Airway Surfactant, a Primary Defense Barrier: Mechanical and Immunological Aspects

Time-series, cross-sectional, and prospective cohort studies have observed associations between mortality and particulate air pollution but have been limited by ecologic design or small number of subjects or study areas. The present study evaluates effects of particulate air pollution on mortality using data from a large cohort drawn from many study areas. We linked ambient air pollution data from 151 U.S. metropolitan areas in 1980 with individual risk factor on 552,138 adults who resided in these areas when enrolled in a prospective study in 1982. Deaths were ascertained through December, 1989. Exposure to sulfate and fine particulate air pollution, which is primarily from fossil fuel combustion, was estimated from national data bases. The relationships of air pollution to all-cause, lung cancer, and cardiopulmonary mortality was examined using multivariate analysis which controlled for smoking, education, and other risk factors. Although small compared with cigarette smoking, an association between mortality and particulate air pollution was observed. Adjusted relative risk ratios (and 95% confidence intervals) of all-cause mortality for the most polluted areas compared with the least polluted equaled 1.15 (1.09 to 1.22) and 1.17 (1.09 to 1.26) when using sulfate and fine particulate measures respectively. Particulate air pollution was associated with cardiopulmonary and lung cancer mortality but not with mortality due to other causes. Increased mortality is associated with sulfate and fine particulate air pollution at levels commonly found in U.S. cities. The increase in risk is not attributable to tobacco smoking, although other unmeasured correlates of pollution cannot be excluded with certainty.

Results are presented from a second cross-sectional assessment of the association of air pollution with chronic respiratory health of children participating in the Six Cities Study of Air Pollution and Health. Air pollution measurements collected at quality-controlled monitoring stations included total suspended particulates (TSP), particulate matter less than 15 microns (PM15) and 2.5 microns (PM2.5) aerodynamic diameter, fine fraction aerosol sulfate (FSO4), SO2, O3, and No2. Reported rates of chronic cough, bronchitis, and chest illness during the 1980-1981 school year were positively associated with all measures of particulate pollution (TSP, PM15, PM2.5, and FSO4) and positively but less strongly associated with concentrations of two of the gases (SO2 and NO2). Frequency of earache also tended to be associated with particulate concentrations, but no associations were found with asthma, persistent wheeze, hay fever, or nonrespiratory illness. No associations were found between pollutant concentrations and any of the pulmonary function measures considered (FVC, FEV1, FEV0.75, and MMEF). Children with a history of wheeze or asthma had a much higher prevalence of respiratory symptoms, and there was some evidence that the association between air pollutant concentrations and symptom rates was stronger among children with these markers for hyperreactive airways. These data provide further evidence that rates of respiratory illnesses and symptoms are elevated among children living in cities with high particulate pollution. They also suggest that children with hyperreactive airways may be particularly susceptible to other respiratory symptoms when exposed to these pollutants.(ABSTRACT TRUNCATED AT 250 WORDS)

This study was designed to investigate the early stages of particle deposition on airway and alveolar surfaces. To do this we used morphometric studies of aerosol deposition, in situ measurements of surface tension, and in vitro assays of particle displacement and mathematical modelling. We observed that latex particles, equal or less than 6 microns in diameter deposited in hamster lungs were submerged in the subphase of the alveolar lining layer and became completely coated with an osmiophilic film. Similar results were obtained for particles deposited in the conductive airways which were also covered with a surface active film, having a surface tension of 32 +/- 2 dyn.cm-1. In vitro experiments showed that pulmonary surfactant promotes the displacement of particles from air to the aqueous phase and that the extent of particle immersion depends on the surface tension of the surface active film. The lower the surface tension the greater is the immersion of the particles into the aqueous subphase. Mathematical analysis of the forces acting on a particle deposited on an air-fluid interface show that for small particles (less than 100 microns) the surface tension force is several orders of magnitude greater than forces related to gravity. Thus, even at the relatively high surface tension obtained in the airways (32 +/- 2 dyn.cm-1) particles will still be displaced into the aqueous subphase. Particles in peripheral airways and alveoli likely are below the surfactant film and submerged in the subphase. This may promote clearance by macrophages. In addition, particle displacement into the subphase is likely to increase the contact between the epithelial cell and particle. Toxic or allergenic particles would be available to interact with epithelial cells and this may be important in the pathophysiology of airway disease.