NATA Frequent Questions
Questions on this page:
General Background Questions
- What are air toxics and what health effects can they cause?
- What is NATA?
- How can I use NATA results?
- How should I NOT use NATA results?
- I understand that NATA is a screening tool. But why doesn’t EPA run a more refined analysis?
- Are there any risks from air toxics that aren't covered by NATA?
- Who is responsible for controlling air toxics?
- What should I do if I am concerned about air toxics in my area?
- How does NATA differ from other screening tools used by EPA? How do I know which tool to use?
Emissions, Modeling, and Methods Questions
- Which air toxics are included in NATA?
- What are the steps in the National Air Toxics Assessment?
- What are CMAQ and AERMOD, and how did EPA use them in NATA?
- Why did you exclude Alaska, Hawaii, Puerto Rico, the Virgin Islands, and other territories from CMAQ modeling?
- Why are all the estimates from 2014 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 the 2014 NATA?
- What kind of changes were made in the 2014 NATA because of the review by the states?
- How did EPA characterize risk from modeled 2014 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?
- Part of the estimated risk is due to "secondary formation," which is widespread across the country. What is secondary formation?
- What does a “1-in-1 million” cancer risk mean?
- What does EPA believe constitutes an acceptable level of risk?
- NATA results also show 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 NATA results?
- What does NATA tell us overall about the risks from air toxics in the United States?
- What do these estimates mean for me?
- NATA shows an elevated risk of cancer in my area. Am I in danger, or am I going to get cancer? What can I do?
- How accurate is the assessment?
- 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 NATA, can EPA show which people or places are at greatest risk from air toxics?
- How does this assessment of 2014 air toxics data compare to previous national-scale assessments?
- Why did risks change in my area from the previous NATA?
- Has U.S. air quality improved?
- Can I use NATA to get risks at an exact place, like my home or my child's school?
- I can search on an address in the NATA Map and get a risk value at that point. How accurate is that value?
- How does NATA treat emissions from fires?
- What does NATA 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 the results from NATA tell us about health risks from exposure to near-road pollution?
- NATA 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 Background Questions
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 187 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 “carcinogeniccarcinogenicCapable 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 effectsadverse 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.
A2: The National Air Toxics Assessment, or NATA, is EPA's review of air toxics in the United States, based on modeled air quality. We developed NATA as a tool for state, local and tribal agencies, and we use its results as well. NATA helps us find out which air toxics, emission sources, and places may need further study to better understand risksrisksThe 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)..
NATA uses the best science and emissions data available to estimate possible health risks from air toxics. But because of its large, national scale, we must simplify some of NATA’s input data and analytical methods. For this reason, we call NATA a “screening tool” – it helps us estimate risks and tells us where to look further.
NATA provides screening-level estimates of the risk of cancer and other serious health effects from breathing (inhaling) 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 NATA.
NATA 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 NATA and the methods used can be found in the NATA Technical Support Document.
You can use NATA 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 NATA 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 NATA 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.
A4: NATA 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,
- to examine trends from one NATA year to another,
- 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 NATA 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, NATA 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.
A5: There are several reasons why we can’t do that right now.
For some source types, we don’t have emissions 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. It already takes us several years to put NATA together. Collecting source data for a more refined NATA would take even longer. By the time we finished, so much about the data would have changed that the results would be meaningless.
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 make a refined NATA, we don't have that just yet. NATA results can, however, inform a more refined, local analysis that uses EPA recommendations and guidance.
A6: Yes. NATA 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 NATA, from 2014), and it assumes that they stay the same throughout one's lifetime. Together, these assumptions mean NATA can’t account for all risks.
Also, NATA 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 medianmedianThe 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 diesel PM);
- 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.
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.
You can also view information on tribal programs and EPA's Regional Tribal Program coordinators.
Q9: How does NATA differ from the other screening tools used by EPA? How do I know which tool to use?
A9: NATA is a national assessment that estimates cancer and noncancer risks from breathing air toxics. NATA is intended as a screening tool to help users prioritize pollutants, types of emission sources, and places of interest for further study. NATA is also a part of other agency screening tools, including 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.
