Unit Risk Values Research Articles

A Simplified Method for the Risk Analysis of Protection Against Lightning: Theory and a Case Study

Lightning strikes can cause physical harm to people and damage inside commercial, industrial, and residential structures. The risk of damage from lightning depends on the dimensional and environmental characteristics of the structure, the number of people and their permanence in the structure, their reaction to a possible fire, and the density of lightning strikes to the ground in the structure location. The assessment of the prospected risk determines the need for protective measures if it is higher than the tolerable value. The standard IEC/EN 62305-2 proposes a method to calculate the probable average annual loss in a structure due to lightning flashes. Since the standard is oriented toward analyzing the greatest number of types of structures, the analysis is complex and laborious because of the multitude of parameters to be used. The aim of this article is to facilitate an easy understanding of the basic parameters to consider and to introduce an analysis aimed at typical cases of buildings in urban environments to simplify the International Electrotechnical Commission (IEC)/EN method. We introduce an effective parameter: the per unit (p.u.) risk value related to the tolerable risk. The applications of the suggested simplified formulas to real cases have provided results that absolutely coincide with the values calculated by applying the IEC/EN formulas. Table 1 list the symbols used in this article.

Use of Biomarker Data and Relative Potencies of Mutagenic Metabolites to Support Derivation of Cancer Unit Risk Values for 1,3-Butadiene from Rodent Tumor Data.

Unit Risk (UR) values were derived for 1,3-butadiene (BD) based upon its ability to cause tumors in laboratory mice and rats. Metabolism has been established as the significant molecular initiating event of BD’s carcinogenicity. The large quantitative species differences in the metabolism of BD and potency of critical BD epoxide metabolites must be accounted for when rodent toxicity responses are extrapolated to humans. Previously published methods were extended and applied to cancer risk assessments to account for species differences in metabolism, as well as differences in mutagenic potency of BD metabolites within the context of data-derived adjustment factors (DDEFs). This approach made use of biomarker data (hemoglobin adducts) to quantify species differences in the internal doses of BD metabolites experienced in mice, rats, and humans. Using these methods, the dose–response relationships in mice and rats exhibit improved concordance, and result in upper bound UR values ranging from 2.1 × 10−5 to 1.2 × 10−3 ppm−1 for BD. Confidence in these UR values was considered high based on high confidence in the key studies, medium-to-high confidence in the toxicity database, high confidence in the estimates of internal dose, and high confidence in the dose–response modeling.

NOA Air-Quality Lessons Learned During Calaveras Dam Replacement Project

ABSTRACT The Calaveras Dam Replacement Project (CDRP) pioneered technical approaches for addressing community exposure to naturally occurring asbestos (NOA) via the inhalation pathway. Over the course of the CDRP, approaches were developed for key issues, including determining the NOA particles of interest, defining the toxicity limits to apply to various types of NOA particles, establishing dust control, and creating appropriate feedback loops for using laboratory data. Specific issues of interest included whether to count only structures above a certain length and the inhalation unit risk value to use for amphiboles. The knowledge gained on the CDRP can and is being used to optimize NOA evaluation and control at other, similar projects.

Ethylene Oxide: Cancer Evidence Integration and Dose-Response Implications.

The International Agency for Research on Cancer (IARC) and the United States Environmental Protection Agency (USEPA) classified ethylene oxide (EtO) as a known human carcinogen. Critically, both noted that the epidemiological evidence based on lymphoid and breast cancers was “limited,” but that the evidence in animal studies was “sufficient” and “extensive” (respectively) and that EtO is genotoxic. The USEPA derived one of the highest published inhalation unit risk (IUR) values (3 × 10−3 per [µg/m3 EtO]), based on results from 2 epidemiological studies. We performed focused reviews of the epidemiological and toxicological evidence on the carcinogenicity of EtO and considered the USEPA’s reliance on a genotoxic mode of action to establish EtO’s carcinogenicity and to determine likely dose–response patterns. Higher quality epidemiological studies demonstrated no increased risk of breast cancers or lymphohematopoietic malignancies (LHM). Similarly, toxicological studies and studies of early effect biomarkers in animals and humans provided no strong indication that EtO causes LHM or mammary cancers. Ultimately, animal data are inadequate to define the actual dose–response shape or predict tumor response at very low doses with any confidence. We conclude that the IARC and USEPA classification of EtO as a known human carcinogen overstates the underlying evidence and that the IUR derived by USEPA grossly overestimates risk.

