Acute toxicity of compound

Chemical safety is the acute toxicity of compounds which needs to be considered thoroughly in view of the increasing potency and the potentially different effects on genetically different subtypes of humans or other entities of the biosphere. 

Lowe, S. (1946) Studies on the pharmacology and acute toxicity of compounds with marijuana activity. J. Pharmacol. Exp. Ther. 88, 154-161. 

Except for polybrominated biphenyls (PBB), a limited number of studies regarding the toxicity of aromatic brominated compounds has been performed. Some experiments suggest a moderate acute toxicity of these compounds (ref. 1). 

Fig. 2. Acute toxicity of organotin compounds to freshwater aquatic organisms.

The acute toxicity of different types of organomercury compounds to mammals,... 

OASIS (optimized approach based on structural indices set) has been developed by Mekenyan and co-workers [87]. Given the activities or toxicities of a set of compounds, it generates large numbers of structural indices for each and develops QSAR correlations. The approach has been used to model the acute toxicity of industrial chemicals [88]. It is claimed [89] that the method can be of use in elucidating mechanisms of action. 

Conventional WWTPs are, therefore, unable to remove wide ranges of pharmaceuticals and other compounds. For pharmaceuticals, although acute toxicity of aquatic organisms or chronic effects are unlikely with the present concentrations due to dilution effects, a wide range of pharmaceuticals are detected in the Ebro, and the overall toxicity of mixed pharmaceuticals may be high. Further studies are therefore required to assess the interactions of different compounds and the consequential health effects. In a similar manner to other pollutants, pharmaceuticals have a clear sensitivity to climate change through dilution effects, and the projected future decrease in annual precipitation could cause certain compound concentrations (e.g. anti-inflammatory diclofenac and p-blocker pranolol) to reach levels which may cause chronic effects [76]. 

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). 

Interaction effects of PCDDs with other polychlorinated compounds or mixtures are not extensively documented. For example, certain polychlorinated hexachlorobiphenyls (PCBs) have a low toxic potency to induce cleft palate deformities in mice (Bimbaum et al. 1985). However, mixtures of 2,3,7,8-TCDD and 2,3,4,5,3, 4 -hexachlorobiphenyl resulted in a tenfold increase in incidence of cleft palate in mice. Thus, the toxicity of compounds such as 2,3,7,8-TCDD may be enhanced by compounds of relatively low acute toxicity, such as selected PCBs. Bimbaum etal. (1985) concluded that the widespread environmental occurrence of such combinations suggests a need for further evaluation of the mechanism of this interaction. 

Kaise, T. and S. Fukui. 1992. The chemical form and acute toxicity of arsenic compounds in marine organisms. Appl. Organometall. Chem. 6 155-160. 

Hunziker, R. W., Escher, B. I. and Schwarzenbach, R. P. (2002). Acute toxicity of triorganotin compounds different specific effects on the energy metabolism and role of pH, Environ. Toxicol. Chem., 21, 1191-1197. 

As mentioned, RMP addresses specific chemicals/materials (compounds) it addresses the accidental release of over one hundred chemical substances. Of the RMP chemicals listed, seventy-seven include acutely toxic chemical compounds and sixty-three flammable gases. Threshold quantity levels range from 500 pounds to 20,000 pounds. USEPA estimates that approximately 100,000+ sources are covered by the rule. The universe includes chemical and most other manufacturers, certain wholesalers and retailers, drinking-water systems, wastewater treatment works, ammonia refrigeration systems, chemical wholesalers and end users, utilities, propane retailers, and federal facilities. 

The acute toxicity of PNA to the sea urchin was measured by immersion of the animals at 12°C in Instant OceanR containing known levels of test compound (Table IV). After 24 hours, the animals were observed and transferred to untreated water,... 

The acute toxicity of aliphatic nitriles, which are important industrial compounds, is ascribed mainly to the liberation of cyanide after oxidative de-nitrilation [118 - 120], The reaction involves cytochrome P450 mediated hy-droxylation of C(a) to form an intermediate cyanohydrin, which then breaks down to inorganic cyanide and an aldehyde ... 

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. 

Keller, A.E. Acute toxicity of several pesticides, organic compounds, and a wastewater effluent to the freshwater mussel, Anodonta Imbecilis, Cerlodaphnla dubla, anA Pimephalespromelas, BuU. Environ. Contam. Toxicol, 51(5) 696-702,1993. 

Mattson, V.R., Arthur, J.W., and Walbridge, C.T. Acute toxicity of selected organic compounds to fathead minnows, Office of Research and Development, U.S. EPA Report 600/3-76-097, 1976. 

Palau-Casellas, A. and Hutchinson, T.H. Acute toxicity of chlorinated organic compounds to the embryos and larvae of the marine worm Fiatynersis rfumen/ii (Polychaete Nereidae), Environ. Toxicol Water Qual, 13(2) 149-155, 1998. 

Tietze, N.S., Hester, P.G., Hallmon, C.F., Olson, M.A., and Shaffer, K.R. Acute toxicity of mosquitocidal compounds to young mosquitofish, Gambusia affinis, J. Am. Mosq. Control Assoc., 7(2) 290-293, 1991. 

It should be noted that all three are lethal, however, and so the acute toxicity of these compounds is not entirely due to C-40 substituent effects. Potency does follow the oxidation series from alcohol to aldehyde to acid vivo, suggesting that perhaps these substituents influence the degree of accessibility of each lipid-solvent soluble toxin to its membrane site of action. Being that the toxins in their natural forms are so soluble in non-polar solvents, and tend to bind to or solubilize in the lipid components of membrane... 

Fairchild EJ, Stokinger HE Toxicologic studies on organic sulfur compounds. 1. Acute toxicity of some aliphatic and aromatic thiols (mercaptans). Am Ind Elyg Assoc J 19 171-189, 1958... 

Johnson GT, Lewis TR, Wagner WD Acute toxicity of cesium and rubidium compounds. Toxicol Appl Pharmacol 32 239-245, 1975... 

Poisonings resulting in convulsions have occurred in manufacturing workers. Recovery after occupational exposures is usually complete within 24 hours. Unlike dieldrin, which persists in the body, endrin is rapidly eliminated from the body and apparently does not accumulate, even in fatty tissue. However, endrin is the most acutely toxic of the cyclodiene compounds, which also include chlordane, heptachlor, dieldrin, and aldrin. ... 

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