Frequently Asked Questions
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. The Clean Air Act identifies 187 air toxics and subjects the sources of their emissions to regulations in order to protect public health. Through appropriate rulemaking, the Clean Air Act list may be modified. For more information on the Clean Air Act, see http://www.epa.gov/air/caa/. For more information on air quality, see www.epa.gov/air/basic.html
A: The National-Scale Air Toxics Assessment (NATA) is EPA's ongoing, comprehensive evaluation of air toxics in the United States. EPA developed the NATA as a tool for EPA and State/Local/Tribal Agencies to prioritize air toxics, 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 that does not incorporate refined information about emission sources, but rather, uses general information about sources to develop estimates of risks using analytical methods that 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 that 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 or populations where the potential for health risks are highest. NATA provides a snapshot of the outdoor air quality and the risks to human health that would result if air toxic emission levels remained unchanged. A more detailed explanation of NATA and the methods used may be found in the Technical Methods Document.
A: Specifically, EPA uses NATA results to:
- identify pollutants and source categories of greatest concern,
- improve understanding of health risks posed by air toxics,
- help set priorities for the collection of additional information,
- set priorities for improving emission inventories,
- expand and prioritize EPA's air toxics monitoring network,
- support communities in designing their own local assessments,
- enhance targeted risk reduction activities,
- link air toxics to the Criteria Pollutant Program, and
- help inform community and local air toxics programs
A: NATA assessments should not be used for the following:
It should also be noted that although results are reported at the census tract level, average risk estimates are far more uncertain at this level of spatial resolution than at the county or state level. Even though some of the methods used to conduct NATA are similar to those used in air-related risk assessments conducted under the Clean Air Act mandate (such as residual risk assessments of hazardous air pollutant (HAP) emissions from point sources, or assessments of exposures to criteria pollutants for evaluations of National Ambient Air Quality Standards), NATA fundamentally differs from such assessments in that it is not a refined assessment, and it is not used as the sole source of information leading to regulations or guiding the enforcement of existing rules.
- as a definitive means to pinpoint specific risk values within a census tract,
- to characterize or compare risks at local levels such as between neighborhoods,
- to characterize or compare risks between states,
- to examine trends from one NATA year to another,
- as the sole basis for developing risk reduction plans or regulations,
- as the sole basis to control specific sources or pollutants, or
- as the sole basis to quantify benefits of reduced air toxic emissions.
A: The 2005 NATA is a national-level risk assessment based on the emissions of air toxics that produces census-tract level estimates of ambient and exposure concentrations for 177 air toxics, plus diesel PM, which EPA assessed for noncancer effects only. Using the concentration estimates for the 177 air toxics plus diesel PM, NATA estimates cancer risk and noncancer hazard for 139 of these. For 39 air toxics, concentration estimates but no health effects information are available. A list of all air toxics assessed and an indication of what types of results were generated for each can be found in the file, 2005 NATA - List of Air Toxics Assessed (PDF) (3pp, 15k).
The following individual listed air toxics were not included in this assessment because either no emission information was reported for them in 2005 or emission estimates useful for modeling could not be determined reliably from their reported emissions (e.g., radionuclides).
- fine mineral fibers,
- parathion, and
A: NATA includes the following four major steps for assessing air toxics across the United States (and also for Puerto Rico and the U.S. Virgin Islands):
- Compile a 2005 national emissions inventory of air toxics from outdoor sources.
EPA compiled measured or estimated emissions data reported by sources, States, and others. EPA also estimated 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), and both onroad and nonroad mobile sources (e.g., cars, trucks, and boats). For 2005, EPA used the NEI as the starting point and developed the 2005 NATA inventory which was used as the source of input information for modeling.
- Estimate ambient air concentrations based on the 2005 emissions.
The 2005 NATA emissions information for all air toxics were used as inputs to the air dispersion models, Human Exposure Model (HEM) for point sources and the ASPEN model for area and mobile sources, to estimate ambient concentrations. The additional secondary formation concentrations of formaldehyde, acetaldehyde, and acrolein and the decay of 1,3-butadiene to acrolein estimated by CMAQ modeling are presented separately from the concentrations of these air toxics estimated by the HEM and ASPEN models. 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. The estimated ambient concentrations are used as inputs to an exposure model, the Hazardous Air Pollution Exposure Model (HAPEM). Estimating exposure is a key step in determining potential health risk. People move from one location to another, for example from outside to inside. Thus, exposure isn't the same as it would be if people stayed in one location. People also breathe at different rates depending on their activity levels, so the amounts of air they take in vary in time. For these reasons, the average concentration of a pollutant that people breathe, or their exposure concentration, might 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.
