Exposure to Hazardous Air Pollutants in the San Francisco Bay Area Prepared for
Rep. George Miller Rep. Nancy Pelosi Rep. Fortney Pete Stark Rep. Anna G. Eshoo Rep. Tom Lantos Rep. Barbara Lee Rep. Mike Thompson Rep. Lynn C. Woolsey Minority Staff Report
Committee on Government Reform
U.S. House of RepresentativesMarch 18, 1999
II. Methodology
A. Sources of Air Quality Monitoring Data and Location of Monitors
B. Determination of Average Exposures
C. Determination of Health Risks from Exposure to Hazardous Air PollutantsIII. Results
A. Residents of the San Francisco Bay Area Are Exposed to Multiple Hazardous Air Pollutants in Ambient Air
B. Levels of Hazardous Air Pollutants Are above the Clean Air Act's Health GoalIV. Sources of Hazardous Air Pollutants
V. Public Health Significance of Exposure to Hazardous Air Pollutants
A. Need for Further Emission Reductions
B. Need for Additional Data
C. Appropriate Interpretation of the Health RisksUnder the 1990 Clean Air Act, 188 chemicals have been designated as hazardous air pollutants because of their potential to cause adverse environmental and health effects, including cancer, neurological damage, and birth defects. Although the U.S. Environmental Protection Agency and others have reported on the level of emissions of these hazardous air pollutants, little is known about the level of hazardous air pollutants in ambient air. Few reports have examined the extent to which the public is actually exposed to these toxic pollutants.
Eight members of Congress from the San Francisco Bay Area asked the minority staff of the Committee on Government Reform of the U.S. House of Representatives to investigate the public's exposure to hazardous air pollutants in the Bay Area. This congressional staff report presents the results of this investigation. It finds that many residents of the San Francisco Bay Area may be exposed to levels of hazardous air pollutants that are over two hundred times higher than the goals of the Clean Air Act.
The findings in this report are based on data from air quality monitors operated in six locations in the San Francisco Bay Area from 1995 to 1998. These data contain over 4,800 monitoring results collected for ten hazardous air pollutants. While previous reports may have discussed the level of emissions of hazardous air pollutants, this is the first report to reveal the concentrations of these pollutants in the ambient air in the San Francisco Bay Area based on recent monitoring data. It is also the first report to estimate the potential health risks from exposure to these hazardous air pollutants.
The quantification of health risks from exposure to hazardous air toxics is an imprecise science. In general, hazardous air pollutants have not been as well studied as ozone, carbon monoxide, and other "criteria" air pollutants subject to national ambient air quality standards. Moreover, the risks examined in this report are cancer risks, and considerable scientific uncertainty surrounds cancer risk estimates. Most cancer risk estimates are based on studies that expose animals to high doses of the hazardous air pollutant. Conservative assumptions are used to extrapolate "upper bound" estimates of the cancer risk to humans. These risk estimates assume that individuals are exposed to the hazardous air pollutant for a lifetime (70 years).
Despite these substantial uncertainties, the results of this study show that many residents of the San Francisco Bay Area are exposed to excessive levels of hazardous pollutants in the air they breathe. The 1990 Clean Air Act established a goal of reducing the lifetime cancer risk from exposure to major sources of hazardous air pollutants to one additional cancer case per million exposed individuals. The data examined in this report show that residents of the San Francisco Bay Area are exposed to levels of hazardous air pollutants that, in combination, may be an average of 208 times higher than this goal. The pollutants that appear to pose the greatest cancer risks are 1,3-butadiene and benzene. At the average levels measured in the San Francisco Bay Area, the lifetime cancer risks for these hazardous air pollutants could be as high as 68 in a million for 1,3-butadiene and 61 in a million for benzene. In total, nine of the ten hazardous air pollutants analyzed in this study appear to present cancer risks that are at or above the Clean Air Act goal (Table 1).
Table 1: Potential cancer risks from ambient exposure to toxic air pollutants in the San Francisco Bay Area exceed Clean Air Act goals by a wide margin.
