Integrating Exposures Across the Lifespan: Early Life Exposure to Trichloroethylene as a Risk Factor for Parkinson’s Disease

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Abstract

Trichloroethylene (TCE) is an organic solvent used in industrial applications worldwide. Despite a recently proposed ban in the US, its usage over the last century produced widespread and long-lasting environmental contamination. TCE has been linked to multiple adverse health outcomes, with evidence growing that is a Parkinson’s disease (PD) risk factor. Exposure to TCE and other solvents in contaminated water at Camp Lejeune, North Carolina is associated with 70% increased PD risk in US veterans who lived on the base. However, little is known about PD risk from TCE in civilian populations, particularly in children who were exposed in early life. Importantly, the developing brain is highly susceptible to toxicant exposure, and previous work shows that exposure to TCE can result in neurodevelopmental deficits that manifest in adolescence and into adulthood. Given the number of individuals who have yet to “age” into idiopathic PD, understanding the mechanisms that underlie neurodegeneration from early life exposure to TCE could help to develop early interventions in at-risk populations. To further examine this, we review the existing literature on environmental exposures to PD-related toxicants during early-life and their long-term consequences. In addition, we discuss the potential for TCE-induced neurotoxic mechanisms to prime the brain for PD risk. Finally, we highlight the need for future studies to evaluate the impact of early-life TCE exposure across the lifespan.

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