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 2005 levels of emissions. It also discusses the uncertainties and limitations of the NATA assessments. More detailed information about these steps can be found in the Technical Methods Document.
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 that specific concentration over 70 years (an assumed lifetime). This risk would be an excess cancer risk that is in addition to any cancer risk borne by a person not exposed to these air toxics.
A: We used 2005 data because emission inventories from that year were the most complete and up-to-date available. Working with industries and States, we update our air toxics emission inventories every 3 years and are now gathering and compiling 2008 data. The risk estimates assume a lifelong exposure to 2005 levels because calculating projected exposures based on projections to more recent years would be substantially more complex and uncertain.
A: This assessment is focused on characterizing one piece of the air toxics risk picture at a particular point in time. NATA looks at human health impacts from estimated, chronic, inhalation exposure due to outdoor sources of air toxics, assuming the emissions upon which NATA are based remain constant throughout one's lifetime, not today's levels or projected levels. NATA does not include:
- Cancer risks associated with diesel particulate matter, which are likely to be substantial (see question 13 below in the Results Section).
- 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 (polychlorinated biphenyls)).
- Exposures and risk very near to specific sources or 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 exposure to be a "typical" 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 that 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.
A: The responsibility is shared among EPA, state, local and tribal air programs. EPA sets national standards for air toxics emissions. The state, local, tribal programs are responsible for implementing these rules. In addition, some state, local, and tribal programs have their own air toxics rules.
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 Tribal programs and EPA's Regional Tribal Program coordinators can be found at : http://www.epa.gov/oar/tribal/where.html
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, comprehensive assessment such as NATA.
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 toxic concentrations is still not practical for all air toxics of interest across all areas of the country. Such measurement data are used and will continue to be used as more become available, however, to evaluate the models to better understand some of the uncertainties in such assessments and to improve modeling tools. For example, in the Section on Limitations, there is a link to the results of the model-to-monitor comparison done for this 2005 assessment.
A: The following changes were incorporated in the 2005 NATA. Many of the changes adopted in the 2002 NATA were carried over to the 2005 NATA: they are not repeated here. See FAQ for the 2002 NATA.
- Point Sources Inventory
- The point source emission inventory was based on 2005 data.
- Risk and Technology Review updates were included.
- Data for 19000 airports were included.
- Nonpoint sources
- The nonpoint source emission inventory was based on 2002 data.
- Forest fires and wildfires were not included.
- Formaldehyde and benzene from pesticides were removed to reflect recent rulemakings.
- Chromium Electroplating sources were moved to the point source inventory.
- Mobile Sources
- The onroad and nonroad inventories were updated to 2005.
- The new "MOVES" model was used for some HAPs.
- The secondary formation of formaldehyde, acetaldehyde, and acrolein were estimated using CMAQ.
- The transformation of 1,3 butadiene to acrolein was accounted for using CMAQ.
- The mobile source modeling approach using AERMOD was improved.
- Emissions buoyancy for certain sources at coke oven facilities was accounted for.
- Risk Characterization
EPA made several methodological changes to the 2005 NATA. Some of these were carried over from the 1999 and 2002 NATA and applied in 2005. Although EPA is continually refining and updating the assessment methods, it is important to remember that NATA is a screening-level assessment. The intent is to identify hazardous air pollutants resulting in high exposures or census tracts where population exposures may be of concern. These areas could then utilize more refined assessments (e.g., monitoring or site-specific risk assessments), to develop a more thorough understanding of these "hot-spot" exposures.
- Dose-response values were updated with latest science (IRIS, CalEPA, ATSDR).
- The formaldehyde unit risk estimate was revised.
