Trichloroethylene Exposure and Usage, Environmental Associations in Parkinson Disease: Samuel M. Goldman, MD, MPH

WATCH TIME: 4 minutes

“There are not a lot of environmental associations with Parkinson disease—which is really important—and the reason for that I believe is largely because it's so difficult to study. Therefore, we need better methods to assess exposures and those are happening right now."

Millions of people worldwide are exposed to the chemical trichloroethylene (TCE) in the air, food, and water. According to research, those exposed to the chemical have an increased risk of developing Parkinson disease (PD). This is further supported by a recently published study of veterans formerly stationed at Camp Lejeune, a Marine Corps base found to have TCE water contaminated.¹

Among 340,489 veterans between 1975 and 1985, PD incidence was higher in those stationed at Camp Lejeune than those at Camp Pendleton (0.33% vs 0.21%), a base with uncontaminated water, resulting in a 70% higher prevalence rate (OR, 1.70; 95% CI, 1.39-2.07). Notably, those at Camp Lejeune were also associated with a statistically significant increased risk of prodromal risk scores (internal: OR, 1.14 [95% CI, 1.03-1.26]; Movement Disorders Society: OR, 1.18 [95% CI, 1.06-1.32]) and an overall increased PD risk of 14% to 20% in men.

Recently, lead author of the study Samuel M. Goldman, MD, MPH, clinical professor in the department of neurology at the University of California, San Francisco sat down in an interview with NeurologyLive® to discuss actions the Environmental Protection Agency is taking regarding the reevaluation of TCE and tetrachloroethylene (PCE). He also talked about how the long latency period of PD poses a challenge in studying environmental risk factors. Furthermore, he spoke about some of the methods being explored to improve the assessment of exposure to environmental factors in PD.

REFERENCES
1. Goldman SM, Weaver FM, Stroupe KT, et al. Risk of Parkinson Disease Among Service Members at Marine Corps Base Camp Lejeune. JAMA Neurol. 2023;e231168. doi:10.1001/jamaneurol.2023.1168