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the regulatory focus shifted from total suspended particles to particles that could readily penetrate and deposit in the tracheobronchial tree, or PM10 (PM with a median aerodynamic diameter of <10 μm). In 1997, the US EPA promulgated 24-hour and annual average standards for PM2.5 (PM with median aerodynamic diameter <2.5 μm), comprising the size fraction that can reach the small airways and alveoli. The existing federal PM10 standards were retained, however, to address health effects that could be related to the “coarse fraction” (PM10 to 2.5). Currently, a separate PM10 to 2.5 standard is under consideration. In general, PM2.5 originates mostly from combustion sources and includes primary and secondary particles, whereas the coarse fraction derives predominantly from natural sources, especially crustal material (including windblown soil) and grinding processes. Important bioaerosols (eg, endotoxin, pollen grains, and fungal spores) are found mostly in the coarse fraction (and larger particles), although both endotoxin (an essential component of the cell wall of Gram-negative bacteria)... Generally, larger particles demonstrate a greater fractional deposition in the extrathoracic and upper tracheobronchial regions, whereas smaller particles (eg, PM2.5) show greater deposition in the deep lung. Although PM2.5 generally behaves as a regional pollutant, there can be considerable small-scale spatial variability due to point source emissions (eg, a smelter) or features such as street canyons in large cities. In addition, prevailing wind patterns can affect human exposures.

More recently, considerable research attention has been devoted to ultrafine particles (UFPs) <100 nm (0.1 μm) in diameter, which result from combustion processes. UFPs tend to be short-lived, because they agglomerate and coalesce into larger particles. However, they demonstrate very high deposition in human alveoli,27 account for a major portion of the actual numbers of particles within PM, and have a high surface area-to-mass ratio, potentially leading to enhanced biological toxicity. UFPs may even be able to pass directly into the circulatory system, which could allow them to be disseminated systemically.28–30