Exposure of Farm Labor to Pesticides

 H. N. Nigg J. H. Stamper
 University of Florida
 Citrus Research and Education Center
 700 Experiment Station Road
 Lake Alfred, FL 33850, USA


 The purpose of this article is to review agricultural pesticide
monitoring methods and suggest ways to protect farm labor
from unnecessary exposure. A comparison of pesticide ex-
posure for various application methods indicates exposure in
the order, airblast > high-boy > low-boy > hand application.
Anatomical regions of the body receive total exposure in the
order, hands > legs > arms > chest > head, with the back and


buttocks generally receiving lower exposure. Urinary
metabolite and blood acetylcholinesterase methods are
generally not definitive for monitoring exposure except in
acute poisoning cases. Possible protective methods suggested
by these exposure studies are outlined, with particular
reference to small farm use.
Keywords: Fieldworker; exposure; pesticides; methods.


 The assessment and minimization of farmworker exposure to
pesticides has been a research effort since the introduction of
organic pesticides in the late 1940's. Research concentrates on two
groups:
 1. agricultural harvester exposure to residual pesticides, and
 2. pesticide exposure of workers mixing, loading, and apply-
 ing pesticides.
Each of these work activities involves special circumstances and
dangers. The small acreage farmer may encounter hazards faced
by both groups.
 Methods for monitoring the exposure of farmworkers to
pesticides were reviewed by Davis (1980). The purpose of this
report is to update and expand that review, discuss problems
relating to pesticide monitoring procedures, and suggest possible
protective methods which small acreage farmers might employ.

Applicator Exposure Methods
 Applicator exposure studies have usually monitored dermal ex-
posure, cholinesterase levels, and urinary metabolites for the
human applicator, often in conjunction with more intrusive
animal experiments. One of the first applicator studies was by
Kay et al. (1952) who measured cholinesterase levels in orchard
parathion applicators. They compared these with cholinesterase
levels from non-spray periods. Plasma cholinesterase was 16%
lower for sprayers reporting physical symptoms and this value was
20% lower than the no-symptom group. Erythrocyte
cholinesterase was depressed 27% for the symptom group vs.
17% for the non-symptom group, but these means were not
statistically different. In 1958 Quinby et al. measured
cholinesterase activity in aerial applicators as well as residues col-
lected on worker clothing and respirator pads. Despite physical
complaints by pilots exposed to organophosphates, their in-
vestigation revealed either normal or only slightly depressed
cholinesterase levels. However, these cholinesterase levels were
compared with the "normal" range for the U.S. population rather
than the pilots' individual "normal" range. Roan et al. (1969)
measured plasma and erythrocyte cholinesterase and serum levels
of ethyl and methyl parathion. Serum levels of the parathion
could not be correlated with cholinesterase levels. However,
serum levels did correlate with the urine concentration of
p-nitrophenol. Drevenkar et al. (1983) measured plasma and
erythrocyte cholinesterase levels and urine concentrations of
organophosphate and carbamate pesticides in formulating plant

VOL. XX-PROCEEDINGS of the CARIBBEAN FOOD CROPS SOCIETY


workers. No correlation could be made between urinary
metabolites and cholinesterase activity. Bradway et al. (1977) ex-
amined cholinesterase, blood residues, and urinary metabolites
in rats exposed to eight organophosphates under a controlled en-
vironment. No correlation was found between cholinesterase ac-
tivity and blood residues or urine metabolite levels. The overall
conclusion from these cited studies is that cholinesterase inhibi-
tion as an exposure indicator contains too many variables, known
and unknown, to be of use (except in a very general sense).
 Urinary metabolites of pesticides have been used for a variety
 of experimental goals. Swan (1969) measured paraquat in the
 urine of spraymen, Gallop and Glass (1979) and Wagner and
 Waring (1974) measured arsenic in timber applicator urine,
 Lieben et al. (1953) measured paranitrophenol in urine after
 parathion exposure as did Durham et al. (1972). Chlorobenzilate
 metabolite (presumably dichlorobenzilic acid) in citrus workers
 (Levy et al., 1982), phenoxy acid herbicide metabolites in farmers
 (Kolmodin-Hedman et al., 1983a) and organophosphate
 metabolites in the urine of the general public exposed to mos-
 quito treatments (Kutz and Strassman, 1977) were detected.
 Davies et al. (1979) used urine metabolites of organophosphates
 and carbamates to confirm poisoning cases. These studies docu-
 ment exposure, but no estimation of exposure can be made from
 urinary metabolites alone. Other studies have used air sampling
 and hand monitoring, combined with urine levels (Cohen et al.,
 1979), and air plus cholinesterase plus urine sampling (Hayes et
 al., 1980).
 The exposure pad method, combined with measurement of
urinary metabolites, has been used to compare the effect of differ-
ent application methods on worker exposure (Wojeck et al., 1983;
Carman et al., 1982), formulating plant worker exposure (Comer
et al., 1975) and homeowner exposure (Staiff et al., 1975).
 Several researchers have used the exposure pad method, calcu-
lated a total estimated dermal dose, and attempted to correlate
urine levels with this estimated dose (Wojeck et al., 1981, 1982,
1983; Franklin et al., 1981; Lavy et al., 1980, 1982). Lavy et al.
(1980, 1982) failed to find any such correlation with 2,4-D and
2,4,5-T. Wojeck et al. (1983) found no paraquat in urine and
consequently no relationship between dermal dose and urine
level. However, the group daily mean concentration of urinary
metabolites of ethion and the group mean total dermal exposure
to ethion on that day correlated at the 97% confidence level
(Wojeck et al., 1981). For arsenic, the cumulative total exposure


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