[LindaH]

The New York Times ran an article today about a worker at a Kentucky industrial plant who developed Parkinson’s, after having been exposed for more than 20 years to the industrial solvent - trichloroethylene. His workmen’s comp claim was turned down because he couldn’t prove without a doubt it was the solvent that caused his PD.

He participated in a study at the Un of Kentucky,that analyzed the incidence of PD amd Parkinsonian symptoms among workers at that plant . They also conducted a parallel study that showed "feeding the solvent to rats resulted in injured neurons in the same area of the brain whose degeneration causes Parkinson’s in humans."

The study was published in the Annals of neurology (feb 2008) and concluded, “These results demonstrate a strong potential link between chronic TCE exposure and Parkinsonism… 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.”

But the researchers could not provide the strict proof required by workmen’s comp, and Ed Abney’s claim was still denied.. Do these laws need to be changed? Or should the burden of proof remain on the stricken workers?

BTW, You might recognize the name Ed Abney. He was one of the Kentucky GDNF trial participants, and took part in the patients’ lawsuit against Amgen for reinstatement of their GDNF treatments. Ed lost that one too.
The full text of the article is at:
http://www.nytimes.com/2009/01/25/us/25toxic.html

from: New York Times, January 25, 2009
Exposed to Solvent, Worker Faces Hurdles
By FELICITY BARRINGER

Also below is the Pubmed abstract for the Annals of Neurology article, Feb 2008
"Trichloroethylene: Parkinsonism and complex 1 mitochondrial neurotoxicity."
Gash DM, Rutland K, Hudson NL, Sullivan PG, Bing G, Cass WA, Pandya JD, Liu M, Choi DY, Hunter RL, Gerhardt GA, Smith CD, Slevin JT, Prince TS.
Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA. dongash@email.uky.edu

"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 parkinson's."

PMID: 18157908 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum