Criteria for attributing lung cancer to asbestos exposure.

The article by Mollo and coworkers1 examines the criteria for attribution of lung cancers to asbestos exposure, suggesting that the number of asbestos-related lung cancers in Italy might be underestimated. Their review of 924 consecutive lobectomies and pneumonectomies for lung cancer in northwest Italy included light microscopic asbestos body counts for asbestos body concentration in addition to histologic examination for asbestosis and asbestos bodies. Their interpretation is that 6% of the lung cancers in their series are attributable to asbestos exposure because of histologic diagnosis of asbestosis. However, they also conclude that another 0.5% of their cases had interstitial fibrosis without asbestos bodies on histologic section but an elevated asbestos body concentration on digestion study. Mollo and coworkers1 raise the possibility that these cases also may be asbestos-related lung cancers. The great majority of lung cancers are caused by tobacco smoke, but a minority of lung cancers are caused by asbestos exposure, virtually always in association with tobacco smoke exposure. One reason to identify the lung cancers caused by asbestos exposure is for establishing occupational and public health policies regarding asbestos or for investigation of lung cancer pathogenesis that, in turn, may provide a basis for new lung cancer therapies. In the individual case, the major reason to determine whether asbestos contributed to the development of a lung cancer is for purposes of compensation, which, in the United States, often is through litigation. Accurate identification of patients deserving compensation is also a primary concern of Mollo and coworkers.1 Before proceeding, we should remind ourselves that risk of a disease and actually having a disease due to that risk are two different things. This is a rather simple observation, but it is important if one is addressing etiology of a disease. Risk has to do with populations studied for relative likelihood of disease due to a common factor not present in a control population. Any membes of the at-risk population may not develop the disease under investigation and may have many individual factors that may modify the risk from the studied factor, be a confounding factor for the risk factor under study, or put them at risk for other diseases. An example can be found with the relationship of tobacco smoke to lung cancer. On the one hand, about 10% of tobacco smokers develop lung cancer as a result of their tobacco smoking. This is a considerably greater risk than the population of never smokers who have a background risk of lung cancer that is less than 1%, probably considerably so. On the other hand, even though most smokers do not develop lung cancer, about 90% of all lung cancers are caused by tobacco smoking.2 A smoker has a risk of lung cancer because of smoking that is much greater than that of individuals who have never smoked, but, even so, that person has a fairly good chance of not developing a lung cancer based on the risk seen in the population of all smokers. If that smoker does develop lung cancer, the lung cancer will be caused by the tobacco smoke and could have been avoided if the person had never smoked. If we look closer at the population of smokers with a risk of lung cancer, we can identify criteria that select those with the most risk of developing lung cancer based on the cumulative dose of tobacco smoke that they are exposed to and to factors of individual susceptibility.3-5 However, the causal association between tobacco smoke and lung cancer is so strong that we seldom do more than obtain a smoking history and do not require a detailed analysis of corroborating evidence to link a smoker’s lung cancer to tobacco smoke in the vast majority of cases.