## 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 (O 3 ) and related photochemical oxidants. The current primary O 3 standard includes an 8

- hour average standard set in 2008 at 75 parts per billion (ppb). The secondary standard for O 3 is equal to the pr imary standard. The current primary NAAQS protects against respiratory health effects incurred after short

- term exposure to O 3 , 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 O 3 . This review builds upo n the findings of previous assessments, and evaluates the relevant results pertaining to the atmospheric science of O 3 ; short

- and long

- term exposure to ambient O 3 ; health effects due to ambient O 3 exposure as characterized in epidemiologic, controlled hum an exposure, and toxicological studies; and ecological or welfare effects; as well as O 3 exposure

- response relationships, mode(s) of action (MOA), and populations at increased risk for O 3 - related health effects. In this ISA, the conclusions and key finding s 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.
C ausality 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
rele vant 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 anddraws 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. T his ISA uses a five

- level hi erarchy 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 integrat ed 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, O 3 acts as a powerful oxidant and can harm living organisms and materials. Tropospheric O 3 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 volati le 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, ligh tning, and geogenic sources. A schematic overview of the major photochemical cycles influencing O 3 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 O 3 precursors emitted directly within the rural areas and from emissions in urban areas that are processed during transport.
Because O 3 is produced downwind of urban s ource areas and O 3 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 ur ban areas.

On a smaller scale, O 3 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, O 3 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 O 3 have been given various def initions in the literature over time. In the context of a review of the NAAQS, it is useful to define background O 3 concentrations in a way that distinguishes between concentrations that result fromprecursor emissions that are relatively less directly con trollable 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 O 3 concentrations is estimated using chemistry transport models. Model

- predicted an nual 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 th e environment, originating from both natural and anthropogenic sources, although few indoor sources exist. As such, people are routinely exposed to O 3 as they participate in normal day

- to

- day activities. A number of factors affect the pattern of personal O 3 exposure. These include: the variation in O 3 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 O 3 ; and i nfiltration of ambient O 3 into indoor microenvironments, which is driven by air exchange rate.

Several approaches have been used to measure or quantify exposure to ambient O 3 , giving an indication of the impact of some of the factors that affect the patte rn of human exposure to O 3 . These approaches include characterizing the correlation and ratio between personal exposure and ambient O 3 concentrations, determining the ratio between indoor and outdoor concentrations, and using models to estimate exposure to O 3 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 O 3 is inhaled, the amount of O 3 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 th e reaction of O 3 with compounds present in the lung lining fluid to produce secondaryoxidation products. On a breath

- by

- breath basis, humans at rest absorb between 80 and 95% of inhaled O 3 . The site of the greatest O 3 dose to the lung tissue is the juncti on of the conducting airway and the gas exchange region, in the deeper portion of the respiratory tract. Additionally, the primary site of O 3 uptake moves deeper into the respiratory tract during exercise when breathing becomes faster and the breathing rou te begins to move from the nose only to oronasal breathing (i.e., through the nose and mouth).

Once O 3 has been inhaled, there are several key events in the toxicity pathway of O 3 in the respiratory tract that lead to O 3 - induced health effects. These incl ude 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 ai rway remodeling. Another key event, systemic inflammation and vascular oxidative/nitrosative stress, may be critical to the extrapulmonary effects of O 3 .



### 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 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 Causal 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

M ortality The evidence is highly suggestive that O 3 directly 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 a ir 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 regar ding 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 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

## 1.6 Integration of Ozone Health Effects

This ISA evaluates and integrates the evide nce 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 span s 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 determinati ons 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 O 3 , and for additional health effects for which there is emerging evidence of
an association with O 3 ; 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 O 3 is provided by studies of respiratory effects. Collectively, a very large amount of evidence spanning several decades supports the causal association between exposure to O 3 and a continuu m 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 O 3 , 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 O 3 and respiratory health effects. This ca usal 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 O 3 exposures with a range of respiratory health endpoints f rom respiratory tract inflammation to respiratory emergency department (ED) visits and hospital admissions (HA) . Across disciplines, short

- term O 3 exposures induced or were associated with statistically significant declines in lung function. An equally str ong body of evidence from controlled human exposure and toxicological studies demonstrated O 3 - induced inflammatory responses, increased epithelial permeability, and airway hyperresponsiveness. Toxicological studies provided additional evidence for O 3 - induc ed impairment of host defenses. Combined, these findings from experimental studies provided support for epidemiologic evidence, in which short

- term O 3 exposure wasconsistently associated with increases in respiratory symptoms and asthma medication
use in asthmatic children, respiratory

- related hospital admissions, and asthma

- related ED
visits. Although O 3 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 short

term O 3 exposure and respiratory effects

.



