Data Available for Evaluating the Risks and Benefits of MTBE and Ethanol as Alternative Fuel Oxygenates

The wide-scale use of methyl tertiary butyl ether (MTBE) in gasoline has resulted in substantial public controversy and action to ban or control its use due to perceived impacts on water quality. Because oxygenates are still required under federal law, considerable research has focused on ethanol as a substitute for MTBE. In this article, we summarize the currently available literature on the air and water quality risks and benefits of MTBE versus ethanol as alternative fuel oxygenates. We find that MTBE-fuel blends are likely to have substantial air quality benefits; ethanol-fuel blends appear to offer similar benefits, but these may be at least partially negated because of ethanol's propensity to increase emissions and ambient concentrations of some air contaminants. Releases of gasoline containing either MTBE or ethanol could have an impact on some drinking water sources, although the impacts associated with MTBE tend to relate to aesthetics (i.e., taste and odor), whereas the impacts associated with ethanol generally relate to health risk (i.e., greater exposure to gasoline constituents such as benzene). It is likely that these water quality impacts will be outweighed by the air quality benefits associated with MTBE and perhaps ethanol use, which affect a much larger population. A lack of data on environmental exposures and associated health impacts hinders the completion of a comprehensive quantitative risk-benefit analysis, and the available air and water quality data should be evaluated in a broader risk-management context, which considers the potential life-cycle impacts, costs, and feasibility associated with alternative fuel oxygenates.     

A Comparative Cancer Risk Evaluation of MTBE and Other Compounds (Including Naturally Occurring Compounds) in Drinking Water in New Hampshire

Methyl tert-butyl ether (MTBE) was added to gasoline in New Hampshire (NH) between 1995 and 2006 to comply with the oxygenate requirements of the 1990 Amendments to the Clean Air Act. Leaking tanks and spills released MTBE into groundwater, and as a result, MTBE has been detected in drinking water in NH. We conducted a comparative cancer risk assessment and a margin-of-safety (MOS) analysis for several constituents, including MTBE, detected in NH drinking water. Using standard risk assessment methods, we calculated cancer risks from exposure to 12 detected volatile organic compounds (VOCs), including MTBE, and to four naturally occurring compounds (i.e., arsenic, radium-226, radium-228, and radon-222) detected in NH public water supplies. We evaluated exposures to a hypothetical resident ingesting the water, dermally contacting the water while showering, and inhaling compounds volatilizing from water in the home. We then compared risk estimates for MTBE to those of the other 15 compounds. From our analysis, we concluded that the high-end cancer risk from exposure to MTBE in drinking water is lower than the risks from all the other VOCs evaluated and several thousand times lower than the risks from exposure to naturally occurring constituents, including arsenic, radium, and radon. We also conducted an MOS analysis in which we compared toxicological points of departure to the NH maximum contaminant level (MCL) of 13 µg/L. All of the MOSs were greater than or equal to 160,000, indicating a large margin of safety and demonstrating the health-protectiveness of the NH MCL for MTBE.     

Air Toxics and Health Risks in California: The Public Health Implications of Outdoor Concentrations

Of the 188 hazardous air pollutants (HAPs) listed in the Clean Air Act, only a handful have information on human health effects, derived primarily from animal and occupational studies. Lack of consistent monitoring data on ambient air toxics makes it difficult to assess the extent of low-level, chronic, ambient exposures to HAPs that could affect human health, and limits attempts to prioritize and evaluate policy initiatives for emissions reduction. Modeled outdoor HAP concentration estimates from the U.S. Environmental Protection Agency's Cumulative Exposure Project were used to characterize the extent of the air toxics problem in California for the base year of 1990. These air toxics concentration estimates were used with chronic toxicity data to estimate cancer and noncancer hazards for individual HAPs and the risks posed by multiple pollutants. Although hazardous air pollutants are ubiquitous in the environment, potential cancer and noncancer health hazards posed by ambient exposures are geographically concentrated in three urbanized areas and in a few rural counties. This analysis estimated a median excess individual cancer risk of 2.7E-4 for all air toxics concentrations and 8600 excess lifetime cancer cases, 70% of which were attributable to four pollutants: polycyclic organic matter, 1,3 butadiene, formaldehyde, and benzene. For noncancer effects, the analysis estimated a total hazard index representing the combined effect of all HAPs considered. Each pollutant contributes to the index a ratio of estimated concentration to reference concentration. The median value of the index across census tracts was 17, due primarily to acrolein and chromium concentration estimates. On average, HAP concentrations and cancer and noncancer health risks originate mostly from area and mobile source emissions, although there are several locations in the state where point sources account for a large portion of estimated concentrations and health risks. Risk estimates from this study can provide guidance for prioritizing research, monitoring, and regulatory intervention activities to reduce potential hazards to the general population. Improved ambient monitoring efforts can help clarify uncertainties inherent in this analysis.     

