EPA Risk Assessment Research Articles

The U.S. Environmental Protection Agency's assessment of risks from indoor radon.

The U.S. Environmental Protection Agency has updated its assessment of health risks from indoor radon, which has been determined to be the second leading cause of lung cancer after cigarette smoking. This risk assessment is based primarily on results from a recent study of radon health effects (BEIR VI) by the National Academy of Sciences. In BEIR VI, the National Academy of Sciences fit empirical risk models to data from 11 cohorts of miners, and estimated that each year about 20,000 lung cancer deaths in the U.S. are radon related. A summary, abstracted from the technical report, is given of the EPA's risk assessment results and methods, including some modifications and extensions to the approach used in BEIR VI. Results include numerical estimates of lung cancer deaths per unit exposure, which had not been provided in BEIR VI.

Toxic metals in sewage sludge-amended soils: has promotion of beneficial use discounted the risks?

Land application of contaminated waste products has been defended as beneficial use by some scientists and regulators, based on the premise that the behavior of any toxins accumulated in soils from this practice is reasonably well understood and will not have detrimental agronomic or environmental impacts into the foreseeable future. In this review, I use the case of toxic metals in sewage sludges applied to agricultural land to illustrate that metal behavior in soils and plant uptake is difficult to generalize because it is strongly dependent on the nature of the metal, sludge, soil properties and crop. Nevertheless, permitted agricultural loadings of toxic metals from sewage sludges are typically regulated using the sole criterion of total metal loading or concentrations in soils. Several critical generalizing assumptions about the behavior of sludge-borne metals in soil-crop systems, built into the US EPA risk assessment for metals, have tended to underestimate risks and are shown not to be well justified by published research. It is argued that, in the absence of a basic understanding of metal behavior in each specific situation, a more precautionary approach to toxic metal additions to soils is warranted.

Untreated abandoned mercury mining works in a scenic area of Asturias (Spain)

Mercury mining was a large and thriving industry during the last century in Asturias (NW Spain). At Brañalamosa, mining activity introduced significant quantities of wastes in spoil heaps located close to the mining operations. In these mining wastes, in addition to mercury, high concentrations of other potentially dangerous elements like As have been found. As a consequence, pollution and dereliction of the local environment occurred. This paper focuses on the environmental impact of these old mining operations and describes a preliminary assessment of the extent of contamination. This includes analytical data from systematic sampling of soils, stream sediments, wastes from spoil heaps, water and herbaceous plants in areas affected by mining activities. The potential risk that spoil materials imply for human health and the environment is documented on the basis of the application of EPA Risk Assessment methodology.

The Market Value of Reducing Cancer Risk: Hedonic Housing Prices with Changing Information

1. Introduction Market evidence on the value of a statistical life invariably consists of cross-sectional evidence on risks and prices or wages at a point in time. If information about the level of risk changes over time and people incorporate this information in a rational manner, there will be a corresponding price response. On the basis of these temporal changes, one can estimate the market price-risk tradeoff, eliminating many confounding time-invariant effects that cannot be controlled for using cross-sectional data. This paper examines the market response to the release of government information about the level of risk at hazardous waste sites and provides insight into the rationality of this response. Studies based on experimental evidence and survey data often find that individual beliefs may deviate from objective risk levels.1 People often overestimate highly publicized risks and mortality risks. In the case of hazardous waste risks, bias in risk beliefs often leads to considerable public reaction and pressure for site cleanups, which may be an inefficient outcome. By using market data, one can examine whether this intense public reaction carries over to contexts in which private money is at stake. Government agencies frequently use information provision as a regulatory device, particularly since the advent of the right-to-know movement of the 1980s. Examples of information provision efforts include the Food and Drug Administration's requirement that many prescription drugs indude information inserts, the Department of Housing and Urban Development's requirement that sellers of houses built before 1950 inform buyers about the presence of lead-based paints, and the Environmental Protection Agency's (EPA) requirement that manufacturing facilities report their annual releases of chemicals above a threshold amount for a list of over 600 substances. Such regulations imply a belief that citizens can learn from information about risk and rationally adjust their prior beliefs towards the objective risk level in light of the information. This article provides market evidence to bolster the results of some survey studies of information transfer that suggest that individuals revise their risk beliefs in response to new information.2 The U.S. federal policy dealing with hazardous waste sites is known as the Superfund program. The most hazardous sites are targeted for cleanup and placed on a government priority roster called the National Priorities List (NPL). Extension of the classic theory of compensating differentials to the housing market implies that environmental disamenities (such as hazardous waste sites) will reduce housing prices (Rosen 1974). The negative impact of hazardous waste sites on the housing prices of nearby residences is well documented. For example, in a previous study (Gayer, Hamilton, and Viscusi 2000), we used an analysis that focused on the sale of 16,928 houses from 1988 to 1993 that surround Superfund sites in Greater Grand Rapids, Michigan. We found that before the EPA released its risk report, a reduction in the cancer risk from neighborhood Superfund sites by the mean level of risk would increase the average value of a house by $238 (in 1996 dollars).3 To estimate this willingness of residents to pay to avoid cancer risks before the release of the EPA's risk report, we assumed that residents' prior beliefs were equal to the objectively measured risks suggested by the report. Thus, this analysis was based on the very strong informational assumption that residents could, in effect, predict the results of the EPA's site-specific risk assessments. Before the release of the report, the price-risk tradeoff implied a value of a statistical cancer case of $51 million. Once the EPA released its risk information, the implied value of a statistical cancer case was $4 million. These results suggest that after the release of the EPA's risk report, revealed preferences for avoiding Superfund risks were consistent with surveys of the value of a statistical life in the labor market. …

