NYC-WTC_000195068

NYC 9/11 Public Portal Document

aSBESTOS MEDITEXT ® - Medical Management Page 4 of 15

1. DEFINmON - Diffuse pleural thickening is a uniform, homogenous, uninterrupted pleural density extending over at least 1/4 of the chest wall with or without accompanying costophrenic angle obliteration (Gefter & Conant, 1988). 2. CAUSES - In a series of 1,373 asbestos-exposed workers, 31.4 percent of the cases were related to asbestos exposure, 25.4 percent to confluent plaques, 33 percent to malignant effusion, trauma, infection, or a combination of these, and 10.3 percent were presumed extensions of parenchymal fibrosis (McLoud et al, 1985). 3. CLINICAL COURSE - Diffuse pleural thickening may develop as an acute, rapidly progressive process associated with chest pain, or it may assume an indolent, asymptomatic course (Gefter & Conant, 1988). Chronic cases may present with significant pulmonary insufficiency and may require surgical decortication (Gefter & Conant, 1988). Patients presenting with stable pleural plagues are at risk for diffuse pleural thickening and subsequent greater ventilatory impairment (Miller & Miller, 1993).

G INTERACTION

1. SMOKING - An apparent synergism exists between asbestos-related pulmonary diseases and smoking. The mechanism for this has yet to be established, although several theories have been postulated and tested (Blanc et al, 1988; deShazo et al, 1988; Hobson et al, 1988; Kronenberg, 1989; Mossman & Gee, 1989; Talcott & Antman, 1988; ATSDR, 1995). a. Those who are occupationally exposed to asbestos and who smoke have a 5 to 6 times greater than expected incidence of pleural plaques on chest x-ray in later years (Hillerdal et al, 1983). b. CASE SERIES - A retrospective review of shipyard workers found cigarette smoking­ asbestos exposure interactions for parenchymal opacities, but not for decreased lung capacity (Blanc et al, 1988). The ILO-interpreted opacities may reflect smoking- associated parenchymal changes among asbestos-exposed smokers. c. Smoking and asbestos exposure were shown to interact and thus decrease mononuclear cell natural killer function (deShazo et al, 1988). d. Smoke-exposed cultures of tracheal implants from rats had a greater number of asbestos fibers in the epithelium and greater proliferative activity, compared to cultures unexposed to cigarette smoke (Hobson et al, 1988). e. Smoking may impair the lung's ability to clear asbestos fibers and thus enhance asbestos- induced fibrogenesis (Mossman & Gee, 1989). f. Lung macrophages, in response to foreign bodies such as asbestos fibers, may release enzymes and oxidants and thus destroy normal lung tissue in the same way that they would react to cigarette smoke (Kronenberg, 1989).

o SPUTUM INCREASED

1. FERRUGINOUS BODIES - have been found in the sputum of asbestos workers (Stewart & Haddow, 1929). a. McLarty et al (1980) demonstrated a significant association between ferruginous (chalybeate) bodies found in the sputum and radiographic findings of interstitial pulmonary disease, pleural fibrosis, and spirometric abnormalities. b. Increased age and smoking were also related to an increased number of ferruginous bodies (McLarty et al, 1980). c. Although hemolytic activity has been said to be a factor influencing pathogenesis, there

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