Peak Exposures in Epidemiologic Studies and Cancer Risks: Considerations for Regulatory Risk Assessment.

We review approaches for characterizing “peak” exposures in epidemiologic studies and methods for incorporating peak exposure metrics in dose–response assessments that contribute to risk assessment. The focus was on potential etiologic relations between environmental chemical exposures and cancer risks. We searched the epidemiologic literature on environmental chemicals classified as carcinogens in which cancer risks were described in relation to “peak” exposures. These articles were evaluated to identify some of the challenges associated with defining and describing cancer risks in relation to peak exposures. We found that definitions of peak exposure varied considerably across studies. Of nine chemical agents included in our review of peak exposure, six had epidemiologic data used by the U.S. Environmental Protection Agency (US EPA) in dose–response assessments to derive inhalation unit risk values. These were benzene, formaldehyde, styrene, trichloroethylene, acrylonitrile, and ethylene oxide. All derived unit risks relied on cumulative exposure for dose–response estimation and none, to our knowledge, considered peak exposure metrics. This is not surprising, given the historical linear no‐threshold default model (generally based on cumulative exposure) used in regulatory risk assessments. With newly proposed US EPA rule language, fuller consideration of alternative exposure and dose–response metrics will be supported. “Peak” exposure has not been consistently defined and rarely has been evaluated in epidemiologic studies of cancer risks. We recommend developing uniform definitions of “peak” exposure to facilitate fuller evaluation of dose response for environmental chemicals and cancer risks, especially where mechanistic understanding indicates that the dose response is unlikely linear and that short‐term high‐intensity exposures increase risk.

Evaluation of hazardous airborne carbonyls in five urban roadside dwellings: A comprehensive indoor air assessment in Sri Lanka

Indoor hazardous airborne carbonyls were quantified in five natural-ventilated roadside dwellings in Colombo, Sri Lanka. The total concentrations of all targeted carbonyls ranged from 13.6 to 18.6 μg/m3. Formaldehyde (C1) was the most abundant carbonyl, followed by acetaldehyde (C2) and acetone (C3K). The concentrations of C1 and C2 ranged from 3.3 to 8.5 μg/m3 and 2.3 to 4.4 μg/m3, respectively, which accounted for 23 to 42% and 18 to 26% respectively, to the total quantified carbonyls. The highest carbonyls levels were obtained in the dwelling located in an urban district with a mixture of industrial, commercial and residential areas. Much lower concentrations of carbonyls were measured in a light local traffic value was counted. Moderate correlations between individual combustion markers from vehicular emissions suggest the strong impacts from traffics to the indoor airs. The concentrations of C1 and C2 were compared with international indoor guidelines established by different authorities. A health assessment was conducted by estimation of inhalation cancer risk, implementing the inhalation unit risk values provided by Integrated Risk Information System (IRIS), associated with C1 and C2, which were 6.2 × 10−5 and 7.7 × 10−6, respectively. Even though the risks did not reach the action level (1 × 10−4), their health impact should not be overlooked. This kick-off indoor monitoring study provides valuable scientific data to the environmental science community since only limit data is available in Sri Lanka.