Physical injury risks associated with drinking water arsenic treatment.

We estimated the number of transportation deaths that would be associated with water treatment in Albuquerque to meet the EPA's recently proposed revisions of the Maximum Contaminant Level (MCL) for arsenic. Vehicle mileage was estimated for ion exchange, activated alumina, and iron coagulation/microfiltration water treatment processes to meet an MCL of 0.020 mg/L, 0.010 mg/L, 0.005 mg/L, and 0.003 mg/L. Local crash, injury, and death rates per million vehicle miles were used to estimate the number of injuries and deaths. Depending on the water treatment options chosen, we estimate that meeting an arsenic MCL of 0.005 mg/L will result in 143 to 237 crashes, 58 to 98 injuries, and 0.6 to 2.6 deaths in Albuquerque over a 70-year period, resulting in 26 to 113 years of life lost. The anticipated health benefits for Albuquerque residents from a 0.005 mg/L arsenic MCL, estimated using either a multistage Weibull or Poisson model, ranged from 3 to 80 arsenic-related bladder and lung cancer deaths prevented over a 70-year period, adding between 43 and 1,123 years of life. Whether a revised arsenic MCL increases or reduces overall loss of life in Albuquerque depends on the accuracy of EPA's cancer risk assessment. If the multistage Weibull model accurately estimates the benefits, the years of life added is comparable or lower than the anticipated years lost due to transportation associated with the delivery of chemicals, disposal of treatment waste, and operation of the water treatment system. Coagulation/microfiltration treatment will result in substantially fewer transportation deaths than either ion exchange or activated alumina.

Growing food crops on sludge‐amended soils: Problems with the U.S. Environmental Protection Agency method of estimating toxic metal transfer

AbstractThe use of sewage sludges as farm fertilizers, encouraged in recent years by changes in U.S. Environmental Protection Agency (U.S. EPA) policy, has raised concerns among some scientists regarding food safety and long‐term soil productivity. The U.S. EPA risk assessment for entry into the human diet of three of the most toxic metals, cadmium (Cd), mercury (Hg), and lead (Pb), utilized uptake coefficients (UCs) to calculate the amount of each metal that could enter food crops from the soil. Each UC was calculated as the increment of metal concentration in the edible part of the crop per unit increase of metal loading to the soil. However, the final UC estimates employed in the risk assessment are biased toward low values by a number of factors. These include the use of geometric means to obtain single‐point averages of UCs for each crop group evaluated, rather than using arithmetic means or probabilistic methods, a systematic analytical or contamination error apparent in the reported metal concentrations of the control crops, and the fact that most of the UC values were derived for soils with pH 6 or higher. For more than 50% of all the soil and cropping conditions represented in the risk assessment, the geometrically averaged Cd UC values used by the U.S. EPA underestimated the actual risk posed by uptake into crops. The UC values for Pb and Hg are uncertain because of analytical or contamination errors, and because of the few data available for a number of crops. These uncertainties and biases in the risk assessment would advise a more cautious approach to agricultural and home garden use of sewage sludge than is permitted by the U.S. EPA 503 rule.

