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Parathion development

Meinke, LJ USDA Western corn rootworm resistance to methyl parathion-development of resistance management strategies... [Pg.172]

The hazards of human poisoning by the parathions have stimulated the development of safer analogues. Two chlorinated derivatives have gready reduced mammalian toxicides. Dicapthon [2463-84-5], 0,0-dimethyl 0-(2-chloro-4-nitrophenyl) phosphorothioate (63) (mp 53°C), has rat LD qS of 400, 330 (oral) and 790, 1250 (dermal) mg/kg. Chlorthion [500-20-8], 0,0-dimethyl 0-(3-chloro-4-nitrophenyl) phosphorothioate (64) (mp 21°C, <71.437), has rat LD qS of 890, 980 (oral) and 4500, 4100 (dermal) mg/kg. These compounds have been used as household insecticides. [Pg.282]

The development of malathion in 1950 was an important milestone in the emergence of selective insecticides. Malathion is from one-half to one-twentieth as toxic to insects as parathion but is only about one two-hundredths as toxic to mammals. Its worldwide usage in quantities of thousands of metric tons in the home, garden, field, orchard, woodland, on animals, and in pubHc health programs has demonstrated substantial safety coupled with pest control effectiveness. The biochemical basis for the selectivity of malathion is its rapid detoxication in the mammalian Hver, but not in the insect, through the attack of carboxyesterase enzymes on the aUphatic ester moieties of the molecule. [Pg.290]

Encapsulated fonofos, a soil insecticide, was developed to coat seeds before they were planted (72). Encapsulation reduces oral toxicity 100-fold and dermal toxicity 10-fold while extending activity of the fonofos. Other encapsulated pesticides available include permethrin and parathion (69). Significantly, all commercial encapsulated pesticides are prepared by interfacial polymeri2ation. [Pg.325]

Developmental Effects. Adverse effects of methyl parathion on hirman fetal development have not been reported. Based on studies in animals, such effects appear to be possible if pregnant women were exposed during the first trimester to high concentrations of methyl parathion that resulted in significant depression of cholinesterase levels, particularly if concomitant signs and symptoms of organophosphate intoxication occur. Such an exposure scenario may occur with occupational exposure, exposure in homes or offices illegally sprayed with methyl parathion, or accidental exposure to methyl parathion, but is less likely as a result of low-level exposure. [Pg.36]

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been made for methyl parathion. An MRL is defined as an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure. MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration within a given route of exposure. MRLs are based on noncancerous health effects only and do not consider carcinogenic effects. MRLs can be derived for acute, intermediate, and chronic duration exposures for inhalation and oral routes. Appropriate methodology does not exist to develop MRLs for dermal exposure. [Pg.40]

Mice that were exposed dermally to residues of methyl parathion in emulsifiable concentrate on foliage, and were muzzled to prevent oral intake, developed inhibition of plasma cholinesterase and erythrocyte cholinesterase after two 10-hour exposures (Skinner and Kilgore 1982b). For the organophosphate pesticides tested in this study, cholinergic signs generally were seen in mice with cholinesterase inhibition >50% results for this end point were not broken down by pesticide. [Pg.79]

Associations between urinary 4-nitrophenol and indoor residential air and surface-wipe concentrations of methyl parathion have been studied in 142 residents of 64 contaminated homes in Uorain, Ohio (Esteban et al. 1996). The homes were contaminated through illegal spraying. A mathematic model was developed to evaluate the association between residential contamination and urinary 4-nitrophenol. There were significant positive correlations between air concentration and urinary 4-nitrophenol, and between maximum surface-wipe concentrations and urinary 4-nitrophenol. The final model includes the following variables number of days between spraying and sample collection, air and maximum surface wipe concentration, and age, and could be used to predict urinary 4-nitrophenol. [Pg.113]

Unusually susceptible populations are those groups of individuals who respond more quickly or at lower exposure levels than the general population to the toxic effects of methyl parathion. These responses may be genetic in origin or may be due to differences in development or life style factors such as nutrition or behavior, or due to preexisting disease states. [Pg.116]

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the Administrator of EPA and agencies and programs of the Public Health Service) to assess whether adequate information on the health effects of methyl parathion is available. Where adequate information is not available, ATSDR, in conjunction with the National Toxicology Program (NTP), is required to assure the initiation of a program of research designed to determine the health effects (and techniques for developing methods to determine such health effects) of methyl parathion. [Pg.120]

A recent method, still in development, for determining total 4-nitrophenol in the urine of persons exposed to methyl parathion is based on solid phase microextraction (SPME) and GC/MS previously, the method... [Pg.170]

