Ozone Excerpts 2

Excerpts Taken From

Integrated Science Assessment for Ozone and
Related Photochemical Oxidants

U.S. Environmental Protection Agency
EPA/600/R-10/076B
September 2011

Excerpted by Michael H. Klein

Chapter 2: Integrated Summary

Page 2-5 line 21 (ARP 97)

This ISA uses a five-level hierarchy that classifies the weight of evidence for causation:

• 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

Page 2-8 line 3 (ARP 100) — O₃ formation

In urban areas, NOX, VOCs and CO are all important for O₃ formation. In nonurban vegetated areas, biogenic VOCs emitted from vegetation tend to be the most important precursor to O₃ formation. In the remote troposphere, methane – structurally the simplest VOC – and CO are the main carbon-containing precursors to O₃ formation. Throughout the troposphere, O₃ is subsequently lost through a number of gas phase reactions and deposition to surfaces…

Page 2-8 line 25 (ARP 100) – Background Concentrations

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. North American (NA) background O₃ can include contributions that result from emissions from natural sources (e.g., stratospheric intrusion, biogenic methane and more short-lived VOC emissions), emissions of pollutants that contribute to global concentrations of O₃ (e.g., anthropogenic methane) from countries outside North America. In previous NAAQS reviews, a specific definition of background concentrations was used and referred to as policy relevant background (PRB). In those previous reviews, PRB concentrations were defined by EPA as those concentrations that would occur in the U.S. in the absence of anthropogenic emissions in continental North America (CNA), defined here as the U.S., Canada, and Mexico. 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 CNA. North American background concentrations so defined facilitate separation of pollution that can be controlled directly by U.S. regulations or through international agreements with neighboring countries from that which would require more comprehensive international agreements, such as are being discussed as part of the United Nations sponsored Convention on Long Range Transboundary Air Pollution Task Force on Hemispheric Air Pollution. There is no chemical difference between background O₃ and O₃ attributable to CNA anthropogenic sources, and background concentrations can contribute to the risk of health effects. However, to inform policy considerations regarding the current or potential alternative standards, it is useful to understand how total O₃ concentrations can be attributed to different source.

Since North American background as defined above is a construct that cannot be directly measured, the range of background O₃ concentrations are estimated using chemistry transport models (CTMs). The 2006 O₃ AQCD provided regional estimates of PRB O₃ concentrations based on a coarse resolution (2°×2.5°, or ~200 km×200 km) GEOS-Chem model. For the current assessment, updated results from a finer resolution (0.5°×0.667°, 20 or ~50 km×50 km) GEOS-Chem model were used. Base-case model performance evaluations comparing 2006 predicted to observed mean O₃ concentrations from March to August showed general agreement to within ~5 ppb at most (26 out of 28) sites investigated. Exceptions included over-prediction of mean O₃ during the summer at a site on the Atlantic coast of Florida and under-prediction of mean O₃ year-round at a site in Yosemite NP. The finer resolution GEOS-Chem model agrees more closely with observations in the intermountain West than earlier versions.

The GEOS-Chem model-predicted North American O₃ seasonal mean concentrations for spring and summer, 2006 are shown in Figure 2-2. As can be seen, North American background concentrations are generally higher in spring than in summer across the U.S., with exception in the Southwest where predictions peak in the summer. Highest estimates are found in the Intermountain West during the spring (less than 47 ppb) and in the 32 Southwest during the summer (less than 49 ppb). Lowest estimates occur over the East in the spring (greater than 23 ppb) and over the Northeast in the summer (greater than 15 ppb).

Page 2-10 line 1 (ARP 102) – Monitoring

The federal reference method (FRM) for O₃ measurement is based on the detection of chemiluminescence resulting from the reaction of O₃ with ethylene gas. However, almost all of the state and local air monitoring stations (SLAMS) that reported data to the EPA’s Air Quality System (AQS) database from 2005 to 2009 used the federal equivalence method (FEM) UV absorption photometer. More than 96% of O₃ monitors met precision and bias goals during this period.

