Pesticide Excretion - Pesticide Biotransformation and Disposition - page 186

discussed ( Fenske et al., 2005; Scher et al., 2007; Faustman et al., 2006; Harris et al.,
2010; Naeher et al., 2010 ). Some of these studies involve single compounds, primar-
ily but not exclusively organophosphorus compounds, and examples are given in Table
8.1 . Other studies are surveys of populations either exposed or potentially exposed
to multiple pesticides. For example, urine samples from 1000 residents of the United
States were analyzed for 12 analytes potentially derived from pesticides, and 6 were
frequently found ( Hill et al., 1995 ). These, with possible parent compounds, were
2,5-dichlorophenol (from 1,4-dichlorobenzene), 2,4-dichlorophenol (from bifenox,
clomethoxyfen, dichlofen-thion, etc.), 1-naphthol (from naphthalene, carbaryl, etc.),
2-naphthol (from naphthalene, etc.), 3,5,6-trichloro-2-pyridinol (from chlorpyrifos,
chlorpyrifos-methyl), and pentachlorophenol (from pentachlorophenol, pentachloro-
nitrobenzene). In another large study of multiple exposure, in tree nursery workers,
only a small number, 42 of 3134, of urine samples were positive, in this case for beno-
myl, bifenox, and carbaryl ( Lavy et al., 1993 ). A summary of all methods, including
measurement of urinary metabolites, of estimating exposure by biomarkers was pub-
lished in 2000 ( Maroni et al., 2000 ), and appropriate analytical methods continue to
be developed (e.g., for organophosphorus pesticides (OPs)) ( De Alwis et al., 2008 ). A
more recent study ( McKone et al., 2007 ) used OP biomarker data to develop insights
into the importance of various exposure sources in a cohort of almost 600. Gosselin
et al. (2005) carried out a toxicokinetic modeling study of parathion and its metabo-
lites ( p -nitrophenol and alkyl phosphates) in humans to facilitate their use in exposure
studies. Toxicokinetic modeling studies have also been carried out for chlorpyrifos and
2,4-D ( Scher et al., 2008 ). Studies of exposure of schoolchildren to and the excre-
tion of pentachlorophenol ( Wilson et al., 2007 ) and cis - and trans -permethrin ( Morgan
et al., 2007; Lu et al., 2009 ) showed good correlation in the case of permethrin, but an
excess of excretion over estimated exposure in the case of pentachlorophenol indicated
that the use of urinary biomarkers is not without problems and may need to be refined
for future studies, depending upon the pesticide in question.
Urinary mercapturic acids have been extensively explored for use as biomarkers of
exposure, and several detailed reviews are available ( De Rooij et al., 1998; Van Welie
et al., 1992 ). The emphasis has been on industrial and environmental chemicals and
this potentially valuable technique has not yet been applied extensively to pesticides.
However, the soil nematocide dichloropropene was included. Methods for the detec-
tion of pyrethroid insecticides, including pyrethrins, are being developed ( Leng and
Greis, 2005 ) and validated ( Barr et al., 2007 ), and the use of biomarkers for pesticides
other than OPs is being expanded.
The effects of pesticides on the excretion of metabolites of endogenous metab-
olism have been explored to some extent. For example, in rats, treatment with
dimethoate decreased the excretion of proline and lysine derivatives known to
be collagen metabolites ( Reddy et al., 1991 ). The mechanism of this effect was not