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Peter S.J. Lees

Bio: Peter S.J. Lees is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Population & Poison control. The author has an hindex of 28, co-authored 73 publications receiving 3306 citations.


Papers
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Journal ArticleDOI
TL;DR: This research presents a meta-analyses of the immune system’s response to exposure to radiation and shows clear patterns of decline in the immune systems of men and women aged 65 and over.
Abstract: Robert E. Chapin, Jane Adams, Kim Boekelheide, L. Earl Gray Jr, Simon W. Hayward, Peter S.J. Lees, Barry S. McIntyre, Kenneth M. Portier, Teresa M. Schnorr, Sherry G. Selevan, John G. Vandenbergh, and Susan R. Woskie Pfizer, Inc., Groton, CT University of Massachusetts, Boston, MA Brown University, Providence, RI U.S. Environmental Protection Agency, Research Triangle Park, NC Vanderbilt University Medical Center, Nashville, TN Johns Hopkins University, Baltimore, MD Schering Plough Research Institute, Summit, NJ American Cancer Society, Atlanta, GA National Institute for Occupational Safety and Health, Cincinnati, OH U.S. Public Health Service (Ret), Silver Spring, MD North Carolina State University, Raleigh, NC University of Massachusetts, Lowell, MA

489 citations

Journal ArticleDOI
TL;DR: The best quantitative evidence to date of the relationship between hexavalent chromium exposure and lung cancer is offered and shows a strong dose-response relationship for lung cancer.
Abstract: Background An elevated risk of lung cancer among workers in chromate production facilities has previously been reported. This excess risk is believed to be the result of exposure to hexavalent chromium. There have been mixed reports about whether trivalent chromium exposure is also associated with an excess lung cancer risk. Previous studies of measured hexavalent chromium exposure and lung cancer risk have not examined cigarette smoking as a risk factor. Methods A cohort of 2,357 workers first employed between 1950 and 1974 at a chromate production plant was identified. Vital status of the workers was followed until December 31, 1992. Work histories of cohort members were compiled from the beginning of employment through 1985, the year the plant closed. Annual average exposure estimates, based on historical exposure measurements, were made for each job title in the plant for the years 1950‐1985. These exposure estimates were used to calculate the cumulative hexavalent chromium exposure of each member of the study population. Following closure of the plant, settled dust samples were collected and analyzed for hexavalent and trivalent chromium. The trivalent/hexavalent concentration ratios in each plant area were combined with historic air-sampling data to estimate cumulative trivalent chromium exposure for each individual in the study cohort. Smoking status (yes/ no) as of the beginning of employment and clinical signs of potential chromium irritation were identified from company records. Results Cumulative hexavalent chromium exposure showed a strong dose‐response relationship for lung cancer. Clinical signs of irritation, cumulative trivalent chromium exposure, and duration of work were not found to be associated with a risk of lung cancer when included in a proportional hazards model with cumulative hexavalent chromium exposure and smoking. Age-specific data on cumulative hexavalent chromium exposure, observed and expected numbers of lung cancer cases, and person-years of observation are provided. Conclusion Cumulative hexavalent chromium exposure was associated with an increased lung cancer risk; cumulative trivalent chromium exposure was not. The excess risk of lung cancer associated with cumulative hexavalent chromium exposure was not confounded by smoking status. The current study offers the best quantitative evidence

417 citations

Journal ArticleDOI
TL;DR: Current occupational standards for hexavalent chromium permit a lifetime excess risk of dying of lung cancer that exceeds 1 in 10, which is consistent with previous risk assessments.
Abstract: The purpose of this investigation was to estimate excess lifetime risk of lung cancer death resulting from occupational exposure to hexavalent-chromium-containing dusts and mists. The mortality experience in a previously studied cohort of 2,357 chromate chemical production workers with 122 lung cancer deaths was analyzed with Poisson regression methods. Extensive records of air samples evaluated for water-soluble total hexavalent chromium were available for the entire employment history of this cohort. Six different models of exposure-response for hexavalent chromium were evaluated by comparing deviances and inspection of cubic splines. Smoking (pack-years) imputed from cigarette use at hire was included in the model. Lifetime risks of lung cancer death from exposure to hexavalent chromium (assuming up to 45 years of exposure) were estimated using an actuarial calculation that accounts for competing causes of death. A linear relative rate model gave a good and readily interpretable fit to the data. The estimated rate ratio for 1 mg/m 3 -yr of cumulative exposure to hexavalent chromium (as CrO3), with a lag of five years, was RR = 2.44 (95% CI = 1.54‐3.83). The excess lifetime risk of lung cancer death from exposure to hexavalent chromium at the current OSHA permissible exposure limit (PEL) (0.10 mg/m 3 ) was estimated to be 255 per 1,000 (95% CI: 109‐416). This estimate is comparable to previous estimates by U.S. EPA, California EPA, and OSHA using different occupational data. Our analysis predicts that current occupational standards for hexavalent chromium permit a lifetime excess risk of dying of lung cancer that exceeds 1 in 10, which is consistent with previous risk assessments.

