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PubMed2001

Dose-response implications of the University of Alabama study of lymphohematopoietic cancer among workers exposed to 1,3-butadiene and styrene in the synthetic rubber industry.

New quantitative cancer risk estimates for exposure to 1,3-butadiene are presented. These estimates are based on the most recent human epidemiologic data developed by Drs Delzell and Macaluso and their colleagues at the University of Alabama at Birmingham. The implications of Poisson regression analyses of the relative rate for leukemia are explored using their updated dose estimates and lymphohematopoietic cancer data. The Poisson regression model in these analyses has the same form as in the U.S. Environmental Protection Agency (EPA)'s draft risk assessment of 1,3-butadiene [U.S. Environmental Protection Agency, Health Risk Assessment of 1,3-Butadiene - External Review Draft, National Center for Environmental Assessment, Office of Research and Development, 63 Fed. Reg. 7167 (February 12, 1998) Publication NCEA-W-0267, Washington, 1998]. Consistent with the proposed cancer risk assessment guidelines of the EPA and the EPA's draft risk assessment, the exploration includes the maximum likelihood estimate of the 'effective concentration' (EC(01)) corresponding to an extra risk of leukemia of 0.01 (1%) from a lifetime continuous exposure to 1,3-butadiene based on a linear dose-response model and the cumulative 1,3-butadiene dose metric (ppm-years). The incorporation of the most recent exposure estimates results in a 2.5-fold decrease in the estimates of leukemia risks computed by EPA. In addition, three changes proposed by the American Chemistry Council (formerly the Chemical Manufacturers Association) to the EPA's Science Advisory Board (SAB) for EPA's draft risk assessment of 1,3-butadiene are incorporated into the calculation. This results in approximately an additional fivefold decrease in the risk estimates of leukemia. The leukemia cancer risk estimates in the EPA's draft risk assessment of 1,3-butadiene decrease by approximately a factor of 13-fold when the updated epidemiologic data and the alternative numbers proposed by industry to the SAB are both incorporated. Specifically, the maximum likelihood estimate of the EC(01) increases from EPA's 1.2 ppm to 2.8 ppm on the basis of the updated epidemiologic data and increases further to 15.1 ppm when the CMA's proposed changes are also incorporated.

Alabama↗

PubMed1987

Risk assessment in environmental policy-making.

Environmental policy-making has become more dependent on formal, quantitative risk assessment because of increasing attention to the prevention of human health damage from toxic chemicals. Risk assessment helps set priorities for regulation of the very large numbers of chemicals that are of potential concern and helps direct limited social and government resources against the most significant risks. Although the scientific basis for risk assessment is often uncertain and the public and its representatives have often been confused by its use in regulatory decisions, the U.S. Environmental Protection Agency currently uses a variety of risk assessment techniques to set priorities, tailor regulations, and make decisions at particular sites. The Environmental Protection Agency also attempts to make the practice of risk assessment more consistent throughout the agency and to improve public understanding of the meaning of risk assessment and risk management.

Environmental Exposure↗

PubMed1996

What can research contribute to regulatory decisions about the health risks of multiple chemical sensitivity?

Multiple Chemical Sensitivity (MCS), which may not be caused by chemicals at all, is a serious medical problem of unknown origin and uncertain etiology that raises many fundamental science and policy questions. Regulators, for example, are confronted with a dilemma: what, if anything, should be done to protect people from the scientifically uncertain health risks of exposures to extremely low levels of environmental chemicals. Regulatory agencies, such as the Environmental Protection Agency, do not have the luxury of waiting until conclusive scientific evidence is available before making a decision; however, our present lack of scientific understanding about MCS is so acute that it is not possible to ascertain whether the cause of MCS-related symptoms is chemical, biological, physical, psychosocial, or some combination thereof. Nevertheless, many MCS sufferers and advocates for the chemically induced hypothesis are clamoring for regulatory action to reduce putative health risks from very-low-level exposures to chemicals in the environment. Unless steps are taken to improve the quantity and quality of the existing scientific data base, we cannot, with any acceptable degree of certainty, evaluate the extent to which regulatory decisions about MCS are either protective of public health or cost-effective. This article examines how research can strengthen the scientific basis for risk-related decisions about MCS, and proposes a framework for establishing research directions and priorities. It is argued that high-priority research on MCS is distinguishable by four attributes: (1) results are valuable for risk-related decisions; (2) findings significantly advance scientific knowledge and understanding; and the hypothesis being tested is both (3) biologically plausible and (4) readily testable.

