AirToxScreen Frequent Questions
Questions on this page:
General Assessment Questions
- What are air toxics and what health effects can they cause?
- What is AirToxScreen?
- How can I use AirToxScreen results?
- How should I NOT use AirToxScreen results?
- Why is AirToxScreen a "screening" tool? Why doesn’t EPA run a more detailed analysis?
- Are there any risks from air toxics that aren't covered by AirToxScreen?
- Who is responsible for controlling air toxics?
- What should I do if I am concerned about air toxics in my area?
- How does AirToxScreen differ from other screening tools used by EPA? How do I know which tool to use?
- How do AirToxScreen results compare with the data in the EJScreen tool?
- Did AirToxScreen replace NATA? How are they different?
- How often does EPA update AirToxScreen emissions and risk results?
Emissions, Modeling, and Methods Questions
- Which air toxics are included in AirToxScreen?
- What are the steps in the AirToxScreen assessment?
- What are CMAQ and AERMOD, and how did EPA use them in AirToxScreen?
- Why did you exclude Alaska, Hawaii, Puerto Rico, the Virgin Islands, and other territories from CMAQ modeling?
- Why are all the estimates from 2019 and not more recent?
- Why is EPA using computer modeling instead of actual measurements to estimate concentrations and exposures?
- What improvements did EPA make in this version of AirToxScreen?
- What kind of changes were made in AirToxScreen because of the review by state, local, and tribal air agencies?
- How did EPA characterize risk from modeled exposure estimates?
- How does EPA estimate cancer risk?
- What are biogenic emissions?
- Why aren't primary biogenic emissions included from Alaska, Hawaii, Puerto Rico and the Virgin Islands?
- Part of the estimated risk is due to “background." What is background?
- Does AirToxScreen account for background concentrations of ethylene oxide?
- Part of the estimated risk is due to "secondary formation," which is widespread across the country. What is secondary formation?
- How does EPA update its emissions data to the latest data year?
- What does a “1-in-1 million” cancer risk mean?
- Why do most of AirToxScreen’s risk estimates seem to be to the nearest 10, like 20- or 30-in-1 million? Weren’t there any 25’s?
- What does EPA believe constitutes an acceptable level of risk?
- AirToxScreen also gives a noncancer "hazard index" for my area. What does that mean?
- How were the cancer risk estimates affected by EPA's Guidelines for Carcinogen Risk Assessment (EPA/630/P-03/001F) and Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens (EPA/630/R-03/003F)?
- Why aren’t results for dioxins included?
- What's the easiest way to review AirToxScreen results?
- What does AirToxScreen tell us overall about the risks from air toxics in the United States?
- What do these estimates mean for me?
- AirToxScreen shows an elevated risk of cancer in my area. Am I in danger? Am I going to get cancer? What can I do?
- How accurate is AirToxScreen?
- How does the cancer risk identified in this assessment compare to a 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?
- Based on AirToxScreen, can EPA show which people or places are at greatest risk from air toxics?
- How does this assessment of air toxics data compare to previous national-scale assessments?
- Why did risks change in my area from the previous national assessment?
- Has U.S. air quality improved?
- Can I use AirToxScreen to get risks at an exact place, like my home or my child's school?
- I can search on an address in the AirToxScreen Mapping Tool and get a risk value at that point. How accurate is that value?
- How does AirToxScreen treat emissions from fires?
- What does AirToxScreen show regarding impacts of wildfires, prescribed fires and agricultural burning?
- What are the uncertainties in risks from fire emissions?
- What is being done to reduce air pollution from fires?
Mobile Source Questions
- What is a "mobile source?" Are there different types?
- How accurate are risk estimates for mobile sources in my area?
- What is EPA doing to reduce emissions of mobile source air toxics?
- Why did EPA only calculate noncancer risks from diesel PM and not cancer risks?
- There has been increased concern about health effects associated with pollution near roads. What can AirToxScreen tell us about health risks from exposure to near-road pollution?
- AirToxScreen results show impacts associated with a port in my community. How accurate are these estimates, and what can be done to reduce the impacts?
General Assessment Questions
Q1: What are air toxics and what health effects can they cause?
A1: Air toxics (also called toxic air pollutants or hazardous air pollutants) are airborne substances that cause or may cause serious health problems. These can include cancer, reproductive problems or birth defects. Air toxics can also cause harmful environmental and ecological effects.
Section 112 of the Clean Air Act lists a set of 188 pollutants as air toxics. This section requires EPA to identify categories of industrial sources for these listed air toxics. It also requires us to take steps to reduce pollution by requiring sources of these air toxics to install controls or change production processes. Learn more at the Overview of the Clean Air Act. Examples of air toxics include benzene, found in gasoline; tetrachloroethylene, emitted from some dry cleaning facilities; and methylene chloride, used as a solvent and paint stripper by several industries.
EPA has classified many of these pollutants as “carcinogenicCapable of causing cancer. to humans,” “likely to be carcinogenic to humans,” or “suggestive evidence of carcinogenic potential.” Air toxics are also associated with many noncancer adverse health effectsA change in body chemistry, body function or cell structure that could lead to disease or health problems.. These include effects on the lungs and other parts of the respiratory system; on the immune, nervous and reproductive systems; and to organs such as the heart, liver and kidneys. These health effects can range from headaches and nausea to respiratory arrest and death. Severity varies with the amount and length of exposure and the nature of the chemical itself (for example, how it interacts with various organs and organ systems). It can even vary due to unique behaviors and sensitivities of individual people. For example, some chemicals pose hazards to people of certain ages or genetic backgrounds.
Q2: What is AirToxScreen?
A2: The Air Toxics Screening Assessment, or AirToxScreen, is EPA's review of air toxics in the United States, based on modeled air quality. We developed AirToxScreen as a tool for state, local and tribal agencies, and we use its results as well. AirToxScreen helps us find out which air toxics, emission sources, and places may need further study to better understand risksThe probability that adverse effects to human health or the environment will occur due to a given hazard, such as exposure to a toxic chemical or mixture of toxic chemicals. We can measure or estimate some risks in numerical terms (for example, one chance in a million)..
AirToxScreen uses the best science and emissions Pollutants released into the air. data available to estimate possible health risks from air toxics. But because of its large, national scale, we must simplify some of AirToxScreen’s input data and analytical methods. That's why we call AirToxScreen a “screening tool” — it helps us estimate risks and tells us where to look further.
AirToxScreen provides screening-level estimates of the risk of cancer and other serious health effects from breathing air toxics. This helps show which air toxics and source types may raise health risks in certain places. Air pollution experts can then study these places in more detail, focusing on where the risks to people may be greatest. They may even choose to perform a smaller-scale local assessment, which allows them to use more detailed data than we can in AirToxScreen.
AirToxScreen gives a “snapshot” of the outdoor air quality as it relates to air toxics. It also suggests the long-term risks to human health if air toxic emissions stay the same. A more detailed explanation of AirToxScreen and the methods used can be found in the AirToxScreen Technical Support Document.
Q3: How can I use AirToxScreen results?
A3: You can use AirToxScreen to:
- learn which air toxics may be of concern to you;
- better understand risks from air toxics;
- open a dialogue with your local air agency about air quality in your area.
Your state, local or tribal agency uses AirToxScreen results to:
- prioritize pollutants and emission source types;
- identify places of interest for further, more detailed study;
- get a starting point for local assessments;
- focus community efforts;
- inform monitoring programs;
- prioritize sensitive locations for outdoor air toxics monitoring.
EPA uses AirToxScreen results to:
- learn which pollutants and source types may be of concern;
- better understand risks from air toxics;
- help decide what other data to collect;
- improve data in emission inventories;
- expand and prioritize EPA's air toxics monitoring network;
- work with communities to design their own assessment;
- help target risk reduction activities.
Q4: How should I NOT use AirToxScreen results?
A4: AirToxScreen assessments should not be used:
- to pinpoint risk or exposure values at a specific place (like a home or school);
- to characterize or compare risks or exposures at local levels (such as between neighborhoods);
- to characterize or compare risks or exposures between states;
- as the sole basis for risk reduction plans or regulations;
- to control specific sources or pollutants; or
- to quantify benefits of reduced air toxics emissions.
