The cytotoxic effects of volatile and water-insoluble organic solvents (ethylbenzene, tetrachloroethylene, n-hexane) were tested on isolated hepatocytes in monolayer culture by using the 3-(4,5 dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) reduction assay. All of the tested compounds inhibited metabolic activity of hepatocytes and this effect depended on the concentration of solvents in the incubatory medium. The presence of fetal calf serum in the medium did not change the cytotoxicity of xenobiotics. IC50 values calculated on the basis of the MTT assay indicated that ethylbenzene was more cytotoxic than tetrachloroethylene and n-hexane. Using hepatocyte monolayer culture and the MTT assay to assess cytotoxicity of organic solvents causes many technical problems. It seems that it cannot be used as a rapid, cheap, and credible method.
Cytotoxicity of resorcinol to 3T3 fibroblast in short- (3 hrs) and long-term (72 hrs or 6 weeks) exposure was investigated. The effects of resorcinol on cell viability (neutral red uptake, NRU assay), mitochondrial function (MTT assay) and total cell protein (Kenacid Blue assay) were estimated. As a model for long-term exposure an INTEGRA CL 6-WELL bioreactor was used. The concentrations of resorcinol producing 20, 50 and 80% inhibition of cell growth in the NRU test were lower than in the MTT test after 3 hrs of exposure. The use of an INTEGRA CL 6-WELL bioreactor allows continuous culturing and exposure to test chemical of cells for several weeks, but the strong adhesiveness of fibroblast and forming aggregates make it difficult to remove them from chambers. Resorcinol in concentration of 1 microg/cm(3) did not decrease the viability of cells to 50% of control in long-term exposure in the bioreactor.
The working environment is the special case of the non-natural environment created by man in which the increased production activity brings about the concentration of stimulators particularly aggressive to the human organism, such as chemical hazards, noise, vibration, extreme temperatures, and finally, intensified psychological and emotional stress. Depending on the nature and intensity, working environment factors have been classified into dangerous, harmful and annoying. The workers are more and more frequently exposed to dangerous chemicals in the working environment. The chemicals cause many diseases including, in the 1st place, respiratory insufficiency, inflammatory skin conditions, psychoneurological disorders and neoplastic diseases. Occupational exposure limit values (OELs), the main criteria for occupational exposure assessment, constitute an important factor for the safe use of chemicals in the working environment. In Poland, to date there are 524 chemical substances and 19 dusts for which maximum admissible concentrations (MAC) have been established. THE HISTORYThe history of establishing occupational exposure levels for agents harmful to health in the working environment in Poland begins around 1956. There were 14 substances for which maximum admissible concentration (MAC) values were established without documentation [1]. The values did not differ from those which were at that time valid in the Soviet Union.
StreszczenieW artykule omówiono zasady ustalania wartości dopuszczalnych stężeń dla czynników rakotwórczych przyjęte w Polsce, Unii Europejskiej i wybranych państwach WE. Substancje rakotwórcze i/lub mutagenne stanowią bezpośrednie zagrożenia życia osób narażonych na ich działanie. Jeżeli nie można ich wyeliminować ze środowiska pracy i życia, narażenie na nie należy ograniczyć do minimum. Ocena ryzyka zdrowotnego ze strony substancji rakotwórczych polega na określeniu prawdopodobieństwa zachorowania na chorobę nowotworową lub zgonu z powodu choroby nowotworowej w następstwie narażenia zawodowego na daną substancję rakotwórczą. Med. Pr. 2013;64(4):541-563 Słowa kluczowe: czynniki rakotwórcze, klasyfikacja, wartości dopuszczalnych stężeń, ocena ryzyka AbstractThe principles of determining exposure limits for carcinogens adopted in Poland, the European Union and in other selected countries of the EC are discussed in this article. Carcinogens and/or mutagens pose a direct health risk to people exposed to them. If carcinogens cannot be eliminated from the work and living environments, their exposure should be kept at the lowest possible level. To assess health risk for carcinogens it is necessary to determine the probability of developing a disease or of death from cancer as a result of occupational exposure to carcinogenic substances. Med Pr 2013;64 (4) WSTĘPCzynniki rakotwórcze (kancerogeny) to czynniki śro-dowiska pracy (chemiczne, fizyczne i biologiczne) powodujące wzrost zapadalności i umieralności na specyficzne choroby nowotworowe w populacji osób narażo-nych w porównaniu z populacją osób nienarażonych. U pracowników narażonych na substancje chemiczne o działaniu rakotwórczym zmiany nowotworowe mogą ujawnić się po upływie wielu lat od chwili pierwszego narażenia. Czas tego opóźnienia jest nazywany okresem latencji i może wynosić 4-40 lat.Nowotwory powstałe w następstwie narażenia zawodowego mogą być zlokalizowane w różnych miejscach organizmu, niekoniecznie ograniczonych do miejsca bezpośredniego kontaktu z substancją chemiczną. Substancje takie, jak arsen, azbest, chrom i nikiel mogą powodować nowotwory płuc. Nowotwory jamy nosowej i zatok nosowych mogą być następ-stwem narażenia na chrom, nikiel, oleje izopropylowe,
Metabolic and toxicodynamic interactions of some organic solvents in rats repeatedly treated with medium dose levels were examined. It was shown that both n-hexane and ethylbenzene significantly inhibited tetrachloroethylene metabolism during a 2-week period. n-Hexane and tetrachloroethylene enhanced metabolism of ethylbenzene whereas ethylbenzene suppressed n-hexane metabolism only at the end of the experiment. Biochemical changes, especially the drop in the level of non-protein sulfhydryl groups in tissues of rats treated with organic solvent mixtures, were significantly less pronounced than those observed after these chemicals were administered separately. These results demonstrate that metabolic interactions between hydrocarbons and chloroalkene may lead to a modification of the biological response to these compounds.
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