Endangerment and Cause or 

Contribute Findings for 

Greenhouse Gases Under 

Section 202(a) of the Clean Air 

Act: 

EPA’s Response to Public 

Comments 

Volume 5: Impacts and Risks to 

Public Health and Welfare: 

Human Health and Air Quality
Impacts and Risks to Public Health 

and Welfare: Human Health and 

Air Quality 

U. S. Environmental Protection Agency 

Office of Atmospheric Programs 

Climate Change Division 

Washington, D.C. 
FOREWORD 

This document provides responses to public comments on the U.S. Environmental Protection Agency’s 

(EPA’s) Proposed Endangerment and Cause or Contribute Findings for Greenhouse Gases Under Section 

202(a) of the Clean Air Act, published at 74 FR 18886 (April 24, 2009). EPA received comments on 

these Proposed Findings via mail, e-mail, and facsimile, and at two public hearings held in Arlington, 

Virginia, and Seattle, Washington, in May 2009. Copies of all comment letters submitted and transcripts 

of the public hearings are available at the EPA Docket Center Public Reading Room, or electronically 

through http://www.regulations.gov by searching Docket ID EPA-HQ-OAR-2009-0171. 

This document accompanies the Administrator’s final Endangerment and Cause or Contribute Findings 

for Greenhouse Gases Under Section 202(a) of the Clean Air Act (Findings) and the Technical Support 

Document (TSD), which contains the underlying science and greenhouse gas emissions data. 

EPA prepared this document in multiple volumes, with each volume focusing on a different broad 

category of comments on the Proposed Findings. This volume of the document provides responses to 

public comments regarding human health and air quality. 

In light of the very large number of comments received and the significant overlap between many 

comments, this document does not respond to each comment individually. Rather, EPA summarized and 

provided a single response to each significant argument, assertion, and question contained within the 

totality of comments. Within each comment summary, EPA provides in parentheses one or more lists of 

Docket ID numbers for commenters who raised particular issues; however, these lists are not meant to be 

exhaustive and EPA does not individually identify each and every commenter who made a certain point in 

all instances, particularly in cases where multiple commenters expressed essentially identical arguments. 

Several commenters provided additional scientific literature to support their arguments. EPA’s general 

approach for taking such literature into consideration is described in Volume 1, Section 1.1, of this 

Response to Comments document. As with the comments, there was overlap in the literature received. 

EPA identified the relevant literature related to the significant comments, and responded to the significant 

issues raised in the literature. EPA does not individually identify each and every piece of literature 

(submitted or incorporated by reference) that made a certain point in all instances. 

Throughout this document, we provide a list of references at the end of each volume for additional 

literature cited by EPA in our responses; however, we do not repeat the full citations of literature cited in 

the TSD. 

EPA’s responses to comments are generally provided immediately following each comment summary. In 

some cases, EPA has discussed responses to specific comments or groups of similar comments in the 

Findings. In such cases, EPA references the Findings rather than repeating those responses in this 

document. 

Comments were assigned to specific volumes of this Response to Comments document based on an 

assessment of the principal subject of the comment; however, some comments inevitably overlap multiple 

subject areas. For this reason, EPA encourages the public to read the other volumes of this document 

relevant to their interests. 

iii 
TABLE OF CONTENTS 

5.0 Impacts and Risks to Public Health and Welfare: Human Health and Air Quality 

5.1 Human Health...............................................................................................................1 

5.2 Air Quality...................................................................................................................56 

iv 
Acronyms and Abbreviations 

ANPR Advance Notice of Proposed Rulemaking 

°C degrees Celsius 

CAIR Clean Air Interstate Rule 

CCSP U.S. Climate Change Science Program 

CDC Centers for Disease Control and Prevention 

CIRAQ Climate Impact on Regional Air Quality 

CH4 methane 

CO2 carbon dioxide 

D8H daily 8-hour average 

ENSO El Niño Southern Oscillation 

EPA U.S. Environmental Protection Agency 

GCM general circulation model 

GHG greenhouse gas 

GIT Georgia Institute of Technology 

HFC hydrofluorocarbon 

IA integrated assessment 

ICAP Intercontinental transport and Climatic effects of Air Pollutants 

IPCC Intergovernmental Panel on Climate Change 

MDA8 maximum daily 8-hour 

N2O nitrous oxide 

NAAQS National Ambient Air Quality Standards 

NERL National Exposure Research Laboratory 

NIPCC Nongovernmental International Panel on Climate Change 

NOx nitrogen oxides 

O3 ozone 

OAQPS Office of Air Quality Planning and Standards 

ORD Office of Research and Development 

PAN peroxyacetylnitrate 

PFC perfluorocarbon 

PM particulate matter 

PM2.5 fine particulate matter (particles less than 2.5 micrometers in diameter) 

ppb parts per billion 

ppm parts per million 

RIA regulatory impact analysis 

SRES IPCC Special Report on Emissions Scenarios 

TAR IPCC Third Assessment Report 

TBE tick-borne encephalitis 

TSD Technical Support Document 

UK United Kingdom 

USGCRP U.S. Global Change Research Program 

VOC volatile organic compound 

WHO World Health Organization

v 
5.0 Impacts and Risks to Public Health and Welfare: Human Health and Air Quality 

5.1 Human Health 

General Issues 

Comment (5-1):

Commenters (e.g., 0329, 2750, 3136.1, 3394.1, 3462.1, 3449.1:10, 3747.1, and 7020) state that specific 

aspects of the climate impacts evidence summarized in the Technical Support Document (TSD) with 

respect to human health do not support the Administrator’s endangerment finding. 

Response (5-1):

The specific issues that underlie these comments are addressed in the responses throughout this volume, 

and other volumes of the Response to Comments document. With regard to the commenters' conclusion 

that the current science does not support an endangerment finding with respect to human health and air 

quality, we disagree based on the scientific evidence before the Administrator. See the Findings, Section 

IV.B, “The Air Pollution is Reasonably Anticipated to Endanger Both Public Health and Welfare,” for 

details on how the Administrator weighed the scientific evidence underlying her endangerment 

determination in general, and with regard to the human health and air quality in particular. 

Comment (5-2): 

A commenter (3394.1) acknowledges the paucity of studies addressing “the interaction effects of multisector climate impacts (they may be nonlinear) or of interactions between climate change health impacts 

and other kinds of local, regional, and global changes,” and indicates that the U.S. Environmental 

Protection Agency’s (EPA’s) analysis demonstrates that the Agency assumes that such studies would 

demonstrate additional negative impacts as opposed to possible benefits or the potential for mitigation. 

The commenter notes EPA may not properly substitute speculation for adequate information. 

Response (5-2): 

The sentence the commenter is quoting was taken from the introduction of Section 7 of the TSD 

associated with the Advanced Notice of Proposed Rulemaking (ANPR) for this action. We have revised 

this statement in response to these comments and it now reads: “There are few studies that address the 

interactive effects of multiple climate change impacts or of interactions between climate change health 

impacts and other kinds of local, regional, and global socioeconomic changes (Field et al., 2007).” The 

commenter interprets this statement as evidence that the Agency is speculating in the absence of adequate 

information. 

We disagree, and note that the next sentence following the one highlighted by the commenter summarizes 

another key finding from the Intergovernmental Panel on Climate Change (IPCC): “For example, climate 

change impacts on human health in urban areas will be compounded by aging infrastructure, maladapted 

urban form and building stock, urban heat islands, air pollution, population growth, and an aging 

population (Field et al., 2007).” In addition, the TSD summarizes the U.S. Climate Change Science 

Program (CCSP) findings that vulnerability is the summation of all the factors of risk and resilience that 

determine whether individuals experience adverse health impacts, and that climate change is very likely 

to accentuate the disparities already evident in the American health care systems, as many of the expected 

health effects are likely to fall disproportionately on the poor, the elderly, the disabled, and the uninsured 

(Ebi et al., 2008). 

EPA has not speculated that there would be negative impacts. We have carefully reviewed the TSD, and 

conclude we have summarized the conclusions of the scientific assessment literature for both positive and 

1 
negative impacts. We note that the commenter has failed to cite any scientific literature to the contrary. 

Further, we note EPA has summarized both beneficial and adverse impacts of climate change that 

throughout the TSD. The assertion that the Agency is focusing on negative impacts and ignoring 

beneficial impacts is incorrect. 

Finally, see the Findings, Section III.C, “Adaptation and Mitigation,” for our response to comments on 

the treatment of adaptation and mitigation in the Findings. 

Comment (5-3): 

At least one commenter (3497.1) indicates that EPA in the endangerment finding has failed to consider 

health benefits from increases in carbon dioxide (CO2). The commenter argues that any reductions in CO2

increase the potential loss of agricultural product and threaten sufficient food supply and that we must 

maintain and increase our ability to produce food and fiber for a growing population. The commenter 

states that not having food, i.e. starvation, is a real human health hazard. Similarly, another commenter 

(2818) states that “if there is not enough food, if there is not enough water, then chronic diseases, heart 

disease, diabetes, as serious as those problems are, they really don’t mean as much if there is not enough 

food and water to go around.” 

 

Response (5-3): 

We examined the TSD and Findings in light of this comment, and conclude that the issues the commenter 

raises are addressed. First, the TSD addresses the beneficial and adverse effects of climate change on food 

production and agriculture in Section 9, and the scientific literature on CO2 fertilization is discussed 

therein. See Volume 6 of the Response to Comments document for responses to comments on issues 

associated with food production and agriculture. Second, the impacts of climate change on water quantity 

and quality are discussed in Section 11 of the TSD, and responses to comments on these issues are 

provided in Volume 7 of the Response to Comments document. 

Lastly, see the Findings, Section IV.B, “The Air Pollution Is Reasonably Anticipated to Endanger Both 

Public Health and Welfare,” for our response to comments on how the Administrator weighed the 

scientific evidence underlying her endangerment determination. In addition, see Response to Comments 

Volume 9 for our responses to other significant comments on how evidence of specific climate impacts 

was considered in the Administrator’s endangerment finding. Also see the Findings, Section III.C, 

“Adaptation and Mitigation,” for our response to comments on the treatment of adaptation and mitigation 

in the Findings. 

Comment (5-4):

A commenter (1468) states that if increased concentrations of the minor greenhouse gases (GHGs) 

including CO2 have any significant warming effect (which is highly debatable), they could conceivably 

contribute to a warmer world that would be more propitious for human beings. 

Response (5-4): 

EPA disagrees with the commenter’s assertion that the scientific literature does not suggest that increased 

concentrations of GHGs such as CO2 affect temperatures. See Volume 3 of the Response to Comments 

document, “Attribution of Observed Climate Change,” for responses to comments on the attribution of 

climate warming. 

2 
With respect to the commenter’s general assertion that a warmer world would be better for human beings, 

we note that many commenters provided specific comments on this issue. See responses to other 

comments in this volume regarding the health impacts associated with a warmer world. 

Comment (5-5):

A commenter (4003) indicates that perhaps the most significant indicator of all that the U.S. population 

does not seem to have been adversely affected by any vulnerabilities, risks, and impacts that may have 

arisen as the result of human-induced climate change is the increase in life expectancy, and provided the 

figure below. Similarly, several commenters cite the Nongovernmental International Panel on Climate 

Change (NIPCC) (Idso and Singer, 2009), which concludes that observations demonstrate that if the 

increases in temperature and CO2 concentrations of the past two centuries were bad for our health, their 

combined negative influence was minuscule compared to whatever else was at work in promoting this 

vast increase in worldwide longevity. 

Source: Commenter 4003, from Carlin, 2009 

Response (5-5):

In light of this comment, we have reviewed the cited literature and examined the issue in the context of 

this action. We note that life expectancy over the last century in the United States (and globally) is 

determined by several factors, many of which are non-climatic (i.e., advances in health care, 

infrastructure, technology, and wealth). The chart provides no insight into the risk or trend of any specific 

factor on life expectancy. We also conclude that this measure is of limited meaning in the context of the 

evaluation of risks due to a changing climate, which can occur via various pathways. The single metric of 

life expectancy does not convey or provide information on the risks associated with changes in climate 

and whether or not they are increasing, either in the past or in the future. For example, were a particular 

epidemic to occur within this trend it may or may not be evident; however, this does not mean it is not of 

serious concern to public health. 

While the commenter notes that this increase in life expectancy has occurred despite increasing 

temperatures and CO2 levels, it does not represent future conditions in which climate is likely to become 

warmer and with likely more variable precipitation. The fact that public health measures are very 

effective (i.e., we do not have many cases of certain diseases) does not mean that the risk is not present or 

increasing. In addition, our prevention measures are not 100% effective and there remain concerns about 

potential risks (e.g., new diseases), growing resistance to antibiotics, reduction in effectiveness of vectorcontrol measures over time, and an aging sanitation and drinking water infrastructure. See the Findings, 

Section IV.B, “The Air Pollution Is Reasonably Anticipated to Endanger Both Public Health and 

Welfare,” for our response to comments on how the Administrator weighed the scientific evidence 

underlying her endangerment determination. 

3 
Comment (5-6):

A commenter (11348) indicates that we need more research on direct and indirect health effects of climate 

change, and more effort in adaptation, given the impossibility of preventing natural events. 

Response (5-6):

Though EPA agrees more research would be valuable on the direct and indirect health effects of climate 

change, the current state of knowledge of the current and future risks of climate change and public health 

provides sufficient support basis for the Administrator’s determination. Please refer to the Findings, 

Section III.A, “The Science on Which Decisions Are Based,” and Section IV.B, “The Air Pollution Is 

Reasonably Anticipated to Endanger Both Public Health and Welfare,” for our response to comments on 

how the Administrator weighed the scientific evidence underlying her endangerment determination. See 

the Findings, Section III.C, Adaptation and Mitigation, for our response to comments on the treatment of 

adaptation and mitigation in the Findings. 

Comment (5-7): 

A commenter (3136.1) asks why EPA includes the parenthetical “but may be modulated by public health 

measures” after the expanded range of vector-borne and tick-borne disease in the ANPR TSD. This 

applies equally to all of the other bullets in this section. The commenter states that there is conclusive 

evidence that public health measures have successfully reduced our sensitivity to heat waves (Davis et al., 

2003a, 2003b). 

Another commenter (3722) indicates that the fundamental factor which EPA repeatedly discounts or 

ignores in its Proposed Findings is human adaptability to temperature change. This adaptability, which 

underlies the increased life expectancy and improved health in U.S. cities and cities throughout the world 

over the last 100 years, despite increases in temperatures (of 4°C or more), is the single most important 

factor which has to be taken into account in predicting the health effects of future warming. In addition, 

studies in the United States indicate the importance of human adaptation in mitigating the mortality 

effects of climate. The commenter references Davis et al. (2003), which indicates that a 74% drop in heatrelated deaths occurred despite an average increase in temperature of 1.0°C during the same period. 

Response (5-7): 

See the Findings, Section III.C, “Adaptation and Mitigation,” for our response to comments on the 

treatment of adaptation and mitigation in the Findings. 

With respect to the specific comment regarding the referenced parenthetical, we note that it is based on a 

specific IPCC (Field et al., 2007) finding and associated underlying scientific literature. Thus, we disagree 

with the commenter that it applies to all of the other bullets in this particular section. However, we note 

that Section 7(c) of the April 2009 version of the TSD, also notes an Intergovernmental Panel on Climate 

change (IPCC) conclusion that indicates more broadly that human health risks from climate change will 

be strongly modulated by changes in health care, infrastructure, technology, and accessibility to health 

care (Field et al., 2007). In response to these comments, and in acknowledgment that measures to 

modulate human health risks apply more broadly, we have revised the final TSD by moving the following 

language toward the beginning of Section 7: 

“The IPCC concludes that human health risks from climate change will be strongly modulated by 

changes in health care, infrastructure, technology, and accessibility to health care (Field et al., 

2007). The aging of the population and patterns of immigration and/or emigration will also 

strongly influence risks (Field et al., 2007).” 

4 
While EPA finds that risks to human health can be reduced by investments in countermeasures, we 

conclude that this does not eliminate risk, especially to populations vulnerable to the array of direct and 

indirect health effects associated with climate change. EPA is familiar with the studies by Davis et al. 

(2003a, 2003b) but notes that net mortality is based on several factors beyond the influence of 

preventative and adaptive measures. Please refer to responses 5-24 and 5-48 for further discussion of 

Davis et al. (2003a; 2003b) in the context of temperature effects. 

Comment (5-8): 

A commenter (0329) asks the following questions: “Will the EPA recommend to U.S. lawmakers that 

population within the borders of the U.S. be limited by artificial means to further reduce emission of 

greenhouse gases? Can the EPA guarantee that if the U.S. curtails its production of greenhouse gases that 

citizens will see a notable and measurable improvement in the economic, social and medical standard of 

living within the U.S.? If GHG are “hazardous” to human health how many days/months/years will the 

average life expectancy of U.S. citizens be increased by implementation of controls?” Another 

(2818_GGG) wonders if EPA will require permits for having children given the contributions of 

human respiration and digestion to CO2 and CH4. One commenter (3712.1) claims that regulating 

CO2 will regulate all activities, increasing prices for the poor and elderly, and restricting the amount of 

life that can be allowed to exist. Similarly, commenter (9717) worries that because people emit CO2 in 

proportion to their weight that fat people will be taxed. 

Response (5-8): 

EPA notes that all of the commenters’ questions focus on methods and implications of greenhouse gas 

(GHG) controls, which are not the focus of this action. This action concerns the Administrator’s 

determination regarding whether GHG pollution is reasonably anticipated to endanger public health and 

welfare. In this action, EPA is not recommending any specific responses be taken to reduce greenhouse 

gases, and questions regarding the nature and effectiveness of measures to reduce greenhouse gas 

emissions are outside the scope of this action. When and if EPA proposes regulatory action to control 

greenhouse gas emissions, it would be accompanied by a regulatory impact analysis which would 

examine the costs and benefits of the specific proposed regulatory actions, and the public would have the 

opportunity to comment on any proposals. 

We also want to state clearly that EPA has not, is not and does not plan to recommend any of the concepts 

raised by commenters (e.g., limiting population “by artificial means”, requiring “permits for having 

children”, “restricting the amount of life that can exist”). Further, it is unclear to us where the 

commenters got these ideas, as it is well known that CO2 emissions from human respiration are not an 

emission source of concern, and are not contributing to the atmospheric buildup of CO2. Human 

respiration of CO2 is part of a closed system. There can be no net addition of CO2 to the atmosphere 

because the amount of CO2 people exhale cannot be greater than the carbon people put into their bodies 

by eating plants, or eating animals that eat plants. 

Comment (5-9): 

A commenter (11350) indicates that global warming could lead to human extinction, and the 

Administrator is justified in taking the most extreme measures to stop GHG pollution. The commenter 

references a book by Brian Fagan, “A Long Hot Summer” (Fagan, 2004) as evidence of “how Global 

Warming could lead to the extinction of Homo Sapiens by the year 2030.”

Response (5-9): 

5 
EPA acknowledges that the risks and impacts of climate change are occurring now and will continue to 

increase over this century; however, EPA notes that the underlying scientific literature does not include 

predictions of human extinction. 

Comment (5-10): 

A commenter (4946) indicates that EPA’s Proposed Findings make the case for action by demonstrating 

that climate change threatens “virtually every facet of the living world around us” and that its effects 

include “sickness and death.” While coal plants are a major source of global warming pollution, it is clear 

that emissions from new motor vehicles and new motor vehicle engines contribute to global warming 

pollution too. The commenter applauds EPA for using its authority under the Clean Air Act to take action 

to protect us from the pollution that causes global warming and urge you to move rapidly by finalizing 

these determinations and issuing strong new rules to control global warming pollution and provide a 

sound foundation for our economy. 

Response (5-10):

The commenters’ view that this action demonstrates that climate change threatens human health is 

consistent with the Findings. The comments on GHG emission sources are generally consistent with the 

scientific literature summarized in the TSD on this issue. 

 

Comment (5-11): 

A commenter (8320) submits information and references on the potential health effects of global climate 

change. The commenter discusses the following topics: extreme heat events, wildfires, vector-borne 

diseases, water-borne diseases, air quality and human heath, aeroallergens and allergies, environmental 

justice, and the vulnerability of children to effects from air quality. The commenter stresses that “climate 

change will alter the global environment and present major challenges to the health and welfare of 

children.” 

Response (5-11): 

EPA has reviewed the submitted comments and associated references, and finds that they include several 

very recent and relevant studies (e.g., St. Louis and Hess, 2008; Patz et al., 2008; Jerret et al., 2009) that 

confirm the scientific support for health related impacts summarized in the TSD. 

In one example, Luber and McGeehin (2008) call extreme heat events “the most prominent cause” of 

weather-related human mortality in the United States, noting that they are responsible for more deaths 

annually than hurricanes, lightning, tornadoes, floods, and earthquakes combined. We note that the 

recently released U.S. Global Change Research Program (USGCRP) report (Karl et al., 2009) also 

concludes that mortality from heat is the number one weather-related cause of death and cites an analysis 

of nine U.S. cities showing that deaths rise with increases in temperature and humidity with no 

confounding or effect modification due to air pollution (Zanobetti and Schwartz, 2008). 

Another recent study (Jerret et al., 2009) provided by the commenter indicates that high levels of groundlevel ozone can increase the risk of asthma-related hospital visits and premature mortality and that the 

effect of long-term exposure to ozone on air pollution–related mortality was not known. The study 

indicates that ozone exposure is associated with the risk of death from respiratory causes, and that longterm, low-level exposure can be lethal. Researchers studied the outcomes of almost 500,000 adults in 96 

metropolitan regions who enrolled in the American Cancer Society Cancer Prevention Study in 1982 and 

1983 and were tracked for an average of 18 years. In addition, the study by Jerrett et al. (2009) looked at 

associations between ozone concentrations and the risk of death, in a single-pollutant model and in a two6 
pollutant model with fine particulate matter (PM2.5). In two-pollutant models, researchers demonstrated a 

significant increase in the risk of death from respiratory causes in association with an increase in ozone 

concentration. The study found that every increase in 10 parts per billion (ppb) in average ozone 

concentrations was associated with a roughly 4% increase in mortality from respiratory causes. This 

translated in Los Angeles to a 43% increase in the risk of dying from respiratory causes. Eastern cities 

like New York and Washington had an average increased risk of about 25% to 27%. EPA concludes this 

study fills important knowledge gaps in health impact literature from increases in ozone exposure (at low 

levels). 

Another study provided by the commenter provides evidence of vector-borne disease shift attributed to 

climate. For example, in Europe, geographic shifts in the tick’s distribution have been attributed to 

climate change. An expansion of the tick’s range into higher elevations in the Czech Republic 

corresponded to rising temperatures. A shift toward higher latitudes in Sweden corresponded to a 

reduction in the number of very cold winter days (Gage et al., 2008). 

Based on review of the cited literature from the commenter, we conclude that the information provided is 

generally consistent with, and in several cases even stronger than the assessment literature summarized in 

the TSD. 

Comment (5-12):

A commenter (3402) indicates that the Earth is a dynamic system of balance, and all living things have a 

stake in the health of our shared atmosphere. While CO2 as a gas is as critical as oxygen to life on Earth, 

like oxygen it becomes a toxin when the balance of concentration is disrupted. We must achieve 

atmospheric balance to protect not only human health, but also that of all living things. The commenter 

also indicates that her son is sensitive to air quality and notes there is a strong correlation between his sick 

days and poor air quality. The commenter indicates that, to protect public health and wellbeing, we must 

reduce health risks to those suffering from allergies. The commenter notes that warming climates have 

resulted in an earlier and longer allergic pollen season. She states: “Global warming pollution threatens 

the well being of today’s youth as well as the future generations. Increased GHG emissions and climate 

change are putting more and more of our cities and communities in violation of air pollution standards. 

Children are most susceptible to these changes, particularly African American children who are more 

likely to be affected by asthma than their Caucasian counterparts.” 

Response (5-12):

We note the commenter’s perspective and recognize that the risks and impacts mentioned by the 

commenter, while not supported by specific scientific literature, are in some cases the same impacts as 

those based on the scientific literature and summarized in the TSD. For example, the TSD notes that 

specific subpopulations may experience heightened vulnerability to climate-related health effects. As 

summarized in the TSD, climate change is very likely to accentuate the disparities already evident in the 

American health care system as many of the expected the health effects are likely to fall 

disproportionately on the poor, the elderly, the disabled, and the uninsured. The CCSP (Ebi et al., 2008) 

also notes that “climate can also affect the incidence of diseases associated with air pollutants and 

aeroallergens (Bernard et al., 2001).” The TSD summarizes the IPCC on the impact of climate change on 

ozone and particulate matter (PM), which states that “future climate change may cause significant air 

quality degradation by changing the dispersion rate of pollutants, the chemical environment for ozone and 

PM generation and the strength of emissions from the biosphere, fires and dust.” 

Comment (5-13): 

7 
Commenter(s) (2895) indicate that the World Health Organization (WHO) estimates that global warming 

is already responsible for 150,000 deaths and 5 million illnesses each year. The commenters note that 

these have come in the form of malnutrition, diarrhea, and vector-borne diseases like malaria and dengue 

fever. So far they have occurred predominantly in poor and developing countries; ironically, the countries 

that contribute the least to global warming are the most susceptible. The health impact of climate change 

is also evident here in the developed world, the commenters state, and will be increasingly felt if we do 

not take action. 

The commenters state that there are four main categories of health effects: 

Increased frequency, duration, and intensity of heat waves. The associated health problems of 

heat cramps, heat exhaustion, and heat stroke will be become increasingly common. The very old 

and very young are especially vulnerable, as well as those who are poor, socially isolated or who 

have chronic illnesses. 

Increased air pollution. Increased temperatures cause increased production of ground level 

ozone, the main component of smog. This will increase rates of asthma and other respiratory 

diseases. It also makes breathing difficult for those who already have cardiac or respiratory 

ailments. Pollen production and allergies are also increasing as a result of increased CO2

concentrations. 

Infectious diseases. Climate change is altering the range of disease-carrying organisms. West Nile 

virus carried by mosquitoes was not as prevalent in the United States until recently. More than 

25,000 cases and more than 1,000 deaths have been recorded. 

Extreme weather events. This includes severe storms, increases in both drought and flooding, and 

associated features such as erosion and wild fires. The commenter indicates that we simply do not 

have the public health capacity to respond to increasing numbers of large-scale disasters that are 

difficult to predict. 

Response (5-13):

EPA acknowledges the health effect categories as listed by the commenter and recognizes the rapid 

emergence of research and published literature on health effects associated with climate change. The TSD 

summarizes key conclusions of IPCC (2007), based on their review of over 500 articles on the effects of 

heat and cold; wind, storms, and floods; drought, nutrition, and food security; food safety; water and 

disease; air quality and aeroallergens and disease; vector-borne, rodent-borne, and other infectious 

diseases; occupational health; and ultraviolet radiation. The TSD also summarizes the conclusions of the 

recently released USGCRP report (Karl et al., 2009), which describes global climate change impacts for 

the United States. This report provides further evidence of the scope and magnitude of health effects, both 

direct (e.g., increased morbidity from heat waves or floods) and non-direct (e.g., increased or alteration in 

the spread and transmission rates of infectious diseases). As noted by the commenter, the literature shows 

poor countries and communities are likely to be disproportionately impacted by climate change health 

risks. For example, IPCC notes that adverse health impacts will be greatest in low-income countries and 

those at greatest risk include—in all countries—the urban poor, the elderly and children, traditional 

societies, subsistence farmers, and coastal populations (high confidence, Confalonieri et al. 2007). 

Comment (5-14): 

Commenters (3226, 3248, 4036.5) cite and submit a 2009 report published in Lancet (Costello et al., 

2009). Similarly, a commenter (3226) submits an article from the Grist Web site entitled “New Lancet 

Report on Health and Social Effects of Climate Change” (Roberts, 2009). The commenters highlight the 

importance of the findings in the report with regard to public health effects from climate change. 

8 
Specifically, the commenters note from the report that “climate change is the biggest global health threat 

of the 21st century.” 

Response (5-14):

EPA has carefully reviewed the cited reference and notes that it relies heavily on IPCC (2007) reports and 

other sources of information summarized in the TSD. We note that the although the report (Costello et al., 

2009) focuses on global health and the TSD has a primary focus on U.S. impacts, the overall conclusions 

on impacts and effects to human health and vulnerable populations are generally consistent with the TSD. 

Comment (5-15): 

A commenter (3574.1) indicates that ozone is detrimental to human health and references a book as 

evidence of impacts to lung function as a result of high ozone concentration (Casarett and Doull, 1991). 

Response (5-15):

We have reviewed the reference and note the well-documented effects of ozone to lung function at 

concentrations of sufficient levels. The TSD notes climate change is expected to increase regional ozone 

pollution, with associated risks in respiratory illnesses and premature death. 

Comment (5-16):

Several commenters (0296, 0489, 1470, 1529, 1548, 1582, 1586, 1672, 1807, 3280.1, 3501, 10298, 

11249) express their support for the findings (and/or strong action on climate change) and describe 

various health impacts resulting from climate change, including increased heat-related illnesses and 

mortality, respiratory diseases, and both vector- and water-borne infectious diseases. Several commenters 

(2040, 3680.1, 4171) note that multiple and severe effects of climate change on health have been 

documented by numerous governmental and scientific bodies, including IPCC, CCSP, the World Health 

Organization (WHO), and/or the American Public Health Association. Several commenters (4171, 11249) 

provide WHO statistics regarding the number of annual deaths attributable to climate change and note 

that this number is expected to rise. 

Response (5-16):

EPA has carefully considered the commenters’ views, many of which are based on the same sources of 

information relied upon by to summarize science impacts and risk from climate change in the TSD. As 

stated in the findings, the Administrator has evaluated various health impacts, both direct (temperature 

effects) and indirect (e.g., changes in climate-sensitive diseases) that occur through human-induced 

climate change. For more specific information, see our responses to comments on topics throughout this 

volume of the Response to Comments document. 

Comment (5-17):

A commenter (6749) states that environmental factors contribute to a multitude of cancers, and expressed 

concern that clean air, nutrient-rich foods, and clean drinking water are threatened by climate change. One 

commenter (6733) notes an increase in skin cancers resulting from ozone depletion. 

Response (5-17):

Summarizing the assessment literature, Sections 7 and 8 of the TSD summarize health effects associated 

with climate change and attendant changes in air quality. The assessment literature does not highlight 

changes in cancer as a likely effect of climate change. 

