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Mortality risk in Hoechst Celanese Corporation cellulose triacetate fiber production workers women's health danbury ct order generic premarin pills, Rock Hill menstruation in islam premarin 0.625 mg sale, South Carolina: 1 women's health clinic central coast buy 0.625mg premarin with mastercard,271 men and women employed 1954�1977, followed through 1990. Cancer mortality risk in Hoechst Celanese Corporation cellulose triacetate fiber production workers, Cumberland, Maryland: 2,909 men and women employed 1970�1981, followed through 1989. Incidences of histopathologic changes in livers of male and female F344 rats exposed to dichloromethane in drinking water for 90 days. Incidences of histopathologic changes in livers of male and female B6C3F1 mice exposed to dichloromethane in drinking water for 90 days. Incidence data for mammary gland tumors and internal doses based on different dose metrics in male and female F344 rats exposed to dichloromethane via inhalation for 2 years. Exposure response array for chronic (animal) or occupational (human) inhalation exposure to dichloromethane (log Y axis) (M = male; F = female. Predicted (logistic model) and observed incidence of noncancer liver lesions in male F344 rats exposed to dichloromethane in drinking water for 2 years (Serota et al. Predicted and observed incidence of animals with hepatocellular carcinoma or adenoma in male B6C3F1 mice exposed to dichloromethane in drinking water for 2 years, using liver-specific metabolism dose metric (Serota et al. Predicted and observed incidence of animals with hepatocellular carcinoma or adenoma in male B6C3F1 mice exposed to dichloromethane in drinking water for 2 years, using whole-body metabolism dose metric (Serota et al. Predicted and observed incidence of animals with hepatocellular carcinoma or adenoma in male B6C3F1 mice exposed by inhalation to dichloromethane for 2 years, using whole-body metabolism dose metric (Mennear et al. Predicted and observed incidence of animals with carcinoma or adenoma in the lung of male B6C3F1 mice exposed by inhalation to dichloromethane for 2 years, using whole-body metabolism dose metric (Mennear et al. It is not intended to be a comprehensive treatise on the chemical or toxicological nature of dichloromethane. The intent of Section 6, Major Conclusions in the Characterization of Hazard and Dose Response, is to present the major conclusions reached in the derivation of the reference dose, reference concentration and cancer assessment, where applicable, and to characterize the overall confidence in the quantitative and qualitative aspects of hazard and dose response by addressing the quality of data and related uncertainties. The discussion is intended to convey the limitations of the assessment and to aid and guide the risk assessor in the ensuing steps of the risk assessment process. Formerly of the National Center for Environmental Assessment Office of Research and Development Allan Marcus, Ph. National Center for Environmental Assessment Office of Research and Development U. National Health and Environmental Effect Research Laboratory Office of Research and Development U. Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy University of Georgia xxii David W. Department of Pharmacology and Toxicology, Division of Toxicology Indiana University School of Medicine Kannan Krishnan, Ph. Departement de sante environnementale et sante au travail, Faculte de medicine Universite de Montreal Harihara M. Department of Toxicology, College of Pharmacy the University of Louisiana at Monroe Martha M. Air Toxicology and Epidemiology Branch, Office of Environmental Health Hazard Assessment California Environmental Protection Agency xxiii 1. The RfD and RfC, if derived, provide quantitative information for use in risk assessments for health effects known or assumed to be produced through a nonlinear (presumed threshold) mode of action. The RfD (expressed in units of mg/kg-day) is defined as an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of 3 deleterious effects during a lifetime. The inhalation RfC (expressed in units of mg/m ) is analogous to the oral RfD, but provides a continuous inhalation exposure estimate. The inhalation RfC considers toxic effects for both the respiratory system (portal-of-entry) and for effects peripheral to the respiratory system (extrarespiratory or systemic effects. Reference values are generally derived for chronic exposures (up to a lifetime), but may also be derived for acute (24 hours), short-term (>24 hours up to 30 days), and subchronic (>30 days up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of continuous exposure throughout the duration specified. Unless specified otherwise, the RfD and RfC are derived for chronic exposure duration. The carcinogenicity assessment provides information on the carcinogenic hazard potential of the substance in question and quantitative estimates of risk from oral and inhalation exposure may be derived.