Decision Making↗

PubMed1990

Identifying ecological indicators: an environmental monitoring and assessment program.

The U.S. Environmental Protection Agency is initiating the Environmental Monitoring and Assessment Program (EMAP) to monitor the status and trends of the nation's near-coastal waters, forests, freshwater wetlands, surface waters, agroecosystems, and arid lands. This program is intended to evaluate the effectiveness of Agency policies for protecting ecological resources within these systems. Monitoring data collected for all ecosystems will be integrated for national status and trends assessments.

Environmental Monitoring↗

PubMed1995

Passive smoking and lung cancer.

Evidence that environmental tobacco smoke may be a risk factor for lung cancer among individuals who themselves have never smoked tobacco products has been the subject of expert review over the last decade by several United States and international agencies. The most recent comprehensive review, published in 1993 by the United States Environmental Protection Agency, concluded that environmental tobacco smoke is a Group A (known human) carcinogen. This report, coming in the midst of rapid social and political change in attitudes towards public policy implications for protecting human health, has been the subject of considerable discussion. Issues involved in these discussions, as well as more recently published studies on the topic, are reviewed with respect to current thinking about the risk of lung cancer in passive smokers, particularly women, who are lifetime never-smokers.

Epidemiologic Factors↗

PubMedDate not supplied

Research integrity: a government perspective.

What is research integrity? At the United States Environmental Protection Agency (U.S. EPA) research integrity can be defined as conducting and fostering research to define, anticipate, and understand environmental problems; and generating sound, appropriate, credible, and effective solutions to those problems. Whether in government, academia, or industry, integrity is required at all stages of research--from data generation to data analysis. What constitutes research integrity? Simply put, Did we do the right thing? Did we do it the right way? Did we honestly document what we did? This is especially important if the research is used as a basis for public policy. The extensive and intensive use of the results of science in EPA's standard setting, regulatory, and enforcement responsibilities means that scientific misconduct can lead to costly and inappropriate actions through unnecessary expenditure or inadequate protection. The soundness, effectiveness, and credibility of EPA's regulations ultimately rest on the scientific and technical bases for these actions. Careful attention to research record keeping can help ensure data quality and integrity. The U.S. Environmental Protection Agency, its research requirements, and the work of the National Health and Environmental Effects Research Laboratory are discussed below.

Environmental Monitoring↗

PubMed1994

National and regional distributions of airborne radon concentrations in U.S. homes.

The National Residential Radon Survey was conducted during 1989 and 1990 to provide data on the frequency distribution of annual average radon concentrations in U.S. residences nationwide, in U.S. Environmental Protection Agency defined Regions, and in subgroups of the housing stock. The National Residential Radon Survey also provided housing and demographic data and a preliminary assessment of the relationship of housing and geographical characteristics to residential radon concentrations. This paper focuses solely on the national and regional estimates of annual average radon concentrations. A stratified, three-stage sampling procedure was used to select housing units for the survey. Data were collected through personal interviews with residents and placement of alpha track detectors in each level of the residences for 12 mo. The survey found an arithmetic annual average radon concentration in U.S. homes of 46.3 +/- 4.4 Bq m-3 (1.25 +/- 0.12 pCi L-1). About 6.0 +/- 1.4% of homes (5.8 million) had radon levels greater than the U.S. Environmental Protection Agency's action level for mitigation of 148 Bq m-3 (4 pCi L-1). Concentrations varied significantly across Environmental Protection Agency Regions. A lognormal distribution was found to closely approximate the major distributions of radon concentrations.

Air Pollutants, Radioactive↗

PubMed1988

Dust emissions in cattle feedlots.