Compound Average
Concentration
(yg/m3)Potential Cancer Risk (X10-6) 1.3-Butadiene 0.40 68 Benzene 2.06 61 Carbon Tetrachloride 0.57 24 Chromium VI 0.00017 24 Formaldehyde 2.65 16 1,4-Dichlorobenzene 0.78 9 Methylene Chloride 3.09 3 Perchloroethylene 0.51 3 Chloroform 0.15 1 Trichloroethylene 0.11 0 Total Potential Cancer Risk 208 Clean Air Act Goal 1 According to the most recent toxicity estimates from the California Environmental Protection Agency, ambient concentrations above 0.0059 micrograms per cubic meter (yg/m3) for 1,3-butadiene and 0.034 yg/m3 for benzene could cause lifetime cancer risks to exceed one in one million. The actual concentrations of these pollutants exceeded these benchmarks, however. The average monitored concentration was 0.40 yg/m3 for 1,3-butadiene and 2.06 yg/m3 for benzene.
One important cancer-causing pollutant, diesel particulates, was not included in this analysis because recent monitoring data was not available. In August 1998, the California EPA designated diesel particulates as a toxic air pollutant with a substantial cancer potency. The exclusion of diesel particulates means that the aggregate cancer risks from toxic air pollution could potentially exceed those estimated in this report.
This report also sought to identify the sources of the hazardous air pollutants posing the highest risks. Under the 1990 Clean Air Act, the U.S. EPA has issued over 40 standards to control major sources of hazardous air pollutants, such as chemical plants and oil refineries. Since 1990, the U.S. EPA and the State of California have also established standards for cleaner automobiles and gasoline. Although these actions have substantially lowered emissions, millions of tons of hazardous air pollutants continue to be released into the atmosphere each year. In the case of the hazardous air pollutants studied in this report, the most significant sources of emissions appear to be mobile sources, such as cars, trucks, and off-road vehicles. According to 1993 emissions estimates -- the most recent estimates available -- mobile sources are responsible for 68% of 1,3-butadiene emissions and 67% of benzene emissions.
I. BACKGROUND
Under the 1990 Clean Air Act, 188 air pollutants are listed as hazardous air pollutants.1 These pollutants were designated as hazardous because of their potential to cause adverse health effects such as cancer, neurotoxicity, or reproductive toxicity. The Act required the United States Environmental Protection Agency to control the emissions of hazardous air pollutants from major sources such as factories and refineries, smaller stationary sources, and motor vehicles.2 The Act required that over time U.S. EPA regulations for major sources should "provide an ample margin of safety to protect public health." In the case of cancer risks from major sources of hazardous air pollutants, this was defined as a lifetime cancer risk no greater than one in a million.3
Considerable attention has been focused on reporting releases of hazardous air pollutants from major sources. Each year, over 25,000 large sources provide detailed reports on emissions of over 650 toxic chemicals to U.S. EPA's Toxic Release Inventory. According to U.S. EPA's National Toxics Inventory, 8.1 million tons of air toxics were released in 1993, the most recent year for which this data is available.4
Unfortunately, there has been relatively little attention devoted to the issue of human exposure to hazardous air pollutants. According to U.S. EPA, "presently there is no national ambient air quality monitoring network designed to perform routine measurements of air toxics levels."5 This is a critical data gap. Ultimately, what matters most to human health is the degree to which individuals are actually exposed to these toxic emissions.
Eight members of Congress from the San Francisco Bay Area asked the minority staff of the Committee on Government Reform to help fill this gap by investigating exposure to hazardous air pollutants and the risks that this exposure poses to the residents of San Francisco. This report presents the results of this investigation.
A. Sources of Air Quality Monitoring Data and Location of Monitors
The monitoring data used in this analysis were obtained from the U.S. EPA's Aerometric Information Retrieval System (AIRS) database, the Agency's central repository of air quality information. Data on hazardous air pollutants are voluntarily reported to the AIRS system by state air quality agencies, and these state agencies are responsible for the accuracy and reliability of the data reported to U.S. EPA.
