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Acute toxicity of organophosphates

Chambers JE and Carr RL (2001) Acute toxicities of organophosphates and carbamates. In Massaro EJ (ed.) Handbook of Neurotoxicology, pp. 3-16. Totowa, NJ Humana Press. [Pg.1895]

Acute Toxicity of Organophosphate Chemical Threat Agents...139... [Pg.135]

Organophosphates. The acute toxicity of organophosphate pesticides is basically derived from the anticholinesterase property of these chemicals. This property, which results in accumulation of acetylcholine at synapses and myoneural junctions, is responsible for both the insecticidal activity and mammalian toxicity. Early symptoms of organophosphate poisoning in humans include, among others, miosis (pinpoint pupils) and blurred vision, and a response known as the SLUD (salivation, lacrimation, urination, and diarrhea) syndrome all of these are the result of muscarinic effects (12-15). Clinical manifestations of more severe poisoning involve predominantly nicotinic and central effects which include convulsions, paralysis, depressed respiration and cardiovascular functions, and coma (12-15). Death is usually due to respiratory failure, accompanied by cardio-vascular failure (13). [Pg.23]

Fawcett, W.P., Aracava, Y., Adler, M., et al, 2009. Acute toxicity of organophosphate compounds in guinea pig is sex- and age-dependent and cannot be solely accounted for by acetylcholinesterase inhibition. J. Pharmacol. Exp. [Pg.515]

Studies on the scaleless chicken are underway examining its suitability as a model for assessing toxicity of organophosphates. The first compound selected for field trials was the defoliant DEF (S,S,S-tributylphosphorotrithioate) used during the harvesting of cotton in California and Arizona in the fall (October-November) when air movements are frequently restricted by inversions. DEF has been the subject of sufficient complaints to place it on the pre-RPAR list, although there are no reports of acute or delayed neurotoxicity in humans when it and related chemicals are used according to recommendations. It both inhibits cholinesterases and causes delayed neurotoxicity in hens (3,6). [Pg.192]

Anklcy el a . (1991) discovered that the co-ad mini strut ion of PBO effectively reduced the acute toxicity of four mctabolically activated organophosphate... [Pg.308]

Chambers, J. (1992). The role of target site activation of phospho-rothionates in acute toxicity. In Organophosphate.s Chemistry, Fate, and Effects (J. Chambers and R Levi, Eds.), pp. 229-329. Academic Press, New York,... [Pg.156]

Agent GA (tabun) is an organophosphate ChE inhibitor similar to other nerve agents in mode of action and toxic effects, and it is toxic by all possible exposure routes ingestion, inhalation, and ocular and percutaneous absorption (DA 1974). By the inhalation exposure route, GA is only half as toxic as GB however, at low concentrations it has a greater effect on the eyes (DA 1974). The acute toxicity of GA and other nerve agents has been reviewed in several earlier reports (Carnes and Watson 1989 Dacre 1984 Munro et al. 1994 Sidell 1992 ... [Pg.66]

Toxicities of organophosphate plasticizers are compiled in the hazardous substances data bank of the National Libraiy of Medicine s Toxicological Data Netwoik. All of the organophosphates mentioned in this chapter show a low acute toxicity for mammals, but seem to have weak serum cholinesterase inhibiting properties. Some of them are skin or eye irritants (e.g., TEHP, TCEP) or sensitizers (e.g., DPEHP). [Pg.580]

J. E. Chambers, The role of target site activation of phosphorothionates in acute toxicity in Organophosphates, Chemistry, Fate and Effects, ed, J. E. Chambers and P. E. Levi, Academic Press, New York, 1992, pp. [Pg.77]

Enzyme Inhibition. Some materials produce toxic effects by inhibition of biologically vital enzyme systems, leading to an impairment of normal biochemical pathways. The toxic organophosphates, for example, inhibit the cholinesterase group of enzymes. An important factor in thek acute toxicity is the inhibition of acetylocholinesterase at neuromuscular junctions, resulting in an accumulation of the neurotransmitter material acetylcholine and causing muscle paralysis (29) (see Neuroregulators). [Pg.228]

Skinner CS, Kilgore WW. 1982a. Acute dermal toxicities of various organophosphate insecticides in mice. J Toxicol Environ Health 9 491-497. [Pg.231]

Reliable NOAELs and LOAELs for intermediate oral exposure are restricted to a 90-day NOAEL of 50 mg/kg/day for systemic toxicity in rats (a species that is not sensitive to the neuropathic effects of organophosphate esters) exposed to Pydraul 90E for 90 days and NOAELs and LOAELs for delayed neuropathy in chickens exposed to Durad 110. In chickens exposed to Durad 110 for 28 days, a NOAEL of444 mg/kg/day and LOAEL of 1,333 mg/kg/day were identified (FMC 1986) when the duration was increased to 90 days, the NOAEL was 20 mg/kg/day and the LOAEL was 90 mg/kg/day (FMC 1986). These data are inadequate for derivation of an intermediate oral MRL for organophosphate ester hydraulic fluids. As discussed under the acute-duration oral MRL section, there is uncertainty regarding extrapolation of chicken doses to human doses. [Pg.193]

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. [Pg.3]

This is the only available well conducted intermediate-duration inhalation study for diazinon. In an acute-duration study in which rats were exposed to 2,300 mg/m3 diazinon for four hours (Holbert 1989), mild signs of organophosphate toxicity were noted (nasal discharge, salivation). NIOSH recommends an occupational exposure level of 0.1 mg/m3, approximately 100-fold higher than the MRL. [Pg.217]


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See also in sourсe #XX -- [ Pg.103 ]




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