Dust emissions were measured at three Texas cattle feedlots on 15 occasions in 1987 to determine concentrations of total suspended particulate matter (TSP) and dust with 10 microns or less aerodynamic particle size (PM-10). Net feedlot dust concentrations (downwind minus upwind) ranged from 15.7 to 1,700.1 micrograms per m3 and averaged 412.4 +/- 271.2 micrograms per m3, which is about 37 per cent less than was determined in feedlot dust research in California approximately 17 years earlier. Upwind concentrations averaged 22 per cent of the downwind concentrations. Feedlot dust concentrations were generally highest in early evening and lowest in early morning. Using the Wedding and Andersen-321A PM-10 samplers, the PM-10 dust concentrations were 19 and 40 per cent, respectively, of mean TSP concentrations in direct comparisons. There was good correlation between PM-10 and TSP concentrations. Although dust concentrations decreased with increasing moisture, the correlation coefficients were relatively low. Odor intensity appeared to increase with decreasing net dust concentrations, perhaps due to moisture influences. Mean particle sizes of feedlot dust were 8.5 to 12.2 microns on a particle volume basis and 2.5 to 3.4 microns on a population basis. Respirable dust (below 2 microns) represented only 2.0 to 4.4 per cent of total dust on a particle volume basis. Under conditions of these experiments, the feedlots often exceeded both state and federal (U.S. Environmental Protection Agency) standards for TSP concentrations and for PM-10 concentrations measured using the Andersen-321A sampler. However, feedlots were below the new U.S. Environmental Protection Agency standards when the Wedding PM-10 sampler was used for measuring dust emissions.

Animals↗

PubMed2005

The tobacco industry and pesticide regulations: case studies from tobacco industry archives.

Tobacco is a heavily pesticide-dependent crop. Because pesticides involve human safety and health issues, they are regulated nationally and internationally; however, little is known about how tobacco companies respond to regulatory pressures regarding pesticides. In this study we analyzed internal tobacco industry documents to describe industry activities aimed at influencing pesticide regulations. We used a case study approach based on examination of approximately 2,000 internal company documents and 3,885 pages of U.S. Environmental Protection Agency documents obtained through Freedom of Information Act requests. The cases involved methoprene, the ethylene bisdithiocarbamates, and phosphine. We show how the tobacco industry successfully altered the outcome in two cases by hiring ex-agency scientists to write reports favorable to industry positions regarding pesticide regulations for national (U.S. Environmental Protection Agency) and international (World Health Organization) regulatory bodies. We also show how the industry worked to forestall tobacco pesticide regulation by attempting to self-regulate in Europe, and how Philip Morris encouraged a pesticide manufacturer to apply for higher tolerance levels in Malaysia and Europe while keeping tobacco industry interest a secret from government regulators. This study suggests that the tobacco industry is able to exert considerable influence over the pesticide regulatory process and that increased scrutiny of this process and protection of the public interest in pesticide regulation may be warranted.

Conflict of Interest↗

PubMed1987

A critical evaluation of the use of mutagenesis, carcinogenesis, and tumor promotion data in a cancer risk assessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Regulatory agencies in the Western Hemisphere are currently assessing the potential human health risks of environmental contamination by 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). Some U.S. agencies such as the Environmental Protection Agency (EPA) and Centers for Disease Control (CDC) have assumed that TCDD behaves as a tumor initiator in animals and have used linear low-dose mathematical extrapolation models for estimating any human risk. In contrast, the Ontario Ministry of the Environment, the State Institute of National Health of The Netherlands, and the Federal Environmental Agency of the Federal Republic of Germany have concluded that TCDD does not have initiator activity; these agencies have advocated a risk extrapolation approach which applies a safety factor to a no-observable-effect level. Estimations of the potential risk obtained by these two approaches can differ by three to four orders of magnitude and have a major impact on the allocation of resources within the affected countries. This paper critically reviews the TCDD bacterial, animal, and human data on mutagenesis, carcinogenesis, and tumor promotion and concludes that the scientific evidence does not support risk estimations which are based on TCDD as a tumor initiator. Rather, the animal data overwhelmingly support TCDD as a tumor promoter. Risk estimations which incorporate tumor promotion activity more accurately reflect the scientific understanding of TCDD's mechanism of action and provide better estimates of its risk.