The need for transparency and reproducibility in documenting values for regulatory decision making and evaluating causality: The example of formaldehyde

Reproducibility and transparency in scientific reporting is paramount to advancing science and providing the foundation required for sound regulation. Recent examples demonstrate that pivotal scientific findings cannot be replicated, due to poor documentation or methodological bias, sparking debate across scientific and regulatory communities. However, there is general agreement that improvements in communicating and documenting research and risk assessment methods are needed. In the case of formaldehyde, the peer-review conducted by a National Academy of Sciences (NAS) Committee questioned the approaches used by the Integrated Risk Information System (IRIS) in developing draft unit risk values. Using the original data from the key study (Beane Freeman et al., 2009) and documentation provided in the draft IRIS profile, we attempted to duplicate the reported inhalation unit risk values and address the NAS Committee's questions regarding application of the appropriate dose-response model. Overall, documentation of the methods lacked sufficient detail to allow for replication of the unit risk estimates, specifically for Hodgkin lymphoma and leukemias, the key systemic endpoints selected by IRIS. The lack of apparent exposure-response relationships for selected endpoints raises the question whether quantitative analyses are appropriate for these endpoints, and if so, how results are to be interpreted.

Comparison of hydrofluorosilicic acid and pharmaceutical sodium fluoride as fluoridating agents—A cost–benefit analysis

Abstract Water fluoridation programs in the United States and other countries which have them use either sodium fluoride (NaF), hydrofluorosilicic acid (HFSA) or the sodium salt of that acid (NaSF), all technical grade chemicals to adjust the fluoride level in drinking water to about 0.7–1 mg/L. In this paper we estimate the comparative overall cost for U.S. society between using cheaper industrial grade HFSA as the principal fluoridating agent versus using more costly pharmaceutical grade (U.S. Pharmacopeia – USP) NaF. USP NaF is used in toothpaste. HFSA, a liquid, contains significant amounts of arsenic (As). HFSA and NaSF have been shown to leach lead (Pb) from water delivery plumbing, while NaF has been shown not to do so. The U.S. Environmental Protection Agency's (EPA) health-based drinking water standards for As and Pb are zero. Our focus was on comparing the social costs associated with the difference in numbers of cancer cases arising from As during use of HFSA as fluoridating agent versus substitution of USP grade NaF. We calculated the amount of As delivered to fluoridated water systems using each agent, and used EPA Unit Risk values for As to estimate the number of lung and bladder cancer cases associated with each. We used cost of cancer cases published by EPA to estimate cost of treating lung and bladder cancer cases. Commercial prices of HFSA and USP NaF were used to compare costs of using each to fluoridate. We then compared the total cost to our society for the use of HFSA versus USP NaF as fluoridating agent. The U.S. could save $1 billion to more than $5 billion/year by using USP NaF in place of HFSA while simultaneously mitigating the pain and suffering of citizens that result from use of the technical grade fluoridating agents. Other countries, such as Ireland, New Zealand, Canada and Australia that use technical grade fluoridating agents may realize similar benefits by making this change. Policy makers would have to confront the uneven distribution of costs and benefits across societies if this change were made.

Biological monitoring versus air monitoring strategies in assessing environmental–occupational exposure

Assessment of environmental and occupational exposure to chemicals can be performed with environmental monitoring (EM) and biological monitoring (BM). Biological monitoring was for a long time considered as a method complementary to environmental monitoring. At present this attitude is changing and in certain areas biological monitoring is applied as the method of choice for exposure and health-risk assessment. This paper examines advantages and disadvantages of those two approaches. In occupational settings environmental monitoring of exposure to VOCs seems to be superior to biological monitoring (possibility of simultaneous determination of components of mixtures, simple interpretation, possibility of evaluation of short-term exposure to local irritants). In the case of this group of compounds BM can be useful in selected cases such as evaluation of dermal absorption or efficiency of protective measures. In the case of metals both forms of monitoring can be used depending on the available methods for interpretation of results. BM of exposure may be considered as superior for evaluating the effects of exposure to lead, cadmium and mercury. However, quantitative evaluation of cancer risk after exposure to arsenic or chromium is possible only on the basis of determination in the air and the use of unit risk values. Both environmental and biological monitoring are useful for evaluation of occupational and environmental exposure to polycyclic aromatic hydrocarbons (PAHs). In certain areas such as evaluation of exposure to external tobacco smoking, cytostatic drugs, and pesticides, biological monitoring is the method of choice used for individual exposure assessment or tracing the trends of environmental exposure.