The air quality information presented in this report is based on data collected at six monitors operated by the California Environmental Protection Agency in four counties in the San Francisco Bay Area air basin. There are three monitors located in Contra Costa County, in the cities of Concord, Richmond, and San Pablo. There are also monitors located in Santa Clara County (in the city of San Jose), San Francisco County (in the city of San Francisco), and Alameda County (in the City of Fremont). According to the California EPA, the monitors in Concord, San Jose, and Fremont are located near residential areas, the monitors in Richmond and San Pablo are located near a commercial area, and the monitor in San Francisco is located near an industrial area. The locations of the air quality monitors are shown in Appendix B.
In order to ensure that only the most recent data was included, this report analyzed only data collected after January 1, 1995. The AIRS database contains over 4,800 daily average monitoring results for ten hazardous air pollutants monitored at these six locations between January 1995 and May 1998. These data were collected in a seasonally representative fashion. The ten hazardous air pollutants monitored at the six locations were benzene, 1,3-butadiene, carbon tetrachloride, chloroform, chromium, 1,4-dichlorobenzene, formaldehyde, methylene chloride, perchloroethylene, and trichloroethylene.
B. Determination of Average Exposures
Exposure estimates for the hazardous air pollutants were based on average ambient concentrations observed at air monitors. Simple average concentrations were determined for each pollutant at each of the six monitoring sites, and these were used to determine average exposures in each county. The average exposures for the San Francisco Bay Area as a whole were estimated by averaging the results from the four counties together. All "nondetects" were treated as being equal to zero, an assumption that tends to underestimate exposure.
C. Determination of Health Risks from Exposure to Hazardous Air Pollutants
The primary health impact analyzed in this report is the increased risk of cancer from exposure to hazardous air pollutants. In order to estimate this cancer risk, the report uses the most recent risk estimates developed by the California EPA.
For each cancer-causing compound, the California EPA determines a potency: the relationship between the level of exposure and the cancer risk. In determining these potencies, California EPA incorporates conservative assumptions and considers the potencies to be "upper bound" estimates, meaning that actual risks are unlikely to be greater and may be lower. Using these potencies, the Agency then calculates the concentration of the compound that could pose a lifetime risk that exceeds the Clean Air Act goal of one additional cancer case per million exposed individuals. This is known as the benchmark concentration. The benchmark concentrations used in this analysis are shown in Appendix A.
To estimate the potential cancer risks from the exposures observed in this analysis, the average concentration was compared to the benchmark concentration. For example, the benchmark concentration for benzene is 0.034 micrograms per cubic meter ( yg/m3). This means that for an individual exposed for 70 years to an average benzene concentration of 0.34 yg/m3 ten times the benchmark concentration -- the lifetime cancer risk could be as high as ten in one million.
To determine the total cancer risks from exposure to the ten pollutants, the report used an additive model, summing the individual cancer risks from each pollutant together. This methodology is consistent with the National Academy of Science's recommendations for risk assessment.6
A. Residents of the San Francisco Bay Area Are Exposed to Multiple Hazardous Air Pollutants in Ambient Air
The data collected for the ten hazardous air pollutants at the six monitoring locations in the San Francisco Bay Area showed that all ten of these compounds were frequently detected in ambient air (Table 2).
Methylene chloride was found at the highest average concentration (3.09 yg/m3), followed by formaldehyde (2.65 yg/m3), benzene (2.06 yg/m3), 1,4-dichlorobenzene (0.78 yg/m3), and carbon tetrachloride (0.57 yg/m3).
Table 2: Average Concentrations of Hazardous Air Pollutants in the San Francisco Bay Area.