A: EPA appreciates the time taken by State, local, and tribal air agencies to preview and comment on the preliminary results of this assessment. It is thorough reviews such as these that enable us to continually improve our assessments, thereby increasing the benefit to all users of the results. For this review, we received more than 5000 sets of comments from nearly 100 State, local, and tribal agencies. These comments resulted in over 25000 revisions to the NEI and NATA inventories. These comments covered the areas of:
- Facility changes:
- Addition and deletion of facilities
- Location address, facility coordinates, and facility name changes
- Corrections to closure date information
- Removal of duplicate facility information
- Revisions to stack parameters
- Revisions to MACT and SCC codes
- Emission changes:
- Additions, deletions, and recalculations
- Deletions and revisions of NEI and State IDs
Most of the comments were addressed by making the appropriate changes to the 2005 NEI and NATA inventories, and the final 2005 NATA now reflects these changes. Additional comments focused on methodological and toxicological questions, many of which are addressed or answered in various sections of the NATA webpage. A detailed summary of comments received and actions taken may be found in the NATA2005 Summary of Comments (MSACCESS format - 257KB).
A: Based on the results of this NATA 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 2005 NATA estimates most individuals' risks to be between 1 in a million and 100 in a million, although a small number of localized areas show risks to be higher than 100 in a million risk. Individuals and communities may be concerned about this. It is important to remember, however, that NATA 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. Also, it should be noted that the risks estimated by NATA do not consider ingestion exposure or indoor sources of air toxics, and that NATA estimates cancer risks for only 80 of the 177 air toxics plus diesel PM that were assessed. Therefore, these cancer risk estimates may represent only a subset of the total potential cancer risks associated with air toxics. For noncancer effects, the picture is similar. Only 110 of the air toxics assessed have noncancer dose-response values (e.g., reference concentrations needed for estimating noncancer effects).
Historical data show that approximately 1 out of every 3 Americans (or 336,000 in a million) will contract cancer during their lifetime when all causes are taken into account. The 2005 NATA results (the average national cancer risk is estimated to be 50 in a million) suggest that the inhalation of air toxics contributes less than 0.1% due to the risk of contracting cancer. For comparison purposes, the national risk of contracting cancer from radon exposure is about 1 in 500 (or 2,000 in a million).
A: Unlike other pollutants that 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, the rule set an upper limit of risk acceptability of about 1 in 10,000 (or 100 in 1 million) lifetime cancer risk for the most exposed individual. In the 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 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. These determinations called for considering other health and risk factors, including the uncertainty in the risk assessment, in making an overall judgment on risk acceptability.
Unlike cancer risk, there currently is no framework for determining the acceptability of noncancer risks . Aggregate exposures equal to or below a hazard index (HI) of 1.0 derived using target organ specific hazard quotients likely will not result in adverse noncancer health effects over a lifetime of exposure and would ordinarily be considered acceptable. However, an HI greater than 1.0 does not necessarily suggest a likelihood of adverse effects nor does it imply an unacceptable level of effect. Instead, the acceptability of exceedances is evaluated on a case-by-case basis, considering such factors as the confidence level of the underlying health data, the uncertainties , the slope of the dose-response curve (if known), the magnitude of the exceedances, and the numbers or types of people exposed at various levels above the RfC.
NATA was not designed to be a definitive tool for assessing the acceptability of risks because 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. Such exposures are different from the exposures experienced by the most exposed individuals in a tract, which would be the focus of the more detailed analysis supporting a NESHAP-related regulation. The national-scale assessment contains uncertainties in emissions levels, exposure concentrations, and dose-response information, and lacks the level of refinement that might 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.
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 of the total amount of air toxics in an area for 2005 as well as a general estimate of the geographic patterns of potential risk within each State and county in the U.S. in 2005.
A:Uncertainties are inherent in analyses like this (uncertainty in the emissions, actual population exposures, and dose-response or health effects information). Thus, the results are appropriate to answer questions such as which pollutants or source sectors might be associated with higher risks than others but not for determining exactly how many people are exposed to certain levels of absolute risk, or to determine what's safe and what's not.
A: The 2005 NATA estimates that, on average, approximately 1 out of every 20,000 Americans (50 in one million) could contract cancer from breathing air toxics if exposed to 2005 emission levels for 70 years. These risks are unevenly distributed.
This may be compared with estimates that approximately 1 out of every 3 Americans (or 336,000 in a million) will contract cancer in their lifetimes and about 570,000 out of the nearly 1.5 million cancer cases annually will die from their disease. Of these cancer deaths, almost one-third can be attributed to tobacco use alone, and another third can 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; in some they are not.
Note that these cancer projections are based on actuarial data that are much more certain than risk estimates provided by NATA, 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, that is , it is intended to address some questions but not others. The risks estimated 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 may represent only a subset of the total potential cancer risk associated with air toxics. NATA risk estimates may be compared with but should not be confused with actual reported cases of cancer.