Assessing Risk of Inorganic Arsenic in Drinking Water in the United States

Limitations of the current EPA risk assessment for inorganic arsenic in drinking water in the U.S. are discussed. An empirical approach is suggested that would sample survey the populations in regions with the highest arsenic levels in drinking water for signs of arsenicism, which has been much more prevalent and appeared much earlier in exposed populations than cancer (e.g., of the skin). Biomarkers of exposure, such as arsenic content in urine, nails, hair, and skin scales, may provide even earlier indications of subpopulations with excessive arsenic exposure and identify individuals at risk. Further study is needed to evaluate fully the potential for use of biomarkers, focusing on the accuracy and reliability of analytical methods, the utility of biomarkers as indicators of short-term and long-term exposure and as precursors to clinical signs of arsenicism, and the use of “normal” ranges of biomarkers for interpretation of field observations.

Recent developments in the investigation of thyroid regulation and thyroid carcinogenesis.

This review covers new mechanistic information spanning the past 10 years relevant to normal and abnormal thyroid growth and function that may assist in the risk assessment of chemicals inducing thyroid follicular cell neoplasia. Recent studies have shown that thyroid regulation occurs via a complex interactive network mediated through several different messenger systems. Increased thyroid-stimulating hormone (TSH) levels activate the signal transduction pathways to stimulate growth and differentiation of the follicular cell. The important role of TSH in growth as well as in function helps to explain how disruptions in the thyroid-pituitary axis may influence thyroid neoplasia in rodents. New investigations that couple mechanistic studies with information from animal cancer bioassays (e. g., sulfamethazine studies) confirm the linkage between prolonged disruption of the thyroid-pituitary axis and thyroid neoplasia. New initiation/promotion studies in rodents also support the concept that chronic stimulation of the thyroid induced by goitrogens can result in thyroid tumors. Some of these studies confirm previous suggestions regarding the importance of chemically induced thyroid peroxidase inhibition and the inhibition of 3,3',5, 5'-tetraiodothyronine (T4, thyroxine) deiodinases on disruption of the thyroid-pituitary axis leading to thyroid neoplasia. Some comparative physiologic and mechanistic data highlight certain differences between rodents and humans that could be expected to confer an increased vulnerability of rodents to chronic hypersecretion of TSH. New data from epidemiologic and molecular genetic studies in humans contribute further to an understanding of thyroid neoplasia. Acute exposure to ionizing radiation, especially in childhood, remains the only verified cause of thyroid carcinogenesis in humans. Iodine deficiency studies as a whole remain inconclusive, even though several new studies in humans examine the role of dietary iodine deficiency in thyroid cancer. Specific alterations in gene expression have been identified in human thyroid neoplasia, linked to tumor phenotype, and thus oncogene activation and tumor-suppressor gene inactivation may also be factors in the development and progression of thyroid cancer in humans. An analysis by the U.S. EPA Risk Assessment Forum, prepared as a draft report in 1988 and completed in 1997, focused on the use of a threshold for risk assessment of thyroid follicular tumors. New studies, involving several chemicals, provide further support that there will be no antithyroid activity until critical intracellular concentrations are reached. Thus, for chemically induced thyroid neoplasia linked to disruptions in the thyroid-pituitary axis, a practical threshold for thyroid cancer would be expected. More information on thyroid autoregulation, the role of oncogene mutations and growth factors, and studies directly linking persistently high TSH levels with the sequential cellular development of thyroid follicular cell neoplasia would provide further confirmation.

A Native American exposure scenario.

EPA's Risk Assessment Guidance for Superfund (RAGS) and later documents provide guidance for estimating exposures received from suburban and agricultural activity patterns and lifestyles. However, these methods are not suitable for typical tribal communities whose members pursue, at least in part, traditional lifestyles. These lifestyles are derived from a long association with all of the resources in a particular region. We interviewed 35 members of a Columbia River Basin tribe to develop a lifestyle-based subsistence exposure scenario that represents a midrange exposure that a traditional tribal member would receive. This scenario provides a way to partially satisfy Executive Order 12,898 on environmental justice, which requires a specific evaluation of impacts from federal actions to peoples with subsistence diets. Because a subsistence diet is only a portion of what is important to a traditional lifestyle, we also used information obtained from the interviews to identify parameters for evaluating impacts to environmental and sociocultural quality of life.

