Animals acute effects

Fazekas 1971) exposed by various routes. Because of a lack of toxicokinetic data, it cannot be assumed that the end points of methyl parathion toxicity would be quantitatively similar across all routes of exposure. The acute effects of dermal exposures to methyl parathion are not well characterized in humans or animals. Therefore, additional dermal studies are needed. 

The data in animals are insufficient to derive an acute inhalation MRL because serious effects were observed at the lowest dose tested (Hoechst 1983a). No acute oral MRL was derived for the same reason. The available toxicokinetic data are not adequate to predict the behavior of endosulfan across routes of exposure. However, the limited toxicity information available does indicate that similar effects are observed (i.e., death, neurotoxicity) in both animals and humans across all routes of exposure, but the concentrations that cause these effects may not be predictable for all routes. Most of the acute effects of endosulfan have been well characterized following exposure via the inhalation, oral, and dermal routes in experimental animals, and additional information on the acute effects of endosulfan does not appear necessary. However, further well conducted developmental studies may clarify whether this chemical causes adverse developmental effects. 

Further information gained from accidental human exposures could be utilized in defining the lowest air level that affects humans. Similarly, studies on the acute effects of dermal exposure to trichloroethylene in animals may be useful in determining the risk for these exposures in humans at hazardous waste sites. However, there appear to be sufficient data available on neurological effects after acute inhalation exposure. 

M usculoskeletal Effects. Accidental exposure of a worker to 241 Am resulted in histological signs of fibrosis, bone cell depletion, and bone marrow atrophy. Degenerative changes in bone have also been observed in animals acutely exposed to 241 Am via inhalation and intravenous administration. 

Some values for tests on rats are given in Table 9.1. Estimates of the LD50 for man are based on tests on animals. The LD50 measures the acute effects it gives only a crude indication of the possible chronic effects. 

Effects observed in animals are similar to those that have been observed in humans. Death has occurred in animals after inhalation of high concentrations of hydrogen sulfide. Acute inhalation exposures to hydrogen sulfide have also resulted in respiratory, cardiovascular, neurological, hepatic, body weight, and developmental effects in animals. Gastrointestinal effects have been noted in animals after oral exposure to hydrogen sulfide. 

Intake can be expressed either as a pollutant mass per unit time, as discussed above, or as a mass per kg of body weight per unit time. The latter expression facilitates comparison to health effects data, especially laboratory animal data, which are commonly reported in equivalent units. Similarly, depending on the route of exposure, intake may be estimated on an annual basis to address chronic effects, or on a smaller time scale for addressing acute effects including lethality, teratogenesis, reproductive and neurotoxic effects. 

Lupien, S. J. and McEwen, B. S. The acute effects of corticosteroids on cognition integration of animal and human model studies. Brain Res. Rev. 24 1-27,1997. 

Neurological Effects. The central nervous system is the primary target for cyanide toxicity in humans and animals. Acute-duration inhalation of high concentrations of cyanide provokes a brief central nervous... 

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. 

Aqueous and sedimentary TBT and TFT cause chronic and acute effects in algae, zooplankton, Crustacea, mollusks, fish, and animals. These effects have been local in nature, occurring mostly in harbors near industrialized lands. TBT is bioaccumulated in many species, which is unfortunate as it is a potent endocrine disrupter. The enrichment factor in mussels, snails, and oysters ranges from 10,000 to 60,000. As mentioned in Section 28.7.1, TBT induces imposex in marine gastropods. 

One feature of the response to oxidants (in particular, ozone) that has stimulated considerable interest is the apparent development of tolerance to the acute effects of short-term exposure to these agents in laboratory animals. Fairchild reviewed possible mechanisms of this phenomenon. Tolerance has been defined as the increased capacity of an organism that has been pre-exposed to oxidant to resist the effects of later exposures to ordinarily lethal (or otherwise injurious) doses of the same agent or of different agents (cross-tolerance) with similar toxicologic properties. 

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