Distributions of metabolic menstrual bleeding cheap premarin, physiological breast cancer youngest age generic premarin 0.625 mg online, and partitioning parameters in the mouse and human models were updated by using Bayesian methods with data for mice and humans in published studies of mouse and human physiology and dichloromethane kinetic behavior pregnancy 5 months ultrasound discount 0.625 mg premarin mastercard. Monte Carlo simulations were then used with the refined probabilistic model to predict human liver cancer risk estimates at several dichloromethane exposure levels using an algorithm similar to 26 the one used by El-Masri et al. Development of these models used multiple mouse and human data sets in a Bayesian hierarchical statistical structure to quantitatively capture population variability and reduce uncertainty in model dosimetry and the resulting risk values. Metabolic kinetic parameters (VmaxC, Km, kfC, ratio of lung Vmax to liver Vmax [A1], and ratio of lung kfC to liver kfC [A2]) (Table 3-5) were calibrated with this Bayesian methodology by using several experimental data sets. These partition coefficients were derived by using a vial equilibration method similar to that used by prior investigators (Andersen et al. Tissue:air partition coefficients were approximately 2�3 times lower than previously utilized values with the exception of the liver coefficient, which was similar to previous values (Table 3-5. Posterior distributions from the first Bayesian analysis were used as prior distributions for the second step, and posterior distributions from the second step were used as prior distributions for the final updating. Final results from the Bayesian calibration of the mouse probabilistic model are shown in Table 3-5. Resultant values were three- to fourfold higher than values calculated with the Andersen et al. The only available data for levels of dichloromethane in fat came from the study of Engstrom and Bjurstrom (1977) (described in Section 3. Means for partition coefficients, the A1 ratio, and the A2 ratio were those used by Andersen et al. Estimates of the population mean values for the fitted parameters from the Bayesian calibration with the combined kinetic data for individual subjects are shown in Table 3-7. Thus, that narrowing should only be interpreted as indicating a high degree of confidence in the population mean. A component of quantitative uncertainty arises in examining the results of David et al. The authors reported Bayesian posterior statistics for the population mean parameters when calibration was performed either with specific published data sets or the entire combined data set. But according to the text and distribution prior statistics specified, the upper bound for kfC 0. Given the convergence problems with the combined data set when parameter values were unbounded, it is possible that convergence had not actually been reached after parameter bounds were introduced, and a higher value for kfC would have been obtained had the chain been continued longer. Setting this uncertainty aside, since the parameter statistics shown in Table 3-7 [values reported by David et al. Thus, to fully account for both the population variability and parameter uncertainty, a Monte Carlo statistical sampling should first sample the 0. Blood:air partition measured using human samples; other partition coefficients based on estimates from tissue measures in rats. The resulting set of parameter distribution characteristics, including those used as defined by David et al. Those values, however, reflect the in vitro differences originally quantified by Lorenz et al. In examining the derivation of the rat values, however, it appeared that Andersen et al. Once this adjustment was performed, the rat value was found to be 20-fold lower than the value used by Andersen et al. These interspecies differences in A1 and A2 are based on independent measurements of tissue-specific metabolic capacity; while the specific values for mouse and human were refined through Bayesian analysis, the ultimate (posterior) values used are within a reasonable range of the in vitro measurements and so do not appear to be artifactual. The data used for model parameter estimation are primarily measurements of parent dichloromethane kinetics (e. Metabolic parameters were re-optimized against the inhalation data of Andersen et al. However the extent of the error appears quite limited in the rat and more predominant at high exposures versus low exposures in the mouse. When extrapolated from in vitro to in vivo, the apparent values of the oxidative saturation constant, Km, identified by Reitz et al. This apparent discrepancy is partly explained by the disparate concentration ranges investigated: Reitz et al. In particular, the oxidation of dichloromethane could involve two oxidative processes, one with a high affinity (low Km) corresponding to the nonlinearity observed in vivo and one with a low affinity (high Km) corresponding to the nonlinearity observed in vitro. Another possible explanation which supports the findings observed in Kim and Kim (1996), as well as Reitz et al.
