Acute general effects

Deals with those effects which can occur during or shortly after exposure and at a place other than the place of exposure. 

Damage to, or changes in, an organ can occur even in the absence of immediate symptoms (which may develop later). 

Some substances which display little toxicity if ingested can be aspirated (entering the lungs as a result of choking, vomiting etc.), subsequently causing pneumonia. 

Prolonged or repeated contact can cause skin disorders 

As already indicated (under Can cause... damage), non-acute effects can be delayed. Repeated exposure to certain substances can also be harmful, leading to skin/lung disorders, many of them (e.g. eczema) occasioned by an allergic reaction. Persons found to be allergic should avoid all further contact with the substance. 

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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. 

Assessments of these new chemicals are made by teams of multidisciplined scientists, and are based on limited firm data, comparisons to similar chemicals and estimations of exposure to humans and the environment. Generally, these PMNs contain some information on acute health effects but relatively scant information on chronic health and environmental effects. 

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. 

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... 

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... 

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. 

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 adverse effects seen after phenytoin administration usually result from overdosage. They are generally characterized by nystagmus, ataxia, vertigo, and diplopia (cerebellovestibular dysfunction). Higher doses lead to altered levels of consciousness and cognitive changes. 

Abecarnil is a partial agonist at the benzodiazepine -GABA receptor complex, and is used in generalized anxiety disorder. Its pharmacology suggests that it may be less likely to produce sedation and tolerance, but data thus far have not shown clear differences in its adverse effects from those of classical benzodiazepines, such as alprazolam, diazepam, and lorazepam. As expected, both acute adverse effects and tolerance are dose-related. 

The hazard classification should lead directly to labelling of acute health effects, environmental and physical hazards. The labelling approach that involves a risk assessment should only be applied to chronic health hazards, e.g. carcinogenicity, reproductive toxicity, or target organ systemic toxicity based on repeated exposure. The only chemicals it may be applied to are those in the consumer product setting where consumer exposures are generally limited in quantity and duration ... 

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