Please keep a few other things in mind when using AirToxScreen results. While results are reported at the census tract level, average exposure and risk estimates are far more uncertain at this level than at the county or state level. Also, AirToxScreen is a screening tool, not a refined assessment. It shouldn’t be used as the sole source of information to regulate sources or enforce existing air quality rules.
In addition, while we do allow users to view results from both the current and previous AirToxScreen assessments in our AirToxScreen Mapping Tool, you should keep some things in mind when comparing different assessments. Over the years, we have improved the source inventory, made modeling changes, revised background calculations, and updated some health benchmarks. Also, each assessment uses a particular year of weather data in the air models that we use to calculate risks, which can also influence results. That’s why it can be misleading to compare this version of AirToxScreen with previous assessments.
Q5: Why is AirToxScreen a "screening" tool? Why doesn’t EPA run a more detailed assessment?
A5: Because of AirToxScreen's broad national scale, we must simplify some of its input data and our analytical methods. That's why we call AirToxScreen a “screening tool”—it's designed to help guide where to look in more detail at air toxics risks.
As for the second question, there are several reasons why we can’t run a detailed, or refined, national analysis right now.
For some source types, we don’t have emissions Pollutants released into the air. data at a precise enough level. For example, we don’t know the exact location of widespread, numerous sources such as emissions from homes and gas stations, or exactly how auto emissions are spread across an area. That means we can’t calculate the precise impacts from those sources at a specific point, something needed in a refined analysis.
It would also take lot of time to collect source data at the level of detail needed for a refined assessment. Starting with the 2017 AirToxScreen and continuing through this latest release, EPA is updating this assessment every year. Right now, we can’t update that kind of large, refined dataset annually.
We would need several other things, including local weather data to use in modeling, more detailed human activity-pattern data for better exposure estimates, and more. So, while perhaps one day we will have the data and resources needed to do a refined assessment, we don't have that just yet. AirToxScreen results can, however, inform a more refined, local analysis that uses EPA recommendations and guidance.
Q6: Are there any risks from air toxics that aren't covered by AirToxScreen?
A6: Yes. AirToxScreen looks at just one facet of the air toxics picture — potential health effects due to breathing air toxics from outdoor sources over many years. It also just looks at one point in time: air toxics emissions and weather data used are from a single year (in this latest AirToxScreen release, from 2019), and it assumes that they stay the same throughout one's lifetime. Together, these assumptions mean AirToxScreen can’t account for all risks.
Also, AirToxScreen doesn’t include:
- potential cancer risks associated with diesel particulate matter (PM), which may be large (see question 3 below in the Mobile Sources section);
- non-inhalation exposures, such as ingestion and skin exposures. These pathways are important for pollutants that stay in the environment and bioaccumulate (build up in tissues of organisms) such as mercury and polychlorinated biphenyls;
- exposures and risks very close to specific sources or at highly localized “hotspots” (such as some types of workplace-related or near-roadway-related exposures);
- individual exposure extremes. We base all risk estimates on exposure estimates for the medianThe middle value of a set of ordered values (i.e., half the numbers are less than or equal to the median value). A median is the 50th percentile of the data. individual in each census tract. EPA considers this to be a “typical” exposure for that tract. Some people may have higher or lower exposures based on where they live or spend most of their time within that tract;
- emissions from indoor sources of air toxics. For certain air toxics and for certain indoor situations, exposure to indoor sources can influence and sometimes dominate total long-term human exposures;
- risk estimates for chemicals without adequate dose-response information (for example, cancer risk from cobalt emissions);
- impacts of nonroutine increases in facility emissions due to things like equipment startups, shutdowns, malfunctions and upsets;
- assessment of adverse environmental effects or other welfare effects.
Q7: Who is responsible for controlling air toxics?
A7: EPA, state, local and tribal air programs share responsibility. EPA sets national standards for some sources of air toxics emissions. State, local and tribal programs implement these rules. Some state, local and tribal programs also set their own air toxics rules and conduct their own studies.
Q8: What should I do if I'm concerned about air toxics in my area?
A8: Please contact your state, local or tribal air program. View a list of state and local programs.
You can also view information on tribal programs and EPA's Regional Tribal Program coordinators.
Q9: How does AirToxScreen differ from the other screening tools used by EPA? How do I know which tool to use?
A9: AirToxScreen is a national assessment that estimates cancer and noncancer risks from breathing air toxics. AirToxScreen is intended as a screening tool to help users prioritize pollutants, types of emission sources, and places of interest for further study. AirToxScreen risk results are included in the EJScreen tool. EPA has designed other tools, such as EnviroAtlas and NEPAssist, to meet certain needs.
Which tool to use depends on your main area of interest. For a quick-look comparison, visit the Other Environmental Risk Screening Tools web page.
Q10: How do AirToxScreen results compare with the data in the EJScreen tool?
A10: EJScreen includes cancer risk, respiratory hazard index, and diesel PM concentrations results provided by AirToxScreen in its data layers. But EJScreen groups and displays these results differently than AirToxScreen.
AirToxScreen shows results at the census tract level, as described in more detail in the Results section of these Frequent Questions. EJScreen shows the air toxics results at the census block group level, which generally includes several city blocks. But as we mentioned, since these data came from AirToxScreen and are only shown at the census tract, all census block groups in EJScreen within a particular census tract will show the same values.
Also, EJScreen's risk maps look different than the AirToxScreen's Mapping Tool's, despite using the same data. This is because EJScreen groups and displays risk by percentile, while AirToxScreen's maps group and display actual risk values. AirToxScreen also provides additional detailed air toxics information, such as risks and concentrations from individual pollutants.
Q11: Did AirToxScreen replace NATA? How are they different?
A11: The Air Toxics Screening Assessment, or AirToxScreen, is a part of EPA's Air Toxics Strategy, which is focused on improving public access to air toxics information and data. AirToxScreen falls under the umbrella of our Air Toxics Data Update, which also includes the National Emissions Inventory of air toxics sources.
While AirToxScreen has similarities to previous versions of the National Air Toxics Assessment, or NATA, it is designed to be a more dynamic, flexible, and timely assessment. In addition, the new name distinguishes this new approach and highlights that, like NATA, this is a screening level assessment. The biggest change going forward is that EPA is releasing a new Air Toxics Data Update and new AirToxScreen assessment annually. This started with the 2017 emissions-year release.
Frequency of Release
Every 3 to 4 years
Spatial Resolution of Information
Census tract level
Census tract level (In future years, finer resolution census block level for certain sources.)
Release of Information
Initially available on EPA’s air toxics website and incorporated into EJScreen, and eventually included in the annual Air Trends Report
Q12: How often does EPA update AirToxScreen?
A12: Starting with the 2017 update that was released in March 2022, EPA plans to release a new AirToxScreen assessment for every data year. In the year 2022, we released three updates to AirToxScreen, one each for data-years 2017, 2018, and 2019, as we "caught up to the calendar." Starting in 2023 with the data-year 2020 release, we intend to have one update per year that includes the latest available data.
Emissions, Modeling, and Methods Questions
Q1: Which air toxics are included in AirToxScreen?
A1: AirToxScreen estimates ambientThe open air. In AirToxScreen, ambient concentrations describe how much of a pollutant is in the air as an amount, or mass, of pollutant per certain volume of air. and exposure concentrationsConcentrations of air pollutants that a person might breathe over time. Exposure concentration differs from ambient concentration in that it considers the time a typical person in an area spends indoors or outdoors as well as traveling from one area to another. for 180 air toxics plus diesel particulate matter (PM), which we assess for noncancer effects only. Using the concentration estimates for the 180 air toxics plus diesel PM, AirToxScreen estimates cancer risks and noncancer hazards for 138 of these. For the other air toxics, AirToxScreen gives concentration estimates, but no health-effects data are available. You can find a list of all air toxics assessed and the types of results generated for each in Appendix B of the AirToxScreen Technical Support Document.
EPA did not include the following air toxics in this assessment because either no emissions Pollutants released into the air. data were reported for them in 2019 or we couldn’t reliably make emission estimates useful for modeling from their reported emissions. We also don't include the air toxic chromium III from the assessment because there are no risk values for that specific compound (only the chromium VI portion of chromium emissions were assessed).