In 2010, there were 1250 SLAMS O₃ monitors reporting data to AQS. Ozone is required to be monitored at SLAMS during the local “ozone season” which varies by state. In addition, National Core (NCore) is a new multipollutant monitoring network implemented to meet multiple monitoring objectives and each state is required to operate at least one NCore site. The NCore network consists of 60 urban and 20 rural sites nationwide (See Figure 3-16). The densest concentrations of O₃ sites are located in California and the eastern half of the U.S.

Page 2-11 line 7 (ARP 103) – Ambient Concentrations

Ozone is the only photochemical oxidant other than NO2 that is routinely monitored and for which a comprehensive database exists. Other photochemical oxidants are typically only measured during special field studies. Therefore, the concentration analyses in Chapter 3 are limited to widely available O₃ data obtained directly from AQS for the period from 2007 to 2009. The median 24-h average, 8-h daily maximum, and 1-h daily maximum O₃ concentrations across all U.S. sites reporting data to AQS between 2007 and 2009 were 29, 40, and 44 ppb, respectively.

Page 2-12 line 6 (ARP 104)

According to the 2010 National Air Quality Status and Trends report (U.S. EPA, 2010e), O₃ concentrations have declined over the last decade; with the majority of this decline occurring before 2004. A noticeable decrease in O₃ between 2003 and 2004 coincides with NOX emissions reductions resulting from implementation of the NOX SIP Call rule, which began in 2003 and was fully implemented in 2004. This rule was designed to reduce NOX emissions from power plants and other large combustion sources in the eastern U.S. As noted in the 2006 O₃ AQCD, trends in national parks and rural areas are similar to nearby urban areas, reflecting the regional nature of O₃ pollution.

Page 2-18 (ARP 110)

Table 2-1 Summary of evidence from epidemiologic, controlled human exposure, and animal toxicological studies on the health effects associated with short- and long-term exposure to ozone

Recent multicity time-series studies and a multicontinent study consistently demonstrated associations between ambient O₃ and respiratory-related mortality visits across the U.S., Europe, and Canada with supporting evidence from single city studies. Generally, these studies had mean 8-h max O₃ concentrations less than 63 ppb.