Cleanup levels for dioxin‐contaminated soils

AbstractEPA's use of a 1 part per billion (ppb) level for dioxin contamination in residential soils is shown to be too high and not protective of public health. It was derived in a 1984 cancer risk assessment by another federal agency, but it is inconsistent with risk‐based levels of 2 to 4 parts per trillion (ppt) obtained by using EPA's standard risk assessment methods. EPA has called the 1 ppb level a policy‐based level, which correctly distinguishes it from a risk or health‐based cleanup standard. The 1984 assessment is shown in this article to have considerable shortcomings. For over a decade, dioxins have been left in soils at levels posing health risks and sometimes at levels that EPA is legally required to address. Moreover, noncancer effects have been ignored, but recent work has shown them to support action at low ppt levels. To protect public health, be consistent with current scientific knowledge and other EPA policies, reduce confusion in the environmental management community, and be responsive to public demands for stringent dioxin cleanups, new EPA policy guidance for dioxin soil cleanups is needed, and key elements are presented in this article. In an ad hoc fashion, EPA Region 4 has recently used a 200 ppt dioxin cleanup level for residential soil, acknowledged to correspond to a one‐in‐ten‐thousand cancer risk, at two Superfund sites, which environmental professionals should be aware of. This suggests a shift in EPA policy.

Understanding Phytotoxicity Thresholds for Trace Elements in Land‐applied Sewage Sludge

AbstractSewage sludge contains trace elements. With repeated sludge applications as crop fertilizer, these trace elements may accumulate in the soil to phytotoxic concentrations. My objective was to assess the scientific basis for the current cumulative loading limits for Cu, Ni, and Zn in land‐applied sewage sludge. An overview of the USEPA's phytotoxicity risk assessment, the basis for these loading limits, was presented, discussed, and compared in the context of the underlying principles of phytotoxicity thresholds. I concluded that EPA phytotoxicity thresholds in immature plants were arbitrarily selected, and extrapolations to field applications of sewage sludge were not substantiated. Variability in plant accumulation rates and soil sorption capacities of trace elements were not adequately considered in the EPA analysis. Because of the assumptions, simplifications, and extrapolations introduced into the phytotoxicity analysis, the final results, that is, EPA's cumulative loading limits for Cu, Ni, and Zn, are not substantiated by the analysis. The phytotoxicity analysis does not represent an appropriate application of underlying scientific principles. A more appropriate basis for regulating trace element applications in sewage sludge would reflect an understanding of site‐specific characteristics, possibly including concentration limits for trace elements in plant tissue, soil, and/or groundwater. Additional research would be required to substantiate EPA's conclusions about the cumulative pollutant loading limits, as derived from EPA's phytotoxicity risk assessment.

A Mechanistic Interpretation of the Oncogenicity of Chlorothalonil in Rodents and an Assessment of Human Relevance

Chronic dietary treatment of rodents with the fungicide chlorothalonil causes an increased incidence of papillomas and carcinomas of the forestomach squamous epithelium (rats and mice, both sexes) and adenomas and carcinomas of the renal proximal tubule epithelium (rats, both sexes; mice, males only); the product elicits no tumorigenic response in dogs. As a result, chlorothalonil is classified by EPA as a Group B2 “probable human carcinogen.” However, chlorothalonil is not genotoxic and there is strong evidence that both the forestomach and renal tumors observed in rodents result from cytotoxicity followed by compensatory cell proliferation and hyperplasia. In the case of the forestomach, cytotoxicity results from sustained irritation of the squamous epithelium by chlorothalonil leading to inflammation, ulceration, and restorative hyperplasia. Cytotoxicity in the renal tubular epithelium is associated with formation of di- and trithiols that arise through the action of renal β-lyase on cysteine S-conjugates derived from the corresponding glutathione conjugates of chlorothalonil. Renal cytotoxicity and cell necrosis in rodents result from the ability of the di- and trithiols to inhibit kidney mitochondrial respiration and disrupt cellular integrity. There is strong evidence that this mechanism is not operative in other species such as dogs and monkeys. The progression from cytotoxicity to hyperplasia to neoplasia is becoming increasingly well-recognized as a threshold-based mechanism of carcinogenesis. Unless exposure is excessively prolonged or intense, the cytotoxic effects will be fully reversible. Furthermore, the effects observed in rodents are not appropriate for evaluating the potential human cancer risk from chlorothalonil. Humans do not possess an organ equivalent to the rodent forestomach and the rat is a poor model for evaluating potential human risk for the renal tumorigenicity of chlorothalonil. Humans are likely to be very much less sensitive than rats to the nephrotoxic effects of chlorothalonil. In view of the fact that the tumorigenic effects of chlorothalonil are mediated through a well-understood, nongenotoxic, threshold-based mechanisms of little or no relevance to humans, chlorothalonil should be a prime candidate for re-review under EPA's new risk assessment guidelines. Expert committees in both Europe and Canada have concluded that human risks to chlorothalonil should be evaluated by means of the NOEL/safety factor approach usually employed for noncarcinogenic materials.