9 
Comment (5-18):

A commenter (0293) indicates that reducing atmospheric CO2 would have the co-benefit of reducing the 

disease burden of criteria pollutants, hazardous air pollutants, and other toxics, including cardiovascular 

disease, pulmonary disease, cancer, neurodegenerative disorders, immunosuppression, premature birth, 

and infant mortality. 

Response (5-18): 

See the Findings, Section III.C, “Adaptation and Mitigation,” for our response to comments on the 

treatment of adaptation and mitigation in the Finding. 

Comment (5-19): 

A commenter (3921.1) submits the first page of a research paper by Joachim Bormann entitled 

“Memantine is a potent blocker of N-methyl-D-aspartate (NMDA) receptor channels” (1989). The 

commenter provides no comments in association with the reference. 

Response (5-19): 

EPA confirms review of the submitted reference; however, it does not appear to address any elements of 

climate change science discussed in the TSD or the Findings. 

Comment (5-20):

A commenter (3501) indicates that dust storms and forest fires obviously have their own destructive 

impacts on the economy, the ecosystems, and the aesthetics of the region. But they also have an impact on 

public health. 

The commenter indicates that air pollution from forest fires and dust storms has become commonplace in 

the West for several months of the year, even sometimes in the winter, and notes that recent studies have 

demonstrated that PM air pollution from forest forests may be much more toxic than that from typical 

fossil fuel combustion. The commenter also states it is well known that forest fires generate atmospheric 

mercury. 

Response (5-20):

We note the commenter does not provide specific references for studies demonstrating that air pollution 

from forest fires may be much more toxic than that from typical fossil fuel combustion, or that forest fires 

generate atmospheric mercury. The climate change assessment literature does not discuss these issues and 

they are, therefore, not summarized in the TSD. However, we agree with the commenter that forest fires 

can have an impact on public health, and this is well-documented in the assessment literature. 

Summarizing the assessment literature, Section 7(b) of the TSD notes that wildfires can increase eye and 

respiratory illnesses and injuries, including burns and smoke inhalation (Ebi et al., 2008). Further 

evidence comes from a study cited by IPCC (Confalonieri et al., 2007), which indicates that large fires are 

also accompanied by an increased number of patients seeking emergency services for inhalation of smoke 

and ash. Section 8(b) of the TSD provides additional evidence of the effects of PM from forest fires. For 

example, PM emissions from forest fires can contribute to acute and chronic illnesses of the respiratory 

system, particularly in children, including pneumonia, upper respiratory diseases, asthma, and chronic 

obstructive pulmonary diseases (Moore et al., 2006; Confalonieri et al., 2007). 

10 
Comment (5-21):

One commenter (3280.1), in supportive comments regarding the Findings, specifically discusses several 

expected challenges to the health and welfare of children due to climate change. The commenter provides 

a summary of recent studies and statements from organizations and leading officials that detail children’s 

physical and social climate change health risks. The commenter lists several examples including 

respiratory diseases, heat stroke, increased rates of malnutrition, and allergies. 

Response (5-21):

We reviewed the materials submitted and find them generally consistent with the information summarized 

in the TSD. We note that most of the studies and statements submitted (e.g., Frumkin, 2008; American 

Academy of Pediatrics, 2008; Bunyavanich et al., 2003) extensively cite the assessment literature to 

support their findings. 

In Section 7’s summary of the assessment literature (Field et al., 2007), the TSD notes that for heat waves 

populations most vulnerable to illness and death include the very young (children). Furthermore, in 

Section 8(b), the TSD (summarizing Confalonieri et al., 2007) states: “Particulate matter emissions from 

forest fires can contribute to acute and chronic illnesses of the respiratory system, particularly in children, 

including pneumonia, upper respiratory diseases, asthma, and chronic obstructive pulmonary diseases.” 

See other responses to comments in this volume for information on additional effects on human health 

from climate change. 

Comment (5-22):

Many commenters (e.g., 1156.1, 1672, 3383.1,, 3455.1, 3570.1, 3893, 3995, 4171, 4184, 9786, 10809, 

10838) state their support for the findings, noting observed and future changes in heat waves and heat 

stress as one of the environmental effects of climate change. Some commenters (e.g., 2263, 11249) state 

concern for an increase in heat-related illnesses due to global warming associated with heat exposure, 

including heat cramps, heat syncope (fainting), heat exhaustion, and heatstroke. 

Response (5-22):

While the commenters do not provide specific supporting information, we have carefully considered their 

views and statements regarding health effects of increasing temperatures and future changes in heat waves 

and heat stress. We note in the TSD that the IPCC projects that severe heat waves are expected to 

intensify in magnitude and duration over the portions of the United States where these events already 

occur, with potential increases in mortality and morbidity, especially among vulnerable populations (e.g., 

elderly, young and frail). We note that these and other findings in the TSD support the commenters’ 

views with respect to temperature effects and changes in climate. 

Comment (5-23):

A commenter (3347.3) alleges that EPA’s analysis of the temperature effects is flawed and violates the 

Information Quality Act. The commenter contends that EPA is presenting a biased scientific record 

suggesting that potential rising temperatures may cause adverse local or regional public health risks, 

while ignoring equally strong or stronger evidence that rising temperature would provide offsetting 

reductions in public health risk, equal or larger in magnitude according to the highest-quality scientific 

evidence. 

Response (5-23):

11 
Please see Volume 1, Section 1.5 of this Response to Comments document for EPA’s general response to 

the information quality concerns submitted during the public comment process. The science upon which 

the Administrator relied, including a discussion of how the literature was identified, is discussed in 

Section III of the Findings, and our response to comments on this can be found in Volume 1 of the 

Response to Comments document. This section also describes our treatment of new and additional studies 

that are not incorporated into the assessment literature. EPA’s approach is fully consistent with EPA’s 

IQA guidelines in accordance with sound, transparent and objective scientific practices. 

For specific discussion of the balance of warming-related temperature effects and related scientific 

evidence, please refer to responses in the rest of this section, and in particular, responses 5-24 and 5-27. 

Comment (5-24):

Several commenters (e.g., 3347.3, 11453.1, 3187.3) note that the April 2009 TSD indicated that coldrelated deaths presently exceed heat-related deaths in the United States and that this provides evidence 

that a warming climate will have beneficial effects on temperature-related mortality. Commenters note 

that on page 70 of the April 2009 TSD, EPA states that 5,983 heat-related deaths were reported in the 

United States between 1979 and 2002. In the same timeframe, 16,555 people died of extreme cold. A 

commenter (3187.3) provides a paper by Goklany (2007), which indicates that death from extreme cold 

exceed death from extreme heat. 

Response (5-24):

We have revised the TSD’s estimates of heat-related deaths based on the latest findings of the assessment 

literature (Karl et al., 2009). Based on these results, other supporting evidence presented in the TSD, and 

additional evidence cited below, we have determined that the available literature strongly supports the 

conclusion that extreme heat is, on an average annual base, the leading cause of weather-related death in 

the United States. We agree that the April 2009 TSD contained statistics that could be interpreted as 

suggesting that cold-related mortality has recently been higher in the United States than heat-related 

mortality. The cold-related mortality statistics in the TSD from Ebi et al. (2008) are similar to those cited 

by Goklany (2007). However, the methods and data for estimating heat-related mortality were recently 

updated and these revised values are presented in Karl et al. (2009). 

The more recent heat-related mortality numbers from Karl et al. (2009) reflect results from the Centers for 

Disease Control and Prevention (CDC). CDC (2006) reports more than 3,400 deaths from 1999 to 2003 

for which exposure to extreme heat was listed as either a contributing factor or the underlying cause of 

death. This result of roughly 680 heat-related deaths per year is almost identical to the 689 deaths per year 

from cold exposure reported by Ebi et al. (2008) and summarized in the TSD. CDC (2006) suggests that 

even the revised heat-related mortality numbers may underestimate total heat-related mortality, noting: 

“Because heat-related illnesses can exacerbate existing medical conditions and death from heat exposure 

can be preceded by various symptoms, heat-related deaths can be difficult to identify when illness onset 

or death is not witnessed by a clinician. In addition, the criteria used to determine heat-related causes of 

death vary among states. This can lead to underreporting heat-related deaths or to reporting heat as a 

factor contributing to death rather than the underlying cause.” This issue has long been recognized in 

attempting to estimate the mortality impact of extreme heat using information from death certificates 

(American Medical Association Council on Scientific Affairs, 1997). As noted in a subsequent response 

(5-29), cold-related deaths are likely also underestimated. One complication with these death certificate–

based estimates of extreme cold and heat is they are not limited to periods that would be considered heat 

waves or cold snaps in the location where the death occurs. Therefore, while these results are based in a 

consistent methodology and data source, they have an uncertain overlap with the occurrence of the 

weather events of primary interest to the TSD, cold snaps and heat waves. As a result, these data alone do 

not provide strong evidence the heat-related mortality is presently greater than cold-related mortality. 

12 
However, we note that alternative and much higher estimates of heat-related mortality come from 

analyses of daily urban summertime mortality patterns in Kalkstein and Greene (1997) and Davis et al. 

(2003a), which use a different methodology to compute heat-related deaths compared to CDC (2006). 

These studies first define extreme heat events by identifying threshold conditions for an event in a 

location and then calculate the number of extreme heat–attributable deaths based on differences in daily 

deaths on extreme heat days compared to longer-term averages. In these studies, heat’s mortality impact 

is quantified in terms of the excess deaths that result during the extreme heat conditions. By evaluating 

changes in daily deaths attributable to all causes, this approach also effectively eliminates differences or 

restriction in using certain causes of death as potential sources of bias in estimating the extreme heat’s 

mortality impact. This method is also more consistent with the view that heat waves are effectively 

identified through exceptional weather conditions that result in increases in daily mortality (e.g., 

Confalonieri et al., 2007; U.S. EPA, 2006a). Although differences in the time series, definitions of urban 

populations, and other analytical methods prevent an exact comparison of the results in these two studies, 

both studies (Kalkstein and Greene, 1997; Davis et al., 2003a) estimate that there are approximately 

1,700–1,800 excess deaths per year during extreme heat events based on an evaluation of a subset of 

approximately 40 U.S. metropolitan areas (see U.S. EPA, 2006a). These estimates of extreme heat’s 

mortality impact are much higher than the corresponding death certificate–based estimates for heat as 

well as the Ebi et al. (2008) estimate for cold-related mortality summarized in the TSD. 

We also note that Davis et al. (2004) find that the net impact of the observed temperature increase from 

1964 to 1998 (considering both reduced temperature mortality in winter and increased temperature 

mortality in summer) was an extra 2.9 deaths (per standard million) per city per year in 28 major U.S. 

cities. This indicates that extreme heat has been the larger cause of mortality in the recently observed 

record when temperatures have warmed. 

Furthermore, we note that the USGCRP assessment (Karl et al., 2009) specifically refers to a recent study 

by Borden and Cutter (2008), which concludes heat is the most deadly natural hazard in the United States. 

It also cites Medina-Ramon and Schwartz (2007), which found that in 50 U.S. cities between 1989 and 

2000, extreme heat increased death rates 5.7% while extreme cold increased death rates by only 1.6%. 

These results are summarized in the TSD. 

Though we are aware of a recent study by Andersen and Bell (2009) that finds a similar mortality risk for 

extremely hot and cold days based on the synthesis of results from 107 U.S. communities (contrasting 

with Medina-Ramon and Schwartz), Andersen and Bell are clear that cold temperatures more indirectly 

affect mortality than heat. In addition to the longer lag times for exposure incorporated for the effects of 

extreme cold (up to 25 days, compared a one-day lag for heat), they note that infectious diseases, which 

are more common in industrialized countries during colder weather (when people spend more time 

indoors and in proximity) could account for a substantial portion of the cold-related effect. 

Summarizing, both recent studies and the assessment literature provide strong evidence that heat-related 

mortality presently exceeds cold-related mortality in the United States. 

Comment (5-25):

A commenter (3347.3) argues that key studies used by EPA to show higher mortality relating to 

increasing temperature rely on incorrect estimation methods. The comment refers to EPA’s Excessive 

Heat Events Guidebook (U.S. EPA, 2006a), which discusses estimates of heat-related mortality in a set of 

U.S. cities from Kalkstein and Greene (1997) and Davis et al. (2003a). It notes that despite the similarity 

in the aggregate results of those studies (obtained by adding the mortality totals for the cities analyzed), 

there are large differences in the results of the individual cities, which suggests balance was achieved by 

13 
trading off mortality between cities. The commenter concludes that the mortality results are therefore 

sensitive to the methodology and unreliable. 

Response (5-25):

We disagree with the commenter’s conclusion about the reliability of these study results. The methods 

and results of these studies are legitimate. Both studies were peer-reviewed and cited in the assessment 

literature (Kalkstein and Greene, 1997, was cited in IPCC’s Third Assessment Report, McMichael et al., 

2001; Davis et al., 2003a, was cited in IPCC’s Fourth Assessment, Confalonieri et al., 2007, and in CCSP, 

Ebi et al., 2008). We also note that in other comments (see 5-36 and 5-37) the commenter extensively 

relies on the Davis et al. (2004) study which, in fact, is dependent on the allegedly “unreliable” Davis et 

al. (2003a) study. 

While noting that the studies share a similar methodological approach in terms of quantifying the 

mortality impact of extreme heat based on estimates of the excess mortality, we also have recognized the 

city-specific results appear sensitive to the detailed differences in methodologies employed as well as 

other factors (note that U.S. EPA, 2006a, states that there are “differences in the time series, definitions of 

urban populations, and other analytical methods that prevent an exact comparison between the studies”). 

Regardless of these specific differences, the bottom line is that, using an excess mortality–based 

approach, both studies (further discussed in response 5-24) produce heat-related mortality totals that are 

substantially larger than the death certificate-based results described in response 5-24. 

Comment (5-26):

A commenter (3347.3) suggests that since deaths are expected following a heat wave, they are therefore 

more likely to be reported as heat-related. The comment contends that this results in an overestimation of 

mortality attributed to heat waves. 

Response (5-26):

We strongly disagree with this comment. The comment directly conflicts with statements from CDC 

(2006) with respect to the death certificate–based estimates of the mortality impact of extreme heat. 

Response 5-24 summarizes CDC’s (2006) assessment of the difficulties in accounting for heat-related 

deaths that may lead to underestimates using death certificate information. 

This comment also has no validity with respect to estimates of the mortality impact of extreme heat that 

rely on estimates of excess mortality based on all-cause mortality estimates. In these studies (e.g., Davis, 

2003a, Kalkstein and Greene, 1997) differences in all-cause mortality during a period of extreme heat are 

compared with mortality levels during a reference period. As a result, the methodology effectively 

controls for possible bias in assigning the cause of death by considering all deaths on a day. 

Comment (5-27):

Many commenters (e.g., 3347.3, 3449.1, 11453.1) indicate that EPA has not demonstrated that increased 

mortality from heat will exceed decreased mortality from cold in a warming climate and/or that EPA 

concedes that the balance is uncertain and additional research is needed to better understand this issue. 

Some commenters present literature (e.g., Keating et al., 1997; Campbell-Lendrum et al., 2003) that, they 

find, suggests that reduced deaths from cold will outnumber increased deaths from heat in a warming 

climate. 

14 
Response (5-27):

The TSD is very clear that the assessment literature (Confalonieri et al., 2007; Ebi et al., 2008; Karl et al., 

2009) finds that the exact balance between increases in heat-related mortality and decreases in coldrelated mortality is uncertain in a warming climate. However, we note that the latest USGCRP assessment 

(Karl et al., 2009) cites recent research by Medina-Ramon and Schwartz (2007) that concludes that 

increases in heat-related mortality due to global warming are unlikely to be compensated for by decreases 

in cold-related mortality, based on the finding that heat currently results in higher death rates than cold in 

the United States. Additional support for the conclusion that heat is, in fact, the leading cause of 

temperature-related mortality in the United States is given in response 5-24. 

Our review of relevant recent literature and the studies submitted by commenters does not identify flaws 

in our characterization of this issue in either the TSD or the Findings. Recent (post-2001) studies that 

estimate the possible future effects of temperature-related mortality provide varying results: 

Many commenters submitted comments that discuss observed temperature-related mortality 

trends and projections in Europe (e.g. Keating et al., 1997). Those studies are generally not 

germane to the United States for reasons discussed in response 5-39 and 5-40. 

Campbell-Lendrum et al. (2003) project no or a slightly negative net change in the risk of 

temperature-related mortality by 2030 for developed countries under several emissions scenarios 

and varying assumptions about acclimatization. For additional details, refer to response 5-37. 

Davis et al. (2004), who found the net effect of observed increases in temperature between 1964 

and 1988 had resulted in a net increase in mortality (see response 5-24), project mortality results 

in the future will vary depending on the seasonal distribution of warming. They project that a 

uniform 1°C warming (equal warming in summer and winter) would result in a net mortality 

decline of 2.65 deaths (per standard million) per metropolitan area analyzed, a summer-dominant 

warming would generate a net increase in mortality of 3.61 additional deaths (per standard 

million), and that a winter-dominant warming would produce a net decrease in mortality of 8.92 

fewer deaths (per standard million). 

McMichael et al. (2006) suggest that additional heat-related deaths in summer would outweigh 

the extra winter deaths averted globally in 2050 (refer to Figure 2 in that study). 

Deschenes and Greenstone (2007) find under a “business as usual” scenario, climate change will 

lead to an increase in the overall U.S. annual mortality rate ranging from 0.5% to 1.7% by the end 

of the 21st century (depending on choice of climate model). 

Older studies which project future changes in net mortality are discussed in response 5-28. 

Most of the studies above examine temperature changes across the year and then evaluate seasonal 

mortality relationships, which are incorporated to analyze the climate change impact or a summary of 

impacts across all temperatures. To quantitatively address the risk associated with the changes in extreme 

temperature events in a warming climate which tend to be most lethal, it would be necessary to project 

future changes in extremes while holding current conditions constant with respect to thresholds for 

extreme heat and cold and the associated mortality response, taking into account regional variation. The 

current literature lacks such an analysis. 

Comment (5-28): 

Commenter (3747.1) indicates that EPA removed from an earlier version of its TSD a statement 

describing how a majority of studies on the subject showed a larger decrease in cold-related deaths than 

increase in heat-related deaths. 

Response (5-28): 

15 
The version of the TSD the commenter is referring to (from the June 28, 2008, ANPR) stated the 

following: 

In the TAR [Third Assessment Report], the IPCC cited several studies that indicate 

decreases in winter mortality may be greater than increases in summer mortality in some 

temperate countries under climate change (McMichael et al, 2001). However, it cites one 

U.S. study (Kalkstein and Greene, 1997) that estimates increases in heat-related deaths 

will be three times greater than decreases in cold-related deaths. Given the paucity of 

recent literature on the subject and the challenges in estimating and projecting weatherrelated mortality, IPCC concludes additional research is needed to understand how the 

balance of heat-and cold-related deaths might change globally under different climate 

scenarios (Confalonieri et al, 2007). 

We decided to remove the first two sentences of this statement for two primary reasons: 

1) Of the five studies assessing net temperature-related mortality changes in IPCC’s Third 

Assessment Report, only two contained results applicable to the United States. One study showed 

a net decrease in mortality (Martens, 1998) and the other showed a net increase in mortality 

(Kalkstein and Greene, 1997, as described above) under climate change scenarios. So for the 

U.S., the studies in IPCC’s Third Assessment Report did not provide a clear picture with respect 

to the balance of heat and cold-related deaths. The other studies indicating temperature-related 

mortality would decline pertained to Europe (Donaldson et al., 2001; Langford and Bentham, 

1995) and Australia (Guest et al., 1999). 

2) In the April 2009 TSD, we focused on the most recent assessment literature, and relied primarily 

on IPCC’s Fourth Assessment Report (as opposed to the Third Assessment Report) as well as 

findings from the most recent assessment literature from CCSP/USGCRP (Ebi et al., 2008; Karl 

et al., 2009). 

Note that the third sentence in the above statement remains in the TSD. 

Comment (5-29):

A commenter (3347.3) notes the TSD fails to include the Ebi et al. (2008) statement finding that coldrelated mortality is likely underestimated. 

Response (5-29):

We have added to the TSD the statement that “Cold also contributes to deaths caused by respiratory and 

cardiovascular diseases, so the overall mortality burden is likely underestimated (Ebi et al., 2008).” 

Comment (5-30):

Commenters (3411.1, 3347.3, 11348,) suggest that direct effects of possible climate warming on 

temperature-related mortality are likely to be beneficial due to increases in life expectancy. 

Referencing Deschenes and Moretti (2009),1

 commenters (3347.3, 11348,) suggest the increased 

longevity that has arisen from migrations of large populations from the northern to the southern United 

 

1

 Some commenters referred to Deschenes and Moretti (2007), whereas others referred to Deschenes and Moretti 

(2009). These are essentially the same studies. The 2007 paper was published as a working paper; the 2009 paper 

was published in the Review of Economics and Statistics. It is cited as Deschenes and Moretti (2009) in these 

responses to comments. 

16 
States illustrates the benefits of increasing temperatures. A commenter notes that there are similar effects 

beginning in Europe. 

Response (5-30): 

We find that the commenters are drawing inappropriate conclusions from future warming and migration 

trends and inappropriately applying the results from Deschenes and Moretti (2009). 

The assessment literature does not explicitly address temperature effects on life expectancy or longevity. 

While we have reviewed Deschenes and Moretti (2009) and do not dispute migration to a warmer climate 

may have longevity benefits (whether in the United States or in Europe), we reject consideration of the 

estimated benefits from migration to a warmer climate as an appropriate analog to warming from GHGinduced climate change. The fundamental reason for this is that in estimating the health effects of climate 

change scenarios, individuals are explicitly assumed to stay in the same location (and the choice to 

migrate is a planned, adaptive response to temperature; see the Findings, Section III.C, “Adaptation and 

Mitigation,” for our response to comments on the treatment of adaptation and mitigation in the Findings). 

The assessment literature, as summarized in the TSD, is clear that local factors, such as climate, 

topography, heat-island magnitude, demographic and health characteristics of the population, and policies 

that affect the social and economic structures of communities, including urban design, energy policy, 

water use, and transportation planning, are important in determining the underlying temperature-mortality 

relationship in a population. In studies, mid-latitude metropolitan areas with greater summertime 

temperature variability have shown stronger adverse health responses to heat than desert and semitropical cities with less variable weather (e.g., Chestnut et al., 1998; Media-Ramon and Schwartz, 2007; 

Gosling et al., 2007, Davis et al., 2003b). 

Importantly, the longevity increase is expected to be the result of many variables and societal factors 

associated with the more southern areas that are associated with increased average temperature, making it 

hard to isolate the impacts of average temperature. Also, the health effects at issue are not associated with 

the increase in average temperature itself, but with the increased likelihood of changes in temperature 

extremes. 

Comment (5-31):

Commenters (3347.3, 3394.1, 3411.1, 11348) refer to Deschenes and Moretti (2009) and other studies 

(e.g., Kunst et al., 1993; Campbell-Lendrum et al., 2003) which indicate that heat deaths often represent a 

short temporal displacement but deaths due to cold usually result in months to years of life lost. 

Response (5-31):

We disagree with the commenter’s suggestion that there is a consensus with respect to the extent of 

mortality displacement that results from extreme heat or cold. 

“Mortality displacement” refers to forward temporal shift in the rate of mortality in a given population 

resulting from an environmental stressor—often heat or cold. It typically describes a situation where 

weakened people die a few days or weeks sooner than they would have under ordinary circumstances. 

(Such displacement is sometimes also described as “harvesting.”) 

Deschenes and Moretti (2009) use fixed temperature thresholds to define cold and hot days in all 

locations across the United States. They then find that, while hot days appear to have significantly 

increased mortality rates in the days immediately following the event, there is no signal of a lasting 

mortality impact of these hot days after 30 days. Their results for cold days are the opposite. The authors 

interpret these results as indicating that the short-term increases in mortality on hot days are offset in the 

17 
longer run by mortality displacement while cold days have a lasting impact in terms of increasing 

mortality rates. 

However, our review of the literature (including Kunst et al., 1993; Campbell-Lendrum et al., 2003) 

revealed considerable evidence that the concept of temperature-related mortality displacement is complex 

and observed impacts and estimates of the extent of mortality displacement may depend on the 

population/location affected and the characteristics of the heat or cold event. For example, Davis et al. 

(2004) caution that mortality displacement is not a universal feature in all cities, and the topic has not 

been examined systematically in the United States with respect to heat. Similarly, Kalkstein (1997) 

develops a range of estimates for discrete heat events in U.S. cities and finds varying signals with respect 

to the importance of mortality displacement. 

In addition, Medina-Ramon and Schwartz (2007) find evidence of short-term displacement for less 

extreme heat events in the United States but little evidence for short-term mortality displacement for 

extreme heat events. 

Studies following the European heat wave of 2003 found no evidence of short-term mortality 

displacement in France (Pirard et al., 2005) or Spain (Simon et al., 2005), while others have estimated that 

mortality displacement may have accounted for a very small fraction of the excess deaths in this event. 

Specifically, Le Tertre et al. (2006) estimated that less than 10% of the 3,000 excess deaths from nine 

cities in France could be attributed to mortality displacement, although the percentage varied widely 

among the individual cities. 

These studies would suggest that the individuals who died still had substantial periods of life remaining. 

The uncertainties surrounding the issue of mortality displacement and differing assumptions made about 

it contribute to the variability in projections of net mortality described in response 5-27. We note that 

Deschenes and Greenstone (2007), who explicitly apply methodologies to account for displacement, still 

project net increases in temperature-related mortality and decreases in longevity in the United States 

under future climate change scenarios. They indicate that, had they not accounted for the harvesting 

effects of heat and the fact that there is often a delay or lag between cold exposure and health impacts, the 

direct mortality impacts would have been overstated by roughly 47% to 202% (depending on the climate 

model). 

Most importantly, the discussion of mortality displacement with extreme heat and cold recognizes that 

these events result in observable increases in the daily mortality levels of the populations experiencing the 

conditions over different time periods. 

To summarize: given the uncertainty over the distribution and magnitude of mortality displacement, the 

importance we assign to mortality, the other evidence of the relative magnitude of heat versus cold 

mortality, and the precautionary nature of the Findings, we are not discounting the heat wave mortality 

risk in any fashion. 

Comment (5-32): 

A commenter (3136.1) notes: “Just because the IPCC doesn’t cite any studies looking at cold vs. heat 

related deaths in the U.S. in the future doesn’t mean that they don’t exist. For instance, the subject of 

Davis et al. (2004) is precisely this topic.” 

Response (5-32): 

18 
The TSD does not cite results from individual studies unless the specific results have been addressed in 

the assessment literature. We discuss the mortality projections in Davis et al. (2004) in response 5-27. 

Comment (5-33):

A commenter (3347.3) states that researchers have found that for heat waves, an increase above average 

mortality rates sometimes occurs, followed by a counterbalancing decrease in the average mortality rates 

in the following days to a few weeks, and that there is no statistical net effect in mortality incidence from 

exposure to heat waves (Campbell-Lendrum, 2003; Kalkstein, 1993; Huynen et al., 2001; Deschenes and 

Moretti, 2009). 

Response (5-33):

We disagree that the evidence suggests that heat waves result in no statistical net effect in mortality 

incidence. The body of literature cited by the commenter does not support such an assertion. 

Due to the mortality displacement described in response 5-31, it is true that the literature suggests there is 

sometimes a counterbalancing decrease in the average mortality rates in the days to few weeks following a 

heat wave. But “sometimes” is the key qualifier, as the literature contains examples in which there is no 

evidence of mortality displacement as described in response 5-31. 

We reviewed all five studies submitted by the commenter and found that—with one exception—they do 

not conclude that heat waves result in no statistical net effect in mortality incidence. 

Campbell-Lendrum (2003) reports: “There also is evidence for a ‘harvesting effect,’ i.e. a period 

of unusually lower mortality following an extreme temperature period. This indicates that in some 

cases extreme temperatures advance the deaths of vulnerable people by a relatively short period, 

rather than killing people who would otherwise have lived to average life expectancy. However, 

this effect has not been quantified for temperature exposures and is not included in the model.” 

(Italics indicate emphasis added.) 

Kalkstein (1993) reports results from two U.S. cities (New York and St. Louis) that indicate that 

“most extra mortality during heat episodes does reflect deaths that would not have happened 

shortly afterwards had there been no heat wave.” 

Huynen et al. (2001) report: “Our results relating to the heat-induced forward displacement of 

deaths are inconclusive. Some heat waves show a decline in mortality in the longer lag periods 

after the extreme heat, which suggests that heat has a harvesting effect, whereas others do not 

show this decline in the number of deaths.” 

Though Schwartz et al. (2004)2

 conclude that “much of the effect of hot temperatures is shortterm displacement of events,” their study is examining morbidity as opposed to mortality. 

Deschenes and Moretti (2009) do conclude that the “increase in mortality that occurs in the days 

immediately following heat waves appears entirely driven by temporal displacement” and that as a result 

“there is virtually no lasting impact of heat waves on mortality.” However, the authors caution: “Of 

course, every death is harvesting, because we all eventually die. The point here is that in a heat wave, 

some individuals die only a few days earlier than they would have, not a few months or years earlier.” As 

discussed in response 5-27, Deschenes and Greenstone (2007) project net increases in temperature-related 

mortality and life years lost under a warming climate in the United States despite the short mortality 

displacement for heat deaths. 

 

2

 The comment cites Schwartz et al. (2007); the commenter’s bibliography, which we believe is the accurate 

citation, refers to Schwartz et al. (2004). 

19 
In addition, there are other studies (e.g., Medina-Ramon and Schwartz, 2007; Le Tertre et al., 2006) 

whose results suggest that mortality displacement may play a relatively insignificant role in the observed 

excess mortality following a period of exceptional heat (see response 5-31) 

Considering all of these studies and those studies reviewed in response 5-31, we do not find the 

commenter’s statement that there is no net effect in mortality incidence from exposure to heat waves is 

supported by the evidence. 

Comment (5-34):

A commenter (3347.3) states that EPA is incorrect in suggesting that cold-related deaths are 

overestimated because it inappropriately considers influenza. The commenter refers to a study finding that 

influenza-like conditions are strongly correlated with low temperatures (Huynen et al., 2001), a study 

predicting that influenza will decrease with a warming climate (McMichael and Beers, 1994), and a study 

finding that controlling for influenza only diminished the aggregate mortality effect of cold weather by 

34% (Kunst et al., 1993). 