Health Risk Assessment of Personal Exposure to Volatile Organic Compounds in Tianjin, China

PP-29-009 Background/Aims: Exposure to volatile organic compounds (VOCs) can induce a range of adverse human health effects, and draw considerable concern in exposure science. To date, however, personal VOCs exposure and residential indoor and outdoor VOCs levels have not been characterized in the mainland of China, less is known about health risk of personal exposure to VOCs. Methods: In this study, a pilot study was conducted to assess personal exposure to VOCs, and US Environmental Protection Agencys unit risk value was used to assess the inhalation caner health risk. To assess uncertainty of health risk estimate, the Monte Carlo simulation and sensitivity analysis were implemented using Crystal Ball 7.2 software. Personal exposure to 10 VOCs was measured, and simultaneously compared with residential indoor and outdoor VOCs concentrations, workplace and vehicle microenvironment concentrations in Tianjin, China. All VOCs samples were collected using passive samplers for 5 days, and were analyzed using Gas Chromatograph-Mass Spectrometer. Results: As expected for most of the VOC, personal exposures were greater than residential Indoor concentrations, with the exception of carbon tetrachloride. Results of exposure assessment show modeled and measured concentrations are statistically lineally correlated for all VOCs (P < 0.01), except chloroform. According to the risk assessment results, benzene, chloroform, 1,3-Butadiene presented the highest cancer risks of 52, 21 per 1 million population based on personal exposure, respectively. The average cumulative cancer risk based on personal exposure was approximately 78 per million, followed by indoor exposure (57 per million). Conclusion: Accurate exposure estimates are critical inputs to risk assessment in evaluating the severity and probability of health impact. The combination of personal exposure monitoring and risk assessment would possibly reduce some of the current uncertainty associated with risk estimates.

A Comparative Study of Indoor VOC Exposures and Associated Cancer Risk in Four North American Cities

WS4-06 Abstract: Recent studies have shown that indoor exposures to volatile organic compounds (VOCs) can significantly contribute to cancer risk. Although indoor VOC levels may originate from outdoor sources, exposures to these compounds are typically controlled by emissions from numerous indoor sources, including building materials, floor and wall coverings, tobacco smoking, consumer products, and volatilization from indoor water use. Although a detailed source apportionment can be difficult in this context, the coincident collection of indoor, outdoor, and personal samples allows for a determination of the relative contribution of source location(s) for measured compounds. Studies that use these methodologies can be used to understand exposure pathways, set research priorities, and design interventions focused on risk reduction. We present the results from personal exposure studies conducted in 4 large North American cities: Boston, New York, Los Angeles, and Mexico City. These studies used personal, indoor, and outdoor air sampling methods to assess the relative contribution of indoor and outdoor sources to personal exposures. These exposure estimates were used to estimate cancer risk through inhalation using published unit risk values. Despite significant ambient sources in large urban areas, indoor VOC sources were shown to contribute a significant portion of cancer risk across these cities. Exposures that contributed significantly to this risk include: 1,4-dichlorobenzene, chloroform, and several aldehydes, particularly formaldehyde. For example, in both Los Angeles and New York, indoor sources of these compounds accounted for more than 40% of the total cancer risk based on personal exposures. These studies highlight the importance of indoor VOC sources as a contributor to health risk. This comparative analysis presents data on the dominant pathways of exposure, the magnitude of cancer risk from measured exposures, and the observed between-city differences that may shed light on controlling variables such as product types, product use patterns, and differences in housing stock.