Animals↗

PubMed1994

The vegetation-to-air concentration ratio in a specific activity atmospheric tritium model.

Specific activity models are frequently used to estimate the concentration of tritium oxide in vegetation. In such models, a single value represents the ratio (R) of the specific activity of tritium oxide in vegetation to the specific activity of atmospheric tritium oxide. Federal agencies such as the Nuclear Regulatory Commission and the Environmental Protection Agency have not established a consensus default for R. Literature on this topic suggests that a site-specific distribution of R should be developed when feasible. In this study, a distribution of R is established for the Savannah River Site. Environmental tritium concentrations in air and vegetation measured on and around the Savannah River Site over a 9-y period form the basis for the analysis. For dose assessments of chronic atmospheric tritium releases at the Savannah River Site, R is best parameterized by a normal distribution with a mean of 0.54 and one standard deviation of 0.10. The Nuclear Regulatory Commission default for R is approximately equal to the Savannah River Site site-specific estimate. Based on the results, the default value for R recognized by the Environmental Protection Agency overestimates tritium concentrations in vegetation and, therefore, doses from foodstuff consumption pathways at humid sites. For the Savannah River Site, the magnitude of the error is on the order of a factor of 2. This consideration may be important if an estimated dose approaches an as-low-as-reasonably-achievable or regulatory threshold. Conversely, without the benefit of site-specific data, ingestion doses may be underestimated in regions with dry climates.

Atmosphere↗

PubMed1994

Summary of the workshop on issues in risk assessment: quantitative methods for developmental toxicology.

This report summarizes the proceedings of a conference on quantitative methods for assessing the risks of developmental toxicants. The conference was planned by a subcommittee of the National Research Council's Committee on Risk Assessment Methodology in conjunction with staff from several federal agencies, including the U.S. Environmental Protection Agency, U.S. Food and Drug Administration, U.S. Consumer Products Safety Commission, and Health and Welfare Canada. Issues discussed at the workshop included computerized techniques for hazard identification, use of human and animal data for defining risks in a clinical setting, relationships between end points in developmental toxicity testing, reference dose calculations for developmental toxicology, analysis of quantitative dose-response data, mechanisms of developmental toxicity, physiologically based pharmacokinetic models, and structure-activity relationships. Although a formal consensus was not sought, many participants favored the evolution of quantitative techniques for developmental toxicology risk assessment, including the replacement of lowest observed adverse effect levels (LOAELs) and no observed adverse effect levels (NOAELs) with the benchmark dose methodology.

Animals↗

PubMed2003

Non-destructive determination of 224Ra, 226Ra and 228Ra concentrations in drinking water by gamma spectroscopy.

The U.S. Environmental Protection Agency mandates that drinking water showing gross alpha-activity greater than 0.19 Bq L(-1) should be analyzed for radium, a known human carcinogen. The recommended testing methods are intricate and laborious. The method reported in this paper is a direct, non-destructive gamma-spectroscopic method for the determination of 224Ra, 226Ra, and 228Ra, the three radium isotopes of environmental concern in drinking water. Large-volume Marinelli beakers (4.1-L capacity), especially designed for measuring radioactive gases, in conjunction with a low-background, high-efficiency (131%) germanium detector were used in this work. It was first established that radon, the gaseous decay product of radium, and its progeny are quantitatively retained in this Marinelli beaker. The 224Ra, 226Ra, and 228Ra activity concentrations are determined from the equilibrium activities of their progeny: 212Pb, 214Pb (214Bi), and 228Ac; and the gamma-lines used in the analysis are 238.6, 351.9 (and 609.2), and 911.2 keV, respectively. The 224Ra activity is determined from the first 1,000-min measurement performed after expulsion of radon from the sample. The 226Ra activity is determined from the second, 2,400-min measurement, made 3 to 5 d later, and the 228Ra activity is determined from either the first or the second measurement, depending on its concentration level. The method's minimum detectable activities are 0.017 Bq L(-1), 0.020 Bq L(-1), and 0.027 Bq L(-1) for 224Ra, 226Ra, and 228Ra, respectively, when measured under radioactive equilibrium. These limits are well within the National Primary Drinking Water Regulations required limit of 0.037 Bq L(-1) for 226Ra and for 228Ra. The precision and accuracy of the method, evaluated using the U.S. Environmental Protection Agency and the Environmental Resource Associates' quality control samples, were found to be within acceptable limits.