Emissions, Modeling, and Methods Questions
A1: The 2014 NATA estimates ambientambientThe open air. In NATA, 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 concentrationsexposure concentrationConcentrations 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, NATA estimates cancer risks and noncancer hazards for 138 of these. For the other air toxics, NATA 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 2014 NATA Technical Support Document.
EPA did not include the following air toxics in this assessment because either no emissions data were reported for them in 2014 or we couldn’t reliably make emission estimates useful for modeling from their reported emissions:
- Other dioxins/furans
- Fine mineral fibers
- Chromium III
A2: NATA 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 2014 national emissions inventory of air toxics emissions from outdoor sources.
EPA compiled measured or estimated emissions 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).The emission source types in the NEI include major stationary sourcesstationary 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 sourcesarea 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-roadon-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 nonroadnonroadMobile 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), biogenicbiogenicProduced by biological processes. In NATA, biogenic emissions are those from trees, plants and soil microbes. sources, and fires. These emissions data become a major part of the modeling input data used in the next NATA step.
- Estimate ambient air concentrations based on the 2014 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 51 HAPsHAPsAir 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 NATA air toxics in AERMOD. We then combined the results using a hybrid approach that takes advantage of the strengths of both models (the NATA 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 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 NATA: 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 2014 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.
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 the 2014 NATA, EPA used CMAQ for 52 pollutants, with emissions from point and nonpoint sources, mobile sources, and fires.
In addition to CMAQ, we ran the dispersion model AERMOD for all NATA 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 NATA Technical Support Document.
A4: The CMAQ modeling performed for the 2014 NATA 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 the.
A5: We used 2014 data because emission inventories from that year were the most complete and up to date available. Working with industries and states, we update our air toxics emission inventories every 3 years (we are now gathering and compiling 2017 data). The risk estimates assume a lifelong exposure to 2014 levels because calculating exposures based on projections to more recent years would be much more complex and uncertain.
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 very expensive. Instead, we only measure a subset of air toxics concentrations in a few locations. So for large-scale assessments such as NATA, 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 Section 3.7 of the Technical Support Document, Model Evaluation, we explain the results of model-to-monitor comparisons done for the 2014 NATA. In addition, we provide annual statistics for air toxics monitoring data in the NATA Map Application. 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.
A7: The following changes were included in the 2014 NATA. Many of the changes adopted in the 2011 NATA were carried over to the 2014 NATA; they are not repeated here.
- Mobile and nonpoint source emissions now allocated by grid square rather than census tract using improved methods to assign emissions based on known data patterns (called “surrogates”). These new approaches allowed more accurate modeling of these source types.;
- Better estimates of oil and gas emissions achieved through both a more refined allocation of emissions (to a 4-km by 4-km grid in lower 48 states) and an improved breakdown of VOC emissions into specific HAPs.
- Toxics emission factors for nonroad emissions updated based on newer data.
- New “bottom-up” approach to marine vessel emissions used; these emissions are also now allocated to the areas within ports where ships idle and maneuver.
- Updated emission factors used where available.
- Number of air toxics modeled with CMAQ increased to 52.
- New approach used in CMAQ for estimating the impacts of secondary formation and biogenic and fire emissions in Alaska, Hawaii, Puerto Rico and the Virgin Islands.
- Improved method for calculating AERMOD emissions allowed faster calculations and are easier for other researchers to repeat.
- Annual emissions data must be converted to hourly rates for modeling; we adjusted how we did this in AERMOD to be more consistent with CMAQ’s treatment.
- Faster computing allowed a more complete set of weather data to be included in modeling.
- Risk Characterization
- New HAPEM7 model features used, including updated population and commuting patterns, activity-pattern data, and four new commuting-related microenvironments.
- Dose-response values updated with latest science (sources: EPA Integrated Risk Information System (IRIS), California Environmental Protection Agency, Centers for Disease Control’s Agency for Toxic Substances and Disease Registry).
- Several benchmarks updated since the 2011 NATA, including ethylene oxide, benzo(a)pyrene and acrolein.
- Web-based NATA Map improved, making displaying results easier.
These and other improvements that EPA makes between each NATA mean you should not directly compare results from different NATA assessments.
