To further assess the clinical significance of
asbestos-induced pleural
fibrosis, we performed cardiopulmonary exercise testing in 90 subjects who were exposed to
asbestos. Of the 82 subjects without an abnormal resperate exercise, 35 had normal pleura, 33 had circumscribed pleural plaques, and 14 had diffuse pleural thickening. Interstitial
fibrosis (International Labor Organization [ILO]. > or = 1/10) was present in 14 of 35 subjects with normal pleura, 13 of 33 subjects with circumscribed pleural plaques, and 2 of 14 subjects with diffuse pleural thickening. Although pleural
fibrosis did not appear to be related to impaired respiratory function with exercise in our entire cohort, this finding was confounded by a higher proportion of interstitial
fibrosis in subjects with normal pleura. In fact, among study subjects without
asbestosis, significant decreases in gas exchange (higher VD/VT and increased alveolar-arterial
oxygen pressure difference) were observed at maximal exercise among subjects with pleural
fibrosis. Interestingly, neither a higher respiratory rate nor a lower VT/FVC ratio was observed among those with pleural
fibrosis, suggesting that the mechanical effects of pleural
fibrosis on the chest wall do not explain the increased VD/VT. Using multivariate analyses to control for potential confounders, regression models showed that pleural plaques (p = 0.04) and diffuse pleural thickening (p = 0.03) were independently associated with significant increases in dead space ventilation (VD/VT) with maximal exercise. These findings indicate that
asbestos-induced pleural
fibrosis is independently associated with decrements in gas exchange with maximal exercise and suggest that
interstitial lung disease, not detected on the routine chest
x-ray film, may be responsible for this abnormal response to exercise.