- Other dioxins/furans
- Fine mineral fibers
- Chromium III
Q2: What are the steps in the AirToxScreen assessment?
A2: AirToxScreen includes the following four major steps for assessing air toxics across the United States (including Puerto Rico and the U.S. Virgin Islands):
- Compile a 2019 inventory of air toxics emissions from outdoor sources.
EPA compiled measured or estimated emissions Pollutants released into the air. data reported by sources, states and others. We also estimated mobile source and other emissions using models, measurements and a quality-control process. This dataset is called the National Emissions Inventory (NEI). We start with the latest NEI (from 2017) and update it with 2019 emissions (see below). The emission source types in the NEI include major stationary sourcesEmission sources that do not move. Stationary sources include as large industrial sources such as power plants and refineries, smaller industrial and commercial sources such as dry cleaners, and residential sources such as residential wood burning and consumer products usage. (such large waste incinerators and factories), area and other sourcesSources of air pollution that, by themselves, generally have lower emissions than “major sources” of air pollution (like factories). Area sources can include smaller facilities, such as gas stations, or widespread sources like smoke from home fireplaces. (such as gas stations and small manufacturers), on-roadMobile sources used on roads and highways for transportation of passengers or freight. On-road sources include passenger cars and trucks, commercial trucks and buses, and motorcycles. and nonroadMobile sources not used on roads and highways for transportation of passengers or freight. Nonroad sources include aircraft, heavy equipment, locomotives, marine vessels, recreation vehicles (such as snowmobiles and all-terrain vehicles), and small engines and tools (such as lawnmowers). mobile sources (such as cars, trucks and boats), biogenicProduced by biological processes. In AirToxScreen, biogenic emissions are those from trees, plants and soil microbes. sources, and fires. These emissions Pollutants released into the air. data become a major part of the modeling input data used in the next AirToxScreen step.
- Estimate ambient air concentrations based on the 2019 emissions.
We used the emissions data from step 1 as inputs to two air quality models: the American Meteorological Society/Environmental Protection Agency Regulatory Model (AERMOD) and the Community Multiscale Air Quality model (CMAQ). These models estimate ambient concentrations of the emitted toxics. We modeled 52 HAPsAir pollutants that are known or suspected to cause cancer or other serious health effects, such as reproductive effects or birth defects, or adverse environmental effects. plus diesel particulate matter in CMAQ and all AirToxScreen air toxics in AERMOD. We then combined the results using a hybrid approach that takes advantage of the strengths of both models (the AirToxScreen Technical Support Document describes this hybrid approach). To evaluate model performance, we compared estimated ambient concentrations to air toxics monitoring data.
- Estimate population exposures. Next, we used the estimated ambient concentrations as inputs to an exposure model, the Hazardous Air Pollution Exposure Model (HAPEM), version 7. Estimating exposure is a key step in determining potential health risk. People move from one location to another — for example, from outside to inside. Their exposure isn't the same as it would be if they stayed in one place. 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, called their exposure concentration, might be higher or lower than the concentration at a fixed location (ambient concentration). We accounted for this when calculating exposures.
- Characterize potential public health risks due to breathing air toxics.
We characterized cancer risks and noncancer health effects using available information on air toxics health effects, current EPA risk assessment and risk characterization guidelines, and the exposures estimated in the prior step. The result is the heart of AirToxScreen: a national view of potential long-term risks to public health due to breathing air toxics from outdoor emission sources, assuming a lifelong exposure to 2019 emission levels. Along with presenting these numbers, we discuss the assessment’s uncertainties and limitations.You can find more detailed information about these steps in the Technical Support Document.
Q3: What are CMAQ and AERMOD, and how did EPA use them in AirToxScreen?
A3: CMAQ, EPA’s Community Multiscale Air Quality Model, is a computer program that estimates air quality. CMAQ simulates how emissions of multiple air pollutants, emitted by numerous sources at the same time, travel and disperse downwind. From this, it calculates the pollutants’ concentrations across the United States. Not only does CMAQ show how pollutants move and disperse, it also models how they can react with other pollutants and gases in the atmosphere. This is a key difference between CMAQ and some other air quality models.
CMAQ conserves mass (that is, if some pollution blows out of one area, the same amount is tracked into the new area); allows long-range pollutant transport; and estimates concentrations of secondarily-formed pollutants such as formaldehyde. In AirToxScreen, EPA used CMAQ for 52 pollutants, with emissions from point and nonpoint sources, mobile sources, biogenics and fires.
In addition to CMAQ, we ran the dispersion model AERMOD for all AirToxScreen pollutants at all U.S. census tracts for point, nonpoint and mobile sources. Like all similar models, AERMOD uses equations to simulate how the atmosphere disperses pollutants. From this, it can calculate pollutant concentrations at many discrete points (called receptors). Modelers can place these receptors closer together in AERMOD than in CMAQ, a strength of the former model.
We then combined the ambient concentrations estimated by both CMAQ and AERMOD in a hybrid approach, taking advantage of each model’s features and strengths. Detailed information on this approach can be found in Section 3 of the AirToxScreen Technical Support Document.
Q4: Why were Alaska, Hawaii, Puerto Rico, the Virgin Islands, and other territories not included?
A4: The CMAQ modeling performed for AirToxScreen used a single domain that covers the contiguous United States and large portions of Canada and Mexico. However, this domain doesn’t include Alaska, Hawaii, Puerto Rico or the Virgin Islands (consistent with previous regulatory modeling conducted by EPA). To model in these areas using CMAQ, we would have needed very detailed weather and terrain data, and thus many more computing resources. However, EPA did model these areas in AERMOD. You can find more information about air toxics emissions in these areas with theAirToxScreen Mapping Tool.
Q5: Why are all the estimates for the year 2019 and not more recent?
A5: We used 2019 data because emission inventories from that year were the most complete and up to date available when we began putting this AirToxScreen release together. It takes time to gather, quality check, and model these data. Note that EPA is updating AirToxScreen for each data year starting with the 2017 version released in March 2022.
Q6: Why is EPA using computer modeling instead of actual measurements to estimate concentrations and exposure?
A6: Right now, we can’t monitor ambient air toxics across the entire country. It would be extremely expensive. Instead, we only measure a subset of air toxics concentrations in a few locations. So for large-scale assessments such as AirToxScreen, we need to use computer models to estimate ambient air toxics concentrations and population exposures nationwide.
EPA does use measured data to evaluate the models. This helps us better understand some of the uncertainties in assessments and improve modeling tools. For example, in a supplemental data file available in our results area here on the AirToxScreen website, we explain the results of model-to-monitor comparisons done for the 2019 AirToxScreen. In addition, we provide annual statistics for air toxics monitoring data in the AirToxScreen Mapping Tool. You can obtain air toxics monitoring data from the Air Monitoring Archive in multiple formats, including Microsoft Access, for historical data years through 2016. You can use EPA’s Air Quality System (AQS) Data Mart for more recent data.
Q7: What improvements did EPA make in this version of AirToxScreen?
A7: The following changes were included in the 2019 AirToxScreen. Most of the changes adopted for the 2017 and 2018 AirToxScreen assessments were carried over to this 2019 assessment; they are not repeated here.
- Updated emission factors used where available
- Note that 2019 commercial sterilizer ethylene oxide emissions were not based on NEI data, but rather the methodology developed for the commercial sterilizer rule modeling using facility throughputs and control apparatus installations that were valid for calendar year 2019. At the time of data development, these were the best available estimates of year 2019 ethylene oxide emissions from commercial sterilizers.
While EPA continually refines and updates these methods, it’s also important to remember that AirToxScreen is a screening-level assessment. It helps us find out which air toxics, emission sources, and places may need further study. Air quality scientists may need to perform more refined assessments (for example, ambient air monitoring or local risk assessments) to better understand local exposures and risks.
Q8: What kind of changes were made in AirToxScreen because of the review by state, local and tribal air agencies?
A8: EPA appreciates the time taken by state, local and tribal air agencies to preview and comment on the preliminary results of this assessment. Thorough reviews such as these help us continually improve our assessments, which benefits all AirToxScreen users.