Response (5-34):

The commenter has misread the TSD: we do not state that cold-related deaths are overestimated and our 

review of the literature suggests that the strength of the association between temperature and influenza is 

uncertain. 

Summarizing the assessment literature (Ebi et al., 2008; Confalonieri et al., 2007), the TSD states that 

“Projections of cold-related deaths, and the potential for decreasing their numbers due to warmer winters, 

can be overestimated unless they take into account the effects of season and influenza, which is not 

strongly associated with monthly winter temperature.” This statement reflects the fact that there are 

important uncertainties in projecting cold-related mortality relating to the association between cold and 

influenza. 

The CCSP assessment on health (Ebi et al., 2008) states: “...many factors contribute to winter mortality, 

making the question of how climate change could affect mortality highly uncertain. No projections have 

been published that incorporate critical factors such as the influence of influenza outbreaks.” This 

information has been incorporated into the TSD. 

Regarding the literature submitted by the commenter, it does not provide evidence that there is stronger 

association between cold and influenza than implied by the TSD. Huynen et al. (2001) note that cold 

influences influenza “indirectly” and that “the fact that we were not able to correct for the effects of 

influenza is one of the flaws in our models.” We note that McGeehin and Mirabelli (2001) state: 

“influenza contributes to, but does not fully explain, the association between winter temperature and 

mortality.” 

We also reviewed McMichael and Beers (1994) and do not dispute their qualified statement that winter 

deaths from influenza “could be expected to decrease” with global warming. However, we note the study 

offers no details, original analysis, or assessment to accompany this statement. 

The Kunst et al. (1993) reference which finds that controlling for influenza incidence diminishes the 

aggregate mortality effect of cold weather by 34% clearly supports the finding of the assessment literature 

that not taking into account influenza in projections of cold-related mortality will result in an overestimate 

of its effects. 

20 
In summary, the assessment literature as summarized in the TSD appropriately characterizes the uncertain 

relationship between influenza and cold and the importance of accounting for this in projections of coldrelated mortality associated with climate change. 

Comment (5-35):

A commenter (3347.3) states that EPA treats sensitive and susceptible subpopulations differently with 

respect to impacts from heat and cold. The commenter notes that EPA lists the vulnerable populations for 

heat but not for cold. They refer to Deschenes and Moretti (2009), which find that susceptible populations 

for excess cold include older adults, the mentally ill (e.g., homeless), those working outdoors, and the 

socially isolated. 

Response (5-35):

We disagree that we do not identify populations vulnerable to excessive cold. Citing the assessment 

literature (Confalonieri et al., 2007), the TSD states: “Accidental cold exposure occurs mainly outdoors, 

among socially deprived people (e.g., alcoholics, the homeless), workers, and the elderly in temperate and 

cold climates, but cold waves also affect health in warmer climates.” These are essentially the same 

susceptible groups identified by the commenter and Deschenes and Moretti (2009). 

Comment (5-36):

Many commenters (e.g., 3136.1, 3187.3, 3283.1, 3347.3, 3449.1:8, 3596.1, and 4632) indicate that 

technological changes and adaptation have already reduced heat-related health effects and will 

sufficiently reduce an increase in heat-related health effects in the future. Many refer to literature (e.g., 

Kalkstein and Davis, 1989; Lerchl, 1998; Davis et al., 2004) that discusses adaptation to heat and/or its 

benefits. Commenters also indicate that humans physiologically adapt or acclimatize3

 to hotter climates 

over time, citing literature (e.g., Harrison, 1998; Kovats and Jendritzky, 2006) as evidence. 

Response (5-36): 

The assessment literature indicates that physical acclimatization to heat, adaptive measures, and 

technology reduce the human health impact of heat and will continue to do so in the future, but it is 

nonetheless indisputable that heat presently causes substantial mortality in the United States. The 

assessment literature clearly concludes the risk of adverse health effects from heat will increase as the 

climate warms. Therefore, we strongly disagree that technological changes, physical acclimatization, and 

adaptation will “sufficiently” reduce heat-related health risks in the future. 

We have reviewed the literature demonstrating the observed (e.g., Palecki et al., 2001; Fouillet et al., 

2008; Davis et al., 2003a, 2003b) and/or projected (e.g., Guest et al., 1999) benefits of adaptive measures 

in terms of reduced adverse health effects from heat. Many of the studies submitted by commenters are 

cited in the assessment literature and a following key conclusion that is drawn is stated in Section 7 of the 

TSD: “...human health risks from climate change will be strongly modulated by changes in health care, 

infrastructure, technology, and accessibility to health care (Field et al., 2007).” 

We also do not dispute that there is evidence (e.g., Kalkstein and Davis, 1989; Harrison, 1998; Kovats 

and Jendritzky, 2006) that humans physiologically adapt (or acclimatize) to hotter climates over time. In 

fact, the TSD, citing the assessment literature, states: “Estimates of heat-related mortality attributable to 

 

3

 “Heat acclimatization” refers to biological adaptations that reduce physiologic strain (e.g., heart rate and body 

temperature), improve physical work capabilities, improve comfort, and protect vital organs (brain, liver, kidneys, 

muscles) from heat injury. 

21 
climate change are reduced but not eliminated when assumptions about acclimatization and adaptation are 

included in models.” 

Furthermore, we agree technology (e.g., less climate-sensitive architecture and air conditioning) can 

reduce the health impacts of heat but it is not clear that it can eliminate them. Refer to additional 

discussion of air conditioning in response 5-52. 

However, despite the presence of physical acclimatization, technology, and adaptive measures, it is 

indisputable from the health statistics cited in the TSD (as summarized from the assessment literature) 

that heat kills. In fact, heat is the leading cause of temperature-related mortality in the United States, as 

stated in the assessment literature (Karl et al., 2009), summarized in the TSD, and discussed in response 

5-24. 

Under future climate change scenarios in which the United States warms, the argument that increased risk 

from hotter temperatures will be compensated by technology (e.g., air conditioning) and/or adaptation 

(which are interrelated) is not relevant in the context of these Findings. See the Findings, Section III.C, 

“Adaptation and Mitigation,” for our response to comments on the treatment of adaptation and mitigation 

in the Findings. Commenters do not present evidence that acclimatization alone will compensate for heatrelated health effects that have been projected into the future. Physical acclimatization, which is a form of 

autonomous adaptation, is considered relevant. However, a recent study (Kinney et al., 2008) indicates 

the timescales over which individuals or communities acclimate to local weather is not well understood. 

Comment (5-37):

A commenter (3347.3) argues that U.S. society has changed; therefore, past relationships between climate 

and mortality are not a reliable predictive basis for the future. The commenter refers to a Davis et al. 

(2004) study, which finds that on average for the 28 cities analyzed in that study, the number of excess 

deaths on hot and humid days declined from 41.0 in the 1960s and 1970s to 17.3 in the 1980s to only 10.5 

in the 1990s. The comment highlights the Davis et al. (2004) conclusions that temperature currently does 

not have a major influence on monthly mortality rates in the United States and that the lives saved in 

conjunction with warm winters tend to offset the deaths associated with warmer conditions in July and 

August. The comment also refers to a study by Campbell-Lendrum et al. (2003), which investigates the 

direct physiological effects of heat and cold on cardiovascular mortality. The study finds that when 

physiological adaptation and unmitigated emissions are assumed, there is no increase in mortality risk 

from cardiovascular disease attributable to climate change in any region of the world and a decrease in the 

developed world (including the United States). 

Response (5-37):

We do not dispute the general notion that past relationships between climate and mortality are not 

necessarily a reliable indicator for the future. We recognize, as stated in the TSD, that non-climatic 

factors such as changing demographics will influence past as well as future trends along with adaptive 

measures that might be adopted—though these are not germane to the Findings (e.g., see responses 5-36 

and 5-47). However, we disagree the references provided by the commenter provide strong evidence that 

a warming climate will not pose a risk of adverse health effects from heat in the future. 

Regarding the results presented from the Davis et al. (2004) study, we agree that heat-related mortality 

declined from the late 1960s into the 1990s in the major U.S. cities studied and that adaptation 

contributed to the decline. But this decline seems to have leveled off since the mid-1990s according to 

Sheridan et al. (2009). Refer to response 5-48 where this is discussed further. Regarding the finding that 

temperature does not have a major influence on monthly mortality rates in the United States, we note that 

the latest health statistics indicate that there are conservatively over 680 heat-related deaths per year; refer 

22 
to response 5-24 for further discussion. Regarding the Davis et al. (2004) projection that lives saved in 

conjunction with warm winters tend to offset the deaths associated with warmer conditions in July and 

August under certain scenarios (see response 5-27), their own results from the observed record suggest 

that heat deaths exceeded cold deaths from 1964 to 1998 as the climate warmed (see response 5-24). In 

summary, we do not find that Davis et al. (2004) provide evidence that would lead us to conclude that a 

warming climate will not increase the risk of adverse heat-related health effects. 

Reviewing Campbell-Lendrum et al. (2003), we agree that they find little net change in the risk of 

mortality in the scenarios presented for the year 2030. Though they note a very slight decrease in the risk 

of mortality for developed countries, which includes the United States, it is only after they make 

assumptions about physical acclimatization which they concede have “not been formally tested.” 

Furthermore, they note important latitudinal differences that are not resolved on a country-by-country 

basis in their study: “Climate change is expected to affect the distribution of deaths from the direct 

physiological effects of exposure to high or low temperatures (i.e. reduced mortality in winter, especially 

in high latitude countries, but increases in summer mortality, especially in low latitudes). However, the 

overall global effect on mortality is likely to be more or less neutral.” Though this study does not support 

an increased risk in temperature-related mortality in developed countries, its results are equivocal and 

consistent with the conclusions of the assessment literature that the net changes in temperature-related 

mortality are difficult to estimate. Refer to response 5-27 for additional discussion. 

Comment (5-38):

A commenter (11348) asserts that the benefits in life expectancy from warming in cold periods may be 

much more than nine times greater than lifespan lost in warm periods. 

Response (5-38):

The commenter (11348) provides no reference to support the assertion that life expectancy from warming 

in cold periods may be more than nine times greater than lifespan lost in warm periods. See our responses 

throughout this section for specific discussion of the broader issues. 

Comment (5-39):

Commenters refer to studies (Kunst et al., 1993; Langford and Bentham, 1995; Keatinge et al., 1997; 

Martens, 1998; Keatinge et al., 2000; Keatinge and Donaldson, 2004; Deschenes and Moretti, 2009; 

Laaidi et al., 2006) that provide evidence of, document, or project mortality benefits in winter from 

warming temperatures. 

Response (5-39):

We reviewed these studies and do not disagree with their findings that warmer winter temperatures reduce 

mortality during that season. In fact, the TSD summarizes the assessment literature conclusion that coldrelated mortality is projected to decrease under future climate scenarios. 

However, we also note that studies such as Medina-Ramon and Schwartz (2007) only consistently find a 

mortality impact for cold days across U.S. cities when cold days are defined based on the location’s 

annual temperature distribution (i.e. for unusually cold days in that city) instead of by absolute 

temperature levels. This suggests that there may be limited reduction in the mortality impact of cold snaps 

in most U.S. locations as long as these events are defined relative to a location’s weather experience. 

Comment (5-40):

23 
One commenter (11348), referencing a European study (Keatinge et al., 1997), suggests that there will be 

25,000–50,000 fewer deaths in the United States per year for a 1°C temperature rise. The commenter 

compares this to 30,000 deaths per year from breast cancer, 30,000 for prostate cancer, or about 40,000 

from motor vehicle accidents. 

Response (5-40):

We do not find this comment supportable. The temperature-mortality results from specific regions in 

Europe—such as those from Keatinge et al. (1997)—cannot credibly be projected on the entire United 

States. The assessment literature, as summarized in the TSD, clearly reflects that local factors, such as 

climate, topography, heat-island magnitude, demographic and health characteristics of the population, and 

policies that affect the social and economic structures of communities, including urban design, energy 

policy, water use and transportation planning are important in determining the underlying temperaturemortality relationship in a population (Confalonieri et al., 2007; Ebi et al., 2008). 

 

Climate conditions in the United States differ in important ways from Europe in that they are more 

variable with greater heat extremes, not to mention that there are important socioeconomic and 

demographic differences. In addition, Medina-Ramon and Schwartz (2007) report: “Despite a wide range 

of temperatures, the U.S .population seems fully acclimatised to cold temperatures, but not to heat. This 

may reflect the near universality of central heating in the United States, as opposed to central air 

conditioning, which explained a substantial fraction of the heterogeneity between cities in the heat 

effects.” 

Furthermore, the Keatinge et al. (1997) study reported estimated deaths associated with falling winter 

temperatures; it did not assess risks associated with rising summer temperatures, which the commenter 

fails to take into account. Finally, the commenter did not provide attribution for the statistics provided on 

death counts for breast cancer, prostate cancer, and motor vehicle accidents. 

Comment (5-41):

One commenter (11348) cites a report by the Department of Health of the United Kingdom (UK) that 

there was no increase in heat-related deaths from 1971 to 2002 despite warming summers, suggesting that 

the UK population is capable of adapting to warmer conditions. The report also notes that winter deaths 

will continue to decline. 

Response (5-41):

As discussed in previous responses (5-40), we find temperature-mortality studies from Europe should not 

be projected on the United States. 

Furthermore, EPA reviewed the referenced report by the Department of Health of the United Kingdom; 

we note that—directly after the quote provided by the commenter, which indicates that “there was no 

increase in heat-related deaths from 1971-2002”—the report states, “But heat waves still present a serious 

risk” and “While, periods of very cold weather will become less common, periods of very hot weather 

(heat waves) will become more common.” EPA notes the study projects temperature-related mortality out 

to 2012, yet predicts a 1 in 40 chance every year (a 1 in 4 risk in the decade centered on 2012) of a nineday heat wave at 27°C in southeast England. The report indicates that “Without preventive action, this 

could cause more than 3,000 immediate deaths with more than 6,350 heat-related deaths throughout that 

summer (Department of Health UK, 2008).” The authors also note that “in terms of conventional thinking 

about risk to health a risk of 1 in 40 is high.” 

More directly, the 2003 European heat wave was estimated to result in over 2,000 excess deaths in 

England and Wales from August 4 through 13, clarifying the risk of extreme heat in the United Kingdom 

24 
(Koppe et al., 2004). These impacts also resulted in the development of a national heat strategy to address 

heat waves (Department of Health UK, 2009). 

Regarding the report’s finding of a decline in winter deaths in the future, EPA notes that this is consistent 

with the underlying science of the IPCC and USGCRP assessments which EPA relies upon. For instance, 

the USGCRP notes that the number of deaths caused by extremely low temperatures would be expected to 

drop (Karl et al., 2009). 

Comment (5-42): 

A commenter (11348) suggests that the consequences of widespread cooling are likely to be much more 

threatening than warming. 

Response (5-42): 

Climate change projections in the assessment literature do not project cooling and, therefore, the health 

effects of cooling are not relevant to these Findings. 

Comment (5-43):

At least one commenter (11348) refers to studies by Moore (1995, 1998). The commenter claims that the 

1998 study estimated that a temperature increase of 2.5°C in the United States would cause a drop of 

40,000 deaths per year from respiratory and circulatory disease, based on U.S. mortality statistics as a 

function of monthly climate change. 

Response (5-43):

We reviewed the submitted publications and note that their results specific to temperature-related 

mortality are not current, not supported by other peer-reviewed studies, and not cited in the assessment 

literature. We note that IPCC and CCSP/USGCRP assessments had several opportunities to incorporate 

the results of these studies since their publication and declined. Further, though Moore (1998) was 

published in the peer-reviewed literature, Moore (1995) was not. Refer to the Findings, Section III.A., for 

the science on which the decisions are based. 

With respect to specific results from the Moore (1998) study, we note that the study models the 

relationship between monthly and annual mortality rates and monthly and annual temperatures. As the 

impacts of extreme heat events often manifest themselves over a series of days, this is an unsupportable 

assumption. This study, therefore, does not explicitly isolate extreme heat events, which are known to be 

associated with elevated mortality and projected to increase as a result of climate change. 

Therefore, we do not agree the publications of Moore from 1995 and 1998 are relevant, nor that their 

findings are supportable. 

Comment 5-44): 

A number of commenters (e.g., 11348, 3411.1) contend that because all-cause mortality is greater in 

winter than summer in the United States, a warming climate will result in a net decrease in temperaturerelated mortality. 

At least one commenter (11348) disagrees with the McMichael et al. (2006) finding that heat-related 

deaths will increase more than the lives saved by warming of the cold periods. The commenter refers to 

“previous data” showing that U.S. mortality in winter due to cardiac, vascular, and respiratory disease in 

25 
winter is seven times greater than in summer, and also that this ratio is about nine to 10 in Europe, from 

the data of Keatinge et al. (1997). The commenter (11348) further asserts that the most comprehensive 

data on U.S. daily mortality, from all causes, as a function of the day of the year, is found in Deschenes 

and Moretti (2009). The commenter states that these data show a clear relationship, with maximum 

mortality in January and minimum mortality in the warmest months of July and August. The commenter 

contends that these data strongly indicate that warming of average daily temperatures would cause a 

decrease in mortality in winter far greater than the slight increase of mortality from summer heat. 

Other commenters (3187.3, 3411.1, and 4632) also reference the Laaidi et al. (2006) and/or others (i.e., 

Braga et al., 2002) as evidence that winter-related mortality is greater than summer-related mortality. 

Response (5-44): 

Though we do not dispute that all-cause mortality is greater in winter than in summer in the United States, 

this information alone does not and cannot substantiate that a warming climate will result in net 

reductions in mortality. Studies (e.g., Davis et al., 2004; Andersen and Bell, 2009) show that the direct 

relationship between winter temperatures and mortality is much weaker than for summer; this is 

especially true for infectious and respiratory illnesses. In fact, McGeehin and Mirabelli (2001) note: 

“Overall mortality is generally higher in winter than in summer, but there is little convincing evidence 

that weather patterns are solely responsible.” (Regarding the comment stating that U.S. mortality is much 

greater in winter than in summer citing “previous data” we note this comment does not make clear which 

previous data it is referring to.) 

Furthermore, EPA notes that the seasonality highlighted by the commenter and depicted in Figure 1 of 

Deschenes and Moretti (2009) is not representative of regional differences in temperature exposure (for 

example, see Figure 2 in the same study). These data do not convey that people in hotter cities are more 

affected by cold temperatures; on the other hand, it is well documented in the scientific assessment 

literature (Media-Ramon and Schwartz, 2007; Gosling et al., 2007; McMichael et al., 2006; Ebi et al., 

2006; Curriero et al., 2002; Davis et al., 2002) that people in colder cities are more affected by warmer 

temperatures. This finding is also confirmed in the study referenced by the commenter (Laaidi et al., 

2006), which finds that excessive heat is more likely to increase heat-related mortality in colder areas 

since the thermal optimum (critical temperature threshold) is lower for the population in these areas. 

Accordingly, these studies do not warrant rejecting the conclusion that temperature-related mortality may 

increase as stated in McMichael et al. (2006) and Deschenes and Greenstone (2007) (refer to response 5-

27). 

Comment (5-45): 

Commenters (3136.1, 3596.1) provide two side-by-side graphs of U.S. mortality trends and U.S. 

temperature trends from 1980 to 2006 (CDC, http://www.cdc.gov/nchs/data/nvsr/nvsr56/nvsr56_16.pdf; 

National Climatic Data Center, http://climvis.ncdc.noaa.gov/cgi-bin/cag3/hr-display3.pl). These graphs, 

state the commenters, show that we are greatly triumphing over climate change, or perhaps that a warmer 

climate is a healthier climate. The commenters indicate that perhaps the most direct evidence of health 

and welfare is mortality rates, which have improved significantly over the last 100 years, and submit a 

graph of all-cause mortality and U.S. mean surface temperature for the 1980–2006 period in support of 

this point. The commenter notes that it would take a true pessimist to think this strong trend toward 

decreasing mortality rates will reverse itself in the future, no matter what the climate holds in store—

primarily because the impact of climate on human health in the United States is minuscule, according to 

findings by Davis et al. (2004). 

26 
Another commenter (2898.1) indicates that public health and welfare will continue to improve, even in a 

warming world. In support of this view the commenter submits a reference by Indur Goklany (2007) 

entitled, “The Improving State of the World: Why We’re Living Together, Healthier, More Comfortable 

Lives on a Cleaner Planet.” 

Response (5-45): 

EPA reviewed the graphs provided by the commenter, as well as the associated referenced literature, and 

finds that they do not support the commenters’ conclusions with respect to heat-related mortality due to 

climate change. 

These two graphs depict “all cause mortality” and “U.S. mean surface temperature” for the 1980–2006 

period. The metrics of crude and age-adjusted mortality represented in these graphs are influenced by all 

known factors that lead to mortality and do not represent or isolate the role of temperature or any other 

individual factor. Over the period represented in the graphs, mortality has decreased in United States as a 

result of several factors, such as technological and medical advances, improved health care, regulatory 

statutes, increases in life-expectancy, and improved emergency preparedness. In addition, the general 

trend in average annual temperature indicates warming but does not represent the specific weather events 

that are of concern for heat-related mortality. As a result, the trends depicted in the graphs provide little 

information regarding the direct health effects associated with extreme heat exposure or temperature in 

general. Two graphs showing that “all cause” mortality declined do not provide evidence to support a 

claim that mortality from every cause declined. All they would show is that the overall morality declined, 

reflecting changes that reduced mortality outweighing any changes that increased mortality. It does not 

show what changes increased and what changes decreased mortality. Moreover, these graphs do not 

represent conditions in the future in which extreme heat events are expected to increase in frequency, 

duration, and intensity, nor the future drivers affecting vulnerability to heat-related mortality (i.e., urban 

heat island effects, demographic trends of older age brackets). 

We do not dispute that Davis et al. (2004) find that the observed temperature-related mortality rates are 

very low relative to the baseline total (all-cause) death rate. However, as noted in a previous response, 

Davis et al. (2004) find that the net impact of the observed temperature change from 1964 to 1998 was to 

cause an extra 2.9 deaths (per standard million) per city per year in 28 cities, which represents thousands 

of total deaths. 

Regarding the comment that measures to protect public health and welfare will continue to improve, even 

in a warming world based on evidence from Goklany (2007), we conclude for reasons stated above that 

this evidence does not support changing our Findings of the presence of risk or the potential for 

increasing risk in the future from climate change. 

Comment (5-46):

A commenter (3347.3) states that Longstreth (1991) suggests that if, with global warming, populations in 

the northern U.S. cities became like those in the South, then full acclimatization will have occurred and 

little or no impact from global warming is predicted. 

Response (5-46):

We find this comment to be a mischaracterization of the results of Longstreth (1991). In fact, the author 

states: 

Studies based on two general circulation model scenarios in urban areas that include 

several from North America predict that the number of heat-related deaths will double by 

the year 2020 and increase severalfold by 2050. These numbers may be reduced if 

27 
changes in climate occur over an extended time so populations can become acclimatized 

to the new conditions (1,9). Although climate change could also bring milder winters and 

a drop in winter death rates, the predicted increase in death rates from hotter summers 

may be such that there is a net increase in deaths associated with changing climate (21). 

This excerpt from Longstreth (1991) clearly demonstrates that the study does not state acclimatization 

will result in little or no impact from global warming. To the contrary, the study only suggests that there 

may be a decrease in the overall impact from heat stress as a result of acclimatization, and that the net 

effect of climate change may be to increase deaths. 

Comment (5-47):

Commenters indicate the population’s rapid adaptation to heat has been demonstrated after the 1995 

Chicago heat wave (Palecki et al., 2001), after heat waves in Philadelphia in 1993 and 1994, and across 

Europe after the 2003 heat wave event (Fouillet et al., 2008). The commenter notes that it is one thing for 

EPA to state that summer extreme temperatures may be related to global warming; it is another to relate 

them to individual events without elaborating more fully. Furthermore, the commenter that notes a major 

adaptation to heat waves occurred in France as a result of the 2003 disaster. The commenter indicates that 

when a heat wave of similar magnitude struck in 2006, far fewer deaths occurred than were predicted 

(Fouillet et al., 2008). The commenter suggests that the words “depending upon progress in health care” 

in the TSD are an attempt to influence the reader into thinking that people are unlikely to adapt, when in 

fact there is incontrovertible evidence they already have. 

Response (5-47):

Regarding recent heat wave events and the assertion (from commenter 3136.1) that EPA does not provide 

sufficient information about the human response: citing the assessment literature (Confalonieri et al., 

2007; Karl et al., 2009), the TSD has added specific information about the European heat wave in 2003, 

its effects, and implications for the future: 

The excess mortality during the extreme heat wave in Europe in 2003 demonstrates the lethality 

of such events, which led to approximately 15,000 deaths in France alone (Confalonieri et al., 

2007). Karl et al. (2009) report that an analysis of the European summer heat wave of 2003 found 

that the risk of such a heat wave is now roughly four times greater than it would have been in the 

absence of human-induced climate change. 

The specific adaptive responses to the 2003 European heat wave or other individual heat waves such as 

those that occurred in Philadelphia and Chicago are not relevant to these Findings. See the Findings, 

Section III.C, “Adaptation and Mitigation,” for our response to comments on the treatment of adaptation 

and mitigation in the Findings. 

Comment (5-48):

One commenter (3136.1) indicates that he has shown that sensitivity to extreme heat events has been 

declining in major cities across the United States and notes this result is only apparent when you correctly 

standardize the population for changing size and age distribution. Furthermore, the commenter indicates 

that without properly standardizing, it is impossible to compare the climate impacts from one period to 

another (or one place to another) and that once you do standardize you find that extreme heat is having 

less of an impact as we better adapt to its occurrence. The commenter refers to Davis et al. (2003a, 

2003b), who find that heat-related mortality declined in 28 major U.S. cities even as temperatures rose. 

28 
Response (5-48):

We do not dispute the findings of Davis et al. (2003a, 2003b) presented here. In fact, the assessment 

literature, as summarized in the TSD, refers to the Davis et al. (2003a, 2003b) papers; it states that heatrelated mortality in major U.S. cities declined from 1964 to 1998 and that adaptive measure contributed to 

the decline. However, it is not clear that the results of Davis et al. remain relevant. We note that the 

assessment literature, as summarized in the TSD, finds that this decreased sensitivity or decline in heatrelated mortality may not be as pronounced in the future since access to air conditioning is already high in 

most regions (Ebi et al., 2008). We note that recent work by Sheridan et al. (2009) indicates that the 

general decline in heat-related deaths that had been observed since the 1970s leveled off in the mid1990s, which is summarized the latest assessment literature (Karl et al., 2009) and the TSD. Additional 

discussion of air conditioning can be found in response 5-52. 

Comment (5-49): 

A commenter (3136.1) indicates that the TSD’s statement that “possible implications for human health of 

these projected changes in temperature extremes are discussed in Section 7(b)” is misleading, as it 

contains no reference to the highly documented phenomenon of adaptation to increasing heat-wave 

frequency. They suggest that EPA might substitute “some implications,” which they state is more honest 

and also weakens the TSD as support for endangerment. 

 

Response (5-49): 

EPA notes that these comments pertain to the TSD associated with the ANPR released in July 2008. 

Reflecting this comment, we updated the version of the TSD released with the April 2009 proposal to 

include information about heat sensitivity to increasing temperatures in the context where the underlying 

references already take into account certain assumptions about adaptation in the context of climate 

change. 

See the Findings, Section III.C, “Adaptation and Mitigation,” for our response to comments on the 

treatment of adaptation and mitigation in the Findings. 

Comment (5-50): 

A commenter (3136.1) indicates that just because there are more elderly people living now and in the 

future does not mean they are at greater risk. If they were, the commenter indicates, life expectancy could 

not be increasing. The commenter notes that older adults are clearly living longer despite increased 

exposure to heat. The commenter posits that it is a hard argument to make that future heat wave mortality 

will increase despite the fact that historically the trend has been exactly the opposite, even with increasing 

heat and humidity. According to the commenter, the fact that more of the populace tends to live in cities 

but that age-adjusted death rates have not increased over time in these areas actually weakens EPA’s 

argument for CO2 impacts. Another commenter (3347.3) states that EPA incorrectly assumes that heatrelated mortality risks will increase as the U.S. population ages because it ignores the likelihood of further 

development of climate-mitigating technology over this period. 

Response (5-50): 

EPA has reviewed the commenter’s argument and finds that the reasoning is flawed and the conclusions 

are not supported by the scientific assessment literature. EPA notes that life expectancy is increasing in 

the United States and other developed countries for a variety of reasons (e.g., economic growth, public 

health measures, and technology). The fact that life expectancy is increasing does not mean that the 

mortality rate associated with every cause of death is declining, however. To the contrary, we know that 

death rates from some causes can and are increasing while others are decreasing, and that the overall trend 

29 
in recent years has been lower mortality from all causes combined. Thus, EPA concludes that life 

expectancy and heat-related mortality can both increase as long as some other factor(s) exceed(s) the rate 

of change in heat-related mortality. The issue before EPA concerns the impact of temperature-related 

mortality, and how this impact might incrementally affect the otherwise expected trends in life 

expectancy mortality. 

In addition, the assessment literature unambiguously indicates that advanced age represents one of the 

most significant risk factors for heat-related death in the United States, and this is summarized in the 

TSD. Increased life expectancy and projected growth in older age brackets (e.g., the aging baby boomer 

generation, as noted in assessment literature) will increase the overall number of vulnerable individuals 

who may be exposed to more extreme heat conditions in the future (under documented climate change 

scenarios). 

Finally, commenters are assuming that the risks posed to the elderly by an increase in heat waves will be 

modulated by adaptive actions. See the Findings, Section III.C, “Adaptation and Mitigation,” for our 

response to comments on the treatment of adaptation and mitigation in the Findings. 

Comment (5-51): 

Commenters (3136.1, 3316.1, and 3596.1) contend that EPA misinterprets the series of the Davis et al. 

(2002, 2003, and 2004) studies summarized in the TSD (as cited in the assessment literature) due to the 

juxtaposition of the April 2009 statement: 

Estimates of heat-related mortality attributable to climate change are reduced but not 

eliminated when assumptions about acclimatization and adaptation are included in 

models. Confalionieri et al. (2007) cite a series of studies that suggests populations in the 

U.S. became less sensitive to high temperatures over the period 1964 to 1988, in part, due 

to these factors. 

with the statement it precedes: 

On the other hand, growing numbers of older adults will increase the size of the 

population at risk because of a decreased ability to thermo-regulate is a normal part of the 

aging process (Confalonieri et al., 2007). In addition, according to a study in Confalonieri 

et al. (2007), almost all the growth in population in the next 50 years is expected to occur 

in cities where temperatures tend to be higher due to the urban heat island32 effect 

increasing the total number of people at risk of adverse health outcomes from heat. 

