inflammatory responses, increased epithelial permeability, and airway 

### 6

hyperresponsiveness. Toxicological studies provided additional evidence for O 3 - induced 

### 7

impairment of host defenses. Combined, these findings from e xperimental studies 

### 8

provided support for epidemiologic evidence, in which short

- term increases in O 3 

### 9

concentration were consistently associated with increases in respiratory symptoms and 

### 10

asthma medication use in children with asthma, respiratory

- related ho spital admissions, 

### 11

and ED visits for COPD and asthma. Additionally, recent evidence supports the range of 

### 12

respiratory effects induced by O 3 by demonstrating that short

- term increases in ambient 

### 13

O 3 concentrations can lead to respiratory mortality. The combi ned evidence across 

### 14

disciplines supports a causal relationship between short

- term O 3 exposure and 

### 15

respiratory effects. 

### 16

Taken together, the recent epidemiologic studies of respiratory health effects (including 

### 17

respiratory symptoms, new

- onset asthma and resp iratory mortality) combined with 

### 18

toxicological studies in rodents and nonhuman primates, provide biologically plausible 

### 19

evidence that there is likely to be a causal relationship between long

- term exposure 

### 20

to O 3 and respiratory effects. The strongest epidemiologic evidence for a relationship 

### 21

between long

- term O 3 exposure and respiratory effects is provided by studies that 

### 22

demonstrate interactions between exercise or different genetic variants and long

- term 

### 23

measures of O 3 exposure on new

- onset asthma in children; and increased respiratory 

### 24

symptom effects in asthmatics. Additional studies of respiratory health effects and a 

### 25

study of respiratory mortality provide a collective body of evidence supporting these 

### 26

relationships. Studies considering other pollut ants provide data suggesting that the effects 

### 27

related to O 3 are independent from potential effects of the other pollutants. Some studies 

### 28

provide evidence for a positive concentration

- response relationship. Short

- term studies 

### 29

provide supportive evidence wit h increases in respiratory symptoms and asthma 

### 30

medication use, hospital admissions and ED visits for all respiratory outcomes and 

### 31

asthma, and decrements in lung function in children. The recent epidemiologic and 

### 32

toxicological data base provides a compellin g case to support the hypothesis that a 

### 33

relationship exists between long

- term exposure to ambient O 3 and measures of 

### 34

respiratory health effects. 

### 35

### Draft

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The last review concluded that the overall body of evidence was highly suggestive that 

### 1

short

- term exposure to O 3 directly or indirectly contributes to non

- accidental and 

### 2

cardiopulmonary

- related mortality; but that additional research was needed to more fully 

### 3

establish underlying mechanisms by which such effects occur. The evaluation of recent 

### 4

mul ticity studies and a multicontinent study that have examined the association between 

### 5

short

- term O 3 exposure and mortality found evidence that supports the conclusions of the 

### 6

last review (See Section 6.6 ). These recent studies reported consistent positive 

### 7

associations between short

- term O 3 exposure and total (nonaccidental) mortality, with 

### 8

associations being stronger during the warm season. They also a dded support for 

### 9

associations between O 3 exposure and cardiovascular mortality being similar to or 

### 10

stronger than those between O 3 exposure and respiratory mortality. Additionally, these 

### 11

recent studies examined previously identified areas of uncertainty in the O 3 - mortality 

### 12

relationship, and provide evidence that continues to support an association between short



### 13

term O 3 exposure and mortality. The body of evidence indicates that there is likely to be 

### 14

a causal relationship between short

- term exposures to O 3 an d total mortality. 

### 15

Populations Potentially at Increased Risk

The examination of populations potentially at increased risk for O 3 exposure identifies 

### 16

populations that are at increased risk for O 3 - related health effects; these studies do so by 

### 17

examining groups within the study population, such as those with an underlying health 

### 18

condition or genetic variant; categories of age, race, or sex; or by developing animal 

### 19

models that mimic the conditions associated w ith a health effect. Such studies have 

### 20

identifie d a multitude of factors that could potentially contribute to whether an individual 

### 21

is at increased risk for O 3 - related health effects (See Chapter 8 ). The populations 

### 22

identified as having adequate evidence for increased risk of O 3 - related health effects are 

### 23

individuals with asthma, younger and older age groups, individuals with reduced intake 

### 24

of certain nutrients (i.e., V itamins C and E), and outdoo r workers. The evidence for other 

### 25

potential factors, including variations in multiple genes related to oxidative metabolism 

### 26

or inflammation

, sex, socioeconomic status, and obesity is suggestive of an increased 

### 27

risk, but further evidence is needed. 