Projection of Health Benefits from Ambient Ozone Reduction Related to the Use of Methyl tertiary Butyl Ether (MTBE) in the Reformulated Gasoline Program

To estimate potential public health benefits from ozone (O₃) pollution reduction attributable to the use of methyl tertiary-butyl ether (MTBE) in gasoline, O₃ dose-response estimates from the biomedical literature were combined with model estimates of O₃ reduction. Modeling employed EPA MOBILE5a and Complex models to predict emission changes, industry AQIRP techniques to predict ambient O₃ changes, and the National Exposure Model to predict human exposures. Human health effects considered were lung function decrements and respiratory irritant symptoms (using dose-response functions measured in laboratory and field studies), and increased death rates (using concentration-response functions inferred statistically from public-health data). Other reported health effects, such as lung inflammation, increases in asthma attacks, and hospitalizations, were not addressed because of inadequate dose-response information. Even for the health responses considered, quantitation of improvements due to MTBE use is problematical, because MTBE affects only a small percentage of existing O₃ pollution, and because exposure-response relationships are not well understood for population subgroups most likely to be affected. Nevertheless, it is reasonable to conclude that even small MTBE-associated reductions in peak ambient O₃ levels (1–5 ppb, according to model estimates) should yield considerable public health benefits. Tens of millions of Americans are potentially exposed to O₃ in the concentration range associated with health effects. Even if only a small percentage of them are susceptible, any incremental reduction in O₃ (as with MTBE use) must mitigate or prevent effects for a meaningful number of people. Better quantitative estimates of benefit must await a more detailed understanding of each link in the chain of causation.     

The Risk of MTBE Relative to Other VOCs in Public Drinking Water in California

Ongoing publicity about methyl tertiary butyl ether (MTBE) suggests that this chemical is of greater concern than other contaminants commonly found in drinking water. The purpose of this article is to evaluate the available MTBE data in context with other volatile organic compounds (VOCs) that are detected in public drinking water sources in California. We find that of the 28 VOCs with a primary maximum contaminant level (MCL) in California, 21 were found in 50 or more drinking water sources from 1985 to 2002. Over the last 10 years, the most frequently detected VOCs were chloroform, tetrachloroethylene (PCE), and trichloroethylene (TCE), which were found in about 9-15% of all sampled drinking water sources. These same chemicals were found to have the highest mean detected concentrations over the last 5 years, ranging from 13 to 15 microg/L. Many VOCs were also found to routinely exceed state and federal drinking water standards, including benzene and carbon tetrachloride. By comparison, MTBE was found in approximately 1% of sampled drinking water sources for most years, and of those drinking water sources found to contain MTBE from 1998 to 2002, over 90% had detected concentrations below California's primary MCL of 13 microg/L. Relative to the other VOCs evaluated, MTBE has the lowest estimated California cancer potency value, and was found to pose one of the least cancer risks from household exposures to contaminated drinking water. These findings suggest that MTBE poses an insignificant threat to public drinking water supplies and public health in California, particularly when compared to other common drinking water contaminants.     