The commenters state the Davis et al. papers show that heat-related mortality is lowest in U.S. cities that 

have the oldest population distributions (Tampa and Phoenix). The commenters indicate that it is true that 

as the population ages, the number of individuals susceptible to extreme heat effects increases, but this 

has nothing to do with climate change. Further, the commenters indicate that the effects of population age 

structure are accounted for in the Davis et al. (2003) papers and the results indicate that the overall 

population’s sensitivity to extreme heat has been declining across the United States, including for the 

elderly, from the 1960s through the 1990s. The commenters note the TSD indicates 1988 as the ending of 

the time period for this study, whereas it should be 1998. 

Response (5-51):

We have carefully reviewed the TSD and find we have not misinterpreted the findings from Davis et al. 

The fact that some of the cities with the oldest population distributions have the lowest heat-related 

mortality as demonstrated in Davis et al. does not alter the fact that the population of this most vulnerable 

30 
age-group is projected to grow. It is well-established cities like Tampa and Phoenix that have lower heatrelated mortality, as measured in terms of excess deaths, because climate variability is less there and the 

population is generally acclimated to warm temperatures (Curriero et al., 2002). Cities with highest 

climate variability, such as those in the Midwest and Northeast, are likely to experience the greatest 

number of illnesses and deaths in response to changes in summer temperatures (e.g., see McGeehin and 

Mirabelli, 2001; Curriero et al., 2002). 

We agree with the commenters that projections for an increasing elderly population are independent of 

climate change and note the April 2009 and final TSD state: “...non-climatic factors related to 

demographics will have a significant influence on future heat-related mortality.” 

Please refer to response 5-48 for a discussion of the Davis et al. finding that the population’s sensitivity to 

extreme heat has been declining. We also note that recent work by Sheridan et al. (2009) indicates that the 

general decline in heat-related deaths that had been observed since the 1970s leveled off in the mid1990s, which is summarized the latest assessment literature (Karl et al., 2009) and the TSD. 

EPA has updated the final TSD to reflect the study period (1968 to 1998) in reference to the series of 

studies (Davis et al., 2002, 2003, and 2004) cited by IPCC. 

Comment (5-52): 

Commenters (3347.1, 3347.3) assert that EPA incorrectly assumes that routine social and economic 

adaptation to temperature changes will not occur despite the increasing availability of air conditioning 

with increases in income. One of these commenters (3347.3) contends that clear historical evidence shows 

that air conditioning use reduces mortality in extreme heat events and refers to literature demonstrating 

the benefits of air conditioning in terms of reduced health effects from heat (e.g., Kilbourne et al., 1982; 

Kalkstein, 1993; Semenza et al., 1996, Davis et al., 2004; Seretakis et al., 1997; Basu and Samet, 2002). 

The commenter states although the use of air conditioning has grown continuously as Americans’ 

incomes have risen and technology prices have fallen, EPA assumes that growth will now stop. The 

commenter refers to census data showing that the percentage of housing in the United States without air 

conditioning decreased from 46.5% in 1978 to 19.2% in 2005. The commenter cites a study (Stern et al. 

cited in Kalkstein et al., 1997) that projects that air conditioning will be “nearly universal” in 2050 and 

refers to a mathematical relationship between the availability of air conditioning and income (from Issaac 

and van Vuuren, 2009). 

Response (5-52): 

We do not assume that adaptation to temperature change will not occur and we find that the assessment 

literature suggests access to air conditioning is already high, if not reaching near saturation. Nonetheless, 

heat continues to harm or kill people in the United States. 

As discussed in response 5-7, the TSD now states: “human health risks from climate change will be 

strongly modulated by changes in health care, infrastructure, technology, and accessibility to health care 

(Field et al., 2007).” Regarding air conditioning, we agree with the commenter that air conditioning 

reduces mortality in extreme heat events. We have reviewed the literature submitted on this issue and 

concur with findings presented. And we also agree with the statistics cited by the commenter showing that 

the percentage of housing in the United States without air conditioning has decreased. In fact, the TSD 

now states that the assessment literature has found access to air condition is high in most regions of the 

United States (Ebi et al., 2008). 

Despite the increase in air conditioning, the assessment literature refers to Sheridan et al. (2009), which 

finds that the general decline in heat-related deaths observed from the 1970s to the mid-1990s seems to 

31 
have leveled off. This information is now summarized in the TSD. This evidence suggests that people 

remain subject to adverse health effects from heat in spite of increasing access to air conditioning. 

Furthermore, studies and reports from past heat events (e.g., National Weather Service, 2004; Sheridan, 

2007; Luber and McGeehin, 2008) have demonstrated that not everyone with access to air conditioning 

uses it during heat events due to their financial situation and/or cognitive impairments. In other words, 

even if air conditioning prevalence were to increase independent of climate change, the evidence suggests 

that there would still be heat-related mortality risk. 

Accordingly, despite projections in the references submitted for increasing access to air conditioning for 

the future—which we do not dispute—it is not clear that adverse heat-related health outcomes will 

decline. Finally, the argument that increased risk from hotter temperatures will be compensated for by 

technology (e.g., air conditioning) and/or adaptation (which are interrelated) is not relevant in the context 

of these Findings. See the Findings, Section III.C, “Adaptation and Mitigation,” for our response to 

comments on the treatment of adaptation and mitigation in the Findings. 

Comment (5-53): 

Commenters (3502.1, Commonwealth of Massachusetts and the States of Arizona, California, 

Connecticut, Illinois, Iowa, Maine, Maryland, New Jersey, New Mexico, New York, Oregon, Rhode 

Island, Washington, and New York City) submit a 33-page document, including a manuscript of a paper 

accepted for publication in the July 2009 issue of Journal of Epidemiology entitled “Extreme High 

Temperatures and Hospital Admissions for Respiratory and Cardiovascular Diseases” (Lin et al., 2009). 

The commenters indicate that the study found the following: For each degree increase in temperature 

above a threshold (28.9°C), there was a significant increase in hospitalizations due to respiratory diseases 

on the same day (immediate effects). Similarly, for each degree increase above a threshold (29.4°C), there 

was a significant increase several days after exposure in hospitalizations due to cardiovascular diseases 

(likely due to the fact that it can take several days for cardiovascular effects to manifest). The diseases 

most associated with rises in temperature were asthma, chronic pulmonary obstructive disease, ischemic 

heart disease (heart attacks), and abnormal heart rhythms. For respiratory diseases, the risks for Hispanics 

were higher than those for non-Hispanics, and people living in low-income neighborhoods were at higher 

risk than those in high-income neighborhoods. Elderly people also had higher increased hospitalization 

risks for both disease types. 

The commenters indicate that based on the results of the Lin et al. (2009) study, it is reasonable to 

conclude that the number of hospitalizations can be expected to significantly increase in the future due to 

a warming climate. In addition, the commenters indicate the results of this study further confirm EPA’s 

conclusion that GHG emissions endanger public health. The commenters state: “We concur with EPA’s 

approach to its proposed finding as to public health and strongly agree that even though the projected 

risks and impacts to public health are indirect, as opposed to resulting from direct exposure to greenhouse 

gas emissions, they constitute reasonably anticipated endangerment within the meaning of the statute.” 

Response (5-53):

EPA has reviewed the submitted reference and finds that it is consistent with the literature summarized in 

the TSD. The study (manuscript) by Lin et al. (2009) provides information on the association of high 

temperatures and morbidity, which is useful since such data are limited. It supports the TSD summary of 

the assessment literature, which finds: “Hot temperatures have also been associated with increased 

morbidity. A study cited in Field et al. (2007) indicates increased hospital admissions for cardiovascular 

disease and emergency room visits have been documented in parts of North America during heat events.” 

32 
Comment (5-54): 

A commenter (3722) indicates that the health impacts and mortality associated with increased temperature 

are considerably less than those associated with cold; and that anticipated warming over the next 50 to 

100 years will actually decrease mortality. The commenter suggests that this is not a new issue and that 

older literature supports their assertion. The commenter (3722RI0A, B, C, D) submits four references in 

support of their comments (Bull, 1973; Bull and Morton, 1975a, 1975b, 1978). These references are also 

cited by the NIPCC report entitled, “Climate Change Reconsidered” (Idso and Singer 2009) (as 

referenced by commenter 7031, for example), which also contends that these studies suggest mortality 

decreases as temperatures rise. 

Response (5-54): 

EPA has reviewed the submitted references and we do not find they support the commenter’s assertion. 

These studies mainly apply to England and Wales; in the one study that analyzes New York City, the 

results do not imply that warm weather reduces mortality rates. 

These studies were published in the 1970s, and discuss the relationship of temperature changes and 

changes in death rates of specific health conditions. They are primarily focused on studying the 

relationships between temperature change and the health response of myocardial and cerebral infarction, 

particularly in the elderly. 

We first note that the first three of the studies listed above find that changes in temperature typically are 

inversely associated with death rates except for stroke, and the second study (Bull and Morton, 1975a) 

does find that high temperature on the day of onset is associated with an increase in deaths on that day. 

These studies, however, were conducted in England and Wales, which do not experience the same climate 

variability as many parts of the United States; therefore, the results may not be applicable in the United 

States (see response 5-40 for further discussion). 

We note that the most recent of the four studies (Bull and Morton, 1978), which includes New York City 

in its analysis, obtains results that differ importantly from the first three studies. It finds in all three 

locations, but particularly New York, “[a]bove 20°C deaths rise steeply as the temperature rises...,” 

demonstrating the lethal effect of high temperatures, particularly for a U.S. location with a strongly 

variable climate. The study concludes: “there is a close association between temperature and death rates 

from most diseases and at all temperatures.” 

Importantly, these studies do not directly address climate change or long-term trends in health effects 

related to climate variables. Since their publication, many studies that are specifically focused on the 

impacts of climate change on health in the United States have been published, and the findings of this 

literature are summarized in the TSD. 

Comment (5-55): 

A commenter (3187.3) indicates that the claim that warming increases morbidity rates is a myth. The 

commenter states that Dr. Robert Mendelsohn, an environmental economist from Yale University, argues 

that heat-stress deaths are caused by temperature variability, not warming, and that those deaths grow in 

number not as climates warm but as the variability in climate increases. The commenter notes that excess 

deaths are greatest in metropolitan areas among the elderly and when the nighttime readings stay high 

(80o

F or greater) and the heat lasts more than a few days. 

Response (5-55): 

We disagree with the commenter’s contention that warming will not increase morbidity or mortality. 

33 
(We note the comment indicates that morbidity does not increase with climate warming; however, the 

substance of the comment is related to mortality. Although both morbidity and mortality are important in 

terms of human health impacts and risks from climate change, EPA does not view these terms as 

interchangeable.) The assessment literature, as cited in the TSD, is very clear that excessive heat 

contributes to increases in both morbidity and mortality. 

The commenter indicates that Dr. Robert Mendelsohn argues that heat-stress deaths are caused by 

temperature variability and not a warming climate. We disagree with this argument and, furthermore, find 

that the commenter does not substantiate the claim that Mendelsohn makes this argument. Numerous 

studies (e.g., Kalkstein and Greene, 1997; Curriero et al., 2002; Davis et al., 2003a; Laaidi et al., 2006) 

find that temperature-related mortality increases when threshold conditions, typically defined exclusively 

or in large part by temperature measures, are crossed. If climate change increases the probability of a 

location exceeding that threshold, mortality will rise, all else being equal. The commenter refers to 

Mendelsohn’s book (Mendelsohn and Neumann, 1999), but we find no statement in that book to indicate 

that heat-stress deaths are not caused by a warming climate. In the introductory chapter, authors 

Mendelsohn, Smith, and Neumann summarize a study by Kalkstein and Davis (1989) that finds that 

climate change could increase heat stress mortality. However, the authors then state: “These judgments 

about sizable health effects from climate change may be premature. Uncertainties about the role of 

climate variability and human adaptation to heat stress make it difficult to predict the magnitude of the 

effect.” Though the authors express some skepticism about the results of Kalkstein and Davis (1989), this 

is not at all the same as stating that heat stress deaths are not caused by a warming climate. We further 

note the book was published in 1999, and we now have a decade of additional science, which the TSD 

summarizes. 

We agree that the risks from heat waves are highest for older adults and that heat waves of long duration 

with high nighttime minimum temperatures are often deadly. 

Comment (5-56):

A commenter (0300) claims that the greenhouse effect will have beneficial moderation of nighttime low 

temperatures, but no effect on daytime highs, because clouds from water vapor feedback warm at all 

hours but cool during the day. Another commenter (3411.1) refers to the study of Robeson (2002) which 

shows temperature variability has declined with warming in the United States. 

Response (5-56):

We disagree that daytime highs will not increase and that the effects of warming nighttime minimum 

temperature will have beneficial effects on human health. 

While the observational record in the United States has shown greater increases in minimum temperatures 

than maximum temperatures in recent decades (as noted in Robeson, 2002), daytime highs are still rising. 

The TSD, citing the assessment literature (Field et al., 2007; Kunkel et al., 2008) notes in Section 4(c) 

that “daily minimum (nighttime) temperatures have warmed more than daily maximum (daytime) 

temperatures” but also states in Section 4(k) that “the annual percent of days exceeding the 90th, 95th, 

and 97.5 percentile thresholds for both maximum (hottest daytime highs) ... have increased.” These 

statements are further supported by a recent study by Meehl et al. (2009) that finds that the current ratio of 

daily record high maximum temperatures to record low minimum temperatures averaged across the 

United States is about two to one. Refer to Response to Comments Volume 2 for further discussion of 

observed maximum and minimum temperatures in the United States. 

Future projections of climate warming are not limited to nighttime temperatures because a positive water 

vapor feedback does not operate solely at night—and the commenter presents no evidence to the contrary. 

34 
For further discussion of the water vapor feedback, please refer to Response to Comments Volume 4. We 

note Robeson (2002) finds: “Although the variability of air temperature may decrease or remain 

unchanged at most locations in the contiguous USA [under climate change], the probability of extremely 

high air temperatures should still increase...” In fact, climate model projections indicate substantial 

daytime warming. Summarizing the assessment literature in Section 6(e), the TSD notes: “Karl et al. 

(2008) find for a mid-range scenario (A1B) of future GHG emissions, a day so hot that it is currently 

experienced only once every 20 years would occur every three years by the middle of the century over 

much of the continental United States; by the end of the century, it would occur every other year or 

more.” Furthermore, 

As noted in the previous comment and response (5-55), high minimum temperatures also contribute to 

heat stress. A number of studies (e.g., Kalkstein, 1991; Chestnut et al., 1998; Dixon, 1999; Basu and 

Samet, 2002) have linked high minimum (nighttime) temperatures with elevated mortality. For example, 

Basu and Samet (2002) noted several temperature-mortality studies identified a minimum temperature 

above which effects of temperature on mortality were observed and that these temperatures varied by 

location. 

To summarize: both daytime and nighttime temperatures are projected to increase, and the evidence 

suggests that both will result in increasing risk of adverse health effects. 

Comment (5-57):

A commenter (3187.3) states that the risk of heat-related deaths may be increased by policies that limit 

reliable traditional energy sources in favor of renewable energy such as wind power, which increase the 

likelihood of brownouts and blackouts. The comment notes that it is during the normal heat waves that 

energy demand is the greatest. The commenter asserts that during extremes of heat and cold, high 

pressure dominates, causing winds to be below the threshold for energy generation, and that this has 

already been shown in Texas, California, and the UK. The commenter states that this type of policy, not 

the weather, puts the population at enhanced risk. 

Response (5-57):

Regarding the commenter’s perspective that policies favoring renewable energy are responsible for 

impacts during extreme weather, EPA notes that this action does not propose any policies concerning 

mitigation and considers this issue beyond the scope of the Findings.

Comment (5-58):

A commenter (3347.3) contends that EPA cites U.S.-specific heat-related mortality projections from 

IPCC that suffer from exposure mischaracterization. The commenter indicates that the projections are 

based on a “place-time” model which assumes that outdoor temperature is a surrogate for personal 

exposure to heat, even though people in the United States generally spend most of their time indoors. 

They suggest these projections should use the “micro-environmental” model, which uses a time-weighted 

sum of heat exposure to project mortality, citing Basu and Samet (2002). 

Response (5-58):

We disagree that the projections of heat-related mortality for the United States referred to in the TSD 

suffer from exposure mischaracterization. Contrary to the commenter’s assertions, the methodology used 

to project heat-related mortality does not assume people are spending most of their time outdoors. 

35 
In the TSD, EPA summarizes mortality projections described in IPCC (Field et al., 2007) from one study 

(Hayhoe et al., 2004). In the study, heat-related mortality projections for Los Angeles are developed using 

algorithms that are based on the historical, empirically developed relationships between mortality and air 

mass characteristics (e.g., temperature and humidity) in that city. Because the projections are based on 

empirically based associations, it is not necessary to control for exposure using methods described in 

Basu and Samet (2002). 

Comment (5-59):

Some commenters (e.g., 1543, 3353, 5379, 6510, 6941, 11249) express concern about the effects that 

extreme weather—such as heat waves, droughts, floods, wildfires, and hurricanes—has had or would 

have on the safety and health of humans. The commenters state that such events can result in the spread of 

infectious disease, malnutrition, and poor air and water quality because runoff from these events contains 

agricultural wastes, metals, pesticides, pathogens, dangerous chemicals, and fecal indicator bacteria. 

Response (5-59): 

We have carefully reviewed the commenters’ concerns regarding the effects of extreme weather events 

(heat waves, droughts, floods, wildfires, and hurricanes). We note that the TSD contains information on 

the human health effects of extreme events as well as information on the vulnerabilities of populations, 

communities, and locations to such events. In addition, we note that the TSD summarizes the scientific 

literature with regard to observations and projections of extreme events in Sections 4 and 6, respectively.

Comment (5-60): 

A commenter (3475.10) submits a reference by Delfino et al. (2009) entitled, “The Relationship of 

Respiratory and Cardiovascular Hospital Administrations to the Southern California Wildfires of 2003.” 

The commenter summarizes the study’s general conclusions with respect to wildfire-related PM2.5 leading 

to increased respiratory hospital admissions, especially asthma, and suggesting that better preventive 

measures are required to reduce morbidity among vulnerable populations. 

Response (5-60): 

EPA reviewed this study and finds its conclusions on the health impacts of wildfires to be consistent with 

the assessment literature summarized in Section 7(b) of the TSD. For example, the TSD indicates a study 

cited by IPCC (Confalonieri et al., 2007) indicating that large fires are also accompanied by an increased 

number of patients seeking emergency services for inhalation of smoke and ash. See also the discussion 

of wildfire frequency in Sections 8(b) and 10(b) of the TSD, and response to comments on this issue in 

Volume 6 of the Response to Comments document. 

See the Findings, Section III.C, “Adaptation and Mitigation,” for our response to comments on the 

treatment of adaptation and mitigation in the Findings. 

Comment (5-61): 

A commenter (3722) indicates that it is true that flood, severe storms, fire, and disease can cause human 

injury and death; however, the fundamental issue with this portion of the TSD is that of causation. The 

commenter indicates that EPA has not established elsewhere in the TSD that climate change that is 

occurring is in fact having a material impact on these kinds of disastrous events, or that human 

contribution to climate change is the causative factor in such impacts. This fundamental issue, states the 

commenter, undercuts Sections 7 and 8 of the TSD. The commenter provides an example of the extreme 

36 
event impacts from floods and storms as compared to the evidence provided in the TSD. The commenter 

refers to the following information in the TSD (as paraphrased by the commenter): 

The IPCC projects a very likely increase in heavy precipitation event frequency over 

most areas as described in Sections 6. Increases in the frequency of heavy precipitation 

events are associated with increased risk of deaths and injuries as well as infectious, 

respiratory and skin diseases. Flood health impacts include deaths, injuries, infectious 

diseases, intoxications and mental health problems. 

The commenter then, referring to Figure 2c in study, notes that despite projections of increased flooding 

in the United States, no increased trends in flood-related damages have been detected (Downton et al., 

2005) while temperatures and CO2 have been rising. 

Response (5-61):

We have carefully reviewed the comments and referenced literature provided by the commenter. We note 

that the Downton et al. (2005) study also provides two additional graphics (Figures 2a and 2b of that 

study) related to flooding trends. They both appear to support an upward (increase) trend flooding over 

the past century. Further, we conclude that this information does not convey an evaluation of risks 

associated with flooding and storms in future conditions of a warming climate. We will continue to rely 

on the science summarized in the TSD on this issue. Please also refer to Volume 7 of these responses to 

comments for further discussion of the changes in flood damage over time versus the increased risk of 

flood. 

The commenter also appears to be challenging the notion of attribution of observed climate change and 

extreme events as the basis for projected climate change impacts. See Volume 2, “Attribution of 

Observed and Measured Climate,” and Volume 3, “Change and Validity of Future Projections,” of this 

Response to Comments document for our responses to comments on these issues. See Volume 9 for 

EPA’s responses on the Administrator’s determination, in general and with respect to climate impacts. 

Comment (5-62):

A commenter (3283.1) indicates that EPA cites floods, storms, droughts, and wildfires as human health 

risks. The risks listed are death, injury, disease, intoxications, increased exposure to smoke and ash, and 

mental health problems. The commenter notes that while disease is a public health issue, in the future, 

improved medical technology will all but eliminate elevated disease risks due to extreme events. 

Similarly, the commenter indicates that improved forest management practices can be used to minimize 

health risks due to wildfires. 

Response (5-62):

As noted in the TSD and summarized from the scientific literature, human health risks from climate 

change will be strongly modulated by changes in health care, infrastructure, technology, and accessibility 

to heath care (Field et al., 2007). However, the commenter fails to provide any supporting evidence that 

improved medical technology will all but eliminate elevated disease risks due to extreme events. 

Similarly, the commenter fails to provide supporting information that improved forest management 

practices will effectively reduce health risks. In addition, see the Findings, Section III.C, “Adaptation and 

Mitigation,” for our response to comments on the treatment of adaptation and mitigation in the Findings. 

 

Comment (5-63): 

37 
A commenter (10050.1) submits brief comments and several references on the subject of the impacts of 

global warming on the mental health of those impacted. The commenter indicates that as GHG emissions 

continue to soar and fuel the problems associated with climate change, severe harm will come to the 

mental wellbeing of millions of Americans and citizens around the world. The commenter further states 

that while we often hear that the public’s physical health will face increasing threats from droughts, 

floods, storms, food shortages, higher temperatures, and climate change’s related repercussions, many 

more members of the public will experience increased rates of anxiety, depression, conflict, and other 

psychological problems that damage lives and spirits for years to come. 

The commenter indicates that WHO, CDC, and even the U.S. military now recognize that climate change 

is on track to be one of the most significant contributors to behavioral problems on the planet. In support 

of the proposed endangerment finding, the commenter indicates that projected climate impacts including 

rising temperatures, water scarcity, devastating storms (i.e., hurricane Katrina), air pollution, and a rise in 

infectious diseases will adversely affect society and the psychological wellbeing of millions of people 

around the world. 

Another commenter (3421) notes that an important health consequence not mentioned in the TSD is the 

risk to mental health. The commenter states that the toll on mental health from surviving an extreme 

weather event, deprivation of food and water, forced relocation, and worry about “what comes next” can 

be expected to far surpass the physical injuries and illnesses of climate change. 

Response (5-63): 

EPA has reviewed and considered the submitted references concerning mental health effects. We note the 

commenter provides a study indicating that severe weather events, such as coastal areas experienced with 

hurricane Katrina in 2005, engender severe anxiety, depression, grief, anger, family problems, work 

problems, conflict, and, potentially, post-traumatic stress disorder that can last for years (Galea et al., 

2007). 

EPA agrees with commenter that climate change effects, particularly those related to some extreme 

events, may pose mental health risks. We conclude the commenter’s views are supported in the TSD. For 

example, the assessment literature, as summarized in the TSD, refers to mental health problems that arise 

from flood impacts (Confalonieri et al., 2007), which are projected to become more extreme (Karl et al., 

2009). The TSD also notes the IPCC (2007b) finding that intense hurricanes—which are projected to 

increase—are linked to increases in post-traumatic stress disorder. These findings are generally consistent 

with the literature as referenced by the commenter (e.g., Bourque et al., 2006; Kessler et al., 2008; Weems 

et al., 2007; Weisler et al., 2006), which documents mental health problems that arise from certain 

extreme weather events. 

Comment (5-64): 

A commenter (2818) indicates that EPA’s technical documents did not really mention the mental health 

effects of climate change. The commenter indicates that mental health problems, although much harder to 

see, are likely to impact far more people than just injury and illness. The commenter states that mental 

health impacts would manifest themselves in things like depression, anxiety, and post-traumatic stress 

disorder from living through traumatic events. The commenter notes that hurricane Katrina demonstrated 

that people who have lived through a traumatic event such as that have far greater problems with medical 

conditions as well as mental health conditions; their health indicators have gone down precipitously. 

Response (5-64): 

EPA agrees with the commenter that mental health effects associated with extreme events are an 

important consideration, and notes that this issue is addressed in Section 7 of the TSD, though briefly. 

38 
Section 7(b) summarizes scientific findings that flood health impacts include deaths, injuries, infectious 

diseases, intoxications, and mental health problems (Confalonieri et al., 2007). Further the TSD notes, in 

Section 7, that high-impact events can overwhelm and disrupt social organizations, which can leave 

people displaced and without necessary post-event assistance. In addition, the TSD notes increased 

deaths, injuries, infectious diseases, and stress-related disorders and other adverse effects associated with 

social disruption and migration from more frequent extreme weather (Field et al., 2007). Our review of 

the assessment literature has also found that there is limited information on the mental health impacts 

associated with climate change. 

Comment (5-65):

Some commenters specifically mention the migration of tropical diseases (0311) such as West Nile virus 

(3893, 4184, 11249) and malaria and dengue fever (1507, 3680.1, 10838, 11357). One commenter (6510) 

mentions the spread of disease-carrying vectors into new habitats as a specific impact, which will increase 

health-related morbidity and mortality. One commenter (6733) discusses the rise in the number of 

disease-carrying mosquitoes. 

Response (5-65):

While the commenters do not provide specific references for these observations and views, we note that 

they are generally consistent with the scientifically based findings summarized in the TSD, especially in 

Section 6. We note that several human and other diseases are sensitive to climate. As indicated in the 

TSD, there are several important associations between climate and water-, vector-, and food-borne 

diseases. Based on the science and research from major assessments (IPCC, USGCRP), we conclude that 

certain disease may occur more often and affect new populations, as a result of changes in temperature 

and precipitation that allow these pathogens to expand into new geographic regions. 

Comment (5-66): 

Commenters (e.g., 3347.3, 3921.1) indicate that dengue fever and other vector-borne diseases have 

become an endangerment to American public health because of climate change. Commenters state that 

vectors and infectious agents are cold-blooded, and because breeding sites have increased due to changing 

temperature and precipitation, vector and agent development has accelerated, their geographic range has 

shifted to higher latitudes and altitudes, and their seasonal period of disease risk has lengthened. The 

commenters state that these diseases are only one piece of the huge threat to the United States and urge 

EPA to take action. 

Response (5-66): 

We agree that climate increases the risk of certain diseases to spread or emerge in areas where they had 

previously been limited or not existed, and we find that these risks are appropriately summarized in the 

TSD as reflected in the assessment literature. We also agree with the commenter that in addition to risks 

associated with infectious diseases, there are various other risks due to climate change. Please see the 

appropriate volumes of this Response to Comments document for our responses to comments on other 

impacts of climate change that affect public health and welfare. 

Comment (5-67): 

A number of commenters (e.g., 0339, 0700.1, 3283.1, 3316.1, 3347.3, 3449.1:10, 3722, and 10158) argue 

that statements made in the TSD regarding the spread of infectious and vector-borne diseases as a result 

of temperature and precipitation changes are speculative, that they are not scientifically supportable, 

and/or that there is there is no demonstrated link between climate change and disease. Some commenters 

39 
suggest that the TSD relies on inferred health effects based on temperature sensitivity as a proxy for 

public health impacts in the United States. 

Response (5-67): 

We have reviewed the assessment literature in light of these comments, and we find that the TSD’s 

summary of the current state of the science on this topic as reflected in the assessment literature is 

accurate and sound. The assessment literature is clear that certain vector-borne diseases and other 

infectious diseases are sensitive to climate and that climate change increases the risk of exposure in a 

number of ways. As noted in the TSD, the incidence of airborne infectious diseases (e.g., 

coccidioidomycosis) varies seasonally and annually, due partly to climate variations such as drought 

(Field et al., 2007; Karl et al., 2008). It also notes that waterborne disease outbreaks are distinctly 

seasonal, suggesting potential underlying environmental or weather control, clustered in particular 

watersheds, and associated with heavy precipitation. It further states that food-borne diseases show some 

relationship with temperature based on Confalonieri et al. (2007). 

The CCSP assessment Analyses of the Effects of Global Change on Human Health and Welfare and 

Human Systems includes additional detail on this topic, stating that “[s]everal important pathogens that 

are commonly transmitted by food or water may be susceptible to changes in replication, survival, 

persistence, habitat range, and transmission under changing climatic and environmental conditions” (Ebi 

et al., 2008). Similarly, IPCC (Confalonieri et al., 2007; Field et al., 2007) references a number of studies 

documenting links between climate and disease. 

Based upon our careful review of the literature, we have determined that the comment that the TSD relies 

only on inferred health effects is incorrect. Our review of the assessment literature indicates that there are 

documented links between climate change and disease, and that these are appropriately summarized in the 

TSD. As the TSD notes, studies discussed in Field et al. (2007) linked above-average temperatures in the 

United States during the summers of 2002–2004 to the greatest transmissions of West Vile virus. The 

TSD also reports that associations between temperature and precipitation and tick-borne Lyme disease are 

noted by IPCC (Field et al., 2007), as well as the finding from CCSP (2008b) that there will likely be an 

increase in the spread of several foodborne and waterborne pathogens among susceptible populations 

depending on the pathogens’ survival, persistence, habitat range, and transmission under changing 

environmental conditions. 

