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Frequent Questions

Information provided for informational purposes onlyNote: EPA no longer updates this information, but it may be useful as a reference or resource.
General Background
  1. What are air toxics?
  2. What is the national-scale assessment?
  3. Which air toxics are included in the national-scale assessment?
  4. What are the steps in the national-scale assessment?
  5. What does a "1 in a million" cancer risk mean?
  6. How do EPA and its regulatory partners at the state and local level use the results of national-scale assessments?
  7. Why are all the estimates from 1999 -- and not more recent?
  8. Are there any risks from air toxics that are not covered by the national-scale assessment?
  9. Who is responsible for controlling air toxics?
  10. What should I do if I am concerned about toxics in my area?
  11. Why is EPA using computer modeling techniques instead of actual measurements to estimate concentrations and exposure?
Results
  1. Does the assessment show that the risk is high?
  2. What does EPA believe constitutes an acceptable level of risk?
  3. What do these estimates mean to me?
  4. How accurate is the assessment?
  5. How does the cancer risk identified in this assessment compare to lifetime cancer risk from all causes?
  6. You show risk data/maps down to the census tract level. Are the results accurate enough to draw conclusions at this scale?
  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)?
  8. Based on this national-scale assessment, can EPA determine which areas and/or populations are at greatest risk from air toxics?
  9. 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?
  10. How does this assessment of 1999 air toxics data compare to the 1996 national-scale assessment?
  11. Do you see improvement in air quality?
  12. The contribution of nonroad equipment to overall risk is substantially lower in the 1999 national-scale assessment than it was in 1996. Is this due to changes in methodology or real reductions?
  13. Why are only noncancer risks calculated for diesel PM? Isn't there a cancer unit risk available?
  14. Why didn't EPA use the (higher) unit risk estimate (URE) for formaldehyde reported in the Agency's Integrated Risk Information System (IRIS)?
  15. How did EPA treat Coke Oven facilities in the assessment?
  16. Why aren't results for dioxin included?

General Background

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.

EPA is required to control 188 hazardous air pollutants based on a list initially defined by the Clean Air Act Amendments of 1990. Five important air pollutants are not included in the list of air toxics because the Clean Air Act addresses them separately as "criteria pollutants:" particulate matter (PM), nitrogen oxides (NOx), sulfur oxides (SOx), and carbon monoxide. (Lead is both a criteria pollutant and an air toxic).

Examples of toxic air pollutants include benzene, which is found in gasoline; perchlorethlyene, 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 six common pollutants or air toxics, see www.epa.gov/air/basic.html)

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2: What is the national-scale air toxics assessment?

A: The national-scale air toxics assessment is designed to help EPA, state, local and tribal governments and the public better understand and set priorities among hazardous air pollutants and their sources. The assessment focuses on a single year, and includes four steps:
  1. An inventory of air toxics emissions (1999 in this case),
  2. Estimates of annual average outdoor air toxics concentrations,
  3. Estimates of exposure concentrations (what people are estimated to breathe),
  4. A characterization of potential public health risks.

The 1999 national-scale air toxics assessment (released in 2005) is an update to the 1996 national-scale assessment (released in 2002). EPA expects to release a new national-scale assessment about every three years.

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3: What air toxics are included in the 1999 national-scale assessment?

A: The 1999 national-scale assessment includes emissions and ambient concentrations for 177 air toxics plus diesel PM. It also includes an exposure and risk assessment (cancer risk and noncancer hazard) for 133 of these air toxics (this subset is identified in the list of 178 pollutants in the assessment), plus an exposure and noncancer hazard assessment for diesel PM. EPA was able to characterize the cancer risk and noncancer hazard from this subset of 133 air toxics and diesel PM since these pollutants have health data based on chronic exposure. It should be noted that in December 2005 the EPA removed Methyl Ethyl Ketone (MEK) from the Clean Air Act list of HAPs, However, NATA was conducted prior to this action, thus MEK was included in the assessment.

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4: 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):
  1. Compiling a 1999 national emissions inventory of air toxics emissions 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 emissions 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).

  2. Estimating 1999 ambient air concentrations based on an air dispersion model (the ASPEN model) using 1999 emissions as input to the model. EPA also included estimated background concentrations (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.