Causality Assessment of the Acute Health Complaints Reported in Association with Oxygenated Fuels

In some areas where oxygenated fuel programs have been implemented, there have been widespread complaints of non-specific health effects attributed to the gasoline. There are a number of hypotheses that can account for this apparent association. This paper examines the hypothesis that the use of oxy-fuel (either oxygenated gasoline or reformulated gasoline) results in exposure of the general population to one or more chemicals at concentrations that cause toxicologic injury. Although several oxygenates can be used in oxy-fuels, this analysis focuses on MTBE because it is the most widely used oxygenate and because the database of relevant toxicologic data is greatest for this oxygenate. The causal assessment is based on an evaluation of the qualitative and quantitative plausibility that oxygenated fuel-related exposures have toxicological effects, and the epidemiologic studies that directly test the hypothesis that the use of oxygenated fuels causes adverse health effects. The plausibility that chemical exposures related to oxy-fuel use cause toxicological effects is very low. This determination is based on consideration of the exposure-response and time-action profiles for relevant toxicological effects of MTBE in animals, experimental MTBE exposure studies in humans, and the possibility that the addition of MTBE to gasoline results in toxicologically significant qualitative and/or quantitative changes in gasoline-related exposures. Similarly, the epidemiologic studies of oxy-fuel exposed cohorts do not support a causal relationship between oxy-fuel use and adverse health effects. Although the data are insufficient to rule the possibility of unique sensitivity in a small segment of the population, the strength of the evidence and the availability of other more plausible explanations for the health complaints reported in association with oxy-fuels support a high degree of confidence in the conclusion that MTBE-containing oxygenated fuels are not the cause of acute toxicity in the general population.     

Validation of a Novel Air Toxic Risk Model with Air Monitoring

Three modeling systems were used to estimate human health risks from air pollution: two versions of MNRiskS (for Minnesota Risk Screening), and the USEPA National Air Toxics Assessment (NATA). MNRiskS is a unique cumulative risk modeling system used to assess risks from multiple air toxics, sources, and pathways on a local to a state‐wide scale. In addition, ambient outdoor air monitoring data were available for estimation of risks and comparison with the modeled estimates of air concentrations. Highest air concentrations and estimated risks were generally found in the Minneapolis‐St. Paul metropolitan area and lowest risks in undeveloped rural areas. Emissions from mobile and area (nonpoint) sources created greater estimated risks than emissions from point sources. Highest cancer risks were via ingestion pathway exposures to dioxins and related compounds. Diesel particles, acrolein, and formaldehyde created the highest estimated inhalation health impacts. Model‐estimated air concentrations were generally highest for NATA and lowest for the AERMOD version of MNRiskS. This validation study showed reasonable agreement between available measurements and model predictions, although results varied among pollutants, and predictions were often lower than measurements. The results increased confidence in identifying pollutants, pathways, geographic areas, sources, and receptors of potential concern, and thus provide a basis for informing pollution reduction strategies and focusing efforts on specific pollutants (diesel particles, acrolein, and formaldehyde), geographic areas (urban centers), and source categories (nonpoint sources). The results heighten concerns about risks from food chain exposures to dioxins and PAHs. Risk estimates were sensitive to variations in methodologies for treating emissions, dispersion, deposition, exposure, and toxicity.     

Route-to-Route Extrapolation of the Toxic Potency of MTBE

MTBE is a volatile organic compound used as an oxygenating agent in gasoline. Inhalation from fumes while refueling automobiles is the principle route of exposure for humans, and toxicity by this route has been well studied. Oral exposures to MTBE exist as well, primarily due to ground-water contamination from leaking stationary sources, such as underground storage tanks. Assessing the potential public health impacts of oral exposures to MTBE is problematic because drinking water studies do not exist for MTBE, and the few oil-gavage studies from which a risk assessment could be derived are limited. This paper evaluates the suitability of the MTBE database for conducting an inhalation route-to-oral route extrapolation of toxicity. This includes evaluating the similarity of critical effect between these two routes, quantifiable differences in absorption, distribution, metabolism, and excretion, and sufficiency of toxicity data by the inhalation route. We conclude that such an extrapolation is appropriate and have validated the extrapolation by finding comparable toxicity between a subchronic gavage oral bioassay and oral doses we extrapolate from a subchronic inhalation bioassay. Our results are extended to the 2-year inhalation toxicity study by Chun et al. (1992) in which rats were exposed to 0, 400, 3000, or 8000 ppm MTBE for 6 hr/d, 5 d/wk. We have estimated the equivalent oral doses to be 0, 130, 940, or 2700 mg/kg/d. These equivalent doses may be useful in conducting noncancer and cancer risk assessments.     

