Parkinson's disease (PD) is the second most common neurodegenerative disorder, primarily affecting older adults. Given the projected growth and aging trend of the population, the prevalence of PD is expected to double by the year 2040, highlighting the imperative need for a better understanding of the disease. It is generally accepted that the development of idiopathic PD is multifactorial, involving both genetic and environmental factors; however, relatively little is known about specifi c exposures. An association between TCE exposure and increased PD risk has been suggested by several case reports/clusters, and recently, the fi rst epidemiologic study found a signifi cant six-fold increased risk of PD associated with occupational TCE exposure. Data from animal studies also support a plausible mechanistic pathway, with rodent models demonstrating TCE-induced neurotoxic effects similar to those occurring in PD. Given that TCE is ubiquitous, even a modest increased risk could have enormous population-level neurological health implications.