ABSTRACT
The vast majority of Parkinson’s disease (PD) is etiologically multifactorial, with important contributions from both genetic and environmental determinants. Very few cases of PD can be attributed to single gene disorders (1-5). For PD without single gene Mendelian inheritance, relative risks as high as 14 for first-degree relatives of PD cases have been reported (6), but most studies have found more modest risks, on the order of two-to fourfold (7-10). Tanner et al. (11), in a study of a World War II cohort of monozygotic (MZ) and dizygotic (DZ) twins, with at least one of each pair with PD, found no difference in concordance between MZ and DZ twins diagnosed after the age of 50, when most PD occurs (12-15). While these studies suggest that, on a population level, a major genetic contribution to
PD is unlikely, there is a potentially important role for genetic susceptibility to environmental exposures in both sporadic and familial cases (16-18). Therefore, to increase our understanding of the etiology of PD, future analytical PD epidemiological studies must focus on better defining environmental factors that confer risk or protection, identifying genetic factors that modify risk, and determining the roles played by these factors, alone and interactively. In this chapter, we will review research on environmental factors implicated in PD, initially with a focus on methodology, and thereafter with a concentration on selected analytical epidemiological studies.