These comments covered the areas of:
- Facility changes:
- Geographic coordinate changes
- Revisions to stack parameters
- Emission changes:
- Additions, deletions, and recalculations
- Changes to chromium speciation, hexavalent chromium percentage
Most of the comments were addressed by making the appropriate changes to the 2017 NEI and 2019 AirToxScreen inventories and/or directly to AERMOD input files for AirToxScreen modeling. The final 2019 AirToxScreen now reflects these changes. Additional comments focused on methodological and toxicological questions, many of which are addressed or answered in various sections of the AirToxScreen website.
Q9: How did EPA characterize risk from the modeled exposure estimates?
A9: To evaluate a chemical's potential to cause cancer and other adverse health effects, we:
- examine the adverse effects the chemical causes (a “hazard identification”);
- determine the exposure to the population (an “exposure assessment”); and
- evaluate the specific exposures at which these effects might occur (a “dose-response assessment”).
The chemical’s evaluation is based on studies of humans, animals, and microorganisms, and is usually published in peer-reviewed scientific journals. In this national assessment, we combined information from dose-response assessments with modeled exposure estimates in a “risk characterization” to describe the potential that real-world exposure to air toxics might cause harm. We also looked at the uncertainties of risk characterization.
Q10: How does EPA estimate cancer risk?
A10: EPA typically assumes a linear relationship between the level of exposure and the lifetime probability of cancer from an air toxic (unless research suggests a different relationship). We express this dose-response relationship for cancer in terms of a “unit risk estimate.” The unit risk estimate (URE) is an upper-bound estimate of a person’s chance of contracting cancer over a lifetime of exposure to a particular concentration: one microgram of the pollutant per cubic meter of air. Risks from exposures to concentrations other than one microgram per cubic meter are usually calculated by multiplying the actual concentration to which someone is exposed by the URE.
For example, EPA may determine the URE of an air toxic to be 1 in 10,000 per microgram per cubic meter. This means that a person who breathes air containing an average of 1 microgram per cubic meter for 70 years would have (as an upper bound) 1 chance in 10,000 (or 0.01 percent) of contracting cancer as a result. So, in this example, if the modeled concentration in AirToxScreen for this air toxic is 0.5 micrograms per cubic meter for a particular tract, the risk would be 0.5 times the URE, or a 1-in-20,000 cancer risk.
EPA has developed UREs for many substances, and continues to re-examine and update them as knowledge improves. More information on UREs can be found in EPA's Integrated Risk Information System. The UREs used in this assessment are included in the AirToxScreen Supplemental Data folder.
Q11: What are biogenic emissions?
A11: In AirToxScreen, biogenic emissions are those from trees, plants and soil microbes. Biogenic sources emit formaldehyde, acetaldehyde and methanol; formaldehyde and acetaldehyde are key risk drivers in AirToxScreen. Biogenic sources also emit large amounts of other volatile organic compounds. These compounds are not hazardous, but they can react in the air with certain human-caused emissions to form hazardous pollutants.
In AirToxScreen, the biogenic emissions source group only includes primary emissions, or those directly emitted into the air by natural sources. Some compounds emitted by natural sources also react chemically in the air with compounds emitted by humans to make other pollutants; these are included in the Secondary source group; (see question 15 below).
For AirToxScreen, a model computes biogenic emissions using vegetation and land use data for an area. It also uses data such as air temperature and the amount of sunlight received. More information about how we compute and model biogenic emissions in AirToxScreen can be found in Section 2 of the AirToxScreen Technical Support Document.
Q12: Why aren't primary biogenic emissions included from Alaska, Hawaii, Puerto Rico, and the Virgin Islands?
A12: We modeled primary biogenic emissions only with the CMAQ air quality model. Alaska, Hawaii, Puerto Rico, the Virgin Islands, and other territories are not currently included in CMAQ. See the answer to question 4 for more information.
Q13: Part of the estimated risk is due to "background." What is background?
A13: In AirToxScreen, background risk represents:
- the contributions to outdoor air toxics concentrations from natural sources not modeled directly as biogenic emissions;
- persistence in the environment of past years’ emissions; and
- long-range transport from distant sources.
Background concentrations represent levels of pollutants that would be found in a year even if there had been no recent human-caused emissions. For example, a main contributor to risk from background concentrations is carbon tetrachloride, a common pollutant that now has few emissions sources but persists in the air due to its long half-life.
For AirToxScreen, we estimated background using remote concentration estimates from monitoring and emissions.
Q14: Does AirToxScreen account for background concentrations of ethylene oxide?
A14: AirToxScreen incorporates only known emissions sources of ethylene oxide (EtO). To learn more, please see EPA's Work to Understand Background Levels of Ethylene Oxide.
Q15: Part of the estimated risk is due to "secondary formation," which is widespread across the country. What is secondary formation?
A15: Some hazardous air pollutants form when compounds called VOCs (short for volatile organic compounds) react chemically in the air with other compounds emitted by humans (usually oxides of nitrogen, or NOx). This is known as secondary formation.
During the summer months, most of the VOCs come from actively growing trees and other biogenic sources; in winter, when plant growth slows, wood burning from homes and auto exhaust provide most of the VOCs. Year-round, most NOx comes from the burning of fossil fuels by autos and industry.
Formaldehyde and acetaldehyde are common secondary HAPs (the criteria pollutant ozone also is another secondary pollutant). For AirToxScreen, we estimated secondary formation using the CMAQ model.
Q16: How does EPA update its emissions data to the latest data year?
A16: When putting together the emissions data for AirToxScreen, we start with the latest National Emissions Inventory, or NEI. However, the NEI only comes out every three years; the most recent one was in 2017. But we're able to use that NEI because each emission sector is represented for the inventory year being modeled.
For point sources, many of the largest point sources are reported to the NEI annually by state, local, and tribal agencies, and their emissions have been updated in the AirToxScreen modeling platform for 2019. For smaller point sources, emissions are either carried forward from the most recent NEI year or marked as closed and removed, if applicable. Airports were projected to 2019 using the FAA’s Terminal Area Forecast data, except for military airports which were unchanged from 2017. For nonpoint sources, the emissions would remain mostly unchanged from the 2017 NEI. However, some nonpoint sources were updated using appropriate activity data (e.g., area fugitive dust was projected to 2019 using 2019 vehicle miles traveled trends). Onroad mobile emissions were projected from 2017 to 2019 mostly using Federal Highway administration annual data, and railway emissions were projected from 2017 to 2019 using activity-based factors. Fire emissions and biogenic emissions were both updated to 2019 using their respective emission models and methodology.
More information about how each emission sector was estimated for 2019 can be found in the 2019 Emissions Modeling Platform TSD.
Q1: What does a "1-in-1 million" cancer risk mean?
A1: A lifetime cancer risk of 1-in-1 million means that, for every 1 million people who are continuously exposed to a certain level of a pollutant over 70 years, one person may develop cancer. These risks are on top of any other cancer risks from other sources.
Q2: Why do most of AirToxScreen’s risk estimates seem to be to the nearest ten, like 20- or 30-in-1 million? Weren’t there any 25’s?
A2: In AirToxScreen, as in most of our air toxics risk assessments, we round calculated risks to one significant figure in the last step of the risk calculation. Significant figures are the digits of a number that are meaningful in terms of accuracy or precision. Usually, that's the non-zero digits. So a number with one significant figure has just one non-zero digit.
Let’s look at an example. In AirToxScreen, we round all calculated risks from 25-in-1 million through 34 in-1-million to 30-in-1 million. The “3” is the one significant figure in this number.
Why do we do this? It’s because of the uncertainty that’s part of all our assessments. Our results can only be as precise as the input data we use to calculate risk. We could show risk out to two significant figures or more, but that’s “false precision.” We simply aren’t that certain about things like the precise location and amounts of pollutant releases, the meteorological data, and other inputs. There are also some uncertainties in the air models that we use. Therefore, we aren't that certain about the final calculated risks.
By the way, the larger the risk, the larger the rounding to get to one significant figure. For example, if we calculate a risk of 145-in-1 million, this is rounded down to 100-in-1 million in AirToxScreen. If the risk is 155-in-1 million, it’s rounded up to 200-in-1 million. Again, we always round to one significant figure.
Q3: What does EPA believe constitutes an acceptable level of risk?
