Selenium exposure

As visualized by the different radiation constants of 0.48 ( iridium) and 0.203 ( Selenium) exposure times differ by an approximate factor of 2.5 with slight variations depending on the actual material thicknesses under inspection. 

Diskin CJ, Tomasso CL, Alper JC, Glaser ML, Fhegel SE. Long-term selenium exposure. Arch Intern Med 1979 139(7) 824-6. 

Very high amounts of selenium have resulted in decreased sperm counts, increased abnormal sperm, changes in the female reproductive cycle in rats, and changes in the menstrual cycle in monkeys. The relevance of the reproductive effects of selenium exposure in animals studied to potential reproductive effects in humans is not known. Selenium compounds have not been shown to cause birth defects in humans or in other mammals. 

There is no evidence to support a causal association between selenium compounds and cancer in humans. In fact, some epidemiological and experimental evidence suggests that selenium exposure under certain conditions may contribute to a reduction in cancer risk. Currently, the chemopreventive potential of selenium is under research. Selenium sulfide and ethyl selenac are the only selenium compounds that have been shown to be carcinogenic upon oral administration in rodents however, significant exposure to these forms of selenium is extremely unlikely. 

Pancreatic toxicity has been observed following excess selenium exposure. Cytoplasmic flocculation was observed in lambs treated with a single oral dose of selenite, and pancreatic damage, which was not further described, was noted in rats following chronic oral treatment with selenate or selenite. Pancreatic toxicity associated with excessive selenium exposure is likely related to the unique ability of that organ to accumulate the element. 

Information concerning possible neurological effects caused by inhalation of selenium or selenium compounds is limited. Severe frontal headaches were reported by workers exposed during an accident to high concentrations of selenium fumes (compound not stated) for approximately 2 minutes (Clinton 1947). Workers at a selenium rectifier plant reported symptoms of malaise and irritability when working with selenium (exposure probably to selenium dioxide and elemental selenium, but form was not stated) (Glover 1967). The symptoms resolved whenever the workers were moved to other work. Urinary concentrations of selenium were about 0.08 mg/L, compared to 0.024—0.034 mg/L in unexposed workers. 

Some epidemiological studies report data from populations exposed to selenium in the food chain in areas with high selenium levels in soil. It is likely that selenite, selenate, and the selenium found in food and in dietary supplements comprise the majority of selenium compounds to which oral, off-site selenium exposures will occur at or near hazardous waste sites. Aside from the variation in effective dose, the health effects from exposure to selenate, selenite, and dietary selenium are not expected to differ greatly. However, oral exposures to many other compounds of selenium could occur (primarily through soil or edible plant ingestion) if those compounds were deposited at the site, or if local environmental conditions greatly favor transformation to those forms. Heavy metal selenides, aluminum selenide, tungsten diselenides, and cadmium selenide are used in industry and may end up in waste sites. 

Excess incidence of melanoma was reported for a cohort of 2,065 individuals exposed to selenium as selenate that contaminated the municipal water supply in Reggio Emilia, Italy from 1972 until 1988 (Vinceti et al. 1998). Eight individuals among the exposed cohort developed melanoma compared with 128 in the remainder of the municipal population (total number of individuals not given). The SMRs were 5.0 (95% CI=1.6-12.0) for males and 3.2 (95% CI=1.0-7.7) for females. The authors estimate the general dietary intake of selenium in the area to be 45-50 pg/day and the excess selenium supplied in the contaminated tap water to be 10-20 pg/day. However, the study is limited by the fact that no individual measurements of selenium exposure were made, and individuals were classed as exposed or unexposed depending on their place of residence. 

The antigenotoxic effects generally occur at lower selenium exposure levels than the frank genotoxicity. This discussion will focus on genotoxic effects only. In vitro studies of the genotoxicity of selenium compounds are summarized in Table 3-4, and in vivo studies of the genotoxicity of selenium compounds are summarized in Table 3-5. 

