1 EXECUTIVE SUMMARY

1.1 Introduction

This Integrated Science Assessment (ISA) is a synthesis and evaluation of the most 

policy-relevant science that forms the scientific foundation for the review of the primary 

(health-based) and secondary (welfare-based) national ambient air quality standard 

(NAAQS) for ozone (O3) and related photochemical oxidants. The current primary O3

standard includes an 8-hour average standard set in 2008 at 75 parts per billion (ppb). The 

secondary standard for O3 is equal to the primary standard. The current primary NAAQS 

protects against respiratory health effects incurred after short-term exposure to O3, while 

the secondary NAAQS protects against damage to vegetation and ecosystems.

1.2 Scope

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

and drawing conclusions regarding air pollution-related health and welfare effects. This 

ISA is focused on health and welfare effects resulting from current ambient 

concentrations of O3. This review builds upon the findings of previous assessments, and 

evaluates the relevant results pertaining to the atmospheric science of O3; short- and 

long-term exposure to ambient O3; health effects due to ambient O3 exposure as 

characterized in epidemiologic, controlled human exposure, and toxicological studies; 

and ecological or welfare effects; as well as O3 exposure-response relationships, mode(s) 

of action (MOA), and populations at increased risk for O3-related health effects. In this 

ISA, the conclusions and key findings from previous reviews provide the foundation for 

the consideration of evidence from recent studies. Conclusions are drawn based on the 

synthesis of evidence from recent studies and building upon the extensive evidence 

presented in previous reviews. 

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

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

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

Causality determinations are based on the evaluation and synthesis of evidence from 

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

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

relevant literature, building upon evidence available during the previous NAAQS 

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

exposures and health or welfare effects. EPA also evaluates the quantitative evidence and 
draws scientific conclusions, to the extent possible, regarding the concentration-response 

relationships and the loads to ecosystems, exposure doses or concentrations, duration and 

pattern of exposures at which effects are observed. This ISA uses a five-level hierarchy 

that classifies the weight of evidence for causation, not just association. This weight of 

evidence evaluation is based on various lines of evidence from across the health and 

environmental effects disciplines. These separate judgments are integrated into a 

qualitative statement about the overall weight of the evidence and causality. The causal 

determinations are:

 Causal relationship 

 Likely to be a causal relationship 

 Suggestive of a causal relationship 

 Inadequate to infer a causal relationship 

 Not likely to be a causal relationship 

1.3 Atmospheric Chemistry and Ambient Concentrations

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

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

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

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

present not only in polluted urban air, but throughout the globe.

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

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

atmosphere by photochemical reactions involving sunlight and precursor pollutants 

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

attributed to natural sources is formed through the same photochemical reactions 

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

biomass burning, lightning, and geogenic sources. A schematic overview of the major 

photochemical cycles influencing O3 in the troposphere and the stratosphere is shown in 

the figure to the right.
Figure 1-1 Schematic overview of photochemical processes influencing 

stratospheric and tropospheric ozone.

Ozone in rural areas is produced from emissions of O3 precursors emitted directly within 

the rural areas and from emissions in urban areas that are processed during transport.

Because O3 is produced downwind of urban source areas and O3 tends to persist longer 

in rural than in urban areas as a result of lower chemical scavenging, the result is 

substantial cumulative exposures for humans and vegetation in rural areas, that are often 

higher than cumulative exposures in urban areas.

On a smaller scale, O3 can be influenced by local meteorological conditions, circulation 

patterns, emissions, and topographic barriers, resulting in heterogeneous concentrations 

across an individual urban area. On a larger scale, O3 persists in the atmosphere long 

enough that it can be transported from continent to continent and around the globe. The 

degree of influence from intercontinental transport varies greatly by location and time.

Background concentrations of O3 have been given various definitions in the literature 

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

concentrations in a way that distinguishes between concentrations that result from 
precursor emissions that are relatively less directly controllable from those that are 

relatively more directly controllable through U.S. policies. For this document, we have 

focused on the sum of those background concentrations from natural sources everywhere 

in the world and from anthropogenic sources outside the U.S., Canada and Mexico, i.e., 

North American background. Since North American background is a construct that 

cannot be measured, the range of North American background O3 concentrations is 

estimated using chemistry transport models. Model-predicted annual average North 

American background estimates are typically less than 50 ppb across the country with 

highest concentrations in the Intermountain West during the spring and the Southwest 

during the summer.

