Toxic exposure acute

Safety. Hydrogenated terphenyls are low in toxicity as the following data (78) indicate. Single exposure (acute) studies show ... 

Neurotoxicity. Information in both humans and animals indicates that the nervous system is the major target of methyl parathion-induced toxicity following acute exposure by any route (Daly 1989 Dean et al. 1984 EPA 1978e Fazekas 1971 Gupta et al. 1985 Nemec et al. 1968 Roberts et al. 1988 Suba 1984 Yamamoto et al. 1982 Youssef et al. 1987). The most prominent signs of acute exposure to methyl... 

No animal or human data were available for inhalation exposure. There are no data regarding effects in humans after oral exposure. Information is available in animals regarding health effects following acute, intermediate, and chronic oral ingestion of diisopropyl methylphosphonate. The animal data obtained after oral exposure indicate that diisopropyl methylphosphonate is moderately toxic after acute bolus exposure but has a lower order of toxicity after intermediate and chronic exposures in food. No data were found on the toxicity of diisopropyl methylphosphonate after exposure in drinking water. Further, diisopropyl methylphosphonate is rapidly metabolized and excreted and does not accumulate. It does not appear to have reproductive or developmental effects. At the doses tested, it does not appear to be an acetylcholinesterase inhibitor, although this issue has not been resolved yet. Limited data are available for dermal exposure in humans and animals. Diisopropyl methylphosphonate does not appear to be a... 

Acute-Duration Exposure. Acute oral LD50 data are available for mice and rats (Hart 1976) and for ducks (Aulerich et al. 1979). Acute oral toxicity studies, including histopathological observations, are available for ducks, mice, rats, dogs, and mink (Aulerich et al. 1979 Hardisty et al. 1977 Hart 1976, 1980). Limited acute dermal toxicity are available for rats (Hart 1976). These data suggest a relatively low toxicity. However, a clear relationship between dose and effect has not been elucidated. Inhalation data of any kind were not identified, and dermal data were very limited. 

Donham KJ, Knapp LW, Monson R, et al. 1982b. Acute toxic exposure to gases from liquid manure. J OccupMed 24 142-145. 

The human experience regarding the toxicity of acute exposures to monomethylhydrazine exposure is limited. The study by MacEwen et al. (1970) found that a 10-min exposure to monomethylhydrazine at 169 mg/m3 (90 ppm) resulted in minor ocular and upper respiratory tract irritation. 

The following factors have been suggested as alternatives to consider when presented with a potential case of exposure to carbon monoxide diabetic ketoacidosis, hypothyroidism and myxedema coma, labyrinthitis, and lactic acidosis toxic exposures resulting in methemoglobinemia ingestion of alcohols or narcotics and diseases that cause gastroenteritis, encephalitis, meningitis, and acute respiratory distress syndrome. 

Very toxic by acute exposure (by oral, dermal or inhalation administration)... 

Clinical signs in humans and animals related to acute toxic exposure to 1,2-dibromoethane are depression and collapse, indicative of neurologic effects, and erythema and necrosis of tissue at the point of contact (oral and pharyngeal ulcers for ingestion, skin blisters and sloughing for dermal exposure). Neurologic signs are not seen in animals exposed to nonlethal doses. 

Death. 1,2-Dibromoethane can be fatal to humans after oral or dermal exposure. Acute deaths following toxic doses are related to cardiopulmonary arrest or, if affected individuals survive for a period of time, to hepatic and renal failure. These results are supported by animal studies in which acute death occurred after oral, dermal, and inhalation exposure. 

Death. Occupational mortality studies of pesticide workers exposed to heptachlor have not revealed an excess number of deaths in these cohorts compared to the general U.S. population. This may possibly be explained as a healthy worker effect. The ERA has described human case reports in which convulsions and death were reported following suicidal ingestion of technical-grade chlordane, which typically contains 6-30% heptachlor, but these effects cannot be attributed to heptachlor or heptachlor epoxide. There are no controlled, quantitative human data for any route of exposure. Acute lethality data were located for animals exposed via the oral and dermal routes. Both heptachlor and heptachlor epoxide may be considered very toxic via the oral route on the basis of acute animal data in rats and mice. Intermediate oral exposure to these compounds also caused up to 40% and 100% mortality in rats and mice, respectively. There appear to be differences in sensitivity in males and females in some species with the males being most sensitive. Heptachlor epoxide is more toxic than heptachlor. Heptachlor may be considered very toxic to extremely toxic via the dermal route on the basis of acute lethality data in rats and mice. The severity of acute effects may possibly depend upon the extent of formation of heptachlor epoxide and the species tested. 

Symptoms of exposure Acute toxic symptoms include hematuria, vomiting, convulsions, and respiratory arrest (Patnaik, 1992). 

Already in 1937 Roholm [40], originator of modern fluoride research, distinguished between chronic and acute toxicity of inorganic fluorides. Chronic toxicity is the result of continuous or repeated exposure of an organism to a toxic substance. Acute toxicity involves harmful effects in an organism through a single or short-term exposure to a toxic substance. 

Signs of methyl bromide toxicity following acute exposure include irritation of the eyes and respiratory tract, tremor, incoordination, depression of the central nervous system and convulsions. Long-term exposure induces pulmonary congestion, central nervous system effects, and renal and hepatic lesions. After oral administration to rats, hyperplasia and hyperkeratosis (and squamous-cell carcinomas) of the forestomach were observed (lARC, 1986). 

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