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Occupational exposure to pesticides menstruation odor purchase premarin canada, reproductive hormone levels and sperm quality in young Brazilian men menopause gynecologist safe 0.625mg premarin. Porphyria turcica due to hexachlo- robenzene: A 20 to 30 year followup study on 204 patients menstrual yoga poses buy premarin no prescription. Arsenic speciation in bile and urine fol- lowing oral and intravenous exposure to inorganic and organic arsenics in rats. The role of tobacco smoke in bladder and kidney carcinogenesis: A comparison of exposures and meta-analysis of incidence and mortality risks. M ortality patterns among women Vietnam-era veterans: Results of a retrospective cohort study. M ortality patterns of Army Chemical Corps veterans who were occu- pationally exposed to herbicides in Vietnam. Herbicide exposure, Vietnam service, and hypertension risk in Army Chemical Corps veterans. Stillbirth: Case defnition and guidelines for data collection, analysis, and presentation of maternal immunization safety data. A comparison of infant mortality rates between two Vietnamese villages sprayed by defoliants in wartime and one unsprayed village. Cancer mortality patterns among women who served in the military: the Vietnam experience. Thyroid function and plasma con- centrations of polyhalogenated compounds in Inuit adults. Estimated dietary dioxin exposure and breast cancer risk among women from the French E3N prospective cohort. Aryl hydrocarbon receptor imported into the nucleus following ligand binding is rapidly degraded via the cytosplasmic proteasome following nuclear export. Arsenic as an endocrine disruptor: Arsenic disrupts retinoic acid receptor-and thyroid hormone receptor-mediated gene regulation and thyroid hormone-mediated amphibian tail metamorphosis. Ovarian tumors in rats induced by chronic 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment. Pesticides and other occupational exposures are associated with airway obstruction: the Lifelines Cohort Study. Parental occupational exposures to chemicals and incidence of neuroblastoma in offspring. Parental occupational exposures to electromagnetic felds and radiation and incidence of neuroblastoma in offspring. Persistent organochlorine chemi- cals in plasma and risk of non-Hodgkins lymphoma. Rheumatoid arthritis among women in the Agricultural Health Study: Risk associated with farming activities and exposures. Self-reported health status of Viet- nam veterans in relation to perceived exposure to herbicides and combat. Targeting of aryl hydrocarbon receptor-mediated activation of cyclooxygenase-2 expression by the indole-3-carbinol metabo- lite 3,3-diindolylmethane in breast cancer cells. Prenatal exposure to environmental contaminants and body composition at age 7�9 years. Human exposure to endocrine disrupting chemicals and fertility: A case-control study in male subfertility patients. Exactly the same but differ- ent: Promiscuity and molecular mechanism of action of the aryl hydrocarbon (dioxin) receptor. Pesticide use and cutaneous mela- noma in pesticide applicators in the Agricultural Health Study. The health and medical status of M aine veter- ans: A report to the Bureau of Veterans Services, Commission of Vietnam and Atomic Veterans. Lack of effects of postnatal exposure to a mixture of aryl hydrocarbon-receptor agonists on the development of methylnitrosourea-induced mammary tumors in Sprague-Dawley rats. M ortality from Alzheimers disease, Parkinsons disease, and dementias in France and Italy: a comparison using the multiple cause-of-death approach. New evidence concerning the nervous site of action of a chemical herbicide causing professional intoxication.
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