### 28



## Integrat ion of Effects on Vegetation and Ecosystems

The most policy

- relevant information pertaining to the review of the NAAQS for the 

### 29

effects of O 3 on vegetation and ecosystems are evaluated and synthesized, integrating key 

### 30

findings about plant physiology, bioche mistry, whole plant biology, ecosystems and 

### 31

### Draft

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- response relationships. The welfare effects of O 3 can be observed across spatial 

### 1

scales, starting at the cellular and subcellular level, then the whole plant and finally, 

### 2

ecosystem

- level processes. Ozone effects at small spatial scales, such as the leaf of an 

### 3

individual plant, can result in effects at a continuum of larger spatial scales. These effects 

### 4

include altered rates of leaf gas exchange, growth and reproduction at the individual plant 

### 5

level and ca n result in changes in ecosystems, such as productivity, carbon storage, water 

### 6

cycling, nutrient cycling, and community composition. The conclusions from the 

### 7

previous NAAQS review and the causality determinations from this review are 

### 8

summarized in the tabl e below. Further discussion of these conclusions is provided below 

### 9

for visible foliar injury, growth, productivity, and carbon storage, reduced yield and 

### 10

quality of agricultural crops, water cycling, below

- ground processing, community 

### 11

composition, and O 3 e xposure

- response relationships; discussion for all relevant welfar e 

### 12

effects is provided in Chapter 9

. 

### 13

Table 1

- 2 Summary of ozone causal determination for welfare effects

Vegetation and Ecosystem Effects Conclusions from Previous Review Conclusions from

2012 3rd Draft

ISA

Visible Foliar Injury Effects on Vegetation Data published since the 1996 O 3 AQCD strengthen previous conclusions that there is strong

evidence that current ambient O 3 concentrations cause impaired aesthetic quality of many native plants and trees by increasing foliar injury. Causal Relationship

Re duced Vegetation

Growth Data published since the 1996 O 3 AQCD strengthen previous conclusions that there is strong evidence that current ambient O 3 concentrations cause decreased growth and

biomass accumulation in annual, perennial and woody plants, includ ing agronomic crops, annuals, shrubs, grasses, and trees. Causal Relationship

Reduced Productivity in Terrestrial Ecosystems There is evidence that O 3 is an important stressor of ecosystems and that the effects of

O 3 on individual plants and processes are scaled up through the ecosystem, affecting net primary productivity. Causal Relationship

Reduced Carbon (C) Sequestration in Terrestrial Ecosystems Limited studies from previous review Likely to be a Causal

Relation ship

Reduced Yield and Quality of Agricultural Crops Data published since the 1996 O 3 AQCD strengthen previous conclusions that there is strong evidence that current ambient O 3 concentrations cause decreased yield and/or nutritive quality in a large number of agronomic and forage crops. Causal Relationship

Alteration of Terrestrial Ecosystem Water Cycling Ecosystem water quantity may be affected by O 3 exposure at the landscape level. Likely to be a Causal Relationship

Alteration of Below

ground Biogeochemical Cycles Ozone

- sensitive species have well known responses to O 3 exposure , including altered C

allocation to below

- ground tissues, and altered rates of leaf and root production, turnover, and decomposition. These shifts can affect overall C and N loss from the ecosystem in terms of respired C, and leached aqueous dissolved organic and inorganic C and N. Causal Relationship

Alteration of Terrestrial Community Composition Ozone may be affecting above

- and below

- ground community com position through impacts on both growth and reproduction. Significa nt changes in plant community composition resulting directly from O 3 exposure have been demonstrated. Likely to be a Causal Relationship

### Draft

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- 9 June 2012 Visible Foliar Injury

Visible foliar injury resulting from exposure to O 3 has been well characterized and 

### 1

documented over several decades on many tree, shrub, herbaceous and crop species. 

### 2

Ozone

- induced visible foliar injury symptoms on certain plant species are considered 

### 3

diagnostic of exposure to O 3 , as experimental evidence has clearly established a 

### 4

consistent association, with greater exposure often resulting in greater and more prevalent 

### 5

injury. Additional sensitive species showing visible foliar injury continue to be identified 

### 6

from field survey s and verified in controlled exposure studies (See Section 9.4.2 ). 

### 7

Overall, evidence is sufficient to conclude that there is a causal relationship between 

### 8

ambient O 3 exposure and the occurrence of O 3 induced visible foliar injury on 

### 9

sensitive vegetation across the U.S. 