Compound Number of
Samples
CollectedAverage
Concentration
(yg/m3)Maximum
Concentration
(yg/m3)Methylene Chloride 537 3.09 30.5 Formaldehyde 291 2.65 10.1 Benzene 547 2.06 19.0 1,4-Dichlorobenzene 537 0.78 9.70 Carbon Tetrachloride 488 0.57 1.14 Perchloroethylene 537 0.51 7.48 1,3-Butadiene 545 0.40 2.89 Chloroform 543 0.15 0.15 Trichloroethylene 537 0.11 6.49 Chromium VI 480 0.00017 0.0005 Maximum concentrations were often much higher than average concentrations. The maximum benzene concentration was 19.0 yg/m3, detected in Richmond in January 1996. 1,3-butadiene was found at a maximum concentration of 2.89 yg/m3 in San Jose in November 1995. Maximum concentrations of methylene chloride and formaldehyde were 30.5 and 10.1 yg/m3, respectively.
B. Levels of Hazardous Air Pollutants Are above the Clean Air Act's Health Goal
Nine of the ten hazardous air pollutants analyzed in this study were detected at levels at or above the health goal of one additional cancer case per million exposed individuals established for major sources of hazardous air pollutants in the Clean Air Act. When added together, the total average lifetime risk from exposure to these ten compounds in ambient air could be as high as 208 additional cancer cases per million exposed individuals. This represents a risk that is more than 200 times higher than the health goal established in the Clean Air Act (Table 1).
Cancer risks from exposure to hazardous air pollutants were far above the health goal in all four counties with monitoring stations (Table 3). Potential risks were 268 times higher than the Clean Air Act's health goal at the monitoring site in Santa Clara County, 199 times higher than the Clean Air Act's health goal at the monitoring site in Alameda County, and 182 and 178 times higher than the Clean Air Act's health goal in Contra Costa and San Francisco Counties, respectively.
Table 3: Potential Cancer Risks Were Above Clean Air Act Health Goals at All San Francisco Bay Area Monitoring Stations.
County Potential Cancer
Risk (X10-6)Santa Clara
Alameda
Contra Costa
San Francisco268
199
182
178Average Potential
Cancer Risk208 Clean Air Act
Health Goal1 The majority of the risk comes from two compounds: 1,3-butadiene and benzene (Figure 1). The potential cancer risks from exposure to 1,3-butadiene at the average levels monitored in the San Francisco Bay Area are 68 times the Clean Air Act's health goal. 1,3-butadiene is a by- product of combustion that, in animal studies, has been found to cause cancer in multiple sites, including the heart, lung, mammary glands, ovaries, stomach, liver, pancreas, thyroid, and testes.7 Benzene is a known human carcinogen that has been found to cause leukemia and cancers of the lymphoid system, skin, ovary, lung, and mammary glands.8 The potential risks from benzene exposure are 61 times the Clean Air Act goal.
IV. SOURCES OF HAZARDOUS AIR POLLUTANTS
Information on local sources of hazardous air pollutants is not readily available. However, U.S. EPA's National Toxics Inventory provides national estimates of emissions of hazardous air pollutants from various sources.9 This inventory is based on 1993 data but remains the most current national information available on sources of hazardous air pollutants. Overall, large stationary sources, such as chemical plants and oil refineries, account for 61% of all hazardous air pollutant emissions, while mobile sources and smaller area sources contribute 21% and 18% respectively.10
Although stationary sources emit more total hazardous air pollutants than mobile sources, they do not appear to be the primary source of the elevated cancer risks in the San Francisco Bay Area. Table 4 shows the most significant national sources of the two hazardous air pollutants which pose the most risk in the San Francisco Bay Area. On-road motor vehicles are the largest source for both pollutants. Off-road vehicles and equipment are the second largest source for both benzene and 1,3-butadiene.
Taken together, mobile sources represent the biggest national source of these two hazardous air pollutants. Overall, on- and off-road vehicles account for 68% of 1,3-butadiene emissions and 67% of benzene emissions.
Natural sources can also contribute to exposure to certain hazardous air pollutants. In the case of benzene, natural sources include forest fires, volcanos, and some plants that naturally produce the compound. U.S. EPA estimates indicate that these background concentrations may pose a lifetime cancer risk of approximately four in one million. 11 In contrast, in the case of 1,3- butadiene, there are virtually no natural sources.
