Exposure dichlorvos

Animals exposed to dichlorvos vapor were found to absorb at least 50% of the total material by the respiratory route. Dichlorvos can also be absorbed through the oral and dermal routes. Following oral exposure, dichlorvos is rapidly detoxified in the liver. Metabolites include 0,0 -dimethyl phosphate, monomethyl phosphate, 0-methyl-0-2,2-dichlorovinyl phosphate (desmethyl dichlorvos), and inorganic phosphate. Detoxification processes for dichlorvos are also found in plasma. 

Even though all OP insecticides have a common mechanism of action, differences occur among individual compounds. OP insecticides can be grouped into direct and indirect ACHE inhibitors. Direct inhibitors are effective without any metabolic modification, while indirect inhibitors require biotransformation to be effective. Moreover, some OP pesticides inhibit ACHE more than PCHE, while others do the opposite. For example, malathion, diazinon, and dichlorvos are earlier inhibitors of PCHE than of ACHE. In these cases, PCHE is a more sensitive indicator of exposure, even though it is not correlated with symptoms or signs of toxicity. 

Most insecticides, especially the organophosphate group, cause neurotoxicity as their major mode of action. Assessment of the neurotoxicity includes neurochemical endpoints such as cholinesterase (including acetylcholinesterase, which is the major neurotransmitter in vertebrates such as fish, and other enzymes such as butyrylcholinesterase) inhibition and behavioral endpoints such as swimming speed [79]. Studies done in rats show the neurotoxic action of insecticides such as dimethoate, methyl parathion, dichlorvos, ethyl parathion or propoxur after a prolonged exposure [80,81]. 

Although several epidemiological studies have suggested a positive association between dichlorvos exposure and cancer, conclusions are limited because all have involved small study groups and exposure to several agents. In animal studies chronic gavage administration of dichlorvos caused a dose-related increase in papillomas of the forestomach in mice and a dose-related increase in mononuclear-cell leukemia and an increased incidence of pancreatic acinar cell adenomas in male rats. The lARC has determined that there is sufficient evidence for the carcinogenicity of DDVP in experimental animals and inadequate evidence in humans. ... 

Menz M, Luetkemeir H, Sachsse K Longterm exposure of factory workers to dichlorvos (DDVP) insecticide. Arch Environ Health 28 72-76, 1971... 

Metrifonate is an organophosphorous compound that is effective only in the treatment of S. haematobium The active metabolite, dichlorvos, inactivates acetylcholinesterase and potentiates inhibitory cholinergic effects. The schistosomes are swept away from the bladder to the lungs and are trapped. Therapeutic doses produce no untoward side effects except for mild cholinergic symptoms. It is contraindicated in pregnancy, previous insecticide exposure, or with depolarizing neuromuscular blockers. Metrifonate is not available in the United States. 

If a keyword consists of a phrase which contains a word identical to a Boolean operator, this word must be changed (e.g., AID can be substituted for AND). This is important to remember when using the terms describing biological end points as listed in Table 3. A search for craniofacial defects resulting from dichlorvos exposure can be worded ETIC AND 62-73-7 AND CRANIUM AID FACE (KW). 

Malathion, trichlorophen, Dichlorvos Silica gel Chloroform G ethyl acetate containing (9 1) silver nitrate or in the case Extracted from water with chloroform. Rf. Trichloronhon Spray with butter yellow then expose to UV Malathion exposure to bromine vapour 1-2 Mg [82]... 

The fabric samples for exposure to dichlorvos were placed in a wooden, glass-topped museum case along with one No-Pest Strip in such a manner that the strip would not touch the samples. The time of duration to the dichlorvos vapor was four weeks, after which the fabric samples were removed from the museum case for testing. 

Cross-resistance refers to a situation in which a strain that becomes resistant to one insecticide automatically develops resistance to other insecticides to which it has not been exposed. For example, selection of a strain of Spodoptera littoralis with fenvalerate resulted in a 33-fold increase in tolerance to fenvalerate. The resistant strain also showed resistance to other pyrethroids (11- to 36-fold) and DDT (lower than for the pyrethroids). Exposure of Cidex qninquefasciatus to fenitrothion resulted in the development of resistance to the carbamate insecticide propoxur. Similarly, selection of a housefly strain with permethrin resulted in a 600-fold increase in resistance to permethrin. The resistant strain also showed resistance to methomyl, DDT, dichlorvos, and naled (Hassall, 1990). 

Das, Y.T., P.K. Taskar, H.D. Brown and S.K. Chattopadhyay (1983). Exposure of professional pest control operators to dichlorvos (DDVP) and residue on house structures, Toxicol. Lett., 17, 95-99. 

Gold, R.E. and T. Holcslaw (1985). Dermal and respiratory exposure of applicators to dichlorvos-treated residences, in Dermal Exposure Related to Pesticide Use, R.C. Honeycutt, G. Zweig and N.N. Ragsdale (Eds), ACS Symposium Series 273, American Chemical Society, Washington, DC, USA, pp. 253-264. 

