- Alcohol
- Evidence (epidemiological)
- Exposure (asbestos)
- Exposure (formaldehyde)
- Smoking (second-hand smoke)
- Cancer (throat)
The sole issue before the Panel was the worker's entitlement for hypopharyngeal cancer.
The appeal was denied. The Panel acknowledged that hypopharyngeal cancer is a relatively rare cancer and, thus, more resistant to epidemiological study. It was not disputed that the worker was at significantly increased risk of developing hypopharyngeal cancer resulting from his smoking and alcohol consumption history.The Panel noted that, although cancer of the hypopharynx is rare, the roles that alcohol and smoking play are well established. There was a lack of sufficient evidence that exposure to asbestos causes cancer in the pharynx in humans. IARC did not support a causal role for formaldehyde in relation to hypopharyngeal cancer. There was also limited evidence of a casual association between exposure to second hand smoke and hypopharyngeal cancer. The most favourable data was from the Marchand study with a relative risk of 1.8 with a relatively small cohort of subjects exposed to asbestos. The Vice-Chair noted that the Marchand study did not meet the criteria of a relative risk of 2. With respect to the applicability of the Demers report, if this were a case where there were studies of several substances, each of which exhibited a slightly increased risk of developing lung cancer, then the model would be applicable to the facts of this case. However, the evidence was not such that each of the worker's workplace exposures put him at a slightly increased risk. There was no clear trend in the studies to suggest an increased risk. The Panel noted that it was not that the evidence had not reached medical certainty; rather, it had not reached a probability.In conclusion, there was insufficient evidence for the Panel to infer that there was a likely causal relationship between the workplace exposures, considered together, and the development of the worker's hypopharyngeal cancer. There existed a possibility, but this was not sufficient. The Panel found that the epidemiological evidence of a causal relationship between alcohol/smoking and the development of hypopharyngeal cancer was so strong that the workplace exposures in this case, even accepting that they might possibly have played a minor role, had been reduced to a de minimis contribution.