Previous studies report that PM triggers the generation of reactive oxygen species or ROS mainly from dysfunctional mitochondria [27, 28] , and we also noticed the massive generation of ROS by this PM sample is also mainly from mitochondria (unpublished observation). The high iron level of this particular PM might also contribute to the ROS generated via Fenton reactions. ROS released endogenously, have been implicated in the pathophysiology of several lung diseases, including asthma and COPD, as the biochemical mechanisms underlying the urban PM-induced airway inflammation and toxicity [29] . ROS are highly reactive and cause deleterious gene, protein, and tissue effects. ROS are increased in BAL or exhaled breath condensate from patients with inflammatory lung injuries and from people with cardiopulmonary disease who have been exposed to PM [30, 31] . This response may reflect the high oxidative potential of fine and ultrafine particulates. Residual oil fly ash (ROFA) and PM1.7-3.5 cause pulmonary inflammation mediated by oxidative stress [32, 33] . In vivo, exposing rats to PM leads to the formation of free radicals in the lung [34] . Since cardiovascular disease is considered a risk factor of PMrelated mortality and morbidity, it is interesting to note that spontaneously hypertensive rats, when exposed to PM, were more susceptible to pulmonary (inflammatory injury) and cardiovascular complications (acute depression of ECG activity) in an oxidant-dependent manner [35] . Besides ROS, PM might trigger adverse outcomes via other potential mechanisms including nonselective phosphatase inhibition (by vanadium) or competitive ion channel inhibition (by nickel) due to the complex and variable chemical components.