Use of genetic toxicology data in U.S. EPA risk assessment: the mercury study report as an example.

Assessment of human health risks of environmental agents has often been limited to consideration of the potential for the agent to cause cancer or general systemic toxicity after long-term exposure. The U.S. Environmental Protection Agency (U.S. EPA) is increasingly moving toward the development of integrated assessments, which consider all potential health end points including developmental toxicity, neurotoxicity, immunotoxicity, reproductive effects, and germ cell mutagenicity. The U.S. EPA has a responsibility to assess risks to nonhuman species or ecosystems when appropriate data are available. An example of a recent integrated human health and ecological risk assessment can be found in the U.S. EPA Mercury Study Report to Congress. This report covers the following topics in separate volumes: an inventory of anthropogenic mercury emissions in the United States; an exposure assessment using measured and predicted values and including indirect dietary exposure; an evaluation of human health risks; an assessment of ecologic risk wherein water criteria are presented for several wildlife species; an overall integrated characterization of human and nonhuman risk; and a discussion of risk management considerations. In the evaluation of human health risk, genetic toxicology data were considered for three forms of mercury: elemental, inorganic (divalent), and methylmercury. These data were used in judgments of two types of potential health effects (carcinogenicity and germ cell mutagenicity). In assessment of potential carcinogenicity of inorganic and methylmercury, genetic toxicity data were key. Data for clastogenicity in the absence of mutagenicity supported the characterization of inorganic and methylmercury as materials that produce carcinogenic effects only at high, toxic doses. The evidence for clastogenicity, coupled with information on metabolism and distribution, resulted in a judgment of a moderate degree of concern (or weight of evidence) that inorganic mercury can act as a human germ cell mutagen. For methylmercury, the degree of concern for germ cell mutagenicity is high.

Use of Genetic Toxicology Data in U.S. EPA Risk Assessment: The Mercury Study Report as an Example

Use of Genetic Toxicology Data in U.S. EPA Risk Assessment: The Mercury Study Report as an Example

Developmental Toxicity Risk Assessment: Consensus Building, Hypothesis Formulation, and Focused Research

Risk assessment for developmental toxicity has become more defined over the last decade and the most recent EPA guidelines for developmental toxicity risk assessment were published in 1991. Development of approaches for risk assessment in this area have relied on building of consensus opinion among experts about the interpretation of developmental toxicity data. These discussions have aided in strengthening the scientific basis for risk assessment for developmental toxicity, including the default assumptions that must be used when more complete information on mechanisms of action and pharmacokinetics are unavailable. Such discussions continue on both a national and international basis. The EPA risk assessment guidelines outlined several major areas of research needed to strengthen risk assessment for developmental toxicity and led to the formulation of hypotheses to be tested in focused research projects. Several major research efforts have focused on dose-related mechanisms and biologically based modeling of specific agents, physiologically based pharmacokinetic models of pregnancy that can be scaled across species, and the influence of dose and duration of exposure on developmental outcomes, as well as the delineation of specific biomarkers of adverse developmental effects. Although such research initiatives will require a long-term effort, it is important that attention be focused now on those approaches that can improve the risk assessment process to avoid continued reliance on default approaches that have been used for the past 30 years or more. The impact of the EPA Guidelines for Developmental Toxicity Risk Assessment has been widespread. One of the main purposes for developing risk assessment guidelines by EPA was to communicate procedures to risk assessors inside the agency in an effort to promote consistency. In addition, the guidelines were to communicate to those outside the agency in private industry and other regulatory agencies how EPA would evaluate and interpret data. The developmental toxicity guidelines have standardized terminology used in developmental toxicity risk assessments. They also have influenced the revision of testing guidelines and the writing of new guidelines, such as the developmental neurotoxicity testing guidelines. More extensive use of developmental toxicity data within the RfD/RfC process was influenced by the guidelines, as well. More recently, the risk assessment guidelines have had a major impact on the harmonization of international testing and risk assessment guidelines through cooperative efforts with the World Health Organization under the auspices of the International Program on Chemical Safety (IPCS) and the Organization for Economic Cooperation and Development (OECD). We foresee these types of interagency and international cooperative efforts continuing as we attempt to make more efficient use of the limited resources available for testing, risk assessment, and research to better understand and prevent developmental toxicity.

