Acute toxicity measures

NIOSH publishes IDLH concentrations to be used as acute toxicity measures for common industrial gases. An IDLH exposure condition is defined as a condition that poses a threat of... 

Chronic toxicity may be quantitated in a similar manner to acute toxicity, using the TD50 concept. Measurement of chronic toxicity in comparison with acute toxicity measurements may reveal that the compound is accumulating in vivo and may therefore give a rough approximation of the probable whole-body half-life of the compound. 

Acute Toxicity Measure Acute toxicity of a chemical may be measured through different routes and by systemic exposures by injections such as subcutaneous, intravenous, intramuscular, and intratracheal, which are all used in experimental and medical support. Appropriate knowledge about measures and acute toxicity warnings of chemicals are necessary to contain chemical hazards vis-a-vis to achieve chemical safety and human health. 

Acute toxicity and short-term bioaccumulation. Studies of acute toxicity measure the lethal response after 24 or 96 h of exposure in various bodies of water. Test species should be chosen from amongst most commonly used organisms and standardized procedures should be applied. The test should include at least three different trophic levels, namely primary producers, primary consumers and secondary consumers. Normally, organisms such as green algae, daphnids and fish are utilized. 

IDLHs. The National Institute for Occupational Safety and Health (NIOSH) publishes Immediately Dangerous to Life and Health (IDLH) concentrations to be used as acute toxicity measures for common industrial gases. An IDLH exposure condition is defined as a condition that poses a threat of exposure to airborne contaminants when that exposure is likely to cause death or immediate or delayed permanent adverse health effects or prevent escape from such an environment (NIOSH, 1994). IDLH values also take into consideration acute toxic reactions, such as severe eye irritation, that could prevent escape. The IDLH is considered a maximum concentration above which only a highly reliable breathing apparatus providing maximum worker protection is permitted. If IDLH values are exceeded, all unprotected workers must leave the area immediately. 

Carcinogenicity of DGEBPA or DGEBPA-based resins, as measured by topical appHcation, has not been shown by a majority of the studies (45). Advanced DGEBPA resins exhibit low systemic toxicity either by dermal or oral routes and inhalation of these resins is unlikely because of low volatihty. The acute oral LD q in rats has been reported to be >2000 mg/kg (46). Acute dermal studies show these materials have alow potential for absorption through the skin in acutely toxic amounts. No evidence of carcinogenicity has been found in animals or humans for advanced DGEBPA resins (47,48). 

Many methods have now been developed for measuring the potential harmful effects chemicals can have. Common tests include those for irritancy, mutagenic effects, reproductive effects and acute toxicity. 

The purified tetraethyl pyrophosphate is a colorless, odorless, water-soluble, hygroscopic liquid (24, 4 )- It possesses a very high acute toxicity (28), exceeding that of parathion, and is rapidly absorbed through the skin. There is no spray-residue problem, however, for tetraethyl pyrophosphate hydrolyzes even in the absence of alkali to nontoxic diethyl phosphoric acid. Hall and Jacobson (24) and Toy (47) have measured its rate of hydrolysis, which is a first-order reaction. Its half-life at 25° C. is 6.8 hours and at 38° C. is 3.3 hours. Coates (10) determined the over-all velocity constant at 25° C. k = 160 [OH-] + 1.6 X 10 3 min.-1 Toy (47) has described an elegant method for preparing this ester as well as other tetraalkyl pyrophosphates, based upon the controlled hydrolysis of 2 moles of dialkyl chlorophosphate ... 

Organophosphate insecticides also inhibit RBC-ACHE and PCHE. Inhibition of ACHE in erythrocytes is assumed to mirror inhibition of ACHE in the nervous system, which is the receptor of the toxic action, to some extent. Therefore, measurements of RBC-ACHE and PCHE are used for biological monitoring of exposure to OP insecticides (Maroni, 1986). Inhibitions of RBC-ACHE and PCHE activities are correlated with intensity and duration of exposure, although at different levels for each OP compound. Blood ACHE, being the same molecular target as that responsible for acute toxicity in the nervous system, is a true indicator of effect, while PCHE can only be used as an indicator of exposure. 

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. 

In all cases, the concentrations of malathion and fenitrothion measured in water (up to 5.8 and 1.2 pg/L, respectively) were below the LC50 (lethal concentration 50%) values reported for these compounds in oysters and mussels, which range between 2.7 and 278 mg/L in the case of malathion, and between 10.3 pg/L and 123 mg/L in the case of fenitrothion (http //www.pesticideinfo.org). However, it has to be stressed that these LC50 values express acute toxicity, that both malathion and fenitrothion might be bioaccumulated by molluscs (as their detection in biota suggests), and that aquatic organisms are exposed to a variety of contaminants, some of which could show synergetic or additive effects [40]. Further matters of... 

Pharmacologically, carbofuran inhibits cholinesterase, resulting in stimulation of the central, parasympathetic, and somatic motor systems. Sensitive biochemical tests have been developed to measure cholinesterase inhibition in avian and mammalian brain and plasma samples and are useful in the forensic assessment of carbamate exposure in human and wildlife pesticide incidents (Bal-lantyne and Marrs Hunt and Hooper 1993). Acute toxic clinical effects resulting from carbofuran exposure in animals and humans appear to be completely reversible and have been successfully treated with atropine sulfate. However, treatment should occur as soon as possible after exposure because acute carbofuran toxicosis can be fatal younger age groups of various species are more susceptible than adults (Finlayson et al. 1979). Carbofuran labels indicate that application is forbidden to streams, lakes, or ponds. In addition, manufacturers have stated that carbofuran is poisonous if swallowed, inhaled, or absorbed through the skin. Users are cautioned not to breathe carbofuran dust, fumes, or spray mist and treated areas should be avoided for at least 2 days (Anonymous 1971). Three points are emphasized at this juncture. First, some carbofuran degradation... 

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

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