Academic journal article Environmental Health Perspectives

Pesticides and Parkinson's Disease-Is There a Link?

Academic journal article Environmental Health Perspectives

Pesticides and Parkinson's Disease-Is There a Link?

Article excerpt

Parkinson's disease (PD) is an idiopathic disease of the nervous system characterized by progressive tremor, bradykinesia, rigidity, and postural instability. It has been postulated that exogenous toxicants, including pesticides, might be involved in the etiology of PD. In this article we present a comprehensive review of the published epidemiologic and toxicologic literature and critically evaluate whether a relationship exists between pesticide exposure and PD. From the epidemiologic literature, there does appear to be a relatively consistent relationship between pesticide exposure and PD. This relationship appears strongest for exposure to herbicides and insecticides, and after long durations of exposure. Toxicologic data suggest that paraquat and rotenone may have neurotoxic actions that potentially play a role in the development of PD, with limited data for other pesticides. However, both the epidemiology and toxicology studies were limited by methodologic weaknesses. Particular issues of current and future interest include multiple exposures (both pesticides and other exogenous toxicants), developmental exposures, and gene-environment interactions. At present, the weight of evidence is sufficient to conclude that a generic association between pesticide exposure and PD exists but is insufficient for concluding that this is a causal relationship or that such a relationship exists for any particular pesticide compound or combined pesticide and other exogenous toxicant exposure. Key words: epidemiology, literature review, Parkinson's disease, pesticides, toxicology. doi: 10.1289/ehp.8095 available via http://dx.doi.org/ [Online 7 September 2005]

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Parkinson's disease (PD) is an idiopathic disease of the nervous system characterized clinically by parkinsonism: chronic progressive tremor, bradykinesia, rigidity, and postural instability. The major pathologic feature of PD is the profound loss of pigmented neurons, mainly in the pars compacta of the substantia nigra (SN). Associated with this neuronal loss is the presence of large eosinophilic inclusions, called Lewy bodies, within the remaining pigmented neurons, made up of a series of proteins, including neurofilaments, [alpha]-synuclein fibrils, ubiquitin, parkin, and proteasomal elements. The first clinical signs of PD, however, become apparent only after the loss of about 70-80% of dopaminergic neurons (Schapira 1999), and although the diagnosis of PD is entirely clinical, histopathology on autopsy is the only way to definitively confirm a diagnosis.

The mean age of onset of PD is typically between 60 and 65 years, and in Europe the prevalence of PD has been estimated to be 1.8% in persons [greater than or equal to] 65 years of age (de Rijk et al. 2000), with an incidence of approximately 16-19 per 100,000 per year (Twelves et al. 2003). Although age is unequivocally associated with increasing PD risk, the underlying process of PD is distinct from the natural aging process (Goldman and Tanner 1998). PD prevalence is also similar among ethnic groups living in the same location (Morens et al. 1996), but may differ among ethnic groups living in different locations (Schoenberg et al. 1988). Genetic factors can influence the risk of PD, and higher rates of PD have been found in relatives of those with PD (Foltynie et al. 2002). However, twin studies have consistently shown low rates of concordance (5-8%) in monozygotic and dizygotic twins (Foltynie et al. 2002), suggesting that other factors play a part in the etiology of PD. The exception to this is young-onset PD (onset before 50 years of age), where concordance in monozygotic twins was 100%, suggesting a primarily genetic basis (Tanner 2003). Several specific loci have been identified that result in PD, including mutations in the PARK 1 to PARK 8 genes, although these forms of PD are rare and usually display atypical features of the disease (Foltynie et al. 2002).

A number of causative factors have been found to induce parkinsonism similar to that of idiopathic PD, including vascular insults to the brain, repeated head trauma, neuroleptic drugs, and manganese toxicity (Adler 1999). …

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