External and internal exposure of wine growers spraying methyl parathion.

Organophosphates, used in agriculture, are readily absorbed through the skin. We investigated the relationship between dermal and inhalative methyl parathion exposure and the plasma levels. Twenty-three healthy wine growers sprayed the insecticide for 50 min. Fluorescent brilliant sulfoflavin was added to the spraying fluids and filter papers were fixed on the subjects. The filter papers were used to evaluate the amount of brilliant sulfoflavine on the unprotected skin fluorometrically. Inhalative exposure was measured with personal air sampler. Plasma concentrations of methyl parathion and its metabolite methyl paraoxon were determined with gas chromatography. Cholinesterase activity in serum and erythrocytes was measured before and after exposure. Some wine growers wore protective clothes, none protective gloves. Dermal exposure ranged up to 12,044 microg, inhalative to 22 microg. Maximum plasma concentration of methyl parathion was 12.1 microg/l. Methyl paraoxon was not detectable. Cholinesterase activity did not decrease. Dermal exposure correlated with the methyl parathion plasma level (Spearman's rho=0.72, p<0.001). In conclusion, dermal exposure exceeded inhalative exposure considerably. Measuring dermal deposition with the brilliant sulfoflavin technique may provide a good estimate of the internal load with methyl parathion. Preventive measures should be improved as toxic effects of repeated exposure to low doses of methyl parathion cannot be excluded.

Evaluation of potential adverse health effects resulting from chronic domestic exposure to the organophosphate insecticide methyl parathion.

Methyl parathion (MP) was used illegally to spray homes for insect control over approximately an 8-yr period. In an attempt to determine if there were any adverse health effects from this, health-screening evaluations were performed on 353 individuals living in homes that were illegally sprayed. The average subject spent 15.5 h a day in the home. Subjects from homes with high levels of MP (exposure group) were compared to controls that lived in homes with minimal or no MP. Subjects were aware of the levels of MP found in their homes and recall bias was likely. There were no significant differences in the symptoms reported or by the physician assessment of subacute or chronic toxicity between those in the exposure group and controls. No significant differences were found in growth and developmental evaluations. Three subjects were identified who most likely suffered acute toxicity from the initial exposure and were not appropriately diagnosed and treated. Cholinesterase determinations also did not differ between those in the exposure group and controls. When subjects from the exposure group were stratified by the level of MP in their home, those from homes with the highest levels appeared to have an increased likelihood of subacute toxicity and reported an increased number of neuropsychiatric symptoms (OR 2 for both evaluations).

[The profiles of free organophosphorus poisons in the bile of rabbits poisoned with different organophosphates].

OBJECTIVE: To study the process and significance of the distribution of free organophosphorus poisons (FOPs) in the blood and bile of rabbits poisoned with organophosphates. METHODS: Seventy two livid blue rabbits, male, 2 - 2.5 kg in weight, were divided into 3 groups: trichlorfon (556.0 mg/kg), monocrotophos (11.12 mg/kg) and methyl parathion (37.05 mg/kg). Each group consisted of 24 rabbits. All organophosphates were administered by subcutaneous route. Blood and bile were collected at time intervals of 1, 6, 24, 96 hours after administration. Blood cells and plasma were separated. Acetylcholinesterase (AChE) activity was measured with dithiobisnitrobenzoic acid (DTNB) enzyme kinetic method. The levels of FOPs in plasma and bile were determined with enzyme inhibited method. RESULTS: From 1 h to 96 h after administration negative correlation was found between time and FOP concentration in plasma (trichlorfon, r = -0.74, P < 0.01; monocrotophos, r = -0.55, P < 0.01; methyl parathion, r = -0.69, P < 0.01), and it was also found in bile between time and FOP concentration of trichlorfon (r = -0.97, P < 0.01) and monocrotophos (r = -0.71, P < 0.01). There is no linear correlation between time and concentration of methyl parathion in bile (r = -0.14, P > 0.05). When FOPs in plasma were not detectable at 96 h after administration, high levels of FOPs could still be detected in bile [trichlorfon (300.3 +/- 174.44) IU/L; monocrotophos (362.8 +/- 136.62) IU/L; methyl parathion (101.0 +/- 75.85) IU/L]. CONCLUSION: The bile is the most important store for FOPs in animal. FOPs can exist in bile over 96 h. The process of poisoning is a changing process of absorption, distribution and redistribution and it is different owing to various physical and chemical properties of organophosphates.

Cholinesterase reactivation in organophosphorus poisoned patients depends on the plasma concentrations of the oxime pralidoxime methylsulphate and of the organophosphate.

We measured in nine patients, poisoned by organophosphorus agents (ethyl parathion, ethyl and methyl parathion, dimethoate, or bromophos), erythrocyte and serum cholinesterase activities, and plasma concentrations of the organophosphorus agent. These patients were treated with pralidoxime methylsulphate (Contrathion), administered as a bolus injection of 4.42 mg.kg-1 followed by a continuous infusion of 2.14 mg.kg-1/h, a dose regimen calculated to obtain the presumed "therapeutic" plasma level of 4 mg.l-1, or by a multiple of this infusion rate. Oxime plasma concentrations were also measured. The organophosphorus agent was still detectable in some patients after several days or weeks. In the patients with ethyl and methyl several days or weeks. In the patients with ethyl and methyl parathion poisoning, enzyme reactivation could be obtained in some at oxime concentrations as low as 2.88 mg.l-1; in others, however, oxime concentrations as high as 14.6 mg.l-1 remained without effect. The therapeutic effect of the oxime seemed to depend on the plasma concentrations of ethyl and methyl parathion, enzyme reactivation being absent as long as these concentrations remained above 30 micrograms.l-1. The bromophos poisoning was rather mild, cholinesterases were moderately inhibited and increased under oxime therapy. The omethoate inhibited enzyme could not be reactivated.

Cytogenetic study of workers exposed to methyl-parathion.

When compared with non-exposed controls, a group of pesticide plant workers chronically exposed to methyl-parathion did not show an increased frequency of chromosome aberrations in lymphocyte cultures. Although methyl-parathion increased chromosome aberrations in cases of intoxication, a chronic exposure to small doses in the work place did not seem to produce the same effect.

Kinetic analysis of the fate of methyl parathion in the dog.

Methyl parathion (1, 3, 10 and 30 mg.kg-1) was injected intravenously in dogs and the serum concentrations were followed in function of time. For each dose the serum level data were fitted to a two- or tri-exponential equation by means of a non-linear least-squares regression analysis computer program. During the first hours after injection a rapid and important decrease of the serum levels was observed, whereas afterwards the levels decreased more slowly with a harmonic mean terminal half-life of 7.2 h (range 6.6-8.8 h) for the 10 mg.kg-1 dose. Simulations using the kinetic parameters obtained for the dose of 10 mg.kg-1 show that elimination of methyl parathion from the body is fast (5 h after injection only 30% of the dose is still present in the body) and that the fraction remaining is mainly located in the peripheral compartments.