1.4 Human Exposure

Ozone is ubiquitous throughout the environment, originating from both natural and 

anthropogenic sources, although few indoor sources exist. As such, people are routinely 

exposed to O3 as they participate in normal day-to-day activities. A number of factors 

affect the pattern of personal O3 exposure. These include: the variation in O3

concentrations at various spatial and temporal scales; individual’s activity patterns, 

particularly time spent outdoors, which may involve changes in personal behavior to 

avoid known high exposure to O3; and infiltration of ambient O3 into indoor 

microenvironments, which is driven by air exchange rate.

Several approaches have been used to measure or quantify exposure to ambient O3, 

giving an indication of the impact of some of the factors that affect the pattern of human 

exposure to O3. These approaches include characterizing the correlation and ratio 

between personal exposure and ambient O3 concentrations, determining the ratio between 

indoor and outdoor concentrations, and using models to estimate exposure to O3 based on 

ambient concentrations. The factors affecting the pattern of personal exposure, as well as 

the types of approaches used for quantification of exposure, may have implications for 

epidemiologic studies.

1.5 Dosimetry and Modes of Action

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

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

as well as how quickly and deeply a person is breathing. Another factor involves the 

reaction of O3 with compounds present in the lung lining fluid to produce secondary 
oxidation products. On a breath-by-breath basis, humans at rest absorb between 80 and 

95% of inhaled O3. The site of the greatest O3 dose to the lung tissue is the junction of 

the conducting airway and the gas exchange region, in the deeper portion of the 

respiratory tract. Additionally, the primary site of O3 uptake moves deeper into the 

respiratory tract during exercise when breathing becomes faster and the breathing route 

begins to move from the nose only to oronasal breathing (i.e., through the nose and 

mouth).

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

the respiratory tract that lead to O3-induced health effects. These include formation of 

secondary oxidation products in the lung, activation of neural reflexes, initiation of 

inflammation, alterations of epithelial barrier function, sensitization of bronchial smooth 

muscle, modification of innate and adaptive immunity, and airway remodeling. Another 

key event, systemic inflammation and vascular oxidative/nitrosative stress, may be 

critical to the extrapulmonary effects of O3.

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

and health outcome

Health Outcome Conclusions from Previous Review Conclusions from 

2011 2nd 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

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

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
1.6 Integration of Ozone Health Effects

This ISA evaluates and integrates the evidence from short-term (i.e., hours, days, weeks) 

or long-term (i.e., months to years) exposure studies across scientific disciplines (i.e., 

controlled human exposure studies, toxicology, and epidemiology) in interpreting the 

health effects evidence that spans all lifestages, and varies in severity from minor 

subclinical effects to death. The results from the health studies evaluated in combination 

with the evidence from atmospheric chemistry and exposure assessment studies 

contribute to the causal determinations made for the health outcomes discussed in this 

ISA. The conclusions from the previous NAAQS review and the causality determinations 

from this review are summarized in the table below. Additional details are provided here 

for respiratory health effects and mortality, for which there is the strongest evidence of an 

effect from O3, and for additional health effects for which there is emerging evidence of 

an association with O3; details for all health effects are provided in the ISA.

1.6.1 Respiratory Effects

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

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

several decades supports the causal association between exposure to O3 and a continuum

of respiratory effects (See figure below). The majority of this evidence is derived from 

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

toxicological studies and recent epidemiologic evidence demonstrate that long-term 

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

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

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

association was substantiated in this ISA by the coherence of effects observed across 

controlled human exposure, epidemiologic, and toxicological studies indicating 

associations of short-term O3 exposures with a range of respiratory health endpoints from 

respiratory tract inflammation to respiratory emergency department (ED) visits and 

hospital admissions (HA). Across disciplines, short-term O3 exposures induced or were 

associated with statistically significant declines in lung function. An equally strong body 

of evidence from controlled human exposure and toxicological studies demonstrated O3-

induced inflammatory responses, increased epithelial permeability, and airway 

hyperresponsiveness. Toxicological studies provided additional evidence for O3-induced 

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

provided support for epidemiologic evidence, in which short-term O3 exposure was 
consistently associated with increases in respiratory symptoms and asthma medication 

use in asthmatic children, respiratory-related hospital admissions, and asthma-related ED 

visits. Although O3 was consistently associated with nonaccidental and cardiopulmonary 

mortality, the contribution of respiratory causes to these findings was uncertain. The

combined evidence across disciplines supports a causal relationship between shortterm O3 exposure and respiratory effects. 

