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1 EXECUTIVE SUMMARY

Introduction and Purpose

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

2 evaluation of the most policy-relevant science that forms the scientific foundation for the 

3 review of the primary (health-based) and secondary (welfare-based) national ambient air 

4 quality standard (NAAQS) for ozone (O3) and related photochemical oxidants. The ISA 

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

6 thereby support decisions by the EPA Administrator on the NAAQS for O3 (See Figure I 

7 in Preamble). The current primary O3 standard includes an 8-hour average standard set in 

8 2008 at 75 parts per billion (ppb). The secondary standard for O3 is equal to the primary 

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

10 after short-term exposure to O3, while the secondary NAAQS protects against damage to 

11 vegetation and ecosystems.

Scope and Methods

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

13 and drawing conclusions regarding air pollution-related health and welfare effects, which 

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

15 of O3. Building upon the findings of previous assessments, this review includes 

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

17 the atmospheric science of O3; short- and long-term exposure to ambient O3; health 

18 effects due to relevant O3 concentrations as characterized in epidemiologic, controlled 

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

20 O3 concentration-response relationships, mode(s) of action, and populations at increased 

21 risk for O3-related health effects. The conclusions and key findings from previous 

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

23 studies published since the completion of the 2006 O3 AQCD). Conclusions are drawn 

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

25 upon the extensive evidence presented in previous reviews. 

26 EPA has developed a consistent and transparent approach to evaluate the causal nature of 

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

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

29 Causality determinations are based on the evaluation and synthesis of evidence across 

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

31 determinations will vary by pollutant or assessment. EPA assesses the entire body of 
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1 peer-reviewed literature, building upon evidence available during the previous NAAQS 

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

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

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

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

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

7 A five-level hierarchy is used to classify the weight of evidence for causation, not just 

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

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

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

11 causality. The causal determinations are:

12  Causal relationship 

13  Likely to be a causal relationship 

14  Suggestive of a causal relationship 

15  Inadequate to infer a causal relationship 

16  Not likely to be a causal relationship 

Ambient Ozone Concentrations

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

18 blocking harmful ultraviolet radiation from the Sun, and preventing the majority of this 

19 radiation from reaching the surface of the Earth. However, in the troposphere, O3 acts as 

20 a powerful oxidant and can harm living organisms and materials. Tropospheric O3 is 

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

22 by local meteorological conditions, circulation patterns, emissions, and topographic 

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

24 larger scale, O3 persists in the atmosphere long enough that it can be transported from 

25 continent to continent. 

26 Ozone in the troposphere originates from both anthropogenic (i.e., man-made) and 

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

28 atmosphere by photochemical reactions involving sunlight and precursor pollutants 

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

30 attributed to natural sources is formed through the same photochemical reactions 

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

32 biomass burning, and lightning. Because O3 is produced downwind of urban source areas 

33 and O3 tends to persist longer in rural than in urban areas as a result of lower chemical 
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1 scavenge, resulting in concentrations in rural areas that are often higher than those in 

2 urban areas.

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

4 concentrations in a way that distinguishes between concentrations that result from 

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

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

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

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

9 background is a construct that cannot be measured, NA background O3 concentrations are 

10 estimated using chemistry transport models. Seasonal mean daily maximum 8-h average 

11 NA background O3 concentrations are generally higher in spring than in summer across 

12 the U.S. The highest estimates are found in the Intermountain West during the spring and 

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

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

Human Exposure to Ozone

15 The widespread presence of O3 in the environment results in exposure as people 

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

17 ambient concentration measured at fixed-site monitors can be described in terms of 

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

19 mangnitude. Personal-ambient O3 correlations are generally moderate (0.3-0.8), although 

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

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

22 Ratios of 0.1-0.3 between personal exposure and ambient concentration have been 

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

24 workers. Evidence suggests that some groups, particularly children, older adults, and 

25 those with respiratory problems, change their behavior on high-O3 days to reduce 

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

27 estimates in epidemiologic studies that do not account for averting behavior on high-O3

28 days. Variation in O3 concentrations occurs over multiple spatial and temporal scales, and 

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

30 epidemiologic studies evaluating the influence of spatial scale and monitor selection find 

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

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

33 different levels of personal-ambient associations. This suggests that there is no clear 

34 indication that a particular method of exposure assessment produces stronger 

35 epidemiologic results.
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Dosimetry and Modes of Action

1 When O3 is inhaled, the amount of O3 that is absorbed is affected by a number of factors 

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

3 as well as how quickly and deeply a person is breathing. The site of the greatest O3 dose 

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

5 the deeper portion of the respiratory tract. Additionally, the primary site of O3 uptake 

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

7 and the breathing route changes from the nose only to oronasal breathing (i.e., through 

8 the nose and mouth) (See Section 5.2). 