Equipment Design↗

PubMed1998

Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer.

BACKGROUND: Heavy industrial exposure to asbestos causes lung cancer and mesothelioma, but it remains unknown whether much lower environmental exposure to asbestos also causes these cancers. Nevertheless, regulatory agencies, including the Environmental Protection Agency (EPA), have assessed the risk of lung cancer by extrapolating known risks from past industrial exposure to asbestos to today's much lower environmental asbestos levels (roughly 100,000 times lower). We also tested the EPA's model for predicting the risk of asbestos-induced lung cancer in a population of women with relatively high levels of nonoccupational exposure to asbestos. METHODS: Mortality among women in 2 chrysotile-asbestos-mining areas of the province of Quebec was compared with mortality among women in 60 control areas, and age-standardized mortality ratios were derived. With the help of an expert panel, we estimated past exposure to asbestos among women in the mining areas and used these data with the EPA's model to predict the relative risk of lung cancer. We then compared this prediction with the observed mortality ratios. RESULTS: On the basis of the estimated exposure in the asbestos-mining areas, a relative risk of death due to lung cancer of 2.1 was predicted by the EPA's model, amounting to about 75 excess deaths from lung cancer in this population. By contrast, we calculated a standardized mortality ratio of 1.0 and a standardized proportionate mortality ratio of 1.1 (P> 0.05), suggesting that there were between 0 and 6.5 excess deaths from lung cancer among the women with nonoccupational exposure to asbestos. Seven deaths from pleural cancer were observed (relative risk=7.63; P<0.05). CONCLUSIONS: We found no measurable excess risk of death due to lung cancer among women in two chrysotile-asbestos-mining regions. The EPA's model overestimated the risk of asbestos-induced lung cancer by at least a factor of 10.

Adult↗

PubMedDate not supplied

Estimation of fish consumption and methylmercury intake in the New Jersey population.

Despite scientific attention to the toxicology of methylmercury (MeHg), little is known about population-based exposure to this compound. In this study, fish consumption and MeHg intake were estimated based on a seven-day recall survey of fish consumption among 1000 randomly selected New Jersey residents. Survey data were reported on a per-meal basis, and the fish species/dishes consumed at each meal were identified. Portion sizes for each meal were reported or estimated. To correct a possible bias due to underrepresentation of infrequent consumers, several schemes for weighting fish consumption data were investigated. MeHg concentration for most fish species was estimated from the National Marine Fisheries Service database or from recent United States Food and Drug Administration data. Commercial fish accounted for about 95% of all consumption. Mean fish consumption is estimated for all New Jersey adult consumers at 50.2 g/day (90th percentile = 107.4 g/day) and for women 18-40 years old (childbearing age) at 41.0 g/day (90th percentile = 88.1 g/day). Mean MeHg intake is estimated for all New Jersey adult consumers at 7.5 micrograms/day (90th percentile = 1.79 micrograms/day) and for women 18-40 at 6.3 micrograms/day (90th percentile = 14.8 micrograms/day). When MeHg concentrations are adjusted to account for the possible overestimation of current concentrations by the 20-year-old National Marine Fisheries Service database, it is estimated that MeHg intakes may be about 70-80% of unadjusted estimates. Based on these analyses, it is estimated that 21-30% of New Jersey women 18-40 and 5-8% of all New Jersey adults exceed their respective U.S. Environmental Protection Agency Reference Doses for MeHg. Because of uncertainty associated with the Reference Doses, exceeding the U.S. Environmental Protection Agency guidelines does not necessarily correspond to adverse effects on consumers or their fetuses.

