- What are air toxics?
- What is the national-scale assessment?
- How can NATA information be used?
- Which air toxics are included in the national-scale assessment?
- What are the steps in the national-scale assessment?
- What does a "1 in a million" cancer risk mean?
- Why are all the estimates from 2002 and not more recent?
- Are there any risks from air toxics that are not covered by the
- Who is responsible for controlling air toxics?
- What should I do if I am concerned about toxics in my area?
- Why is EPA using computer modeling techniques instead of actual
measurements to estimate concentrations and exposure?
- What improvements have been made in the 2002 NATA?
- What kind of changes were made in the 2002 NATA as a result of the review by the States?
- Does the assessment show that the risk is high?
- What does EPA believe constitutes an acceptable level of risk?
- What do these estimates mean to me?
- How accurate is the assessment?
- How does the cancer risk identified in this assessment compare to lifetime cancer risk from all causes?
- You show risk data down to the census tract level.
Are the results accurate enough to draw conclusions at this scale?
- How were the cancer risk estimates affected by EPA's recently revised Guidelines for Carcinogen Risk Assessment (EPA/630/P-03/001F) and new Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens (EPA/630/R-03/003F)?
- Based on this national-scale assessment, can EPA determine which areas
and/or populations are at greatest risk from air toxics?
- Given the assessment identifies benzene as a relatively large "driver" for cancer risk, and a large proportion of the emissions come from mobile sources, what is the Agency doing to reduce benzene emissions from mobile sources?
- What is EPA doing to reduce other mobile source emissions?
- How does this assessment of 2002 air toxics data compare to previous national-scale assessments?
- Do you see improvement in air quality?
- The contribution of nonroad equipment to overall risk is substantially lower in the 2002 national-scale assessment than it was in 1996. Is this due to changes in methodology or real reductions?
- Why are only noncancer risks calculated for diesel PM? Isn't there a cancer unit risk available?
- Why didn't EPA use the (higher) unit risk estimate (URE) for formaldehyde reported in the Agency's Integrated Risk Information System (IRIS)?
- Why aren't results for dioxin included?
- There has been increased concern in recent years about health effects associated with pollution near roads. What can results of the NATA assessment tell us about communities potentially at greater health risk from exposure to near-road pollution?
- Can the NATA assessment results be used to evaluate exposures at specific points of interest,(e.g., near schools, day care centers, hospitals, etc.)?
- I am able to locate a specific facility location from the map and get a risk at that location. How accurate is that risk value?
- I'm familiar with the assessments EPA performed for coke ovens to support their residual risk rulemaking in 2006. The NATA results for those same coke ovens don't seem to match those from the rulemaking. Why is that?
1: What are air toxics?
A: Air toxics, also known as toxic air pollutants or hazardous air pollutants, are those pollutants that cause or may cause cancer or other serious health effects, such as reproductive effects or birth defects, or adverse environmental and ecological effects.
Examples of toxic air pollutants include benzene which is found in gasoline; tetrachloroethylene which is emitted from some dry cleaning facilities; and methylene chloride which is used as a solvent and paint stripper by a number of industries. Through appropriate rulemaking, the Clean Air Act list can be modified. For more information on the Clean Air Act, see http://www.epa.gov/air/caa/.
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2: What is the national-scale air toxics assessment?
The National-Scale Air Toxics Assessment (NATA) is EPA's ongoing comprehensive evaluation of air toxics in the U.S. EPA developed the NATA as a tool for EPA and State/Local/Tribal Agencies to prioritize pollutants, emission sources and locations of interest for further study in order to gain a better understanding of risks. NATA is a state-of-the-science screening tool which does not incorporate refined information about emission sources, but rather, uses general information about sources to develop estimates of risks which are more likely to overestimate impacts than underestimate them. NATA assessments provide screening-level estimates of the risk of cancer and other serious health effects from breathing (inhaling) air toxics in order to inform both national and more localized efforts to identify and prioritize air toxics, emission source types and locations which are of greatest potential concern in terms of contribution to population risk. This in turn helps air pollution experts focus limited analytical resources on areas and or populations where the potential for health risks are highest. Assessments provide a snapshot of the outdoor air quality and the risks to human health that would result if air toxic emission levels remained unchanged.
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3: How can NATA information be used?
EPA uses the results of these assessments in many ways, including:
- To work with communities in designing their own local-scale assessments,
- To set priorities for improving data in emissions inventories,
- Inform the deployment of local air toxics monitoring efforts
States use NATA too. For example, Oregon has used NATA results to help target areas for further study and data gathering, and States such as Washington, Delaware, and New Jersey have provided discussions of NATA results and links to NATA directly from their websites.
NATA assessments can not be used to identify near-source or "hotspot" risks, i.e., risks to individuals living near emitting sources. Also NATA results alone are not used for regulatory purposes.
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4: What air toxics are included in the 2002 national-scale assessment?
A:The 2002 national-scale assessment is a national-level risk assessment based on the emissions of air toxics and produces census-tract level estimates of ambient and exposure concentrations for 181 air toxics, including diesel PM, which we assessed for noncancer effects only. The following individual listed HAPs were not included in this assessment: chloramben, 2,3,7,8-tetrachlorodibenzo-p-dioxin, N-nitroso-N-methylurea, asbestos, fine mineral fibers, radionuclides, and 2-acetylaminofluorene. The individual cresols (o,m,p-cresols) and individual xylenes (o,m,p- xylenes) were included in the modeling, but the results were combined into the mixture category for both. Therefore, only the results for the mixtures (identified as the mixed isomers) may be found in the results section.
Using the concentration estimates for the 181 air toxics, NATA estimates cancer risk and noncancer hazard (only the respiratory and neurologic endpoints) for 124 of these. For 57 air toxics, we have concentration estimates, but no health effects information. A list of all air toxics assessed and an indication of what types of results were generated for each may be found in the file, 2002 NATA - List of Air Toxics Assessed (PDF) (3pp, 15k).
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5: What are the steps in the national-scale assessment?
A: The national-scale assessment includes the following four major steps for assessing air
toxics across the United States (also Puerto Rico and the Virgin Islands):
- Compile a 2002 national emissions inventory of air toxics from outdoor sources. EPA compiles measured or estimated emissions data reported by sources, States, and others. EPA also estimates mobile source and other emissions using models, measurements, and a quality-control process. This compilation of information is called the National Emissions Inventory (NEI). The types of emission sources in the inventory include major stationary sources, (e.g., large waste incinerators and factories), area and other sources, (e.g., dry cleaners, small manufacturers, wildfires), and both onroad and nonroad mobile sources (e.g., cars, trucks, boats).
- Estimate ambient air concentrations based on the 2002 emissions.
Using the 2002 NEI emissions information as input to the air dispersion models, i.e., Human Exposure Model (HEM) for point sources and the
ASPEN model for area and mobile sources, EPA estimates ambient concentrations. These emission inputs also included estimates of
background concentrations which consider contributions from distant or natural sources based on existing air quality measurements. As part of this modeling exercise, EPA compared estimated ambient concentrations to available ambient air toxics monitoring data to evaluate model performance.
- Estimate population exposures based on a screening-level exposure model,
The estimated ambient concentrations (from the HEM or ASPEN models) are used as input to the exposure model. Estimating exposure is a key step in determining potential health risk. People move from one location to another, outside to inside, etc., so exposure isn't the same as concentration at a static site. People also breathe at different rates depending on their activity levels, so the amounts of air they take in vary. For these reasons, the average concentration of a pollutant that people breathe (i.e., exposure concentration) may be higher or lower than the concentration at a fixed location (i.e., ambient concentration).
- Characterize potential public health risks due to inhalation of air toxics.Chronic cancer and noncancer health effects were characterized using available information on air toxics health effects, current Agency risk assessment and risk characterization guidelines, and estimated population exposures. This characterization quantifies, as appropriate, potential cumulative risks to public health due to inhalation of air toxics from outdoor emission sources assuming a lifelong exposure to 2002 levels of emissions. It also discusses the uncertainties and limitations of the NATA assessments.
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6: What does "1 in a million" risk mean?
A:A risk level of 1 in a million implies a likelihood that one person, out of one million equally exposed people, would contract cancer if exposed continuously (24 hours per day) to the specific concentration over 70 years (an assumed lifetime). This risk would be an excess cancer risk that is in addition to any cancer that might occur in a person not exposed to these air toxics.
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7: Why are all the estimates for the year 2002 and not more recent?
A: We used 2002 data because emissions inventories from that year were the most complete and up-to-date available. Working with industries and States, we update our air toxics emissions inventories every 3 years and are now gathering and compiling 2005 data. The risk estimates assume a lifelong exposure to 2002 levels because calculating projected exposures would be substantially more complex and uncertain.
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8: Are there any risks from air toxics that are not covered by the national-scale assessment?
A: This assessment is focused on characterizing one piece of the air toxics risk picture at a particular point in time, (i.e., 2002). It looks at human health impacts from outdoor, inhalation, chronic exposures and is based on 2002 emission rates, assuming they remain constant throughout one's lifetime (not today's levels or projected levels). It does not include:
- Cancer risks associated with diesel particulate matter, which are likely to be substantial (see question 12 below).
- Non-inhalation exposures, such as ingestion and dermal exposures. These additional pathways are especially important for pollutants that persist in the environment and bioaccumulate, e.g., mercury and PCBs.
