Pulmonary function and pleural fibrosis: Quantitative relationships with an integrative index of pleural abnormalities

Abstract

Pleural fibrosis due to asbestos exposure was fully appreciated considerably later than pulmonary interstitial fibrosis due to similar exposure. This is well exemplified by the fact that pleura face on was included in the International Labour Office's International Classification of Radiographs of Pneumoconioses only in the last revision of the Classification. The functional relevance of pleural fibrosis, in particular circumscribed pleural fibrosis, has remained controversial. Since pleural fibrosis can occur at various sites (diaphragmatic plaques, chest wall in profile and face on, mediastinal) and can be of different thickness and extent, a comprehensive integrative assessment of pleural fibrosis was undertaken in order to permit a quantitative study of relationships between pleural fibrosis and pulmonary function. This approach was used for chest X-ray films of 1,584 asbestos insulation workers examined (1981-1983); 1,185 (75%) had pleural fibrosis. The distribution pattern of the integrative pleural index was found to be different in the subgroup with circumscribed (n = 975) from that with diffuse (n = 197) pleural fibrosis, with a higher profusion of high INDEX values in the latter. Stepwise regression analysis indicated that there was a significant inverse relationship between forced vital capacity (FVC) and the integrative index of pleural fibrosis in the subgroup with circumscribed pleural fibrosis. In the subgroup with diffuse pleural fibrosis, the obliteration of costophrenic angle(s), even with pleural fibrosis of limited extent, resulted in marked decrement in FVC% predicted; higher values of INDEX did not result in additional significant reductions of FVC. In those with both parenchymal and pleural abnormalities (n = 862) the pleural index was found to make a significant contribution, independent of that of parenchymal abnormalities, to decrements of FVC. Since pleural fibrosis has gradually become the predominant radiologically detectable abnormality in asbestos exposed workers, establishing its quantifiable functional relevance is useful.

Baseline Serum β-carotene Concentration and Mortality among Long-Term Asbestos-Exposed Insulators

“…Since the durational measurement of asbestos exposure had been already used as a means of assessing asbestos exposure in previous studies (14)(15)(16)(17)(18)(19)22) and because asbestos-exposed workers were insulators, an assumption was made that all had the same intensity of exposures at varying time intervals. However, because 75% of the NAIC had !29 years of asbestos-exposure levels, with the lowest duration being 3 years, the dataset may not have been conducive for an accurate assessment of an effect modification between high and low levels of asbestos exposure and serum b-carotene.…”

“…Clinical examinations took place in 19 U.S. cities from November 1981 to November 1983. They encompassed chest radiography, pulmonary function, standard laboratory tests (19), and special serological studies (20) that included measurement of serum b-carotene concentration. Workers who had taken b-carotene supplements were excluded from study participation.…”

Asbesto, asbestose e câncer: critérios diagnósticos

“…Corpos ou fibras de asbesto são freqüentemente encontrados na pleura visceral, no parênquima subjacente, ou em ambos. Há três mecanismos diferentes envolvidos na fibrose pleural difusa (20)(21)(22) . O primeiro é a confluência de grandes placas pleurais fibrosas ocorrendo em 10 a 20% dos casos.…”

The molecular epidemiology of asbestos and tobacco in lung cancer

“…Asbestos fibers promote the formation of hydroxyl radicals (Maples and Johnson, 1992;Schapira et al, 1994;Weitzman and Graceffa, 1984) a process catalyzed by the presence of fiber-bound metals (Fubini and Mollo, 1995;Lund and Aust, 1992;Park and Aust, 1998;Zalma et al, 1987), and asbestos exposure results in elevated 8-OHdG DNA adducts, a biomarker of ROS exposure, both in vitro and in vivo (Adachi et al, 1992(Adachi et al, , 1994Chao et al, 1996;Chen et al, 1996;Fung et al, 1997;Marczynski et al, 2000;Murata-Kamiya et al, 1997;Nejjari et al, 1993;Takahashi et al, 1997;Takeuchi and Morimoto, 1994;Xu et al, 1999) Smoking also induces cell proliferation, inflammation, and the production of ROS. In fact, very early radiographic changes that mimic an early fibrotic pattern are associated with smoking (Lilis et al, 1991). The combination of smoking and asbestos exposure has been shown to increase the occurrence of both lung fibrosis (Lilis et al, 1991) and cell proliferation (Sekhon et al, 1995).…”

“…In fact, very early radiographic changes that mimic an early fibrotic pattern are associated with smoking (Lilis et al, 1991). The combination of smoking and asbestos exposure has been shown to increase the occurrence of both lung fibrosis (Lilis et al, 1991) and cell proliferation (Sekhon et al, 1995). In addition, cigarette smoking may enhance the lifetime accumulation of asbestos fibers (Churg and Stevens, 1995).…”