CCSP (Ebi et al., 2008) includes extensive discussion of this topic that is consistent with the TSD’s 

summary. Table 2.2 in Ebi et al. lists a number of pathogens, the climate-related driver, the possible 

influence of climate change, the likelihood of changes, the basis for assessment, and the peer-reviewed 

references underlying the assessment. It reports, among other things, that increasing temperature is likely 

to be associated with increasing clinical cases of Salmonella. It also reports that increasing temperature is 

extremely likely to be associated with higher environmental prevalence of Vibrio species and associated 

disease, and very likely to be associated with range expansion. 

 

Comment (5-68):

Several commenters (e.g., 7031) referred to the NIPCC report (Singer and Idso, 2009) which contends 

that the projected spread of tick-borne diseases is based on a speculative assumption of steadily increasing 

temperature and other assumptions. 

Response (5-68): 

We have reviewed the assessment literature in light of this comment, and we disagree that the projected 

spread of tick-borne disease is “speculative.” The assessment literature, as summarized in the TSD, 

clearly demonstrates relationships between tick-borne diseases and climate. IPCC (Field et al., 2007) 

40 
reports on studies indicating that Lyme disease, a prevalent tick-borne disease in North America, has an 

association with temperature (Ogden et al., 2004) and precipitation (McCabe and Bunnell, 2004). IPCC 

refers to a study (Ogden et al., 2006) that projects that the northern range limit for the tick responsible for 

transmitting Lyme disease could shift north by 200 kilometers by the 2020s, and 1,000 kilometers by the 

2080s (based on model projections under IPCC Special Report on Emissions Scenarios (SRES) A2 

emissions scenario) (Field et al., 2007). CCSP (2008b) reinforces these statements, reporting that studies 

suggest that temperature influences the distributions of Ixodes species ticks that transmit pathogens 

causing Lyme disease in the United States (Brownstein et al., 2003) and Canada (Ogden et al., 2006). 

EPA concludes that the TSD’s summary of the current state of the science on this topic as reflected in the 

assessment literature is accurate and sound. 

Please refer to Volume 4 for EPA’s responses to comments specific to the validity of future projections of 

climatic variables important for disease transmission such as temperature and precipitation. 

Comment (5-69):

A commenter (3136.1) indicates that most tropical diseases occur in the tropics not because the weather is 

warm, but because public health measures are poor. Similarly, a commenter (3722) notes that EPA 

ignores the fact that public health advancements, availability of health care, and other socioeconomic 

factors unrelated to climate change play a far greater role in the spread of disease than warming 

temperatures. Commenters (e.g., 3136.1, 3283.1, and 3316.1) note that prior to public health intervention 

(such as in the late 1800s), malaria was common in non-tropical areas (including high latitudes). They 

indicate that the spread of malaria is easily preventable and that public health measures are far more 

effective at controlling disease outbreaks than attempting to control global climate. Commenters (3136.1, 

3316.1) contend that malaria is weakly related to climate but strongly related to poverty, arguing that the 

resurgence of malaria in some developing countries is related to the ban of DDT, anti-malaria drug 

resistance, and the breakdown of public health systems, not any ascertainable changes in climate. 

Commenters also note that EPA acknowledges that locally acquired cases of malaria in the United States 

have been virtually eliminated, and thus the Agency relies on the effects to other countries under the guise 

of public health impacts in the United States. One commenter (4509) submitted an interview with Paul 

Reiter entitled “Global Warming Won’t Spread Malaria (EIR, 2007). Another commenter indicates that 

the NIPCC book Climate Change Reconsidered states that the global spread of malaria related to CO2-

induced warming is not supported in the scientific literature. 

Response (5-69):

Commenters are correct when they note that the TSD states that locally acquired cases of malaria have 

been virtually eliminated in the United States, in part due to effective public health interventions. We also 

agree that public health interventions have reduced malaria in other parts of the world. EPA never states 

that temperature is the only determinant in the transmission of malaria and the TSD is clear that a number 

of factors impact transmission. However, we disagree with commenters who dismiss the possibility that 

climate change may impact the spread of malaria in some areas (globally) based on our review of the 

assessment literature. 

IPCC (Confalonieri et al., 2007), citing several studies (Hay et al., 2002a; Craig et al., 2004), reports the 

spatial distribution, intensity of transmission, and seasonality of malaria is influenced by climate in subSaharan Africa. It notes that studies have reported associations between interannual variability in 

temperature and malaria in the African highlands. IPCC (Confalonieri et al., 2007) also indicates that 

malaria risk is well associated with climatic factors such as rainfall patterns and the El Niño Southern 

Oscillation (ENSO) in Southern Asia and South America. IPCC (Confalonieri et al., 2007) concludes that 

there are known causal links between climate and malaria transmission dynamics, but that there is still 

41 
much uncertainty about the potential impacts of climate change on malaria at local and global scales 

because of the paucity of concurrent detailed historical observations of climate and malaria, the 

complexity of malaria diseases dynamics, and the importance of non-climatic factors, including 

socioeconomic development, immunity, and drug resistance, in determining infection and infection 

outcomes. Accordingly, we find the TSD’s qualified discussion of possible linkages between climate 

change and malaria (in Sections 7 and 16b), appropriately summarizes the assessment literature. 

See the Findings, Section III.C, Adaptation and Mitigation, for our response to comments on the 

treatment of adaptation and mitigation in the Findings. 

Comment (5-70):

A commenter (3136.1) argues that climate change has nothing to do with the reason why West Nile virus 

now exists in the United States, and that the reason it was not found in the United States in the past was 

simply that it had not been introduced until recently. 

Response (5-70):

The assertion that climate change has nothing to do with why West Nile virus currently exists in the 

United States is irrelevant when considering the effects climate change has on the transmission of this 

disease now and in the future. We have reviewed the assessment literature in light of this comment and 

we find that the TSD’s summary is accurate. The TSD notes that a study cited by Field et al. (2007) 

linking above-average temperatures in the United States during the summers of 2002–2004 to the greatest 

transmissions of West Nile virus. 

The assessment literature includes additional detail on this topic that is consistent with the TSD’s overall 

discussion of climate-sensitive diseases. Karl et al. (2009) cite a study (Kilpatrick et al., 2008) which 

found that transmission of both strains of West Nile virus accelerated sharply with increasing 

temperature, such that small increases in temperature had relatively large effects on transmission. This 

laboratory study suggests that both viral evolution and temperature influence the distribution and intensity 

of transmission of West Nile virus, and provides a model for predicting the impact of temperature and 

global warming on virus transmission (Kilpatrick et al., 2008). Karl et al. (2009) report that the study 

suggests that greater risks from West Nile virus may result from increases in the frequency of heat waves, 

but note that the risk will also depend on the effectiveness of mosquito control programs. 

Comment (5-71):

One commenter (3136.1) indicates that there is no evidence linking climate change to past or future Saint 

Louis encephalitis outbreaks in the United States. The comment contends the TSD makes unsubstantiated 

claims of increased risk of Saint Louis encephalitis during La Niña weather events. 

Response (5-71):

The TSD does not state that there is explicit evidence linking Saint Louis encephalitis and climate change, 

but rather summarizes a study (Cayan et al., 2003) cited by IPCC (Field et al., 2007) finding a 

relationship between Saint Louis encephalitis and hot, dry La Niña years. We, therefore, disagree with the 

assertion that the TSD makes unsubstantiated claims on this topic. Rather, we find that it appropriately 

summarizes the conclusions of the assessment literature. 

Comment (5-72): 

42 
A number of commenters (e.g., 3347.3, 3449.1:10, and 3747) state that many factors other than climate, 

such as the availability of an adequate health system, are more important to the incidence of disease than 

climate, or that the impacts of climate on food and water-borne pathogens are not the only factors 

determining the risk of human injuries, illness, and death. Some commenters state that the risk of disease 

following flooding in developed countries is generally low. 

Response (5-72): 

We agree that many non-climate factors are important for the incidence of disease. The TSD includes 

information from the assessment literature on this topic, noting, for example, the IPCC (Field et al., 2007) 

conclusion that human health risks from climate change will be strongly modulated by changes in health 

care, infrastructure, technology, and accessibility to health care. 

The fact that many factors are important to the incidence of disease does not mean that climate change is 

not one of them. As discussed throughout this section of the Response to Comments document, the 

assessment literature clearly indicates that some diseases transmitted by food, water, and insects are likely 

to increase due to climate change (Karl et al., 2009). 

In regard to the risk of disease due to flooding, the TSD notes that the United States has successful 

programs to protect water quality under the Safe Drinking Water Act and the Clean Water Act but adds 

that some contamination pathways and routes of exposure do not fall under regulatory programs (e.g., 

dermal absorption from floodwaters, swimming in lakes and ponds with elevated pathogen levels). The 

TSD additionally notes that the primary climate-related factors that affect these pathogens include 

temperature, precipitation, extreme weather events, and shifts in ecological regimes, adding that 

consistent with the latest understanding of climate change on human health, the impact of foodborne and 

waterborne pathogens will seldom be the only factor determining the burden of human injuries, illness, 

and death (CCSP, 2008b). 

CCSP (Peterson et al., 2008) assesses this issue in more detail. It reports that “Floods directly promote 

transmission of water-borne diseases by causing mingling of untreated or partially treated sewage with 

freshwater sources, as well as indirectly from the breakdown of normal infrastructure causing post-flood 

loss of sanitation and fresh water supplies (Atherholt et al., 1998; Rose et al., 2000; Curriero et al., 2001; 

Patz et al., 2003; O’Connor, 2002).” The report goes on to report the following: 

Analyses of the U.S. indicate that the assumption that developed countries have low 

vulnerability may be premature, as independent studies have repeatedly concluded that 

water and food-borne pathogens (that cause diarrhea) will likely increase with projected 

increases in regional flooding events, primarily by contamination of main waterways 

(Rose et al., 2000; Ebi et al., 2006). 

A U.S. study documented that 51% of waterborne disease outbreaks were preceded by 

precipitation events in the top 10% of occurrences, with 68% of outbreaks preceded by 

precipitation in the top 20% (Curriero et al., 2001). These outbreaks comprised mainly 

intestinal disorders due to contaminated well water or water treatment facilities that 

allowed microbial pathogens, such as E. coli, to enter drinking water. In 1993, 54 people 

in Milwaukee, Wisconsin died in the largest reported flood-related disease outbreak 

(Curriero et al., 2001). The costs associated with this one outbreak were $31.7 million in 

medical costs and $64.6 million in productivity losses (Corso et al., 2003). 

CCSP (2008b) also includes an analysis of the potential impacts of flooding, noting that “[f]ixed 

infrastructure itself has the potential to be adversely impacted by climate change, which can increase 

43 
vulnerability to climate change. For example, flooding can overwhelm sanitation infrastructure and lead 

to water related illnesses (Grambsch and Menne, 2003).” 

To better explain the link between flooding and climate-sensitive diseases and incorporate the CCSP 

assessment of this topic, we have modified the summary of Section 7(c) of the TSD to read as follows: 

Waterborne disease outbreaks are distinctly seasonal (which suggests potential 

underlying environmental or weather control), clustered in particular watersheds, and 

associated with heavy precipitation. IPCC (Confalonieri et al., 2007) reports that the risk 

of infectious disease following flooding in high-income countries is generally low, 

although increases in respiratory and diarrheal diseases have been reported after floods. 

However, CCSP (Peterson et al., 2008) finds that analyses of the United States indicate 

that the assumption that developed countries have low vulnerability may be premature, 

citing to studies that “have repeatedly concluded that water and food-borne pathogens 

(that cause diarrhea) will likely increase with projected increases in regional flooding 

events, primarily by contamination of main waterways.” In another report, CCSP (2008b) 

notes that flooding can overwhelm sanitation infrastructure and lead to water-related 

illnesses. A U.S. study documented that 51% of waterborne disease outbreaks were 

preceded by precipitation events in the top 10% of occurrences, with 68% of outbreaks 

preceded by precipitation in the top 20% (Curriero et al., 2001, cited in Peterson et al., 

2008). After hurricanes Katrina and Rita in 2005, contamination of water supplies with 

fecal bacteria led to many cases of diarrheal illness and some deaths (Ebi et al., 2008; 

CDC, 2005; Confalonieri et al., 2007). 

This new text replaces the previous text from the April 2009 version that read: 

Waterborne disease outbreaks are distinctly seasonal (which suggests potential 

underlying environmental or weather control), clustered in particular watersheds, and 

associated with heavy precipitation. The risk of infectious disease following flooding in 

high-income countries is generally low, although increases in respiratory and diarrheal 

diseases have been reported after floods (Confalonieri et al, 2007). For example, after 

Hurricanes Katrina and Rita in 2005, contamination of water supplies with fecal bacteria 

led to many cases of diarrheal illness and some deaths (Ebi et al., 2008; CDC, 2005; 

Confalonieri et al, 2007) 

As the CCSP findings quoted above show, there is considerable evidence that high-precipitation events 

associated with climate change are likely to increase the likelihood of waterborne disease outbreaks in 

parts of the United States. Therefore, EPA concludes that the TSD’s summary of the current state of the 

science on this topic as reflected in the assessment literature is accurate and sound. 

Comment (5-73):

A commenter (3347.3) asserts that EPA ignores important contrary scientific conclusions on climatesensitive disease. The commenter points to a statement in the CCSP assessment on health effects (Ebi et 

al., 2009) not in the April 2009 TSD that concludes: “For the U.S., it is not anticipated that climate 

change will lead to loss of life or years of life due to chronic illness or injury from waterborne or 

foodborne illnesses.” The commenter requests that EPA add this statement to the TSD.

Response (5-73):

We have added this statement from Ebi et al. (2008) to Section 7c of the TSD. However, as stated in the 

TSD, Ebi et al. (2008) indicate that there will likely be an increase in the spread of several foodborne and 

44 
waterborne pathogens among susceptible populations depending on the pathogens’ survival, persistence, 

habitat range, and transmission under changing climate and environmental conditions (CCSP 2008b). As 

noted in response 5-72, deaths were attributed to water contamination in the wake of Hurricanes Katrina 

and Rita. 

Comment (5-74):

One commenter (1616.1) indicates that diseases naturally vary with climate and that as climate changes, 

diseases will undoubtedly change, but there is no reason to think there will be a net change for the worse 

in the future. 

Response (5-74): 

We disagree with this comment and note that it provides no references to substantiate its assertion that 

climate change will not make diseases worse. As discussed in response 5-67, the assessment literature 

(e.g., Ebi et al., 2008; Karl et al., 2009) finds that some diseases transmitted by food, water, and insects 

are likely to increase due to climate change. 

Comment (5-75): 

A commenter (3501) indicates that of unique concern in the western United States are rates of valley 

fever (coccidioidomycosis), which have quadrupled in the last 10 years, primarily due to weather pattern 

changes which will likely continue as the climate warms. The commenter also indicates that ocean 

temperature changes directly influence waterborne disease distribution; in particular, outbreaks of the 

waterborne disease cholera are directly linked to warmer ocean temperatures. The commenter indicates 

that studies have shown that ENSO events and associated warming of regional ocean surface waters 

induce algae blooms that harbor the pathogen Vibrio cholerae, ultimately leading to disease outbreaks in 

coastal areas. The commenter also indicate that rising temperatures directly impact urban air quality by 

accelerating ozone formation and heat-related illness in urban areas is also on the rise and states that 

approximately 70,000 people in Europe died during the 2003 heat wave. The commenter states that 

numerous studies show a clear relationship between temperature and such things as hospitalizations for 

respiratory diseases as well as sudden cardiac death, but does not reference any specific studies. 

Response (5-75):

We agree that climate change will affect human health in a variety of ways and find that these comments 

are generally consistent with the underlying scientific literature summarized in the TSD; however, we 

note that the statements in the comment do not in all cases employ the careful qualifying language the 

TSD uses in summarizing the conclusions of the assessment literature. Please see other responses in this 

section for our responses to comments on specific diseases discussed in the TSD. Please see responses 5-

11, 5-20, 5-86, and 5-92 for some example responses to comments on links between climate change and 

respiratory diseases. 

Comment (5-76):

One commenter (3347.3) claims that “EPA often fails to adequately explain the context of research results 

that could significantly affect the applicability of those results to estimates from climate change,” citing as 

an example the TSD’s treatment of links between temperature and the incidence of human disease from 

food- and water-borne pathogens such as the Salmonella and Vibrio species. The commenter states that a 

study cited by Confalonieri et al. (2007) (Mclaughlin et al., 2005) includes important relevant information 

omitted by EPA, such as that the oysters involved were consumed raw. 

45 
Response (5-76): 

We have reviewed our summary of the assessment literature in light of this comment. On the basis of our 

review, we have determined that the commenter’s claim that we failed to adequately explain the context 

of research results that could significantly affect the applicability of those results to estimates from 

climate change is incorrect and not substantiated by the evidence cited. 

We have reviewed the assessment literature’s treatment of links between temperature and the incidence of 

human disease from food- and water-borne pathogens such as the Salmonella and Vibrio species and the 

source study referenced by the commenter. On the basis of this review, we have concluded that the TSD 

accurately summarizes this information. The fact that the outbreak at issue involved oysters consumed 

raw is in no way inconsistent with the TSD’s summary of assessment literature conclusions on this issue, 

which is as follows: 

 

Vibrio spp. infections from shellfish consumption may also be influenced by temperature 

(Confalonieri et al., 2007). For example, Confalonieri et al. (2007) cited a study 

documenting a 2004 outbreak of V. parahaemolyticus linked to atypically high 

temperatures in costal water. 

This statement is fully consistent with the conclusions of other assessment reports. Karl et al. (2009), for 

example, note that “[t]here is a close association between temperature, Vibrio sp. abundance, and clinical 

illness.” 

EPA concludes that the TSD’s summary of the current state of the science on this topic as reflected in the 

assessment literature is reasonable and sound. 

Comment (5-77): 

With regard to EPA’s summary of assessment literature conclusions on West Nile virus, one commenter 

(3347.3) states that “The incidence of infectious disease has a complex etiology, and cannot be ascribed to 

one factor alone.” The commenter adds that “the incidence of a disease is not evidence of causation.” 

Response (5-77): 

We agree that incidence of infectious disease has a complex etiology and cannot be ascribed to one factor 

alone. The TSD does not claim that West Nile Virus or any other infections disease will be affected by 

climate change acting in isolation. Rather, it notes that the study discussed in Field et al. (2007) linked 

above-average temperatures in the United States during the summers of 2002-2004 to the greatest 

transmissions of West Nile virus. Consistent with Field et al. (2007), the statement uses the world 

“linked” rather than “caused” but is still clearly in general agreement with the conclusion from Karl et al. 

(2009) that some diseases transmitted by food, water, and insects are likely to increase due to climate 

change. The term “likely” indicates the degree of certainty about the causal link between climate change 

and the increased transmission of some diseases. 

Comment (5-78):

One commenter (3347.3) argues that statements in the TSD regarding Lyme disease are questionable and 

not well supported by existing research. The commenter states that “[r]ecent research shows that climate 

change is projected to decrease the geographic range of tick-borne encephalitis (TBE) in areas of lower 

latitude and elevation if transmission expands Northward (Randolph, 2004, Randolph and Rogers, 2000 

in CCSP). These same researchers also found that changing patterns of TBE in Europe are not 

consistently related to changing climate.” The commenter then references research in the Baltics (Sumilo 

46 
et al., 2007) that, according to the commenter, finds that a sudden jump in climate suitability for TBE in 

1989 did not result in a landscape-wide increase in incidence. The commenter concludes that climate 

change alone cannot explain recent increases in the incidence of tick-borne diseases in North America, 

citing Confalonieri et al. (2007). The commenter asserts that the incidence of tick-borne diseases could 

decrease in areas where they are currently endemic, due to climate-related changes in habitat. 

Response (5-78): 

We have reviewed the relevant assessment reports in the light of this comment and disagree that 

statements in the TSD regarding Lyme disease are “questionable and not well supported by existing 

research.” The relevant statements from the TSD on this topic are as follows: “Associations between 

temperature and precipitation and tick-borne disease are also noted by IPCC (Field et al., 2007). A study 

cited in Field et al. (2007) found that the northern range limit of Ixodes scapularis, the tick that carries 

Lyme disease, could shift north by 120 mi (200 km) by the 2020s and 620 mi by the 2080s.” 

These statements are consistent with both Field et al. (2007) and Ebi et al. (2008). The statements do not 

imply that recent changes in tick-borne diseases are due to climate change alone, nor do they imply that 

the incidence of tick-borne diseases will not decrease in some areas. 

Ebi et al. (2008) assessed the Randolph (2004) and Randolph and Rogers (2000) studies referenced by the 

commenter. To further summarize the conclusions of the assessment literature on the regionally variable 

nature of potential changes in tick distribution, and to incorporated the findings of Randolph (2004) 

(which relates specifically to Europe) and Randolph and Rogers (2000), as assessed by the CCSP, we 

have added the following detail on this topic to the TSD: 

According to Ebi et al. (2008), studies suggest that higher minimum temperatures 

generally were favorable to the potential of expanding tick distributions and greater local 

abundance of these vectors. However, Ebi et al. (2008) add that: “changing patterns of 

tick-borne disease in Europe are not consistently related to changing climate (Randolph, 

2004a). Climate change is projected to decrease the geographic range of TBE (tick-borne 

encephalitis) in areas of lower latitude and elevation as transmission expands northward 

(Randolph and Rogers, 2000).” 

Comment (5-79): 

One commenter (3347.3) argues that “the TSD includes statements regarding food-borne diseases that 

cannot be supported by the science.” The commenter cites a recent CDC report (CDC, 2009) that suggests 

the incidence of food-borne illnesses over the past three years has hit a plateau. The commenter 

additionally states that “significant declines since 1996 were reported in the incidence rates involving 

numerous, other food-borne infections.” The commenter adds that Kovats et al. (2005) find that 

campylobacteriosis rates peak before high annual temperatures and that according to CCSP (2008b), 

pathogenic species of Campylobacter cannot replicate in the environment and will not persist long under 

non-microaerophilic conditions, suggesting that high ambient temperatures would not contribute to 

increased replication in water or in food products. The commenter concludes that “[e]xisting scientific 

evidence does not support the notion that increasing global temperatures will increase rates of all foodborne diseases.” 

Response (5-79):

We have reviewed the assessment literature in light of this comment and the referenced studies, and we 

find that the TSD’s summary of this issue appropriately reflects the judgment of the scientific community 

as reflected in the assessment literature. Therefore, we disagree with the comment that the TSD includes 

information regarding food-borne disease that “cannot be supported by the science.” 

47 
The TSD does not state or imply that increasing global temperatures will increase rates of all food-borne 

diseases. Rather, it includes a much more qualified conclusion based on Confalonieri et al. (2007): 

“Foodborne diseases show some relationship with temperature (e.g., increased temperatures have been 

associated with increased cases of Salmonellosis).” This statement is fully consistent with the CCSP 

analysis (Ebi et al., 2008), which states that “[E]vidence supports the notion that increasing global 

temperatures will likely increase rates of salmonellosis,” noting that studies in North America and several 

countries across Europe “report striking similarities in correlations between peak ambient temperatures 

(controlled for season) and peak in clinical cases of salmonellosis.” 

We find that the commenter’s discussion of Campylobacter is largely consistent with the assessment 

report the commenter cites (CCSP, 2008b), which references the Kovats et al. (2005) study cited by the 

commenter. However, the commenter did not mention that Campylobacter transmission can be affected 

by factors other than replication in water or food products. CCSP (Ebi et al., 2008) concludes that it is 

more likely than not that increasing temperatures may expand typical peak season of clinical infection, or 

result in earlier peak. It also assesses that it is about as likely as not that increasing temperatures will 

result in shorter development times for flies, contributing to increased transmission by this proposed 

vector. 

With regard to the CDC report referenced by the commenter, we note that a three-year period is not 

sufficient for analyzing long-term trends in food-borne illness and that the incidence of some food-borne 

infections could well change due to non-climate factors such as public awareness advances, food 

processing changes, or changes in eating habits. This does not mean that the incidence of food-borne 

diseases will not increase due to climate change—all else being equal—but rather, as the TSD notes, that 

other factors will also play a role. EPA concludes that the TSD’s summary of the current state of the 

science on this topic as reflected in the assessment literature is accurate and sound. 

Comment (5-80):

Several commenters (2633, 3077, 3961, 4791, 4818, 4820, 4923, and 9345) cite the increase in asthma 

cases as a health concern due to climate change. Many (3077, 4818, 4820, 4923, 9345) are specifically 

concerned about asthma in children. One commenter (3961) states that researchers have found that 

asthma incidence has quadrupled in the United States since 1980 and that the “drivers” include “rising 

CO2 which increases the allergenic plant pollens and some soil fungi, and dust clouds containing particles 

and microbes coming from expanding deserts, compounding the effects of air pollutants and smog from 

the burning of fossil fuels.” Another commenter (2633) notes that today nearly 30 million adults and 

children in the United States have been diagnosed with asthma. 

One commenter (11249) notes that as temperatures increase historic seasonal patterns change, leading to 

an earlier and potentially longer allergy season. The commenter (11249) cites that allergic diseases are the 

sixth leading cause of chronic disease in the United States and impose a substantial burden on the U.S. 

population, noting that the global rise in asthma is an early health effect of climate change. 

Response (5-80):

As indicated in the TSD, climate change, including change in CO2 concentrations, could impact the 

production, distribution, dispersion, and allergenicity of aeroallergens and the growth and distribution of 

weeds, grasses, and trees that produce them (McMichael et al., 2001; Confalonieri et al., 2007). We also 

note the commenter’s point that an earlier and potentially longer allergy season is consistent with 

information in the TSD that was reaffirmed in the recent USGCRP report (Karl et al., 2009). While the 

commenter does not provide a reference for chronic diseases in the United States, it is true that a 

48 
significant number of people suffer from allergic diseases. However, projections of the possible impacts 

of climate change on allergenic diseases are difficult to assess. 

Comment (5-81):

Numerous commenters (e.g., 2750, 3347.1, 3347.3, 3394.1, 3449.1, 3509.1, 3722, 3747.1) contend that 

the proposed endangerment finding offers no support regarding the effect of GHG levels on aeroallergenrelated health risks, and that the scientific literature does not provide definitive data or conclusions on 

how climate change might impact allergenicity and aeroallergens. This includes the incidence, 

prevalence, distribution, and severity of allergic disorders. Commenters note that there are numerous 

factors that affect aeroallergen levels and the prevalence of associated allergenic illnesses, such as 

changes in land use, air pollution, and adaptive responses, many of which are difficult to assess. One 

commenter (3722) additionally criticizes the indefinite language used (the word “could”) and EPA’s 

acknowledgment that the scientific literature lacks “definitive data or conclusions,” as “reduc[ing] this 

issue to the level of speculation.” Commenters suggest that the EPA has made a predetermination about 

the effect of GHG levels on aeroallergen-related health risks based completely on unfounded, 

scientifically unsupported, and hypothetical harms. Without evidence, the issue of aeroallegens should not 

figure into the calculation of harm at all. One commenter (3722) states that “it is surprising that EPA 

gives any weight whatsoever to aeroallergens in the Proposed Rule.” Another (3349.1) states that EPA 

“reaches an arbitrary and capricious conclusion.” Another (3347.3) asks EPA to revise the TSD to 

accurately portray scientific knowledge, and present that knowledge objectively. This commenter goes on 

to state that the TSD section on aeroallergens “does not meet the standard of objectivity because it 

includes only scattered information suggestive of a potential link, and it presents this information with a 

notable bias that exaggerates the likely effect of climate change.” 

Response (5-81): 

EPA disagrees with the commenters that the TSD was developed without sensitivity to uncertainties in 

this area, that EPA did not accurately portray scientific knowledge, or that EPA presented “scattered 

information” with a “notable bias” that exaggerates the likely effect of climate change. A review of 

Section 7(d) of the TSD confirms that it accurately conveys the findings of the scientific literature. The 

TSD clearly states in Section 7(d) that “the scientific literature does not provide definitive data or 

conclusions on how climate might impact aeroallergens and subsequently the prevalence of allergenic 

illnesses in the U.S.” The TSD notes that numerous other factors affect aeroallergen levels and the 

prevalence of associated allergenic illnesses. Consistent with the scientific literature, EPA describes the 

impacts of elevated temperature and CO2 on aeroallergens, including IPCC’s conclusion that “pollens are 

likely to increase with elevated temperature and CO2,” as well as discussion of impacts on season length 

and allergenic content of pollens. We agree with the commenters, and state in the TSD, that numerous 

factors affect aeroallergen levels and the prevalence of associated allergenic illnesses. The information 

provided in the section is not scattered, but rather presents the scientific assessment on a range of climate 

change impacts on aeroallergens. Additionally, the information is presented objectively and in an 

unbiased fashion. All of the references cited by EPA in the aeroallergen section of the TSD are from 

IPCC or CCSP, and thus are part of the body of peer-reviewed assessment literature upon which EPA 

relies for the TSD. See Section III.A., “The Science on Which the Decisions Are Based,” for our response 

to comments on the use of the assessment literature and our treatment of new and additional scientific 

literature provided through the public comment process. 

We disagree with the assertion by the commenter that EPA’s use of “indefinite language (the word 

‘could’),” and EPA’s statement that the scientific literature lacks definitive data or conclusions, means 

that the TSD’s conclusions on aeroallergens are speculative. We clearly characterize the existing level of 

scientific uncertainty regarding climate change impacts upon aeroallergens, based upon the peer-reviewed 

assessment literature. For a response to comments regarding EPA’s characterization of scientific 

49 
certainty, please see Volume 1, Section 1.2, “Level of Scientific Certainty,” in this Response to 

Comments document. 

We also disagree with the commenters that EPA reached a predetermined or arbitrary and capricious 

conclusion. EPA conducted a careful review of the peer-reviewed assessment literature, which is reflected 

in the TSD, and upon which the Administrator based her judgment on aeroallergens. See the Findings, 

Section IV.B, “The Air Pollution Is Reasonably Anticipated to Endanger Both Public Health and 

Welfare,” for our response to comments on how the Administrator weighed the scientific evidence 

underlying her endangerment determination. 

 

Finally, we note that commenters did not submit any evidence that shows the TSD’s discussion and 

conclusions to be inaccurate. Thus, EPA finds the discussion of aeroallergens in the TSD to be reasonable 

and sound. 