Risk Characterization of Methyl tertiary Butyl Ether (MTBE) in Tap Water

Methyl tertiary butyl ether (MTBE) can enter surface water and groundwater through wet atmospheric deposition or as a result of fuel leaks and spills. About 30% of the U.S. population lives in areas where MTBE is in regular use. Ninety-five percent of this population is unlikely to be exposed to MTBE in tap water at concentrations exceeding 2 ppb, and most will be exposed to concentrations that are much lower and may be zero. About 5% of this population may be exposed to higher levels of MTBE in tap water, resulting from fuel tank leaks and spills into surface or groundwater used for potable water supplies. This paper describes the concentration ranges found and anticipated in surface and groundwater, and estimates the distribution of doses experienced by humans using water containing MTBE to drink, prepare food, and shower/bathe. The toxic properties (including potency) of MTBE when ingested, inhaled, and in contact with the skin are summarized. Using a range of human toxic potency values derived from animal studies, margins of exposure (MOE) associated with alternative chronic exposure scenarios are estimated to range from 1700 to 140,000. Maximum concentrations of MTBE in tap water anticipated not to cause adverse health effects are determined to range from 700 to 14,000 ppb. The results of this analysis demonstrate that no health risks are likely to be associated with chronic and subchronic human exposures to MTBE in tap water. Although some individuals may be exposed to very high concentrations of MTBE in tap water immediately following a localized spill, these exposures are likely to be brief in duration due to large-scale dilution and rapid volatilization of MTBE, the institution of emergency response and remediation measures to minimize human exposures, and the low taste and odor thresholds of MTBE which ensure that its presence in tap water is readily detected at concentrations well below the threshold for human injury.     

Development of a Unit Risk Factor for 1,3-Butadiene Based on an Updated Carcinogenic Toxicity Assessment

The Texas Commission on Environmental Quality (TCEQ) has developed an inhalation unit risk factor (URF) for 1,3-butadiene based on leukemia mortality in an updated epidemiological study on styrene-butadiene rubber production workers conducted by researchers at the University of Alabama at Birmingham. Exposure estimates were updated and an exposure estimate validation study as well as dose-response modeling were conducted by these researchers. This information was not available to the U.S. Environmental Protection Agency when it prepared its health assessment of 1,3-butadiene in 2002. An extensive analysis conducted by TCEQ discusses dose-response modeling, estimating risk for the general population from occupational workers, estimating risk for potentially sensitive subpopulations, effect of occupational exposure estimation error, and use of mortality rates to predict incidence. The URF is 5.0 × 10⁻⁷ per μg/m³ or 1.1 × 10⁻⁶ per ppb and is based on a Cox regression dose-response model using restricted continuous data with age as a covariate, and a linear low-dose extrapolation default approach using the 95% lower confidence limit as the point of departure. Age-dependent adjustment factors were applied to account for possible increased susceptibility for early life exposure. The air concentration at 1 in 100,000 excess leukemia mortality, the no-significant-risk level, is 20 μg/m³ (9.1 ppb), which is slightly lower than the TCEQ chronic reference value of 33 μg/m³ (15 ppb) protective of ovarian atrophy. These values will be used to evaluate ambient air monitoring data so the general public is protected against adverse health effects from chronic exposure to 1,3-butadiene.     

Consideration of Background Exposures in the Management of Hazardous Waste Sites: A New Approach to Risk Assessment

The current approach to health risk assessment of toxic waste sites in the U.S. may lead to considerable expenditure of resources without any meaningful reduction in population exposure. Risk assessment methods used generally ignore background exposures and consider only incremental risk estimates for maximally exposed individuals. Such risk estimates do not address true public health risks to which background exposures also contribute. The purpose of this paper is to recommend a new approach to risk assessment and risk management concerning toxic waste sites. Under this new approach, which we have called public health risk assessment, chemical substances would be classified into a level of concern based on the potential health risks associated with typical national and regional background exposures. Site assessment would then be based on the level of concern for the particular pollutants involved and the potential contribution of site contaminants to typical background human exposures. While various problems can be foreseen with this approach, the key advantage is that resources would be allocated to reduce the most important sources of human exposure, and site remediation decisions could be simplified by focussing on exposure assessment rather than questionable risk extrapolations.     

