Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
700905
Reference Type
Journal Article
Title
Trichloroethylene: Parkinsonism and complex 1 mitochondrial neurotoxicity
Author(s)
Gash, D; Rutland, K; Hudson, N; Sullivan, P; Bing, G; Cass, W; Pandya, J; Liu, M; Choi, D; Hunter, R; Gerhardt, G; Smith, C; Slevin, J; Prince, T
Year
2008
Is Peer Reviewed?
Yes
Journal
Annals of Neurology
ISSN:
0364-5134
EISSN:
1531-8249
Volume
63
Issue
2
Page Numbers
184-192
Language
English
PMID
18157908
DOI
10.1002/ana.21288
Abstract
Objective: To analyze a cluster of 30 industrial coworkers with Parkinson's disease and parkinsonism subjected to long-term (8-33 years) chronic exposure to trichloroethylene.
Methods: Neurological evaluations were conducted on the 30 coworkers, including a general physical and neurological examination and the Unified Parkinson's Disease Rating Scale. In addition, fine motor speed was quantified and an occupational history survey was administered. Next, animal studies were conducted to determine whether trichloroethylene exposure is neurotoxic to the nigrostriatal dopamine system that degenerates in Parkinson's disease. The experiments specifically analyzed complex 1 mitochondrial neurotoxicity because this is a mechanism of action of other known environmental dopaminergic neurotoxins.
Results: The three workers with workstations adjacent to the trichloroethylene source and subjected to chronic inhalation and dermal exposure from handling trichloroethylene-soaked metal parts had Parkinson's disease. Coworkers more distant from the trichloroethylene source, receiving chronic respiratory exposure, displayed many features of parkinsonism, including significant motor slowing. Neurotoxic actions of trichloroethylene were demonstrated in accompanying animal studies showing that oral administration of trichloroethylene for 6 weeks instigated selective complex 1 mitochondrial impairment in the midbrain with concomitant striatonigral fiber degeneration and loss of dopamine neurons.
Interpretation: Trichloroethylene, used extensively in industry and the military and a common environmental contaminant, joins other mitochondrial neurotoxins, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and some pesticides, as a risk factor for parkinsonism.
Tags
IRIS
•
Trichloroethylene (TCE) (Final, 2011)
All References
Hazard
Neuro
Dose-Response
Non-Cancer
OPPT REs
•
OPPT_Trichloroethylene (TCE)_F. Human Health
Total – title/abstract screening
On topic
Peer review
Primary source
Cited in IRIS document or IRIS HERO page
On topic - additional tags for titles/abstracts
Human hazard ID
Animal hazard ID
MOA
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity