Acute toxicity effects

Sodium nitrite is poisonous and prolonged contact with dry sodium nitrite or its solutions can cause irritation to the skin, eyes, and mucous membranes. The LD q (oral, rat) is 85 mg per kg body weight (11). Inhalation or ingestion of significant quantities of dust or mist may result in acute toxic effects such as nausea, cyanosis, and low blood pressure, which can lead to possible coUapse, coma, and even death. 

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. 

Overexposure to acryhc mbbers is not likely to cause significant acute toxic effects. ACM however may contain residual monomers, mainly acrylate monomers, vapors of which are known to cause eye and/or skin irritation. 

Male rodents have been shown to be more susceptible to acute toxic effects of methyl parathion than females (EPA 1978e Murphy and Dubois 1958). 

In summary, neurotoxic effects of endosulfan are usually apparent only after acute ingestion of relatively high doses. Cumulative neurotoxicity does not appear to be significant. If the animal survives the acute toxic effects, then no long-term neurotoxic effects are evident from behavioral, gross, and microscopic observations. However, some impairment may occur that can be detected only by specialized neurobehavioral testing. 

Bechmann, R.K. 1994. Use of life tables and LC50 tests to evaluate chronic and acute toxicity effects of copper on the marine copepod Tisbe furcata (Baird). Environ. Toxicol. Chem. 13 1509-1517. 

Lock, E.A. and J. Ishmael. 1979. The acute toxic effects of paraquat and diquat on the rat kidney. Toxicol. 

Most commonly, bioassays for the evaluation of the acute toxic effects of pesticides are based on single aquatic species selected to be representative of a range of taxonomic and functional groups, i.e., bacteria, algae, invertebrates or fish [ 53,54]. Generally, toxicity evaluation using a single species is the alternative of choice rather than the use of multiple species, because extrapolation of effects to an ecosystem is more difficult and can often lead to incorrect conclusions. 

Rhodes, C. (2000). Principles of Tseting for Acute Toxic Effects. In General and Applied Toxicology (Ballantyne, B., Marrs, T. and Szversen, T., Eds.) Macmillan References, Ltd., London, pp. 33-54. 

Persons with a history of convulsive disorders would be expected to be at increased risk from exposure to endrin. Children may be more sensitive than adults to the acute toxic effects of endrin. In an endrin poisoning episode in Pakistan, children 1-9 years old represented about 70% of the cases of convulsions (Rowley et al. 1987). The causative factor responsible for the outbreak was not identified, however, and the age distribution of cases could be explained by age-specific exposure situations. In general, following oral administration, female animals appear to be more susceptible to endrin toxicity than males (Gaines 1960 Treon et al. 1955). The difference may be due to the more rapid excretion of endrin by male versus female rats (Hutson et al. 1975 Klevay 1971 Korte et al. 1970). A sex-related difference in toxicity was not apparent following dermal exposure (Gaines 1960, 1969). No sex-based differences in endrin-related... 

Egle JL Jr, Guzelian PS, Borzelleca JF. 1979. Time course of the acute toxic effects of sublethal doses of chlordecone (Kepone). Toxicol Appl Pharmacol 48 533-536. 

Alexeeff GV, Kilgore WW, Munoz P, et al. 1985. Determination of acute toxic effects in mice following exposure to methyl bromide. J Toxicol Environ Health 15 109-123. 

At the initial stages of a release, when the benzene-derived compounds are present at their highest concentrations, acute toxic effects are more common than they are later. These noncarcinogenic effects include subtle changes in detoxifying enzymes and liver damage. Generally, the relative aquatic acute toxicity of petroleum will be the result of the fractional toxicities of the different hydrocarbons present in the aqueous phase. Tests indicate that naphthalene-derived chemicals have a similar effect. 

Humans are susceptible to the acute toxic effects of 1,2-dibromoethane from various routes of exposure. Except for adverse reproductive effects in men after occupational exposure, chronic effects of 1,2-dibromoethane exposure have not been documented in humans. Based on data derived from animal studies, mechanisms of action of 1,2-dibromoethane at a cellular level, toxicokinetics, and genotoxicity tests, there is a potential for certain adverse health effects in humans exposed chronically to low environmental levels of 1,2-dibromoethane that could exist near hazardous waste sites or areas of former agricultural use. 

Benzene is shipped in tank cars, tank trucks, barges, and drums. Transfers from one vessel to another are in dosed systems because benzene is a poisonous substance with acute toxic effects. It ll kill you in 5—10 minutes if you breathe too much. Red DOT flammable liquid labels are required. 

Threshold Limit Value-Short Term Exposure Limit (TLV-STEL) - the concentration to which workers can be exposed continuously for a short period of time without suffering from (1) irritation (2) chronic or irreversible tissue damage or (3) narcosis of sufficient degree to increase the likelihood of accidental injury, impair self-rescue, or materially reduce work efficiency, provided that the daily TLV-TWA is not exceeded. It is not a separate independent exposure limit rather, it supplements the TWA limit where there are recognized acute toxic effects from a substance whose toxic effects are primarily of a chronic nature. STELs are recommended only where toxic effects have been reported from high short-term exposures in either humans or animals. 

Symptoms of exposure Produces skin burns. Causes eye irritation on contact. Inhalation may cause irritation of the respiratory tract. Acute toxic effects following ingestion may include corrosion of mouth and gastrointestinal tract, vomiting, diarrhea, ulceration, bleeding from intestines and circulatory collapse (Patnaik, 1992 Windholz et al., 1983). An irritation concentration of 25.00 mg/m in air was reported by Ruth (1986). 

Information from case reports is primarily on acute toxic effects and the clinical symptoms can in some cases be rather well described. For some substances, however, effects may be observed only after a latency period and therefore, may not be recognized as being linked to the poisoning incident. 

In poisoning cases, the exposure concentration or dose is often unknown and thus, a dose-effect relationship is difficult to evaluate. Therefore, information from poisoning cases generally has a limited use in the hazard assessment. An exception is identification of acute toxic effects. Furthermore, poisoning cases can also indicate whether a substance can become systemically available ... 

Acute toxic effects are considered as being threshold effects, i.e., effects for which there are expected to be a threshold of substance concentration below which the effects will not be manifested. For the hazard and risk assessment, it is important to identify those dose levels at which signs of acute toxicity are observed, and the dose level at which acute toxicity is not observed, i.e., to derive a NOAEL for acute toxicity. However, it should be noted that a NOAEL is usually not derived in the classic acute toxicity smdies, partly because of the limitations in smdy design. 

Lock EA, Ishmael J. 1979. Original investigations The acute toxic effects of hexachloro-1 3-butadiene on the rat kidney. Arch Toxicol 43 47-57. 

Thallium chloride is highly toxic. Acute toxic effects are those of thallium poisoning. 

Intensive intermittent schedules of drug treatment should allow time for recovery from the acute toxic effects of antineoplastic agents, primarily bone marrow toxicity. The use of non-myelosuppressive agents can be considered during the recovery period, especially for treatment of fast-growing cancers. 

E. Intensive intermittent schedules allow time for recovery from the acute toxic effects of the antineoplastic agents. If a drug has no activity by itself, it is not likely to be beneficial in a combination. It is important not to include two drugs with the same dose-limiting toxicity. Most curable tumors require at least six to eight cycles of therapy. 

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