Exposure to dichlorvos vapor can result in exposure through not only the respiratory route but also the dermal and oral routes (e.g., through contamination of feed). 

Under most conditions, dichlorvos is not detectable in any tissues. Dichlorvos is not stored in tissues, it does not accumulate in secretions (e.g., milk), and it is below detection levels in the blood of various species at exposure levels in excess of 10 times those effective for insect control. At exceptionally high concentrations (90mgm or about 2000 times normal exposure levels), dichlorvos was detectable in various tissues of the rat. 

Dichlorvos is rapidly metabolized and excreted by mammals following any route of exposure. 

The toxicity of dichlorvos is due to inhibition of acetylcholinesterase and the signs of toxicity are generally similar to those caused by other organo-phosphorus insecticides. Dichlorvos is a direct inhibitor of cholinesterases thus, toxicity rapidly follows exposure and recovery is also rapid. With inhalation exposures, airway acetylcholinesterase inhibition is possible in the absence of significant blood enzyme inhibition. The fly head acetylcholinesterase appears more sensitive to inhibition by dichlorvos relative to mammalian brain acetylcholinesterase. At high doses, dichlorvos may cause hyperglycemia and abnormal glucose tolerance. 

Inhalation, dermal, or oral exposure to dichlorvos can result in systemic toxicity through inhibition of acetylcholinesterase. Symptoms of acute exposure to dichlorvos may include blurred vision, nausea, headache, and shortness of breath. 

Increased risk from exposure to dichlorvos will occur in persons who have reduced lung function, convulsive disorders, liver disorders, or recent exposure to cholinesterase inhibitors. 

Symptoms of chronic exposure to dichlorvos are similar to those of acute exposure, in addition to which there could be tension, insomnia, loss of appetite, apathy, trembling, and confusion. 

In humans, the plasma cholinesterase appears more sensitive than erythrocyte cholinesterase to inhibition by dichlorvos thus, discrimination between these two activities may be warranted during assessment of exposures. 

Mehl, A., Rolseth, V., Gordon, S., Bjoraas, M., Seeberg, E., and Fonnum, F. 2000. Brain hypoplasia caused by exposure to trichlorfon and dichlorvos during development can be ascribed to DNA alkylation damage and inhibition of DNA alkyltransferase repair. Neurotoxicology, 21, 165-173. 

TRICHLOROPHON or TRICHLORO-PHON FN (52-68-6) C4HgCi304P Contact with alkaline materials (e.g., lime, lime sulfur) causes decomposition to dichlorvos. Incompatible with acids and bases (toxic fume formation) prolonged exposure to moisture or elevated temperatures + water. Conosive to many metals, including iron and steel. 

A total exposure of several times the acute LDs ) dose over a prolonged period can be tolerated by rodents when exposed repetitively to OP compounds such as schradan (Rider et at.. 1952), demeton (Barnes and Denz 1954a,b), disiilfoion (Brodeur and Dubois, 1964 Stavinoha ei al., 1969), DFP (Glow et al., 1966 Russel ef at., 1975), paraoxon (Weeker et at., 1977), dichlorvos (Sterri, 1981), sarin (Fonnum and Steni, 1981 Sterri, 1981), or soman (Sterri et al., 1980, 1981 Fonnum and Sterri, 1981 Sterri, 1981). For several of these compounds, the spontaneous reactivation of inhibited AChE may explain part of the tolerance. For soman, however, the tolerance cannot be related to any recovery of AChE since sornan is a completely irreversible AChE inhibitor (Coult ef /.. 1966). 

Sarin, 5, and Gill, K. D, (199B). Biochemical and behavioral deficii.s in adult rat following chronic dichlorvos exposure. Piuirmacol. Biochem. Beha 59, 1081-1086. 

The effect of dichlorvos exposure on lipid peroxidation and the antioxidant defense system in different regions of the rat central nervous system was also studied. Inhibition of AChE activity was used as an index of dichlorvos... 

It is estimated that 18% of all new Wilms tumours, affecting the kidneys of Brazilian children, are attributable to pesticide exposure of their parents. Consistently elevated risks were seen among children whose fatlier or mother carried out farm work which involved the frequent use of pesticides. As elsewhere, many pesticides are used in Brazil and researchers estimated that 73 insecticides, 42 fungicides and 59 herbicides are in use. Atrazine and dichlorvos are particularly widely used and both are rated as possibly carcinogenic by the International Agency for Research in Cancer. 

Berger-Preiss et al. (2002) measured indoor pyrethroid exposure in 80 homes with woollen textile floor coverings. While permethrin concentrations in house dust were high (mean 53.7 pg g ), the permethrin concentrations in suspended particles were very low (mean 2.8 ng m ). Roinestad et al. (1993) identified 30 pesticides in household dust ranging from 80 (diazinon) to 15000 (chlorpyrifos) ng g . Permethrin levels decreased from 2550-3850 (just after application) to 550-675 ng g 8 weeks after pesticide application. However, dichlorvos and... 

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