9 Once O3 has been absorbed, there are several key events in the toxicity pathway of O3 in 

10 the respiratory tract that lead to O3-induced health effects (See Section 5.3). These 

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

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

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

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

15 stress, may be critical to the extrapulmonary effects of O3.

16 Overall, biological responses to O3 exposure are common across many species (See 

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

18 of potential O3-mediated health effects.

Integration of Ozone Health Effects

19 The body of evidence from short-term (i.e., hours, days, weeks) or long-term 

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

21 disciplines (i.e., controlled human exposure studies, toxicology, and epidemiology) and 

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

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

24 supported by the evidence from atmospheric chemistry and exposure assessment studies, 

25 contribute to the causal determinations made for the health outcomes. The conclusions 

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

27 summarized in Table 1-1. Additional details are provided here for respiratory health 

28 effects and mortality, for which there is the strongest evidence of an effect from O3; 

29 details for a wider range of health effects are provided subsequent chapters.
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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 O3

Respiratory effects The overall evidence supports a causal relationship between acute ambient O3

exposures and increased respiratory morbidity outcomes.

Causal Relationship

Cardiovascular effects The limited evidence is highly suggestive that O3 directly and/or indirectly contributes to 

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

substantiate the association.

Suggestive of a Causal 

Relationship

Central nervous system 

effects

Toxicological studies report that acute exposures to O3 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 O3 directly or indirectly contributes to nonaccidental and cardiopulmonary-related mortality.Likely to be a Causal 

Relationship

Long-term Exposure to O3

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

long-term O3 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 O3 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 O3 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 O3 exposure 

and increased risk for mortality in humans.

Suggestive of a Causal 

Relationship

Respiratory Effects

1 The clearest evidence for health effects associated with exposure to O3 is provided by 

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

3 several decades supports a relationship between exposure to O3 and a broad range of 

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

5 derived from studies investigating short-term exposure (i.e., hours to weeks) to O3, 

6 although animal toxicological studies and recent epidemiologic evidence demonstrate 

7 that long-term exposure (i.e., months to years) may also be detrimental to the respiratory 

8 system.

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

10 relationship between short-term exposure to O3 and respiratory health effects. This causal 

11 association is substantiated by the coherence of effects observed across recent controlled 

12 human exposure, epidemiologic, and toxicological studies indicating associations of 
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1 short-term O3 exposures with a range of respiratory health endpoints from respiratory 

2 tract inflammation to respiratory-related emergency department (ED) visits and hospital 

3 admissions. Across disciplines, short-term O3 exposures induced or were associated with 

4 statistically significant declines in lung function. An equally strong body of evidence 

5 from controlled human exposure and toxicological studies demonstrated O3-induced 

6 inflammatory responses, increased epithelial permeability, and airway 

7 hyperresponsiveness. Toxicological studies provided additional evidence for O3-induced 

8 impairment of host defenses. Combined, these findings from experimental studies 

9 provided support for epidemiologic evidence, in which short-term increases in O3

10 concentration were consistently associated with increases in respiratory symptoms and 

11 asthma medication use in children with asthma, respiratory-related hospital admissions, 

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

13 respiratory effects induced by O3 by demonstrating that short-term increases in ambient 

14 O3 concentrations can lead to respiratory mortality. The combined evidence across 

15 disciplines supports a causal relationship between short-term O3 exposure and 

16 respiratory effects.