A3: Unlike other pollutants that EPA regulates, air toxics have no universal, predefined risk levels that clearly represent acceptable or unacceptable thresholds. However, EPA has made case-specific determinations and made general presumptions that apply to certain regulatory programs. As explained below, we use levels that come from these rulings to guide how we interpret risk in AirToxScreen.
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.
First, the rule sets an upper limit of acceptable risk at about a 1-in-10,000 (or 100-in-1 million) lifetime cancer risk for the most exposed person. As the rule explains, “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 rule set a target of protecting the most people possible to an individual lifetime risk level no higher than about 1-in-1 million. These determinations called for considering other health and risk factors, including risk assessment uncertainty, in making an overall judgment on risk acceptability.
Q4: AirToxScreen results also show a noncancer “hazard index” for my area. What does that mean?
A4: To estimate noncancer health impacts, EPA calculates what’s known as a hazard index. This index accounts for potential noncancer health effects to certain human organs and organ systems due to long-term exposure to air toxics. It accounts for impacts from all air toxics that affect a target organ system in the same (or similar) way, summing a hazard quotientThe ratio of the potential exposure to the substance and the level at which no adverse effects are expected. A hazard quotient less than or equal to one indicates that adverse noncancer effects are not likely to occur, and thus can be considered to have negligible hazard. calculated for each air toxic.
A hazard index (HI) of 1 or lower means air toxics are unlikely to cause adverse noncancer health effects over a lifetime of exposure. However, an HI greater than 1 does not necessarily mean adverse effects are likely. Instead, EPA evaluates this on a case-by-case basis. We consider the confidence level of the underlying health data, the uncertainties, the slope of the dose-response curveA way to express the relationship between the dose, or amount, of a pollutant to which a person may be exposed and how their body responds. (if known), the magnitude of the exceedances, and the numbers or types of people exposed at various levels above the Reference ConcentrationAn estimate of a continuous inhalation exposure unlikely to cause adverse health effects during a person’s lifetime. This estimate includes sensitive groups such as children, asthmatics and the elderly. (RfC).
Q5: How were the cancer risk estimates affected by EPA's Guidelines for Carcinogen Risk Assessment (EPA/630/P-03/001F) and Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens (EPA/630/R-03/003F)?
A5: AirToxScreen is consistent with the methods for estimating cancer risks to children recommended by the 2005 revised Cancer Guidelines and the Supplemental Guidance.
For the following HAPs, we applied a risk factor of 1.6 (see source of factor below) to account for the increase in lifetime cancer risk due to childhood exposures:
- Coke oven emissions
- Ethyl carbamate
- Ethylene oxide
- Methylene chloride
We used this factor because research shows these HAPs 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 (see explanation below).
In contrast, vinyl chloride does have chemical-specific data available regarding children’s exposure and risk. EPA used these data to derive the unit risk estimateAn upper-bound estimate of a person’s chance of contracting cancer over a lifetime of exposure to a particular concentration: one microgram of the pollutant per cubic meter of air. Risks from exposures to concentrations other than one microgram per cubic meter are usually calculated by multiplying the actual concentration to which someone is exposed by the URE., or URE (see the IRIS website for a more thorough explanation). Therefore, the vinyl chloride URE used in AirToxScreen (see Appendix H of the AirToxScreen Technical Support Document) already reflects the risk due to childhood exposures; no further adjustment is necessary.
For trichloroethylene, a carcinogen with a mutagenic mode of action, the age-dependent adjustment factor for the URE only applies to the part of the slope factor reflecting risk of kidney cancer. For lifetime exposure to a constant level of trichloroethylene, we adjusted the URE by a factor of 1.12.
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 (cause cancer by damaging genes) and linear (direct-acting) mode of action. Where available data for the chemical are adequate (such as with vinyl chloride), 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 tenfold for children up to 2 years old, and threefold for children from 2 through 15 years old. These adjustments have the aggregate effect of increasing by about 60 percent (a factor of 1.6), the estimated risk for a 70-year (lifetime) constant inhalation exposure.
It’s important to keep in mind that EPA recommends making the default adjustments 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 assessments will reflect adjustments for those substances.
Q6: Why aren't results for dioxin included?
A6: We did not evaluate exposure and risk related to dioxins in AirToxScreen because we did not evaluate the completeness or accuracy of the state, local and tribal agency data for dioxins. The most significant exposure route for dioxins is ingestion, not inhalation. So dioxins’ relative contribution to AirToxScreen’s risk estimates likely would be small.
Q1: What's the easiest way to review AirToxScreen results?
A1: The AirToxScreen Mapping Tool displays cancer risks, emissions Pollutants released into the air. data, and ambient concentrations data on a map and dashboard. The map allows you to examine places of interest anywhere in the country. Key features of the mapping tool include tracts sorted by total risk, risk by source type, facility-level emissions information, and air toxics monitoring data. You can easily change the displayed data type by toggling the different map layers. You can also download all AirToxScreen data and results, and run queries to find the information you want.
The AirToxScreen mapping tool includes the following layers (note: some of these layers are still to be added to the tool):
- all emissions sources modeled in AirToxScreen;
- cancer risks by pollutant and source
- long-term noncancer hazard indexes
- modeled ambient concentrations and exposure concentrations (tract level); and
- air toxics monitoring sites with monitoring data.
You can use the AirToxScreen Mapping Tool on a computer or mobile device.
Q2: What does AirToxScreen tell us overall about the risks from air toxics in the United States?
A2: The 2019 AirToxScreen estimates most people’s risks to be between 1-in-1 million and 100-in-1 million. The estimates for a small number of localized areas are higher than 100-in-1 million (see question 2 of the Risk section for more on what this means). People and communities may be concerned about this. It’s important to remember, however, that AirToxScreen wasn’t designed as a final means to pinpoint specific risk values at local levels. The results are best used as a tool to help learn which pollutants, types of emissions sources and places should be studied further.
We should note that AirToxScreen risk estimates do not consider ingestion exposure or skin contact with toxics. They also don’t include indoor sources of air toxics. Because we don’t have health-effects data for some air toxics, out of about 180 toxics modeled, we only assessed 129 for risk. (Diesel particulate matter risk was only assessed for noncancer effects.) Therefore, these risk estimates may represent only some of the total potential risks associated with air toxics.
While air quality continues to improve nationwide, 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.
Q3: What do these estimates mean for me?
A3: AirToxScreen’s results estimate the amount of air toxics in an area and show general patterns of potential risk for each state and county in the United States. They are best used to help show which pollutants, emissions sources and places should be studied in more detail.
AirToxScreen wasn’t designed to be a final tool for assessing risks. Because of its national scale, it has some limitations in data and methods. Some of these will cause AirToxScreen to report higher risk estimates for an area than may truly exist. At the same time, the most-exposed people in an area may run a higher risk than AirToxScreen calculates.
This means you should avoid using AirToxScreen results as an absolute measure of your risk from air toxics. Instead, perhaps you can discuss the results for your area with your state, local or tribal air agency. These agencies often use AirToxScreen as the starting point for a more refined assessment in an area. The National Association of Clean Air Agencies keeps a list of state and local programs that can help you find your agency. You can get information about tribal programs and EPA's Regional Tribal Program coordinators online as well.
Q4: AirToxScreen shows an elevated risk of cancer in my area. Am I in danger? Am I going to get cancer? What can I do?
A4: First, keep in mind that EPA did not design AirToxScreen to pinpoint specific risk values at any one place. AirToxScreen results show general patterns of potential risk. They shouldn’t be used as an absolute measure of whether any one person’s risk is elevated.
It’s also important to understand that an elevated risk in AirToxScreen does not necessarily mean you are in immediate danger. AirToxScreen risk results are based on breathing air toxics over a very long time — a lifetime, in fact. AirToxScreen can’t tell us much about health risks over shorter periods. We didn’t design it to do that. That said, the amount of a pollutant in the air needed to put a person in any immediate danger is generally much higher than the amount needed to raise long-term risks.
For AirToxScreen, our primary concern is people being exposed to air toxics concentrations associated with elevated cancer risk over many years. Any cancer-causing chemical is potentially dangerous, but just how dangerous depends on:
- the toxicity of the chemical;
- the concentration to which a person is exposed; and
- how long a person is exposed to the chemical.
There are resources available to help answer your questions about air toxics exposure and health.