A proposed methodology for selecting a trichloroethylene inhalation unit risk value for use in risk assessment

U.S. EPA’s 2001 draft assessment of trichloroethylene (TCE) toxicity reviews the existing human and animal data on TCE carcinogenicity and proposes a 20-fold range of cancer potency values for use in risk assessment. Each value in the range is derived from a different source of data, either animal bioassays or epidemiology studies, and thus the range does not represent a distribution which can be characterized by statistical parameters such as a mean or 95% confidence interval. The U.S. EPA suggests users choose a single slope factor from among those it describes as appropriate for the population of interest and mode of exposure, but little guidance is given for making this choice. We propose an approach for determining the most scientifically defensible carcinogenic inhalation unit risk estimate from the range of slope factors developed by U.S. EPA, one that relies on accepted principles for evaluating scientific studies. Based on these considerations, we identify the most appropriate interim unit risk for low-level inhalation exposure as 9 × 10 −7 per μg/m 3. This approach may have fairly broad utility if U.S. EPA elects to use a similar approach in future assessments of other chemicals.

Addressing Nonlinearity in the Exposure‐Response Relationship for a Genotoxic Carcinogen: Cancer Potency Estimates for Ethylene Oxide

Ethylene oxide (EO) has been identified as a carcinogen in laboratory animals. Although the precise mechanism of action is not known, tumors in animals exposed to EO are presumed to result from its genotoxicity. The overall weight of evidence for carcinogenicity from a large body of epidemiological data in the published literature remains limited. There is some evidence for an association between EO exposure and lympho/hematopoietic cancer mortality. Of these cancers, the evidence provided by two large cohorts with the longest follow-up is most consistent for leukemia. Together with what is known about human leukemia and EO at the molecular level, there is a body of evidence that supports a plausible mode of action for EO as a potential leukemogen. Based on a consideration of the mode of action, the events leading from EO exposure to the development of leukemia (and therefore risk) are expected to be proportional to the square of the dose. In support of this hypothesis, a quadratic dose-response model provided the best overall fit to the epidemiology data in the range of observation. Cancer dose-response assessments based on human and animal data are presented using three different assumptions for extrapolating to low doses: (1) risk is linearly proportionate to dose; (2) there is no appreciable risk at low doses (margin-of-exposure or reference dose approach); and (3) risk below the point of departure continues to be proportionate to the square of the dose. The weight of evidence for EO supports the use of a nonlinear assessment. Therefore, exposures to concentrations below 37 microg/m3 are not likely to pose an appreciable risk of leukemia in human populations. However, if quantitative estimates of risk at low doses are desired and the mode of action for EO is considered, these risks are best quantified using the quadratic estimates of cancer potency, which are approximately 3.2- to 32-fold lower, using alternative points of departure, than the linear estimates of cancer potency for EO. An approach is described for linking the selection of an appropriate point of departure to the confidence in the proposed mode of action. Despite high confidence in the proposed mode of action, a small linear component for the dose-response relationship at low concentrations cannot be ruled out conclusively. Accordingly, a unit risk value of 4.5 x 10(-8) (microg/m3)(-1) was derived for EO, with a range of unit risk values of 1.4 x 10(-8) to 1.4 x 10(-7) (microg/m3)(-1) reflecting the uncertainty associated with a theoretical linear term at low concentrations.

Acute toxicity and cancer risk assessment values for tert-butyl acetate

tert-Butyl acetate (TBAc) is an industrial chemical with potential uses as a degreaser and in architectural coatings. Limited chronic toxicity data exist for TBAc. However, acute inhalation exposure data are available for TBAc. Additionally, TBAc has been demonstrated to be substantially metabolized to tert-butanol (TBA) in rats, and a positive TBA genotoxicity study suggests that TBA may cause oxidative DNA damage. TBA has been shown to induce tumors in both rats and mice, and the Office of Environmental Health Hazard Assessment has calculated an oral cancer potency factor (CSF) for TBA of 3 × 10 −3 (mg/kg-day) −1. Therefore, TBAc should be considered to pose a potential cancer risk to humans because of the metabolic conversion to TBA. An acute 1-h reference exposure level of 1 mg/m 3 can be calculated from the extrapolated no observed adverse effect level of 50 mg/m 3. A CSF of 0.002 (mg/kg-day) −1 can be derived for TBAc, assuming 100% metabolism of TBAc to TBA. An inhalation unit risk value for TBAc of 4 × 10 −7 (μg/m 3) −1 can then be derived from the CSF value for TBAc by assuming a human breathing rate of 20 m 3/day, 70% fractional absorption, and an average human body weight of 70 kg.