Health Outcome	Conclusions from 2006 O3 AQCD	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
Lung function	Results from controlled human exposure studies and animal toxicological studies provide clear evidence of causality for the associations observed between acute (= 24 h) O3 exposure and relatively small, but statistically significant declines in lung function observed in numerous recent epidemiologic studies. Declines in lung function are particularly noted in children, asthmatics, and adults who work or exercise outdoors.	Recent controlled human exposure studies demonstrate group mean decreases in FEV1 in the range of 2 to 3% with 6.6 h exposures to as low as 60 ppb O3. The collective body of epidemiologic evidence demonstrates associations between short-term ambient O3 exposure and decrements in lung function, particularly in asthmatics, children, and adults who work or exercise outdoors.
Airway hyperresponsiveness	Evidence from human clinical and animal toxicological studies clearly indicate that acute exposure to O3 can induce airway hyperreactivity, thus likely placing atopic asthmatics at greater risk for more prolonged bouts of breathing difficulties due to airway constriction in response to various airborne allergens or other triggering stimuli.	A limited number of studies have observed airway hyperresponsiveness in rodents and guinea pigs after exposure to less than 300 ppb O3. As previously reported in the 2006 O3 AQCD, increased airway responsiveness has been demonstrated at 80 ppb in young, health adults, and at 50 ppb in certain strains of rats, suggesting a genetic component.
Pulmonary inflammation, injury and oxidative stress	The extensive human clinical and animal toxicological evidence, together with the limited available epidemiologic evidence, is clearly indicative of a causal role for O3 in inflammatory responses in the airways.	Epidemiologic studies provided new evidence for associations of ambient O3 with mediators of airway inflammation and oxidative stress and indicate that higher antioxidant levels may reduce pulmonary inflammation associated with O3 exposure. Generally, these studies had mean 8-h max O3 concentrations less than 73 ppb.
Respiratory symptoms and medication use	Young healthy adult subjects exposed in clinical studies to O3 concentrations = 80 ppb for 6 to 8 h during moderate exercise exhibit symptoms of cough and pain on deep inspiration. The epidemiologic evidence shows significant associations between acute exposure to ambient O3 and increases in a wide variety of respiratory symptoms (e.g., cough, wheeze, production of phlegm, and shortness of breath) and medication use in asthmatic children.	The collective body of epidemiologic evidence demonstrates positive associations between short-term exposure to ambient O3 and respiratory symptoms (e.g., cough, wheeze, production of phlegm, and shortness of breath) in asthmatic children. Generally, these studies had mean 8-h max O3 concentrations less than 69 ppb.
Lung host defenses	Toxicological studies provided extensive evidence that acute O3 exposures as low as 80 to 500 ppb can cause increases in susceptibility to infectious diseases due to modulation of lung host defenses. A single controlled human exposure study found decrements in the ability of alveolar macrophages to phagocytose microorganisms upon exposure to 80 to 100 ppb O3.	Recent studies in human subjects demonstrate the increased expression of cell surface markers and alterations in sputum leukocyte markers related to innate adaptive immunity with short-term O3 exposures of 80-400 ppb. Recent studies demonstrating altered immune responses and natural killer cell function build on prior evidence that O3 can affect multiple aspects of innate and acquired immunity with short-term O3 exposures as low as 80 ppb.
Allergic and asthma related responses	Previous toxicological evidence indicated that O3 exposure skews immune responses toward an allergic phenotype, and enhances the development and severity of asthma-related responses such as AHR.	Recent studies in human subjects demonstrate enhanced allergic cytokine production in atopic individuals and asthmatics, increased IgE receptors in atopic asthmatics, and enhanced markers of innate immunity and antigen presentation in health subjects or atopic asthmatics with short-term exposure to 80-400 ppb O3, all of which may enhance allergy and/or asthma. Further evidence for O3-induced allergic skewing is provided by a few recent studies in rodents using exposure concentrations as low as 200 ppb.
Hospital admissions, ED visits, and physician visits	Aggregate population time-series studies observed that ambient O3 concentrations are positively and robustly associated with respiratory-related hospitalizations and asthma ED visits during the warm season.	Strong evidence demonstrated associations of ambient O3 with respiratory hospital admissions and ED visits in the U.S., Europe, and Canada with supporting evidence from single city studies. Generally, these studies had mean 8-h max O3 concentrations less than 60 ppb.
Respiratory Mortality	Aggregate population time-series studies specifically examining mortality from respiratory causes were limited in number and showed inconsistent associations between acute exposure to ambient O3 exposure and respiratory mortality.
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 non-accidental 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
New onset asthma	No studies at this time.	Evidence for a relationship between different genetic variants (HMOX, GST, ARG) that, in combination with O3 exposure, are related to new onset asthma. These results were observed when subjects living in areas where the mean annual 8-h max O3 concentration was 55.2 ppb, compared to those who lived where it was 38.4 ppb.
Asthma hospital admissions	No studies at this time.	Chronic O3 exposure was related to first childhood asthma hospital admissions in a positive concentration-response relationship. Generally, these studies had mean annual 8-h max O3 concentrations less than 41 ppb.
Pulmonary structure and function	Epidemiologic studies observed that reduced lung function growth in children was associated with seasonal exposure to O3; however, cohort studies of annual or multiyear O3 exposure observed little clear evidence for impacts of longer-term, relatively low-level O3 exposure on lung function development in children. Animal toxicological studies reported chronic O3-induced structural alterations in several regions of the respiratory tract including the centriacinar region. Morphologic evidence from studies using exposure regimens that mimic seasonal exposure patterns report increased lung injury compared to conventional chronic stable exposures.	Evidence for pulmonary function effects is inconclusive, with some new epidemiologic studies (mean annual 8-h max O3 concentrations less than 65 ppb). Information from toxicological studies indicates that long-term maternal exposure during gestation (100 ppb) or development (500 ppb) can result in irreversible morphological changes in the lung, which in turn can influence pulmonary function.
Pulmonary inflammation, injury and oxidative stress	Extensive human clinical and animal toxicological evidence, together with limited epidemiologic evidence available, suggests a causal role for O3 in inflammatory responses in the airways.	Several epidemiologic studies (mean 8-h max O3 concentrations less than 69 ppb) and toxicology studies (as low as 500 ppb) add to observations of O3-induced inflammation and injury.
Lung host defenses	Toxicological studies provided evidence that chronic O3 exposure as low as 100 ppb can cause increases in susceptibility to infectious diseases due to modulation of lung host defenses, but do not cause greater effects on infectivity than short exposures.	Consistent with decrements in host defenses observed in rodents exposed to 100 ppb O3, recent evidence demonstrates a decreased ability to respond to pathogenic signals in infant monkeys exposed to 500 ppb O3.
Allergic responses	Limited epidemiologic evidence supported an association between ambient O3 and allergic symptoms. Little if any information was available from toxicological studies.	Evidence relates positive outcomes of allergic response and O3 exposure but with variable strength for the effect estimates; exposure to O3 may increase total IgE in adult asthmatics. Allergic indicators in monkeys were increased by exposure to O3 concentrations of 500 ppb.
Respiratory mortality	Studies of cardio-pulmonary mortality were insufficient to suggest a causal relationship between chronic O3 exposure and increased risk for mortality in humans. A single study demonstrated that exposure to O3 (long-term mean O3 less than 104 ppb) elevated the risk of death from respiratory causes and this effect was robust to the inclusion of PM2.5.
Cardiovascular Effects	No studies at this time.	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	Toxicological studies reported 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. 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 exposure and increased risk for mortality in humans.</td.	Suggestive of a Causal Relationship