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

18 respiratory symptoms, new-onset asthma and respiratory mortality) combined with 

19 toxicological studies in rodents and nonhuman primates, provide biologically plausible 

20 evidence that there is likely to be a causal relationship between long-term exposure 

21 to O3 and respiratory effects. The strongest epidemiologic evidence for a relationship 

22 between long-term O3 exposure and respiratory effects is provided by studies that 

23 demonstrate interactions between exercise or different genetic variants and long-term 

24 measures of O3 exposure on new-onset asthma in children; and increased respiratory 

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

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

27 relationships. Studies considering other pollutants provide data suggesting that the effects 

28 related to O3 are independent from potential effects of the other pollutants. Some studies 

29 provide evidence for a positive concentration-response relationship. Short-term studies 

30 provide supportive evidence with increases in respiratory symptoms and asthma 

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

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

33 toxicological data base provides a compelling case to support the hypothesis that a 

34 relationship exists between long-term exposure to ambient O3 and measures of 

35 respiratory health effects. 
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Mortality Effects

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

2 short-term exposure to O3 directly or indirectly contributes to non-accidental and 

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

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

5 multicity studies and a multicontinent study that have examined the association between 

6 short-term O3 exposure and mortality found evidence that supports the conclusions of the 

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

8 associations between short-term O3 exposure and total (nonaccidental) mortality, with 

9 associations being stronger during the warm season. They also added support for 

10 associations between O3 exposure and cardiovascular mortality being similar to or 

11 stronger than those between O3 exposure and respiratory mortality. Additionally, these 

12 recent studies examined previously identified areas of uncertainty in the O3-mortality 

13 relationship, and provide evidence that continues to support an association between short14 term O3 exposure and mortality. The body of evidence indicates that there is likely to be 

15 a causal relationship between short-term exposures to O3 and total mortality.

Populations Potentially at Increased Risk

16 The examination of populations potentially at increased risk for O3 exposure identifies 

17 populations that are at increased risk for O3-related health effects; these studies do so by 

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

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

20 models that mimic the conditions associated with a health effect. Such studies have 

21 identified a multitude of factors that could potentially contribute to whether an individual 

22 is at increased risk for O3-related health effects (See Chapter 8). The populations 

23 identified as having adequate evidence for increased risk of O3-related health effects are 

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

25 of certain nutrients (i.e., Vitamins C and E), and outdoor workers. The evidence for other 

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

27 or inflammation, sex, socioeconomic status, and obesity is suggestive of an increased 

28 risk, but further evidence is needed.

Integration of Effects on Vegetation and Ecosystems

29 The most policy-relevant information pertaining to the review of the NAAQS for the 

30 effects of O3 on vegetation and ecosystems are evaluated and synthesized, integrating key 

31 findings about plant physiology, biochemistry, whole plant biology, ecosystems and 
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1 exposure-response relationships. The welfare effects of O3 can be observed across spatial 

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

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

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

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

6 level and can result in changes in ecosystems, such as productivity, carbon storage, water 

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

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

9 summarized in the table below. Further discussion of these conclusions is provided below 

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

11 quality of agricultural crops, water cycling, below-ground processing, community 

12 composition, and O3 exposure-response relationships; discussion for all relevant welfare 

13 effects is provided in Chapter 9.

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 O3 AQCD strengthen previous conclusions that there is strong 

evidence that current ambient O3 concentrations cause impaired aesthetic quality of many 

native plants and trees by increasing foliar injury.

Causal Relationship

Reduced Vegetation 

Growth

Data published since the 1996 O3 AQCD strengthen previous conclusions that there is 

strong evidence that current ambient O3 concentrations cause decreased growth and 

biomass accumulation in annual, perennial and woody plants, including agronomic crops, 

annuals, shrubs, grasses, and trees.

Causal Relationship

Reduced Productivity in 

Terrestrial Ecosystems

There is evidence that O3 is an important stressor of ecosystems and that the effects of 

O3 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 

Relationship

Reduced Yield and 

Quality of Agricultural 

Crops

Data published since the 1996 O3 AQCD strengthen previous conclusions that there is 

strong evidence that current ambient O3 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 O3 exposure at the landscape level. Likely to be a Causal 

Relationship

Alteration of Belowground Biogeochemical 

Cycles

Ozone-sensitive species have well known responses to O3 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 composition through impacts 

on both growth and reproduction. Significant changes in plant community composition 

resulting directly from O3 exposure have been demonstrated.

Likely to be a Causal 

Relationship
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Visible Foliar Injury

1 Visible foliar injury resulting from exposure to O3 has been well characterized and 

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

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

4 diagnostic of exposure to O3, as experimental evidence has clearly established a 

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

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

7 from field surveys and verified in controlled exposure studies (See Section 9.4.2).