Development of a Screening Approach to Interpret Human Biomonitoring Data on Volatile Organic Compounds: Reverse Dosimetry on Biomonitoring Data for Trichloroethylene

A screening approach is developed for volatile organic compounds (VOCs) to estimate exposures that correspond to levels measured in fluids and/or tissues in human biomonitoring studies. The approach makes use of a generic physiologically-based pharmacokinetic (PBPK) model coupled with exposure pattern characterization, Monte Carlo analysis, and quantitative structure property relationships (QSPRs). QSPRs are used for VOCs with minimal data to develop chemical-specific parameters needed for the PBPK model. The PBPK model is capable of simulating VOC kinetics following multiple routes of exposure, such as oral exposure via water ingestion and inhalation exposure during shower events. Using published human biomonitoring data of trichloroethylene (TCE), the generic model is evaluated to determine how well it estimates TCE concentrations in blood based on the known drinking water concentrations. In addition, Monte Carlo analysis is conducted to characterize the impact of the following factors: (1) uncertainties in the QSPR-estimated chemical-specific parameters; (2) variability in physiological parameters; and (3) variability in exposure patterns. The results indicate that uncertainty in chemical-specific parameters makes only a minor contribution to the overall variability and uncertainty in the predicted TCE concentrations in blood. The model is used in a reverse dosimetry approach to derive estimates of TCE concentrations in drinking water based on given measurements of TCE in blood, for comparison to the U.S. EPA's Maximum Contaminant Level in drinking water. This example demonstrates how a reverse dosimetry approach can be used to facilitate interpretation of human biomonitoring data in a health risk context by deriving external exposures that are consistent with a biomonitoring data set, thereby permitting comparison with health-based exposure guidelines.     

Diesel Emissions and Lung Cancer1

This paper uses two different methods to assess the potential risk of human lung cancer from exposure to diesel engine emissions. One method analyzes the best available epidemiological evidence on the lung cancer risks of persons exposed in their occupations to diesel engine emissions. The second conducts a comparative analysis of laboratory and epidemiological data on diesel engine emissions and two chemically related environmental exposures–coke oven emissions and roofing tar emissions. The estimates of potential risk derived from these two distinct methods are compared. The sources of uncertainty in each method are explicitly characterized. The value of these estimates for comparing the potential lung cancer risks from exposure to diesel engine emissions with other personal and societal risks are discussed. Also considered are the limitations of these results in predicting the possible excess incidence of lung cancer from ambient exposure to diesel emissions.     

Potential Exposure and Cancer Risk from Formaldehyde Emissions from Installed Chinese Manufactured Laminate Flooring

Lumber Liquidators (LL) Chinese‐manufactured laminate flooring (CLF) has been installed in >400,000 U.S. homes over the last decade. To characterize potential associated formaldehyde exposures and cancer risks, chamber emissions data were collected from 399 new LL CLF, and from LL CLF installed in 899 homes in which measured aggregate indoor formaldehyde concentrations exceeded 100 μg/m³ from a total of 17,867 homes screened. Data from both sources were combined to characterize LL CLF flooring‐associated formaldehyde emissions from new boards and installed boards. New flooring had an average (±SD ) emission rate of 61.3 ± 52.1 μg/m²‐hour; >one‐year installed boards had ∼threefold lower emission rates. Estimated emission rates for the 899 homes and corresponding data from questionnaires were used as inputs to a single‐compartment, steady‐state mass‐balance model to estimate corresponding residence‐specific TWA formaldehyde concentrations and potential resident exposures. Only ∼0.7% of those homes had estimated acute formaldehyde concentrations >100 μg/m³ immediately after LL CLF installation. The TWA daily formaldehyde inhalation exposure within the 899 homes was estimated to be 17 μg/day using California Proposition 65 default methods to extrapolate cancer risk (below the regulation “no significant risk level” of 40 μg/day). Using a U.S. Environmental Protection Agency linear cancer risk model, 50th and 95th percentile values of expected lifetime cancer risk for residents of these homes were estimated to be 0.33 and 1.2 per 100,000 exposed, respectively. Based on more recent data and verified nonlinear cancer risk assessment models, LL CLF formaldehyde emissions pose virtually no cancer risk to affected consumers.     