Table 4: Sources of 1,3-Butadiene and Benzene
Compound Mobile Resources:
On-Road VehiclesMobile Resources:
Non-Road VehiclesStationary and
Other SourcesTotal 1993
Emissions1,3-Butadiene 36,660 tons
46.9%16,630 tons
(21.2%)24,940 tons
(31.9%)78,230
tonsBenzene 207,300 tons
(47%)90,000 tons
(20%)145,100 tons
(33%)442,400
tonsV. PUBLIC HEALTH SIGNIFICANCE OF EXPOSURE TO HAZARDOUS AIR POLLUTANTS
A. Need for Further Emission Reductions
Since passage of the 1990 Clean Air Act, the focus of U.S. EPA's hazardous air pollution program has been to reduce emissions of hazardous air pollutants from major sources. To date, U.S. EPA has established standards for 47 major sources of hazardous air pollutants under the Clean Air Act's maximum available control technology (MACT) program. These standards require that facilities meet emission standards that are no less stringent than the emission control that is achieved in practice by the best controlled similar source. 12 U.S. EPA estimates that these standards will reduce emissions of hazardous air pollutants by 980,000 tons per year when fully implemented.13 In addition, U.S. EPA has established more stringent emissions standards for automobiles and required the use of reformulated gasoline in some areas. Both of these efforts have reduced the risks from hazardous air pollutants. U.S. EPA estimates that from 1993 to 1996, emissions of hazardous air pollutants from mobile sources have decreased by 16%, and emissions from large stationary sources have decreased by 13%. 14 U.S. EPA is also beginning several new efforts, such as its Residual Risk Program and its Urban Air Toxics Strategy, to further reduce exposure to hazardous air pollutants.15
The results from this investigation show that these efforts, while substantially improving air quality, have not reduced potential cancer risks sufficiently to meet the goal of the Clean Air Act. In 1990, Congress established a health-based goal for the Clean Air Act: to reduce lifetime cancer risks from major sources of hazardous air pollutants to one in one million. In 1996, Congress reaffirmed this basic goal when it passed the Food Quality Protection Act, which established new standards for cancer-causing pesticides in food. This legislation directed that standards for acceptable pesticide levels in food provide a "reasonable certainty that no harm will result,"16 which in the case of cancer-causing pesticides, Congress understood to be a "one-in-one million lifetime risk."17
Unfortunately, the data examined in this report show that San Francisco Bay Area residents face a cancer risk from exposure to hazardous air pollutants that may be more than 200 times higher than the Clean Air Act's health goal.
The Presidential/Congressional Commission on Risk Assessment and Risk Management recommended in 1997 that U.S. EPA establish a tiered approach for addressing environmental cancer risks. The Commission recommended that U.S. EPA give priority to lifetime cancer risks to individuals that are greater than ten in one million.18 This recommendation suggests that, because of the exposure to the hazardous air pollutants examined in this study, the San Francisco Bay Area should be a priority for U.S. EPA attention.