### 10

Growth, Productivity, Carbon Storage and Agriculture

Ambient O 3 concentrations have long been known to cause decreases in photosynthe tic 

### 11

rates and plant growth. The O 3 - induced effects at the plant scale may translate to the 

### 12

ecosystem scale, and cause changes in productivity and C storage. The effects of O 3 

### 13

exposure on photosynthesis, growth, biomass allocation, ecosystem production and 

### 14

ecosystem C sequestration were reviewed for natural ecosystems (See Section 9.4.3 ), and 

### 15

crop productivity and crop quality were reviewed for agricu ltural ecosystems (See 

### 16

Section 9.4.4 ). There is strong and consistent evidence that ambient concentrations of O 3 

### 17

decrease plant photosynthesis and g rowth in numerous plant species across the U.S. 

### 18

Studies conducted during the past four decades have also demonstrated unequivocally 

### 19

that O 3 alters biomass allocation and plant reproduction. Studies at the leaf and plant 

### 20

scales showed that O 3 reduced photos ynthesis and plant growth, providing coherence and 

### 21

biological plausibility for the reported decreases in ecosystem productivity. In addition to 

### 22

primary productivity, other indicators such as net ecosystem CO 2 exchange and 

### 23

C sequestration were often assesse d by modeling studies. Model simulations consistently 

### 24

found that O 3 exposure caused negative impacts on those indicators, but the severity of 

### 25

these impacts was influenced by multiple interactions of biological and environmental 

### 26

factors. Although O 3 general ly causes negative effects on ecosystem productivity, the 

### 27

magnitude of the response varies among plant communities. Overall, evidence is 

### 28

sufficient to conclude that there is a causal relationship between ambient O 3 

### 29

exposure and reduced native plant growth and productivity, and a likely causal 

### 30

relationship between O 3 exposure and reduced carbon sequestration in terrestrial 

### 31

ecosystems. 

### 32

The detrimental effect of O 3 on crop production has been recognized since the 1960’ s, 

### 33

and current O 3 concentrations across the U.S. are high enough to cause yield loss for a 

### 34

### Draft

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- 10 June 2012 variety of agricultural crops including, but not limited to, soybean, wheat, potato, 

### 1

watermelon, beans, turnip, onion, lettuce, and tomato. Continued increases in O 3 

### 2

concentration may further decrease yield in these sensitive crops while also initiating 

### 3

yield losses in less sensitive crops. Research has linked increasing O 3 concentration to 

### 4

decreased photosynthetic rates and accelerated senescence, which are related t o yield 

### 5

(See Section 9.4.4 ). Evidence is sufficient to conclude that there is a causal relationship 

### 6

between O 3 exposure and reduced yield and qualit y of agricultural crops. 

### 7

Water Cycling

Ozone can affect water use in plants and ecosystems through several mechanisms 

### 8

including damage to stomatal functioning and loss of leaf area. Possible mechanisms for 

### 9

O 3 exposure effects on stomatal functioning includ e the build

- up of CO 2 in the 

### 10

substomatal cavity, impacts on signal transduction pathways and direct O 3 impact on 

### 11

guard cells. Regardless of the mechanism, O 3 exposure has been shown to alter stomatal 

### 12

performance, which may affect plant and stand transpirat ion and therefore may affect 

### 13

hydrological cycling (See Section 9.4.5 ). Although the direction of the response differed 

### 14

among studies, the evidence is sufficient to conclude that there is likely to be a causal 

### 15

relationship between O 3 exposure and the alteration of ecosystem water cycling. 

### 16

Below Ground Processes

Below

- ground processes are tightly linked with above

- ground processes. The responses 

### 17

of above

- ground process to O 3 exposure, such as reduced photosynthetic rates, increased 

### 18

metabolic cost, and reduced roo t C allocation, have provided biologically plausible 

### 19

mechanisms for the alteration of below

- ground processes. These include altered quality 

### 20

and quantity of C input to soil, microbial community composition, and C and nutrient 

### 21

cycling (See Section 9.4.6 ). The evidence is sufficient to conclude that there is a causal 

### 22

relationship between O 3 exposure and the alteration of below

- ground 

### 23

biogeochemical cycl es. 