A Physiologically-Based Pharmacokinetic Model Assessment of Methyl t-Butyl Ether in Groundwater for a Bathing and Showering Determination

Methyl t -butyl ether (MTBE) is a gasoline additive that has appeared in private wells as a result of leaking underground storage tanks. Neurological symptoms (headache, dizziness) have been reported from household use of MTBE-affected water, consistent with animal studies showing acute CNS depression from MTBE exposure. The current research evaluates acute CNS effects during bathing/showering by application of physiologically-based pharmacokinetic (PBPK) techniques to compare internal doses in animal toxicity studies to human exposure scenarios. An additional reference point was the delivered dose associated with the acute Minimum Risk Level (MRL) for MTBE established by the Agency for Toxic Substances and Disease Registry. A PBPK model for MTBE and its principal metabolite, t -butyl alcohol (TBA) was developed and validated against published data in rats and humans. PBPK analysis of animal studies showed that acute CNS toxicity after MTBE exposure can be attributed principally to the parent compound since the metabolite (TBA) internal dose was below that needed for CNS effects. The PBPK model was combined with an exposure model for bathing and showering which integrates inhalation and dermal exposures. This modeling indicated that bathing or showering in water containing MTBE at 1 mg/L would produce brain concentrations ˜1000-fold below the animal effects level and twofold below brain concentrations associated with the acute MRL. These findings indicate that MTBE water concentrations of 1 mg/L or below are unlikely to trigger acute CNS effects during bathing and showering. However, MTBE's strong odor may be a secondary but deciding factor regarding the suitability of such water for domestic uses.     

Uncertainty and Variation in Indirect Exposure Assessments: An Analysis of Exposure to Tetrachlorodibenzo-p-Dioxin from a Beef Consumption Pathway

Indirect exposures to 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) and other toxic materials released in incinerator emissions have been identified as a significant concern for human health. As a result, regulatory agencies and researchers have developed specific approaches for evaluating exposures from indirect pathways. This paper presents a quantitative assessment of the effect of uncertainty and variation in exposure parameters on the resulting estimates of TCDD dose rates received by individuals indirectly exposed to incinerator emissions through the consumption of home-grown beef. The assessment uses a nested Monte Carlo model that separately characterizes uncertainty and variation in dose rate estimates. Uncertainty resulting from limited data on the fate and transport of TCDD are evaluated, and variations in estimated dose rates in the exposed population that result from location-specific parameters and individuals'behaviors are characterized. The analysis indicates that lifetime average daily dose rates for individuals living within 10 km of a hypothetical incinerator range over three orders of magnitude. In contrast, the uncertainty in the dose rate distribution appears to vary by less than one order of magnitude, based on the sources of uncertainty included in this analysis. Current guidance for predicting exposures from indirect exposure pathways was found to overestimate the intakes for typical and high-end individuals.     

Quantitative Cancer Risk Estimation for Formaldehyde

Of primary concern are irreversible effects, such as cancer induction, that formaldehyde exposure could have on human health. Dose-response data from human exposure situations would provide the most solid foundation for risk assessment, avoiding problematic extrapolations from the health effects seen in nonhuman species. However, epidemiologic studies of human formaldehyde exposure have provided little definitive information regarding dose-response. Reliance must consequently be placed on laboratory animal evidence. An impressive array of data points to significantly nonlinear relationships between rodent tumor incidence and administered dose, and between target tissue dose and administered dose (the latter for both rodents and Rhesus monkeys) following exposure to formaldehyde by inhalation. Disproportionately less formaldehyde binds covalently to the DNA of nasal respiratory epithelium at low than at high airborne concentrations. Use of this internal measure of delivered dose in analyses of rodent bioassay nasal tumor response yields multistage model estimates of low-dose risk, both point and upper bound, that are lower than equivalent estimates based upon airborne formaldehyde concentration. In addition, risk estimates obtained for Rhesus monkeys appear at least 10-fold lower than corresponding estimates for identically exposed Fischer-344 rats.     

