Solvent exposure at work, home may increase risk of Parkinson’s disease.

Feb 21, 2012

Goldman, SM, PJ Quinlan, GW Ross, C Marras, C Meng, GS Bhudhikanok, K Comyns, M Korell, AR Chade, M Kasten, B Priestly, KL Chou, HH Fernandez, F Cambi, JW Langston and CT Tanner. 2011. Solvent exposures and Parkinson disease risk in twins. Annals of Neurology http://dx.doi.org/10.1002/ana.22629.



Synopsis by Steven Neese and Wendy Hessler

 

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Even relatively limited exposure to some common chemical solvents at work or through hobbies may increase the risk of having Parkinson's disease (PD), report researchers who found a higher risk regardless of the number of exposures, their duration or lifetime totals. They also found that the first symptoms of the disease – the second most common neurodegenerative disease in the United States – may not surface until decades after exposure.

Animal research and limited studies with people suggest exposure to environmental contaminants may play a role in PD. This study of twins supports that idea by providing the first population-based evidence that links exposure to specific solvents – including TCE, PERC, and CCI4 – and the risk of PD. The highest risk was seen with TCE, a degreaser and a chemical used in dry cleaning that contaminates up to a third of U.S. drinking water.

The ubiquitous nature these chemicals in the environment suggests more research is needed to confirm and better understand the possible link between human exposures and PD risk.


Context

Research suggests that exposure to some common workplace chemicals – including pesticides (Wang et al. 2011) – may lead to Parkinson’s disease (PD), but few studies have assessed this relationship in people.

PD afflicts more than 700,000 people in the United States. Hallmarks of this disease include body tremors and stature problems resulting from a loss of dopaminergic cells in the brain.

Solvents are widely used in a variety of products, including glue, paints and cleaning products. Some – such as TCE, PERC and CCl4 – may play a role in PD.

These three chemicals have been used for decades in many industrial and consumer uses. For instance, millions of pounds of TCE is still used mainly as a metal degreaser, and its use in dry cleaning and as an additive in glues, carpet cleaners and other products has been extensive. Like TCE, PERC is a dry cleaning agent and degreaser. CCI4 continues to be used in industry but no longer is used as a dry cleaner solvent, as a pesticide and to make refrigerants.

Even though their use in consumer products has declined in recent years, these chlorinated chemicals can stick around, accumulating in the environment and in people. They are measured in the air, water and human tissues.

Laboratory research shows that TCE can kill dopaminergic brain cells (Liu et al. 2010). PERC and CCI4 can also damage and kill brain cells (Manibusan et al. 2007; Toraason et al. 1999). The studies provide compelling evidence that these chemicals can alter neurochemical functions in the brain.

No treatments exist to delay or prevent PD. It is therefore important to determine if exposure to environmental contaminants are linked to this disease.

What did they do?

Ninety-nine male twin pairs where only one brother was diagnosed with PD were recruited from the National Academy of Sciences/National Research Council World War II Veteran Twins Registry. Since twins are genetically similar (fraternal) or identical, studying twins helps rule out the role of genetics in the risk of PD and allows for a more direct measure of environmental influences on the risk of the disease.

Through questionnaires, participants provided lifetime occupational and hobby exposure to six solvents linked to PD – xylene, toluene, n-hexane, carbon tetrachloride (CCI4), trichloroethylene (TCE) and perchloroethylene (PERC). The researchers inferred exposures based upon job descriptions and length of time the work or hobby occurred. Occupational histories included any job held for longer than six months beginning at 10 years of age.

The inferred solvent exposures were classified in two ways: 1) as ever being in contact with a solvent (at least 1 hour per week) and 2) the intensity of exposure (low, medium or high). An index of cumulative lifetime exposures was calculated based these two criteria.

Smoking habits and incidence of head injury were assessed and factored in as these lifestyle factors may influence PD risk.

What did they find?

The broad job categories with associations were industrial machinery repairer and industrial worker. Electricians and dry cleaners tended to be occupations with the most extensive contact with TCE, PERC and CCI4.

"Ever" exposure to TCE was associated with a significant 6-fold increase in the odds of having PD, while "ever" exposure to PERC or CCI4 also increased the disease risk.

Combined exposures to TCE and PERC increased disease risk by nine fold.

Duration of exposures did not alter PD risk. That is, exposure to these chemicals for any length of time increased the risk of the disease.

PD risk was similar when considering ever/never exposure, duration and lifetime cumulative exposure with these chemicals. Exclusion of hobby-related contact or inclusion of head injury or smoking habits also failed to alter this relationship.

What does it mean?

This study shows that exposure to certain solvents at work or in hobbies increases the risk of Parkison's disease in men. The chemicals with the highest risk were TCE, PERC and CCI4. In some cases, decades passed between exposure and when the first disease symptoms appeared.

Worldwide, the use of these three chemicals is extensive and stretches back several decades. Their longtime use and the reported latency makes the results of this report of particular concern.

The connection between TCE and PD only surfaced after a long period of time had passed between the exposures and the first disease symptoms. The results show the lag can be up to 40 years. This suggests exposures can result in a variety of unseen toxic effects on the brain with clinical symptoms appearing much later in life.

The study is important because the results on a population level are in line with prior animal studies and human research using different methods. Since twins share similar genetic profiles, using twins helps tease apart the links between environmental exposures and disease risk.

The occupations of industry workers had the highest risk, most likely because they have had and continue to have some of the highest exposures to solvent chemicals. Importantly,  "artists" – which is a career and often a hobby – also reported high exposures to PERC, suggesting even hobby contact can be an important risk factor for PD.

TCE is primarily used as a degreasing agent, but this chemical was used as a general anesthetic and to decaffeinate coffee until 1977. Still today, more than 50 million pounds are released annually into the environment. The chemical is frequently measured in groundwater and taints drinking water supplies.

PERC is still found in many household products – including spot removers. While CCI4 has limited industry applications, it can also persist for months in the environment. 

This study is limited by the fact that the results were derived from a small sample, based upon recalled exposures. They do not represent a causal link.

Overall, the findings from this study suggest that exposure to a variety of solvents can increase PD risk. Despite the decreased use of some of these chemicals, human exposure at home and at work is still likely because they are still used in industry and can persist in the environment.


Resources

Liu, M, DY Choi, RL Hunter, JD Pandya, WA Cass, PG Sullivan, HC Kim, DM Gash and G Bing, 2010. Trichloroethylene induces dopaminergic neurodegeneration in Fischer 344 rats. Journal of Neurochemistry 112: 773-783.

Manibusan, MK, M Odin and DA Eastmond. 2007. Postulated carbon tetrachloride mode of action: a review. Journal of Environmental Science and Health Part C 25:185-209.

Toraason, M, J Clark, D Dankovic, P Mathias, S Skaggs, C Walker and D Werren. 1999. Oxidative stress and DNA damage in Fischer rats following acute exposure to trichloroethylene or perchloroethylene. Toxicology 138:43-53.

Wang, A, S Costello, M Cockburn, X Zhang, J Bronstein and B Ritz. 2011. Parkinson’s disease risk from ambient exposure to pesticides. European Journal of Epidemiology 26:547-555.

 

 

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