A: EPA recommends that 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 risk information was provided only at the county level, the results would be less informative because they would show one risk number to represent each county. Information on the potential variability of risk within each county would be lost.
We developed NATA as a tool to inform both national and more localized efforts to collect air toxics information and characterize emissions (e.g., to prioritize pollutants and geographic areas of interest for more refined data collection such as monitoring). We feel reasonably confident that the patterns (i.e., relatively higher and lower 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.
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: NATA 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, acrylamide, and PAHs by applying a risk factor of 1.6 to account for the increase in lifetime cancer 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 regarding children’s exposure and risk. 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 for vinyl chloride 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 4 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 (e.g., vinyl chloride). 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% (i.e.,a factor of 1.6), 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.
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.
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.
In addition, on May 21, 2010, the President also directed EPA to review the adequacy of emissions standards for new motor vehicles and fuels for criteria pollutants and toxics (This was part of a Presidential Memorandum largely focused on future vehicle and truck greenhouse gas (GHG) and fuel economy standards). If EPA finds new regulations are necessary, the Agency is to promulgate such regulations as part of a comprehensive approach toward regulating motor vehicles. We are currently assessing potential new vehicle and fuel controls which would address air toxics.
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.
In addition, 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.
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.
A:EPA has established standards that will dramatically reduce emissions from new vehicles and engines over the next two decades. However, millions of diesel engines already in use will continue to emit large amounts of nitrogen oxides, particulate matter and air toxics, which contribute to serious public health problems. EPA's Diesel Emissions Reduction Program (known as "DERA") was created to deploy pollution-controlling technologies in diesel fleets. Clean diesel projects yield an immediate public health and air quality benefit. EPA estimates that for every dollar invested in reducing diesel exhaust, a community may achieve up to 13 dollars in public health benefits. For more information, visit www.epa.gov/cleandiesel.
In the longer term, there will be substantial emission reductions in all mobile-source-related toxics as older vehicles and engines are replaced with cleaner ones that meet new emission standards. EPA estimates that existing programs will result in 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. There will also be large on-highway diesel PM emission reductions in that timeframe. The highway mobile source programs include fuel programs such as the MSAT rule, lead phase-out, 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, as well as large ocean-going vessels. EPA estimates that gaseous air toxics emissions from nonroad equipment will be reduced almost 60% between 1999 and 2030, despite significant increases in activity. Locomotive and marine engine standards promulgated in 2008 will result in additional gaseous hydrocarbon reductions. These reductions are not reflected in this current estimate but will affect future NATA assessments.
In addition, on May 21, 2010, the President also directed EPA to review the adequacy of emissions standards for new motor vehicles and fuels for criteria pollutants and toxics. (This was part of a Presidential Memorandum largely focused on future vehicle and truck greenhouse gas (GHG) and fuel economy standards.) If EPA finds new regulations are necessary, the Agency is to promulgate such regulations as part of a comprehensive approach toward regulating motor vehicles. We are currently assessing potential new vehicle and fuel controls which would address air toxics.
A:: Due to the extent of improvements in our methodology (e.g.,inventory improvements, modeling changes, background calculation revisions, and changes in health benchmarks), it is not meaningful to directly compare the 2005 assessment with previous assessments. Before changes in risk levels may be attributable to specific reduction efforts, these assessment changes must be considered. For example, the estimated average national cancer risk increased from 36 in a million in 2002 to 50 in a million in 2005. Most of this difference is attributable to a change in the formaldehyde unit risk estimate used in this 2005 assessment. For the previous NATA assessment, EPA selected the CIIT (now called the Hamner Institutes for Health Sciences) - derived unit risk estimate (an estimate of cancer potency) of 5.9 x 10-9 per µg/m3. The EPA's Office of Research and Development (ORD) now believes there is sufficient published, peer-reviewed research to advise against the continued use of the Hamner Institutes potency estimate. Therefore, for this assessment and in the near-term, EPA is using the existing IRIS URE value for formaldehyde. That URE is 1.3 x 10-5 per ug/m3. In addition to the change in the formaldehyde URE, the 2005 NATA used the CMAQ model to estimate the additional ambient concentration of formaldehyde due to its secondary formation in the atmosphere. The effect of using the higher URE and the addition of formaldehyde due to secondary formation is that the national cancer risk average is 50 in a million with formaldehyde contributing 22 in a million to that total. This contrasts with the contribution of formaldehyde risk of less than 1 in a million to the 36 in a million national average estimated in 2002.
