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NYC 9/11 Public Portal Document

ASBESTOS MEDITEXT ® - Medical Management Page 2 of 15

et al, 1988; Davies et al, 1991).

3.6 RESPIRATORY

3.6.1 ACUTE EFFECTS

A. ASBESTOSIS 1. DEFINITION - Asbestosis is defined as an irreversible diffuse bilateral interstitial fibrosis primarily affecting the lower 2/3 of the lung (ATSDR, 1990; Newhouse, 1983). Either heavy exposure for a short time or lower-level exposure over a longer period may result in asbestosis; cases have resulted from intense exposure of one day's duration (ATSDR, 1990). 2. CLINICAL MANIFESTATIONS - Pleural asbestosis generally develops from chronic, low-level exposure; parenchymal asbestosis is related to higher-level exposures (ATSDR, 1990). a. Signs and symptoms include dyspnea on exertion, finger clubbing, clicking, and rales (bilaterally in the posterior axillae) (ILO, 1983; Newhouse, 1983). Persistent pleuritic pain may be a manifestation of asbestos-induced pleural disease (Miller, 1990). b. Cough is usually not present except in the late stages when distressing paroxysms occur (ELO, 1983). Increased sputum production is not present unless there is concomitant smoker's bronchitis (ELO, 1983). c. Early x-rays may not be diagnostic (Newhouse, 1983; Talcott & Antman, 1988). d. Clinical manifestations typically appear 10 to 40 years after onset of exposure (ATSDR, 1990; Demers et al, 1990). However, radiologic changes can occur before 20 years. e. Signs, symptoms, and abnormalities increase with longer duration of exposure (Demers et al, 1990; Selikoff et al, 1990). The typical restrictive pulmonary dysfunction can be obscured by chronic obstructive pulmonary disease due to smoking (Mossman & Gee, 1989). f. A long latency period of at least a decade exists between onset of histologic lesions and radiologically detectable stigmata (Kagan, 1988). 3. CLINICAL COURSE - Pleural thickening progresses at the greatest rate among crocidolite miners and millers who develop early thickening after exposure. This progression decreases with time so that no progression may be noted more than 15 years after onset (de Klerk et al, 1989). a. Asbestosis may progress even after exposure terminates (Kagan, 1988; Talcott & Antman, 1988). b. Although asbestosis progresses slowly and may cease at any time, death may occur from cor pulmonale or from lung cancer (Newhouse, 1983). c. Progressive restrictive pleural fibrosis in a small proportion of patients can cause severe dyspnea, decreased vital capacity, total lung capacity, residual volume, and diffusing capacity, with eventual ventilatory failure and death (Miller et al, 1983; Mossman & Gee, 1989). d. Asbestosis patients may also present with superimposed infections because of increased susceptibility caused by immunologic derangements (ATSDR, 1990). e. CLINICAL PREDICTORS OF OUTCOME - In a review of 74 cases of asbestos deaths, the 10 year risk of death was increased in the presence of increasing interstitial fibrosis as seen on baseline chest x-ray, dyspnea, low forced vital

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