Comment (5-82):

One commenter (7020) states that the TSD conclusion on aeroallergens shows that there are offsetting 

effects that cannot be resolved in one direction or the other that the EPA must improve this section to 

address offsetting effects, and that if this balance cannot be resolved, then aeroallergens cannot influence 

a potential endangerment finding. The commenter defines offsetting effects as when one mechanism 

produces an adverse effect and another mechanism produces a beneficial effect.

Response (5-82):

We disagree that the TSD conclusions presented on aeroallergens, which summarize the peer-reviewed 

assessment literature, are invalid because the TSD does not present a full accounting of “adverse” and 

“beneficial” effects. The TSD clearly describes the current state of scientific understanding on the issue of 

climate change impacts on aeroallergens. We also note that the commenter did not identify any potential 

beneficial effect from aeroallergens for us to consider. For EPA’s discussion on the consideration of net 

effects in the TSD, please see Volume 1, Section 1.4: “Net (Adverse and Beneficial) Effects,” of this 

Response to Comments document. 

Comment (5-83):

One commenter (3283.1) states that EPA has not been able to cite any quantifiable risk with regard to 

aeroallergens, and that risks must be quantified before a massive regulatory structure is implemented to 

reduce this risk.

Response (5-83):

We disagree that climate change impacts must be quantified for inclusion in the TSD and consideration 

with regard to an endangerment finding. We note that the peer-reviewed assessment literature, on which 

we rely for the TSD, is limited with regard to projections of aeroallergen impacts, and thus we provide a 

qualitative, not quantitative, evaluation of this issue. We also note that the commenter did not cite any 

new literature for us to consider with regard to quantifying the risk to aeroallergens from climate change. 

For EPA’s discussion on the quantification of climate change impacts in the TSD, please see Volume 1, 

Section 1.4, “Net (Adverse and Beneficial) Effects,” of this Response to Comments document. 

Comment (5-84):

One commenter (3283.1) states that “medical technology has developed techniques to minimize many 

allergic reactions” and that “new medicines will be available to nullify allergic reactions.” 

50 
Response (5-84):

The commenter’s implication seems to be that new medical techniques and medicines would serve as 

adaptation measures that would offset any adverse health effects from climate change impacts upon 

aeroallergens. See Section III.C, “Adaptation and Mitigation,” of the Findings for our response to 

comments on the treatment of adaptation and mitigation in the Findings. 

Comment (5-85):

One commenter (3347.3) states that the following statement from the TSD is unsupported: “Climate 

change, including changes in CO2 concentrations, could impact the production, distribution, dispersion 

and allergenicity of aeroallergens and the growth and distribution of weeds, grasses, and trees that 

produce them (McMichael et al., 2001; Confalonieri et al., 2007). These changes in aeroallergens and 

subsequent human exposures could affect the prevalence and severity of allergy symptoms.” The 

commenter states that relatively small increases in pollen exposure may have a protective effect against 

acquiring allergic rhinoconjunctivitis or asthma. The commenter cites one study in support of this (Burr et 

al., 2003), and states that the study reports a weak but consistent tendency for the prevalence of allergic 

symptoms to be inversely associated with pollen exposure. The commenter states that based upon this it 

seems that high pollen exposure either has no effect on the risk of acquiring allergic rhinoconjunctivitis or 

may even confer some protection against it. The commenter notes that this conclusion is backed up by the 

study, which cites evidence from several countries suggesting that the prevalence of hay fever and asthma 

is lower in rural than urban areas. 

Response (5-85):

We disagree that the IPCC statement quoted by the commenter lacks adequate support and note that the 

commenter provides no evidence that counter the IPCC statement. See Section III.A., “The Science on 

Which the Decisions Are Based,” for our response to comments on the use of the assessment literature 

and our treatment of new and additional scientific literature provided through the public comment 

process. 

The commenter cites only one study (Burr et al., 2003) to support the assertion that the TSD statement 

was unsupported. However, this study does not contradict and in fact supports the information presented 

in the TSD. The study was cited in the peer-reviewed assessment literature (Ebi et al., 2008). As the Burr 

et al. (2003) study states in its concluding paragraph: 

Overall, it seems very unlikely that high exposure to pollen increases the risk of acquiring 

allergic rhinoconjunctivitis or asthma, despite its action in provoking attacks in 

susceptible persons. The associations in this study were very weak, and it may be that 

pollen exposure has no influence on the prevalence of atopic disease. Nevertheless, the 

degree of consistency in the negative direction of these associations suggests the 

possibility of a protective effect. 

EPA concludes that IPCC’s statement on aeroallergen impacts from climate change is reasonable and 

sound. To the extent there is a protective effect, this would mean that climate change would not be 

expected to increase the risk of acquiring these illnesses, and EPA does not rely on any such increased 

risk in making the findings. However, the literature does support the concern that climate change could 

increase the incidence of allergy-related symptoms or illness for those susceptible persons who do have 

allergic rhinoconjunctivitis or asthma. 

51 
Comment (5-86): 

One commenter (3447.3) states that the following statement from the TSD lacks adequate support: “The 

IPCC concluded that pollens are likely to increase with elevated temperature and CO2 (Field et al., 

2007).” A number of other factors influence aeroallergen levels, including “changes in the spatial 

distribution of natural vegetation, introduction of invasive species, changes in land use, air pollution, 

adaptive responses, water availability, disturbance, nutrients, and meteorological factors (e.g. rainfall, 

humidity, wind).” The commenter notes that most studies focus only on the effects of increasing CO2

concentrations and temperature increase without considering any other factors, and are thus misleading. 

More studies are needed on the combined effects of CO2 and temperature that also consider other 

interactions with other variables, and three studies are presented to highlight the importance of other 

factors: 

1. Schenk et al. (1995) is cited as looking at the effects of CO2 enrichment and intraspecies 

competition on a range of plant attributes, with results showing that some plant attributes changed 

in response to CO2 concentration, but other plant attributes were dependent on plant density. 

2. Ziska et al. (2007) is cited as “indicat[ing] that CO2/temperature differences associated with 

urbanization may increase initial ragweed productivity and pollen production, but suggest that 

long-term, multi-year persistence of ragweed may not occur in the urban macro-environment due 

to the influence of other factors.” 

3. Curtis and Wang (1998) is cited as showing that stress effects significantly reduce overall woody 

plant biomass accumulation from heightened CO2. 

Response (5-86):

We disagree that the IPCC statement quoted by the commenter lacks adequate support and note that the 

evidence provided by the commenter does not demonstrate that there is inadequate support for the IPCC 

statement. See Section III.A., “The Science on Which the Decisions Are Based,” for our response to 

comments on the use of the assessment literature and our treatment of new and additional scientific 

literature provided through the public comment process. 

We have reviewed the three studies cited by the commenter and find that two of them (Curtis and Wang, 

1998; Schenk et al., 1995) do not directly assess pollen production and thus offer no direct support for the 

substance of the comment. We find that the third study (Ziska et al., 2007) indeed suggests that multi-year 

persistence of ragweed in the urban macro-environment may be dependent on factors other than CO2

concentrations; however, we note that the study took place in one specific location at the urban-rural 

interface and furthermore found that urbanization may increase initial ragweed productivity and pollen 

production. 

We note that the Van de Water (2008) study cited elsewhere by the commenter is highly consistent with 

the assessment literature conclusion on this topic. We further note that the most recent assessment report 

to address this issue, Karl et al. (2009), finds that “Rising temperatures and carbon dioxide concentrations 

increase pollen production and prolong the pollen season in a number of plants with highly allergenic 

pollen, presenting a health risk.” 

Additionally, Field et al. (2007) base their assessment on several peer-reviewed studies and state that 

“Warming and climate extremes are likely to increase respiratory illness, including exposure to pollen and 

ozone.” EPA concludes that the IPCC (Field et al., 2007) conclusion that pollens are likely4

 to increase 

with elevated temperature and CO2, as summarized in the TSD, is accurate and sound. 

 

4

 According to IPCC terminology, “likely” conveys a 66% to 90% probability of occurrence. See Box 1.2 of the 

final TSD for a full description of IPCC’s uncertainty terms. 

52 
Comment (5-87):

One commenter (3447.3) criticizes the following statement from the TSD as lacking support: “The IPCC 

(Confalonieri et al., 2007) noted that climate change has caused an earlier onset of the spring pollen 

season in North America and that there is limited evidence that the length of the pollen season has 

increased for some species. However, it is unclear whether the allergenic content of these pollens has 

changed.” The commenter also states that “there is little evidence to support an increase of the length of 

the allergy season and changes in the pollen content that may increase its health impact.” The commenter 

makes numerous points: 

Data are lacking to support an overall increase in the length of the pollen season or a change in 

intensity. The commenter cites WHO (2003) in noting that the observed trends in the end of the 

season phases as a result of climate change are unclear; therefore, it is uncertain how the pollen 

season length will be affected. 

Changes in the pollen season may differ for different plant species, and the length of the pollen 

season may shorten in certain geographical regions. The commenter cites an example from WHO 

(2003) in stating that “For example, increased snowfall (due to increased precipitation) takes 

longer to melt and may cause a later onset of flowering in Northern latitudes.” 

“[T]he burden of immune-mediated (IgE) allergic diseases is related to the length of pollen 

season as well as the total pollen counts and the number/height of the pollen peaks and 

bioallergen availability.” The commenter cites WHO (2003) as presenting several possibilities 

with regard to aeroallergens from climate change. Additionally, the commenter states that 

depending on the actual effects, it remains uncertain how they will impact the severity of 

symptoms: 

o An earlier start of the season, but with several smaller peaks. 

o Seasons are prolonged, but also divided into multiple sub-seasons with smaller peaks. 

o Winter temperature influences the waking of trees leading to effects on the size of the 

peak of the pollen season. 

It is unclear if the allergenic content of the pollen type has changed. The commenter cites Levetin 

and Van de Water (2008) as noting that data from U.S. sampling stations are limited. 

Response (5-87):

We disagree that the IPCC statement from the TSD lacks support. The IPCC references three separate 

studies in support of its conclusion. The commenter, by contrast, did not provide any literature that 

contradicts the IPCC conclusion. We have reviewed the submitted references and on the basis of our 

review find that they are consistent with the relevant IPCC conclusions. 

The TSD does not state that length of the pollen season has increased. Rather, it notes that climate change 

has caused an earlier spring pollen season in the Northern Hemisphere and that there is “limited evidence 

that the length of the pollen season has increased for some species.” Neither of these statements is 

inconsistent with any of the WHO (2003) conclusions cited by the commenter. In fact, while the WHO 

report in question does discuss a number of uncertainties, its overall conclusions are clearly directionally 

consistent with the assessment literature as summarized in the TSD. The report states that “Evidence is 

growing that climate change might facilitate the geographical spread of particular plant species to new 

areas as they become climatically suitable. Warming is likely to further cause an earlier onset and may 

extend the duration of flowering and pollen season, for some species (such as grasses and weeds).” 

Finally, the commenter’s note with regard to increased snowfall potentially causing a later onset of 

flowering in northern latitudes is the only example given for shorter pollen seasons in certain geographic 

regions, and it is worth noting that this report was written specific to Europe. Thus, we find that the report 

does not provide support for the commenter’s claim that “there is little evidence to support an increase of 

53 
the length of the allergy season and changes in the pollen content that may increase its health impact, 

either as a general conclusion or one relevant to the U.S.” 

We have reviewed the Levetin and Van de Water (2008) study and find that it is highly consistent with 

the assessment literature as reflected in the TSD. The study does not state that data from U.S. sampling 

stations are “limited,” though it does note that “Plant phenology data for North America are not as widely 

available as European datasets.” The authors conclude that “Elevated levels of atmospheric carbon 

dioxide and other greenhouse gases have resulted in global warming. The effect of these changes has 

impacted plant production, with increases in plant biomass, number of flowers, pollen per plant, and 

potential changes in pollen per anther. These effects have been shown in select plants through studies at 

elevated carbon dioxide levels.” 

EPA concludes that the TSD’s summary of the current state of scientific knowledge on this topic as 

reflected in the assessment literature is accurate and sound. See Section III.A., “The Science on Which the 

Decisions Are Based,” for our response to comments on the use of the assessment literature and our 

treatment of new and additional scientific literature provided through the public comment process. 

Comment (5-88):

One commenter (3447.3) criticizes the following statement from the TSD as poorly supported: “The 

IPCC concluded that introductions of new invasive plant species with high allergenic pollen present 

important health risks, noting that ragweed (Ambrosia artemisiifolia) is spreading in several parts of the 

world (Confalonieri et al., 2007).” The commenter notes that, in addition to climate change, there are 

other influences on vegetation patterns, which include land use and land cover change as well as 

“socioeconomic changes such as the impact of agricultural policy on plant species composition.” The 

commenter states that EPA failed to separate out these influences. 

Response (5-88):

We agree that a variety of factors can influence vegetation patterns, including that of ragweed. However, 

regardless of the underlying cause(s), the increased spread of ragweed that has been observed could have 

important implications for aeroallergen impacts as the climate changes. As noted by IPCC (Confalonieri 

et al., 2007): “Several laboratory studies show that increasing CO2 concentrations and temperatures 

increase ragweed pollen production and prolong the ragweed pollen season.” 

EPA concludes that IPCC’s statement that the spread of invasive plant species with high allergenic pollen 

presents important health risks is reasonable and sound. See Section III.A., “The Science on Which the 

Decisions Are Based,” for our response to comments on the use of the assessment literature and our 

treatment of new and additional scientific literature provided through the public comment process. 

Comment(5-89):

One commenter (3447.3) states that EPA must recognize that factors unrelated to aeroallergen levels have 

been implicated in allergic disease onset and susceptibility. The commenter cites WHO (2003) in making 

the following statement: “infections in early life, microbial exposure, exposure to endotoxins, indoor and 

outdoor air pollution as environmental tobacco smoke or traffic-related air pollution, poor indoor/outdoor 

climates, allergen exposure and nutrition seem to coincide with the onset of allergic disease. When the 

disease is established, some of these factors may also act as triggers of symptoms.” 

Response (5-89):

54 
We have reviewed the WHO report referenced by the commenter and we agree that factors unrelated to 

aeroallergen levels can affect disease onset and susceptibility. The TSD addresses this point, stating that 

“there are numerous other factors that affect aeroallergen levels and the prevalence of associated 

allergenic illnesses, such as changes in land use, air pollution, and adaptive responses, many of which are 

difficult to assess (Ebi et al., 2008).” EPA concludes that the TSD’s summary of the assessment literature 

conclusions on this topic is reasonable and sound. 

Comment (5-90): 

Commenters (0553, 3394.1, 3722, 7031, and 10158) indicate that it is well known that CO2 is not a health 

hazard for humans or animals at atmospheric concentrations reasonably expected to ever be reached, even 

if all known fossil fuel reserves are combusted and CO2 atmospheric retention times are several centuries. 

Commenters note that this does not support endangerment. One commenter notes that greenhouse 

operations use elevated CO2 concentrations to promote plant growth, yet greenhouse workers are 

completely unaffected. One commenter notes that Occupational Safety and Health Administration limits 

for air contaminants indicate that human exposure to CO2 should not exceed 5,000 parts per million 

(ppm) during an 8-hour work day, which is well above ambient concentrations of CO2. Another 

commenter notes the maximum allowed CO2 concentrations for U.S. submarines is 8,000 ppm and many 

office buildings register greater than 1,000 ppm CO2 levels with no harmful effects. 

Response (5-90): 

EPA agrees with the commenter that exposure to current and projected elevated CO2 concentrations in the 

atmosphere would not have direct adverse impacts on human health, and notes that the science on this 

issue is summarized in Section 3, “Direct Effects of Elevated Greenhouse Gas Concentrations,” as well as 

in Appendix C: “Direct Effects of Ambient GHG Concentrations on Human Health.” The TSD also 

summarizes health effects associated with climate impacts caused by elevated GHGs. See the Findings, 

Section IV.B.1(f), for our response to comments on the consideration of health impacts stemming from 

climate change impacts as relevant to a determination on endangerment of public health impacts. 

Comment (5-91): 

Commenter (3607.1) indicates that the TSD’s Appendix C, “Direct Effects of Ambient GHG 

Concentrations on Human Health,” which discusses direct effects of the six ambient GHG concentrations 

on human health, indicates that “both current and projected atmospheric concentrations of these GHGs do 

not pose exposure risks on human respiratory systems (i.e., breathing/inhalation).” Further, the 

commenter indicates that EPA notes that the projected concentrations in 2100 are “well below” the 

thresholds for adverse effects; however, this conclusion is rather obscure and is in the last sentence of the 

discussions for CO2, methane (CH4), and nitrous oxide (N2O). The commenter indicates that EPA should 

move this conclusion to the first sentence of each of these sections as it has done for the fluorinated gases 

section. 

Response (5-91): 

EPA notes that the Executive Summary of the TSD states, “Current ambient air concentrations of CO2

and other GHGs remain well below published exposure thresholds for any direct adverse health effects, 

such as respiratory or toxic effects.” In addition, the first sentence of Appendix C in the TSD states: 

“Greenhouse gases, at both current and projected atmospheric concentrations, are not expected to pose 

exposure risks on human systems (i.e., breathing/inhalation).” Thus, we find that the TSD clearly states 

the known relationship between atmospheric GHG concentrations and human exposure risks. In addition, 

this point was made explicit in the proposed endangerment finding under the discussion of public health 

impacts. Therefore, we do not find that a change to the TSD is necessary. 

55 
5.2 Air Quality 

Comment (5-92):

Two commenters (2123, 2633) state that breathing polluted air can cause burning eyes and throat 

irritation, and that tiny airborne particles and ground-level ozone can trigger respiratory problems, 

especially for people with asthma. These commenters (2123, 2633) note that some toxic chemicals 

released in the air such as benzene or vinyl chloride are highly toxic and can cause cancer, birth defects, 

long-term injury to the lungs, as well as brain and nerve damage. 

Response (5-92):

We note the comments regarding respiratory illness and other health effects are associated with PM and 

ground-level ozone. We concur with the commenter regarding the health effects associated with these 

pollutants and note that Section 8(c) of the TSD summarizes the health effects due to CO2-induced 

increases in tropospheric ozone and PM. Regarding toxic chemicals such as benzene or vinyl chloride we 

note these chemicals and their emissions are outside the scope of this action. This action pertains to the 

well-mixed GHGs identified in the Findings, which include CO2, CH4, N2O, hydrofluorocarbons (HFCs), 

perfluorocarbons (PFCs) and sulfur hexafluoride. 

Comment (5-93):

Several commenters (2898.1, 3136.1, 3283.1, 3347.1, 3347.3, 3347.4, 3394.1, 3449.1, 3603.1, 3722, 

3747.1) indicated that the TSD analyses of the impact of GHG emissions on air quality should include 

scenarios that assume future emission control programs. The commenters indicate that EPA should 

conduct a robust national-scale risk assessment that considers the impact of climate change on ozone and 

PM under current conditions versus future conditions, including the impact of ongoing regulatory 

emission control programs. Until such an analysis is available, they state, it is not possible to determine if 

climate change will negatively affect health due to changes in air quality. According to these commenters, 

these future emission reduction programs (e.g., the Clean Air Act’s National Ambient Air Quality 

Standards [NAAQS] implementation measures) will ensure no adverse impact on public health due to 

climate change. By excluding consideration of highly relevant modeling showing a much different future 

outcome for ozone and PM, these commenters argue, EPA undermines the link between credible science 

and the endangerment proposal. 

Similarly, several commenters (2898.1, 3136.1, 3477, 3596.2, 4003, 9863, and 10499) ask how EPA can 

support an IPCC claim that declining air quality is a “virtual certainty” when, partly because of EPA 

efforts, air quality has been improving in the United States in a warming climate. Commenters note that 

ozone pollution in the United States as measured by the EPA continues to decline, and the assertion that 

ozone pollution will increase is not supported by these trends. One commenter (4003) submits a figure 

from EPA’s Air Quality Trends Web site which indicates a 21% decrease in ozone based on annual 

fourth-highest 8-hour average5

 in support of their point that ozone concentrations have been decreasing 

since 1970. Commenters state that EPA’s current description fails to capture the nature of observed trends 

in ground-level ozone concentrations during a period of increasing temperatures across the United States 

and describes projections that seemingly are oblivious to the existence of such trends. These comments 

question the utility of these projections in addressing the potential future of low-level ozone 

concentrations across the United States, and contend that EPA is making an endangerment finding that is 

not based upon the most relevant data. The commenters note that lacking any strong guidance that climate 

 

5 http://www.epa.gov/airtrends/ozone.html

56 
change will somehow act to more than offset the gains through regulatory actions into the future, the best 

indication of what is to come should be gained from what we have observed—that is, declines in PM 

concentrations despite increases in human GHG emissions, increasing temperatures, and increasing trends 

in wildfire activity. 

Commenters suggest that the TSD and EPA’s integrated assessment (IA) of the impacts of global change 

on regional U.S. air quality ignored the National Exposure Research Laboratory (NERL) modeling of the 

companion FUT2 simulation; this scenario entails ozone precursor emissions reductions across the United 

States consistent with the 2015 implementation of the Clean Air Interstate Rule (CAIR). One comment 

(3347) suggested that a variety of future baseline ozone and PM reduction scenarios should be fully 

examined. 

Response (5-93):

Contrary to the assertion of the commenters, EPA has conducted a national-scale assessment of the 

impact of climate change on air quality as represented in the IA and reflected in the TSD, and this 

assessment included available results on the combined impacts of climate change and changes in 

emissions of criteria pollutants. 

The IA notes the challenges associated with developing spatially detailed, plausible scenarios of future 

U.S. and worldwide emissions of criteria pollutants. For example, the IA states that: 

Future emissions scenarios that are consistent across pollutants and geographic scales and 

that incorporate important processes such as fire, land use, biogenic emissions, and 

technological change are lacking, limiting the kinds of studies that can be accomplished 

at this time...Plausible scenarios for future emissions need to be developed that account 

for changes in urbanization, population growth, migration, industrialization, fuel, 

technology, etc. 

Therefore, the current uncertainty in future ozone precursor emission scenarios is large, limiting their 

application for the purpose of determining the sensitivity of ozone air quality to GHG emissions 

compared to scenarios that hold ozone precursor emissions constant (and therefore allow the research 

community to isolate the signal of the sensitivity of ozone to climate change). 

Despite these caveats, the IA fully considered available results from all of the modeling groups whose 

simulations included both climate and criteria pollutant emissions changes. For example, EPA considered 

all the results from the NERL CIRAQ effort that was singled out for comment. These results are reported 

on and extensively discussed in the IA (e.g., in the key synthesis chapter and conclusions), and all of the 

published results from the NERL CIRAQ, including the FUT2 scenario, are considered by EPA in the IA 

and are included in the literature summarized in the TSD. Additional details of the CIRAQ effort 

including the FUT2 scenario are provided in response 5-95 below. Beyond the NERL CIRAQ results 

upon which the commenters focus, the IA also considered all available results on combined climate and 

criteria pollutant emissions changes from the other regional modeling groups, including the Columbia, 

Georgia Tech, University of Illinois, and Washington State teams. Synthesizing across all these results, 

the IA concludes: “Preliminary work suggests that the impacts of climate change on future U.S. regional 

O3 [ozone] concentrations remain significant when also considering possible future anthropogenic O3

precursor emissions changes.” Therefore, these results, in aggregate, support the overall finding that 

climate change will negatively affect health due to changes in air quality. Furthermore, the IA goes on to 

state (about the results from the studies just mentioned): 

A number of the modeling teams whose results are discussed in this report also carried 

out simulations with modified future air pollutant emissions generally derived from the 

57 
assumptions used to formulate the various IPCC GHG emissions scenarios. These 

preliminary tests found that the combined effects of climate and anthropogenic precursor 

emissions changes are highly sensitive to the assumptions about future emissions 

trajectories. 

To summarize, the commenters’ assertion that alleged EPA selectivity about which studies to consider 

“undermines the link between credible science and the endangerment proposal” is demonstrably false. As 

described above, the IA, considered available simulation results that included scenarios of changes in 

criteria pollutant emissions along with climate change, when drawing their conclusions, and the findings 

of the IA are accurately summarized in the TSD. 

At the same time, EPA properly recognized that such modeling of future climate change with future 

emission control programs does not isolate the impacts of GHGs on air quality. Because of this EPA also 

considered modeling of future climate change without future emissions control programs, to isolate the 

impacts of GHGs on air quality. Many of the projections of ozone increases and related mortality and 

morbidity are tied to modeling that focuses on isolating the impact of climate change, and this modeling 

shows significant adverse impacts from climate change, typically resulting from the combination of 

climate associated increases in biogenic emissions of volatile organic compounds (VOCs), climate change 

impacts on temperature and atmospheric chemistry, and climate change impacts on atmospheric 

circulation. Climate change can have an important impact on past trends in ozone reduction as well as 

future projections of ozone. For example, Leibensperger et al. (2008) use detailed analysis of long-term 

observations and conclude: 

...[T]he decrease in mid-latitude cyclones over the period 1980–2006 has offset half of 

the air quality gains in the Northeast U.S. that should have been achieved from reduction 

of anthropogenic emissions over that period. This suggests that climate change has 

already had a major effect on the accountability of emission control strategies over the 

past 2–3 decades, preventing achievement of the ozone air quality standard. It 

demonstrates the potential of climate change to dramatically affect air quality on decadal 

scales relevant to air quality policy. 

The challenge that “EPA’s current description fails to capture the nature of observed trends in ground 

level ozone concentrations during a period of increasing temperatures across the U.S. and describes 

projections that seemingly are oblivious to the existence of such trends” is not supported by the results 

presented in the IA and summarized in the TSD. First, the IA explicitly notes the observed trend of 

generally decreasing U.S. ground-level ozone concentrations and explicitly recognizes the contribution of 

EPA’s regulatory efforts to this trend (in Section 1 of the IA). Second, while the process of coupling 

climate with atmospheric chemical processes in modeling systems presents considerable scientific and 

technical challenges, because of the large number of physical, chemical, and biological processes 

involved, the complex interactions between them, and the scientific uncertainties associated with each, the 

modeling systems whose results are synthesized in the IA have been shown to be able to capture the 

observed historical trends in U.S. ozone concentrations to which the commenters refer (as described in 

Section 3 of the IA). From the perspective of the IA’s research questions, however, the major advantage 

of these modeling systems is that they permit the detailed exploration of the potential responses of air 

quality to climate change over the next few decades in a way that would be difficult or impossible with 

other approaches—most saliently the air quality implications of climate changes well outside the 

envelope of historical experience. It is precisely because 1) GHG-induced climate change over the next 

several decades is expected to be greater than over the last few decades and 2) there are large 

uncertainties associated with modeling future U.S. and worldwide criteria pollutant emissions changes (as 

described in the paragraphs above) that these model simulations are considered useful in providing 

58 
scientific support for the TSD. Under these circumstances they are able to provide useful information that 

is not obtained by just looking to observations or trends of the past. 

Finally, substantial challenges remain with respect to achieving the air quality protection under the 

NAAQS for ozone, and these challenges will likely be exacerbated by climate change. See the Findings, 

Section IV.B.1.f and Volume 9 of this Response to Comments document for EPA’s response to 

comments on the relevancy of NAAQS in the context of the Administrator’s endangerment finding. 

Comment (5-94):

One commenter (2898.1) states that the only way to isolate the “global warming effect” on ozone 

pollution would be to compare ozone levels in warming and non-warming scenarios based on realistic 

projections of precursor emissions in the 2020s, 2050s, and 2080s. 

Response (5-94):

See response 5-93 in this section regarding the rationale for the most appropriate method for isolating the 

effect of climate in the selection of modeling scenarios.

Comment (5-95):

A number of commenters (3347.1, 3347.3, and 3347.4) contend that the TSD fails to mention the results 

of three important EPA-sponsored projects that considered the impact of climate change in conjunction 

with existing emission control programs: the Georgia Tech Phase I STAR Grant Project, the EPA Climate 

Impact on Regional Air Quality (CIRAQ) Project, and the EPA Intercontinental transport and Climatic 

effects of Air Pollutants (ICAP) project. The commenters state that these three research programs show 

that the impact of climate change alone on U.S. regional air quality is minor when compared to the effects 

of continued Clean Air Act regulatory strategies for emissions control. The CIRAQ future case FUT2 

modeling clearly demonstrates that maximum daily 8-hour (MDA8) ozone levels in 2050 are likely to 

decrease as the result of continued regulatory programs, notwithstanding the countervailing effects of 

climate change. This EPA modeling shows reductions in 2050 8-hour ozone concentrations as large as 12 

to 15 ppb over several sub-regions of the country. 

The commenters state that, in sum, the Georgia Tech or Georgia Institute of Technology (GIT) ozone 

modeling shows that the combined effect of climate change and emission reductions lead to overall ozone 

reductions up to 15 ppb. The Georgia Institute of Technology projected 2050 emissions reductions of 

more than 60% in nitrogen oxides (NOx) and sulfur dioxide in 2050 as the result of control programs and 

the A1B global growth scenario. In percentage terms, there is likely to be a 20% decrease in the mean 

summer MDA8 ozone mixing ratios. Regionally, the eastern United States appears to benefit more than 

the rest of the country from reductions in mean daily 8-hour average (D8H) ozone because of both spatial 

variations in the meteorological and emissions changes. The commenters indicate that reductions in the 

higher 8-hour maximum ozone concentrations were calculated for all U.S. sub-regions and there are likely 

to be fewer days with D8H ozone above the level of the former NAAQS (85 ppb) in a number of 

metropolitan areas. Further, the commenter indicates that independent modeling by EPA’s Office of 

Research and Development (ORD) (Nolte et al., 2008, 20096

) and Office of Air Quality Planning and 

Standards (OAQPS) (Jang et al., 2008) corroborate the Georgia Tech results. On the other hand, the 

commenter also noted that the Georgia Tech results include finding that climate change by itself has 

mixed effects on the 8-hour ozone levels, but the maximum daily 8-hour ozone levels are anticipated to 

generally increase. 

 

6

 Nolte et al. (2009) refers to a poster presentation which references the Nolte et al. (2008) study. 

59 
Response (5-95):

We disagree with the commenter that studies that consider emission controls in conjunction with climate 

change were not considered in the development of the IA and reflected in the TSD. Other studies (e.g., 

Georgia Tech STAR grant project and the EPA CIRAQ project) were undertaken as part of the IA. The 

results from both projects (along with STAR projects at the University of Illinois, Washington State 

University, Carnegie Mellon University, Harvard University, University of California–Berkeley, and 

Columbia University) are discussed in the key synthesis chapter of the IA and build the foundation of the 

conclusions of the report. Thus, we confirm these studies are considered by the IA and the literature 

underlying the TSD. 