### 24

Community Composition

Ozone exposure changes competitive interactions and leads to loss of O 3 - sensitive 

### 25

species or genotypes. Studies at the plant level found that the severity of O 3 damage to 

### 26

growth, reproduction

, and foliar injury varied among specie s, which provided the 

### 27

biological plausibility for the alteration of community composition (See Section 9.4.3 and 

### 28

Section 9.4.7 ). For example, there is a tendency for O 3 exposure to shift the biomass of 

### 29

grass

- legume mixtures in favor of grass species. Ozone exposure not only altered 

### 30

### Draft

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- 11 June 2012 community com position of plant species, but also microorganisms: research since the last 

### 1

review has shown that O 3 can also alter community composition and diversity of soil 

### 2

microbial communities. Shifts in community composition of bacteria and fungi have been 

### 3

observed in both natural and agricultural ecosystems, although no general patterns could 

### 4

be identified. The e vidence is sufficient to conclude that there is likely to be a causal 

### 5

relationship between O 3 exposure and the alteration of community composition of 

### 6

some ecosystems. 

### 7

Ozone Exposure

- Response Relationships

Previous reviews of the NAAQs have included exposur e

- response functions for the yield 

### 8

of many crop species, and for the biomass accumulation of tree species. They were based 

### 9

on large

- scale experiments designed to obtain clear exposure

- response data, and are 

### 10

updated by using the W126 metric to quantify expo sure. In recent years, extensive 

### 11

exposure

- response data obtained in more naturalistic settings have become available for 

### 12

yield of soybean and growth of aspen. The exposure

- response median functions are 

### 13

validated based on previous data by comparing their pr edictions with the newer 

### 14

observations (See Section 9.6 ). The functions supply very accurate predictions of effects 

### 15

in naturalistic settings. Recent meta

- analyses of large sets of crop and tree studies do not 

### 16

give rise to exposure

- response functions, but their results are consistent with th e 

### 17

functions presented in Section 9.6 . It is important to note that although these median 

### 18

functions provide reliable models for groups of species or group of genotypes within a 

### 19

species, the original data and recent results consistently show that some species, and 

### 20

some genotypes within species are much more severely affected by exposure to O 3

. 

### 21



## The Role of Tropospheric Ozone in Climate Change and

UV

- B Effects

Atmospheric O 3 plays an important role in the Earth’s energy budget by interacting with 

### 22

incoming solar radia tion and outgoing infrared radiation. Tropospheric O 3 makes up only 

### 23

a small portion of the total column of O 3 , but it has important incremental effects on the 

### 24

overall radiation budget. Perturbations in tropospheric O 3 concentrations can have direct 

### 25

effects on climate and indirect effects on health, ecology, and welfare by shielding the 

### 26

earth’s surface from solar ultraviolet (UV) radiation. 

### 27

Radiative Forcing and Climate Change

Tropospheric O 3 is a major greenhouse gas, third in importance after CO 2 and CH 4 

### 28

a ccording to the IPCC (See Section 10.3 ). Models calculate that the global average 

### 29

### Draft

– Do Not Cite or Quote 1

- 12 June 2012 concentration of tropospheric O 3 has doubled since the preindustrial era, while 

### 1

observations indicate that in some regions O 3 may have increased by factors as great as 4 

### 2

or 5. These increases are tied to the rise in emissions of O 3 precursors from human 

### 3

activity, mainly fossil fuel consu mption and agricultural processes. There are large 

### 4

uncertainties in the radiative forcing estimate attributed to tropospheric O 3 , making the 

### 5

effect of tropospheric O 3 on climate more uncertain than the effect of the long

- lived 

### 6

greenhouse gases. Overall, th e evidence supports a causal relationship between 

### 7

changes in tropospheric O 3 concentrations and radiative forcing. 

### 8

Radiative forcing does not take into account the climate feedbacks that could amplify or 

### 9

dampen the actual surface temperature response. Quan tifying the change in surface 

### 10

temperature requires a complex climate simulation in which all important feedbacks and 

### 11

interactions are accounted for. As these processes are not well understood or easily 

### 12

modeled, the surface temperature response to a given r adiative forcing is highly uncertain 

### 13

and can vary greatly among models and from region to region within the same model. In 

### 14

light of these uncertainties, the evidence indicates that there is likely to be a causal 

### 15

relationship between changes in tropospheric O 3 concentrations and effects on 

### 16

climate. 

### 17

UV

- B Effects

UV radiation emitted from the Sun contains sufficient energy when it reaches the Earth to 

### 18

have damaging effects on living organisms and materials (see Section 10.4 ). Atmospheric 

### 19

O 3 plays a crucial role in reducing exposure to UV radiation at the Earth’s surface. Ozone 

### 20

in the stratosphere is responsible for the majority of this shielding, but O 3 in the 

### 21

troposphere provides supplemental shielding of UV radiation in the mid

- wavelength 

### 22

range (UV

- B), thereby influencing human and ecosystem health and materials damage. 