  3. Estimating 1999 population exposures based on a screening-level inhalation exposure model (HAPEM5) and the estimated ambient concentrations (from the ASPEN model) as input to the exposure model. Estimating exposure is a key step in determining potential health risk. People move around 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 significantly higher or lower than the concentration at a fixed location (i.e., ambient concentration).

  4. Characterizing potential public health risks due to inhalation of air toxics. This includes both cancer and noncancer health effects, 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 1999 levels of emissions. It also discusses the uncertainties and limitations of the assessment, and identifies other potential risks to public health from air toxics that are beyond the scope of this quantitative assessment.

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5: What does "1 in a million" risk mean?

A: A risk level of 1 in a million implies a likelihood that up to 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 would be in addition to those cancer cases that would normally occur in an unexposed population of one million people. Note that this assessment looks at lifetime cancer risks, which should not be confused with or compared to annual cancer risk estimates. If you would like to compare an annual cancer risk estimate with the results in this assessment, you would need to multiply that annual estimate by a factor of 70 or alternatively divide the lifetime risk by a factor of 70.

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6: How do EPA and its regulatory partners at the state and local level use the results of national-scale assessments?

A: EPA 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/types of sources/locations for more refined data collection such as monitoring, etc.). More specifically, the national-scale assessment results are used:

  • As a starting point for EPA, states and communities to conduct more refined local assessments to help develop tailored risk reduction strategies to effectively address specific local problems. Since 2002 (year EPA released its 1996 national-scale assessment), many community-level air toxics reduction projects have used the national-scale assessment to identify potential air toxics and sources to investigate.
  • To set priorities for EPA, state and locals to improve quality control and completeness of emission inventories. For example, as a result of EPA's 1996 national-scale assessment, state and locals have provided more complete emissions inventory information on Chromium 6, which helps refine risk estimates for this pollutant.
  • As continued input for making decisions regarding where additional air quality monitoring may be appropriate and which pollutants should be monitored. This includes prioritization of monitoring method development. For example, as a result of the 1996 national-scale assessment, EPA is in the process of developing a better monitoring method for acrolein, a top pollutant identified by both the 1996 and 1999 national-scale assessments for noncancer hazard (respiratory effects).

All of this together will enable the air toxics program to more effectively target risk reduction activities.

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7: Why are all the estimates from 1999 -- and not more recent?

A: We used 1999 data because emissions inventories from that year are the most complete and up-to-date available. Working with the states, we update our air toxics emissions inventories every 3 years and are now gathering and compiling 2002 data. The risk estimates assume a lifelong exposure to 1999 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., 1999). It looks at human health impacts from outdoor, inhalation, chronic exposures and is based on 1999 emissions rates, assuming they remain constant throughout one's lifetime (not today's levels or projected levels). It does not include:
  • Cancer risk 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 for exposure are especially important for pollutants that persist in the environment and bioaccumulate, such as mercury and PCBs.
  • Exposures and risk very close to specific sources (highly-localized "hotspot" levels), such as some types of occupational or roadway-related exposures. The national-scale assessment estimates aggregated impacts of a facility.
  • Individual extremes in exposure. All risk estimates are based on exposure estimates for the median individual within each census tract, which EPA considers to be a "typical" exposure. Some individuals may have substantially higher or lower exposures based on where they spend their time.
  • Emissions from indoor sources of air toxics. For certain air toxics, total long-term human exposures can be significantly influenced and sometimes dominated by exposures from indoor sources.
  • Risk estimates for chemicals that do have EPA toxicity values (e.g., assessment does not quantify cancer risk from diesel PM; other chemicals lacking sufficient data are not assessed).
  • Impacts of short-term deviations at facilities such as startups, shutdowns, malfunctions, and upsets.
  • Ecological impacts, or other welfare effects.

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9: Who is responsible for controlling air toxics?

A: The responsibility is shared between EPA, state, local and Tribal air programs. EPA sets standards for air toxics emissions, which state and local programs are responsible for carrying out. 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 Exit EPA disclaimer

Information on the Tribal programs and EPA's Regional Tribal Program coordinators can be found at : http://www.epa.gov/oar/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.

