Liver kidney toxicity caused

Figure 6. Liver and kidney toxicity caused by chloroform is thought to result from phosgene, a metabolite which at low levels may be rendered harmless by glutathione conjugation and further metabolism to yeild 2-oxothia2olidine-4-carboxylic acid (OTZ).

Toxicity. It is a lacrymator and irritates the skin mucous membranes, especially of the respiratory tract (Ref 26). Prolonged exposure to vapors causes damage to liver, kidneys, and other organs. Concn in air of 0.1 ppm is fatal and 3.3ppm or higher are rapidly fatal (Ref 47, p 1156). Its threshold limit value in air is set at lppm (Ref 47, p 22)... 

No information is available on the adverse health effects of hexachloroethane in humans. Animal studies revealed that hexachloroethane primarily causes liver and kidney toxicity. Effects on the nervous system and lungs have also been reported. The mechanism by which these effects are mediated is not well characterized. Reductive metabolism by cytochrome P-450 and production of a free radical intermediate have been suggested as factors in hexachloroethane-induced hepatotoxicity (Nastainczyk et al. 1982a Thompson et al. 1984 Town and Leibman 1984). Accordingly, one possible approach may be to reduce free radical injury. To that end, oral administration of N-acetylcysteine can be used as a means of reducing free radical injury. Also, oral administration of vitamin E and vitamin C may be of value since they are free radical scavengers. 

Concentrations of V, Mn, Fe, Cr, Co, Cu, Zn, As, Se, Mo, Ag, Cd, Tl, Hg, Pb, and organic mercury (Org-Hg) were determined in liver, kidney, and muscle of healthy Caspian seals (Phoca caspica) collected in 1998. These concentrations were compared with those of seals infected with canine distemper virus (CDV) found stranded along the coastal areas in 2000 (Table 1). Concentrations of toxic elements (As, Ag, Cd, Tl, Hg, Pb, and Org-Hg) in Caspian seals stranded in 2000 were comparable or lower than those of samples collected in 1998 and in other pinnipeds. Thus it may be inferred that these elements were not the causative agents in the deaths of the seals. In contrast, concentrations of Zn and Fe were much higher in diseased Caspian seals than those in other pinnipeds. Zinc concentrations in all tissues of Caspian seals also increased during 1993-2000. Furthermore, negative correlations were found between blubber thickness and hepatic and renal Zn concentrations. These results imply the disturbance... 

Death. Clinical reports in humans and studies in animals demonstrate that death due to central nervous system toxicity is the primary acute lethal effect associated with endrin exposure. A lethal dose of endrin in humans has not been identified, but 0.2-0.25 mg endrin/kg body weight is sufficient to cause convulsions (Davies and Lewis 1956). Liver, kidney, heart, and brain damage were reported following oral and inhalation exposures. Since endrin is no longer used commercially, the general public is not... 

Several cases of ingestion have shown cresol to be corrosive to body tissues and to cause toxic effects on the vascular system, liver, kidneys, and pancreas. ... 

Continuous exposure of rats by inhalation to 0.0055 and 0.3mg/m for 100 days resulted in methemoglobinemia, lowered erythrocyte hemoglobin, leukopenia and reticulocytosis, and reduced muscle chronaxie. Doses up to 500mg/kg administered by gavage to rats and mice for 13 weeks caused cyanosis and decreased motor activity, as well as hemosiderosis in the spleen liver, kidney, and testes. Bone marrow hyperplasia was observed in rats, and mice had increased hematopoiesis in the liver. In general, all toxic effects could be attributed to chronic methemoglobinemia, erythrocyte destruction, and erythrophagocytosis. 

The LCso for a 7-hour exposure of mice was 18,354ppm. Exposure 7 hours/day to 11,300 ppm for 1 week caused mild eye and nose irritation, incoordination, and light narcosis after 4 hours the exposure was fatal to 6 of 50 mice. Animals exposed to toxic concentrations often developed marked fatty changes in the liver, kidney, and heart and inflammatory changes in the lungs. Rats were unaffected by eight 6-hour exposures to 4000 ppm. ... 

Animal studies have shown MEK to enhance the development of or increase the severity of neurotoxic effects due to methyl n-butyl ketone, ethyl butyl ketone, -hexane, and 2,5-hexanedione."MEK exposure did not, however, potentiate the neurobehavioral test decrements produced by acetone. Exposure to 200 ppm MEK or 100 ppm MEK plus 12 5 ppm acetone for 4 hours did not produce any significant effects in a variety of behavioral performance tests, whereas exposure to 250 ppm acetone caused some mild decrements. The liver and kidney toxicity of haloalkane solvents may also be potentiated by MEK. ... 

Acute exposure of rats to 1,2-dichloroethane caused disseminated haemorrhagic lesions, mainly in the liver chronic exposure caused degeneration of the liver and tubular damage and necrosis of the kidneys (lARC, 1979). The limited organ toxicity of... 

Methyl chloride causes toxicity in rodents in the liver, kidney and central nervous system. It may deplete glutathione in tissues. 

Health and Safety Factors. Mesityl oxide is more toxic than saturated ketones and is highly irritating to all tissues on vapor or liquid contact and for this reason sales of mesityl oxide ceased in the United States in 1986. It is absorbed through intact skin, and prolonged exposure can damage liver, kidneys, and lungs. Repeated exposure to vapors can cause anemia and leukopenia (187) however, the odor is so intolerable that long-term exposure is unlikely. Mesityl oxide is still produced, but is consumed captively as an intermediate in the production of MIBK, methyl isobutyl carbinol, and isophorone. 

Other than in sensitive individuals, the aromatic nitro compounds are only moderately irritating to the skin, but very toxic to the liver, kidneys and nervous system. The basic mechanism of toxicity is stimulation of oxidative metabolism in cell mitochondria through interference with the normal coupling of carbohydrate oxidation to phosphorylation (ADP to AT ). The increased oxidative metabolism leads to pyrexia, tachycardia, dehydration and the ultimate depletion of fat stores. The most severe toxicity occurs when workers are concurrently exposed to hot, humid environments. Pyrexia and direct action on the brain cause cerebral edema, clinically evidenced by toxic psychosis and, at times, convulsions. Degenerative changes occur in the liver parenchyma, and renal tubules, and clinical signs of renal injury appear (albuminuria, hematuria, pyuria, increased BUN). 

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