© 2005 American Thoracic Society
Diagnosis and Initial Management of Nonmalignant Diseases Related to AsbestosTo the Editor:The American Thoracic Society (ATS) publishes official statements with the expectation that these statements will be balanced, scientifically rigorous, and reflect a comprehensive review of the medical literature. In our opinion, the recent ATS Statement, "Diagnosis and initial management of nonmalignant diseases related to asbestos" (1), did not fully consider alternative points of view and all of the available literature in several important areas. Since space does not permit a point-by-point rebuttal of the Statement, we have elected to briefly consider examples of the Committee's treatment of two high-impact asbestos-related issues: the question of benign pleural thickening as a risk factor for future malignancy, and whether clinically relevant chronic obstructive pulmonary disease is a likely consequence of asbestos exposure. In the case of the former, the Committee's citing of evidence is selective, and with the latter, there are internal inconsistencies that are likely to leave readers confused and unable to independently draw their own evidence-based conclusions. With regard to pleural plaques being associated with increased malignancy risk, the authors state, "The presence of plaques is associated with a greater risk of mesothelioma and of lung cancer compared with subjects with comparable histories of asbestos exposure who do not have plaques.... Therefore, the presence of pleural plaques should be interpreted as a marker for elevated risk of malignancy, which may be higher than the occupational history alone might suggest." To support this point, two studies were cited (2, 3). Weaknesses of these studies have been pointed out in a more recent publication (4). In addition, other (one could argue, more powerful) data were not included in the Statement. For instance, in a longitudinal study of asbestos cement workers, the presence of pleural plaques (in the absence of asbestosis) was not associated with an increased lung cancer risk (5). The strength of this study was its prospective cohort design in which radiographic and exposure data were available in a large at-risk population subsequently followed for cause-specific mortality. Additionally, a meta-analysis by Weiss (6) concluded that the weight of the evidence favors the position that persons with asbestos-related pleural plaques do not have an increased risk of lung cancer in the absence of asbestosis. This viewpoint is not considered in the Statement. Further, although risk of malignancy is considered in relation to pleural plaques, the question of whether asbestosis is required to attribute lung cancer to asbestos exposure is not addressed. Given that the most persuasive scientific evidence (5, 7, 8), extensively reviewed by Weiss (9), supports the hypothesis that asbestosis is required to assign causation of lung cancer to asbestos, it is a glaring omission that this document chose not to review this area of the literature. Instead, the document addressed only the unproven association between pleural plaques and malignancy. In the section on chronic airway obstruction, the Statement implies that clinically significant chronic airway disease can be caused by asbestos exposure alone. However, the studies cited are unable to support that conclusion given their lack of dose–response information and failure to control for other factors (e.g., smoking, radiographic abnormalities, and age) that impact lung function. Despite this, the Committee reached conclusions that are contradictory and that were not based on a comprehensive review of the available literature. As an example of the former, the Committee states, "In general, the magnitude of the asbestos effect on airway function is relatively small. This effect, by itself, is unlikely to result in functional impairment or the usual symptoms and signs of chronic obstructive pulmonary disease." We agree. However, in the next paragraph, the Committee states, "Asbestos exposure independently contributes to accelerated decline in airflow over time, whether or not exposure ceases...." Finally, in the concluding paragraph of the airway disease section, the claim is made that "[t]he association between airway obstruction and exposure to asbestos has been well demonstrated in nonsmokers...." However, when excluding nonsmoking patients with radiographic evidence of asbestos-related lung disease and when adhering to the definition of COPD (reduced FEV1/FVC ratio) as put forth by the GOLD initiative (10), there is no evidence of an association between clinically significant airway obstruction and asbestos exposure alone. Comments made by the Committee to the contrary are misleading and are not based on the published data. There is very little doubt that asbestos inhalation can cause small airway abnormalities, detected both histologically (11) and physiologically (12). But when the Committee cited studies suggesting the presence of obstruction in exposed populations (either by small reductions in midexpiratory flow rates, FVC, or FEV1/FVC ratio), it made strong assertions about the clinical implications of these changes with very little evidence to support its claims. In fact, contrary to the opinion sometimes expressed in the Statement, these changes lack proven clinical importance, and the airway effects of asbestos exposure alone are small compared with the effects of cigarette smoking, when the latter causes symptomatic, progressive chronic airway obstruction (COPD). It has been demonstrated in a study with exposure and radiographic and pulmonary function information that no decrement in FEV1/FVC ratio was seen in relation to exposure, even while showing dose-dependent declines in FEF25–75 (e.g., see Reference 12). The Statement did not include these data. We take no satisfaction in concluding that the process leading to this Statement has failed to result in a useful and credible summary of current knowledge on causal aspects of asbestos-related health effects. The ATS imprimatur demands great rigor in the development of official statements, particularly those that have substantial potential influence on assessment of public and occupational health risks and related public policy decision-making, and are likely to be controversial if they are not balanced.
a University of Colorado Health Sciences Center Denver, Colorado FOOTNOTES Conflict of Interest Statement: D.W. is involved in consulting and testifying for parties involved in litigation regarding occupational lung diseases; H.W. for many years has consulted with and occasionally testified for interested parties in litigation involving occupational lung diseases including those caused by asbestos. REFERENCES
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