### Figure 1

- 2 T he 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 O 3 exposure and respiratory morbidity comes from a single cohort demonstrating associations between long

- term

measures o f O 3 exposure and new

- onset asthma in children and increased respiratorysymptom effects in asthmatics. While the evidence may be limited, this multi

- community cohort demonstrates that asthma risk is affected by interactions between genetic variability, en vironmental O 3 exposure, and behavior. Other recent studies provide coherent evidence for long

- term O 3 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 O 3 and respiratory morbidity. The evidence for
effects of short

- term exposure to O 3 on respiratory endpoints provides coherence and biological plausi bility for the effects of long

- term exposure to O 3 . 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 O 3 and respiratory health effects

.



### 1.6.2 Mortality Effects

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

- term exposure to O 3 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
multi city studies that have examined the association between short

- term O 3 exposure and mortality found evidence which supports the conclusions of the last review. These recent studies reported consistent positive associations between short

- term O 3 exposure and total (nonaccidental) mortality, with associations being stronger during the warm season. They also added support for associations between O 3 exposure and cardiovascular mortality being similar to or stronger than those between O 3 exposure and respiratory mortality. Additionally, these new studies examined previously identified areas of uncertainty in the O 3 - mortality relationship, and provide evidence that continues to support an association between short

- term O 3 exposure and mortality. The body of
eviden ce indicates that there is likely to be a causal relationship between short

- term exposures to O 3 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 exis ted to adequately characterize the relationships with exposure to O 3 . However, recent evidence indicates that O 3 may impart health effectsthrough 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 O 3 and cardiov ascular effects

.

 Recent toxicological studies add to earlier evidence that short

- and long

- term exposures to O 3 can produce a range of effects on the central nervous system
and behavior. The single epidemiologic study conducted showed that long

term expos ure to O 3 affects memory in humans as well. Together the evidence
from studies of short

- and long

- term exposure to O 3 is suggestive of a causal relationship between O 3 exposure and adverse central nervous system
effects

.

 There is limited though positive toxicological evidence for O 3 - induced developmental effects. Limited epidemiologic evidence exists for an
association with O 3 concentration and decreased sperm concentration and associations with reduced birth weight and restricted fetal growth. Overall, t he
evidence is suggestive of a causal relationship between long

- term exposures to O 3 and reproductive and developmental effects

.

 Several recent studies provide evidence of an association between long

- term exposure to O 3 and mortality, especially respirator y mortality. Collectively,
the evidence is suggestive of a causal relationship between long

- term O 3 exposures and mortality

.



### 1.6.4 Populations at Increased Risk

The examination of populations potentially at increased risk for O 3 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 O 3 - related health effects; these studies do so by examining groups
within the st udy 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 mu ltitude of factors that could potentially contribute to whether an individual
is at increased risk for O 3 - related health effects. The populations identified that are most
at risk for O 3 - related health effects are individuals with influenza/infection, indiv iduals with asthma, and older age groups. Other potential factors, including preexistingconditions such as chronic obstructive pulmonary disease and cardiovascular disease, young age, sex, and variations in multiple genes (such as GSTM1, GSTP1, HMOX

- 1, NQ O1, 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 O 3 with morbidity and mortality is the shape of the concentration

- re sponse relationship across the O 3 concentration range. In this ISA, studies have been identified that attempt to characterize the shape of the O 3 concentration

- response curve along with possible O 3 “ thresholds ” (i.e., O 3 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 O 3 concentrations greater than 30 or 40 ppb, thus if a threshold exists, it is likely at the lo wer end of the range of ambient O 3 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 O 3 on vegetation and ecosystems. It integr ates key findings about plant physiology, biochemistry, whole plant biology, ecosystems and exposure

response relat i onships. The welfare effects of O 3 can be observed across spatial scales, starting at the cellular and subcellular level, then the whole pla nt and finally, ecosystem

level 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 r eproduction 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 O 3 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 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

Reduced 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, including 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) Seque stration 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 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 rat es 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 O 3 exposure have been demonstrated. Li kely to be a Causal Relationship



### 1.7.1 Visible Foliar Injury

Visible foliar injury resulting from exposure to O 3 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 O 3 , as experimental evidence has clearly established a consistent association, with greater exposure often resulting in greater and more prevalent injury. Additional sensi p ti ve 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 O 3 exposure and the occurrenc e of O 3 - induced visible foliar injury on sensitive vegetation across the U.S.