- Exposures and risk very close to specific sources (highly-localized "hotspot" levels), such as some types of occupational or near roadway-related exposures.
- Individual extremes in exposure. All risk estimates are based on exposure estimates for the median individual within each census tract. EPA considers this to be a "typical" exposure for that tract. Some individuals may have substantially higher or lower exposures based on where they live within that tract or spend the majority of their time.
- Emissions from indoor sources of air toxics. For certain air toxics and for certain indoor situations, total long-term human exposures can be significantly influenced and sometimes dominated by exposures from indoor sources.
- Risk estimates for chemicals which do not have adequate dose-response information, (e.g., assessment does not quantify cancer risk from diesel PM).
- Impacts of non-routine increases in facility emissions due to, for example, equipment startups, shutdowns, malfunctions, and upsets.
- Assessment of adverse environmental effects, or other welfare effects.
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9: Who is responsible for controlling air toxics?
A: The responsibility is shared among EPA, State, local and Tribal air programs.
EPA sets National standards for air toxics emissions. The State and local programs are responsible for
implementing these rules. In addition, some State and local programs have their own air toxics rules.
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10: What should I do if I am concerned about toxics in my area?
A: Contact your State, local or Tribal air program. A list of state and local programs is available at: http://www.4cleanair.org
Information on the Tribal programs and EPA's Regional Tribal Program coordinators may be found at : http://www.epa.gov/air/tribal/where.html
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11: Why is EPA using computer modeling techniques instead of actual
measurements to estimate concentrations and exposure?
A: The assessment approach is fundamentally based on using computer models to estimate
ambient air toxics concentrations and population exposures nationwide.
The ability to directly measure ambient air toxics concentrations is currently limited. Such measurements are available for only a subset of air toxics in relatively few locations and for small study populations. Therefore, computer models are needed to conduct a large scale assessment such as this one.
Although EPA is working to expand the number and locations of ambient air toxic monitors and the study of personal exposures, direct measurement of air toxics concentrations is not practical for all air toxics of interest across all areas of the country. Over time, such measurement data have been and will be used, however, to evaluate the models to better understand some of the uncertainties in such assessments and to improve modeling tools.
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12: What improvements have been made in the 2002 NATA?
A: The EPA made several methodological changes to the 2002 NATA. Some of these were carried over from the 1999 NATA and applied again in 2002. EPA is continually refining or updating the assessment methods, but it is important to remember that these assessments are screening-level assessments. Their intent is to identify hazardous air pollutants resulting in high exposures or census tracts where population exposures may be of concern. These areas would then require more refined assessments, e.g., monitoring or site-specific risk assessments to develop a more through understanding of these "hot-spot" exposures. The list below summarizes the changes made.
- Improvements in NEI inventory
- Improved chromium speciation
- Increased number of PAHs included
- Risk and Technology Review improved the information used for modeling certain source categories
- Integration of hazardous air pollutants and criteria air pollutants (currently no criteria pollutants are included in NATA assessments)
- Improved QA/QC
- Improved point source characterization
- Major stationary point sources modeled with HEM3 (AERMOD)
- Modeled at census block level
- Retained individual source contribution
- Improved non-point source characterization
- Modeled area and mobile sources with ASPEN
- Modeled at census tract level
- Area sources grouped into 27 area source bins
- Mobile sources grouped into 9 source bins
- Major airports modeled as point sources using airport-specific geographic features, i.e., runway configurations
- Updated exposure approach
- Used exposure ratios estimated from the 1999 NATA to estimate exposure concentrations versus remodeling with HAPEM5
- Retained individual source contribution to exposure concentration
- Improved background concentration characterization
- 33 air toxics included versus 28 in 1999 NATA
- Updated method using monitoring data and emission inventory data
- Updated monitoring sites included, e.g., NATTS sites
- Improved regional representation
- Improved risk characterization
- Updated the cancer and noncancer dose-response information used
- Results on 180 air toxics plus diesel PM presented
- Includes ambient and exposure concentrations, cancer and noncancer results
- All cancer risk results presented (not just risks above 1 in a million)
- Only the respiratory and neurologic HQs presented for noncancer results versus only HQs above 1
- Census tract risk results and source identifications presented in Google Earth format
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13: What kind of changes were made in the 2002 NATA as a result of the review by the States?
