Report from the Sub-comittee on the environment and health

Neurotoxicity
Neurotoxicity in children
126
There are too few studies on <strong>the</strong> relationship between exposure to
pesticides and developmental effects. This also applies to <strong>the</strong> potential of
pesticides and fertilisers in contaminated groundwater to produce
reproductive and developmental toxic effects in humans.
The term neurotoxicity is used to describe a substance’s potential to
change <strong>the</strong> structure or function of <strong>the</strong> nervous system, defined by
neurochemical, neuropathological organ changes, behaviour and specific
psychological processes such as sense perception, learning and memory.
Many of <strong>the</strong>se disturbances can be directly measured with
neurochemical, neurophysiological and neuropathological methods,
whereas o<strong>the</strong>rs can only be interpreted by looking at <strong>the</strong> behaviour. The
action mechanism of many groups of pesticides – particularly <strong>the</strong>
insecticides – <strong>the</strong> intended target of which is <strong>the</strong> peripheral nervous
system, leads directly to consideration of <strong>the</strong>ir potential neurotoxicity,
whereas <strong>the</strong> neurotoxic potential of o<strong>the</strong>r groups is less clear. Studies of
neurotoxic effects are difficult to perform and interpret, for which reason
<strong>the</strong>re are very few conclusive studies.
Experimental studies have shown that <strong>the</strong> nervous system is more
vulnerable to exposure to chemical substances during development than
when it is fully developed. Animal tests have shown that neurotoxicity as
a consequence of low-dose exposure to such pesticides as
organophosphates, pyrethroids, DDT and paraquat during development
of <strong>the</strong> brain can lead to irreversible changes in <strong>the</strong> adult brain and induce
behavioural and cholinergic changes in <strong>the</strong> adult animal, whereas
exposure of an adult to <strong>the</strong> same substance has little or no effect
(Eriksson 1997; Williams et al. 1997). Exposure to chemical substances
during development of <strong>the</strong> nervous system can vary, both qualitatively
and quantitatively, depending on <strong>the</strong> phase of development of <strong>the</strong>
nervous system (non-linear dose-response curve). It can <strong>the</strong>refore be
difficult to assess <strong>the</strong> effects of long term low-dose exposure on <strong>the</strong> basis
of short-term studies. In addition, <strong>the</strong> development of <strong>the</strong> nervous system
depends on <strong>the</strong> endocrine systems, which are responsible for sexual
development and growth and are closely associated with <strong>the</strong> presence of
circulating thyroid hormones. Moderate to major changes in <strong>the</strong>
concentration of thyroid hormone during development result in motoric
dysfunction, cognitive defects and o<strong>the</strong>r neurological abnormalities
(Porterfield, Hendrich 1993). As stated, it can be difficult to assess
neurotoxic effects. The National Research Council (1993) found that <strong>the</strong>
present strategy for testing toxicity was inadequate for assessing toxicity
to several organ systems, including neurological development processes.
In several epidemiological studies, Parkinson’s disease has been linked
to pesticide use (including Semchuk et al. 1992). The main suspect was
paraquat, <strong>the</strong> chemical structure of which is somewhat similar to a
chemical (MPTP), which can induce parkinsonian symptoms in
laboratory animals. There are no studies specifically elucidating <strong>the</strong>
effect of paraquat.
There are very few studies of children and neurotoxic effects as a
consequence of exposure to pesticides, and clear conclusions cannot be
drawn <strong>from</strong> <strong>the</strong>m. There seems to be insufficient documentation of