Asbestos-related disorders. A realistic perspective.

difficulty. First, since asbestosis is a dose-related disease and workplace asbestos exposures have decreased over the last several decades, past occurrence data for asbestosis do not apply to present cohorts.1 Second, the clinical diagnosis of asbestosis encompasses criteria of variable specificity.2 Therefore, the frequency of diagnosing asbestosis varies inversely with the degree of specificity applicable to the criteria utilized. Without utilizing uniform criteria, occurrence data between different studies are not comparable. Although various approaches to diagnosing asbestosis have been outlined,3 three criteria should be emphasized.4 First, asbestos exposure of significant intensity, duration, and latency must have occurred. A simple dichotomous response of “yes” to the question “have you been exposed to asbestos?” is insufficient in fulfilling this criterion. To assess whether significant exposure has taken place, a thorough understanding of the specifics of an individual’s occupation is mandatory. This understanding encompasses determining the direct or indirect nature of the asbestos exposure, whether the work site was open or enclosed, what (if any) protective equipment was worn, etc. Next, it is imperative to confirm that fibrosis exists. When the interstitial changes on chest radiograph are considered minimal or even absent, how is documentation of fibrosis made? It has been demonstrated that high-resolution CT (HRCT) is a sensitive tool for this purpose.5,6 However, the linear and irregular parenchymal opacities present on HRCT in association with interstitial fibrosis lack specificity for diagnosing asbestosis.7 A multitude of other diseases and conditions similarly affect the lung parenchyma, producing these abnormalities. Thus, while documenting the presence of fibrosis is essential, and HRCT is useful in this respect, the predictive value of these findings alone is low for establishing the existence of asbestosis. Obviously, their predictability increases when they occur in association with asbestos-related bilateral pleural plaques. It follows from this discussion that a third criterion must be met when considering the diagnosis of asbestosis, namely the exclusion of confounders for the presence of pulmonary fibrosis. This criterion was outlined in the American Thoracic Society statement,2 emphasized by Jones,4 and shown to be important by Gaensler.8 Gaensler investigated a population in which the diagnosis of asbestosis had been made on clinical grounds, but was not subsequently established pathologically. Rather, idiopathic pulmonary fibrosis, bronchiolitis obliterans, and other conditions accounted for the presence of fibrosis. As Gaensler pointed out, while the prevalence for nonasbestos-induced interstitial lung disease in this select study population was low (5.1%), the future occurrence of such cases will be increasing because asbestosis is a disappearing disease. It should be noted that among these individuals with nonasbestos-induced interstitial lung disease, when compared to matched controls, their work histories were consistent with indirect asbestos exposure of lower intensity.3 Thus, before establishing the diagnosis of asbestosis, asbestos exposure must have been deemed sig*From University Occupational Health Center at Landerbrook, University Hospitals of Cleveland. Manuscript received June 11, 1996; revision accepted October 15, 1996. Reprint requests: Dr. David Rosenberg, University Health Center at Landerbrook, 5850 Landerbrook Drive, Mayfield Heights, OH 44124 debate in print