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Asbestos Exposure and Laryngeal Cancer: Is there an Association?

1140 • www.entjournal.com Medicine is replete with assumptions and myths based on faulty reasoning. It is important for all of us to be aware of this problem and diligent about assessing evidence to draw the best possible conclusions. One of the most frequent errors results from posthoc ergo propter hoc reasoning. This classic error in logic assumes that because Event B happens after Event A, Event B is caused by Event A. Proof of causation requires considerably more rigorous evidence. The suggestion that asbestos exposure can cause laryngeal cancer appears to be an example of this flaw in logic. It was estimated that in 2008, laryngeal carcinoma would affect 12,250 adults, of whom 3,670 would die. The median age of diagnosis of laryngeal carcinoma is 65 years, and the mean age of death caused by this tumor is 69 years.' Known risk factors for laryngeal carcinoma include cigarette smoking and ethanol use. These factors have been shown to have a synergistic effect in the development of carcinoma. In addition, a possible association between asbestos exposure and laryngeal carcinoma has been evaluated throughout the years. However, there are numerous conflicting reports, and a link between asbestos and laryngeal cancer has not been proven. In 1975, Stell and McGill were the first authors to propose a link between asbestos exposure and laryngeal carcinoma. ' One hundred nineteen patients with squamous cell carcinoma of the larynx were identified. Compared to agematched controls, a greater proportion of patients had significant asbestos exposure (27.7 vs. 2.5%; P< 0.001), but this study failed to account for risk factors such as smoking. Stell and McGill do mention that the patient group had a greater incidence of smoking than the control group, and they suggest that smoking is a cofactor in the development of laryngeal carcinoma, but the failure to account for known risk factors in their analysis undermines the credibility of the study. Griffiths and Molony reviewed 60 articles published between 1973 and 2001.3 They cited postmortem studies by Roggli et aJ,4 which noted that asbestos bodies but no dysplasia was found in the larynges of patients who had been exposed to asbestos. Others performing similar studies reviewed by Griffiths and Molony' demonstrated hyperplasia but no dysplasia in exposed larynges. Based on these studies, Griffiths and Molony conclude that asbestos is an irritant but that it cannot be deemed a causative agent in laryngeal carcinoma. Griffiths and Molony also reviewed case-control studies.' Of the 14 studies reviewed, 3 (including that of Stell and McGilF) were found to have a statistically significant correlation between asbestos exposure and laryngeal carcinoma. However, none of these studies 'adjusted for the smoking risk associated with larynge al carcinoma. The remaining studies failed to demonstrate a statistically significant link after adjusting for smoking and alcohol exposure. A study by Gustavsson et aI, not included in the Griffiths study, evaluated 545 patients with laryngeal cancer who admitted to occupational exposure to asbestos.' A dose-dependent relationship between exposure and risk of laryngeal