| Toxizitätsübersicht | IDENTIFICATION: There are 75 possible congeners of chlorinated naphthalenes. Commercial products are generally mixtures of several congeners and range from thin liquids to hard waxes to high melting point solids. Their main uses have been in cable insulation, wood preservation, engine oil additives, electroplating masking compounds, capacitors and refractive index testing oils and as a feedstock for dye production. HUMAN EXPOSURE: The major sources of release of chlorinated naphthalenes into the environment are likely from waste incineration and disposal of items containing chlorinated naphthalenes to landfill. In the past, chlorinated naphthalene concn of up to 14.5 mg/cu m have been measured in the workplace, while levels of 25-2900 ng/cu m have been recorded in out door air in vicinity of manufacturing sites. More recently, monitoring studies have revealed chlorinated naphthalene concn up to 150 pg/cu m at semirural sites and 1-40 pg/cu m at remote sites. A single study on chlorinated tap water revealed 0.44 ng monochloronaphthalene/l. Chlorinated naphthalenes can be absorbed via oral, inhalative and dermal routes, with absorption and distribution over the whole body after oral admin. Chlorinated naphthalenes, especially the dioxin-like congeners, have been detected in adipose tissue, liver, blood and breast milk samples from the general population at concn in the ng/kg lipid range. Severe skin reactions (chloracne) and liver disease have been reported after occupational exposure to chlorinated naphthalenes. Chloracne was common among workers who handling chlorinated naphthalenes in the 1930's to 1940's. A cohort study on workers exposed to chlorinated naphthalenes at a cable manufacturing plant found an excess of deaths from cirrhosis of the liver. However, individuals with chloracne did not show a higher mortality due to liver cirrhosis compared with other workers. The mortality from all cancers was slightly but significantly elevated among all exposed men (standardized mortality ratio =1.18), but was not more elevated in the subcohort with chloracne. This subcohort showed statistically significant excess mortality from cancer of the esophagus and from benign and unspecified neoplasms. Symptoms described in workers exposed to chlorinated naphthalenes included irritation of the eyes, fatigue, headache, anemia, hematuria, impotency, anorexia, vomiting and severe abdominal pain. ANIMAL STUDIES: Chlorinated naphthalenes have been shown to be highly bioaccumulative in fish, but less so in shrimp and algae. The amount of bioaccumulation observed incr with the degree of chlorination of the chlorinated naphthalenes. The most highly chlorinated naphthalenes do not appear to bioaccumulate. Monochloronaphthalenes appear to be readily degradable by soil and water microorganisms under aerobic conditions. Chlorinated naphthalene concn in fish range up to a maximum of around 300 ug/kg lipid weight. Monitoring studies with seabird eggs have revealed a decr in chlorinated naphthalene levels between 1974 and 1987. Hydroxy metabolites have been identified mostly for the lower chlorinated naphthalenes (mono- to tetra-) in experimental animals. There are also preliminary indications for the occurrence of methylthio- or methyl sulfoxide chloronaphthalene metabolites in the feces of rats. Elimination of the parent compounds and/or metabolites occurs via feces and urine. The higher chlorinated congeners appeared to be more toxic than the lower chlorinated ones. Long term and carcinogenicity studies with chlorinated naphthalenes have not been performed. 1-Monochloronaphthalene was not mutagenic in the Salmonella Ames test. Like related cmpd, chlorinated naphthalenes have been demonstrated to be inducers of the cytochrome p450 (CYP) dependent microsomal enzymes. Chlorinated naphthalenes were also found to change lipid peroxidation and antioxidant enzyme activities in rats in a manner indicative of oxidative stress. At least some of the biological and toxic responses of chlorinated naphthalenes are believed to be mediated via the cytosolic Ah receptor, resembling those of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related cmpd. All chlorinated naphthalenes tested cause skin irritations in laboratory animals. Chlorinated napthalenes appear to be of moderate to high acute toxicity to aquatic organisms. /Chlorinated naphthalenes, Monochloronaphthalenes/ |
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