Exposure to Toxic Substances at Work – Guideline Court of Appeal Ruling

29/11/2023


Exposure to toxic substances at work is often cited as a possible cause of diseases developed later in life. However, as an important Court of Appeal ruling made plain, establishing the plausibility of such causal links may not, by itself, be enough to succeed in an occupational injury claim.

The case concerned a man who developed Parkinson’s disease after working for an industrial employer for almost 40 years. After he launched a personal injury claim, a judge found that he had been exposed on the shop floor to significant levels of an organic solvent, trichloroethylene (TCE), which was used to clean and degrease engineering components.

Before the judge, it was not the man’s case that such exposure merely increased the risk of him developing Parkinson’s disease. Rather, he asserted that TCE did, in fact, cause or materially contribute to his condition. The judge upheld his claim, finding his former employer liable to compensate him for all the consequences of the disease.

Ruling on the employer’s challenge to that outcome, the Court noted that there is no doubt that TCE is neurotoxic. It is also now recognised as a carcinogen. The man was not required to show that a causal link between TCE and Parkinson’s disease had been scientifically proved. It was sufficient for him to establish that such a link was more likely than not.

Upholding the appeal, however, the Court observed that the causation of Parkinson’s disease is poorly understood. A wide range of genetic and environmental factors had been postulated, exposure to TCE amongst them. TCE is one of many compounds that have been suggested to be capable of causing the disease. However, a number of controlled, high-quality studies had, to date, not produced consistent results or substantiated such a cause-effect relationship.

The evidence of such a causal link, as summarised by the judge, was weak. It did no more than establish that TCE is a risk factor for Parkinson’s disease and that there is a plausible mechanism, based on studies involving rodents, for a finding that TCE may cause or materially contribute to the development of Parkinson’s disease. Overall, the evidence did not justify a conclusion that, on the balance of probabilities, such wrongful exposure to TCE as the man experienced made a material contribution to the onset of the disease.


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