U.S. EPA is taking additional steps to further reduce emissions of hazardous air pollutants. The Office of Management and Budget is presently reviewing U.S. EPA-proposed rules that would establish stricter emissions standards for automobiles and sport utility vehicles, potentially reducing hydrocarbon emissions by more than 50% for some vehicles.19 These new standards would also require cleaner fuels, reducing the levels of sulfur in fuel by almost 90%, from an average of 330 parts per million (ppm) to an average of 30 ppm. 20 Because sulfur interferes with catalytic converters on automobiles, reducing their efficiency and increasing emissions, reducing sulfur levels in gasoline will make motor vehicles run cleaner. According to U.S. EPA analyses, establishing the new sulfur standard would reduce hydrocarbon emissions by 13% (for older vehicles) to 46% (for newer vehicles).21
The State of California has also acted to reduce emissions of hazardous air pollutants. Under the Clean Air Act, California is given authority to establish automobile emissions standards that are more stringent than U.S. EPA's national standards, and the California EPA has used this authority to reduce exposure to air toxics. The California Low-Emission Vehicle (LEV) program requires that automobiles sold in California meet emissions standards for hydrocarbon emissions that are more stringent than the comparable U.S. EPA standards. Since 1996, state regulations have required the use of cleaner-burning, low-sulfur gasoline which has substantially reduced emissions of hazardous air pollutants from automobiles.22 Without these actions, the public's exposure to hazardous air pollutants in the San Francisco Bay Area would be even higher than the levels found in this analysis. In fact, the California EPA estimates that the introduction of cleaner gasoline has reduced cancer-causing emissions from automobiles in California by 30% - 40%.23
Like the U.S. EPA, California is continuing to move forward to reduce exposure to hazardous air pollutants. In November 1998, the California EPA announced that the Agency would require more stringent emissions and evaporative standards for automobiles and light trucks, further reducing emissions of hazardous air pollutants in California.24
There are many gaps in scientific understanding of both the health effects of hazardous air pollutants and their average concentrations in ambient air. This report examines risks from only ten hazardous air pollutants. There is no recent data on the level of other hazardous air pollutants in the air in the San Francisco Bay Area. In particular, this report does not include the potentially significant cancer risks from exposure to diesel particulates, which were designated as a toxic air contaminant by the California EPA in August 1998.25 The California EPA's estimates of the cancer potency of diesel particulates, and their pervasiveness in ambient air, suggest that these particulates alone could pose a significant additional cancer risk. 26
In addition, this analysis includes only cancer risks. It does not consider acute risks or reproductive risks such as birth defects. According to U.S. EPA, however, there is some evidence of reproductive or developmental effects for nearly 30% of hazardous air pollutants, and approximately 60% may affect the central nervous system. 27
Scientific research is also lacking on whether there are synergistic effects from exposure to multiple hazardous air pollutants. The risk model used for this analysis assumed that there was no interaction between the multiple contaminants to which the public is exposed. Some scientific data, however, indicate that there could be synergistic effects from exposure to many toxics at the same time, further increasing risks.28
The risk estimates for the San Francisco Bay Area were based on measurements from six monitors, all in the southern Bay Area. While this represents the best data available on ambient concentrations of hazardous air pollutants, additional monitors would allow more precise estimates of the risks from exposure to hazardous air pollutants in the San Francisco Bay Area. State air pollution control officials have taken an important first step by monitoring and reporting to U.S. EPA the level of the ten hazardous air pollutants examined in this report. These actions were taken voluntarily by the state, as federal law does not require monitoring or reporting of hazardous air pollutants. Without significant additional efforts, however, the public's "right to know" the risks of exposure to hazardous air pollutants will not be fulfilled.
C. Appropriate Interpretation of the Health Risks
While the results of this study show a significant exposure to hazardous air pollutants in the San Francisco Bay Area, there are several important caveats that should be considered in interpreting the estimates of health risks.
First, there is considerable scientific uncertainty about the cancer risk estimates for hazardous air pollutants. Most of the cancer risk estimates for these compounds are based on animal studies which have used high doses of the compounds. California EPA uses conservative assumptions in extrapolating risks from animals to humans and from high to low doses. The risk estimates presented in this report therefore represent what could be described as the "upper bounds" of the risk. Moreover, the hazardous air pollutants examined in this analysis have, in general, not been as well studied as ozone, carbon monoxide, and other "criteria" air pollutants subject to national ambient air quality standards.
Due to these uncertainties, the seeming numerical precision associated with specific risk estimates can be misunderstood. Cancer risk estimates should be viewed as indicators of the general level of risk, not as precise quantifications. In fact, different environmental agencies can derive significantly different risk estimates for individual hazardous air pollutants on the basis of the same exposure data because the agencies use different estimates of the cancer potency of the compounds.29 California EPA, U.S. EPA, and other public health agencies continue to update the cancer risk estimates in response to new data and new scientific theories. These revisions can lead to substantial changes in the risk estimates.30
Moreover, although some data indicate that hazardous air pollutants are occasionally present at concentrations that can cause acute effects such as respiratory irritation, the vast majority of risks from these toxics are chronic risks, such as cancer, that require long-term exposure. The risk estimates presented in this report are based on the assumption that individuals experience 70 years of exposure. No individual is likely to get cancer from a single day, or even a single year, of exposure to these hazardous air pollutants. Instead, these compounds generally only cause cancer after many years of exposure.