A:: EPA appreciates the time taken to preview and comment on the results of this assessment. It is thorough reviews such as these that allow us to continually improve our assessments, thereby increasing the benefit to all users of the results. For this review, we received comments from 12 States. These comments covered the following areas:
- 67 comments on coordinate correction, (i.e., location) - 6 States
- 6 comments on inventory emission corrections - 4 States
- 10 comments on changes to source categories - 3 States
- 19 comments to change the State location of a facility - 1 State
- 2 comments concerning the results on "fires" - 2 States
Most of the comments above were addressed by making the appropriate changes to the 2002 NEI inventory, and the 2002 NATA has been redone to reflect these changes. Additional comments focused on methodological and toxicological questions, many of which are addressed or answered in various sections of the NATA webpage. It should be noted that although pieces of the 2002 NEI were changed, the emissions inventory data presented on the results page have not, but the new concentration, cancer, and noncancer results do reflect these changes. A detailed summary of comments received and actions taken may be found in the NATA2002 Summary of Specific Comments.xls.
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1: Does the assessment show that the risk is high?
A: Based on the results of this national-scale assessment and other studies, millions of people live in areas where air toxics may pose potential health concerns. While air quality continues to improve, more needs to be done to meet the Clean Air Act's requirements to reduce the potential exposure and risk from these chemicals.
EPA will continue to develop air toxic regulations as well as cost-effective pollution prevention and other control options to address indoor and urban pollutant sources that significantly contribute to risk.
The national-scale assessment estimates most individuals' risks to be between 100 in a million and 1 in a million, although a small number of localized areas show higher than 100 in a million risk. Individuals and communities may be concerned about this. However, the assessment was not designed as a definitive means to pinpoint specific risk values at local levels. The results are best used as a tool to prioritize pollutants, emissions sources and locations of interest for further investigation. It should also be noted that the risks estimated by the assessment do not consider ingestion exposure or indoor sources of air toxics. Also, the national-scale assessment estimates cancer risks for only 80 of the 181 air toxics assessed. Therefore, these cancer risk estimates represent only a subset of the total potential cancer risks associated with air toxics. For noncancer effects, the picture is similar. Only 68 of the 181 air toxics have noncancer dose-response values, (e.g., reference concentrations) needed for estimating noncancer effects.
Approximately one out of every three Americans (336,000 in a million) will contract cancer during their lives when all causes are taken into account. These assessment results (average national cancer risk = 36 in a million) suggest that the risk of contracting cancer increased less than 0.1% due to inhalation of air toxics. In addition, the national risk of contracting cancer from radon exposure is on the order of 1 in 500 (2,000 in a million). Note that any risk comparison often considers the voluntary or involuntary nature of the risk and whether the emissions are human-made or naturally-occurring, in addition to its numerical value.
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2: What does EPA believe constitutes an acceptable level of risk?
A: Unlike other pollutants which EPA regulates, air toxics have no universally-applicable, pre-defined risk levels that clearly represent acceptable or unacceptable thresholds. However, EPA has made case-specific determinations and described certain general presumptions that apply to particular regulatory programs. The 1989 Benzene National Emission Standard for Hazardous Air Pollutants (NESHAP) rule set up a two step, risk-based decision framework for the NESHAP program. This rule and framework are described in more detail in EPA's 1999 Residual Risk Report to Congress (PDF) (225pp, 2.3 MB). First, it set an upper limit of acceptability of 1 in 10,000 (i.e., 100 in 1 million) lifetime cancer risk for the most exposed individual. In the Benzene NESHAP rule, we explained, "The EPA will generally presume that if the risk to that individual [the Maximum Individual Risk] is no higher than approximately 1 in 10 thousand, that risk level is considered acceptable and EPA then considers the other health and risk factors to complete an overall judgment on acceptability." Second, the benzene NESHAP rule set a target of protecting the greatest number of persons possible to an individual lifetime risk level no higher than approximately 1 in 1 million. In addition, these determinations called for considering other health and risk factors, including the uncertainty in the risk assessment, in making an overall judgment on acceptability.
The national-scale assessment, however, was not designed to be a definitive tool for assessing the acceptability of risks since it has many limitations in data and methods. In addition, this assessment estimates risks associated with a modest range of individual behaviors using ambient levels averaged across a given census tract and averaged across multiple emissions points at a given local facility. This is different than the exposures experienced by the most exposed individuals in a tract, which would be the focus of the more detailed analysis in a NESHAP-related regulation. The national-scale assessment contains uncertainties, (e.g., emissions levels, exposure concentrations, dose-response information), and lacks the level of refinement that would enable us to adequately assess the highest exposures found in localized "hot spots, (i.e., exposures to individuals who live close to emitting sources).
Consequently, the results should not be used as an absolute measure of whether risks are acceptable. Rather, they should be used to focus or target more refined measurement and assessment activities.
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3: What do these estimates mean to me?
A: EPA does not have an extensive network to monitor levels of toxic air pollutants across the country. Therefore, the results of NATA assessments provide estimates that give an idea of the total amount of air toxics in an area for 2002 as well as a general estimate of the geographic patterns of potential risk within each State and county in the U.S. in 2002.