While such computer models necessarily require simplifying assumptions and introduce significant uncertainties, they are needed to conduct such a large scale assessment since direct measurements of ambient air toxics concentrations are limited, and direct personal exposure measurements are even more limited. Such measurements are available for only a subset of air toxics in relatively few locations and for small study populations.

Although EPA is working to expand the number and locations of ambient air toxics 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 has been and will be used, however, to evaluate the models so as to better understand some of the uncertainties in such assessments and to improve modeling tools.

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Results

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 toxics 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 is not designed as a definitive means to pinpoint specific risk values at local levels. The results are best used to 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 the 78 air toxics that EPA is currently able to quantify with available dose-response data. Therefore, these risk estimates may represent only a subset of total risks associated with air toxics.

One out of every three Americans (330,000 in a million) will contract cancer during a lifetime, when all causes are taken into account. These assessment results suggest that the risk of contracting cancer is increased less than 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, for air toxics there are 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 part risk-based decision framework for the NESHAP program. First, it set an upper limit of acceptability of 1 in 10,000 (i.e., 100 in 1 million) lifetime cancer risk for highly exposed individuals. 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 1,000,000. 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, is 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 significant uncertainties, e.g., emissions levels, exposure concentrations, toxicity, and lacks the level of refinement that would enable us to adequately assess the highest exposures found in localized "hot spots."

Consequently, the results should not be used as absolute measures to determine whether risks are acceptable. Rather, they should be used to focus or target further measurement and assessment activities.

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3: What do these estimates mean to me?

A: Since EPA does not have an extensive network to monitor levels of toxic air pollutants across the country, the results of the assessment provide estimates that will give you an idea of the total amount of air toxics in your area for 1999 as well as a general estimate of the geographic patterns of potential risk within your state and county in 1999.

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4: How accurate is the assessment?

A: Large uncertainties, e.g., emissions levels, exposure, toxicity, are inherent in this analysis; therefore, we suggest interpreting the results in a relative rather than absolute manner. 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. See more information on these issues.

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5: How does the cancer risk identified in this assessment compare to lifetime cancer risk from all causes?

A: The 1999 national-scale assessment estimates that, on average, approximately one out of every 25,000 Americans (40 in one million) could contract cancer from breathing air toxics if exposed to 1999 emissions levels for 70 years. This may be compared with estimates that one out of every three Americans (333,000 in one million) will contract cancer during a lifetime, when all causes are taken into account.

These risks are unevenly distributed. For example, for over 10 million Americans in 1999, these estimated risks were at least two times higher.

In 2005, the American Cancer Society estimates that nearly 1.4 million Americans will discover they have cancer and about 570,000 will die from the 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. (http://www.cancer.org/docroot/STT/stt_0.asp Exit EPA disclaimer ) In some of these cases -- smoking for example -- these are voluntarily chosen risk factors.

Note that these cancer projections are based on historical risks which are much more certain than risk estimates provided by the national-scale assessment. The assessment 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 cancer risks for the 78 air toxics that EPA is currently able to quantify with available dose-response data. Therefore, these risk estimates may represent only a subset of total risks associated with air toxics.

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6: You show risk data/maps down to the census tract level. Are the results accurate enough to draw conclusions at this scale?

A:We recommend the census tract data/maps 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 maps 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 which occur 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:The revised Guidelines were released after the risk calculations for the national-scale assessment were completed. However, the effective guidance at the time we calculated the risks (an earlier draft of the revised Guidelines) was consistent in most ways with the revised document. There was one important exception to this consistency, however. The cancer guidelines now include Supplemental Guidance that makes new recommendations with regard to estimating cancer risks to children. These recommendations have not been implemented for the chemicals included in the national-scale assessment, with the exception of vinyl chloride.

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, as EPA has already done for vinyl chloride (and which are already reflected for that chemical in the national-scale assessment). 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, however, and can vary from pollutant to pollutant, according to its sources.

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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 projects that mobile source benzene emissions will decrease by about 60% between 1999 and 2020, as a result of motor vehicle standards, fuel controls, standards for nonroad engines and equipment, and motor vehicle inspection and maintenance programs. Most of these programs reduce benzene by reducing volatile organic compounds more generally.

