Progress and Prospects in Parkinson's Research/Causes/Toxins/Trichloroethylene

Background edit

Trichloroethylene (C2HCl3) is a chlorinated hydrocarbon commonly used as an industrial solvent. It is a clear, non-flammable liquid with a sweet smell.

It is also known as TCE, 1,1,2-Trichloroethene, 1,1-Dichloro-2-Chloroethylene, 1-Chloro-2,2-Dichloroethylene, Acetylene Trichloride, TCE, Trethylene, Triclene, Tri, Trimarand Trilene.

It was introduced by the UK Company Imperial Chemical Industries (ICI) in the 1920s as an anaesthetic and was widely used as an analgesic in childbirth, but was phased out owing to doubts about its toxicity.

Other uses for the product are:-

  • extracting vegetable oils from plants such as coconuts, palms and soy;
  • coffee decaffeination;
  • a dry cleaning solvent;
  • cleaning machines in the film industry;
  • preparation of flavouring extracts;
  • degreasing metals;
  • cleaning rocket engines;
  • the manufacture of hydrocarbon refrigerants.
  • cleaning military weapons during the Gulf War.

Among the toxic effects noted on humans are:-

  • anaesthesia (dizziness);
  • tachypnea (rapid breathing);
  • irregular heartbeat;
  • headaches;
  • cranial nerve dysfunction;
  • facial numbness;
  • hepatoxicity (liver damage);
  • renal failure (kidneys);

Considerable concern has been expressed in the United States about the contamination of well water by TCE.

Research edit


Bringmann et al [1] postulated that the hypnotic chloral reacts chemically with tryptamine and tryptophan in the human body under physiological conditions to form TCE.


Bringmann et al ,[2] established that TCE formed endogenously in humans after administration of the hypnotic chloral hydrate

Guehl et al [3] describe the case of a 47 year old woman, who contracted PD after 7 years’ exposure to TCE. The researchers were able to reproduce the condition in laboratory mice, and concluded,

“The environmental trichlorethylene pollution, as well as other unspecific neurotoxic solvents, could potentially contribute to the genesis of some cases of Parkinson's disease."


Kochen et al [4] examined the possible causative links between Volatile Organic Solvents (VOS) and neurodegenerative diseases. Their conclusions state,

“The onset of Parkinson's disease in three chronic TRI-exposed individuals during the postexposure period could be associated with the presence of TaClo [TCE] in ng-range. Consequently, determination of TaClo and its derivatives in blood of humans exposed to chlorinated VOSs may serve as a marker of risk indicating either causative or supportive processes of neurodegeneration that may lead to manifestation of PD after many years.”


Akundi et al [5] evaluated TCE. Their conclusions state,

“Earlier studies have revealed the relative permeability of the molecule through the blood-brain barrier and its ability to induce Parkinson-like symptoms in rats. In this study, we report that TaClo induces an apoptotic pathway in the human neuroblastoma cell line, SK-N-SH, involving the translocation of mitochondrial cytochrome c to the cytosol and activation of caspase 3. TaClo-induced apoptosis shows considerable differences from that mediated by other Parkinson-inducing agents such as MPTP, rotenone and manganese.”


Gash et al [6] analysed the cases of 30 industrial co-workers with PD, who had been exposed to TCE for periods ranging from 8 to 33 years. They found that the severity of the Parkinson symptoms was proportionate to the degree of exposure to TCE.

“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.”


Researchers at the Parkinson’s Institute and Clinical Center, Sunnyvale, Californis [7] studied the job histories of 99 pairs of twins, where one had contracted PD and the other had not. This was done to try to eliminate genetic factors from the investigation. They found that individuals who had the greater exposure to trichloroethylene were six times more likely to contract Parkinson’s Disease.


Zaheer & Slevin [8] evaluated the evidence linking TCE to the incidence of PD. The indication was that TCE induced mitochondrial failure in nigral neurons.

