LONGITUDINAL CHANGES IN LUNG-FUNCTION AMONG ASBESTOS-EXPOSED WORKERS

Citation
Da. Schwartz et al., LONGITUDINAL CHANGES IN LUNG-FUNCTION AMONG ASBESTOS-EXPOSED WORKERS, American journal of respiratory and critical care medicine, 150(5), 1994, pp. 1243-1249
Citations number
65
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
150
Issue
5
Year of publication
1994
Pages
1243 - 1249
Database
ISI
SICI code
1073-449X(1994)150:5<1243:LCILAA>2.0.ZU;2-V
Abstract
To prospectively identify the determinants of persistent or accelerate d loss of lung function among workers occupationally exposed to asbest os and assess the relative contribution of cigarette smoking, asbestos -induced pleural fibrosis, and specific findings from bronchoalveolar lavage and high resolution CT scans, we examined the determinants of l ung function changes in 117 subjects occupationally exposed to asbesto s for at least 1 yr in a high exposure setting. A minimum of 20 yr was required between the first exposure to asbestos and entry into the st udy. Baseline studies included an independent assessment of dyspnea, l ung volumes, diffusing capacity of carbon monoxide (DL(CO)), a chest r adiograph, a high resolution CT (HRCT) scan, and bronchoalveolar lavag e (BAL). Subjects were observed for an average of 2 yr (range, 0.5 to 4.0 yr), and lung function was measured on at least two separate occas ions (mean, 4.1 separate tests). During the period of observation, the re was an average 1.5% decrease in the TLC and 2.5% decrease in the DL (CO). In this longitudinal data set, after controlling for age, height , pack-years of cigarette smoking, and follow-up time, persistently lo wer measures of TLC were independently related to moderate to severe d yspnea (p = 0.005), diffuse pleural thickening (p = 0.007), and higher concentrations of fibronectin in BAL fluid (p = 0.01). Interstitial l ung disease either on the chest radiograph or HRCT scan was not indepe ndently associated with persistently lower measures of TLC during the period of observation. However, none of the clinical variables we exam ined were associated with an accelerated decline in TLC. After control ling for age, height, and follow-up time persistently lower measures o f DL(CO) were independently related to moderate to severe dyspnea (p = 0.006), increased pack-years of cigarette smoking (p = 0.00001), hone ycombing on HRCT scan (p = 0.0009), and higher concentrations of lymph ocytes (p = 0.0008), neutrophils (p = 0.0005), eosinophils (p = 0.03), and fibronectin (p = 0.02) in the BAL fluid. Importantly, higher conc entrations of neutrophils and eosinophils in the BAL fluid were signif icantly associated with an accelerated decline in gas exchange during the period of observation. These results indicate that among asbestos- exposed subjects, prognostically important risk factors include sympto ms of dyspnea, cigarette smoking, diffuse pleural thickening, honeycom bing on HRCT scan, and higher concentrations of inflammatory cells and fibronectin in the BAL fluid.