If you think you are being exposed to elevated levels of air toxics in the outdoor air, be sure you keep up with routine health screenings and doctor’s visits. If you have health concerns that you believe are related to air toxics exposure, start by contacting a healthcare provider. In addition, the Agency for Toxic Substances and Disease Registry (ATSDR) can tell you the location of occupational and environmental health clinics. These clinics specialize in recognizing, evaluating, and treating illnesses resulting from exposure to hazardous substances. You can reach ATSDR at: 1-800-CDC-INFO · 888-232-6348 (TTY) or click the website link above.
If you are concerned about air toxics and your child’s health, contacting your health care provider is a good place to start. If your provider is not familiar with the chemical of concern, they can work with you to contact the Pediatric Environmental Health Specialty Unit (PEHSU) that serves your area. EPA and the TSDR help fund the PEHSUs, which are a source of medical information and advice on environmental conditions that influence reproductive and children’s health. If you don’t have a doctor, you can contact the PEHSU for your area directly.
- Find PEHSUs in your area: https://www.pehsu.net/findhelp.html
- Read more information about the PEHSU program: https://www.pehsu.net/About_PEHSU.html
As a reminder, because AirToxScreen is designed to identify areas for further examination, you may first want to contact your state, local or tribal air agency with any questions or concerns you have about the results. These agencies usually enforce air toxics rules. Often, they also carry out any localized air quality studies needed to get a more precise picture of the air quality in a particular neighborhood.
The National Association of Clean Air Agencies keeps a list of state and local programs that can help you find your agency.
For information about tribal air programs, you may wish to contact the tribal air coordinator for your region. A list is available at EPA's Regional Tribal Program coordinators website.
Q5: How accurate is AirToxScreen?
A5: EPA uses the best available science and emissions Pollutants released into the air. data to build AirToxScreen. But because of its large, national scale, we must simplify some of AirToxScreen’s input data and analytical methods. This means that AirToxScreen assessments provide “screening-level" estimates of the risk of cancer and other serious health effects from breathing air toxics. These estimates help inform efforts to learn which air toxics, emission source types, and places may need further study to assess population risk.
Uncertainties in emissions, actual population exposures, and dose-response or health-effects data are common in assessments like AirToxScreen. For example, the smaller the area, the more uncertain the results. Thus, AirToxScreen results are useful to show which pollutants, source types, or places might be associated with higher risks than others. They are not designed to determine exactly how many people are exposed to precise levels of risk or if a certain area is “safe” or not.
Even with these assumptions, we have found good agreement for many pollutants when comparing AirToxScreen concentration results to measured concentrations. You can learn more about these model-to-monitor comparisons in section 3.7 of the AirToxScreen Technical Support Document.
Q6: How does the cancer risk identified in this assessment compare to lifetime cancer risk from all causes?
A6: The 2019 AirToxScreen estimates that, on average, one out of about every 30,000 Americans (or 20-in-1 million) could contract cancer from breathing air toxics if exposed to 2019 emission levels for 70 years. That’s a national average: In some places, the risks are higher; in others, lower. That risk is on top of any other risks to which a person might be exposed.
Note that AirToxScreen risk estimates are subject to limitations in the data, modeling and assumptions used routinely in any risk assessment. For example, AirToxScreen doesn’t consider ingestion exposures or indoor sources of pollutants. Also, AirToxScreen only estimates long-term cancer risks for air toxics for which EPA has dose-response data. Therefore, these risk estimates may represent only part of the total potential cancer risk associated with air toxics. Use caution when comparing AirToxScreen results to other estimates of risk.
Q7: You show risk data down to the census tract level. Are the results accurate enough to draw conclusions at this scale?
A7: EPA recommends that you use the census tract data to get patterns of risks within counties rather than to pinpoint specific risk values for each census tract. We feel reasonably confident that the patterns — areas of relatively higher and lower levels of exposure and risk within a county — represent actual changes in overall average population risks within the county. We are less confident that the assessment pinpoints the exact locations where higher exposures and risks exists or captures the highest exposures and risks in a county. Keep in mind, we developed AirToxScreen as a screening tool to help identify pollutants and locations that may need further study.
Q8: Based on AirToxScreen, can EPA show which people or places are at greatest risk from air toxics?
A8: Within its limits, yes. Usually, air toxics emissions are higher in areas with more people. Not surprisingly, AirToxScreen results suggest that larger urban areas often carry larger risk burdens than smaller urban and rural areas. This trend is not universal. It can vary from pollutant to pollutant and by source. It may also be affected by exposures and risk from non-inhalation and indoor sources of exposure, which AirToxScreen does not consider.
But keep in mind that AirToxScreen wasn’t designed to pinpoint precise risk values at any one place. AirToxScreen results show general patterns of potential risk. They shouldn’t be used as an absolute measure of whether any one person’s risk is elevated.
Q9: How does this assessment of air toxics data compare to previous national-scale assessments?
A9: Many of the assessment methods we use in AirToxScreen are similar to our previous 2014 and earlier NATA assessments. But we have improved the source inventory, made modeling changes, revised background calculations, and updated some health benchmarks. Also, each assessment uses a particular year of weather data in the air models that we use to calculate risks, which can also influence results. That’s why it can be misleading to compare this version of AirToxScreen with previous assessments.
Q10: Why did results change in my area from the previous national assessment?
A10: As we discuss in the previous answer, there are many reasons why a certain place’s estimated risk might change from one to the next.
In many places, estimated health risks are higher or lower in the this data-year version of AirToxScreen than in previous versions. This may be because of real emissions changes. But it may also be because of changes in our methods or because we use a particular year of weather data in the models that we use to calculate risks (as explained above).
New research can also trigger changes. For example, EPA updated its risk value for the air toxic ethylene oxide in 2016. So when we released the National Air Toxics Assessment (NATA) in 2018, we used the new health-effects data for ethylene oxide. Largely because of this change, more areas showed elevated risks driven by ethylene oxide in that assessment than were shown in previous assessments. This continues to be the case in AirToxScreen. This does not mean there is more of this compound in the air in these places than before. Even if emissions in an area are the same—or possibly even if they are lower—the new stricter health-effects level often means a higher risk estimate.
In the same way, new data can mean lower risk estimates. For example, starting with the 2014 NATA released in August 2018, our assessments have shown that noncancer health hazards are lower across much of the nation than in previous years. This is at least partly due to new health-effects data for acrolein, one of three air toxics that drive most of the noncancer risk in our assessments, that we began using in that 2014 NATA. These data suggest that higher acrolein levels are needed to cause elevated health risks than we once thought. So for the same amount in the air, the health risks from acrolein are lower in AirToxScreen than in past assessments.
These examples help show why you should use caution when comparing one assessment's results to another.
Q11: Has U.S. air quality improved?
A11: Overall, yes. Levels of six key criteria air pollutants continue to fall, and since 1990, EPA has also made great progress in reducing air toxics emissions. We finalized the 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 nearly two million fewer tons of air toxics released every year.
EPA has also completed all the required emissions standards for smaller sources, known as area sources. Gas stations and dry cleaners are examples of area sources. Individual area source facilities often have low emissions. But there are a lot of them, including many in heavily populated cities. In some urban areas, toxic emissions from area sources can be much greater than those from major sources.
Measured from the 1990 baseline inventory, EPA has set standards for nearly all area sources of urban air toxic pollutants and seven potentially bioaccumulative toxic pollutants (those that can build up in humans and wildlife). We estimate that nearly all emissions from regulated area sources now meet these standards.
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. Mobile source emissions dropped by about 70 percent—close to 2 million tons of HAPs—between 1990 and 2014. With more fleet turnover, including more electric vehicles on the road, we expect these reductions to increase to 80 percent by the year 2030. In addition, EPA projects that mobile-source diesel particulate matter will decrease by roughly 90 percent from 2005 to 2030 as mobile source rules targeting diesel engines continue to take effect. Also, benzene emissions from mobile sources continue to decrease, as monitoring data confirms.
How much these emissions reductions improve public health will depend on several things, including which chemicals were reduced and where the reductions occurred relative to where people live and work.
Q12: Can I use AirToxScreen to get risks at an exact place, like my home or my child's school?