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4: How accurate is the assessment?
A: Uncertainties are inherent in analyses like this, (e.g., uncertainty in the emissions, actual population exposures, and dose-response or health effects information). See more information on the limitations of the assessment. Thus, the results are appropriate to answer questions such as which pollutants or source sectors may be associated with higher risks than others (e.g., priority setting for data collection), but not for determining exactly how many people are exposed to certain levels of absolute risk (e.g., to determine what's safe and what's not). In addition, there are some potential issues with the emissions inventory which affect the results for some States and pollutants.
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5: How does the cancer risk identified in this assessment compare to lifetime cancer risk from all causes?
A: The 2002 national-scale assessment estimates that, on average, approximately one out of every 28,000 Americans (36 in one million) could contract cancer from breathing air toxics if exposed to 2002 emissions levels for 70 years. These risks are unevenly distributed.
This may be compared with estimates that approximately one out of every three Americans (336,000 in a million) will contract cancer and about 570,000 out of the nearly 1.5 million cancer cases will die from their disease. Of these cancer deaths, almost one-third can be attributed to tobacco use alone, and another third will be related to lifestyle factors such as poor nutrition, physical inactivity, and obesity. (See http://www.cancer.org/docroot/STT/stt_0.asp
) In some of these cases, e.g., smoking, these risks are voluntary.
Note that these cancer projections are based on historical risks that are much more certain than risk estimates provided by the national-scale assessment which is subject to limitations in data, modeling and default assumptions used routinely in any risk assessment. In addition there are limitations in the overall design of the assessment (intended to address some questions but not others). The risks estimated by the assessment do not consider ingestion exposure or indoor sources. Also, the assessment estimates chronic cancer risks for only those air toxics that EPA is currently able to quantify with available dose-response data. Therefore, these risk estimates represent only a subset of the total potential cancer risk associated with air toxics.
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6: You show risk data down to the census tract level. Are the
results accurate enough to draw conclusions at this scale?
A: We recommend the census tract data be used to determine geographic patterns of risks within counties rather than to pinpoint specific risk values for each census tract. If we only provided the risk information at the county level, the results would be less informative because they would show one risk number to represent each county. Information on variability of risk within each county would be lost.
We developed the national-scale assessment as a tool to inform both national and more localized efforts to collect air toxics information and characterize emissions (e.g., prioritize pollutants/geographic areas of interest for more refined data collection such as monitoring, etc.). We feel reasonably confident that the patterns (i.e., relatively higher levels of risk within a county) represent actual fluctuations in overall average population risks within the county. We are less confident that the assessment pinpoints the exact locations where higher risk exists, or that the assessment captures the highest risks in a county.
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7: How were the cancer risk estimates affected by EPA's recently revised Guidelines for Carcinogen Risk Assessment (EPA/630/P-03/001F) and new Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens (EPA/630/R-03/003F)
A: This assessment is consistent with the revised cancer guidelines and the new Supplemental Guidance that makes recommendations with regard to estimating cancer risks to children. The recommendations concerning children's risk have been implemented for the following HAPs: benzidine, ethyl carbamate, and PAHs by applying a risk factor of 1.6 to account for the increase in risk due to childhood exposures. This was done because these HAPs have been shown to have a mutagenic mode of action and because there is no chemical-specific data to show that there are differences between children and adults in the way they respond to exposure to these agents.
In contrast, vinyl chloride does have chemical-specific data available. These data were used in the derivation of the unit risk estimate (URE) (see the IRIS website for a more thorough explanation). Therefore, the URE that is presented in the toxicity tables on the OAQPS website, already reflects the risk due to childhood exposures, and no further adjustment (as was done for the other 3 HAPs) is necessary. A brief explanation of the adjustments to risk follows.
The Supplemental Guidance recommends that risks to children be adjusted for carcinogenic
chemicals acting through a mutagenic and linear mode of action, (i.e., chemicals that cause cancer by damaging genes). Where available data for the chemical are adequate, they should be used to develop age-specific potency values. Where available data do not support a chemical-specific evaluation of differences between adults and children, the Supplemental Guidance recommends the use of the following default adjustment factors for early-life exposures: increase the carcinogenic potency by 10-fold for children up to 2 years old, and 3-fold for children from 2 to 15 years old. These adjustments have the aggregate effect of increasing by about 60% the estimated risk for a 70-year (lifetime) constant inhalation exposure.
It is important to keep in mind that EPA recommends that the default adjustments be made only
for carcinogens (1) acting through a mutagenic mode of action, (2) for which a linear dose response has been assigned, and (3) for which data to evaluate adult and juvenile differences are not available. The default adjustments are not recommended for carcinogens whose mode of action is unknown. EPA will determine as part of the IRIS assessment process which substances meet these criteria, and future national-scale assessments will reflect adjustments for those substances.