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

9 ambient O3 exposure and the occurrence of O3 induced visible foliar injury on 

10 sensitive vegetation across the U.S.

Growth, Productivity, Carbon Storage and Agriculture

11 Ambient O3 concentrations have long been known to cause decreases in photosynthetic 

12 rates and plant growth. The O3-induced effects at the plant scale may translate to the 

13 ecosystem scale, and cause changes in productivity and C storage. The effects of O3

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

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

16 crop productivity and crop quality were reviewed for agricultural ecosystems (See 

17 Section 9.4.4). There is strong and consistent evidence that ambient concentrations of O3

18 decrease plant photosynthesis and growth in numerous plant species across the U.S. 

19 Studies conducted during the past four decades have also demonstrated unequivocally 

20 that O3 alters biomass allocation and plant reproduction. Studies at the leaf and plant 

21 scales showed that O3 reduced photosynthesis and plant growth, providing coherence and 

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

23 primary productivity, other indicators such as net ecosystem CO2 exchange and 

24 C sequestration were often assessed by modeling studies. Model simulations consistently 

25 found that O3 exposure caused negative impacts on those indicators, but the severity of 

26 these impacts was influenced by multiple interactions of biological and environmental 

27 factors. Although O3 generally causes negative effects on ecosystem productivity, the 

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

29 sufficient to conclude that there is a causal relationship between ambient O3

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

31 relationship between O3 exposure and reduced carbon sequestration in terrestrial 

32 ecosystems.

33 The detrimental effect of O3 on crop production has been recognized since the 1960’s, 

34 and current O3 concentrations across the U.S. are high enough to cause yield loss for a 
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1 variety of agricultural crops including, but not limited to, soybean, wheat, potato, 

2 watermelon, beans, turnip, onion, lettuce, and tomato. Continued increases in O3

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

4 yield losses in less sensitive crops. Research has linked increasing O3 concentration to 

5 decreased photosynthetic rates and accelerated senescence, which are related to yield 

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

7 between O3 exposure and reduced yield and quality of agricultural crops.

Water Cycling

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

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

10 O3 exposure effects on stomatal functioning include the build-up of CO2 in the 

11 substomatal cavity, impacts on signal transduction pathways and direct O3 impact on 

12 guard cells. Regardless of the mechanism, O3 exposure has been shown to alter stomatal 

13 performance, which may affect plant and stand transpiration and therefore may affect 

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

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

16 relationship between O3 exposure and the alteration of ecosystem water cycling.

Below Ground Processes

17 Below-ground processes are tightly linked with above-ground processes. The responses 

18 of above-ground process to O3 exposure, such as reduced photosynthetic rates, increased 

19 metabolic cost, and reduced root C allocation, have provided biologically plausible 

20 mechanisms for the alteration of below-ground processes. These include altered quality 

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

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

23 relationship between O3 exposure and the alteration of below-ground 

24 biogeochemical cycles.

Community Composition

25 Ozone exposure changes competitive interactions and leads to loss of O3-sensitive 

26 species or genotypes. Studies at the plant level found that the severity of O3 damage to 

27 growth, reproduction, and foliar injury varied among species, which provided the 

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

29 Section 9.4.7). For example, there is a tendency for O3 exposure to shift the biomass of 

30 grass-legume mixtures in favor of grass species. Ozone exposure not only altered 
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1 community composition of plant species, but also microorganisms: research since the last 

2 review has shown that O3 can also alter community composition and diversity of soil 

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

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

5 be identified. The evidence is sufficient to conclude that there is likely to be a causal 

6 relationship between O3 exposure and the alteration of community composition of 

7 some ecosystems.

Ozone Exposure-Response Relationships

8 Previous reviews of the NAAQs have included exposure-response functions for the yield 

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

10 on large-scale experiments designed to obtain clear exposure-response data, and are 

11 updated by using the W126 metric to quantify exposure. In recent years, extensive 

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

13 yield of soybean and growth of aspen. The exposure-response median functions are 

14 validated based on previous data by comparing their predictions with the newer 

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

16 in naturalistic settings. Recent meta-analyses of large sets of crop and tree studies do not 

17 give rise to exposure-response functions, but their results are consistent with the 

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

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

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

21 some genotypes within species are much more severely affected by exposure to O3.

