Detailed Occupational History
The Cornerstone in Diagnosis of Asbestos-related Lung Disease

Raymond Bégin

University of Sherbrooke, Sherbrooke, PQ, Canada

John W. Christman

Vanderbilt University School of Medicine, Nashville, Tennessee

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The pulmonary response to inorganic dust is thought to be proportional to the amount and duration of exposure that contributes to the retention of dust in the distal airspace. The biologic tissue reaction to retained dust involves alterations in signal transduction and mediator production by target cells that initiate or perpetuate pulmonary inflammation and fibrosis. In exposed populations, the dust burden in the lung cannot be directly measured and is most accurately, but indirectly, assessed by a detailed occupational history. In some cases the occupational history can be verified by personal or static environmental measurement of respirable dust in the workplace. The intensity and duration of exposure are combined with indirect measurements of lung inflammation and fibrosis to develop a crude, but reasonably accurate, exposure-response relationship. Exposure-response relationships are useful for population-based epidemiologic studies and for developing safe "threshold limit values" (TLVs), below which dust levels are unlikely to be associated with disease over a worker's lifetime. However, a pneumoconiosis cannot be completely excluded because the exposure to dust is considered too remote, too short, or in a safe industrial environment, as less defined individual factors may determine dust retention and disease susceptibility. These considerations have led to a search for objective, independent measurement of dust exposure and disease activity. Among candidates are bronchoalveolar lavage (BAL) in conjunction with mineral dust measurements and high-resolution computed tomography (HRCT). Although BAL measurements of dust in the airspace have a marginal predictive value in silicosis (1), they are less useful in asbestosis (2- 4). Although HRCT is remarkably sensitive in detecting mineral disease compared with conventional radiography (5), it is not yet a "gold standard" because an exposure-response relationship has not yet been clearly established.

Pleural plaques are considered diagnostic of asbestos exposure but it is unclear that there is a relationship between cumulative dust exposure and the extent of pleural disease. In this issue of the Journal (pp. 705-710), Van Cleemput and collegues use computed tomography (CT) scanning to measure the exact surface area of localized pleural plaques and compare this with objective measurements of cumulative dust exposure in a group of asbestos workers (6). Their data confirm previous reports that CT scanning is more sensitive for the measuring pleural plaques than conventional radiography (7). These authors showed that the extent of pleural plaques is related to the best objective measurements of workplace ambient dust concentrations, which were used to calculate cumulative exposure during the work history of the individual subjects. They have shown no correlation between the total surface of localized pleural plaques and lung function values. The original and most interesting finding of this work is the lack of correlation of the size and surface area of localized pleural plaques with the cumulative asbestos exposure index or the cumulative cigarette smoke exposure index. This observation is important because pleural plaques are often used as a surrogate for past asbestos exposure, particularly when bilateral, and this is useful in establishing a relationship with mesothelioma (8). The presence of pleural plaques without asbestosis is associated with an increased risk (1.4-fold) of lung carcinoma (9). Outside the primary asbestos production industry, the cumulated asbestos exposure of workers is often ill defined and one may be tempted to use the extent of pleural plaques as an indicator of past asbestos exposure. This is particularly true in brief, but sometimes intense, exposures in the armed services or in other industries prior to modern dust control measures. The investigation by Van Cleemput and coworkers in this issue of the Journal clearly establishes that the size and surface of pleural plaques do not correlate with the cumulative asbestos exposure index or the cumulative cigarette smoke exposure index, and thus should not be used as an indicator of past asbestos exposure. The best indicator of past asbestos exposure (the gold standard) remains the detailed past work history (8). In cases of uncertainty, the mineral fiber content of lungs, which necessitates an open lung biopsy, can give a useful indicator of past asbestos exposure when compared with a reference population and with a population with asbestos-related diseases (10). In the evaluation of a probability relationship between dust exposure and lung cancer in an asbestos-exposed worker outside the primary industry, when a detailed past work history is unclear regarding the asbestos exposure, the mineral fiber content of lungs can provide the best available indicator to assess the relative risk of lung cancer associated with the patient's work and thus permit a sound basis for medical expertise. At this time, the pleural plaques cannot provide an index of cumulative asbestos exposure but remain a useful surrogate for past asbestos exposure.

The presence of asbestosis would suggest a cumulated asbestos exposure above the generally accepted threshold limit level of 25 fiber · yr/cm³ but the absence of asbestosis does not establish an exposure level below 25 fiber · yr/cm³, as only a small fraction of exposed workers at that cumulated level develop asbestosis and/or lung cancer. Thus, beyond the debate of the last decade on the subject of the necessity of having asbestosis to develop an asbestos-related lung cancer, asbestos causation of lung cancer in an individual should be based on intensity and duration of exposure based on a detailed occupational history (13, 14).

	References

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