Acute toxicity toxic signs

Acute toxic signs evident after each administration, but complete recovery within 30 min no measurable adverse effects after 15 months LD50... 

Humans exposed at high concentrations of some halogenated hydrocarbons can develop cardiac arrhythmias. The cardiac sensitization test in dogs is considered an effective determination of potential cardiac sensitization in humans. Cardiotoxicity was observed at concentrations well below those associated with any acute toxic signs but only in the presence of greater-than-physiological doses of exogenous epinephrine. 

There have been descriptions of the acute toxic effects in humans that follow high-dose exposure (>LD5o) to the nerve agents soman (Lekov et al., 1966 Sidell, 1974), sarin (Sidell, 1974 Inoue, 1995 Nakajima et al., 1998), and VX (Nozaki et al., 1995). The same cluster of behavioral symptoms that are reported following lower doses (anxiety, psychomotor depression, intellectual impairment, and sleep disturbances) dominate the clinical picture in the immediate period following resolution of the acute toxic signs of intoxication and then slowly fade with time, sometimes taking months to fiiUy resolve. 

Latent effects occur either only after there has been a significant period free of toxic signs following exposure, or after resolution of acutely toxic effects which appeared immediately following exposure. They are also referred to as delayed-onset effects. 

Fohc acid is safe, even at levels of daily oral supplementation up to 5—10 mg (97). Gastrointestinal upset and an altered sleep pattern have been reported at 15 mg/day (98). A high intake of foHc acid can mask the clinical signs of pernicious anemia which results from vitamin deficiency and recurrence of epilepsy in epileptics treated with dmgs with antifolate activity (99). The acute toxicity (LD q) is approximately 500 and 600 mg per kg body weight for rats and mice, respectively (100). 

Kakkar et al. (1992) exposed six male Wistar rats to a single nominal concentration of 15,302 ppm for 10 min the animals were sacrificed 24 h later. Earlier studies (not presented) had shown this to be the highest concentration tolerated without any mortality or acute toxicity. Biochemical changes in the brains of these rats suggested impairment of antioxidant defenses. No other signs of toxicity were reported. The exposure was performed under static conditions, and the measurement method was not described. 

Organic cyanide compounds, or nitriles, have been implicated in numerous human fatalities and signs of poisoning — especially acetonitrile, acrylonitrile, acetone cyanohydrin, malonitrile, and succinonitrile. Nitriles hydrolyze to carboxylic acid and ammonia in either basic or acidic solutions. Mice (Mus sp.) given lethal doses of various nitriles had elevated cyanide concentrations in liver and brain the major acute toxicity of nitriles is CN release by liver processes (Willhite and Smith 1981). In general, alkylnitriles release CN much less readily than aryl alkylnitriles, and this may account for their comparatively low toxicity (Davis 1981). 

Neurotoxicity of Pyrethroids 1.1 Acute Toxicity and Clinical Signs... 

Few data were available that met the definitions of AEGL end points. One inhalation study with 20 human subjects described headaches and slight loss of balance at exposure concentrations of 0.1 to 1.5 ppm for exposure durations of up to 8 h (Stewart et al. 1974). Acute exposure of monkeys for 6 h at concentrations ranging between 70 and 100 ppm resulted in severe signs of toxicity including convulsions but no deaths (Jones et al. 1972). In the same study, exposure of rats at a higher concentration, 189 ppm for 4 h, resulted in no toxic signs. Examination of the relationship between exposure duration and concentration for both mild and severe headaches in humans over periods of 1 to 8 h determined that the relationship is C xt=k. 

Pulskamp K, Diabate S, Krug HF (2007). Carbon nanotubes show no sign of acute toxicity but induce intracellular reactive oxygen species in dependence on contaminants. Toxicol. Lett. 168(1) 58-74. 

Guo et al. (2007) have used water-soluble MWNTs labelled with 99l"Tc for biodistribution study in mice. There was no sign of renal or other severe acute toxicity responses consistent with the results of Singh et al. (2006). This work also suggests that functionalization of CNTs might improve their biocompatibility of CNTs. 

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. 

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