While EPA continually refines and updates these methods, it’s also important to remember that NATA 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.
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 NATA users. The 2014 NEI v1 review led to changes by more than 50 state, local and tribal agencies that were incorporated in the final 2014 NEI. These comments covered the areas of:
- Facility changes:
- Removal of facilities (duplicates or closed prior to 2014)
- Geographic coordinate changes
- Facility changes
- Facility NAICS and SCC changes
- Revisions to stack parameters
- Emission changes:
- Additions, deletions, and recalculations
- Revisions to emissions allocations
- Changes to chromium speciation, hexavalent chromium percentage
- Revision of TRI emissions which were based on midpoint of range (for facilities reporting a range estimate to TRI)
- Removal of estimates based on older, outdated methodology (ethylene oxide sterilizers)
Most of the comments were addressed by making the appropriate changes to the 2014 NEI and NATA inventories, and the final 2014 NATA now reflects these changes. Additional comments focused on methodological and toxicological questions, many of which are addressed or answered in various sections of the NATA website.
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.
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 toxics compound 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.
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 NATA Supplemental Data folder, available on the NATA website.
A11: In NATA, 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 2014 NATA. 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 NATA, the biogenic emissions source group only includes the primary emissions, or those directly emitted into the air. Some compounds emitted by natural sources also form pollutants by reacting chemically in the air with compounds emitted by humans; these are included in the Secondary source group; (see question 14 below).
For NATA, 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 NATA can be found in Section 2 of the NATA 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.
A13: In NATA, 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 NATA, we estimated background using remote concentration estimates from monitoring and emissions.
Q14: Part of the estimated risk is due to "secondary formation," which is widespread across the country. What is secondary formation?
A14: 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 NATA, we estimated secondary formation using the CMAQ model.
A1: A cancer risk level of 1-in-1 million implies that, if 1 million people are exposed to the same concentration of a pollutant continuously (24 hours per day) over 70 years (an assumed lifetime), one person would likely contract cancer from this exposure. This risk would be in addition to any cancer risk borne by a person not exposed to these air toxics.
A2: 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 NATA.
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.
A3: 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 quotienthazard 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 curvedose-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 ConcentrationReference 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).
Q4: Why did EPA use the higher potency or unit risk estimate (URE) for formaldehyde reported in the Agency's Integrated Risk Information System (IRIS)?
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 estimateunit 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 the 2014 NATA (see Appendix H of the NATA 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.
A5: We did not evaluate exposure and risk related to dioxins in the 2014 NATA 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 NATA’s risk estimates likely would be small.
A1: The NATA Map Application displays risks, emissions and monitoring data on a map. While very powerful, the NATA Map can also quickly display risks and other NATA data: simply click on the map. The map’s search tool lets you “zoom” to places of interest anywhere in the country. You can easily change the displayed data type by toggling the different map layers. You can also download all NATA data and results, and run queries to find just the information you want.
NATA Map layers include:
- all emissions sources modeled in NATA;
- cancer risks and noncancer hazard indexes
- annual ambient concentrations; and
- air toxics monitoring sites with monitoring data and NATA modeling results at each monitor.
You can use the NATA Map on a computer or mobile device.
A2: The 2014 NATA 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 NATA 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 NATA 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.
A3: NATA’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.
NATA 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 NATA 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 NATA calculates.
This means you should avoid using NATA 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 NATA 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 programsExitthat can help you find your agency. You can get information about tribal programs and EPA's Regional Tribal Program coordinators online as well.
Q4: NATA shows an elevated risk of cancer in my area. Am I in danger, or am I going to get cancer? What can I do?
A4: First, keep in mind that EPA did not design NATA to pinpoint specific risk values at any one place. NATA 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 NATA does not necessarily mean you are in immediate danger. NATA risk results are based on breathing air toxics over a very long time – a lifetime, in fact. NATA 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 NATA, our primary concern is people being exposed to concentrations associated with elevated cancer risk for their entire lifetime. 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.
