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Outdoor particulate matter (PM 10 ) exposure is carcinogenic to humans. The cellular mechanism by which PM 10 is associated specifically with lung cancer includes oxidative stress and damage to proteins, lipids, and DNA in the absence of apoptosis, suggesting that PM 10 induces cellular survival. We aimed to evaluate the PI3K/AKT/FoxO3a pathway as a mechanism of cell survival in lung epithelial A549 cells exposed to PM 10 that were subsequently challenged with hydrogen peroxide (H 2 O 2 ). Our results showed that pre-exposure to PM 10 followed by H 2 O 2 , as a second oxidant stimulus increased the phosphorylation rate of pAKT Ser473 , pAKT Thr308 , and pFoxO3a Ser253 2.5-fold, 1.8-fold, and 1.2-fold, respectively. Levels of catalase and p27 kip1 , which are targets of the PIK3/AKT/FoxO3a pathway, decreased 38.1% and 62.7%, respectively. None of these changes had an influence on apoptosis; however, the inhibition of PI3K using the LY294002 compound revealed that the PI3K/AKT/FoxO3a pathway was involved in apoptosis evasion. We conclude that nontoxic PM 10 exposure predisposes lung epithelial cell cultures to evade apoptosis through the PI3K/AKT/FoxO3a pathway when cells are treated with a second oxidant stimulus.

Airborne Particulate Matter (PM10) Inhibits Apoptosis through PI3K/AKT/FoxO3a Pathway in Lung Epithelial Cells: The Role of a Second Oxidant Stimulus