Ambient atmospheric particles in the airways of human lungs.

Epidemiologic studies linking particulate matter (PM) air pollution and adverse respiratory and cardiovascular effects have focused attention on the interactions of PM and lung cells. Information on the types, numbers, composition, sizes, and distribution of ambient particles in the airways is potentially useful for correlations with pathological and/or physiological changes, but relatively little is known about the extent to which ambient particles actually enter airway epithelial cells and are retained in airway walls and even less information is available about correlations with pathologic changes. Since many ambient particles are colorless and/or well below the level of resolution of light microscopy, definitive evaluation of particle burden in the airway wall requires analytical electron microscopy. Studies from the authors' laboratory suggest that in Vancouver, a city with relatively low PM levels, particle loads in the airway mucosa are nonetheless numerically substantial, typically in the range of 10(7) particles/g dry tissue. In most individuals particle concentrations in the larger airways show a clear increase in concentration with increasing airway generation (smaller airway diameter) as expected from deposition models; however, smoking disrupts this pattern in some subjects. Respiratory bronchioles accumulate particularly high particle loads, typically 25-100 times the concentrations seen in the mainstem bronchus. Similarly high concentrations are found in the large airway carinas, suggesting that these locations are likely sites for particle toxicity. The majority of particles in the airways in Vancouver lungs appear to be crustal in origin, with particular accumulation of silica in the airways compared to the parenchyma. Ultrafine particles, which have been postulated to be important in PM toxicity, are present in small numbers as singlet particles and are largely metals, perhaps representing combustion products, but carbonaceous chain aggregates are rarely found. Mean particle aerodynamic diameters vary from about 0.3 to 0.6 microm in different parts of the airways and, overall, the airways retain PM2.5 rather than PM10, a finding supporting the observation that, in some studies, adverse health effects appear to correlate better with PM2.5 than with PM10 concentrations. Preliminary examination of lungs of subjects from Mexico City, a location with relatively high ambient particle concentrations, indicates that the airway mucosa retains relatively large numbers of carbonaceous chain aggregates of ultrafine particles that appear to be combustion products and that presumably produce the numerous adverse effects documented for such products. Limited published data correlating visible particle load and airway mucus secretion, inflammation, and mural fibrosis suggest that high levels of air pollutant particles can induce chronic fibrotic responses in the airways, a phenomenon that might be linked to chronic airflow obstruction; this observation needs confirmation as well as correlation with specific types of particles.