Pesticides methyl parathion

Garcia-Repetto R, Martinez D, Repetto M. 1997. Biodisposition study of the organophosphorus pesticide, methyl-parathion. Bull Environ Contam Toxicol 59 901-908. 

Sultatos LG. 1987. The role of the liver in mediating the acute toxicity of the pesticide methyl parathion in the mouse. Drug Metab Disp 15 613-617. 

The pesticide methyl parathion (Folidol-M) is leached into a stream from an abandoned disposal site. Is photolysis likely to be a significant sink for this chemical If the travel time to the ocean is 5 days, what fraction of the chemical would you predict to reach the ocean ... 

Chronic peripheral nervous system effects have been reported in farmers who applied the organophosphate pesticides methyl parathion (2.86), azinphos-methyl (2.75), and tetraethylpyrophosphate (0.45) pesticides in xylene (3.15) solutions and were exposed to levels below those known to produce acute or subacute symptoms. Similar effects were described in another study of low level exposure to organophosphate pesticidesJ49l In both cases, it is hypothesized that the lipophilic solvent (xylene) facilitated the absorption of greater than expected quantities of the more hydrophilic pesticides. 441... 

Ellison, C.A., Tian, Y., Knaak, J.B., et al., 2012. Human hepatic cytochrome P450-specific metabolism of organophosphorus pesticides methyl parathion and diazinon. Drug Metab. Dispos. 40,1-5. 

The pesticide methyl parathion (Folidol-M) is leached into a... 

Reduction of Nitro Substituents. These reactions are very common in anaerobic environments and result in amine-substituted pesticides anaerobic bacteria capable of reducing nitrate to ammonia appear to be primarily responsible. All nitro-substituted pesticides appear to be susceptible to this transformation, eg, methyl parathion (7) (eq. 9), triduralin, and pendimethalin. 

Methyl parathion is a pesticide that is used to kill insects on crops. Usually, it is sprayed on the crops. Methyl parathion comes in two forms a pure form of white crystals and a technical-grade solution (brownish liquid), which contains methyl parathion (80%) and inactive ingredients in a solvent. The technical-grade methyl parathion smells like rotten eggs or garlic. Methyl parathion is a manufactured chemical, so it is found in the environment only as a result of its manufacture or use. Methyl parathion has been manufactured in the United States since 1952 and has been used to kill insects on many types of crops since this time. Because methyl... 

Methyl parathion is approved only for use on crops. The maximum amount of methyl parathion residue allowed by the Food and Drug Administration (FDA) and EPA on crops used as food is 0.1-1 ppm. The FDA has monitored the food supply for pesticides for a number of years. FDA purchases many kinds of foods through Market Basket Surveys and analyzes them for residue levels of pesticides. These FDA studies allow scientists to estimate the daily intake of pesticides. Generally, the FDA monitoring studies conclude that the U.S. food supply contains only very small amounts of pesticides that are not a concern. However, there have been some reports of the illegal use of methyl parathion inside homes. For more information, see Section 1.7 and Chapter 6. 

Children are likely to be exposed to methyl parathion in the same ways as adults, mainly by eating foods or drinking milk or water that contain residues of this chemical. Because of their smaller weight, children s intake of methyl parathion per kilogram of body weight may be greater than that of adults. The FDA and EPA permit residues of pesticides to be present in crops used as food, and these amounts are considered to be safe. The EPA, however, has recently used stricter regulations and has canceled the use of methyl parathion on food crops... 

Families should also be aware that sometimes methyl parathion has been illegally sprayed inside the home to kill insects. Your children may be exposed to methyl parathion if an unqualified person applies pesticides containing it around your home. In some cases, the improper use of pesticides banned for use in homes has turned homes into hazardous waste sites. Make sure that any person you hire is licensed and, if appropriate, certified to apply pesticides. Your state licenses each person who is qualified to apply pesticides according to EPA standards and further certifies each person who is qualified to apply restricted use pesticides. Ask to see the license... 