A12: No. AirToxScreen isn’t designed to predict actual risks at a specific place. It’s a screening tool that simplifies some of its source emissions and other input data and averages risks over a census tract. This means AirToxScreen can show general areas where risks may be elevated. But it doesn’t use detailed emissions Pollutants released into the air. data or include other information we would need to estimate risks at a specific location.
That said, AirToxScreen can still be useful to you. If AirToxScreen projects low risks for an area, and we are confident that we have modeled the main emission sources nearby, then we can be confident that risks actually are low. There is probably no need to develop a more detailed assessment for that area. But if AirToxScreen shows elevated risks in an area, we know that refined assessments may be needed to accurately show the risks there.
This screening approach helps EPA and other air agencies focus resources on areas where the potential for health risks is greatest.
Q13: I can search on an address in the AirToxScreen Mapping Tool and get a risk value at that point. How accurate is that value?
A13: The AirToxScreen Mapping Tool does show the risks that AirToxScreen estimates for each census tract. But these risks are average risks for the entire tract. Since a census tract can be fairly large, risks can vary across a tract. This means that AirToxScreen's tract-level risks may not reflect the impacts at any one point. You should use the results to find patterns in your general area instead of focusing on the risk values or concentrations at any one point. More focused assessments (for example, air toxics monitoring or local-scale risk assessments) would be needed to better define any concentrations and risks.
Q1: How does AirToxScreen treat emissions from fires?
A1: We include from prescribed fires, wildfires and agricultural burning in AirToxScreen. EPA worked with the U. S. Forest Service to develop emissions estimates for wildfires and prescribed fires for our data inventory. Some wildfire and prescribed fire data came from EPA estimates based on satellite data, ground-based incident reports, and other national datasets that describe various aspects of fire activity and state activity data. Some states submitted emissions. Emissions estimates for agricultural burning came from state-submitted emissions data or estimates based on satellite detects. For more information on how EPA estimated emissions from wild and prescribed fires, see Section 2 of the AirToxScreen Technical Support Document.
In AirToxScreen, we model fires only with CMAQ. CMAQ can use details specific to the fires included. For example, we used day-specific emissions data for wildfires and fires from prescribed burning; by contrast, EPA only has annual average emissions estimates for other types of emission sources. Also, CMAQ lets us model the extra lift that a very hot fire gives an emission plume (a bit like heating up a hot-air balloon) and how that hot plume spreads as it moves through the air.
Q2. What does AirToxScreen show regarding impacts of wildfires, prescribed fires and agricultural burning?
A2: AirToxScreen looks at combined risk from exposure to smoke from wildfires, prescribed fires and agricultural burns. In nearly all of the country in 2019, that estimated risk was less than 10 in a million. (For comparison, the national average risk from air toxics exposure in 2019 was 30-in-1 million from all pollutants examined.)
AirToxScreen's risk estimates are based on being exposed to air toxics for 24 hours a day, 365 days a year, for 70 years. The same is done to estimate risk from fires: AirToxScreen takes the level of air toxics that were in smoke in 2019 and assumes people would be exposed at that same level continuously for 70 years.
Washington and California saw significant wildfires in 2017, including the Jolly Mountain fire in Washington and the Sonoma Complex fires in California. These fires resulted in elevated cancer risks (at or above 100-in-1 million) in these areas in the 2017 AirToxScreen assessment. But because it’s unlikely that a wildfire will burn in the same location for a person’s entire lifetime, the risks AirToxScreen showed in these areas were likely higher than actual risk would be. Thus, we believe that the cancer risks from air toxics in wildfire smoke in these two states were likely overestimated in the 2017 AirToxScreen. And in fact, cancer risks in these areas from fire were much lower both the 2018 and 2019 AirToxScreen assessments.
That being said, climate change has already led to an increase in wildfire season length, wildfire frequency and burned area. This could affect future risks. Learn more at EPA's Climate Change Indicators: Wildfires website. Also, wildfire smoke can be harmful to health from the fine particles in the smoke. Learn more at How Smoke from Fires Can Affect Your Health.
There are steps you can take to protect yourself when wildfire smoke is in the air near you. The AirNow Fire and Smoke Map can give you information about air quality near you during fires, along with steps to take to reduce your smoke exposure.
Q3. What are the uncertainties in risks from fire emissions?
A3: Unlike many air toxics sources, the size and location of fires often varies from year to year. AirToxScreen only uses one year of emissions Pollutants released into the air. data; this includes fire emissions. So the places where fires happened to occur in that one year may bias the risks estimated by AirToxScreen toward those locations.
Further, in risk assessments such as AirToxScreen, we assume a 70-year continuous exposure to air toxics when calculating risk. Because it’s unlikely that a fire will burn in the same location for a person’s entire lifetime, the risks that AirToxScreen calculates due to air toxics found in smoke from fires are likely higher than actual risk would be. This means that cancer risks due to wildfires in are likely overestimated in AirToxScreen.
In addition to these uncertainties, the CMAQ model includes only the 48 contiguous United States, so we approximated concentrations from fires in Alaska, Hawaii and Puerto Rico using CMAQ-calculated concentrations from CONUS states with similar fire emissions. You can read more about this technique in Section 3.6.3 of the AirToxScreen Technical Support Document.
Q4. What is being done to reduce air pollution from wildfires and prescribed fires?
A4: Wildland vegetation management can reduce the threat from wildfires. Prescribed fires are one tool that land managers use to reduce fuel load, unnatural understory and tree density. This helps reduce the risk of catastrophic wildfires, which are frequently of long duration and wide impact and can produce large amounts of air pollutants. Even allowing some wildfires to continue can reduce the chance of a more catastrophic wildfire, which may reduce smoke impacts and related health effects in the long term.
EPA is committed to working with federal land managers, other federal agencies, tribes and states to effectively manage prescribed fire and reduce the impact of wildfire-related emissions. Most prescribed fires are managed using Basic Smoke Management Practices and smoke management programs. USDA and DOI both support efforts to conduct more research into smoke management through the Joint Fire Sciences Program and support broad interagency efforts to address smoke from both wildfires and prescribed fires through the National Wildland Fire Coordinating Group and their Smoke Committee.
EPA is also working to reduce the impacts of climate change. Climate change has already led to an increase in wildfire season length, wildfire frequency and burned area. Learn more about what EPA is doing to tackle the climate crisis at our Climate Change website.
Mobile Source Questions
Q1: What is a "mobile source?" Are there different types?
A1: Mobile sources are air pollution sources that can move from place to place. They are divided into two categories: (1) on-road and (2) nonroad vehicles and engines.
On-road vehicles include:
- passenger cars and trucks;
- commercial trucks and buses; and
Nonroad vehicles and engines include
- heavy equipment;
- marine vessels;
- recreational equipment (snowmobiles, all-terrain vehicles, etc.); and
- small engines and tools (lawnmowers, etc.).
Q2: How accurate are risk estimates for mobile sources in my area?
A2: As we discuss in question 3 of the Results section above, EPA uses the best available science and emissions Pollutants released into the air. data in AirToxScreen. But we also simplify some of these data to make running this national-scale assessment possible. So like all of AirToxScreen’s risk estimates, you should treat those from mobile sources as a screening-level estimate of risks. We are confident that AirToxScreen does a good job treating regional-level risks from mobile sources. As we’ll explain, risks at the census tract level are less certain.
Accurately capturing emissions for sources that move from place to place is challenging, particularly over small areas. For on-road traffic such as cars, trucks, buses and motorcycles, we use roadways to place running emissions in grid cells using estimates of average daily traffic. These estimates usually come from traffic demand models, which include some uncertainties. Also, a large share of highway-vehicle emissions doesn’t even occur on roads — it occurs when vehicles are started and during idling. We use different surrogates for these emissions, but they may inaccurately reflect actual emission locations over small areas. For this reason, we average the concentrations across grid cells.
Nonroad source emissions — such as those from construction equipment, lawn and garden equipment, and off-road recreational equipment — are more uncertain than on-road emissions. Often, we must estimate equipment population, age and activity values. In addition, nonroad source emissions are often placed by land-use type. Even though we’ve improved these over time, surrogates used to allocate emissions to grid cells in some cases may not always capture differences in local activity.
In short, results for mobile sources are very uncertain at the census tract level and you should interpret them with caution.