A recent method, still in development, for determining total 4-nitrophenol in the urine of persons exposed to methyl parathion is based on solid phase microextraction (SPME) and GC/MS previously, the method has been used in the analysis of food and environmental samples (Guidotti et al. 1999). The method uses a solid phase microextraction fiber, is inserted into the urine sample that has been hydrolyzed with HCl at 50° C prior to mixing with distilled water and NaCl and then stirred (1,000 rpm). The fiber is left in the liquid for 30 minutes until a partitioning equilibrium is achieved, and then placed into the GC injector port to desorb. The method shows promise for use in determining exposures at low doses, as it is very sensitive. There is a need for additional development of this method, as the measurement of acetylcholinesterase, the enzyme inhibited by exposure to organophosphates such as methyl parathion, is not an effective indicator of low-dose exposures. [Pg.177]

Organophosphates, such as methyl parathion, are known to inhibit cholinesterase activity. A method has been developed to measure the extent of this inhibition and relate it to organophosphate exposure (EPA 1980d Nabb and Whitfield 1967). In this EPA-recommended method, blood is separated into plasma and red blood cell fractions. The fractions are treated with saline solution, brought to pH 8 with sodium hydroxide, and dosed with acetylcholine perchlorate. The ensuing acetic acid releasing enzyme reaction... [Pg.177]

In a study of the metabolism of methyl parathion in intact and subcellular fractions of isolated rat hepatocytes, a high performance liquid chromatography (HPLC) method has been developed that separates and quantitates methyl parathion and six of its hepatic biotransformation products (Anderson et al. 1992). The six biotransformation products identified are methyl paraoxon, desmethyl parathion, desmethyl paraoxon, 4-nitrophenol, />nitrophenyl glucuronide, and /wiitrophenyl sulfate. This method is not an EPA or other standardized method, and thus it has not been included in Table 7-1. [Pg.178]

Basha PM, Nayeemunnisa. 1993a. Effect of methyl parathion on Na, K, and Mg adenosine triphosphatase activity in developing central nervous system in rats. Indian J Exp Biol 31 785-787. [Pg.194]

Basha PM, Nayeemunnisa. 1993b. Methyl parathion induced alterations in GABAergic system during critical stage of central nervous system development in albino rat pups. Indian J Exp Biol 31 369-372. [Pg.194]

Gupta RC, Rech RH, Lovell KL, et al. 1985. Brain cholinergic, behavioral, and morphological development in rats exposed in utero to methyl parathion. Toxicol Appl Pharmacol 77 405-413. [Pg.211]

Holm HW, Kollig HP, Proctor LM, etal. 1982. Laboratory ecosystems for studying chemical fate An evaluation using methyl parathion. Athens, GA U.S. Environmental Protection Agency, Office of Research and Development. EPA-600/S3-82/020. [Pg.213]

Kumar KBS, Devi KS. 1992. Teratogenic effects of methyl parathion in developing chick embryos. Vet Flum Toxicol 34 408-410. [Pg.217]

The main purpose of this work is development of small-scale and mobile dsMmposition system of these chemicals. A number of studies on decomposition of organophosphorus insecticides have been conducted [1-3]. It is well known that or nophosphorus insecticides are decomposed by hydrolysis under alkaline condition, and its meciianisms have been studied [4], Even so, relatively few papers have address the devdopment of kinetic equations for reactor desipi. In this study, we aim to get kinetic equaticms for their decomposition under alkaline condition. As organophosphtous, we used parathion, fenitrothion, diazinon, malathion and phenthoate. [Pg.829]

The first application of immunologically based technology to pesticides was not reported until 1970, when Centeno and Johnson developed antibodies that selectively bound malathion. A few years later, radioimmunoassays were developed for aldrin and dieldrin and for parathion. In 1972, Engvall and Perlman introduced the use of enzymes as labels for immunoassay and launched the term enzyme-linked... [Pg.623]

The complexity of the new insecticidal chemicals brings many other problems. Synthetic organic chemicals are not effective against all pests. There is a marked selectiveness in action even between closely related species of insects. Some insects have already developed resistance to some of the newer materials. The idea of insects developing resistance to certain chemicals is not new. The over-all principle is well established in a few cases. The early development of flies resistant to DDT, a chemical which had been highly and universally effective for fly control, came as a surprise. Other cases of resistance to DDT are being indicated, and at least one kind of mite has developed resistance against another of the newer chemicals—parathion. [Pg.11]


See other pages where Parathion development is mentioned: [Pg.63]    [Pg.80]    [Pg.74]    [Pg.63]    [Pg.80]    [Pg.74]    [Pg.279]    [Pg.279]    [Pg.290]    [Pg.300]    [Pg.325]    [Pg.141]    [Pg.26]    [Pg.36]    [Pg.49]    [Pg.69]    [Pg.70]    [Pg.74]    [Pg.78]    [Pg.106]    [Pg.111]    [Pg.118]    [Pg.125]    [Pg.130]    [Pg.140]    [Pg.171]    [Pg.14]    [Pg.193]    [Pg.293]    [Pg.989]   
See also in sourсe #XX -- [ Pg.20 ]




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