Experimental animals also efficiently absorb selenium compounds from the gut independent of the level of selenium exposure. Several studies have reported absorption of 80-100% in rats given dietary selenium administered as sodium selenite, sodium selenate, selenomethionine, or selenocystine (Furchner et al. 1975 Thomson and Stewart 1973). Other animal species also readily absorb orally administered selenium compounds. Furchner et al. (1975) estimated that over 90% of an oral dose of selenious acid was absorbed in mice and dogs, although monkeys absorbed less of the administered dose (amount unspecified). Using an in vivo perfusion method in which selenite was added directly to the duodenal end of the small intestine, the absorption of selenite was found to be linear (slope=0.0386) over the concentration range of 1-200 pM (Chen et al. 1993). 

Other possible examples of endocrine disruption due to selenium exposure include pancreatic damage in sheep and rats fed selenium as sodium selenite, sodium selenate, or seliniferous wheat (Halverson et al. 1966 Harr et al. 1967 Smyth et al. 1990) and decreased plasma glucose (an insulin-like effects) in rats injected with sodium selenate. However, these are isolated reports and it is not clear what relevance they have for selenium toxicity in humans. 

Field studies have used primarily blood or urine levels to indicate the degree of selenium exposure. Valentine et al. (1978) found a significant correlation between selenium levels in well water used for drinking and urine selenium excretion measured for 35 residents in a New Mexico community. 

Data concerning human subpopulations with unusual susceptibility to the toxic effects of selenium were not located. Epidemiologic studies have identified populations with very low or very high nutritional status, and these groups are expected to have very different responses to selenium exposures. Pregnant and nursing women are believed to require more selenium than the general public (NRC 1989). 

Cretins or other individuals with iodine or thyroid deficiencies may be more sensitive to adverse health effects from selenium exposure (Contempre et al. 1991b, 1992). Iodine supplementation of these individuals without selenium supplementation may further exacerbate the effects. The elderly may be less susceptible to the negative effects of selenium and more prone to selenium deficiencies. A number of researchers have reported lower absorption of selenium and lower selenium tissue concentrations in the elderly compared to younger adults (Martin et al. 1991 Morisi et al. 1989). 

As seen in Figure 3-10, very little quantitative information is available regarding the health effects in humans exposed to selenium compounds via inhalation. The only quantitative inhalation studies in humans that relate selenium exposure levels or selenium body levels to health effects following inhalation exposure are epidemiological cancer studies. Fatalities following inhalation exposure to selenium compounds have not been reported. Despite the large number of cases of reported inhalation exposures in occupational settings, characterization of exposure concentrations and the selenium... 

Exposure. Selenium exposure can be correlated with concentrations detected in human blood, blood components, urine, hair, and nails. Selenium concentrations found in these biomarkers in the general population can be found in Table 3-7. However, these markers vary greatly among different populations (Longnecker et al. 1991). Levels of plasma, erythrocyte and platelet GSH-Px activity, as well as selenoprotein P may serve as better markers of selenium deficiency than selenium concentrations. 

Additional research into markers of selenium status in populations and how they may be used to estimate an additional selenium exposure that would be safe would be helpful. 

Holness DL, Taraschuk IG, Nethercott JR. 1989. Health status of copper refinery workers with specific reference to selenium exposure. Arch Environ Health 44(5) 291-297. 

Rajotte BJP, P an AYS, Malick A, et al. 1996. Evaluation of selenium exposure in copper refinery workers. J Toxicol Environ Health 48 239-251. 

Valentine JL, Faraji B, Kang HK. 1988. Human glutathione peroxidase activity in cases of high selenium exposures. Environ Res 45 16-27. 

Van Noord PAH, Maas MJ, De Bruin M. 1992. Nail keratin as monitor-tissue for selenium exposure. Trace Elements in Medicine 9(4) 203-208. 

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