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The agent is unknown, but several environmental exposures have been associated with PD.

Here, we summarize and examine the evidence for such environmental exposures.

Primary human research articles from peer-reviewed scientific journals were found from databases including Pub Med and Google Scholar by typing in search phrases such as “environment and Parkinson’s disease” and “case-control Parkinson’s” with each of the environmental agents until April 2016 (Table 1).

Over five billion pounds of pesticides were used worldwide in 2007 [20].

Human exposure occurs through ingestion of pesticide residues in food, drinking water, and most significantly, in occupational use including in agricultural field workers and workers in the pesticide industry.

In addition, follow up of the drug addicts exposed to MPTP who developed Parkinsonism revealed the stable, and not progressive, course of their symptoms, along with no Lewy Body pathology in postmortem studies [18].

Interestingly, postmortem tissue analysis has also revealed active, ongoing inflammation with the presence of microglia, extracellular melanin, and neurodegeneration years after MPTP exposure, leading to the theory of “long-latency neurotoxicity” after agent exposure [18].

Oxidative stress and ongoing inflammation leading to nigral cell loss have been hypothesized as the mechanism for the progressive and continued degeneration.

A frequent finding of epidemiologic studies is that PD is associated with farming as an occupation, rural living, and well-water exposure.

While the pathologic agent has yet to be identified, several environmental exposures have been associated with PD.

In this review, we summarize and examine human epidemiologic and case-control evidence for individual environmental agents associated with PD.

MPTP was associated with rapid-onset Parkinsonism when young drug abusers presented in Northern California with severe and irreversible Parkinsonism responsive to dopamine therapy [13].

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