Smoking and duration of asbestos exposure in the production of functional and roentgenographic abnormalities in shipyard workers.

Functional and roentgenographic abnormalities in 131 asbestos-exposed shipyard workers were assessed in terms of duration of asbestos exposure and smoking history to determine the relative contributions of these factors. Both exposure and smoking contributed to the frequency of abnormalities in FEV1 and FVC. In contrast, airways obstruction (FEV1/FVC less than 70%) was unrelated to exposure but correlated closely with smoking. Abnormalities in DLCO were minimally associated with asbestos exposure, but were strongly related to smoking history, suggesting that diffusion impairment in these workers is more likely to be related to smoking and emphysema than to interstitial disease. Significant roentgenographic pleural abnormalities were associated with both duration of exposure and smoking. Interstitial disease did not correlate with exposure and was only mildly associated with smoking. Smoking contributes to many of the functional and roentgenographic abnormalities in asbestos-exposed workers.

Ventilatory and neuromuscular responses to inspiratory positive pressure during CO2 breathing.

We studied the effects of assisting respiration with inspiratory positive pressure (IPP) during air and CO2 breathing by measuring ventilatory and mouth occlusion (P0.1) responses in 15 normal human subjects. Switching from spontaneous breathing to IPP without added CO2 did not cause a significant change in mean PACO2, P0.1, or V1. During CO2 breathing, switching to IPP did not significantly alter tidal volume or frequency. The mean ventilatory response to CO2 during spontaneous breathing was 1.02 liters/min/mm Hg. With IPP at pressure limits of 5 and 7 cm H2O, the mean responses were 0.93 and 0.89 liters/min/mm Hg, respectively, not significantly different from spontaneous breathing. The mean spontaneous P0.1 response to CO2 was 0.32 cm H2O/mm Hg. With IPP at 5 and 7 cm H2), the responses were 0.29 and 0.36 cm H2O/mm Hg, also not significantly different from spontaneous breathing. Reduction of muscular work of breathing by IPP in normal human subjects does not induce a measurable change in either respiratory drive or ventilation, which appears to remain dependent on chemoreceptor input. Inspiratory effort continues during IPP, even though it may be less than during spontaneous breathing.

Exercise performance and functional impairment in asbestos-exposed workers.

Eighty-eight shipyard workers with extensive asbestos exposure were evaluated in terms of dyspnea, smoking history, x-ray film abnormalities, static pulmonary function, and exercise performance. Pulmonary function abnormalities and roentgenographic pleuropulmonary disease were more frequent in smokers. Significant dyspnea was present in 41 percent of the workers and did not correlate with smoking history, pulmonary function, or exercise performance. Despite this high frequency of dyspnea, 70 percent of all workers had normal exercise tolerance by history of exercise testing. Of the 26 workers with exercise impairment, only nine had pulmonary mechanical or gas exchange limitation. Two of these workers had asbestosis, while the other had airways obstruction without asbestosis. The prevalence of both asbestosis and asbestos-related exercise impairment in this population was 2.3 percent.

Diaphragmatic EMG and occlusion pressure response to elastic loading during CO2 rebreathing in humans.

The effects of external elastic loading (EL) (19 cmH2O/l), applied continuously (C) and intermittently (I) during CO2 rebreathing, on diaphragmatic electromyogram (EMGdi), mouth occlusion pressure (P0.15), and ventilation (VI) were studied in normal subjects. EMGdi was analyzed as moving time average and quantitated in terms of peak (mean p) and average rate of rise of inspiratory activity (mean p/TI). CEL resulted in an increased mean p/TI response to CO2 in all subjects with P0.15 increasing in proportion to EMGdi. Tidal volume (VT) during rebreathing was decreased in all cases with VI being preserved in four of six runs due to increased breathing frequency (f). Although mean p was increased for a given end-tidal CO2 (PACO2) level during CEL, for a given rate of rise of inspiratory activity mean p was decreased in three of five subjects, indicating a diminished threshold for inspiratory "off-switch." CEL results in an augmented inspiratory drive that serves to increase muscle output and stabilize VT; the increased drive and decrease inspiratory off-switch threshold shorten TI mediating the compensatory increase in f. The first breath IEL resulted in decreased VT and mean p without change in mean p/TI, and all increased with subsequent loaded breaths independent of changes in PCO2. Load compensation for externally applied EL is mediated by neural mechanisms independent of chemical drive.