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8: Based on this national-scale assessment, can EPA determine which areas
and/or populations are at greatest risk from air toxics?
A: This assessment has not focused on the identification of geographic areas or populations that have significantly higher risks than others. Rather, it has focused on characterizing geographic patterns and ranges of risks across the country. However, in general, we see that larger urban areas tend to carry larger risk burdens than smaller urban and rural areas because the emissions of air toxics tend to be higher in areas with more people. This trend is not universal and can vary from pollutant to pollutant, according to its sources, and may also be affected by exposures and risk from non-inhalation and indoor sources of exposure. Note that NATA estimates risks from the inhalation of air toxics only.
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9: Given the assessment identifies benzene as a relatively large "driver"
for air-toxic cancer risk, and a large proportion of the emissions come from mobile sources, what is the Agency doing to reduce benzene emissions from mobile sources?
A: EPA has taken aggressive action to reduce benzene emissions from mobile sources. EPA estimates that existing programs will result in an about a 65 percent reduction in emissions of benzene from highway mobile sources between 1999 and 2030, despite large increases in vehicle miles traveled. In addition, as a result of nonroad equipment emission controls, EPA estimates that benzene emissions from nonroad equipment will be reduced by over 60% between 1999 and 2030, despite significant increases in activity.
First, programs put in place primarily to reduce ozone through volatile organic compound (VOC) controls, and thereby to help States and localities come into attainment with the national ambient air quality standards (NAAQS), have reduced and will continue to reduce emissions of benzene and other air toxics dramatically.
EPA's most recent program specifically targeted at air toxics emissions, including benzene, is the Control of Hazardous Air Pollutants from Mobile Sources (Mobile Source Air Toxics or "MSAT") Final Rule, promulgated in 2007. This rule will lower emissions of benzene and other air toxics in three ways: (1) by lowering the benzene content of gasoline (beginning in 2011); (2) by reducing exhaust emissions from passenger vehicles operating at cold temperatures (under 75 degrees), beginning in 2010; and (3) by reducing emissions that evaporate from, and permeate through, portable fuel containers (beginning in 2009). Taken together, the standards will reduce total emissions of mobile source air toxics by 330,000 tons in 2030, including 61,000 tons of benzene.
The highway mobile source programs that are reducing benzene include fuel programs such as the MSAT rule, reformulated gasoline (RFG) and anti-dumping standards, gasoline toxics emissions performance standards as required by the 2001 mobile source air toxics rule, and low-sulfur gasoline and diesel requirements. Vehicle programs include our MSAT rule, national low emission vehicle (NLEV) program; our Tier 2 motor vehicle emissions standards; inspection and maintenance programs, on-board diagnostics, and our heavy-duty engine and vehicle standards.
Nonroad equipment emission reductions result from the recently finalized additional emissions controls for small spark-ignition engines and recreational marine engines, the recent locomotive and commercial marine vessel rule, the clean air nonroad diesel rule, and other nonroad standards.
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10: What is EPA doing to reduce other mobile source emissions
EPA estimates that existing programs will result in an about a 65 percent reduction in emissions of gaseous air toxics from highway mobile sources between 1999 and 2030, despite large increases in vehicle miles traveled. By 2030, EPA expects to see on-highway diesel PM emission reductions of over 90 percent from 2001 levels. The highway mobile source programs include fuel programs such as the MSAT rule, lead phaseout, reformulated gasoline (RFG) and anti-dumping standards, gasoline toxics emissions performance standards as required by the 2001 mobile source air toxics rule, and low-sulfur gasoline and diesel requirements. Vehicle programs include our MSAT rule, national low emission vehicle (NLEV) program; our Tier 2 motor vehicle emissions standards and gasoline sulfur control requirements; inspection and maintenance programs, on-board diagnostics, and our heavy-duty engine and vehicle standards.
As a result of the recent Locomotive and Commercial Marine Vessel rule, the Clean Air Nonroad Diesel Rule and other nonroad standards, nonroad diesel PM emissions in 2030 will be reduced by over 80% from year 2001 levels. EPA has also recently finalized additional emissions control for small spark-ignition engines and recreational marine engines. EPA estimates that gaseous air toxics emissions from nonroad equipment will be reduced almost 60% between 1999 and 2030, despite significant increases in activity. EPA is currently developing a proposal to control emissions from the largest ocean-going vessels.
EPA is also assisting States, communities and citizens in identifying and implementing voluntary programs, such as diesel retrofits and Clean School Bus USA to achieve additional reductions.
