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Teresa M. Schnorr

Bio: Teresa M. Schnorr is an academic researcher from National Institute for Occupational Safety and Health. The author has contributed to research in topics: Population & Poison control. The author has an hindex of 23, co-authored 45 publications receiving 2276 citations. Previous affiliations of Teresa M. Schnorr include United States Department of Health and Human Services.

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

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TL;DR: Mortality from respiratory cancer and from nonmalignant gastrointestinal disease was significantly greater among the cadmium workers than would have been expected from U.S. rates, and a statistically significant dose-response relationship was observed between lung cancer mortality and cumulative exposure to cad mium.
Abstract: A previous retrospective mortality study of 292 U.S. cadmium production workers employed for a minimum of 2 years showed increased mortality from respiratory and prostate cancer and from nonmalignant lung disease. To examine further the mortality experience of these workers, investigators from the National Institute for Occupational Safety and Health extended the study to include 602 white males with at least 6 months of production work in the same plant between 1940 and 1969. Vital status was determined through 1978, which included the addition of 5 years to the original follow-up. Cause-specific mortality rates for seven causes of death potentially related to cadmium exposure were compared between the overall cohort and U.S. white males and between subgroups. Mortality from respiratory cancer and from nonmalignant gastrointestinal disease was significantly greater among the cadmium workers than would have been expected from U.S. rates. All deaths from lung cancer occurred among workers employed for 2 or more years. A statistically significant dose-response relationship was observed between lung cancer mortality and cumulative exposure to cadmium. A 50% increase in lung cancer mortality, which was not statistically significant, was observed even among workers whose cumulative exposure to cadmium was between 41 and 200 micrograms/m3 over 40 years. Since the previous investigation, no new deaths from prostate cancer and no excess of deaths from nonmalignant respiratory disease have been observed.

161 citations

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TL;DR: The results support the animal literature in which dioxin-related effects have been observed on the hypothalamic-pituitary-Leydig-cell axis and on testosterone synthesis and offer human evidence of alterations in male reproductive hormone levels associated with dioxIn exposure.
Abstract: Human reproductive endocrine data may be an important source of epidemiologic information in regard to the toxic potential of 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin). The association of serum dioxin with total serum testosterone, luteinizing hormone, and follicle-stimulating hormone was examined in 248 chemical production workers from New Jersey and Missouri plants and 231 nonexposed neighborhood referents who participated in a medical evaluation in 1987. In linear regression analyses, current serum dioxin was positively and significantly related to luteinizing hormone and follicle-stimulating hormone and inversely related to total testosterone after adjustment for potential confounders (p 28 IU/liter), high follicle-stimulating hormone (> 31 IU/liter), and low testosterone (< 10.4 nmol/liter) by serum dioxin quartiles. There was a greater prevalence of high luteinizing hormone among workers in the second (odds ratio (OR) = 1.9, 95% confidence interval (CI) 0.7-5.5), third (OR = 2.5, 95% CI 0.9-7.3), and fourth (OR = 1.9, 95% CI 0.7-5.0) quartiles of serum dioxin compared with referents. For follicle-stimulating hormone, the authors observed a greater prevalence of high follicle-stimulating hormone among workers in the fourth quartile (OR = 2.0, 95% CI 0.7-5.6) compared with referents. Similarly, the prevalence of low testosterone was two to four times greater among workers in the second (OR = 3.9, 95% CI 1.3-11.3), third (OR = 2.7, 95% CI 0.9-8.2), and fourth quartiles (OR = 2.1, 95% CI 0.8-5.8) than among referents. The trends observed in these data offer human evidence of alterations in male reproductive hormone levels associated with dioxin exposure. The results support the animal literature in which dioxin-related effects have been observed on the hypothalamic-pituitary-Leydig-cell axis and on testosterone synthesis.

158 citations

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TL;DR: The lifetime excess lung cancer risk at the current Occupational Safety and Health Administration standard for cadmium fumes of 100 micrograms/m3 is approximately 50 to 111 lung cancer deaths per 1000 workers exposed to Cadmium for 45 years.

