Establishment of reentry intervals for organophosphate-treated cotton fields based on human data: III. 12 to 72 hours post-treatment exposure to monocrotophos, ethyl- and methyl parathion

Abstract

Five human volunteers entered methyl parathion, ethyl parathion, or monocrotophos treated cotton fields for five-hr exposure periods when the residues of the respective pesticides had aged 12 hr, 24 and 48 hr and 72 hr. Foliage residues of methyl parathion disappeared fastest, those of monocrotophos slowest. Personal exposure to pesticide was evaluated from contamination of skin, clothing, and ambient air, while actual absorption of chemical was assessed from pesticide concentration in blood, urinary metabolite excretion, and effects on blood cholinesterase activities. There was good correspondence between magnitudes of foliar residue, estimates of personal contamination, and measures of chemical absorption. Field exposures caused no symptoms or clinical signs of organophosphate poisoning and depressed averaged blood cholinesterase activities by no more than 14% of pre-exposure levels.

Application of a dermal self‐exposure model to worker reentry

“…This lack of correlation between ChE depression and inhalation exposure agrees with the human reentry results of Ware et al (1975) and Spear et al (1977). Tables 2 and 3 summarize the results of studies designed to characterize the ability of the muzzled self-exposure system to generate responses to foliar residues.…”

“…35% of workers had significant depression in one or both blood indicators. cotton scouts for 50 h to cotton treated at rates approximately three times those in the Ware et al (1975) study (but also utilizing a 0-1 d reentry interval) produced 30% and 25% depressions in ChE and AChE, respectively (Burns and Parker, 1975). Azinphos-methyl and mevinphos did not produce human responses at levels of 2.8 and 0.96 jug/cm 2 and exposure intervals of 9 and 5 d, respectively.…”

Percutaneous penetration of [14C] parathion in the mouse: Effect of anatomic region

“…Widespread exposure of workers to toxicants exists in agricultural field reentry, where cholinesterase inhibition may result from dermal exposure to foliar pesticide residues (Ware et al, 1975;Wolfe et al, 1975;Spear et al, 1977). In the past two decades, cases of reenetry poisoning have been most numerous in citrus orchards sprayed with parathion (Gunther et al, 1977).…”

Effects of Single or Repeated Dermal Exposure to Methyl Parathion on Behavior and Blood Cholinesterase Activity in Rats

“…High temperatures increase skin absorption, as does the presence of dermatitis [25]. Dermal absorption has been identified as the primary route of methyl parathion intake as a consequence of occupational exposure [29,42,43]. Lack of immediate recognition of exposure to methyl parathion, coupled with poor decontamination, is characteristic of recent widespread human exposure to illegal methyl parathion spray; also, transdermal absorption of methyl parathion may have been a significant feature of these exposures [1,17].…”