A Reevaluation of the Literature Regarding the Health Assessment of Diesel Engine Exhaust

While the International Agency for Research on Cancer (IARC) classified diesel exhaust (DE) as a “probable” carcinogen in 1989 based primarily on “sufficient” animal data, other investigators have since concluded that the lung tumors found in the rat studies were a result of particle overloading. Subsequent health risk assessments of DE have not used the rat cancer data. The U.S. Environmental Protection Agency (EPA), in developing its 2002 Health Assessment Document (HAD) for DE, primarily considered the epidemiology studies of railroad workers and truck drivers to develop health risk assessments of DE. However, both sets of epidemiology studies have serious weaknesses that make them unsuitable for cancer risk assessment. Major shortcomings were the lack of contemporaneous measurements of exposures to DE, difficulties with exposure history reconstruction, and adequately accounting for other exposures such as gasoline exhaust and cigarette smoke. To compound these problems, there was not, and there is still not, a specific exposure marker for DE. Interestingly, in the underground mining industry, where diesel exposures are much higher than observed in railroad workers and truck drivers, there was no increase in lung cancer. These problems and concerns led the U.S. EPA to conclude that while DE was a “likely” carcinogen, a unit risk value or range of risk cannot be calculated from existing data and that the risk could be zero. In addition, the DE emissions have changed and continue to change with the implementation of new emission control technologies. The HAD recognized this fact and noted that further studies are needed to assess new diesel engine emissions. Recent chemical characterization studies on low-emitting diesel engines with catalyzed particulate filters have shown emissions rates for several chemicals of concern that are even lower than comparable compressed natural gas (CNG)-fueled engines. With lower emissions, better fire safety, and improved cost-effectiveness of new low-emitting diesels compared to CNG, current efforts to restrict use of low-emitting diesels seems misguided.

Evaluation of the Carcinogenicity of 1,1-Dichloroethylene (Vinylidene Chloride)

The U.S. Environmental Protection Agency has classified 1,1-dichloroethylene (vinylidene chloride; VDC) as a “C” carcinogen and has developed an inhalation unit risk value and an oral cancer slope factor for this chemical. The development and use of these cancer potency estimates for risk assessment purposes are questionable. The inhalation unit risk value is based on increased kidney adenocarcinomas in Swiss mice from one study. This type of cancer was not increased in female mice or in rats or hamsters in the same study nor in male mice of a similar strain in another study with higher VDC exposures. The VDC oral cancer slope factor is based on a non-statistically significant increase in adrenal pheochromocytomas in male rats following oral exposure in a standard National Toxicology Program chronic bioassay. Both human and animal literature relevant to VDC carcinogenicity was reviewed according to the USEPA draft Guidelines for Carcinogen Risk Assessment with the objective of determining the weight-of-evidence for VDC carcinogenicity. We conclude that information currently available for VDC is most appropriately characterized in a weight-of-evidence narrative by the descriptor “inadequate for an assessment of human carcinogenic potential.” For chemicals with this descriptor, dose–response assessment is not indicated. Under this guidance, quantitative estimates of cancer risks associated with VDC exposure are inappropriate until additional, more definitive evidence for human carcinogenicity becomes available.