Certainly, if NATA shows elevated risks in your area, we understand your concern. We suggest you contact your state, local or tribal agency with any questions or concerns you have about NATA 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 programsEXITthat can help you find your agency. You can get information about tribal programs and EPA's Regional Tribal Program coordinators online as well.
A5: EPA uses the best available science and emissions data to build NATA. But because of its large, national scale, we must simplify some of NATA’s input data and analytical methods. This means that NATA assessments provide “screening-level,” or first-pass, estimates of the risk of cancer and other serious health effects from breathing (inhaling) 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 NATA. For example, the smaller the area, the more uncertain the results. Thus, NATA 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 NATA concentration results to measured concentrations. You can learn more about these model-to-monitor comparisons in section 3.7 of the NATA Technical Support Document.
Q6: How does the cancer risk identified in this assessment compare to lifetime cancer risk from all causes?
A6: The 2014 NATA estimates that, on average, one out of about every 33,000 Americans (30-in-1 million) could contract cancer from breathing air toxics if exposed to 2014 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 NATA risk estimates are subject to limitations in the data, modeling and assumptions used routinely in any risk assessment. For example, NATA doesn’t consider ingestion exposures or indoor sources of pollutants. Also, NATA 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 NATA results to other estimates of risk.
Q7: NATA presents 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 NATA as a screening tool to help identify pollutants and locations that may need further study.
A8: Within its limits, yes. Usually, air toxics emissions are higher in areas with more people. Not surprisingly, NATA 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 NATA does not consider.
But keep in mind that NATA wasn’t designed to pinpoint specific risk values at any one place. NATA 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 2014 air toxics data compare to previous national-scale assessments?
A9: We continue to improve NATA’s methods. We have improved the NATA source inventory, made modeling changes, revised background calculations, and updated some health benchmarks. That’s why it’s not meaningful – and sometimes it’s even misleading – to directly compare the 2014 NATA with previous assessments.
Lower risk levels in an area might be due to real emissions reductions. But they could also be due to changes in our methods. Some of these improvements include:
- improved emissions inventory;
- better method used to place nonpoint and mobile-source emissions;
- better data for oil and gas wells;
- improved ways to model emissions from marine vessels;
- more complete weather data;
- now 52 air toxics modeled using combined CMAQ/AERMOD hybrid approach;
- updated data on health-effect levels for some air toxics.
A10: As we discuss in the previous answer, there are many reasons why a certain place’s estimated risk might change from one NATA to the next.
In many places, estimated health risks are higher or lower in this NATA than in the last one. This may be because of real emissions changes. But it may also be because of changes in our methods (as explained above).
New research can also trigger changes. In the 2014 NATA, we used new health-effects data for several air toxics. One of these is ethylene oxide. EPA updated its risk value for ethylene oxide in 2016. So for this NATA, we updated our cancer risk calculations to reflect these new data.
Largely because of these changes, more areas show elevated risks driven by ethylene oxide in this NATA than in the 2011 NATA. 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, the 2014 NATA suggests that noncancer health hazards are lower across much of the nation. 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 NATA. These new 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 the 2014 NATA results than in past assessments.
These examples help show why you should avoid comparing one NATA’s results to another.
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 1.7 million fewer tons of air toxic emissions 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 bio-accumulative toxic pollutants. 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 50 percent – close to 1.5 million tons of HAPs – between 1990 and 2008. With additional fleet turnover, we expect these reductions to increase to 80 percent by the year 2030. In addition, mobile-source diesel particulate matter decreased by about 27 percent from 1990 to 2005. We project more reductions (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.
A12: No. NATA 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 NATA can show general areas where risks may be elevated. But it doesn’t use detailed emissions data or include other information we would need to estimate risks at a specific location.
That said, NATA can still be useful to you. If NATA 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 NATA shows elevated risks in an area, we know that refined assessments may be needed to accurately characterize 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 NATA Map and get a risk value at that point. How accurate is that value?
A13: The NATA Map app can show the risk levels estimated for each census tract. The concentrations and estimated risk are averaged across the tract. That means they may not reflect the possible impacts at any one point. You should use the results more 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 NATA treat emissions from fires?
