Association of Pesticide Exposure With Neurologic Dysfunction and Disease

Freya Kamel; Jane A. Hoppin

Disclosures

Environ Health Perspect. 2004;112(9) 

In This Article

Neurotoxicity of High-Level Exposure

Most types of pesticides, including OP, carbamate, and organochlorine insecticides as well as fungicides and fumigants, can be neurotoxic, but only OPs have been studied in detail (Keifer and Mahurin 1997). The response to OPs can occur within minutes. Less severe cases of OP poisoning display symptoms including headache, dizziness, nausea, vomiting, pupillary constriction, and excessive sweating, tearing, and salivation. More severe cases develop muscle weakness and twitches, bronchospasm, and changes in heart rate and can progress to convulsions and coma. The mechanism of OP neurotoxicity in most cases involves overstimulation of postsynaptic cholinergic receptors after inhibition of AChE (Keifer and Mahurin, 1997), although other macromolecular targets may also be involved (Pope 1999). An intermediate syndrome, occurring 1-4 days after exposure, is characterized by muscle weakness and can be fatal if respiratory muscles are affected. Two to five weeks after exposure, some patients develop OP-induced delayed polyneuropathy, a well-characterized syndrome involving sensory abnormalities, muscle cramps, weakness, and even paralysis, primarily in the legs. These symptoms are a consequence of axonal death following OP inhibition of a neural enzyme called neuropathy target esterase and may be irreversible (Keifer and Mahurin 1997).

Several studies have shown that OP poisoning has additional long-term sequelae. Studies of individuals with a history of pesticide poisoning—farmworkers (London et al. 1998; McConnell et al. 1994; Rosenstock et al. 1991; Wesseling et al. 2002), farmers (Stallones and Beseler 2002), rescue workers (Nishiwaki et al. 2001), or individuals identified from hospitals or pesticide registries (Miranda et al. 2002; Savage et al. 1988; Steenland et al. 1994)—have found that increased symptom prevalence, deficits in cognitive and psychomotor function, decreased vibration sensitivity, and motor dysfunction can occur long after the immediate episode is resolved. In some cases, effects were observed ≥ 10 years after poisoning (Savage et al. 1988), suggesting that the residual damage is permanent. Even less severe poisoning can have long-term consequences: Banana farm workers who had been treated for intoxication with OPs or carbamates but did not require hospitalization performed worse on tests of cognitive and psychomotor function than did nonpoisoned workers when tested > 2 years later (Wesseling et al. 2002).

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