The Role of Tropospheric Ozone in Climate Change and 

UV-B Effects

22 Atmospheric O3 plays an important role in the Earth’s energy budget by interacting with 

23 incoming solar radiation and outgoing infrared radiation. Tropospheric O3 makes up only 

24 a small portion of the total column of O3, but it has important incremental effects on the 

25 overall radiation budget. Perturbations in tropospheric O3 concentrations can have direct 

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

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

Radiative Forcing and Climate Change

28 Tropospheric O3 is a major greenhouse gas, third in importance after CO2 and CH4

29 according to the IPCC (See Section 10.3). Models calculate that the global average 
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1 concentration of tropospheric O3 has doubled since the preindustrial era, while 

2 observations indicate that in some regions O3 may have increased by factors as great as 4 

3 or 5. These increases are tied to the rise in emissions of O3 precursors from human 

4 activity, mainly fossil fuel consumption and agricultural processes. There are large 

5 uncertainties in the radiative forcing estimate attributed to tropospheric O3, making the 

6 effect of tropospheric O3 on climate more uncertain than the effect of the long-lived 

7 greenhouse gases. Overall, the evidence supports a causal relationship between 

8 changes in tropospheric O3 concentrations and radiative forcing.

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

10 dampen the actual surface temperature response. Quantifying the change in surface 

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

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

13 modeled, the surface temperature response to a given radiative forcing is highly uncertain 

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

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

16 relationship between changes in tropospheric O3 concentrations and effects on 

17 climate.

UV-B Effects

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

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

20 O3 plays a crucial role in reducing exposure to UV radiation at the Earth’s surface. Ozone 

21 in the stratosphere is responsible for the majority of this shielding, but O3 in the 

22 troposphere provides supplemental shielding of UV radiation in the mid-wavelength 

23 range (UV-B), thereby influencing human and ecosystem health and materials damage. 

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

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

26 exposure resulting from perturbations in tropospheric O3 concentrations. While the 

27 effects are expected to be small, they cannot yet be critically assessed within reasonable 

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

29 exists between changes in tropospheric O3 concentrations and effects on health and 

30 welfare related to UV-B shielding.

31 The conclusions from the previous NAAQS review and the causality determinations from 

32 this review relating climate change and UV-B effects are summarized in the table below 

33 (Table 1-3), with details provided in Chapter 10.
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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 O3 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 O3 await further advances in monitoring and chemical transport modeling, 

the overall body of scientific evidence suggests that high concentrations of O3 on the 

regional scale could 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 O3 concentrations on 

UV-induced health outcomes cannot yet be critically assessed within reasonable 

uncertainty.

Inadequate to Determine if 

a Causal Relationship 

Exists

Conclusion

1 The clearest evidence for human health effects associated with exposure to O3 is provided 

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

3 spanning several decades in support of a causal association between exposure to O3 and a 

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

5 investigating short-term O3 exposure (i.e., hours to weeks), although animal toxicological 

6 studies and recent epidemiologic evidence demonstrate that long-term exposure 

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

8 consistent positive associations between short-term O3 exposure and total (nonaccidental) 

9 mortality have helped to resolve previously identified areas of uncertainty in the 

10 O3-mortality relationship, indicating that there is likely to be a causal relationship 

11 between short-term exposures to O3 and total mortality. Taken together, the recent 

12 epidemiologic studies of respiratory health effects (including respiratory symptoms, new13 onset asthma and respiratory mortality) combined with toxicological studies in rodents 

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

15 a causal relationship between long-term exposure to O3 and respiratory effects. 

16 Recent evidence is suggestive of a causal relationship between long-term O3

17 exposures and total mortality. The evidence for these health effects indicates that the 

18 relationship between concentration and response is linear along the range of O3

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

20 less certainty in the shape of the concentration-response curve at O3 concentrations 

21 generally below 20 ppb. The populations identified as having increased risk of O3-related 

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

23 certain dietary deficiencies, and outdoor workers. 
Draft – Do Not Cite or Quote 1-14 June 2012

1 There has been over 40 years of research on the effects of O3 exposure on vegetation and 

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

3 studies have clearly shown that exposure to O3 is causally linked to visible foliar injury, 

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

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

6 ambient O3 exposures can affect ecosystem productivity, crop yield, water cycling, and 

7 ecosystem community composition. And on a global scale, tropospheric O3 is the third 

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