It should be noted that EPA has recently added nonroad equipment emissions into Motor Vehicle Emission Simulator (MOVES) and plans to update activity estimates for nonroad equipment in future versions of the model. EPA is actively looking for data related to nonroad populations and activity, including geographic allocation data. EPA recognizes that these data can influence AirToxScreen results and therefore welcomes suggestions.
Q3: What is EPA doing to reduce emissions of mobile source air toxics?
A3: Mobile source emissions dropped by about 70 percent — close to 2 million tons of HAPs — between 1990 and 2014. as a result of EPA programs. With additional fleet turnover, we expect these reductions to increase to 80 percent by the year 2030. In addition, EPA projects that mobile-source diesel particulate matter will decrease by roughly 90 percent from 2005 to 2030 as mobile source rules targeting diesel engines continue to take effect.
EPA’s most recent regulatory programs that will greatly reduce mobile source air toxics are Tier 3 vehicle and fuel standards. These standards, issued in 2014, will cut emissions of air toxics from motor vehicles between 10 and 30 percent by 2030 (depending on the pollutant). In addition, EPA issued a final rule in 2021 to strengthen greenhouse gas emission standards for passenger cars and light trucks; it's estimated that this rule will bring about substantial reductions in VOCs, which include many mobile source air toxics.
The 2007 mobile source air toxics rule controlled the benzene content of gasoline, vehicle emissions at cold temperatures, and emissions from portable fuel containers. A recent assessment in Anchorage, Alaska, found a reduction in ambient benzene of more than 50 percent, and the fuel-benzene standard was a major factor.
Other programs reducing mobile source air toxics are:
- low-sulfur gasoline and diesel requirements;
- heavy-duty engine and vehicle standards;
- controls for small spark-ignition engines and recreational marine engines;
- the locomotive and commercial marine rule;
- standards for nonroad diesel engines; and
- the North American and Caribbean Emission Control Areas (ECAs), established to reduce emissions from ships.
Several nonregulatory programs are also reducing mobile source air toxics. Examples include EPA's Diesel Emissions Reduction Act (DERA), SmartWay, and Ports Initiative programs. For example, in fiscal years 2008 to 2016, EPA awarded $629 million under DERA to retrofit or replace 67,300 diesel engines, which yield an immediate public health and air quality benefit. EPA estimates that every federal dollar invested in reducing diesel exhaust has leveraged as much as three dollars from other government agencies, private organizations, industries, and nonprofit organizations, generating between 11 and 30 dollars in public health benefits. Projects include vehicle and engine replacements of older diesel on highway vehicles and nonroad; retrofits such as catalysts or filters; and idling reduction equipment. View more information on EPA's DERA Program website.
Learn more about EPA's programs to reduce air toxics from mobile sources.
Q4: Why are only non-cancer risks calculated for diesel PM and not cancer risks?
A4: EPA has not developed or adopted a cancer unit risk estimate (URE) for diesel exhaust. In the 2002 Health Assessment Document for Diesel Engine Exhaust, EPA concluded that diesel exhaust is likely to be carcinogenic to humans at environmental levels of exposure, but found that data from the health studies available at the time were not suitable for estimating cancer potency.
However, EPA has concluded that diesel exhaust is among the substances that the national assessment suggests pose the greatest cancer risk. The 2002 Health Assessment Document evaluated several studies linking increased lung cancer risk with diesel PM. Exposures in several of these studies are in the same range as ambient exposures throughout the United States.
Several large studies have been published that strengthen the weight of evidence that diesel exhaust is carcinogenic to humans. Two of these studies included quantitative estimates of exposure. Partly based on these studies, the International Agency for Research on Cancer (IARC) elevated its classification of diesel exhaust to “carcinogenic to humans” (Class 1) in 2012.
In 2012, EPA and industry asked the Health Effects Institute (HEI) to convene a panel to review recently published epidemiology studies of occupational exposures to diesel engine exhaust. It was hoped that the panel could determine whether new studies could be used in a quantitative risk assessment (QRA) to calculate a cancer unit risk estimate (URE). In a final report published in late 2015 , the panel concluded that newer studies progressed toward addressing major limitations in previous epidemiologic studies of diesel engine exhaust. Although uncertainties remain, they concluded that the newer studies gave a basis for a QRA of diesel engine exhaust exposures, specifically to diesel engine exhaust from older diesel engines.
Currently there are no plans at the EPA to conduct a QRA for diesel engine exhaust. However, EPA continues to act to reduce diesel emissions through standards for heavy trucks and engines. For example, because of EPA actions, on-road diesel engines manufactured in 2007 and later have much more advanced emission control systems. This results in much lower emissions with different composition than the diesel engines that formed the basis of the currently available epidemiology studies. Thus, a cancer potency based on available epidemiology studies may not be relevant to highway diesel engines that meet these most recent standards.
The studies reviewed by HEI show why it’s important to continue reducing emissions and exposures to diesel exhaust. EPA continues to implement diesel exhaust emission standards reducing exposures. Programs like the Diesel Emissions Reduction Act, Smartway and the Ports Initiative also help reduce emissions from the legacy diesel engine fleet.
Also, EPA has designated a chronic Reference ConcentrationAn estimate of a continuous inhalation exposure unlikely to cause adverse health effects during a person’s lifetime. This estimate includes sensitive groups such as children, asthmatics and the elderly. (RfC) for diesel PM of 5 micrograms per cubic meter. This level is based on specific noncancer effects found in several animal studies, which showed adverse changes in lungs such as inflammation and lesions. AirToxScreen uses this value to estimate the diesel PM hazard quotientThe ratio of the potential exposure to the substance and the level at which no adverse effects are expected. A hazard quotient less than or equal to one indicates that adverse noncancer effects are not likely to occur, and thus can be considered to have negligible hazard..
You can learn more about this subject on EPA’s Mobile Source Pollution and Related Health Effects website.
Q5: There has been increased concern about the health effects associated with pollution near roads. What can AirToxScreen tell us about health risks from exposure to near-road pollution?
A5: Research consistently finds that people who spend a lot of time near high-traffic roads are at greater risk for several adverse health effectsA change in body chemistry, body function or cell structure that could lead to disease or health problems.. Motor vehicle pollutant concentrations tend to be higher closer to the road, with the highest levels generally within the first 500 feet (about 150 meters) of a roadway and reaching background levels within approximately 2,000 feet (about 600 meters) of a roadway, depending on the pollutant, time of day, and surrounding terrain.
For a given location, AirToxScreen’s exposure estimates near major roads may be inaccurate due to limitations in our data. Also, AirToxScreen’s air quality modeling can’t pinpoint high concentrations along specific roadways. However, HAPEM exposure modeling does account for near-road impacts based on average census tract exposures. This means AirToxScreen can estimate where people may be exposed to higher levels of air toxics from heavy traffic near where they live and work. Refined modeling or monitoring studies can then give a more precise picture of air quality in these areas.
EPA has a website focused on near-roadway air pollution and health, as well as a website about ongoing near-source air pollution research.
Q6: AirToxScreen results show impacts associated with a port in my community. How accurate are these estimates, and what can be done to reduce the impacts?
A6: As with other sources, AirToxScreen results for ports highlight places where a more refined analysis may be needed. AirToxScreen’s analysis of ports has some uncertainties and limitations:
- Although pollutant concentrations in ports comes from many sources’ emissions, AirToxScreen only includes emissions from commercial marine vessels within ports.
- Port emissions for those vessels come from state and local agency submittals or, in most cases, EPA’s estimates.
- Due to its national scale, AirToxScreen simplifies port boundaries more than a local assessment would (see Section 2 of the AirToxScreen Technical Support Document).
- We have limited data on which to base emission estimates for toxics from commercial marine vessels.
Despite these limitations, AirToxScreen findings suggest that people who live and work near ports may experience elevated risks. EPA has taken many actions that have reduced risks in recent years. These actions include Tier 2 and Tier 3 standards on oceangoing marine vessels, sulfur control on marine fuel oil, and designation of an emission control area (ECA) off our coasts. Finally, EPA's Ports Initiative program helps speed up the use of cleaner technologies, promotes clean air planning practices such as emissions inventories, and spurs community engagement to address diesel emissions at ports across the country.