In areas of agricultural methyl parathion usage, both outdoor and indoor air levels of methyl parathion of approximately 12 ng/m have been measured, and household dust was found to contain 21 ppb of methyl parathion. Outdoor and indoor air concentrations of methyl parathion as high as 0.71 and 9.4 pg/m, respectively, have been measured at the homes of individuals employed as pesticide formulators. 

Dermal exposure to methyl parathion is not likely to be a health concern to the general population, with the possible exception of individuals in the immediate vicinity of a field during application of the pesticide. Dermal exposure, however, is a major source of exposure for workers directly involved in the manufacture, application, and cleanup of the chemical, and for field workers. Laundry workers cleaning the clothing of such workers may also be exposed. 

Erythrocyte cholinesterase levels were monitored in two men exposed dermally to methyl parathion after entering a cotton field that had been sprayed with this pesticide (Nemec et al. 1968). The field was entered on two separate occasions twice within 2 hours after an ultra-low-volume spraying and a third time within 24 hours after spraying. Dermal methyl parathion residues 2 hours after spraying were 2-10 mg on the arms dermal residues 24 hours after spraying were 0.16-0.35 mg on the arms. The exposed individuals did not have signs of cholinergic toxicity, but erythrocyte cholinesterase levels after the third exposure were 60-65% of preexposure levels. 

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. 

In a case-control study of pesticide factory workers in Brazil exposed to methyl parathion and formulating solvents, the incidence of chromosomal aberrations in lymphocytes was investigated (De Cassia Stocco et al. 1982). Though dichlorodiphenyltrichloroethane (DDT) was coformulated with methyl parathion, blood DDT levels in the methyl parathion-examined workers and "nonexposed" workers were not significantly different. These workers were presumably exposed to methyl parathion via both inhalation and dermal routes however, a dose level was not reported. The exposed workers showed blood cholinesterase depressions between 50 and 75%. However, the baseline blood cholinesterase levels in nonexposed workers were not reported. No increases in the percentage of lymphocytes with chromosome breaks were found in 15 of these workers who were exposed to methyl parathion from 1 week to up to 7 years as compared with controls. The controls consisted of 13 men who had not been occupationally exposed to any chemical and were of comparable age and socioeconomic level. This study is limited because of concomitant exposure to formulating solvents, the recent history of exposure for the workers was not reported, the selection of the control group was not described adequately, and the sample size was limited. 

The lymphocytes from 31 patients exposed to various organophosphate pesticides were examined for chromosomal aberrations (Van Bao et al. 1974). Five of the patients were exposed to methyl parathion only. Blood samples were taken 3-6 days after exposure and again at 30 and 180 days. A significant (p<0.05) increase was noted in the frequency of stable chromosomal aberrations in acutely intoxicated persons (although such cells are eventually lost from the cell population). Two of the methyl parathion-exposed persons had taken large doses orally in suicide attempts. The study limitations include small sample size, absence of a control group, lack of quantification of exposure levels, and possible... 

The controls were patients who had undergone appendicitis or hernia surgery, and were matched for sex, age, and socioeconomic status with a larger set of 31 pesticide poisoning eases, of whieh the methyl parathion eases were a subset. Limitations of this study include the small number of methyl parathion eases, and the use of appendieitis and other surgery patients as eontrols. 

Although the extent of absorption was not measured, the above evidence suggests that absorption in humans occurs rapidly following dermal exposure to commercial pesticide formulations of methyl parathion. 

For methyl parathion, most of the information on health effects in humans is derived from cases of acute exposure to relatively high concentrations of the pesticide. Such reports have not addressed the issue of the potential endocrine-disrupting capacity of methyl parathion in humans. An added complication in determining whether methyl parathion has endocrine-disrupting capabilities in humans is the fact that humans are seldom exposed to a single pesticide. 