EPA is developing a new mobile source air toxics rule under Clean Air Act section 202(l), to be proposed in February 2006, which requires motor vehicle and/or fuel standards that reflect the greatest emissions reductions achievable considering technology, cost, and other factors. As directed by the Act, this regulation will apply to emissions of benzene and formaldehyde, at a minimum.

EPA is also considering options to reduce emissions from gas cans as part of the same rulemaking. Evaporation, permeation, and spillage from gas cans all contribute to benzene emissions. When gas cans are stored in attached garages, these benzene emissions can penetrate into homes and thus increase indoor exposure to benzene.

Finally, EPA is also developing standards for small gasoline engines (e.g., used in lawn and garden equipment), that would also decrease benzene emissions. These standards are likely to be proposed in 2006.

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10: How does this assessment of 1999 air toxics data compare to the 1996 national-scale assessment?

A: Due to the extent of improvements in our methodology (e.g., almost double the number of point sources in the emissions inventory, inclusion of over 100 additional air toxics, updated unit risk estimates), it is not meaningful to compare the two national-scale assessments. This is because any change in emissions, ambient concentrations, or risks may be due to either improvements in methodology or to real changes.

We have made progress in reducing air toxics from stationary, mobile, and indoor sources. For example, by the end of 2004, 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 160 categories of industrial sources. Many of these standards came into effect after 1999 and the air toxics reductions are not reflected in the results. When fully implemented, these rules collectively will reduce between one and two million tons of toxic air emissions compared to the 1990 baseline emissions. The public health improvement associated with this reduction 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. In addition, current mobile source programs will reduce air toxic emissions by another 2.4 million tons in 2020, compared to 1990 levels. Learn more about air toxics reductions from industrial, mobile and indoor sources.

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11: 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 2004 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 160 categories of industrial sources. By 2007, these rules will result in 1.7 million fewer tons of air toxic emissions every year than were emitted in 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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12: The contribution of nonroad equipment to overall risk is substantially lower in the 1999 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 this reduction. These include several methodological changes:
  • For the 1996 national-scale assessment, EPA used the Integrated Risk Information System (IRIS) cancer potency estimate for formaldehyde, which is several orders of magnitude higher risk than the CIIT-based value used in the 1999 version of assessment. Learn more.
  • There were improvements in data and methods used to develop nonroad air toxic inventories since the 1996 assessment was conducted. These data changes result in large reductions in emissions for several key pollutants, but do not reflect real emission reductions.
  • There were improvements in how emissions were spatially allocated for several types of nonroad equipment. Some emissions were re-located in lower population areas, which results in lower population exposure estimates and lower risk estimates.

In addition, EPA programs are reducing emissions from nonroad equipment. EPA estimates this reduction at about 13% between 1996 and 1999.

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13: Why are only noncancer risks calculated for diesel PM? Isn't there a cancer unit risk available?

A: 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). (The cancer unit risk is a health assessment value that can be combined with environmental exposure data to estimate environmental risk.)

EPA cannot provide a quantitative estimate of potential cancer risk associated with environmental exposures to diesel particulate matter as it has for the other carcinogens in the 1999 national scale assessment.

First, the Agency has concluded that it is a likely human carcinogen. In addition, 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 risks from exposure to diesel exhaust may exceed one in one hundred thousand (1/100,000) and could be as high as one in one thousand (1/1,000), 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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14: 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, considerable work on the part of EPA has been performed 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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15: How did EPA treat Coke Oven facilities in the assessment? A:The 1999 NATA estimates risks from 22 coke ovens facilities in 13 states. The assessment includes some but not all air toxics emissions from coke plants. It includes emissions from the coke ovens themselves, but not from pushing (pushing the coke out of the oven), quenching (cooling the coke with water) and combustion stacks (which are attached to the coke oven itself). The reasons for not including all emission points are (1) In some cases, coke ovens plants did not have data from all the emissions points; and (2) In other cases, there was too much uncertainty in some of the emissions information to include it in the risk assessment. Because the assessment does not include all emissions from coke plants, it may underestimate risks from these facilities. We are currently working to reduce uncertainties with emissions information from coke plants and plan to include all emission points in the next NATA.

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16: Why aren't results for dioxin included?

A: EPA is conducting a separate assessment project specifically for dioxin.

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