Human body burden

Kutz FW, Strassman SC, Stroup CR, et al. 1985. The human body burden of mirex in the southeastern United States. J Toxicol Environ Health 15(3-4) 385-394. 

The changes in metabolite concentrations in human blood, urine, or other appropriate biological media over time may be useful in estimating phenol s rate of metabolism in humans. In some instances, the quantification of metabolites may be useful in correlating the exposure doses to the human body burden. Studies that correlate phenol exposure with levels of metabolites in human biological matrices are not available for this compound, although analytical methods for the quantification of the metabolites are available. 

XZ/N VI RON MENTAL APPLICATIONS OF CHEMOMETRics are of interest because of the concern about the effects of chemicals on humans. The symposium upon which this book is based served as an important milestone in a process we, the editors, initiated in 1982. As members of the Environmental Protection Agency s Office of Toxic Substances (OTS), we have responsibilities for the acquisition and analysis of human and environmental exposure data in support of the Toxic Substances Control Act. OTS exposure studies invariably are complex and range from evaluating human body burden data (polychlorinated biphenyls in adipose tissue, for example) to documenting airborne asbestos levels in schools. 

The quantitative determination of the concentrations of PBBs in blood, serum, adipose tissue, milk, and other body tissues or fluids is important in determining the human body burden of these chemicals. Fat is the largest repository of PBBs in the body, and concentrations in fat can provide an index of body burdens and exposure. It is simpler and less invasive to collect samples of serum or breast milk than body fat. However, the collection of milk and serum for the estimation of possible body burtfen has limitations. Breast milk can be obtained from limited segments of the population. Also the concentration of PBBs in breast milk can show considerable fluctuations because the breast is emptied only periodically (Brilliant et al. 1978 Willett et al. 1988). Serum, however, has lower PBB concentrations than body fat (see Section 3.5.1). 

Dioxin Dioxin in blood or lipid Biomarker to body burden and external dose in humans body burden and external dose to toxicity in animals Biomarker results can estimate human risk exposure intervention possible... 

BECHER G Dietary exposure and human body burden of dioxins and dioxin-like PCBs in Norway , Organohalogen Compounds, 1998 38 79-82. 

Becher, G., Eriksen, G., Lund-Larsen, K., Skaare, J., M, S., Alexander, J., 1998. Dietary exposure and human body burden of dioxins and dioxin-like PCBs in Norway. Organohalo. Compd. 38, 79-82. 

TCDD human body burdens calculated from available serum lipid 2,3,7,8-TCDD levels are presented in Table 2-1. 

Comparison of Estimated Body Burdens Associated with Effects in Experimental Animals and Humans. Estimated average body burdens of 2,3,7,8-TCDD in human populations in which various health effects of 2,3,7,8-TCDD are suspected range from 31 to 6,600 ng/kg (estimated body burdens at the time of exposure termination). See Table 2-1 for more information. The human body burden expected in populations exposed to background environmental levels of 2,3,7,8-TCDD has been estimated to be 1 ng TCDD/kg body weight (DeVito et al. 1995 Orban et al. 1994). This would suggest that effects of 2,3,7,8-TCDD in humans may occur at body burdens that are 30 to 6,600 times greater than background burdens for 2,3,7,8-TCDD. 

DeVito MJ, Bimbaum LS, Farland WH, et al. 1995. Comparisons of estimated human body burdens of dioxin-like chemicals and TCDD body burdens in experimentally exposed animals. Environ Health Perspect 103 820-831. 

Ryan JJ, Gasiewicz TA, Brown Jr JR. 1990. Human body burden of polychlorinated dibenzofiirans associated with toxicity based on the Yusho and Yucheng incidents. Fund Appl Toxicol 15 722-731. 

Aylward LL, Hays S, Finley B. 2002. Temporal trends in intake of dioxins from foods in the U.S. and Western Europe issues with intake estimates and parallel trends in human body burdens. 22nd Int Symp Halogenated Environ Organic Pollutants POPs 55 235-238. 

Sasaki, K., Harada, K., Saito, N., Tsutsui, T., Nakanishi, S., Tsuzuki, H., et al. Impacts of airborne perUuorooctane sulfonate on the human body burden and the ecological system. Bull. Environ. Contam. Toxicol., 71 408-413 (2003). 

The highest CB-77, CB-126, and CB-169 human body burden has been shown in a French study [163]. These levels are higher than what was reported in Yusho victims [33]. A Dutch study involving 198 mothers [164] and a Swedish study involving 1072 mothers (between 1972 and 1989) [165] are, so far, the largest sampled works. A study in Finland involving 237 mothers [166] indicates that the body burden in Nordic countries is more or less the same and is one of the lowest reported (Table 5). Potentially very toxic CB-126 has been reported in all the studies on human beings. Persistency of CB-169 has been confirmed and the metabolizability of CB-77 has been shown. 

Equation (2) was used to calculate apparent half-lives when human body burden data, such as blood, serum, plasma, or adipose tissue concentrations of PCBs are available at two or more time points. 

Approximately 1% of the human body burden of MeHg is excreted daily (Clarkson et al. 1988). In humans, the major routes of excretion are via the bile and feces. About 90% of a given dose of MeHg is eventually excreted in the feces as mercuric Hg in humans and other species. Approximately 10% is excreted as mercuric Hg via the urine. Much of the biliary MeHg is reabsoibed MeHg complexed with glutathione is eliminated via the bile. 

The daily excretion of MeHg is about 1% of the human body burden. It is excreted mainly via the bile and feces as MeHg and mercuric Hg. Complexing with GSH is involved. Urine MeHg concentrations do not accurately reflect MeHg exposure. 

TABLE 7.2 Human Body Burden of BPA (only Studies with Sensitivity < 0.1 Ng/g Reported)... 

Lead is ubiquitous in everyday life - it is in the atmosphere, the soil, and present in varying concentrations in food and drink. When Devergie and Hervy (1838) first suggested that lead was present in the body normally, they initiated a controversy that was not finally resolved until the advent of methods sensitive enough to detect traces of lead with reasonable reliability. Today the presence of the human body burden of lead is unquestioned. 

Sauerhoff, M. W. and Michaelson, I. A. (1973). Hyperactivity and brain catecholamines in lead-exposed developing rats. Science, 182, 1022 Scarborough, J. (1969). Roman Medicine. (New York Cornell University Press) Schlaepfer, W. W. (1969). Experimental lead neuropathy a disease of the supporting cells in the peripheral nervous system. J. Neuropathol. Exp. Neurol., 21, 401 Schroeder, H. A. and Mitchener, M. (1971). Toxic effects of trace elements on the reproduction of mice and rats. Arch. Env. Health, 23, 102 Schroeder, H. A. and Tipton, I. H. (1968). The human body burden of lead. Arch. Env. Health, 17, 965... 

In areas that are significantly contaminated with radionuclides or in areas with elevated rates of transfer of radionuclides from soil to biota, whole body measurement techniques can be applied to determine the human body burden and to assess doses due to the internal exposure of critical groups. Seasonal variations in the content of some radionuclides in the human body should be taken into account when assessing annual doses on the basis of particular whole body measurements. The results of individual measurements should be used mainly for validation of the models applied for the purposes of internal dose assessment. 

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