An Analysis of the Uncertainties in Estimates of Radon-Induced Lung Cancer

A recent report by the National Academy of Sciences estimates that the radiation dose to the bronchial epithelium, per working level month (WLM) of radon daughter exposure, is about 30% lower for residential exposures than for exposures received in underground mines. Adjusting the previously published BEIR IV radon risk model accordingly, the unit risk for indoor exposures of the general population is about 2.2 x 10(-4) lung cancer deaths (lcd)/WLM. Using results from EPA's National Residential Radon Survey, the average radon level is estimated to be about 1.25 pCi/L, and the annual average exposure about 0.242 WLM. Based on these estimates, 13,600 radon-induced lcd/yr are projected for the United States. A quantitative uncertainty analysis was performed, which considers: statistical uncertainties in the epidemiological studies of radon-exposed miners; the dependence of risk on age at, and time since, exposure; the extrapolation of risk estimates from mines to homes based on comparative dosimetry; and uncertainties in the radon daughter levels in homes and in the average residential occupancy. Based on this assessment of the uncertainties in the unit risk and exposure estimates, an uncertainty range of 7000-30000 lcd/yr is derived.     

Potential Health Effects of Light-Duty Diesel Exhaust

The purpose of this paper is to review briefly the evidence for potential human health effects that may result from increased dieselization of the nation's light-duty vehicle fleet. An effort is made to put the potential effects into perspective, both with regard to projected excess cancer deaths, should diesel exhaust be carcinogenic to humans, and in relation to past use of vehicles using leaded gasoline. Certain related research needs are highlighted. Available data concerning the relationship between diesel emissions, ambient air quality, and human health are summarized. On the basis of exposure estimates and relative potency factors, the authors conclude that the best estimate of the number of excess annual U.S. lung cancer deaths as a result of lifetime exposure to light-duty diesel particulate under 1990 conditions is between 80 and 1500. Available data suggest that the carcinogenic hazard of exhaust from vehicles burning leaded gasoline may be an order of magnitude greater, on a per mile basis, than that of diesel engines. The hazard of emissions from diesel are, in turn, probably an order of magnitude greater than that of gasoline engines with catalytic converters burning unleaded gasoline. Important research needs identified by the authors include determining whether diesel exhaust is in fact a human carcinogen, studying the effect of atmospheric chemical transformation of organics in diesel exhaust on the toxicity of the exhaust, making a better determination of the relative carcinogenicity of diesel and gasoline exhausts, and determining whether exposure to diesel exhaust contributes to the development or exacerbation of chronic lung disease or of respiratory illness, especially in the very young and the aged.     

Integrated Uncertainty Analysis for Ambient Pollutant Health Risk Assessment: A Case Study of Ozone Mortality Risk

The U.S. Environmental Protection Agency (EPA) uses health risk assessment to help inform its decisions in setting national ambient air quality standards (NAAQS). EPA's standard approach is to make epidemiologically‐based risk estimates based on a single statistical model selected from the scientific literature, called the “core” model. The uncertainty presented for “core” risk estimates reflects only the statistical uncertainty associated with that one model's concentration‐response function parameter estimate(s). However, epidemiologically‐based risk estimates are also subject to “model uncertainty,” which is a lack of knowledge about which of many plausible model specifications and data sets best reflects the true relationship between health and ambient pollutant concentrations. In 2002, a National Academies of Sciences (NAS) committee recommended that model uncertainty be integrated into EPA's standard risk analysis approach. This article discusses how model uncertainty can be taken into account with an integrated uncertainty analysis (IUA) of health risk estimates. It provides an illustrative numerical example based on risk of premature death from respiratory mortality due to long‐term exposures to ambient ozone, which is a health risk considered in the 2015 ozone NAAQS decision. This example demonstrates that use of IUA to quantitatively incorporate key model uncertainties into risk estimates produces a substantially altered understanding of the potential public health gain of a NAAQS policy decision, and that IUA can also produce more helpful insights to guide that decision, such as evidence of decreasing incremental health gains from progressive tightening of a NAAQS.