Transferable residues from dog fur and plasma cholinesterase inhibition in dogs treated with a flea control dip containing Chlorpyrifos. (Articles).

We studied chlorpyrifos, an insecticide present in a commercial dip for treating ectoparasites in dogs, to estimate the amount of transferable residues that children could obtain from their treated pets. Although the chlorpyrifos dip is no longer supported by the manufacturer, the methodology described herein can help determine transferable residues from other flea control insecticide formulations. Twelve dogs of different breeds and weights were dipped using the recommended guidelines with a commercial, nonprescription chlorpyrifos flea dip for 4 consecutive treatments at 3-week intervals (nonshampoo protocol) and another 12 dogs were dipped with shampooing between dips (shampoo protocol). The samples collected at 4 hr and 7, 14, and 21 days after treatment in the nonshampoo protocol averaged 971, 157, 70, and 26 [micro]g chlorpyrifos, respectively; in the shampoo protocol the samples averaged 459, 49, 15, and 10 [micro]g, respectively. The highest single sample was about 7,000 [micro]g collected at 4 hr. The pretreatment specific activities in the plasma of the dogs were about 75 nmol/min/mg protein for butyrylcholinesterase (BChE), and 9 nmol/min/mg protein for acetylcholinesterase (ACHE). BChE was inhibited 50-75% throughout the study, and AChE was inhibited 11-18% in the nonshampoo protocol; inhibition was not as great in the shampoo protocol. There was no correlation (p [less than or equal to] 0.05) between length of hair and residues measured that would explain the residue differences among dogs. Transferable residues had largely dissipated during the three weeks after treatment, with the largest decrease occurring during the first week. Greater plasma ChE inhibition was observed at 7 days than at 4 hr, probably reflecting the bioactivation of chlorpyrifos to chlorpyrifos-oxon. Plasma cholinesterase activity did not return to control levels during the 3-week period. The differences between the shampoo and nonshampoo protocols were explained by differences in the techniques of the dip applicators. Key words: acetylcholinesterase, butyrylcholinesterase, chlorpyrifos, dog fur, flea control, organophosphate insecticide, pesticide monitoring, transferable residues. Environ Health Perspect 109:1109-1114 (2001). [Online 19 October 2001]

http://ehpnet1.niehs.nih.gov/docs/2001/109p1109-1114boone/abstract.html

Exposure of children to pesticides is a major health concern. Children could be exposed to pesticides from carpet, house dust, and toys from treated houses, from clothing of parents who are farm workers and pesticide applicators, and from playing outside in treated lawns and gardens (1-5). One overlooked but important potential source for pesticide exposure to children is pets treated with parasite control products. These products often contain carbamate, pyrethroid, and organophosphate insecticides.

Organophosphate (OP) compounds have been used commonly as insecticides in and around households, on farm and domestic animals, and on agricultural lands. These compounds are used widely in the United States because of their relatively low mammalian toxicity, their short half-lives, and their ease of use. These insecticides have been used residentially for the control of termites, ants, roaches, ticks, fleas, and other insect and arachnid pests. Thus, there is increased opportunity for children to be exposed by multiple routes, and these aggregate exposures could contribute to significant toxicity. Identification of all possible routes of exposure and the quantification of the magnitude of these exposures may contribute to a more accurate calculation of pesticide risk, and thereby decrease the reliance on uncertain default assumptions in risk assessment.

The amount of exposure data to OP insecticides for children is limited. Most of the risk calculations are for adults and may not consider the potentially greater absorption and sensitivity of children, poorer personal hygiene, potentially lower capacity for detoxication, developing organ systems, and a greater body surface area to volume ratio. Human potential exposures to organophosphate compounds have been documented from several sources, such as carpeting and household dust (2). Children have also been poisoned by OP insecticides through exposure to contaminated items, such as bed linens, clothing, and burlap sacks (3-5). However, the amount of exposure to organophosphate compounds from flea and tick control products on pets, such as dogs and cats, has not been documented.