Exposure Assessment of Taste and Odor Standards Used in the Method of Flavor Profile Analysis

Information on the toxicity of individual chemicals that have been used as known or representative odor standards in the method of Flavor Profile Analysis (FPA) was compiled for an exposure assessment. A full risk assessment was not possible since unit risk values for most of these chemicals do not exist. This study provides a recommendation as to what chemicals can be safely used as known and representative taste and odor standards for the next modification of the Flavor Profile Analysis Standard Method 2170. Excluding any potential odor standard listed as possible or probable carcinogens, there would be no known risk to FPA panelists being exposed to the selected odor reference chemicals at the concentrations used in FPA. Also, the concentrations which panelists are exposed to during an FPA (20 minutes per chemical) are lower than the legal threshold limit values for 8 hour occupational exposures. However, many of the odor reference chemicals have yet to be evaluated for their carcinogenic or noncarcinogenic endpoints. Recommendations are made as to which chemicals should be avoided.

Exposure assessment of taste and odor standards used in the method of flavor profile analysis

Information on the toxicity of individual chemicals that have been used as known or representative odor standards in the method of Flavor Profile Analysis (FPA) was compiled for an exposure assessment. A full risk assessment was not possible since unit risk values for most of these chemicals do not exist. This study provides a recommendation as to what chemicals can be safely used as known and representative taste and odor standards for the next modification of the Flavor Profile Analysis Standard Method 2170. Excluding any potential odor standard listed as possible or probable carcinogens, there would be no known risk to FPA panelists being exposed to the selected odor reference chemicals at the concentrations used in FPA. Also, the concentrations which panelists are exposed to during an FPA (20 minutes per chemical) are lower than the legal threshold limit values for 8 hour occupational exposures. However, many of the odor reference chemicals have yet to be evaluated for their carcinogenic or noncarcinogenic endpoints. Recommendations are made as to which chemicals should be avoided.

The use of toxic equivalency factors in assessing occupational and environmental health risk associated with exposure to airborne mixtures of polycyclic aromatic hydrocarbons (PAHs)

The health risk associated with inhalatory exposure to PAHs either in the occupational atmosphere or in outdoor air is commonly assessed on the basis of benzo(a)pyrene (BaP) concentrations in air. The PAH-related health risk is calculated with the help of epidemiological data from coke oven workers. The proportion of individual carcinogenic PAHs to BaP has been shown to vary in different environments by one to two orders of magnitude. Despite this, the unit risk value for BaP derived from epidemiological studies of coke oven workers is used for risk estimation of these environments. Toxic equivalency factors (TEFs) for individual PAHs were used to estimate human health risk associated with inhalatory exposure to PAHs. Given the uncertainties involved in risk assessment in general, a variability of risk estimation for PAH mixtures based on the toxic equivalency factor concept by a factor 2.6 is low and rather unreasonably precise. This underlines the importance of BaP as a surrogate compound of a PAH mixture.

Current assessment of the carcinogenic hazard of diesel exhaust

Diesel exhaust consists of gases, vapors, and soot, which consists of a carbon matrix with adsorbed organic compounds, inorganic salts, and metals. The carcinogenic hazard of organic extracts of diesel soot has long been known, and concern for human carcinogenesis was elevated during the late 1970s by new mutageniciry data and the anticipated increase in diesel use in the U.S. By the mid‐1980s, inhalation bioassays proved diesel soot to be a pulmonary carcinogen in heavily exposed rats, and epidemiology suggested a small increase in lung cancer in heavily exposed occupations. Evidence that organic compounds might not be the cause of the rat lung tumor response as previously assumed and the need to select a dose equivalence term for estimating unit risk values for human cancer led to recent studies which demonstrated that nearly organic‐free carbon black is equally carcinogenic to diesel soot in rats. Recent cancer risk estimates by EPA have used unit risk values calculated from rat studies using the dose of carbon soot core per unit of lung surface as the equivalence dose term. Using this approach, a very small number of cancers is estimated to occur from environmental exposures. The magnitude of occupational cancer risk from diesel exhaust is uncertain, but estimated to be low.