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. 

Recent evidence for a relationship between long-term O3 exposure and respiratory 

morbidity comes from a single cohort demonstrating associations between long-term 

measures of O3 exposure and new-onset asthma in children and increased respiratory 
symptom effects in asthmatics. While the evidence may be limited, this multi-community 

cohort demonstrates that asthma risk is affected by interactions between genetic 

variability, environmental O3 exposure, and behavior. Other recent studies provide 

coherent evidence for long-term O3 exposure and respiratory morbidity effects such as 

first asthma hospitalization and respiratory symptoms in asthmatics. Generally, the 

epidemiologic and toxicological evidence provides a compelling case for a relationship 

between long-term exposure to ambient O3 and respiratory morbidity. The evidence for 

effects of short-term exposure to O3 on respiratory endpoints provides coherence and 

biological plausibility for the effects of long-term exposure to O3. Building upon 

evidence from studies of short-term exposure, the more recent epidemiologic evidence, 

combined with toxicological studies in rodents and non-human primates, provides

biologically plausible evidence that there is likely to be a causal relationship between 

long-term exposure to O3 and respiratory health effects.

1.6.2 Mortality Effects

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

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

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

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

multicity studies that have examined the association between short-term O3 exposure and 

mortality found evidence which supports the conclusions of the last review. These recent 

studies reported consistent positive associations between short-term O3 exposure and

total (nonaccidental) mortality, with associations being stronger during the warm season.

They also added support for associations between O3 exposure and cardiovascular 

mortality being similar to or stronger than those between O3 exposure and respiratory

mortality. Additionally, these new studies examined previously identified areas of 

uncertainty in the O3-mortality relationship, and provide evidence that continues to 

support an association between short-term O3 exposure and mortality. The body of 

evidence indicates that there is likely to be a causal relationship between short-term 

exposures to O3 and mortality.

1.6.3 Emerging Evidence

In the last review, completed in 2006, there were a number of health effects for which an 

insufficient amount of evidence existed to adequately characterize the relationships with 

exposure to O3. However, recent evidence indicates that O3 may impart health effects 
through exposure durations and biological mechanisms not previously considered. This 

includes: 

 Toxicological studies provide evidence for cardiovascular morbidity, while 

epidemiologic studies provide evidence for cardiovascular mortality, and 

together, this evidence is suggestive of a causal relationship for both 

relevant short- and long-term exposures to O3 and cardiovascular effects. 

 Recent toxicological studies add to earlier evidence that short- and long-term 

exposures to O3 can produce a range of effects on the central nervous system 

and behavior. The single epidemiologic study conducted showed that longterm exposure to O3 affects memory in humans as well. Together the evidence 

from studies of short- and long-term exposure to O3 is suggestive of a causal 

relationship between O3 exposure and adverse central nervous system 

effects.

 There is limited though positive toxicological evidence for O3-induced 

developmental effects. Limited epidemiologic evidence exists for an 

association with O3 concentration and decreased sperm concentration and 

associations with reduced birth weight and restricted fetal growth. Overall, the 

evidence is suggestive of a causal relationship between long-term 

exposures to O3 and reproductive and developmental effects.

 Several recent studies provide evidence of an association between long-term 

exposure to O3 and mortality, especially respiratory mortality. Collectively, 

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

exposures and mortality.

1.6.4 Populations at Increased Risk

The examination of populations potentially at increased risk for O3 exposure allows for 

the NAAQS to provide an adequate margin of safety for both the general population and 

for sensitive populations. Some studies attempt to identify populations that are at 

increased risk for O3-related health effects; these studies do so by examining groups 

within the study population, such as those with an underlying health condition or genetic 

polymorphism; categories of age, race, or sex; or by developing animal models that 

mimic the conditions associated with an adverse health effect. Such studies have 

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

is at increased risk for O3-related health effects. The populations identified that are most 

at risk for O3-related health effects are individuals with influenza/infection, individuals 

with asthma, and older age groups. Other potential factors, including preexisting 
conditions such as chronic obstructive pulmonary disease and cardiovascular disease, 

young age, sex, and variations in multiple genes (such as GSTM1, GSTP1, HMOX-1, 

NQO1, and TNF-α), appear related to susceptibility, but further evidence is needed.