134 citations

Journal ArticleDOI
TL;DR: A retrospective mortality study of 17,321 PCB-exposed workers to determine whether mortality from Parkinson disease, dementia, and amyotrophic lateral sclerosis was elevated compared with the U.S. population finds suggestive of an effect of PCBs on neurodegenerative disease for women.
Abstract: Background:Production of polychlorinated biphenyls (PCBs) ended in the United States in the 1970s, but PCBs persist in the environment and are detectable in the blood of approximately 80% of Americans over age 50. PCBs decrease dopamine levels in rats and monkeys. Loss of dopamine is the hallmark of

131 citations


Cited by
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Journal Article
TL;DR: The International Commission on Non-Ionizing Radiation Protection (ICNIRP)—was established as a successor to the IRPA/INIRC, which developed a number of health criteria documents on NIR as part of WHO’s Environmental Health Criteria Programme, sponsored by the United Nations Environment Programme (UNEP).
Abstract: IN 1974, the International Radiation Protection Association (IRPA) formed a working group on non-ionizing radiation (NIR), which examined the problems arising in the field of protection against the various types of NIR. At the IRPA Congress in Paris in 1977, this working group became the International Non-Ionizing Radiation Committee (INIRC). In cooperation with the Environmental Health Division of the World Health Organization (WHO), the IRPA/INIRC developed a number of health criteria documents on NIR as part of WHO’s Environmental Health Criteria Programme, sponsored by the United Nations Environment Programme (UNEP). Each document includes an overview of the physical characteristics, measurement and instrumentation, sources, and applications of NIR, a thorough review of the literature on biological effects, and an evaluation of the health risks of exposure to NIR. These health criteria have provided the scientific database for the subsequent development of exposure limits and codes of practice relating to NIR. At the Eighth International Congress of the IRPA (Montreal, 18–22 May 1992), a new, independent scientific organization—the International Commission on Non-Ionizing Radiation Protection (ICNIRP)—was established as a successor to the IRPA/INIRC. The functions of the Commission are to investigate the hazards that may be associated with the different forms of NIR, develop international guidelines on NIR exposure limits, and deal with all aspects of NIR protection. Biological effects reported as resulting from exposure to static and extremely-low-frequency (ELF) electric and magnetic fields have been reviewed by UNEP/ WHO/IRPA (1984, 1987). Those publications and a number of others, including UNEP/WHO/IRPA (1993) and Allen et al. (1991), provided the scientific rationale for these guidelines. A glossary of terms appears in the Appendix.

4,549 citations

Journal ArticleDOI
TL;DR: The evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology is presented.
Abstract: Thereisgrowinginterestinthepossiblehealththreatposedbyendocrine-disruptingchemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health. The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor , retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models. Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use. We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness. (Endocrine Reviews 30: 293–342, 2009)

3,576 citations

Journal ArticleDOI
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

27 Oct 1991
TL;DR: In this article, the effects of lead poisoning on the developing developing developing nervous system were investigated, including neurological, neurobehavioral, and developmental effects in children, and toxicity.
Abstract: Essentiality Toxicity Carcinogenicity Lead(Pb) Exposure Toxicokinetics Toxicity Neurologic, Neurobehavioral, and Developmental Effects in Children Mechanisms of Effects on the Developing Nervous System Peripheral Neuropathy Hematologic Effects Renal Toxicity Lead and Gout Effects on Cardiovascular System Immunotoxicity Bone Effects Reproductive Effects Birth Outcomes Carcinogenicity Other Effects Dose Response Treatment Organic Lead Compounds Mercury (Hg) Exposure Disposition and Toxicokinetics Metabolic Transformation Cellular Metabolism Toxicology Biological Indicators Treatment Nickel (Ni) Exposure Toxicokinetics Essentiality Toxicity Nickel Carbonyl Poisoning Dermatitis Indicators of Nickel Toxicity

1,727 citations

Journal Article
TL;DR: This publication replaces the low-frequency part of the 1998 guidelines and some guidance in this document is extended to 10 MHz to cover the nervous system effects in this frequency range.
Abstract: IN THIS document, guidelines are established for the protection of humans exposed to electric and magnetic fields in the low-frequency range of the electromagnetic spectrum. The general principles for the development of ICNIRP guidelines are published elsewhere (ICNIRP 2002). For the purpose of this document, the low-frequency range extends from 1 Hz to 100 kHz. Above 100 kHz, effects such as heating need to be considered, which are covered by other ICNIRP guidelines. However, in the frequency range from 100 kHz up to approximately 10 MHz protection from both, low frequency effects on the nervous system as well as high frequency effects need to be considered depending on exposure conditions. Therefore, some guidance in this document is extended to 10 MHz to cover the nervous system effects in this frequency range. Guidelines for static magnetic fields have been issued in a separate document (ICNIRP 2009). Guidelines applicable to movement-induced electric fields or time-varying magnetic fields up to 1 Hz will be published separately. This publication replaces the low-frequency part of the 1998 guidelines (ICNIRP 1998). ICNIRP is currently revising the guidelines for the high-frequency portion of the spectrum (above 100 kHz).

1,620 citations