Finally, while the potential cancer risks described in this report are far above the Clean Air Act's health goal and present a serious public health problem, they are still substantially lower than risks from certain other causes of cancer, such as smoking. For example, the risks of lung cancer from smoking a pack of cigarettes a day is approximately 450 times higher than the potential risk of cancer from breathing hazardous air pollutants at the levels monitored in the San Francisco Bay Area. Unlike other risks, however, the risks from breathing hazardous air pollutants are "involuntary" risks that are imposed on the exposed individuals from sources beyond their control.
Appendix A
Exposure Levels for Hazardous Air Pollutants that Correspond to Potential Lifetime Cancer Risk of One in One Million
Compound Benchmark Concentration
(yg/m3)Benzene
1,3-Butadiene
Carbon Tetrachloride
Chloroform
Chromium VI
1,4-Dichlorobenzene
Formaldehyde
Methylene Chloride
Perchloroethylene
Trichloroethylene0.034
0.0059
0.024
0.19
0.000007
0.091
0.17
1.0
0.17
0.5Source: California EPA, Air Toxic Hotspot Program Risk Assessment Guidelines (Oct. 1997). www.oehha.org/archive/risk_assess.html
1 Section 112(b)(1) of the Act contains a list of 189 hazardous air pollutants. In 1996, U.S. EPA removed the chemical caprolactam from the list, leaving 188 substances designated as hazardous air pollutants.
2 A major source of hazardous air pollutants is defined in the Act as any stationary source that emits at least 10 tons per year or more of one hazardous air pollutant or 25 tons per year of a combination of hazardous air pollutants. Clean Air Act Section 112(a)(1).
3 Clean Air Act Section 112(f)(2). In addition to establishing that lifetime cancer risks from major sources should not exceed one in a million, the Act contains several other requirements for regulating hazardous air pollutants. For mobile resources, the Act requires that U.S. EPA establish "reasonable requirements to control hazardous air pollutants from motor vehicles and motor vehicle fuels." Clean Air Act Section 202(l). For small stationary sources, the Act requires that U.S. EPA develop an urban air toxics strategy with the goal of reducing overall cancer risks from hazardous air pollutants by 75%. Clean Air Act Section 112(k).
4 U.S. EPA, National Air Quality and Emissions Trends Report, 1997, 74 (U.S. EPA 454/R-98-016) (Dec. 1998).
6 See National Research Council, Pesticides in the Diets of Infants and Children (1993); National Research Council, Complex Mixtures: Methods for In-Vivo Toxicity Testing (1988); see also U.S. EPA, Guidelines for the Health Risk Assessment of Chemical Mixtures, 51 FR 34014 (1986).
7 California EPA, Toxic Air Contaminant Identification List Summaries: 1,3- Butadiene, 144 (Sept. 1997).
8 California EPA, Toxic Air Contaminant Identification List Summaries: Benzene, 95 (Sept. 1997).
9 U.S. EPA, 1993 National Toxics Inventory (1999).
10 National Air Quality and Emissions Trends Report, 1997, supra note 4, at 71.
11 ICF Kaiser, Modeling Cumulative Outdoor Concentrations of Hazardous Air Pollutants, Volume II: Attachments, Report to U.S. EPA, 6 (SYSAPP-98-96/33r1) (Feb. 1998).
12 Clean Air Act Section 112(d)(2).
13 National Air Quality and Emissions Trends Report, 1997, supra note 4, at 75.
14 National Air Quality and Emissions Trends Report, 1997, supra note 4, at 74.
15 U.S. EPA, Second Report to Congress on the Status of the Hazardous Air Pollution Program under the Clean Air Act, Draft (U.S. EPA-453/R-96-015) (Oct. 1997).
