Ultrafine Particles Penetrate Human Airway Epithelium Resulting in Increased Expression of Genes Causally Related to Cell Proliferation and Apoptosis

Extract

Epidemiological studies have associated exposure to airborne particulate matter (PM) with an aerodynamic diameter less than 10 microns, especially the finer fraction PM2.5, with increases in morbidity and mortality in persons with preexisting cardiopulmonary disease. However, whether exposures to PM10 cause lung disease in uncompromised individuals is a topic of debate, especially since mechanistic and toxicological studies have failed to define cause and effect relationships between exposures to PM10 and phenotypic changes associated with the development of pulmonary diseases. PM10 is a complex mixture of soot and natural minerals, metal oxide particles, sea salt grains and aeroallergens (Fig. 1). Our interest lies with the carbonaceous components (Fig. 2), since insoluble particles may be more efficiently retained in the peripheral lung and be potentially more bioreactive due to their accumulation over time. We are interested in the ultrafine (UF) fraction (<1.0um diameter) since the number of particles in this size range are known to increase during pollution episodes and they have a greater reactive surface area per unit weight.