Learn more about EPA's programs to reduce air toxics from mobile sources.
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11: How does this assessment of 2002 air toxics data compare to previous national-scale assessments?
A: Due to the extent of improvements in our methodology, (e.g., inventory improvements, modeling changes, background calculation revisions, changes in health benchmarks), it is not meaningful to directly compare the 2002 assessment with previous assessments. Before changes can be attributable to specific reduction efforts, these assessment changes must be considered. For example the average national cancer risk in 2002 fell from 42 to 36 in a million when compared to the 1999 assessment. Some of this change can be attributable to changes in the methodology used to estimate background concentrations. However, an examination of each source category also shows a reduction in risks between 2002 and 1999. These reductions may be attributable to progress in reducing air toxics from stationary and mobile sources. For example, in 2007, EPA finalized the National Emissions Standards for Hazardous Air Pollutants. These 96 rules, known as MACT standards, reduce toxic emissions from 174 categories of industrial sources by 7.1 million tons annually. Many of these standards came into effect between 2002 and 1999. In addition, current mobile source programs will reduce air toxic emissions by another 2.4 million tons in 2020, compared to 1990 levels.
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12: Do you see improvement in air quality?
A: We have made progress in reducing air toxics from stationary, mobile, and indoor sources. By the end of 2007, EPA made significant progress finalizing National Emissions Standards for Hazardous Air Pollutants. These 96 rules, known as MACT standards, will reduce toxic emissions from over 174 categories of industrial sources. By 2007, these rules will result in 7.1 million fewer tons of air toxic emissions for every year after 1990.
Many motor vehicle, nonroad equipment, and fuel emission control programs of the past have reduced air toxics and will continue to provide significant emission reductions in the future. While many of these programs were put in place primarily to reduce ozone and particulate matter through volatile organic compound (VOC) and diesel PM controls, they have reduced and will continue to reduce emissions of air toxics very significantly. By 2020, these rules will eliminate emissions of 2.4 million tons of air toxics every year, relative to 1990 levels.
The public health improvement associated with these reductions in emissions will depend on a number of factors including which chemicals were reduced and where the reductions occurred relative to where people live and work.
Learn more about air toxics reductions from industrial, mobile and indoor sources.
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13: The contribution of nonroad equipment to overall risk is substantially lower in the 2002 national-scale assessment than it was in 1996. Is this due to changes in methodology or real reductions?
A: There are a number of factors contributing to these reductions. These include several methodological changes.
- EPA used the Integrated Risk Information System (IRIS) cancer potency estimate for formaldehyde which is several orders of magnitude higher than the CIIT-based value used in the 1999 and 2002 assessments.
- There were improvements in data and methods used to develop nonroad air toxics inventories since the 1996 assessment was conducted. These data changes result in larger reductions in emissions for several key pollutants, but may not reflect actual emission reductions.
- There were changes in how emissions were spatially allocated for several types of nonroad equipment. Some emissions were re-located in lower populated areas resulting in lower exposure and risk estimates.
These coupled with actual improvements in nonroad emissions since the 1996 assessment, contribute to the overall reductions seen.
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14: Why are only noncancer risks calculated for diesel PM? Isn't there a cancer unit risk available?
A: There is not a cancer unit risk estimate for diesel PM. While available evidence supports EPA's conclusion that diesel exhaust is likely to be a human carcinogen, EPA has concluded that the available data are not sufficient to develop a confident estimate of cancer potency, (i.e., unit risk estimate or URE), but there is evidence that the general population is exposed to levels close to or overlapping with apparent levels that have been linked to increased cancer risk in epidemiological studies. Furthermore, the Agency has concluded that national average lifetime cancer risk from exposure to diesel exhaust may exceed one in one hundred thousand (1 in 100,000) and could be as high as one in one thousand (1 in 1,000), although the lower end of the risk range includes zero. More information on health effects associated with diesel exhaust can be found in the Health Assessment Document for Diesel Exhaust
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15: Why didn't EPA use the (higher) unit risk estimate (URE) for formaldehyde reported in the Agency's Integrated Risk Information System (IRIS)?
A: EPA is currently updating the Integrated Risk Information System (IRIS) file for formaldehyde to consider new science published in the peer-reviewed literature including risk estimates developed by the CIIT Centers for Health Research (formerly the Chemical Industry Institute of Toxicology) and epidemiologic studies published by the National Cancer Institute and others.
In 2004, EPA selected the CIIT-derived unit risk estimate (an estimate of cancer potency) of 5.9 x 10-9per µg/m3 during the development of the plywood and composite wood products air toxics regulation. Since this decision, EPA has performed considerable work to evaluate the new studies as well as the CIIT modeling. However, at this time the evaluation, and hence the revision to the IRIS file for formaldehyde, is incomplete. Until EPA's evaluation is complete, the Agency will continue using the CIIT value and will revisit this issue when we have more information.
