Airways Obstruction From Asbestos Exposure: Cautions
Few physiologic studies of asbestosis have attempted to integrate structure and function or localize the principal target of the disease. Becklake et al, nearly two decades ago, showed midexpiratory flow and FEVi limitations in men exposed to asbestos and greater reductions in those with asbestosis. Jodoin et al, finding that midflows and FEVi decreased early along with FVC, localized “early” asbestosis to small airways. Begin et al found increased up-stream resistance and increased frequency-dependent compliance and postulated that peribronchial-bronchiolar fibrosis was the primary lesion read more asthma medications inhalers. After irregular opacities appeared, VC decreased.
The walls of membranous and respiratory bronchioles are thickened in hamsters and guinea pigs given chrysotile or amosite intratracheally or by inhalation.’ In one study, air space size increased. Cigarette smoke enhanced the lesions. All 15 sheep given chrysotile by inhalation for 24 months had significant peribronchiolar fibrosis and increased resistance but only 9 developed interstitial disease in this brief interval. Gloyne described similar changes in human lungs from the Merewether factory asbestosis series in 1933.
Asbestos exposure causes airway obstruction and asbestosis increases it. Impairment worsens more rapidly in men who smoke than in those who never smoked. This airways obstruction traps gas which increases residual volume at the expense of VC without reducing TLC. As asbestosis evolves, airway obstruction traps more of the slowly deliverable portion of the VC in the residual volume. Cigarette smoking hastens this evolution. First, we age adjusted spirometric and volume values, as age matching of the unexposed group would have eliminated many subjects and sacrificed statistical power. Although this is not ideal, virtual agreement among predicted values derived from different populations of normal subjects,’ and the actual 15-year decrements for non-smokers equaling those calculated from a cross-sectional study, supported this strategy. Second, the decrements of smokers have not been studied prospectively, but function is affected similarly in never smokers and current smokers with asbestos exposure and asbestosis, differing only in magnitude. This interpretation is supported by finding coefficients for FEVi of —0.016 for years of asbestos exposure, of —0.012 for years of smoking, and —0.041 for years of age (vs 0.058 for height in centimeters in an 8-year prospective study of asbestos cement workers.