Goldman et al [9] carried out extensive lifestyle and case history interviews on 99 pairs of twins, where one sibling had contracted PD and the other had not. They concluded that people with a history of exposure to TCE were 6 times more likely than normal to contract PD. The chemical is prevalent in groundwater in parts of the USA. They also found evidence implicating Perchloroethylene -PERC and Carbon tetrachloride - CCl(4) in the spread of the disease.

Further Reading edit


Huber, F. Z. Unfallmed. Berufskr 62 (4) 226-267.

Clinical aspects and neuropathology of trichloroethylene poisoning.


Goldman, S. M. Expert. Rev. Neurother.10(6):835-7.

Trichloroethylene and Parkinson's disease: dissolving the puzzle.


Use the following links to query the PubMed, PubMed Central and Google Scholar databases using the Search terms:- Parkinson's_Disease Trichloroethylene.

This will list the latest papers on this topic. You are invited to update this page to reflect such recent results, pointing out their significance.

Pubmed (abstracts)

Pubmed_Central (Full_Text)


Related Pages edit

Causes > Toxins

Sub Pages:

Cadmium - Copper - Dieldrin - Manganese - Maneb - Mercury - MPTP - n-Hexane - Paraquat - Rotenone - Toluene - Trichloroethylene - Ziram

References edit

  1. Bringmann, G.; Friedrich, H. And Feineis, D. (1992) J. Neural Transm. Suppl. 39 15-26. Trichloroharmanes as potential endogenously formed inducers of Morbus Parkinson: synthesis, analytics, and first in vivo-investigations.
  2. Bringmann. G.; God, R.; Fähr, S.; Feineis, D.; Fornadi, K. and Fornadi, F. (1999) Anal. Biochem. 270 (1) 167-175. Identification of the dopaminergic neurotoxin 1-trichloromethyl-1,2, 3,4-tetrahydro-beta-carboline in human blood after intake of the hypnotic chloral hydrate.
  3. Guehl, D.; Bezard, E.; Dovero, S.; Boraud, T.; Bioulac, B. and Gross, C (1999) Eur. J. Neurol. 6 (5) 609 – 611. Trichloroethylene and parkinsonism: a human and experimental observation.
  4. Kochen, W.; Kohlmuller, D.; De Biasi, P. And Ramsay, R (2003) Adv. Exp. Med. Biol. 527 253-263. The endogeneous formation of highly chlorinated tetrahydro-beta-carbolines as a possible causative mechanism in idiopathic Parkinson's disease.
  5. Akundi, R. S.; Macho, A.; Muñoz, E.; Lieb, K.; Bringmann, G.; Clement, H. W.; Hüll, M. and Fiebich, B. L. (2004) J. Neurochem. 91 (2) 263-273. 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline-induced apoptosis in the human neuroblastoma cell line SK-N-SH.
  6. Gash, D. M. Rutland, K.; Hudson; N.L.; Sullivan, P. G.; Bing, G.; Cass W. A.; Pandya, J. D.; Liu, M.; Choi. D. Y.; Hunter, R.L.; Gerhardt, G.A.; Smith, C.D.; Slevin, J.T. and Prince, T.S. (2008) Ann. Neurol. 63 (2) 184-192. Trichloroethylene: Parkinsonism and complex 1 mitochondrial neurotoxicity.
  8. Zaheer, F. and Slevin, J. T. (2011) Neurol. Clin. 29 (3) 657-665. Trichloroethylene and Parkinson disease.
  9. Goldman, S.M.; Quinlan, P.J.; Ross, G.W.; Marras, C.; Meng, C.; Bhudhikanok, G.S.; Comyns, K.; Korell, M.; Chade, A.R.; Kasten, M.; Priestley, B.; Chou, K.L.; Fernandez, H.H.; Cambi, F.; Langston, F. and Tanner, C.M. (2011) Ann. Neurol. Solvent exposures and Parkinson disease risk in twins