Page 2-28 line 11 (ARP 120) Mortality Effects

The 2006 O₃ AQCD 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 additional research was needed to more fully establish underlying mechanisms by which such effects occur. The evaluation of new multicity studies that examined the association between short-term O₃ exposure and mortality found evidence which supports the conclusions of the 2006 O₃ AQCD. These new studies reported consistent positive associations between short-term O₃ exposure and total (nonaccidental) mortality, with associations being stronger during the warm season, as well as additional support for associations between O₃ exposure and cardiovascular mortality being similar or larger in magnitude compared to respiratory mortality. Additionally, these new studies examined previously identified areas of uncertainty in the O₃-mortality relationship. Taken together, the body of evidence indicates that there is likely to be a causal relationship between short-term exposures to O₃ and all-cause mortality.

The 2006 O₃ AQCD 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 additional research was needed to more fully establish underlying mechanisms by which such effects occur. The evaluation of new multicity studies that examined the association between short-term O₃ exposure and mortality found evidence which supports the conclusions of the 2006 O₃ AQCD. These new studies reported consistent positive associations between short-term O₃ exposure and total (nonaccidental) mortality, with associations being stronger during the warm season, as well as additional support for associations between O₃ exposure and cardiovascular mortality being similar or larger in magnitude compared to respiratory mortality. Additionally, these new studies examined previously identified areas of uncertainty in the O₃-mortality relationship. Taken together, the body of evidence indicates that there is likely to be a causal relationship between short-term exposures to O₃ and all-cause mortality.

Page 2-31 line 5 (ARP 123)

The populations identified in Chapter 8 that are most at risk for O₃-related health effects are individuals with influenza/infection, individuals with asthma, and younger and older age groups.

Page 2-37 (ARP 129)

Table 2-2 Summary of Ozone Causal Determinations for Vegetation and Ecosystem Effects

Vegetation and Ecosystem Effects	Conclusions from 2006 O3 AQCD	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.</td.	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 Below-ground 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

Page 2-37 line 1 (ARP 129)