Compounds that affect activities of hepatic microsomal enzymes can antagonize the effects of methyl parathion, presumably by decreasing metabolism of methyl parathion to methyl paraoxon or enhancing degradation to relatively nontoxic metabolites. For example, pretreatment with phenobarbital protected rats from methyl parathion s cholinergic effects (Murphy 1980) and reduced inhibition of acetylcholinesterase activity in the rat brain (Tvede et al. 1989). Phenobarbital pretreatment prevented lethality from methyl parathion in mice compared to saline-pretreated controls (Sultatos 1987). Pretreatment of rats with two other pesticides, chlordecone or mirex, also reduced inhibition of brain acetylcholinesterase activity in rats dosed with methyl parathion (2.5 mg/kg intraperitoneally), while pretreatment with the herbicide linuron decreased acetylcholine brain levels below those found with methyl parathion treatment alone (Tvede et al. 1989). 

Permethrin, a pyrethrin pesticide, decreased the inhibition of brain cholinesterase activity by methyl parathion, but methyl parathion decreased the LD50 of permethrin when the two pesticides were simultaneously administered to rats (Ortiz et al. 1995). The potentiation of permethrin lethality may be due to the inhibition by methyl parathion of carboxylesterase, which metabolizes permethrin. 

Figure 3-5 graphically depicts the information that currently exists on the health effects of methyl parathion in humans and animals by various routes of exposure. The available literature reviewed concerning the health effects of methyl parathion in humans described case reports of longer-term studies of pesticide workers and case reports of accidental or intentional ingestion of methyl parathion. The occupational exposure is believed to be via the dermal and inhalation routes. The information on human exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic substances cannot be quantified. 

DOT/UN/NA/IMCO shipping Methyl parathion, liquid (DOT) Methyl parathion mixture, dry (DOT) methyl parathion, solid (DOT) UN 3017 organophosphorus pesticides, liquid, toxic, flammable, not otherwise specified HSDB 1999 RTECS 1989... 

Releases to the atmosphere from production facilities and disposal sites have also been reported. Studies have shown that releases of methyl parathion to the atmosphere occur in the vicinity of pesticide-producing factories. At two predominately downwind sites located 1 mile from a plant producing methyl parathion, average monthly concentrations were <0.57 and <0.64 ng/m (Foster 1974). Air emissions from methyl parathion production facilities have been reported to contain 1.0 kg/1,000 kg pesticide produced. In addition, evaporation from holding ponds for pesticide waste potentially contributes 7.4 mg/1,000 kg pesticide produced to the atmosphere (EPA 1978d). 

Methyl parathion may also be released to soils by improper handling of pesticide formulations during processing or handling. In a sampling of soils collected from processing facilities in Illinois, methyl parathion was detected in soil at 2 of the 49 sites tested (Krapac et al. 1995). 

The solubility of methyl parathion is not sufficient to pose a problem in runoff water as determined by an empirical model of Wauchope and Leonard (1980). Some recent monitoring data, however, indicate that methyl parathion has been detected in surface waters (Senseman et al. 1997). In a study to determine the residue levels of pesticides in shallow groundwater of the United States, water samples from 1,012 wells and 22 springs were analyzed for methyl parathion. No methyl parathion was detected in any of the water samples (Kolpin et al. 1998). In a study of water from near-surface aquifers in the Midwest, no methyl parathion was detected in any of the water samples from 94 wells that were analyzed for pesticide levels (Kolpin et al. 1995). Leaching to groundwater does not appear to be a significant fate process. 

In a study to determine the concentrations of pesticides in air collected during times of peak pesticide use in California, air samples were collected at applications sites and at locations adjacent to the application sites (Baker et al. 1996). Of the samples collected adjacent to the application sites, 50% had levels of methyl parathion greater than the detectable limit of 0.2 ng/m, while 21% had levels of methyl paraoxon... 

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