1.6.5 Ozone Concentration-Response Relationship

An important consideration in characterizing the association of O3 with morbidity and 

mortality is the shape of the concentration-response relationship across the O3 

concentration range. In this ISA, studies have been identified that attempt to characterize 

the shape of the O3 concentration-response curve along with possible O3 “thresholds”

(i.e., O3 levels which must be exceeded in order to elicit a physiological response). These 

studies have indicated a generally linear concentration-response function with no 

indication of a threshold for O3 concentrations greater than 30 or 40 ppb, thus if a 

threshold exists, it is likely at the lower end of the range of ambient O3 concentrations.

1.7 Integration of Effects on Vegetation and Ecosystems

The ISA presents the most policy-relevant information pertaining to the review of the 

NAAQS for the effects of O3 on vegetation and ecosystems. It integrates key findings 

about plant physiology, biochemistry, whole plant biology, ecosystems and exposureresponse relationships. The welfare effects of O3 can be observed across spatial scales, 

starting at the cellular and subcellular level, then the whole plant and finally, ecosystemlevel processes. Ozone effects at small spatial scales, such as the leaf of an individual 

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

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

and can result in changes in ecosystems, such as productivity, C storage, water cycling, 

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

NAAQS review and the causality determinations from this review are summarized in the 

table below. Further discussion of these conclusions is provided below for visible foliar 

injury, growth, productivity, and carbon storage, reduced yield and quality of agricultural 

crops, water cycling, below-ground processing, community composition, and O3

exposure-response relationships; discussion for all relevant welfare effects is provided in 

the ISA.
Table 1-2 Summary of ozone causal determination for welfare effects

Vegetation and 

Ecosystem Effects Conclusions from Previous Review

Conclusions from 

2011 2nd 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

1.7.1 Visible Foliar Injury

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

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

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

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

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

prevalent injury. Additional sensiptive species showing visible foliar injury continue to 

be identified from field surveys and verified in controlled exposure studies. Overall, 

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

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

sensitive vegetation across the U.S.
1.7.2 Growth, Productivity, Carbon Storage and Agriculture

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

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

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

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

ecosystem C sequestration were reviewed for natural ecosystems, and crop productivity 

and crop quality were reviewed for agricultural ecosystems. There is strong and 

consistent evidence that ambient concentrations of O3 decrease plant photosynthesis and 

growth in numerous plant species across the U.S. Studies conducted during the past four 

decades have also demonstrated unequivocally that O3 alters biomass allocation and plant 

reproduction. Studies at the leaf and plant scales showed that O3 reduced photosynthesis 

and plant growth, providing coherence and biological plausibility for the reported 

decreases in ecosystem productivity. In addition to primary productivity, other indicators 

such as net ecosystem CO2 exchange and C sequestration were often assessed by 

modeling studies. Model simulations consistently found that O3 exposure caused 

negative impacts on those indicators, but the severity of these impacts was influenced by 

multiple interactions of biological and environmental factors. Although O3 generally 

causes negative effects on ecosystem productivity, the magnitude of the response varies 

among plant communities. Overall, evidence is sufficient to conclude that there is a 

causal relationship between O3 exposure and reduced plant growth and 

productivity, and a likely causal relationship between O3 exposure and reduced 

carbon sequestration in terrestrial ecosystems.

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

and current O3 concentrations across the U.S. are high enough to cause yield loss for a 

variety of agricultural crops including, but not limited to, soybean, wheat, potato, 

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

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

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

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

Evidence is sufficient to conclude that there is a causal relationship between O3

exposure and reduced yield and quality of agricultural crops.

1.7.3 Water Cycling

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

including damage to stomatal functioning and loss of leaf area. Possible mechanisms for 
O3 exposure effects on stomatal functioning include the build-up of CO2 in the 

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

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

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

hydrological cycling. Although the direction of the response differed among studies, the 

evidence is sufficient to conclude that there is likely to be a causal relationship 

between O3 exposure and the alteration of ecosystem water cycling.

1.7.4 Below Ground Processes

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

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

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

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

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

cycling. The evidence is sufficient to conclude that there is a causal relationship 

between O3 exposure and the alteration of below-ground biogeochemical cycles.