A1: We include emissions from prescribed fires, wildfires and agricultural burning in NATA. EPA worked with the U. S. Forest Service to develop emissions estimates for wildfires and prescribed fires for the 2014 National Emissions Inventory (NEI). 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. Two 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 NATA Technical Support Document.
In the 2014 NATA, we modeled 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 rise that a very hot fire gives an emission plume and how that hot plume spreads as it moves through the air.
Q2. What does NATA show regarding impacts of wildfires, prescribed fires and agricultural burning?
A2: The National Emissions Inventory estimates emissions from each fire type separately, but we modeled prescribed fires, wildfires and agricultural burning together in NATA. That means the resulting ambient concentrations, exposure concentrations, and risks are grouped together and can’t be separated.
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. Each NATA only uses one year of emissions data; this includes fire emissions. So the places where fires happened to occur in that one year may bias the risks estimated by NATA toward those locations. Of course, if fires are common in a place from year to year, the risks that NATA estimates from fire there are likely quite appropriate.
Also, 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 NATA 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 Exitand smoke management programs. USDA and DOI both support efforts to conduct more research into smoke management through the Joint Fire Sciences Program Exitand support broad interagency efforts to address smoke from both wildfires and prescribed fires through the National Wildland Fire Coordinating Group and their Smoke Committee.Exit
Mobile Source Questions
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.).
A2: As we discuss in question 3 of the Results section above, EPA uses the best-available science and emissions data to build NATA. But we also simplify some of these data to make running this national-scale assessment possible. So like all of NATA’s risk estimates, you should treat those from mobile sources as a first-pass, or screening-level, estimate of risks. We are confident that NATA 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 NATA results and therefore welcomes suggestions.
A3: Mobile source hazardous air pollutant emissions dropped by about 50 percent – close to 1.5 million tons – between 1990 and 2008. With additional fleet turnover, we expect these reductions to increase to 80 percent by the year 2030. In addition, mobile source diesel particulate matter decreased by about 27 percent from 1990 to 2005. We project more reductions (roughly 90 percent) from 2005 to 2030 as mobile source rules targeting diesel engines go into 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).
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 the National Clean Diesel Campaign, SmartWay, and EPA’s Ports Initiative. In addition, EPA created the Diesel Emissions Reduction Program (known as “DERA”) to reduce pollution from diesel fleets. EPA has awarded over $700 million under DERA for clean diesel projects, which yield an immediate public health and air quality benefit. EPA estimates that for every dollar invested in reducing diesel exhaust, a community gains between five and 18 dollars in public health benefits. Projects include replacements of older diesel locomotive, vessel, vehicle or equipment engines; retrofits such as catalysts or filters; idling reduction equipment; and replacements of vehicles such as school buses.View more information on EPA's Clean Diesel 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? Isn't there a cancer unit risk available?
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,(669 pp, 8 MB, About PDF), 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.
Recently, 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, Exitthe 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 new 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 (DERA), Smartway Transport Partnership and the Ports Initiative also help reduce emissions from the legacy diesel engine fleet.
Also, EPA has designated a chronic Reference ConcentrationReference 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 µg/m3. This level is based on specific noncancer effects found in several animal studies, which showed adverse changes in lungs such as inflammation and lesions. The 2014 NATA uses this value to estimate the diesel PM hazard quotienthazard 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 the 2014 NATA tell us 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 effectsadverse health effectsA change in body chemistry, body function or cell structure that could lead to disease or health problems.. Air quality measurement studies often find higher air pollution within about 500-600 feet (about 200 meters) of heavily traveled roads and along corridors with heavy truck or rail traffic.
For a given location, NATA’s exposure estimates near major roads may be inaccurate due to limitations in our data. Also, NATA’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 NATA 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.
Q6: NATA 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, NATA results for ports highlight places where a more refined analysis may be needed. NATA’s analysis of ports has some uncertainties and limitations:
- Although pollutant concentrations in ports comes from many sources’ emissions, NATA 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, NATA simplifies port boundaries more than a local assessment would (see Section 2 of the NATA Technical Support Document).
- We have limited data on which to base emission estimates for toxics from commercial marine vessels.
Despite these limitations, NATA 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 has established a ports initiative to develop and implement sustainable ports strategies.