Limitations in the 1996 National-Scale Air Toxics Assessment

EPA performed the variability analysis for the national-scale assessment in the following 9 steps for each air toxic compound considered (steps are numbered so the reader can refer back to previous steps):

1. Division of the geographic region. To account for variability in the concentration of an air toxics compound throughout the U.S., the country was divided into census tracts.
   
   

2. Calculating variation in ambient air concentration. Sources and their emission rates were determined, and the ambient air concentrations were calculated throughout the U.S. using the ASPEN dispersion model for that air toxic compound. These results then were used to estimate the ambient air concentration at the centroid of each census tract defined in the first step. EPA pooled the results from all census tracts inside a geographic region (such as county, state or nation) and the concentrations associated with different percentiles were determined. For example, the combined census tract results for a geographic region were used to estimate the ambient air concentration below which 25% of the tracts in that region fall; 50%; 75%; etc. This information depicts the variation in ambient air toxics concentration between the different census tracts in that geographic region (one estimate for each census tract in that region and each air toxics compound).
   
   

3. Incorporating daily activity patterns. For each census tract, the variation in daily activity patterns (the fraction of time spent in each microenvironment and the fraction of time spent commuting during a day) between individuals was determined for each of the 10 receptor populations. The receptor populations were defined by 5 age groups (a 0-5 year age group; a 6-11 year age group; a 12-17 year age group; an 18-64 year age group; and a 65+ age group) and 2 gender groups (male and female gender groups).
   
   

4. Calculating annual exposures. For each census tract and receptor population, the yearly activity pattern for 30 different random individuals in that receptor population was simulated using Monte Carlo analysis. For the first individual, 365 daily activity patterns (one for each day of the year) were chosen based on the variation in daily activity pattern for that specific receptor population. This was repeated for 30 individuals in that receptor population, always using the same ambient air toxic concentration specific to that census tract. This produced 30 different estimates of the exposure over one year of life for each of the 10 receptor populations in that census tract (a total of 300 estimates in the census tract). From these 30 samples, a median value was calculated and applied to all individuals in that receptor population in that census tract. This median value represents a typical exposure for that receptor population and census tract. One such median value was calculated for each receptor population in each census tract.
   
   

5. Calculating lifetime exposure. For a given census tract, the lifetime exposure was estimated using the results from Step 4. This was calculated by multiplying the exposure in an age group (e.g. the 0-5 year age group) as determined by Step 4 by the fraction of a lifetime spent in that age group (e.g. 5/70 or 0.07 for the 0-5 age group); performing this calculation for each of the 5 age groups; and summing these contributions (one contribution from each age group). This produced a time-weighted average lifetime exposure in each census tract for a typical individual.
   
   

6. Calculating cancer risk. The variation in cancer risk was obtained directly from the results of Step 5. For a given census tract, the lifetime exposure was multiplied by the Unit Risk Estimate to obtain the excess lifetime probability of cancer for that air toxics compound. This process was possible because the URE is not a function of age, gender or race (or at least the function is unknown, and so is assumed to be a constant for all individuals). The result was an estimate of the typical lifetime excess probability of cancer in that census tract. Note that it is not strictly the mean probability for the entire population in that census tract, since it is based solely on calculations of exposure at the centroid of the census tract. This was repeated over all census tracts. From these data, the fraction of census tracts characterized by a typical lifetime excess probability of cancer below any particular value (e.g. 1 in 10,000) was determined. For example, the cancer risk below which 25% of the census tracts fall was determined (as well as other percentiles).
   
   

7. Calculating noncancer risk. The variation in noncancer risk is obtained directly from the results of Step 5. For a given census tract, the lifetime exposure was divided by the Reference Concentration (RfC) to yield the Hazard Quotient (HQ) for that air toxics compound. This process was possible because the RfC is not a function of gender or race (or at least the function is unknown, and so is assumed to be a constant for all individuals). The results are two estimates of the HQ for individuals in that census tract; one for typical young children and one for typical adults. Note that these values are not strictly the mean HQ for the entire population in that census tract, since they are based solely on calculations of exposure at the centroid of the census tract. This was repeated over all census tracts. From these data, the fraction of census tracts characterized by a typical HQ below any particular value (e.g. 0.01) was determined. For example, the HQ value below which 25% of the census tracts fall was determined (as well as other percentiles).
   
   

8. Calculating cumulative cancer risk. A cumulative carcinogenicity risk assessment was performed by summing the lifetime excess probability of cancer across air toxic compounds in a census tract. From the resulting information (produced by performing this calculation in each census tract and then pooling the results from all census tracts), the fraction of census tracts characterized by a typical cumulative lifetime excess probability of cancer below any particular value (e.g. 1 in 10,000) was determined. Separate analyses were performed for carcinogens for which human data exist; carcinogens for which only animal data exist; and all carcinogens combined. For example, the cumulative cancer risk below which 25% of the census tracts fall was determined (as well as other percentiles).
   
   

9. Calculating cumulative noncancer risk. Similarly, a cumulative noncancer risk assessment was performed by summing the HQs across all air toxic compounds in a census tract that act on the same target organ or tissue to yield a Hazard Index (HI). From the information (produced by performing this calculation in each census tract and then pooling the results from all census tracts), the fraction of census tracts characterized by a typical HI below any particular value (e.g. 0.01) was determined. For example, the HI value below which 25% of the census tracts fall was determined (as well as other percentiles).
   
   What are the components of variability?
   Which components of variability did the national-scale assessment include?
   What are the results of the variability analysis
   How can these results be interpreted?
   
   Return to Main Variability Page