16 Federal Food, Drug, and Cosmetic Act Section 408(b)(2)(a).
17 Food Quality Protection Act of 1996, 104th Congress, House Report 104-169, 41 (Aug. 1996).
18 The Presidential/Congressional Commission on Risk Assessment and Risk Management, Risk Assessment and Risk Management in Regulatory Decision-Making, 2, 109 (June 1997).
19 EPA Wants Light Trucks to Meet Car Standards; Air Quality, Costs Could Be Affected, Washington Post, E1 (Feb. 18, 1999).
21 U.S. EPA, EPA Staff Paper on Gasoline Sulfur Issues (U.S. EPA-420-R-98-005) (May 1, 1998). U.S. EPA has not, however, implemented Section 202(l)(2) of the Clean Air Act, which directs U.S. EPA to promulgate "reasonable requirements to control hazardous air pollutants from motor vehicles and motor vehicle fuels."
22 California Air Resources Board, California Reformulated Gasoline: A Cleaner Burning Gasoline, Facts and Frequently Asked Questions, 3 (Nov. 8, 1995).
23 California Air Resources Board, Comparison of Federal and California Reformulated Gasoline, Fact Sheet 3 (Feb. 1996). The use of reformulated gasoline containing MTBE has been found to increase emissions of formaldehyde. However, because reformulated gasoline reduces emissions of benzene, 1,3-butadiene, and other hazardous air pollutants, it has a net effect of reducing risks from emissions of hazardous air pollutants from mobile sources.
24 California Air Resources Board, Summary of Proposed Amendments to California's Low-Emission Vehicle Regulations "LEV II" (Aug. 1998) (available online at www.arb.ca.gov/ msprog/levprog/levii/overview.htm).
25 California EPA, ARB Identifies Diesel Particulate Emissions as a Toxic Air Contaminant (Aug. 27, 1998).
26 Id. According to the California EPA, the average level of diesel particulates in the ambient air in California is 2.2 yg/m3, while the benchmark concentration associated with a 1 in a million lifetime cancer risk is 0.0033 yg/m3. Combining these two estimates indicates that the lifetime cancer risks from exposure to diesel particulates could equal or exceed the cancer risks estimated in this report.
27 National Air Quality and Emissions Trends Report, 1996, 61 (U.S. EPA 454/R-97-013) (Jan. 1998).
28 Complex Mixtures: Methods for In-Vivo Toxicity Testing, supra note 9.
29 The U.S. EPA has developed cancer potencies for some of the hazardous air pollutants examined in this report. In the aggregate, the U.S. EPA risk estimates are similar to the California EPA risk estimates. If the current cancer potencies developed by the U.S. EPA had been used in this report instead of the cancer potencies of the California EPA for the hazardous air pollutants for which U.S. EPA potencies are available, the potential aggregate risk would be estimated as 189 in a million, instead of 208 in a million. In the case of individual hazardous air pollutants, however, the California EPA and the U.S. EPA cancer potencies can differ significantly. For example, the current risk estimates of the California EPA are lower than the current risk estimates of the U.S. EPA for 1,3- and formaldehyde and higher than the current risk estimates of the U.S. EPA for benzene and chromium.
30 For example, the U.S. EPA is presently reassessing risk estimates for toxic air pollutants emitted from motor vehicles as part of its implementation of section 202 of the Clean Air Act, which requires U.S. EPA to evaluate the toxic risks from motor vehicle and promulgate regulations to reduce these risks. Preliminary draft studies prepared by the U.S. EPA indicate that the reassessment could substantially lower U.S. EPA's risk estimates for 1,3-butadiene, and at the same time identify diesel particulates as a significant new cancer risk factor. U.S. EPA, Draft Health Assessment Document for Diesel Emissions (Feb. 1998); U.S. EPA, Draft Review of Health Risk Assessment for 1,3-Butadiene (Jan. 1998).
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