Mercury in soils and crops from fields receiving high cumulative sewage sludge applications: Validation of U. S. EPA's risk assessment for human ingestion

Mercury in soils and crops from fields receiving high cumulative sewage sludge applications: Validation of U. S. EPA's risk assessment for human ingestion

More regulation of dioxin sources sought

Two national groups representing health professionals and environmental activists have called for a national prevention- oriented policy to reduce exposure to dioxin and dioxinlike compounds. Physicians for Social Responsibility (PSR) and the Environmental Defense Fund (EDF) made their plea in a newly released policy document, Putting a Lid on Dioxins. The policy document is in response to, and in anticipation of, the Environmental Protection Agency's dioxin risk assessment, scheduled for official release in the next few months. Part of EPA's risk assessment was prematurely leaked to the media, spawning a great deal of attention (C&EN, May 30, page 13). America has only a patchwork of regulations controlling sources of dioxin emissions, says David P. Rail, a board member of PSR and EDF and former director of the National Institute of Environmental Health Sciences, part of the National Institutes of Health. EPA needs to play a stronger leadership role in preventing the entry of dioxins into ...

Hazardous waste storage, disposal, remediation, and closure

Hazardous waste storage, disposal, remediation, and closure

Assessing Health Risks Associated with DDT Residues in Soils in California: A Proposition 65 Case Study

Population growth in California has increased the pressure to convert agricultural land to commercial, industrial, or residential uses. In the ensuing property transactions, buyers and sellers must address the presence of toxic materials in soils such as pesticides, several of which are known to the State of California to cause cancer under Proposition 65. While this statute does not specifically address soil contaminants, the potential scope of its enforcement is sufficiently broad that owners of former agricultural properties may be obliged to provide warning of exposure to potential buyers, occupants, or construction workers about exposure to residues in soil from pesticide applications. However, Proposition 65 provides no guidance on how to assess exposures to chemicals in soil. The U.S. EPA Risk Assessment Guidance for Superfund (RAGS) provides a method for assessing soil-related exposure pathways that is consistent with the intent of Proposition 65. Using this approach, we have calculated the lifetime average concentrations of DDT in soil corresponding to the no-significant-risk level stipulated under Proposition 65 (1 x 10(-5)) for a hypothetical residential exposure scenario. The concentration of DDT in soil corresponding to a no-significant-risk ranges from 7.9-18.8 mg/kg, depending upon which exposure pathways are deemed to be complete for residential land use. It is argued that Proposition 65 forces the assessment and possible cleanup of such a situation through the threat of creating a health risk perception that could affect the market value of a property.

Ground Water Modeling for Risk Assessment Purposes: Use of a Gaussian‐Distributed Transport Model and a Batch Flush Model

AbstractSeveral state regulatory agencies require that risk assessments be performed at contaminated sites to quantify the contaminant levels that may reach the nearest receptors and to evaluate the health risks associated with exposure to such contaminant levels. Petroleum retail facilities with leaking underground storage tanks are prime examples of sites where risk assessments may be required. Ground water modeling is often necessary when evaluating future completed exposure pathways associated with dissolved contaminants. If the aquifer conditions are relatively homogeneous, analytical contaminant transport models may be used in place of complex numerical models. A two‐dimensional, Gaussian‐distributed boundary condition transport model and a batch flush model may be combined to simulate contaminant transport with linear equilibrium adsorption/desorption and biodegradation effects, This enables a relatively rapid and cost‐effective prediction of contaminant levels at sensitive downgradient receptors. The predicted contaminant levels may then be evaluated through an exposure assessment, toxicity assessment, and risk characterization in accordance with U.S. EPA risk assessment protocols.A case study was presented for a gasoline station with a leaking underground storage tank system. The two‐dimensional, Gaussian‐distributed transport model and batch flush model were used to predict dissolved phase contaminant concentration profiles at a downgradient drinking water well. The predicted contaminant concentrations were subsequently converted to chronic daily intakes which were evaluated in terms of toxicity. Reasonable maximum exposures were developed for both carcinogens and non‐carcinogens. The results of the risk assessment indicated that there were no unacceptable risks posed by the residual ground water contamination at the site. This led to the recommendation that the project be closed out in the absence of a demonstrated need for active ground water remediation. The State Water Control Board concurred with the recommendation.