### 23

There is a lack of published studies that critically examine the incremental health or 

### 24

welfare effects (adverse or beneficial) attributable specifically to changes in UV

- B 

### 25

exposure resulting from perturbations in tropospheric O 3 concentrations. While the 

### 26

effects are expected to be small, they cannot yet be critically assessed within reas onable 

### 27

uncertainty. Overall, the evidence is inadequate to determine if a causal relationship 

### 28

exists between changes in tropospheric O 3 concentrations and effects on health and 

### 29

welfare related to UV

- B shielding. 

### 30

The conclusions from the previous NAAQS re view and the causality determinations from 

### 31

this review relating climate change and UV

- B effects are summarized in the table below 

### 32

( Table 1

- 3 )

, with de tails provided in Chapter 10

. 

### 33

### Draft

– Do Not Cite or Quote 1

- 13 June 2012 Table 1

- 3 Summary of ozone causal determination for climate change and

UV

- B effects.

Effects Conclusions from Previous Review Conclusions from

2012 3rd Draft ISA

Radiative Forcing Climate forcing by O 3 at the regional scale may be its most important impact on climate. Causal Relationship

Climate Change While more certain estimates of the overall importance of global

- scale forcing due to tropospheric O 3 await further advances in monitoring and chemical transport modeling, the overall body of scientific evidence suggests that high concentrations of O 3 on the regional scale c ould have a discernible influence on climate, leading to surface temperature and hydrological cycle changes. Likely to be a Causal Relationship

Health and Welfare Effects

Related to UV

- B Shielding UV

- B has not been studied in sufficient detail to allow for a credible health benefits assessment. In conclusion, the effect of changes in surface

- level O 3 concentrations on

UV

- induced health outcomes cannot yet be critically assessed within reasonable uncertainty. Inadequate to Determine if

a Causal Relationship

Exists



## Conclusion

The clearest evidence for human health effects associated with exposure to O 3 is provided 

### 1

by studies of respiratory effects. Collectively, there is a very large amount of evidence 

### 2

spanning several decades in support of a cau sal association between exposure to O 3 and a 

### 3

broad range of respiratory effects. The majority of this evidence is derived from studies 

### 4

investigating short

- term O 3 exposure (i.e., hours to weeks), although animal toxicological 

### 5

studies and recent epidemiolog ic evidence demonstrate that long

- term exposure 

### 6

(i.e., months to years) may also be detrimental to the respiratory system. Additionally, 

### 7

consistent positive associations between short

- term O 3 exposure and total (nonaccidental) 

### 8

mortality have helped to reso lve previously identified areas of uncertainty in the 

### 9

O 3 - mortality relationship, indicating that there is likely to be a causal relationship 

### 10

between short

- term exposures to O 3 and total mortality. Taken together, the recent 

### 11

epidemiologic studies of respiratory health effects (including respiratory symptoms, new



### 12

onset asthma and respiratory mortality) combined with toxicological studies in rodents 

### 13

and nonhuman primates, provide biologically plausible evidence that there is likely to be 

### 14

a causal relationship between long

- term exposure to O 3 and respiratory effects. 

### 15

Recent evidence is suggestive of a causal relationship between long

- term O 3 

### 16

exposures and total mortality

. The evidence for these health ef fects indicates that the 

### 17

relationship between concentration and response is linear along the range of O 3 

### 18

concentrations observed in the U.S., with no indication of a threshold. However, there is 

### 19

less certainty in the shape of the concentration

- response cur ve at O 3 concentrations 

### 20

generally below 20 ppb. The populations identified as having increased risk of O 3 - related 

### 21

health effects are individuals with asthma, younger and older age groups, individuals with 

### 22

certain dietary deficiencies, and outdoor workers. 

### 23

### Draft

– Do Not Cite or Quote 1

- 14 June 2012 There has been over 40 years of research on the effects of O 3 exposure on vegetation and 

### 1

ecosystems. The best evidence for effects is from controlled exposure studies. These 

### 2

studies have clearly shown that exposure to O 3 is causally linked to visible foliar injury, 

### 3

decreased photosynthesis, changes in reproduction, and decreased growth. Recently, 

### 4

studies at larger spatial scales support the results from controlled studies and indicate that 

### 5

ambient O 3 exposures can affect ecosystem productivity, crop yield, water cycling, and 

### 6

ecosystem community composition. And on a global scale, tropospheric O 3 is the third 

### 7

most important greenhouse gas, playing an important role in climate change. 

### 8