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Assessment Limitations

EPA developed this assessment tool to inform both national and more localized efforts to collect information and characterize/reduce air toxics emissions (e.g., prioritize pollutants/geographic areas of interest for monitoring and community assessments). EPA suggests that the results of this assessment be used cautiously, as the overall quality and uncertainties of the assessment will vary from location to location as well as from pollutant to pollutant. In many cases more localized assessments, including monitoring and modeling, may be needed to better characterize local-level risk. The points below highlight limitations to consider when looking at the results:

  • gaps in data
  • limitations in computer models used
  • default assumptions used routinely in any risk assessment
  • limitations in the overall design of the assessment (intended to address some questions but not others).

The following are important specific limitations to recognize:

The results apply to geographic areas, not specific locations. The assessment focused on variations in air concentration, exposure and risk between geographic areas such as census tracts, counties and states. All questions asked, therefore, must focus on the variations among areas (census tracts, counties, etc.). They cannot be used to identify "hot spots" where the air concentration, exposure and/or risk might be significantly higher within a census tract or county. In addition, this type of modeling assessment cannot address the kinds of questions an epidemiology study might, such as the relationship between asthma or cancer risk, and proximity of residences to point sources, roadways and other sources of air toxics emissions.

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The results do not include impacts from sources in neighboring countries (i.e., Canada or Mexico). Since the assessment did not include the emissions of sources in Canada and Mexico the results for States which border countries would not reflect these potentially significant sources of transported emissions.

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The results apply to groups, not to specific individuals. Within a census tract, all individuals were assigned the same ambient air concentration, chosen to represent a typical ambient air concentration. Similarly, the exposure assessment used activity patterns that do not fully reflect variations among individuals. As a result, the exposures and risks in a census tract should be interpreted as being only typical values rather than as means, medians, etc. They are likely to be values in the midrange for the census tract, and so typical here means something like "in the midrange" of values for all individuals in the census tract.

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The results are restricted to 2002. The assessment used emissions data from 2002. This is because it is the most up-to-date data set on emissions. The risk assessment assumes that these levels remain constant throughout one's lifetime (not today's levels or projected levels). Significant emission reductions have taken place since 2002: (i) mobile source regulations are being phased in over time, (ii) EPA has issued air toxics regulations for major industrial sources, (iii) there are State and industry initiatives, and (iv) some facilities may have closed.

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The results do not reflect exposures and risk from all compounds. Only 124 of the 181 air toxics assessed, have dose-response values. The remaining 57 air toxics do not, and therefore, do not contribute to the aggregate cancer risk or target organ-specific hazard indices. It is particularly significant that the assessment did not quantify cancer risk from diesel PM, although EPA has concluded that the general population is exposed to levels close to or overlapping with apparent levels that have been linked to increase cancer risk in epidemiology studies. Currently, there is no unit risk estimate for diesel PM (for more information, see the qualitative discussion on risk from diesel PM.)

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The results do not reflect all pathways of exposure. The assessment included only risks from direct inhalation of the emitted air toxics compounds. It did not consider air toxics compounds that might then deposit onto soil, water, food, etc, and therefore enter the body through ingestion or skin contact. Consideration of these other routes of exposure should have the effect of raising the exposure and risk.

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The assessment results reflect only compounds released into the outdoor air. The assessment did not include exposure to air toxics compounds produced indoors, such as from stoves or out-gassing from building materials or evaporative benzene emissions from cars in attached garages. For some compounds such as formaldehyde, these indoor sources can contribute significantly to the total exposure for an individual, even if only inhalation exposures are considered. In addition, the assessment did not consider toxics released directly to water and soil. It does take into account transformation of one pollutant into another (i.e., secondary formation) in the atmosphere. In this case, the secondary transformation of aldehydes was considered but only for the modeling done by ASPEN, i.e., the area and mobile source emissions.

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The assessment does not fully reflect variation in background ambient air concentrations. The assessment uses background ambient air concentrations that are average values over broad geographic regions. Much more research is needed before an accurate estimate of background concentrations at the level of census tracts, or even at the higher geographic scales (counties, states, etc), can be made. Since background levels are significant contributors to the overall exposure in this assessment, the lack of detailed information on variations in background exposures probably causes the amount of variation in total exposure and risk between census tracts to be smaller than would otherwise be the case.

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The assessment might systematically underestimate ambient air concentration for some compounds. The ASPEN model and HEM-AERMOD model were used to estimate ambient air concentrations. The ASPEN model has been shown to underestimate measured concentration in many cases. No such bias has been found for the AERMOD model. has been shown to underestimate measured concentration in many cases. This would tend to result in an overall underestimation of the exposure and risk. In any event, The the actual effect of this issue is unknown at present, but some sense of the model's performance in this area may be gauged by comparing the modeled results to monitoring results. See more information on the comparison of modeled to monitored concentrations.

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The assessment used default, or simplifying, assumptions where data were missing or of poor quality. Data on some of the quantities used in the modeling for emissions and dispersion of air toxics compounds (such as stack height, facility location, etc) were not available or were flawed. When this happened, they were replaced by default assumptions. For example, a stack height for a facility might be set equal to stack heights at comparable facilities; the location of the facility might be placed at the center of a census tract; etc. This introduces uncertainty into the final predictions of ambient concentration, exposure and risk.

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The assessment may not accurately capture sources that have episodic emissions (e.g., wildfires and prescribed burning or facilities with short-term deviations such as startups, shutdowns, malfunctions, and upsets). The ASPEN model and HEM-AERMOD models assume emission rates are uniform throughout the year. Some sources have variable rates of emissions which occur within only a few days or weeks each year (episodic). For example, the emissions from prescribed fires and wildfires, which typically last for about a week are averaged over the entire year. Further, when assessing cancer risks these emissions are assumed to occur over a lifetime (i.e., 70 years).

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Estimates of risk are uncertain. Some air toxics are known to be carcinogens in animals but lack data in humans. These have been assumed to be human carcinogens. Second, all the air toxics in this assessment were assumed to have linear relationships between exposure and the probability of cancer (i.e. effects at low exposures were extrapolated from higher, measurable, exposures by a straight line). Third, some estimates of cancer risk are considered to be best estimates of cancer risk (those based on human data); others are "upper bound" estimates (usually based on animal data but sometimes based on human data). In the former case, the estimate of risk is equally likely to overestimate risk as underestimate risk. In the latter case, the estimate is more likely to overestimate risk. Most, but not all, of the cancer risk estimates that EPA develops are "upper bound" estimates. However, EPA cancer risk estimates for several important HAPs such as hexavalent chromium and benzene are "best estimates."

Sources of uncertainty in the development of Reference Concentrations (RfCs) generally are intraspecies extrapolation (animal to human), and interspecies extrapolation (average human to sensitive human). Additional sources of uncertainty can be using a lowest-observed-adverse effect-level in place of a no-observed adverse effect level (the latter is preferred), and for other data deficiencies. Theses uncertainties are taken into account in the derivation of the RfCs. As the RfCs used in the assessment in estimating a Hazard Quotient (HQ) are conservative, meaning that they represent exposures at which no appreciable risk is expected to occur +/- an order of magnitude uncertainty, a value of HQ greater than 1, therefore, should not necessarily be taken to indicate that a health effect is expected. See Variability and Uncertainty in NATA (PDF) (9pp, 34k) for more complete discussion of uncertainty and variability.

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