A: Since 1990, EPA has made significant progress in reducing emissions of air toxics from stationary, mobile, and indoor sources, finalizing nearly 100 National Emissions Standards for Hazardous Air Pollutants, or MACT standards, to reduce toxic emissions from over 174 categories of industrial sources. These rules result in 7.1 million fewer tons of air toxic emissions every year.
In addition, with the completion of the urban area source program's set of regulations by the end of 2010, we project that in 2013, when all these area source categories are expected to be in compliance, more than two million fewer tons of toxic pollutants will be emitted annually than would have occurred in the absence of this regulatory program
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 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.
A: There currently is no 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 EPA 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.
A: In recent NATA analyses (1999 and 2002), EPA utilized a cancer potency for inhalation exposure to formaldehyde derived from modeling sponsored by what was then the Chemical Industry Institute for Toxicology (CIIT), now called the Hamner Institutes for Health Sciences. The EPA's Office of Research and Development (ORD) now believes there is sufficient published, peer-reviewed research to advise against the continued use of the CIIT potency estimate. EPA is currently updating the Integrated Risk Information System (IRIS) file for formaldehyde to consider new science published in the peer-reviewed and epidemiologic literature. This study is not expected to be completed in time for the release of the 2005 NATA. Therefore, for this assessment and in the near-term, EPA is using the existing IRIS URE value for formaldehyde. That URE is 1.3 x 10-5 per ug/m3.
The effect of using this URE is that the national cancer risk average is 50 in a million with formaldehyde contributing 22 in a million (approximately 42%) to that total. This contrasts with the contribution of formaldehyde risk of less than 1 in a million to the 36 in a million national average estimated in 2002.
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.
16: There has been increased concern about the health effects associated with pollution near roads. What can results from NATA 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-traveled 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.
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.
A:Included in the results section of the 2005 NATA are Google Earth maps that show the risk levels estimated for each census tract. Using these maps, it is then possible to identify the locations of specific buildings (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 buildings 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 buildings. More focused assessments (e.g., air toxics monitoring or local-scale risk assessments), would be needed to more accurately determine those concentrations and risks.
19: 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 ?
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 using methods that 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 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 2005 NATA uses a screening approach that estimates the enhanced buoyancy around hot banks of coke ovens by raising the battery "stack height" input to the dispersion models (see the 2005 NATA TMD). This method is not the same, refined method used in the Coke Oven Rule, but it does go beyond what was done in the 2002 and previous NATA assessments. This generally results in risk estimates that are higher than would be expected from a more refined level of analysis, but lower than those seen in previous NATA assessments. See an example of a more refined analysis of a coke oven (PDF) (402pp, 13.5 MB). If the risk estimates from a particular coke oven are high, it does not 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.
A:: There are several reasons why airports comprise a larger proportion of national risk in the 2005 NATA than in previous versions of NATA. A key reason is that dose-response values for certain pollutants emitted by aircraft, such as formaldehyde and PAHs, have recently increased. Most notable is the much higher dose-response value for formaldehyde (see question 14), which is emitted by jet engines. In addition, EPA added about 16,000 general aviation airports to the emission inventory that were not included in previous assessments. We also made other improvements to our modeling of airports, such as updated estimates of aircraft activity and revisions to airport runway configurations. It should be noted that emission inventory estimates at general aviation airports are based on nationwide estimates of the mix of aircraft types using those airports. However, the mix at individual airports can be much different, which could significantly impact results. In general, NATA results are estimates; more detailed assessments may then be needed in order to fully characterize health risks. Once risks are further characterized, air agencies can, where necessary, determine steps to reduce air toxics emissions to effectively reduce health risks.
To reduce aircraft emissions, EPA works with the FAA and the United Nations International Civil Aviation Organization (ICAO) to establish aircraft engine emission standards. There are currently standards for NOx, CO, hydrocarbons, and smoke from jet engines which power commercial aircraft. EPA is now working on a proposed rule to adopt the latest ICAO NOx standards. With respect to piston-engine aircraft, EPA’s current focus relates to lead emissions. In April 2010, EPA issued an Advance Notice of Proposed Rulemaking on lead emissions from piston-engine aircraft using leaded aviation gasoline (www.epa.gov/oms/regs/nonroad/aviation/420f10013.pdf). EPA will continue to consider how aircraft operations are contributing to air pollution and what actions may be appropriate to reduce their impact.