Environmental Toxins
A number of environmental toxins have been linked to occurrence of PD. Much research has implicated pesticide exposure in general as a risk factor for PD (Priyadarshi et al., 2001; Brown et al., 2006; Kasten et al., 2007; Hancock et al., 2008). Although identification of specific pesticides has been challenging, some association with PD has been found with the herbicide paraquat and the fungicide maneb (Thrash et al., 2007; Costello et al., 2009). The chemical 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) - which has some structural similarity to paraquat - was made infamous when it was unintentionally injected by drug users who thought they were taking a closely related synthetic opioid compound. These users rapidly developed a phenotype strongly resembling PD (Langston et al., 1983). Some epidemiological data also exists for the insecticide rotenone (Dhillon et al., 2008). Pre-clinical research models using the pesticides rotenone (Betarbet et al., 2000; Cannon et al., 2009) and paraquat (Brooks et al., 1999) demonstrate clear loss of dopamine neurons and have been used to model this aspect of PD (Bove et al., 2005).
Additional indirect evidence of a role for pesticide exposure comes from the observed increased risk for PD in people living in rural communities and farms, or who drink well water that may contain agricultural runoff (Priyadarshi et al., 2001; Kasten et al., 2007).
There is also evidence linking exposure to heavy metals, such as iron, in the diet to increased risk for PD (Powers et al., 2003; Logroscino et al., 2008). Manganese exposure has also been implicated in PD, but the findings are controversial (Kieburtz and Kurlan, 2005).