### 1.7.2 Growth, Productivity, Carbon Storage and Agriculture

Ambient O 3 concentrations have long been known to cause decreases in photosynthetic rates and plant growth. The O 3 - induced ef fects at the plant scale may translate to the ecosystem scale, and cause changes in productivity and C storage. The effects of O 3 exposure on photosynthesis, growth, biomass allocation, ecosystem production and ecosystem C sequestration were reviewed for n atural ecosystems, and crop productivity and crop quality were reviewed for agricultural ecosystems. There is strong and
consistent evidence that ambient concentrations of O 3 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 O 3 alters biomass allocation and plant reproduction. Studies at the leaf and plant scales showed that O 3 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 CO 2 exchange and C sequestration were often assessed by modeling studies. Model simulations consi stently found that O 3 exposure caused negative impacts on those indicators, but the severity of these impacts was influenced by multiple interactions of biological and environmental factors. Although O 3 generally causes negative effects on ecosystem produc tivity, the magnitude of the response varies among plant communities. Overall, evidence is sufficient to conclude that there is a causal relationship between O 3 exposure and reduced plant growth and productivity, and a likely causal relationship between O 3 exposure and reduced carbon sequestration in terrestrial ecosystems.

The detrimental effect of O 3 on crop production has been recognized since the 1960 ’ s, and current O 3 concentrations across the U.S. are high enough to cause yield loss for a variety of a gricultural crops including, but not limited to, soybean, wheat, potato, watermelon, beans, turnip, onion, lettuce, and tomato. Continued increases in O 3 concentration may further decrease yield in these sensitive crops while also initiating yield losses i n less sensitive crops. Research has linked increasing O 3 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 O 3 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 forO 3 exposure effects on stomatal functioning include the build

- up of CO 2 in the substomatal cavity, impacts on signal transduction pathways and direct O 3 impact on guard cells. Regardless of the mechanism, O 3 exposure has been shown to alter stomatal performa nce, 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 betwee n O 3 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 O 3 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 O 3 exposure and the alteration of below

- ground biogeochemical cycles.



### 1.7.5 Community Composition

Ozone exposure changes competitive interactions and leads to loss of O 3 - sensitive species or genotypes. Studies at the plant level found that the severity of O 3 damage to growth, reproduction and foliar injury varied among species, which provided the biological plausibility for the alteration of community composition. For exa mple, there is

a tendency for O 3 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 tha t O 3 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. T he evidence is sufficient to conclude that there is likely a causal relationship between O 3 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 basedon 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 fo r yield of soybean and growth of aspen. This ISA validates the exposure

response median functions based on previous data by comparing their predictions with the newer observations. The functions supply very accurate predictions of effects in
naturalistic s ettings. 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 pro vide 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 O 3 .



## 1.8 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 incoming solar radiation and outgoing infrared radiation. Tropospheric O 3 makes up only a small p ortion of the total column of O 3 , but it has important incremental effects on the overall radiation budget. Therefore, perturbations in tropospheric O 3 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
O 3 has d oubled since the preindustrial era, while observations indicate that in some regions O 3 may have increased by factors as great as 4 or 5. These increases are tied to
the rise in emissions of O 3 precursors from human activity, mainly fossil fuel consumption and agricultural processes.

### Figure 1

- 3 Schematic illustrating the effects of tropospheric O 3 

### on climate

.

Figure 1

- 3 shows the main steps involved in the influence of tropospheric O 3 on climate.
Emissions of O 3 precursors lead to production of tropospheric O 3 . A change in the
abundance of tropospheric O 3 perturbs the radiative balance of the atmosphere, an effect quantified by the radiative forcing (RF) metric. The earth

- atmosphere

- ocean system responds to the r adiative 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 O 3 and O 3 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 livi ng organisms and materials. Atmospheric O 3 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 O 3 in the troposphere provides supplemental shield ing 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 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 could have a discernable influence on climate, leading to surface temperature and h ydrological 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 O 3 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 exposur e to O 3 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
O 3 and a continuum of respiratory effects. The majority of this ev idence is derived from studies investigating short

- term O 3 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 r espiratory system. Additionally , consistent positive associations between short

- term O 3 exposure and total (nonaccidental) mortality have helped to resolve previously identified areas of uncertainty in the O 3 - mortality relationship, indicating that there i s likely to be a causal relationship between short

- term exposures to O 3 and all

- cause mortality. Recent evidence is suggestive of a causal relationship between long

- term O 3 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 O 3 concentrations under which no effect would be observed. The populations identified as being most at risk for O 3 - rel ated 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 O 3 exposure on vegetation and ecosystems. The best evidence for effects is from controll ed exposure studies. These studies have clearly shown that exposure to O 3 is causally linked to visible foliar injury, decreased photosynthesis, changes in reproduction, and decreased growth. Recently, studies at larger spatial scales support the results f rom controlled studies and indicate that
ambient O 3 exposures can affect ecosystem productivity, crop yield, water cycling, and ecosystem community composition. And on a global scale, tropospheric O 3 is the third most important greenhouse gas, playing an i mportant role in climate change.