The IA clearly acknowledges that results from these two studies show that emission reductions can be 

very effective at reducing air pollution to healthful levels. We also note that the conclusions of the 

Georgia Tech study (Tagaris et al., 2009) are consistent with the summary in the TSD. In particular, 

Tagaris et al. (2009) conclude: “Results suggest that climate change driven air quality-related health 

effects will be adversely affected in more than two-thirds of the continental United States.” 

 

To provide further clarification, as described in the IA and in Nolte et al. (2008), EPA initiated the 

CIRAQ project in 2002 to develop a pilot modeling study to incorporate regional-scale climate effects 

into air quality modeling. Historical values for GHGs were used for 1950–2000, with future GHG forcing 

following the Intergovernmental Panel on Climate Change's A1B SRES scenario. Two future simulations 

were conducted, one with anthropogenic emissions held at 2001 levels (FUT1), and one with 

anthropogenic emissions reduced in accordance with the A1B scenario (in FUT2, emissions of NOx were 

projected to decrease by 45%). Considering just climate change alone, with future anthropogenic 

emissions held at current levels (i.e., FUT1), ozone increases in much of the eastern United States. This is 

consistent with the findings of Hogrefe et al. (2004), who reported ozone increases in summertime for the 

2050s as a result of climate change alone under the A2 GHG scenario. For the future reduced emissions 

case FUT2, however, ozone decreases nearly everywhere in the continental United States. These results 

imply that, at least for the magnitude of emissions control assumed for the United States under the IPCC 

A1B scenario, the decrease in surface ozone due to the change in emissions outweighs the increase due to 

climate change. This conclusion is contrary to that of Hogrefe et al. (2004), who found that climate 

change and future emissions changes under the A2 scenario would both lead to enhanced surface ozone 

levels in the eastern United States. Under the A2 scenario, NOx and VOC emissions increase in the 

United States, which accounts for their dramatically differing results. The authors emphasize that 

although the difference in temperature change at 2050 predicted by a range of global climate models in 

response to the A1B and A2 scenarios is small at about 0.25°C (IPCC, 2001) and as a consequence the 

impact of climate change on regional air quality is similar between these two scenarios, the simulated 

ozone changes are substantially different, and indeed of opposite sign, if changes in ozone precursor 

emissions associated with these two scenarios are considered as well. Nolte et al. (2008) also caution that 

“the uncertainty in the future emission scenarios for ozone precursors is quite large.” 

As stated in the final TSD: 

[T]he results in the IA demonstrate that O3 responds to climate change in a qualitatively 

consistent manner across the simulations from multiple research groups. The patterns of 

relative changes in regional climate vary across the same simulations. Figure 3-11 of the 

IA graphically illustrates the net change in daily average ozone values across the research 

results for summertime ozone. Ozone concentrations increase across most areas of the 

country with decreases limited to some parts of the Southwest. The net increases of ozone 

concentrations in the large population centers of the northeastern and middle Atlantic 

United States are the results with the highest confidence. The net increases in the 

60 
Southeast and the small net changes in the Northwest are the features with the lower 

confidence. 

Response 5-102 below provides Figure 3-11. Thus, the net impact of climate change and emissions 

control programs may be a net decrease or a net increase in ozone levels, depending on the emissions 

control scenario that is modeled. However, in all cases the overall effect of climate change itself is to 

increase ozone levels compared to what would occur without the climate change. See response (5-93 for 

our response to comments regarding the selection of modeling scenarios in the context of the Findings. 

Comment (5-96):

A commenter (3722) indicates that EPA already has all the authority needed and indeed the legal 

obligation, enforceable by citizen suit, to limit ozone to levels protective of human health and welfare. 

Response (5-96):

See the Findings, Section IV.B.1.f, and Volume 9 of this Response to Comments document for EPA’s 

response to comments on the relevancy of the NAAQS in the context of the Administrator’s 

endangerment finding. We note that this action does not concern the scope or effectiveness of current or 

projected EPA authorities; its focus is on assessing the impacts of climate change on the United States 

and providing the foundation for the Administrator to determine whether GHG air pollution endangers 

public health or welfare. 

Comment (5-97): 

A commenter (3347.4) believes that inadequate attention is given to the time and space scales of available 

global and regional modeling results compared to the resolutions needed for reliable health risk 

assessments and ozone/PM2.5 attainment demonstrations. Essentially all of the modeling considered by the 

TSD and IA had a horizontal grid spacing no finer than 36 kilometers. In contrast, EPA’s 8-hour ozone 

attainment test requires that modeled concentrations possess substantially finer time and space resolutions 

and cover at least three contiguous years. The ozone attainment test requires use of the average of the 

fourth-highest 8-hour ozone concentration in the base year within a 3-by-3 array of 4-kilometer grid cells. 

PM2.5 attainment modeling should be applied to grid meshes of 12 kilometers. Thus, the commenter 

concludes that the modeling relied upon in the TSD is too coarse for reliable estimates of NAAQS 

compliance in future years and insufficiently resolved to provide the gridded ground-level concentrations 

needed when performing realistic health risk assessments. 

Response (5-97):

The TSD has been developed to inform the Administrator’s endangerment analysis, not to inform area 

specific health risk assessments or attainment demonstrations (e.g., NAAQS). To support its intended 

purpose, the summary in the TSD properly focuses on the projected impact of global GHG emissions on 

large-scale patterns of air quality via induced climate changes as represented in general circulation models 

(GCMs). Confidence in these projections accordingly decreases the finer the spatial scale and further out 

into the future. Thus, larger grid spacing is utilized to minimize uncertainties associated with methods of 

downscaling and to focus on regional- and national-scale air quality changes, rather than the local-scale 

that is currently used for attainment modeling. We conclude the spatial and temporal scales used in the 

TSD and in the context of the Findings are appropriate and consistent with the scales used by the 

scientific assessment literature. See the Findings, Section IV.A.1.f, and Volume 9 of this Response to 

Comments document for response to comments on the relevancy of NAAQS in the context of the 

Administrator’s endangerment finding. 

61 
Comment (5-98):

Two commenters (3136.1, 3722) state that if the Brewer-Dobson circulation is indeed enhanced via 

increasing CO2 levels, then the related high-latitude ozone increases would 1) mitigate against polar ozone 

depletion issues and the concomitant health impacts from surface ultraviolet radiation and 2) not 

necessarily result in more stratosphere-troposphere exchange. Commenters further state that the latter 

occurs primarily in streamers linked to the coldest winter air masses near the polar jet—a warming of the 

coldest air masses, as is being observed over the Northern Hemisphere, and could just as easily result in a 

decrease in tropospheric ozone levels. Commenters request a correction to delete this issue from the TSD 

given that IPCC’s Fourth Assessment Report is unsettled in this area. 

Response (5-98):

In light of this comment, EPA has reviewed this discussion in Section 8(a) of the TSD, which references 

statements on this topic from IPCC (Denman et al., 2007). We conclude that a correction to the TSD is 

not necessary. We note that the TSD indicates that an influx of ozone from stratosphere to troposphere 

could occur with shifts in large-scale atmospheric circulation shifts in response to climate warming, 

which is based on multiple modeling studies in the scientific assessment literature. Since the commenters 

do not provide supporting literature indicating that high-latitude ozone increases will mitigate against 

polar ozone depletion issues, we conclude that this is currently not supported by available science. 

Additionally, we note that the Denman et al. (2007) statement indicates that ozone concentrations could 

increase via more stratosphere-troposphere exchange and further evidence of shifts in atmospheric 

circulation due to climate warming is provided by CCSP (2008b), which reports that stagnant air masses 

related to climate change are likely to degrade air quality in some densely populated areas. We 

acknowledge that stratosphere-troposphere exchange is associated with colder winter air masses; 

however, the current scientific literature does not support that a warming of polar jets will lead to 

decreases in tropospheric ozone levels. For these reasons we have determined that our discussion of this 

issue in the TSD is accurate and sound.

Comment (5-99):

A few commenters (2972.1, 3136.1, and 3722) suggest that despite the simulation provided by Mickley et 

al. (2004), observations show something different. Commenters cite the study by Strong and Davis 

(2007), which calculated a 0.6% increase (per decade) in the frequency of jet cores and increasing jet 

stream speed over much of central and eastern Canada over the 1958–2004 period in conjunction with a 

regional contraction of the 300-hectopascal circumpolar vortex. Commenters state that given the lack of 

upward trend in pollution episodes over the last 30 years, these observations call into question the 

likelihood of future air quality degradation from climate change. The commenters state that the TSD’s 

inclusion of this issue is not based on the best available science and is inappropriate; therefore, they 

request a correction to the TSD. 

Response (5-99):

This comment concerns the discussion in the TSD regarding statements of increases in the severity and 

persistence of regional pollution episodes in the eastern United States due to the reduced frequency of 

ventilation by storms. These results come from IPCC (Denman et al., 2007) based on the results of 

Mickley et al. (2004). 

We disagree with the commenters’ assertion that observations show something different. The 

commenters’ view of Strong and Davis (2007) is incorrect on this issue. Strong and Davis (2007) report 

changes in the frequency of jet cores and increasing jet stream speed for wintertime (December–

February). The Mickley et al. (2004) results are for summertime, which is the period of interest for high 

62 
ozone pollution episodes. Mickley et al. (2004) do cite multiple peer-reviewed journal articles with 

observed trends that are consistent with the model results of decreasing summertime cyclone frequency. 

More recent work by Mickley and co-investigators (Leibensperger et al., 2008) extends the model results 

through detailed analysis of long-term observations and concludes: 

...[T]he decrease in mid-latitude cyclones over the period 1980–2006 has offset half of 

the air quality gains in the Northeast United States that should have been achieved from 

reduction of anthropogenic emissions over that period. This suggests that climate change 

has already had a major effect on the accountability of emission control strategies over 

the past 2–3 decades, preventing achievement of the ozone air quality standard. It 

demonstrates the potential of climate change to dramatically affect air quality on decadal 

scales relevant to air quality policy. 

Importantly, we note that the Leibensperger et al. (2008) work uses the same dataset as Strong and Davis 

(2007). For these reasons, we conclude that we have accurately reflected the science in the TSD regarding 

observations and the future likelihood of air quality from climate change. We will continue to rely on the 

synthesis reports, including this IPCC (Mickley et al. 2004) conclusion, and no changes to the TSD are 

warranted. 

Comment (5-100):

Several commenters (3136.1, 3347.3, 3394.1, 3411.1, 3596.2, and 3722) argue that the statement in the 

TSD Executive Summary that the directional effect of climate change on ambient PM levels remains 

uncertain is misleading and is inconsistent with the underlying research reported in the rest of the report. 

These comments state that another factor to consider with respect to urban ozone levels is the possibility 

that precipitation will increase over urban areas because of the presence of the urban heat island coupled 

with a moister and more unstable atmosphere, resulting in more wet deposition (see, for example, 

Shepherd, 2005). The commenters claim that if EPA were to proceed to a final endangerment finding, it 

would have to first address the potential health benefits from possible climate change–related PM 

reductions. 

Response (5-100):

The TSD discusses the issue of the directional effect of climate change on ambient PM levels as 

highlighted by commenters in Section 8(b): “The overall directional impact of climate change on PM 

levels in the United States remains uncertain (CENR, 2008), as too few data yet exist for PM to draw firm 

conclusions about the direction or magnitude of climate impacts (CCSP 2008b).” Further, recent analyses 

(e.g., EPA’s IA) indicate a range of increases and decreases in PM concentrations related to changes in 

climate. The literature that we cite in the TSD has assessed several effects climate change could have on 

PM, including the one emphasized by the commenter, and found that the directional effect remains 

uncertain. After extensive review of the TSD and associated underlying scientific literature, we disagree 

with the commenters’ assertion that the TSD is misleading or inconsistent with respect to the influence of 

climate change on PM and find the discussion in the TSD to be accurate and in agreement with the 

scientific literature. 

As stated in the TSD, precipitation is a more important primary meteorological driver of PM than of 

ozone, due to its role in removing PM from the atmosphere (wet deposition). Precipitation, however, is 

particularly difficult to model and shows greater disagreement across simulations than other variables. 

Thus, it is reasonable to conclude that the impacts of climate change on PM will both be affected by wet 

deposition or removal from precipitation. However, model parameterizations of wet deposition are highly 

uncertain and not fully realistic in their coupling to the hydrological cycle (NRC, 2005). For models to 

simulate accurately the seasonally varying pattern of precipitation, they must correctly simulate a number 

63 
of processes (e.g., evaporation, condensation, transport) that are difficult to evaluate at a global scale 

(Randall et al., 2007). We determine these complexities and differences in directional effect for PM 

preclude the overall assessment of health benefits based on this modeling assessment which is consistent 

with the most recent scientific literature. 

Comment (5-101):

A few commenters (3347.3, 3394.1, and 3603.1) cite EPA’s IA report Assessment of the Impacts of 

Global Change on Regional U.S. Air Quality: A Preliminary Synthesis of Climate Change Impacts on 

Ground-Level Ozone (U.S. EPA, 2009d) as evidence that significant regions of the United States are 

likely to see ozone decreases associated with climate change and the science in this area is uncertain with 

respect to both ozone and PM. The commenters state that EPA pays little attention to the basic 

uncertainties underlying its modeling. 

Response (5-101):

We reviewed the IA in light of this comment, and do not agree that EPA paid little attention to the basic 

uncertainties underlying its modeling. We note that uncertainties are fully discussed in the IA. For 

example, directly after the Executive Summary, modeling uncertainties are discussed in the section 

“Summary of Policy Relevant Findings.” For instance, there are large differences across modeling groups, 

and/or across different model configurations used by the same group, in the specific spatial patterns of 

future simulated changes in meteorology that lead to differences in simulated future concentrations of 

ozone. Further, Sections 1.6 and 3 of the IA specifically discuss the uncertainty in the assessment effort. 

Here, the IA discusses the differences in modeling systems among the various groups. Section 3 of the IA 

provides a detailed discussion of the major uncertainties associated with the coupled climate and air 

quality modeling systems upon which rests the synthesis of the science of the report. 

The IA report also states that individual simulations show “some regions of little change, or even 

decreases, in addition to the O3 increases.” We note, however, the report goes on to state, “For nearly 

every region of the country, at least one (usually multiple) of the modeling groups found that climate 

change caused increases in summertime O3 concentrations.” Further, the report clearly indicates these 

modeling studies “show increases in summertime O3 concentrations over substantial regions of the 

country as a result of simulated 2050 climate change.” The TSD clearly summarizes the modeling studies 

discussed in the IA that show simulated climate change causes increases in summer O3 concentrations 

over substantial regions of the country, thought this was not uniform, and some areas showed little change 

or decreases. Therefore, we disagree with the commenters that we pay little attention to the uncertainties 

associated with the modeling analyses of the IA. See response to comment (5-103), which contains 

additional information regarding the various modeling groups. 

Comment (5-102): 

According to some commenters (3394.1, 3411.1, 3449.1, and 3747.1), the endangerment proposal admits 

that current models and studies do not reliably predict future ozone impacts. The TSD cites IPCC’s 2007 

conclusion that there are major discrepancies with observed long-term trends in ozone concentrations 

over the 20th century, and resolving these discrepancies is needed to establish confidence in the models. 

The commenters contend that conclusions drawn from models where discrepancies need to be resolved 

cannot support a health-based endangerment finding. EPA makes clear in its ozone IA, they state, that 

scientific analysis of these issues and the development of models that might project climate-related ozone 

changes are only now in the most preliminary of phases. The commenters suggest that the TSD notes 

various uncertainties without addressing their implications for the document’s assertions, and they ask 

that EPA explain these implications and incorporate them into the Agency’s conclusions. 

64 
Specifically, the commenters note the following uncertainties related to ozone impacts: 

“Relative to the other greenhouse gases, there is less confidence in reproducing the changes in 

ozone associated with large changes in emissions or climate, and in the simulation of observed 

long-term trends in ozone concentrations over the 20th century (Forster et al., 2007).” 

“More frequent occurrences of stagnant air events in urban or industrial areas could enhance the 

intensity of air pollution events, although the importance of these effects is not yet well quantified 

(Denman et al., 2007).” 

The commenters suggest that these weakly stated acknowledgements that climate change will result in 

some ozone decreases and that specific posited effects are uncertain are still insufficiently reflective of the 

actual scientific record, which undermines EPA’s reliance here on any supposed increase in ozone. They 

further state that EPA’s own report, Assessment of the Impacts of Global Change on Regional U.S. Air 

Quality: A Preliminary Synthesis of Climate Change Impacts on Ground-Level Ozone (U.S. EPA, 2009d), 

indicates that there are significant regions of the United States that are indeed likely to see ozone 

decreases associated with climate change; that reductions in ozone precursor emissions likely will 

overwhelm any increases that may result from climate change; and that, ultimately, the science in this 

area is riddled with uncertainties with respect to ozone (and PM). The commenters indicate that the TSD 

and the proposed endangerment finding omit any reference to these facts, even though they were publicly 

reported by the Agency itself in the very month in which it issued the proposed endangerment finding. 

The commenters contend that EPA’s approach here of ignoring or distorting scientific assessments, 

including even its own contemporaneous report, is arbitrary and indefensible. 

Response (5-102):

We have examined the TSD in light of this and other comments, and have determined that the TSD 

accurately conveys current scientific understanding and the associated uncertainties. 

The commenters contend that uncertainties in the scientific literature are “weakly stated” in the TSD. 

However, they do not provide adequate support or specific examples to support this assertion. In fact, the 

examples the commenters cite are actually taken from the TSD itself, which confirms that EPA provided 

a comprehensive discussion. Thus, EPA strongly disagrees with the contention that we omitted references 

to uncertainties or the need for additional research. To the contrary, the IA clearly identifies uncertainties 

and areas where further work is needed, and these findings are summarized in the TSD. We find that the 

commenters’ assertions to be unsupported with specific scientific literature. Uncertainties in our modeling 

are transparently described and quantified; the models are widely accepted and scientifically sound to 

make conclusions on the things that we mention in the TSD and IA. Therefore, based on the discussions 

in the TSD and the IA, we conclude that our summary of this issue in the TSD is reasonable and 

supported by scientific literature. 

We further note that the fact that particular issues are uncertain or could be better understood through 

additional research should not be taken to imply that such issues are not sufficiently well characterized to 

inform the Administrator’s endangerment analysis. As noted in the quote above from the Executive 

Summary of the TSD, our goal has been to provide a complete and accurate summary of the science, 

including uncertainties, to ensure that the Administrator has a comprehensive foundation for her 

endangerment analysis. 

For these reasons, we disagree with the comment that results of modeling studies should be excluded if it 

is also recognized that such results could be improved through additional research. The ozone simulations 

employ state-of-the-art models and up-to-date databases, and the assessment literature has found that the 

models are sufficiently accurate to indicate general increases in summertime ozone concentrations over 

65 
substantial regions of the country as a result of simulated 2050 climate change. The IA, as noted in the 

following excerpts, projects ozone increases over “substantial” regions of the country while “some” 

regions show little change or even decreases, though the decreases tend to be less pronounced than the 

increases. 

The new modeling studies discussed in this report show increases in summertime ozone 

concentrations over substantial regions of the country as a result of simulated 2050 climate 

change. 

For nearly every region of the country, at least one (usually more than one) of the modeling 

groups found that climate change caused increases in summertime ozone concentrations. 

Though in agreement on the results above, the different modeling systems did not necessarily 

simulate the same regional patterns of climate-induced ozone changes. The individual simulations 

showed some regions of little change, or even decreases, in addition to the ozone increases. 

As stated in the final TSD: 

[T]he results in the IA demonstrate that O3 responds to climate change in a qualitatively 

consistent manner across the simulations from multiple research groups. The patterns of 

relative changes in regional climate vary across these same simulations. Figure 3-11 of 

the IA graphically illustrates the net change in daily average ozone values across the 

research results for summertime ozone. Ozone concentrations increase across most areas 

of the country with decreases limited to some parts of the Southwest. The net increases of 

ozone concentrations in the large population centers of the northeast and middle Atlantic 

United States are the results with the highest confidence. The net increases in the 

Southeast and the small net changes in the Northwest are the features with the lower 

confidence. 

Thus, the overall effect of climate change itself is to increase ozone levels compared to what would occur 

without future climate change, over broad areas of the country, especially on the highest ozone days and 

in the largest metropolitan areas with the worst ozone problems. Ozone decreases are projected to be less 

pronounced and to be limited to some parts of one area of the country, with generally less overall 

population. See Fig. 3-11 of the IA, which provides mean ozone changes across all seven modeling 

experiments 

66 
Source: Assessment of the Impacts of Global Change on Regional U.S. Air Quality: A Preliminary 

Synthesis of Climate Change Impacts on Ground-Level Ozone (U.S. EPA, 2009d) 

We further disagree with the commenters’ characterizations of the conclusions of the IA. It does not 

indicate that there are “significant” regions of the United States that are likely to see ozone decreases 

associated with climate change, nor does it indicate that reductions in ozone precursor emissions likely 

will “overwhelm” any increases that may result from climate change. The IA states: “Preliminary work 

suggests that the impacts of climate change on future U.S. regional O3 concentrations remain significant 

when also considering possible future anthropogenic O3 precursor emissions changes.” The IA also states: 

“These preliminary tests found that the combined effects of climate and anthropogenic precursor 

emissions changes are highly sensitive to the assumptions about future emissions trajectories.” As noted 

above, the IA projects ozone increases over “substantial” regions of the country while “some” regions 

show little change or even decreases, though the decreases tend to be less pronounced than the increases 

and to be limited to some parts of the Southwest. 

We also note that the commenter failed to acknowledge an additional statement from IPCC: the TSD 

refers to the IPCC (Denman et al., 2007) conclusion that “the current generation of tropospheric ozone 

models is generally successful in describing the principal features of the present-day global ozone 

distribution.” 

67 
It appears that the commenter is also concerned with how uncertainty in the scientific findings has been 

weighed and evaluated by the Administrator in her endangerment analysis. See the Findings, Section 

IV.B, “The Air Pollution Is Reasonably Anticipated to Endanger Both Public Health and Welfare,” for 

our response to comments on how the Administrator weighed the scientific evidence underlying her 

endangerment determination. 

Comment (5-103): 

A number of commenters (3347.1, 3347.3, and 3347.4) state that the TSD selectively presents research 

findings, giving scant (if any) attention to results that contradict its main theme of large climate-related air 

pollution impacts. One commenter indicates that EPA selectively picked model results that support the 

endangerment proposal’s policy objective. A commenter indicates that well over a hundred conference 

papers, final and “in review” journal papers, PowerPoint presentations, poster papers, STAR grant 

proposals, and project narratives are available that may be used to supplement, and in some cases 

challenge, the information in the TSD and IA. In light of the full array of relevant climate-air quality 

modeling data available by mid-April 2009, the commenters express concern that the TSD science 

foundation has been fashioned largely by information that agrees with the proposed finding of 

endangerment. 

Specifically, a commenter (3347.3) states that the EPA’s conclusions do not reflect the variability of the 

findings and EPA accepts as valid the conclusions of a modeling group when they demonstrate an 

increase in ozone in a certain region; however, when the same modeling group reports a decrease in ozone 

in another region, EPA then relies on another group’s modeling results that show an increase in ozone in 

that particular region. The commenter notes, for example, that even though three of four modeling groups 

report that climate change will decrease ozone in the northwestern United States, EPA concludes climate 

change will increase ozone in this region based on the one positive study. The commenter suggests that 

when there is disagreement in the results across modeling groups in a region, EPA will use results from 

the group showing that ozone will increase due to climate change. The commenter concludes that this 

demonstrates a consistent lack of scientific objectivity, both in the substance and presentation of the 

findings. 

Response (5-103):

EPA disagrees with the comments that analyses in the TSD do not reasonably and adequately reflect the 

current state of knowledge, including uncertainties, on this topic. See our response above (5-95) to 

critiques that EPA’s analyses of the impacts of climate change on U.S. air quality were selective. See 

Section III.A., “The Science on Which the Decisions Are Based,” of the Findings for our response to 

comments on the use of the assessment literature and our treatment of new and additional scientific 

literature provided through the public comment process. Similarly, see Volume 1 of the Response to 

Comments document for responses to comments on the use of major assessment reports as the primary 

scientific basis of the TSD. 

EPA disagrees with the commenter’s general assertion that we have selectively and non-scientifically 

presented the results of modeling studies. EPA’s TSD relies not only on analysis provided by the IA but 

also relies on several peer-reviewed synthesis documents, including findings published by IPCC and 

USGCRP (formerly CCSP). The TSD summarizes findings from the IA, which assessed the results of 

numerous modeling simulations performed by a number of different modeling groups. A large proportion 

of Section 3 of the IA, the key scientific synthesis section upon which the conclusions of the IA are based, 

is devoted to detailed discussions of precisely the sorts of differences among the various modeling results 

that the commenter mentions. The full diversity of ozone results from the various modeling groups were 

explicitly presented in numerous maps and figures in the IA, clearly illustrating which simulations 

showed both climate-induced ozone increases and decreases, and in which parts of the country. Assertions 

68 
that the EPA drew conclusions in the IA such as “even though three of four modeling groups report that 

climate change will decrease ozone in the Northwest U.S. EPA concludes climate change will increase 

ozone in this region based on the one positive study” are false. For example, in Fig.3-11 of the IA 

(above), and as referenced in the TSD, the Northwest part of the country shows generally a neutral impact 

from climate change on ozone levels when the results across all seven different modeling experiments are 

combined. The analysis in the IA showed clearly that there are numerous, important model-based 

uncertainties in simulating the potential sensitivity of ozone to climate change, leading to differences 

among the results from the different models analyzed. These inter-model differences were embraced and 

fully examined in the IA to improve our understanding of the pathways by which meteorological changes 

in an altered climate lead to changes in ozone concentrations and the differences in the way these 

pathways are represented in the modeling systems used in the leading research groups. They were not 

highlighted in order to selectively discount the results from any particular model. 

Nowhere in the IA or the TSD was any judgment made about any model being any “better” or “worse” 

than any other model, and nowhere did the IA give any primacy to any simulation result over any other 

for the purpose of drawing its conclusions. Completely contrary to the commenter’s assertion, no model 

result was discarded, and all contributed equally to the stated conclusions of the IA. For regions for which 

there were larger differences among the models as to the simulated effect of climate change on ozone 

concentrations (i.e., portions of the western and southeastern parts of the United States), this was 

explicitly noted in the IA in the Executive Summary, the Summary for Policy Relevant Findings, and the 

main body of the report (in the conclusions of Section 3). To summarize, the conclusions in the IA that 

climate change has the potential to exacerbate ozone pollution in many parts of the country were arrived 

at from the improved scientific understanding provided by the complete range of available model results 

surveyed, and they flow logically and scientifically from this full diversity of findings. Regarding the 

general comment that there are well over a hundred conference papers, final and “in review” journal 

papers, PowerPoint presentations, poster papers, STAR grant proposals, and project narratives available 

for use, we would note that many of those peer-reviewed studies are already considered in the IA. 

Comment (5-104): 

A commenter (3347.4) states that the TSD relies on the “climate penalty” concept to describe air pollution 

increases under a changed future climate and encourages EPA to promote a more scientifically based, 

balanced means of describing the linkages between air quality and climate change impacts. 

69 
Response (5-104):

While the IA uses the term “climate penalty,” the TSD does not. In any case, “climate penalty” has 

become an accepted term among researchers in this field since its introduction in the literature (introduced 

by Wu et al., 2008; see also Tagaris et al., 2009; Avise et al., 2009; and Bloomer et al., 2009). In general, 

“climate penalty” refers to the incremental impact of climate change on air quality under the assumption 

of constant criteria pollutant emissions, such that the effect of climate change on air quality can be 

isolated. It can be assessed from either simulations that hold air pollution emissions constant, from 

simulations with continuing air pollution emission controls, or from historical measures. The climate 

change penalty for ozone air pollution is the best available scientifically based means to describe linkages 

between air quality-climate change impacts across different emission scenarios. It was originally 

developed by researchers at Harvard and has been widely adopted by scientists working in the areas of 

climate change impacts on air quality. Not only is the climate change penalty for ozone air pollution a 

robust feature in modeling simulations, but a recent journal article (Bloomer et al., 2009) provides 

observational evidence for the climate change penalty consistent with modeling results. This helps to 

isolate the climate signal to understand and describe the linkages between air quality and climate change 

impacts. This serves as a scientifically accepted method for determining air pollution changes under 

future climate conditions, as is consistent with the larger body of scientific literature. 

Comment (5-105): 

A commenter (3347.1) states that inadequate consideration is given to projected future intercontinental 

transport of criteria air pollutants and the roles that sources outside the United States (e.g., China, India, 

and Mexico) will have on ozone and PM2.5 impacts in coming decades. The commenter indicates that for 

the regional air quality models relied upon in the TSD, the impact of intercontinental transport of 

emissions is treated by boundary conditions and the TSD does not consider this subject. The commenter 

continues to note the IA states “...the strong influence of the GCM-simulated climate on the downscaled 

results is inescapable, regardless of the methodological details.” The commenter notes that EPA affirms in 

the IA that interactions between the global and regional models are important for air quality modeling and 

emphasizes the need to quantify the biases and characteristics of the specific global model simulations 

being relied upon for boundary conditions to the air quality models. The commenter states that this need 

is not mentioned at all in the TSD. 

Response (5-105):

The modeling systems from the IA indeed consider the effects of international emissions of criteria 

pollutants or their precursors and the transport of those criteria pollutants or their precursors to the United 

States (for example, via the chemical boundary conditions imposed at the borders of the regional air 

quality modeling domain). The results of the IA are reflected in the TSD along with other findings from 

major scientific assessments thus, we conclude this subject is fully considered by the TSD. For the 

climate-only sensitivity simulations, these international emissions were held constant at present-day levels 

(just like the U.S. emissions). Explicitly teasing apart the combined impacts of changes in future U.S. 

emissions, changes in future intercontinental transport, and changes in future climate was not the primary 

focus of the IA, though the intercontinental transport issue is acknowledged as important, called out as a 

research need, and also investigated somewhat by some of the participating modeling groups (and cited in 

their publications referenced in the IA). 

