Report from the Sub-comittee on the environment and health

Neurotoxicity
Immunotoxicity and
sensitivity
100
an increased risk of spina bifida in children born of mo<strong>the</strong>rs employed in
farming, compared with a control group, but <strong>the</strong> association could not be
explained by use of pesticides (Blatter et al. 1996). However, in a Finnish
study of congenital deformities and mo<strong>the</strong>rs working in farming, <strong>the</strong> risk
to workers exposed to pesticides was found to be no greater than <strong>the</strong> risk
to unexposed farm workers (Nurminen et al. 1995). A recent review
article describes methods and results of studies of occupational exposure
to pesticides, mainly among farm workers, and <strong>the</strong> risk of congenital
deformities. However, on <strong>the</strong> basis of <strong>the</strong> available information, <strong>the</strong>re
seems to be insufficient evidence to date to ei<strong>the</strong>r confirm or disprove a
relationship between exposure to pesticides and deformities (García
1998).
With respect to neurotoxic effects of pesticides in adult populations, it
has been found in several studies of workers exposed to pesticides that
effects can occur in <strong>the</strong> peripheral nervous system in workers with ei<strong>the</strong>r
acute poisoning or with chronic occupational exposure without obvious
neuropathic syndromes (Keifer, Mahurin 1997; Ecobichon 1996). Most
of <strong>the</strong> studies of <strong>the</strong> cognitive effects of exposure to pesticides have
concerned organophosphates because of <strong>the</strong>ir widespread use.
Following acute exposure to high doses of organophosphates, with
repeated, acute, clinically significant intoxication, toxic effects have
occasionally been observed with long-term effects on behaviour and on
mental and visual function (Rosenstock et al. 1991; Ames et al.
1995¸Steenland et al. 1994). However, <strong>the</strong> available data do not indicate
that asymptotic exposure to organophosphates is associated with an
increased risk of delayed or permanent neuropsychopathological effects
(Daniell et al. 1992; Eyer 1995).
Among fungicides, <strong>the</strong> dithiocarbamats have been associated with
neurotoxicity in a few cases. In a study <strong>from</strong> <strong>the</strong> Ne<strong>the</strong>rlands, both
autonomous and peripheral neurotoxic effects were found among
workers chronically exposed to zineb and maneb in flower production
(Ruijten et al. 1994). These pesticides are not <strong>the</strong>mselves suspected of
being peripheral neurotoxins, but carbon-disulphide, which is one of <strong>the</strong>
metabolic products, is a known neurotoxin. Fur<strong>the</strong>rmore, occupational
exposure to pesticides containing manganese has been mentioned as a
possible cause of manganese poisoning of <strong>the</strong> central nervous system
(Ferraz et al. 1988).
In an epidemiological study <strong>from</strong> Calgary, Canada, persons with earlier
occupation exposure to herbicides were found to have a three time
greater risk of Parkinson’s disease (Semchuk et al. 1992).
In an American study of 280 cases of aplastic anaemia, an association
was found with occupational exposure to organochlorine compounds and
organophosphates (Fleming, Timmeny 1993). It can be concluded that
<strong>the</strong>re is evidence of contact hypersensitivity as a consequence of
occupational exposure to pesticides.
Experimental and clinical data have shown that some pesticides
(chlornitrobenzene, carbamats, captan and organophosphates) can induce