219 citations

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TL;DR: Despite following recommended safe-handling practices, workplace contamination with antineoplastic drugs in pharmacy and nursing areas continues at these locations.
Abstract: Objective:This study evaluated health care worker exposure to antineoplastic drugs.Methods:A cross-sectional study examined environmental samples from pharmacy and nursing areas. A 6-week diary documented tasks involving those drugs. Urine was analyzed for two specific drugs, and blood samples were

200 citations

Journal ArticleDOI
TL;DR: Results show that DMT1 is important in iron and cadmium transport in Caco-2 cells but that lead enters these cells through an independent hydrogen-driven mechanism.
Abstract: DMT1 (divalent metal transporter 1) is a hydrogen-coupled divalent metal transporter with a substrate preference for iron, although the protein when expressed in frog oocytes transports a broad ran...

200 citations


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TL;DR: It is concluded that when nonmonotonic dose-response curves occur, the effects of low doses cannot be predicted by the effects observed at high doses, and fundamental changes in chemical testing and safety determination are needed to protect human health.
Abstract: For decades, studies of endocrine-disrupting chemicals (EDCs) have challenged traditional concepts in toxicology, in particular the dogma of “the dose makes the poison,” because EDCs can have effects at low doses that are not predicted by effects at higher doses. Here, we review two major concepts in EDC studies: low dose and nonmonotonicity. Low-dose effects were defined by the National Toxicology Program as those that occur in the range of human exposures or effects observed at doses below those used for traditional toxicological studies. We review the mechanistic data for low-dose effects and use a weight-of-evidence approach to analyze five examples from the EDC literature. Additionally, we explore nonmonotonic dose-response curves, defined as a nonlinear relationship between dose and effect where the slope of the curve changes sign somewhere within the range of doses examined. We provide a detailed discussion of the mechanisms responsible for generating these phenomena, plus hundreds of examples from...

2,475 citations

Journal ArticleDOI
TL;DR: Urine concentrations of total BPA differed by race/ethnicity, age, sex, and household income, and these first U.S. population representative concentration data for urinary BPA and tOP should help guide public health research priorities.
Abstract: Of the more than 2,000 high-production volume chemicals that are manufactured in or imported into the United States in amounts of one million pounds or more per year (U.S. Environmental Protection Agency 2004), many are widely used in consumer products. Among these chemicals are bisphenol A [BPA; 2,2-bis(4-hydroxyphenyl)propane; CAS no. 80-05-7] and 4-tertiary-octylphenol [tOP; 4-(1,1,3,3-tetramethylbutyl)phenol; CAS no. 140-66-9]. BPA is used in the manufacture of polycarbonate plastic and epoxy resins, which can be used in impact-resistant safety equipment and baby bottles, as protective coatings inside metal food containers, and as composites and sealants in dentistry [Center for the Evaluation of Risks to Human Reproduction (CERHR) 2007; European Union 2003]. Exposure to BPA is thought to result primarily from ingestion of food containing BPA (Kang et al. 2006; Vandenberg et al. 2007). tOP is both a degradation product of and an intermediate in the manufacture of octylphenol ethoxylates, which are nonionic surfactants used in detergents, pesticide formulations, and other applications (Ying et al. 2002). Exposure to tOP may occur from contact with personal care products, detergents, water, and food containing tOP. Exposures to tOP can result in developmental and reproductive alterations in aquatic species (Segner et al. 2003) and in laboratory animals (Aydogan and Barlas 2006; Bian et al. 2006; Blake et al. 2004; Nagao et al. 2001; Willoughby et al. 2005). At high doses, BPA demonstrates estrogen-like effects on uterine and prostate organ weights in experimental animals. At doses below the putative lowest observed adverse effect level, exposure to BPA has reportedly resulted in decreased sperm production, increased prostate gland volume, altered development and tissue organization of the mammary gland, altered vaginal morphology and estrous cycles, disruption of sexual differentiation in the brain, and accelerated growth and puberty (Durando et al. 2007; Howdeshell et al. 1999; Kubo et al. 2003; Richter et al. 2007; Rubin et al. 2006; Schonfelder et al. 2002; Timms et al. 2005; vom Saal et al. 1998). At present, the interpretation of the evidence related to the low-dose effects of BPA is a subject of scientific debate (European Union 2003; Goodman et al. 2006; Gray et al. 2004; National Toxicology Program 2001; vom Saal and Hughes 2005). BPA and tOP are of concern to environmental public health because of the high potential for exposure of humans to these phenols and their demonstrated animal toxicity. Information about the concentrations of these compounds in the general population is important for understanding human exposure to BPA and tOP. The National Health and Nutrition Examination Survey (NHANES), conducted continuously since 1999 by the National Center for Health Statistics of the Centers for Disease Control and Prevention (CDC), is designed to measure the health and nutritional status of the civilian noninstitutionalized U.S. population ≥ 2 months of age (CDC 2003). The surveys include household interviews; collection of medical histories; standardized physical examinations; and collection of biologic specimens (e.g., blood and urine from participants ≥ 1 and ≥ 6 years of age, respectively) for clinical chemistry testing, nutritional indicators assessments, and assessment of exposure to environmental chemicals (CDC 2005, 2006). Previously, we analyzed 394 urine samples collected from adult participants of NHANES III, conducted during 1988–1994, to estimate urinary concentrations of total BPA (free plus conjugated species) in selected demographic groups (Calafat et al. 2005). We now report the first estimate of urinary concentrations of total BPA and tOP in NHANES 2003–2004 participants, a representative sample of the noninstitutionalized U.S. population ≥ 6 years of age.