1.7.5 Community Composition

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

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

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

biological plausibility for the alteration of community composition. For example, there is 

a tendency for O3 exposure to shift the biomass of grass-legume mixtures in favor of 

grass species. Ozone exposure not only altered community composition of plant species, 

but also microorganisms: research since the last review has shown that O3 can also alter 

community composition and diversity of soil microbial communities. Shifts in 

community composition of bacteria and fungi have been observed in both natural and 

agricultural ecosystems, although no general patterns could be identified. The evidence 

is sufficient to conclude that there is likely a causal relationship between O3

exposure and the alteration of community composition.

1.7.6 Ozone Exposure-Response Relationships

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

of many crop species, and for the biomass accumulation of tree species. They were based 
on large-scale experiments designed to obtain clear exposure-response data, and are 

updated in this ISA by using the W126 metric to quantify exposure. In recent years, 

extensive exposure-response data obtained in more naturalistic settings have become 

available for yield of soybean and growth of aspen. This ISA validates the exposureresponse median functions based on previous data by comparing their predictions with 

the newer observations. The functions supply very accurate predictions of effects in 

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

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

functions presented in the ISA. It is important to note that although these median 

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

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

within species and some genotypes within species are much more severely affected by 

exposure to O3.

1.8 The Role of Tropospheric Ozone in Climate Change and UV-B 

Effects

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

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

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

overall radiation budget. Therefore, perturbations in tropospheric O3 concentrations can 

have direct effects on climate and indirect effects on health, ecology and welfare by

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

Ozone is an important greenhouse gas, and increases in its abundance in the troposphere 

may contribute to climate change. Models calculate that the global burden of tropospheric 

O3 has doubled since the preindustrial era, while observations indicate that in some 

regions O3 may have increased by factors as great as 4 or 5. These increases are tied to 

the rise in emissions of O3 precursors from human activity, mainly fossil fuel 

consumption and agricultural processes.
Figure 1-3 Schematic illustrating the effects of tropospheric O3 on climate.

Figure 1-3 shows the main steps involved in the influence of tropospheric O3 on climate. 

Emissions of O3 precursors lead to production of tropospheric O3. A change in the 

abundance of tropospheric O3 perturbs the radiative balance of the atmosphere, an effect 

quantified by the radiative forcing (RF) metric. The earth-atmosphere-ocean system 

responds to the radiative forcing with a climate response, typically expressed as a change 

in surface temperature. Finally, the climate response causes downstream climate-related 

health and ecosystem impacts. Feedbacks from both the climate response and 

downstream impacts can, in turn, affect the abundance of tropospheric O3 and O3

precursors through multiple feedback mechanisms as indicated in the figure.

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

have damaging effects on living organisms and materials. Atmospheric O3 plays a crucial 

role in reducing exposure to UV radiation at the Earth’s surface. Ozone in the 

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

provides supplemental shielding of UV radiation in the mid-wavelength range (UV-B), 

thereby influencing human and ecosystem health.
The conclusions from the previous NAAQS review and the causality determinations from 

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

with details provided in the ISA.

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

UV-B effects

Effects Conclusions from Previous Review Conclusions from 

2011 2nd 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 discernable influence on climate, leading to surface 

temperature and hydrological cycle changes.

Likely to be a Causal 

Relationship

UV-B Related Health and 

Welfare Effects 

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

1.9 Conclusion

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

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

evidence spanning several decades in support of a causal association between exposure to 

O3 and a continuum of respiratory effects. The majority of this evidence is derived from 

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

toxicological studies and recent epidemiologic evidence demonstrate that long-term 

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

Additionally, consistent positive associations between short-term O3 exposure and total 

(nonaccidental) mortality have helped to resolve previously identified areas of 

uncertainty in the O3-mortality relationship, indicating that there is likely to be a causal 

relationship between short-term exposures to O3 and all-cause mortality. Recent 

evidence is suggestive of a causal relationship between long-term O3 exposures and 

mortality. The evidence for these health effects indicates that the relationship between 

concentration and response is linear within concentrations present in the U.S., with no 

indication of a threshold of O3 concentrations under which no effect would be observed. 

The populations identified as being most at risk for O3-related health effects are 

individuals with influenza/infection, individuals with asthma, and older age groups.
There has been over 40 years of research on the effects of O3 exposure on vegetation and 

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

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

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

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

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

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

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