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16: Why aren't results for dioxin included?
A: EPA is conducting a separate assessment project specifically for dioxin. A major component of that assessment is to develop an emissions inventory that could be used in subsequent NATA assessments.
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17: There has been increased concern in recent years about health effects associated with pollution near roads. What can results of the NATA assessment tell us about communities potentially at greater health risk from exposure to near-road pollution?
A: There is a large body of research that consistently shows that populations spending a significant amount of time near heavily-travelled roads experience increased risks for a number of adverse health effects. Air quality measurement studies also indicate that elevated levels of pollution can be found near roads. Scientists are researching the relationship between the composition of the complex mixture of air toxics and other pollutants people are exposed to near these roads, and the observed adverse health effects.
These increased risks typically occur in close proximity to roads, within about 150 to 200 meters. NATA is not designed to capture these near-source exposures from individual roadways. However, NATA can be used as a screening tool to help identify populations with higher exposures to air toxics due to a greater density of traffic in the area where they work and live. More refined modeling can be used to characterize areas of potentially elevated exposures to populations near roads.
EPA has a major research program to better understand relationships between near-road air quality, population exposures to these pollutants and adverse health effects. This program is also evaluating impacts of potential mitigation strategies to reduce these adverse health effects.
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18: Can the NATA assessment results be used to evaluate exposures at specific points of interest, (e.g., near schools, day care centers, or hospitals)?
A: NATA is not designed to predict actual risks at a specific location. NATA can be used to identify and prioritize air toxics, emission source types and locations which are of greatest potential concern in terms of contributing to population risk. It is a screening assessment which uses general information about sources along with other information about a facility (how tall the emissions stacks are for example), to develop estimates of risks which are averaged over a census tract. It does not incorporate finely detailed information about emission sources, or other information that would be necessary to estimate risks at a specific location.
If a particular area is projected to experience low risks, and we are reasonably confident that the information on the significant emission sources is accurate, then we are fairly confident that risks actually are low, and there is no need to develop a more detailed assessment for that area. Conversely, if NATA estimated risks in a particular area are high, we know that refined assessments may be needed to accurately characterize risks these risks in that area.
This screening approach helps EPA and other air pollution control agencies to focus resources on areas where the potential for health risks are highest.
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19: I am able to locate a specific facility location from the map and get a risk at that location. How accurate is that risk value?
A: Included in the results section of the 2002 NATA are Google Earth maps that show the risk levels estimated for each census tract. Using these map, it is then possible to locate specific facilities, (e.g., schools, day care centers, hospitals, etc.) by entering their specific location information (address or latitude/longitude data) into the Google Earth query. These facilities will then be located within a specific census tract and the NATA results for that tract are readily seen. It should be noted that the concentrations and risk estimated are averaged across the tract and do not necessarily reflect the possible impacts that could occur in the immediate vicinity of these facilities. More focused assessments, (e.g., air toxics monitoring, local-scale risk assessments) would be needed to more accurately determine those concentrations and risks.
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20: I'm familiar with the assessment EPA performed for coke ovens to support their residual risk rulemaking in 2006. The NATA results for those same coke ovens don't seem to match those from the rulemaking. Why is that?
A: NATA is a screening study. As such, it does not incorporate refined information about emission sources, but rather, uses general information about sources to develop estimates of risks which are more likely to overestimate impacts than underestimate them. Therefore, if a particular area is projected to experience low risks, and we are fairly certain that we have captured the significant emission sources in our assessment, then we are fairly confident that risks actually are low, and there is no need to develop a refined assessment for that area. Conversely, if NATA estimated risks in a particular area are high, we know that refined assessments may be needed to accurately characterize risks these risks in that area. This screening approach helps EPA to focus our refined analytical resources on areas where the potential for health risks is highest. In the case of coke ovens, the NATA approach does not consider site-specific information such as the enhanced buoyancy around hot banks of coke ovens when developing estimates of the health impacts of the emissions. This enhanced buoyancy effect from the coke ovens may increase dispersion of the pollutants. By not considering the enhanced buoyancy around the coke ovens, this helps to ensure that the risk estimates associated with coke oven emissions in NATA are not lower than those expected from a more refined analysis. See an example of a more refined analysis of a coke oven (PDF) (402pp, 13.5 MB). The modeling and monitoring data from this example study indicated that the risk at the census tract was over predicted in NATA by about 70%. If the risk estimates from a particular coke oven are high, it does not immediately mean that risks actually are high, but that more refined analyses such as monitoring or site-specific risk assessment, such as the one referenced above, may be needed to accurately quantify the impacts.
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