1,590 citations

Journal ArticleDOI
TL;DR: Indoor air pollution is a major global public health threat requiring greatly increased efforts in the areas of research and policy-making and research on its health effects should be strengthened, particularly in relation to tuberculosis and acute lower respiratory infections.
Abstract: Around 50% of people, almost all in developing countries, rely on coal and biomass in the form of wood, dung and crop residues for domestic energy. These materials are typically burnt in simple stoves with very incomplete combustion. Consequently, women and young children are exposed to high levels of indoor air pollution every day. There is consistent evidence that indoor air pollution increases the risk of chronic obstructive pulmonary disease and of acute respiratory infections in childhood, the most important cause of death among children under 5 years of age in developing countries. Evidence also exists of associations with low birth weight, increased infant and perinatal mortality, pulmonary tuberculosis, nasopharyngeal and laryngeal cancer, cataract, and, specifically in respect of the use of coal, with lung cancer. Conflicting evidence exists with regard to asthma. All studies are observational and very few have measured exposure directly, while a substantial proportion have not dealt with confounding. As a result, risk estimates are poorly quantified and may be biased. Exposure to indoor air pollution may be responsible for nearly 2 million excess deaths in developing countries and for some 4% of the global burden of disease. Indoor air pollution is a major global public health threat requiring greatly increased efforts in the areas of research and policy-making. Research on its health effects should be strengthened, particularly in relation to tuberculosis and acute lower respiratory infections. A more systematic approach to the development and evaluation of interventions is desirable, with clearer recognition of the interrelationships between poverty and dependence on polluting fuels.

1,574 citations

Journal ArticleDOI
TL;DR: This review examines the chemical and physical nature of woodsmoke; the exposures and epidemiology of smoke from wildland fires and agricultural burning, and related controlled human laboratory exposures to biomass smoke; the Epidemiology of outdoor and indoor woodsm smoke exposures from residential woodburning in developed countries; and the toxicology of woodSmoke, based on animal exposures and laboratory tests.
Abstract: The sentiment that woodsmoke, being a natural substance, must be benign to humans is still sometimes heard. It is now well established, however, that wood-burning stoves and fireplaces as well as wildland and agricultural fires emit significant quantities of known health-damaging pollutants, including several carcinogenic compounds. Two of the principal gaseous pollutants in woodsmoke, CO and NOx, add to the atmospheric levels of these regulated gases emitted by other combustion sources. Health impacts of exposures to these gases and some of the other woodsmoke constituents (e.g., benzene) are well characterized in thousands of publications. As these gases are indistinguishable no matter where they come from, there is no urgent need to examine their particular health implications in woodsmoke. With this as the backdrop, this review approaches the issue of why woodsmoke may be a special case requiring separate health evaluation through two questions. The first question we address is whether woodsmoke should be regulated and/or managed separately, even though some of its separate constituents are already regulated in many jurisdictions. The second question we address is whether woodsmoke particles pose different levels of risk than other ambient particles of similar size. To address these two key questions, we examine several topics: the chemical and physical nature of woodsmoke; the exposures and epidemiology of smoke from wildland fires and agricultural burning, and related

1,358 citations