Adult↗

PubMed1998

Model for estimating population impacts averted through the remediation of contaminated soil.

This is the second in a series of papers that discuss methodologies being developed and employed by the U.S. Environmental Protection Agency in support of its decisions on cleanup levels for radioactively contaminated sites that are to be remediated and released for public use. It describes a model, CU-POP, designed by the U.S. Environmental Protection Agency to obtain estimates of the potential collective radiological health impacts over specific periods of time (100, 1,000 and 10,000 y following cleanup), both on and off site, due to residual radioactive materials in on-site soil. Collective doses and risks are linear in population density for the direct exposure, dust and indoor radon inhalation, and soil ingestion pathways; it is assumed that specific fractions of all food grown and all groundwater pumped at a site are consumed by on- and off-site populations. The model was developed for application to a set of hypothetical "reference" sites; its testing on a simple generic site is discussed briefly here.

Inhalation Exposure↗

PubMed2002

Genetic toxicology: web resources.

Genetic toxicology is the scientific discipline dealing with the effects of chemical, physical and biological agents on the heredity of living organisms. The Internet offers a wide range of online digital resources for the field of Genetic Toxicology. The history of genetic toxicology and electronic data collections are reviewed. Web-based resources at US National Library of Medicine (NLM), including MEDLINE, PUBMED, Gateway, Entrez, and TOXNET, are discussed. Search strategies and Medical Subject Headings (MeSH) are reviewed in the context of genetic toxicology. The TOXNET group of databases are discussed with emphasis on those databases with genetic toxicology content including GENE-TOX, TOXLINE, Hazardous Substances Data Bank, Integrated Risk Information System, and Chemical Carcinogenesis Research Information System. Location of chemical information including chemical structure and linkage to health and regulatory information using CHEMIDPLUS at NLM and other databases is reviewed. Various government agencies have active genetic toxicology research programs or use genetic toxicology data to assist fulfilling the agency's mission. Online resources at the US Food and Drug Administration (FDA), the US Environmental Protection Agency (EPA), the National Institutes of Environmental Health Sciences, and the National Toxicology Program (NTP) are outlined. Much of the genetic toxicology for pharmaceuticals, industrial chemicals and pesticides that is performed in the world is regulatory-driven. Regulatory web resources are presented for the laws mandating testing, guidelines on study design, Good Laboratory Practice (GLP) regulations, and requirements for electronic data collection and reporting. The Internet provides a range of other supporting resources to the field of genetic toxicology. The web links for key professional societies and journals in genetic toxicology are listed. Distance education, educational media resources, and job placement services are also available online in the field of genetic toxicology. As molecular biology and computational tools improve, new areas within genetic toxicology such as structural activity relationship analysis, mutational spectra databases and toxicogenomics, now have resources online as well.

Animals↗

PubMed1987

Radon in homes. Council on Scientific Affairs.

Radon 222 and its radioactive decay products can enter buildings and, through inhalation, expose the inhabitants' pulmonary tissues to ionizing radiation. Studies of radon levels in the United States indicate that variations of 100-fold or greater exist among private dwellings. In one region, 55% of homes had levels exceeding 4 pCi/L (0.15 Bq/L), which is the guidance level recommended by the US Environmental Protection Agency. Ventilation and tightness of construction are important determinants of radon levels. In some instances, fans or heat exchangers can reduce excessive concentrations, but in others more elaborate remedial measures may be required. Physicians may obtain information about radon through Environmental Protection Agency regional offices and state radiation control programs. The risk of radiogenic cancer is believed to increase with exposure to ionizing radiation. According to some estimates, concentrations of radon decay products in US homes could be responsible for several thousand cases of lung cancer per year. Studies of radon levels in representative buildings and guidelines are needed to ensure safe, effective, and cost-effective countermeasures. Architects, contractors, designers, building code administrators, health physicists, and biomedical investigators can help with solutions.

Air Pollutants↗