The use of biological indicators in field surveys to detect phytotoxic levels of O₃ is a longstanding and effective methodology. The USDA Forest Service through the Forest Health Monitoring (FHM) Program (1990-2001) and currently the Forest Inventory and Analysis (FIA) Program has been collecting data regarding the incidence and severity of visible foliar injury on a variety of O₃ sensitive plant species throughout the U.S. The network has provided evidence that O₃ concentrations were high enough to induce visible symptoms on sensitive vegetation. From repeated observations and measurements made over a number of years, specific geographical patterns of visible O₃ injury symptoms can be identified. In addition, a study assessed the risk of O₃-induced visible foliar injury on bioindicator plants in 244 national parks in support of the National Park Service’s Vital Signs Monitoring Network. The results of the study demonstrated that the risk of visible foliar injury was high in 65 parks (27%), moderate in 46 parks (19%), and low in 131 parks (54%). Some of the well-known parks with a high risk of O₃-induced visible foliar injury include Gettysburg, Valley Forge, Delaware Water Gap, Cape Cod, Fire Island, Antietam, Harpers Ferry, Manassas, Wolf Trap Farm Park, Mammoth Cave, Shiloh, Sleeping Bear Dunes, Great Smoky Mountains, Joshua Tree, Sequoia and Kings Canyon, and Yosemite. 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.

Page 2-39 line 23 (ARP 131)

The suppression of ecosystem C sinks results in more CO2 accumulation in the atmosphere. A recent study suggested that the indirect radiative forcing caused by O₃ exposure through lowering ecosystem C sink could have an even greater impact on global warming than the direct radiative forcing of O₃.

Although O₃ generally causes negative effects on ecosystem productivity, the magnitude of the response varies among plant communities (Section 9.4.3.4). For example, O₃ had little impact on white fir, but greatly reduced growth of ponderosa pine in southern California. Ozone decreased net primary production (NPP) of most forest types in Mid-Atlantic region, but had small impacts on spruce-fir forest. Ozone could also affect regional C budgets through interacting with multiple factors, such as N deposition, elevated CO2 and land use history. Model simulations suggested that O₃ partially offset the growth stimulation caused by elevated CO2 and N deposition in both Northeast- and Mid-Atlantic-region forest ecosystems of the U.S. 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.

Page 2-39 line 13 (ARP 132)

In addition, new research has highlighted the effects of O₃ on crop quality. Increasing O₃ concentration decreases nutritive quality of grasses, decreases macro- and micro-nutrient concentrations in fruits and vegetable crops, and decreases cotton fiber quality. These areas of research require further investigation to determine the mechanism and dose-responses (Section 9.4.4.2).

During the previous NAAQS reviews, there were very few studies that estimate O₃ impacts on crop yields at large spatial scales. Recent modeling studies found that O₃ generally reduced crop yield, but the impacts varied across regions and crop species (Section 9.4.4.1). For example, the largest O₃-induced crop yield losses occurred in high-production areas exposed to high O₃ concentrations, such as the Midwest and the Mississippi Valley regions of the U.S. Among crop species, the estimated yield loss for wheat and soybean were higher than rice and maize. Satellite and ground-based O₃ measurements have been used to assess yield loss caused by O₃ over the continuous tri-state area of Illinois, Iowa and Wisconsin. The results showed that O₃ concentrations significantly reduced soybean yield, which correlates well with the previous results from FACE-type experiments and OTC experiments (Section 9.4.4.1).

Evidence is sufficient to conclude that there is a causal relationship between O₃ exposure and reduced yield and quality of agricultural crops.

Page 2-46 line 26 (ARP 138)

The impact of the tropospheric O₃ change since preindustrial times on climate has been estimated to be about 25-40% of anthropogenic CO₂ impact and about 75% of anthropogenic CH₄ impact according to the IPCC, ranking it third in importance among the greenhouse gases. There are large uncertainties in the RF estimate attributed to tropospheric O₃, however, making the impact of tropospheric O₃ on climate more uncertain than the impact of the long-lived greenhouse gases. Despite these uncertainties, the evidence supports a causal relationship between changes in tropospheric O₃ concentrations and radiative forcing.

RF does not take into account the climate feedbacks that could amplify or dampen the actual surface temperature response. Quantifying the change in surface temperature requires a complex climate simulation in which all important feedbacks and interactions are accounted for. As these processes are not well understood or easily modeled, the surface temperature response to a given RF is highly uncertain and can vary greatly among models and from region to region within the same model. In light of these uncertainties, the evidence supports a likely to be a [sic] causal relationship between changes in tropospheric O₃ concentrations and climate change.