Background: Cardiovascular disease (CVD) is the leading cause of mortality and morbidity in the elderly and the ambient concentration of PM_2.5 has been associated with several cardiovascular diseases. Methods: We describe the present state of planetary air pollution, analyze epidemiological studies linking PM_2.5 and CVD, and discuss multiple pathophysiological mechanisms linking PM_2.5 and CVD. Results: A few epidemiological studies show that the elderly appear specifically susceptible to adverse cardiovascular effects triggered by PM_2.5 exposure. Plausible pathophysiological mechanisms include inflammatory dysfunction, oxidative stress, abnormal activation of the hemostatic system and disturbance of the autonomic nervous system. Conclusions: An in-depth knowledge of the chemical compounds, pathophysiological mechanisms, and epidemiological studies of PM_2.5 are recommended to understand this important and modifiable factor contributing to geriatric CVD burden. We offer public health recommendations to reduce this preventable cause of disease and death.

Apigenin (APG), a widely distributed flavonoid in vegetables and fruits, with low toxicity, and a nonmutagenic characteristic, has been reported to have many targets. Evidence indicates that APG can inhibit the proliferation, migration, invasion, and metastasis of some tumor cells, but the mechanism, specifically in lung cancer, is unclear. The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway regulates a diverse set of cellular functions relevant to the growth and progression of lung cancer, including proliferation, survival, migration, and invasion. Our results showed that APG exerted anti-proliferation, anti-migration, and anti-invasion effects in A549 human lung cancer cells by targeting the PI3K/Akt signaling pathway. 3-(4, 5-dimethylthiszol-2-yl)-2, 5-diphenytetrazolium bromide assay and colony formation assay showed that APG suppressed cell proliferation in a dose-dependent and time-dependent manner. Cell motility and invasiveness were assayed using a wound healing and Transwell assay, suggesting that APG inhibited the migration and invasion of A549 cells. Western blot analyses were carried out to examine the Akt signaling pathways. The results confirmed that APG decreased Akt expression and its activation. Then, cells were transfected with Akt-active and Akt-DN plasmids separately. The migration and invasion of A549 cells were significantly changed, constitutively activating Akt or knocking down Akt, indicating that APG can suppress the migration and invasion of lung cancer cells by modulating the PI3K/Akt signaling pathway. Furthermore, the results indicated that APG not only suppressed phosphorylation of Akt, thereby preventing its activation, but also inhibited its downstream gene expression of matrix metalloproteinases-9, glycogen synthase kinase-3β, and HEF1. Together, APG is a new inhibitor of Akt in lung cancer and a potential natural compound for cancer chemoprevention.

Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.