 

Comment (5-106): 

A commenter (3411.1) states that the Center for the Study of Carbon Dioxide and Global Change 

provided EPA with experimental evidence that the increased levels of CO2 in the atmosphere may 

actually reduce the emission of isoprene per unit of biomass. Since isoprene is a highly reactive biogenic 

70 
hydrocarbon that is emitted in copious amounts by vegetation and is a major source of ozone in the 

atmosphere, the commenter requests that EPA permit testimony on how increased levels of CO2 in the 

atmosphere would affect isoprene levels. 

Response (5-106):

We reviewed the source of information provided by commenter and note it is derived from the 

organization’s Web site. We note that this source of information does not specifically reference peerreviewed scientific literature related to this issue. Thus, we conclude that the commenter’s view of 

changes in isoprene emissions is not adequately supported by the scientific assessment literature. We will 

continue to rely on the synthesis reports, including the IPCC finding, and no changes to the TSD are 

warranted. See the Findings, Section III.A., “The Science on Which the Decisions Are Based,” for our 

response to comments on the use of the assessment literature and our treatment of new and additional 

scientific literature provided through the public comment process. 

As noted in the TSD, IPCC (Meehl et al., 2007) reports that biogenic emissions are projected to increase 

by between 27% and 59%, contributing to a 30 to 50% increase in ozone formation over northern 

continental regions (for the 2090–2100 timeframe, relative to 1990–2000). We addressed the issue of 

isoprene in the IA, stating, “Another important impact is that climate change leads to changes in the 

natural emissions of VOCs, e.g., isoprene from vegetation. All of the modeling groups found climateinduced increases in these biogenic VOC emissions over most of the United States, with especially 

pronounced increases in the Southeast.” 

See the Findings, Section I.C.1(e) for our response on the request to permit testimony under a formal 

rulemaking under the Administrative Procedures Act. 

Comment (5-107): 

Commenters (3411.1 and 3347.3) cite Tagaris et al. (2007) and state that this work reported that both 

ozone and fine PM were substantially reduced in the 2050 case, confirming that the nation’s air quality 

will continue to improve in spite of projected climate change. The commenter also indicated that Tagaris 

et al. (2007) included a model simulation in which the projected climate change in 2050 was combined 

with the 2001 emissions and, while this is an unrealistic simulation of the future, it is a direct way to 

separate out the impact of climate change. The commenter indicates that the study found that summer 

ozone over the entire United States was essentially unchanged with climate change, although five 

individual regions had ozone increases or decreases ranging up to 3% and that summer fine PM was 

reduced by about 10% overall with reductions from 2% to 18% in the five regions. 

Response (5-107):

We reviewed this comment and have determined that the Tagaris et al. (2007) study was addressed in the 

IA and appropriately reflected in the TSD. In particular, the findings of this study were taken into account 

in the IA, as part of its “Synthesis of Results Across Groups.” (This journal article comes from the 

Georgia Tech/NESCAUM research group whose activities were funded through an EPA STAR grant and 

analyzed in detail in the IA.). The study confirms that substantial reductions in emissions (more than 

50%) are effective for improving future air quality. We disagree with the commenters’ assertion that the 

study found that the summer ozone over the entire United States was essentially unchanged with climate 

change. Importantly, the study indicates that GHG emissions will increase “the number of days with 

ozone concentrations above 85 ppb in most regions except the Midwest.” A more recent journal article 

from the Georgia Tech/NESCAUM team estimates a net increase in ozone mortality of an additional 300 

deaths per year due to climate change in 2050. This confirms that the results from the Georgia 

Tech/NESCAUM team indicate a net increase in ozone over the United States (Tagaris et al., 2009). 

71 
Thus, we disagree with the commenter that the results of Tagaris et al. (2007) as described the commenter 

were essentially unchanged. 

For both the climate change only and the combined climate and emission changes cases, the magnitude of 

the “climate change penalty” for controlling ozone is found to be consistent with the work of Wu et al. 

(2008). The impact of climate change is to worsen air quality compared to both cases without climate 

change. The findings further suggest that compliance with air quality standards in areas at or near the 

NAAQS in the future would be sensitive to the amount of future climate change. For these reasons we 

find this work (Tagaris et al., 2007) to be consistent with climate-only analysis, thereby supporting the 

TSD’s summary of the IA. 

Comment (5-108): 

A commenter (3347.4) states that “[t]here is no indication that OAQPS staff was involved in the science 

development of the proposed endangerment finding” and “[t]he TSD’s perfunctory treatment of air 

quality-climate change modeling findings from the CIRAQ and ICAP programs suggests inadequate 

communication between the agency’s modeling scientists and policy staff.” 

Response (5-108):

The commenter is in error. The EPA team of TSD authors and reviewers included staff from ORD and 

OAQPS. Further, we disagree that the TSD’s treatment of air quality/climate change modeling findings 

from the CIRAQ and ICAP programs was “perfunctory.” The TSD does not include the ICAP 

information contained in two PowerPoint presentations cited in comments (Jang, 2008, 2004) because, as 

explained in a previous response to comment, EPA is relying on peer-reviewed, synthesis reports such as 

IPCC (2007). The results from the NERL CIRAQ project, as published in Nolte et al. (2008), were a key 

part of the IA analysis and were fully considered in the TSD. We note in the IA report the critical role of 

the CIRAQ project and other offices within EPA had in providing modeling expertise for the 

development of the IA assessment. This assessment team, as identified in the IA report, provides the air 

quality modeling expertise to develop these simulations, to interpret the sensitivity of air quality to the 

future climate changes simulated, and to consider the regulatory implications of potential changes in air 

quality. 

Comment (5-109): 

A commenter (3347.4) asserts that the TSD relies almost exclusively on EPA’s IA report to support 

assertions related to future ozone levels associated with climate change. 

Response (5-109):

The EPA IA represents the current state of the science based on analysis of results from eight research 

groups that examined how climate change may affect U.S. air quality. However, we disagree with the 

commenter’s assertion that the TSD relies almost exclusively on EPA’s IA report for the section on air 

quality. The TSD relies on many studies relating climate change and ozone levels, and includes several 

references to findings of IPCC, USGCRP, and other sources in the assessment literature. 

Comment (5-110): 

One commenter (3347.3) states that EPA’s conclusion on page ES-4 of the TSD fails to acknowledge that 

ozone levels may decrease in rural areas with low nitrogen oxide levels (U.S. EPA, 2009d). Such findings 

have a significant impact on the assessment of potential health impacts of changing air quality due to 

climate change. In regions of the country where ozone levels are expected to decline (e.g., rural and 

72 
certain coastal areas), the commenter asserts that EPA should account for the potential benefits of these 

lower ozone levels in these regions. The commenter further asks EPA to make its estimates of health 

effects from ozone methodologically consistent with the methods EPA uses in the recent ozone regulatory 

REA, or explain why the ozone regulatory impact analysis (RIA) is methodologically biased. 

Response (5-110):

EPA disagrees with the commenter that we do not acknowledge regional changes in ozone levels such as 

in rural and urban locations. We note that the TSD summarizes the IA’s assessment of the differing 

impacts of climate change in clean rural versus polluted rural and urban areas. In the IA and TSD we 

draw directly from the studies cited and do not alter the data or methodology conducted in those studies. 

However, because most of the population resides in urban areas, the overall impact of this aspect (clean 

rural versus urban areas) of climate change on ozone likely will be adverse; i.e., a large part of the 

population experiencing increased ozone levels. Overall, IPCC states that climate change is expected to 

decrease background tropospheric ozone due to higher water vapor and to increase regional and urbanscale ozone pollution due to higher temperatures and weaker air circulation (Denman et al., 2007; 

Confalonieri et al., 2007). 

In addition, we note that climate change is projected to increase surface layer ozone concentrations in 

both urban and polluted rural environments due to decomposition of peroxyacetylnitrate (PAN) at higher 

temperatures (Sillman and Samson, 1995; Liao and Seinfeld, 2006). Further, warming temperatures 

enhances decomposition of PAN, releasing NOx, an important ozone precursor (Stevenson et al., 2005). 

Model simulations (using the high-end A2 emissions scenario) with higher temperatures for the year 2100 

showed that enhanced PAN thermal decomposition caused this species to decrease by up to 50% over 

source regions and ozone net production to increase (Hauglustaine et al., 2005). Thus, there is strong, 

credible scientific evidence that ozone in rural areas may end up higher in the future due to greater PAN 

decomposition. 

We determined that the commenter meant RIA instead of REA and have responded accordingly. The RIA 

method for analyzing ozone attainment is appropriate for analyzing attainment with the NAAQS and EPA 

employs another method to analyze what the NAAQS should be and whether it should be revised. 

However, the present action related to endangerment is not a regulatory action; therefore, the RIA method 

does not apply. In addition, EPA is not trying to quantify the health benefits of a specific change in the 

NAAQS, and the resulting modeling of a certain ozone levels, which the RIA methodology then uses. 

Modeling studies discussed in EPA’s IA show that simulated climate change causes increases in 

summertime ozone concentrations over substantial regions of the country, though this was not uniform 

and some areas showed little change or decreases, though the decreases tend to be less pronounced than 

the increases. For those regions that showed climate-induced increases, the increase in maximum daily 8-

hour average ozone concentration, a key metric for regulating U.S. air quality, was in the range of 2 to 8 

ppb, averaged over the summer season. The increases were substantially greater than this during the peak 

pollution episodes that tend to occur over a number of days each summer. Thus, the overall effect of 

climate change itself is to increase ozone levels, compared to what would occur without future climate 

change, over broad areas of the country, especially on the highest ozone days and in the largest 

metropolitan areas with the worst ozone problems. Ozone decreases are projected to be less pronounced 

and to be limited to some parts of one area of the country, with generally less overall population. 

Comment (5-111): 

A commenter (3347.3) asserts that EPA has failed to cite data for locations other than the eastern United 

States where ozone is predicted to increase and adversely impact air quality and health (e.g., Bell et al., 

2007; Field et al., 2007). On the other hand, the commenter states, EPA does not report findings where 

73 
climate change is expected to produce no change or a decrease in mortality due to no change or a decrease 

in the level of ozone; thus, the Agency only reports on areas for which a trend toward an increase in 

health effects is predicted. The commenter states that this is further evidence of a lack of substantive and 

presentational objectivity because EPA failed to perform a comprehensive nationwide analysis 

considering both the regional variability (increases and decreases) in ozone subsequent to climate change, 

and the regional variability in concentration function responses that are apparent in the health effects data 

(even though EPA possesses the data to do so). The commenter concludes that it is not possible at this 

time to make a definitive conclusion concerning whether, overall, U.S. health effects will increase or 

decrease due to the influence of climate change on ozone. 

Response (5-111):

EPA strongly disagrees with the comment that the IA failed to cite data for locations other than the 

eastern United States with regard to ozone air quality and health effects. The IA extensively discusses the 

changes in ozone across the United States based on nationwide results from seven modeling groups and 

regional results from two additional modeling groups. Results across these modeling groups show greater 

increases than decreases, with the increases more predominant in high-population areas and for high-airpollution episodes. Thus, we strongly disagree that we did not consider national-scale analyses in the 

TSD. The IA is a comprehensive nationwide analysis that considered the regional variability in ozone 

subsequent to climate change. The TSD has been developed to inform the Administrator’s endangerment 

analysis, not to inform attainment demonstrations under the NAAQS. To support its intended purpose, the 

summary in the TSD properly focuses on the projected impact of global GHG emissions on large-scale 

patterns of air quality in the United States via induced climate changes as represented in GCMs. 

The findings described in the IA as well as other peer-reviewed, synthesis documents, including findings 

published by IPCC and USGCRP (formerly CCSP), clearly indicate that ozone concentrations in urban 

and polluted rural areas are expected to increase during summer episodes due to climate changes 

including changes in temperature, wind patterns and chemical mechanisms involving PAN. The TSD also 

indicates that in some areas ozone concentrations are expected to decrease due to the higher absolute 

humidity which decreases ozone concentrations. Because the increases in ozone are projected to occur 

primarily in urban areas, we expect the overall impact to be adverse to public health. For example, the 

results in the IA demonstrate that ozone responds to climate change in a qualitatively consistent manner 

across the simulations from multiple research groups. The patterns of relative changes in regional climate 

vary across these same simulations. Figure 3-11 of the IA graphically illustrates the net change in daily 

average ozone values across the research results for summertime ozone. As mentioned in previous 

responses in the section, ozone concentrations increase across most areas of the country with decreases 

limited to some parts of Southwest. The net increases of ozone concentrations in the large population 

centers of the northeastern and middle Atlantic United States are the results with the highest confidence. 

The net increases in the Southeast and the small net changes in the Northwest are the features with the 

lower confidence. Recent results from the Georgia Tech group (Tagaris et al., 2009) estimate a net 

increase in ozone mortality of an additional 300 deaths per year due to climate change in 2050. 

 

See the Findings, Section IV.B, “The Air Pollution Is Reasonably Anticipated to Endanger Both Public 

Health and Welfare,” for our response to comments on how the Administrator weighed the scientific 

evidence underlying her endangerment determination. 

Comment (5-112):

A commenter (3347.3) states that the EPA also relies heavily and selectively on the study by Jacob and 

Winner (2009). EPA cites this reference to support the conclusion that “there is now consistent evidence 

from models and observations that 21st-century climate change will worsen summertime surface ozone in 

polluted regions of North America compared to a future with no climate change.” According to the 

74 
commenter, EPA fails to note that Jacob and Winner (2009) also state that while most of these models 

predict increases in the Northeast, the results in other regions show “large differences between models.” 

Furthermore, this study did not account for existing regulatory control programs and reductions in 

anthropogenic emissions in making projections of future levels of ozone. 

Response (5-112):

Jacob and Winner (2009) is a journal article that reviews and synthesizes results across all known peerreviewed studies as of late 2008. As such, it provides a very recent representation of the current state of 

knowledge on the impacts of climate change on air quality. It assessed numerous individual studies to 

draw its conclusions that were reviewed not only through the journal’s peer review process, but also by 

EPA, and we have determined the study by Jacob and Winner (2009) has been well-vetted and accurately 

reflects the consensus among knowledgeable peers in the field of climate science and air quality. 

The statement in the TSD that “There is now consistent evidence from models and observations that 21stcentury climate change will worsen summertime surface ozone in polluted regions of North America 

compared to a future with no climate change” accurately reflects the conclusions of Jacob and Winner 

(2009), and this statement does take into account the differences between models. 

Jacob and Winner (2009) discuss several studies that account for existing regulatory control programs and 

reductions in criteria air pollutant emissions. We note that Jacob and Winner state: “Simulations that 

assume emission reductions far beyond the full implementation of current regulations indicate that 

climate change will partly offset the benefit of the emissions reductions (Tao et al., 2007; Tagaris et al., 

2007; Nolte et al., 2008). Wu et al. (2008) refer to this ‘climate penalty’ as the need for stronger emission 

controls to achieve a given air quality standard.” Thus, the EPA finds clear evidence from the scientific 

assessment literature that GHGs will impact air quality adversely in the future. For these reasons we 

conclude the study by Jacob and Winner (2009) is appropriate and reflects the current state of the 

scientific literature on this issue. See response (5-103) for our response to comments on the results and 

reasons for the relative differences between models. 

Comment (5-113): 

One commenter (3347.4) notes that notwithstanding the prodigious amount of modeling data generated 

by EPA and other research programs in the climate science field, certain basic data sets are simply 

unavailable to independent scientists or can only be obtained from participating researchers through timeconsuming data requests. 

Response (5-113):

We are not aware of any instance in which someone formally requested access to modeling data for the 

purpose of the proposed endangerment finding and was denied access. Additionally, most of the models 

used in these studies are publicly available for free download, such as CMAQ, CAMx, MM5, and the 

GISS GCM. 

Comment (5-114): 

A commenter (3347.4) notes that a few literature citations are missing in the reference section of the TSD. 

These include WHO (2002), Bowman and Johnston (2005), and Moore et al. (2006). The citation for 

Brasseur, et al. (2006) should include the page numbers 3932-3951. 

Response (5-114):

75 
We appreciate the commenter’s point of clarification. The TSD was revised to reference the primary 

source of the finding (Confalonieri et al., 2007) and then note additional references therein, rather than 

adding the individual references to reflect the additional sources which contribute to the finding. We note 

this change is consistent with how other supporting conclusions from IPCC are referenced in the TSD. 

Comment (5-115): 

A commenter (3347.4) quotes the following from the TSD: “increased biogenic emissions alone add 1–3 

parts per billion (ppb) to summertime average daily maximum 8-hour ozone concentrations in the 

Midwest and along the eastern seaboard (Hogrefe et al., 2004).” The commenter goes on to state that a 

closer inspection of the Hogrefe et al. (2004) paper reveals that over most of the Midwest and eastern 

United States, the biogenic impact ranges from -1 to 1 ppb. The ozone increases of 1–3 ppb mentioned in 

the TSD are largely confined to a narrow band of grid cells aligned along the Ohio River and along the 

East Coast margin from Philadelphia to Boston. The commenter concludes that the TSD has emphasized 

the high end of the modeled ozone enhancements (1–3 ppb) from biogenic increases, essentially 

neglecting broad regions across the country where ozone perturbations in the -1 to 1 ppb range were 

calculated. 

Response (5-115):

We disagree with the commenter and maintain that the TSD accurately reflects the results reported by 

Hogrefe et al. (2004). The TSD summarizes this study in the context of evidence that the influence of 

climate induced changes of biogenic VOC emissions may be regionally substantial. Hogrefe et al. (2004) 

state: “Results from these simulations are shown in Figures 5a–5c and indicate that increased biogenic 

emissions alone add 1–3 ppb to summertime average daily maximum 8-hour O3 concentrations in the 

Midwest and along the eastern seaboard.” Other regions of the United States may not experience this 

increase, which is consistent with respect to expected overall variability in ozone levels associated with 

climate change. We note that Hogrefe et al. (2004) found the strongest increases in emissions in the 

Southeast, similar to the results from the NERL and Illinois 1 and 2 experiments modeling teams, but 

found that the largest ozone concentration changes that could be attributed to biogenic emissions changes 

occurred instead in parts of the Ohio Valley and coastal Mid-Atlantic. We conclude that the TSD 

accurately reflects these findings from Hoegefe et al. (2004) and we do not emphasize the high end of the 

ozone increases as the commenter implies. 

Comment (5-116): 

A commenter (3347.4) suggests that given differences among mechanism predictions and difficulty in 

proving which one is “correct,” regulatory decisions based on model predictions should account for the 

uncertainty due to differences in chemical representation. The commenter further suggests that this is an 

area where the TSD should be expanded to include 1) the recent chemistry-related modeling studies 

within EPA’s ORD as well as by outside researchers and 2) the range of predictions resulting from 

mechanism comparison studies in order to shed light on the expected range of uncertainty for ozone and 

PM2.5. 

76 
Response (5-116):

The various chemical mechanisms used in several models are described in the IA, and the TSD 

summarizes findings from many references, including the IA. The TSD, for example, indicates that “the 

response of ozone to changes in biogenic emissions depends on how isoprene chemistry is represented in 

the models—models that recycle isoprene nitrates back to NOx will tend to simulate significant O3

concentration increases in regions with biogenic emissions increases, while models that do not recycle 

isoprene nitrates will tend to simulate small changes, or even O3 decreases.” We provide appropriate 

detail on the chemical mechanisms and reflect the associated uncertainties and references in the IA; we 

find it seems unnecessary to provide and repeat the same level of detailed information from the IA in the 

TSD, which is a summary of major conclusions from the underlying scientific assessments. 

Comment (5-117): 

A commenter (3347.4) notes that the TSD briefly mentions an area of increasing importance for reliable 

regional air quality modeling—reactive nitrogen chemistry feedbacks. Given the importance of the 

reactive nitrogen budget for future air quality simulations, the commenter requests that the TSD should be 

expanded to reflect recent research findings as well as a clear explanation of the values of dinitrogen 

pentoxide used in the various platforms employed in the Phase I, CIRAQ, and ICAP modeling (e.g., 

GEOS-Chem, MOZART, CMAQ, CAMx) and the assumptions regarding isoprene nitrate partitioning 

and yields. 

Response (5-117):

In light of this comment and after further review of the TSD, we find these areas are adequately 

summarized in the TSD. Additional detailed discussions of both well understood and highly uncertain 

ozone photochemistry can be found in the U.S. EPA Air Quality Criteria Document for Ozone (U.S. EPA, 

2006). 

Comment (5-118): 

A commenter (3347.4) states that the TSD paints a pessimistic view of the adequacy of state-of-science 

coupled chemistry-aerosol-climate models for providing guidance for decision-making and recommends 

the TSD incorporate this newer perspective of photochemical aerosol modeling capabilities. Although 

much work remains, the modeling tools are useful in their present stage of development to provide useful 

information to public decision-makers. 

Response (5-118):

We agree that the modeling tools are useful in their present stage of development; however, no changes to 

the TSD are warranted. As described in the IA, improvements in our ability to model chemistry of air 

pollution are desirable in a number of areas to better understand the influence of climate change on air 

quality. Notable among these is the ability to introduce simulation of two-way interactions between 

climate and chemistry such as changes in the distribution of particulates resulting from changes in climate 

or emissions could have important impacts on the Earth’s radiation budget, thereby further influencing 

climate. 

Comment (5-119):

A commenter (5846) indicates that EPA has adopted the following false or misleading belief: that climate 

change will lead to degraded air quality specifically, that regional ozone pollution will increase. The 

commenter indicates that ozone is a natural chemical produced by natural processes in quantities much 

greater than any amounts produced by humans and ozone production is driven by natural, not 

77 
anthropogenic, processes. The commenter further indicates that any warming effect of increased ozone on 

health will be offset by a reduction in the severe cold events which are the true drivers of the increased 

rates of most respiratory complaints. The commenter argues that EPA presents the opposite of the most 

likely results of warming as fact and the true consequences are not presented. 

Response (5-119):

EPA does not agree with the commenter that the potential for increases in regional ozone pollution is 

false or misleading. We rely on strong evidence from the scientific literature to support our statements 

regarding climate change and effects on air quality. As indicated in the TSD, tropospheric (including 

ground or surface-level) ozone is both naturally occurring and, as the primary constituent of urban smog, 

a secondary pollutant formed through photochemical reactions involving NOx and VOCs in the presence 

of sunlight. IPCC (Denman et al., 2007) reports that climate change can affect ozone by modifying 

emissions precursors, atmospheric chemistry, and transport and removal. Further, there is now consistent 

evidence from models and observations that 21st century climate change will worsen summertime surface 

ozone in polluted regions of North America compared to a future with no climate change (Jacob and 

Winner, 2009). Thus, EPA considers there to be clear evidence that climate change will likely increase 

ozone pollution, with associated risks to human health from respiratory illness and premature death. 

Comment (5-120): 

A commenter (10116) indicates that this document is an important step for the federal government. 

However, on the issue of air quality and human health, it downplays an important body of work, funded 

by EPA, that represents the first comprehensive assessment of climate change impacts on ozone-related 

and heat-related health impacts in the United States: the New York Climate Health Project. The 

commenter recommends that EPA discuss Kinney et al. (2006, 2008) and Knowlton et al. (2004, 2008) 

and states that the EPA has overlooked the only health-based paper on climate change and health with a 

U.S. focus (Kinney et al., 2008). 

Response (5-120): 

In light of this comment, EPA has reviewed the reference literature in the TSD. We note that some of the 

studies referenced by the commenter (Knowlton et al., 2004) are cited by IPCC (Field et al., 2007) and 

summarized in Section 6 of the TSD section (6) which is referred to by the commenter. Similarly, the 

USGCRP assessment report (Karl et al., 2009) relies on the same findings and associated studies, which 

are also consistent with information summarized in the TSD. Further, we note several of the studies 

reviewed in Kinney et al. (2008) are cited in the assessment literature, TSD and this document. While 

EPA considers the studies referenced by the commenter to be consistent with the assessment literature 

and supportive of conclusions summarized in the TSD, we conclude that revising the TSD to incorporate 

these studies is unnecessary. 

Comment (5-121): 

Commenter (2750) notes that the endangerment proposal indicates climate change can exacerbate 

tropospheric ozone levels in some parts of the United States. However, with more frequent and intense 

storms which clean the atmosphere also projected, how will more ozone be produced? 

Response (5-121): 

EPA disagrees with the commenter’s general assertion that the United States will have more frequent 

storms. Future changes in precipitation due to human-induced climate change are more difficult to project 

than temperature. Further, we note the overall frequency of summertime storms will likely decrease in 

many areas (e.g., Mickley et al., 2004). 

78 
Changes in the frequency and intensity of storms may decrease ozone, but this ignores other possible 

changes such as increasing biogenic emission of ozone precursors or increases in the reaction rates of 

chemical process that form ozone due to higher temperatures. Formation of tropospheric ozone is a 

complex system of chemical and physical processes. This is why the IA relies on comprehensive 

modeling systems to analyze this complex system. Based on this assessment, more ozone will be 

produced over much of the United States under future climate conditions. 

Comment (5-122): 

Commenter (3387.2) submits a study by Corbett et al. (2007), Mortality From Ship Emissions: A Global 

Perspective, on health effects and emissions from marine transport as part of an appendix to comments on 

EPA's Proposed Findings. The commenter indicates that epidemiological studies consistently link 

ambient concentrations of PM to negative health impacts, including asthma, heart attacks, hospital 

admissions, and premature mortality. Corbett et al. estimate global and regional mortalities by applying 

ambient PM increases due to ships to cardiopulmonary and lung cancer concentration risk functions and 

population models. The results indicate that shipping-related PM emissions are responsible for 

approximately 60,000 cardiopulmonary and lung cancer deaths annually, with most deaths occurring near 

coastlines in Europe, East Asia, and South Asia. The study notes that under current regulation and with 

the expected growth in shipping activity annual mortalities could increase by 40% by 2012. 

Response (5-122): 

EPA reviewed this reference and acknowledges the important health effects associated with emissions of 

PM and PM precursors. These findings are concerned with the causes of human-induced climate change. 

Please see Volume 9, Section 9.1.6, “Additional Substances” (black carbon, other substances, under the 

proposed definition of “air pollution”) for our response to comments concerning the contribution to 

climate change of human emissions of black carbon and other short-lived pollutant species beyond the six 

GHGs associated with this action. 

Comment (5-123): 

One commenter (3893) voices support for the Findings, pointing out that global warming will undermine 

efforts to improve air quality, as higher temperatures will accelerate ozone formation during summer 

months. 

Response (5-123):

We note that this is consistent with information summarized in the TSD. For example, increases in 

regional ozone pollution relative to ozone levels without climate change are expected due to higher 

temperatures and weaker circulation in the United States and other world cities relative to air quality 

levels without climate change. As further stated in the TSD, increases in regional ozone pollution relative 

to ozone levels without climate change are expected due to higher temperatures and weaker circulation in 

the United States and other world cities relative to air quality levels without climate change. 

Comment (5-124): 

Commenters (0660, 8320) indicate that reducing atmospheric CO2 concentrations would result in 

significant co-benefits by reducing the disease burden caused by the criteria pollutants and other toxics. 

Knowledge regarding the extensive health consequences of air pollution has expanded exponentially in 

the last decade, with thousands of studies published in the mainstream medical literature. 

79 
Response (5-124): 

See the Findings, Section III.C, “Adaptation and Mitigation,” for our response to comments on the 

treatment of adaptation and mitigation in the Findings. 

Comment (5-125):

Several commenters (2633, 6679, 8874, 11233) express concern over the impacts of climate change on 

the degradation of air quality, specifically, that climate change will lead to higher levels of ozone and 

other air pollution. One commenter (2633) notes that toxic air pollutants and the chemicals that form acid 

rain and ground-level ozone can damage trees, crops, wildlife, aquatic life, lakes and other bodies of 

water, including drinking water supplies. Some commenters (0293, 1507, 11249) express concern that 

climate change led to increased ozone formation and mercury contamination. One commenter (11249) 

notes that global warming will undermine efforts to improve air quality, and states that rising ozone 

concentrations would cause serious respiratory and cardiovascular health problems. The commenter 

(11249) notes that more than 100 million Americans live in areas where ozone levels exceed the 8-hour 

NAAQS. 

Response (5-125):

EPA notes the concerns expressed by the commenters regarding the impacts of climate change on air 

quality, human health, and the environment. We also note the commenters’ concerns regarding current 

levels of air pollutants and ecosystem health. The TSD and supporting information in the Findings cover 

the effects and impacts from climate change across of variety of environmental media (i.e., water, air, 

soil) and pathways. 

Comment (5-126): 

One commenter 72818) stated that just last month, EPA’s USGCRP released its assessment of the 

impacts of global change on regional U.S. air quality, a synthesis of climate change impacts on groundlevel ozone. The commenter indicates that the report finds that climate-induced ozone, averaged over the 

summer season, was in the range of approximately 2 to 8 ppb in the maximum daily 8-hour ozone 

concentration and this is a key metric for regulating U.S. air quality. According to the commenter, the 

study also found that the largest increases in ozone would be during the peak pollution events. The 

commenter believes this study tells us that on average these models agreed that these events will become 

more severe. The commenter further states that some of the modeling groups also found that climateinduced increases in ozone in some regions would extend into the spring and fall, which means that the 

ozone season could become longer. 

Response (5-126):

We have reviewed these comments and note they are generally consistent with EPA’s analyses in the 

Interim Assessment report and as reflected in the final TSD. The TSD now incorporates results from the 

latest USGCRP report. 

Comment (5-127):

A commenter (2895) indicates that the effects of climate change will also be very significant for air 

quality, and in particular for ambient ground-level ozone levels. The commenter notes that this is not just 

a problem in notorious places like Los Angeles or Houston—it is also in Seattle. The commenter notes 

that as temperatures rise, as we can expect with climate change, it’s going to put the area much more at 

risk for exceedances of the ozone standards. This is something that will affect human health; asthmatics 

and others at risk will be particularly severely impacted. Increased ozone will obscure the iconic vistas of 

80 
Mount Rainier. The commenter indicates that these are real effects that clearly show EPA needs to take 

action. And, states the commenter, EPA has a mandate to look at current as well as future risks in 

evaluating what action to take. 

Response (5-127):

We note the concerns of the commenter regarding the risk of increasing ozone concentrations in Seattle, 

Washington. We concur with the commenter that breathing ozone at sufficient concentrations can reduce 

lung function, thereby aggravating asthma or other respiratory conditions. EPA’s IA report, which is 

reflected in the TSD, provides a synthesis of the potential effects of climate change on air quality 

including ground-level ozone based on current and future conditions. 

81 
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