Acute toxicity data definition

In practice, there will sometimes be situations for which saltwater toxicity data are not available. In these situations, it may be deemed necessary to use freshwater data in lieu of data for marine species. However, several regulatory authorities (e.g., Australia, Canada, and the United States) would not extrapolate from freshwater data to set a definitive marine EQS. Based on acute SSDs, Wheeler et al. (2002) concluded that it is possible to use freshwater toxicity data to extrapolate to saltwater effects by applying an appropriate assessment factor. However, they did not propose a value for this factor moreover, looking in detail at their results (see Section 4.6.1), this extrapolation could be overprotective in some cases. 

A battery of tests developed by Dutka et al. 1986 to test the sediments of near-shore sites of Lake Ontario (Canadian part) is used to exemplify the definitions and some results of HDT. In Lake Ontario 55 sediment samples were tested, thus, the set E contains 55 objects. Dutka et al. classified their results and used discrete scores instead of the measured (raw) data. For our analysis we have adopted their classification. Thus, s, denotes the score of the i-th test of the battery. Five specific tests form the actual battery (1) Fecal Coliforms FC , as an indicator designed to control the health state of the sediments, (2) Coprostanol CP and (3) Cholesterol CH both being indicators of loadings by fecals, (4) Microtox tests MT and (5) Genotoxicity tests GT disclosing some kind of acute toxicity and the potential for carcinogenicity, respectively (see Table 3). 

Another important definition and terminology is the so-called application factor , which is applied for converting data from one exposure period or end point to another, e.g. from an acute EC50 (measured) to a chronic NOEC (predicted). For surfactants, application factors from 10 to 1000 are generally used when missing data for chronic toxicity have to be derived from acute toxicity tests. The stringency of the acute test influences the dimension of the application factor. 

A.1.3.6.2.3 In the event that an ingredient with unknown acute toxicity is used in a mixture at a concentration >1%, and the mixture has not been classified based on testing of the mixture as a whole, the mixture cannot be attributed a definitive acute toxicity estimate, in this situation the mixture is ciassified based on the known ingredients oniy. (Note A statement that x percent of the mixture consists of ingredient(s) of unknown toxicity is required on the iabei and safety data sheet in such cases see Appendix C to this section, Aiiocation of Labei Eiements and Appendix D to this section. Safety Data Sheets.)... 

There are no definitive data regarding the metabolism of arsine. Based upon proposed mechanisms of action and the known interaction with RBCs and hemoglobin, metabolism per se may of limited importance relative to acute exposures to arsine. Delayed toxicity and lethality are observed in both humans and animals following acute exposure to arsine, and it is known that increased... 

Data on acute exposures of humans to both isomers of dimethylhydrazine are limited to case reports of accidental exposures. Signs and symptoms of exposure include respiratory irritation, pulmonary edema, nausea, vomiting, and neurologic effects. However, definitive exposure data (concentration and duration) were unavailable for these accidents. The limited data in humans suggest that the nonlethal toxic response to acute inhalation of dimethylhydrazine is qualitatively similar to that observed in animals. No information was available regarding lethal responses in humans. In the absence of quantitative data in humans, the use of animal data is considered a credible approach for developing AEGL values. 

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. 

While there is no definite evidence of a marked effect of therapeutic doses of morphine on the respiration of a normal man, this does not deny that toxic doses of morphine may cause a fatal interference in the respiration of man or that therapeutic doses of morphine may induce extreme respiratory depression in certain sick individuals. It does mean that the effects of therapeutic doses of morphine on factors concerned in the regulation of respiration in healthy individuals are not the proper source for data to explain such acute effects as may occasionally be observed chnically. Tentatively we would suggest that whenever morphine depresses respiration it does so by decreasing metabolism, by a mechanism involving an increase in hydroxyl ions, or by both (1). 

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