The most up-to-date estimate of the global burden of disease indicates that ambient air pollution, including fine particulate matter and ozone, contributes to an estimated 5.2 million deaths each year. In this review, we highlight the challenges in estimating population exposure to air pollution and attributable health risks, particularly in low- and middle-income countries and among vulnerable populations. To protect public health, the evidence so far confirms urgent needs to prioritize interdisciplinary research on air pollution exposure and risk assessment and to develop evidence-based intervention policies and risk communication strategies. Here, we synthesize the emerging evidence supporting the monitoring and evaluation of the progress in implementation of the Global Air Quality Guidelines prepared by the World Health Organization.

Particulate matter with an aerodynamic diameter less than 2.5μM (PM_2.5) is one of the major environmental pollutants in China. In this study, we carried out a metabolomics profile study on PM_2.5-induced inflammation. PM_2.5 from Beijing, China, was collected and given to rats through intra-tracheal instillation in vivo. Acute pulmonary injury were observed by pulmonary function assessment and H.E. staining. The lipid metabolic profile was also altered with increased phospholipid and sphingolipid metabolites in broncho-alveolar lavage fluid (BALF) after PM_2.5 instillation. Organic component analysis revealed that benzo[a]pyrene (BaP) is one of the most abundant and toxic components in the PM_2.5 collected on the fiber filter. In vitro, BaP was used to treat A549 cells, an alveolar type II cell line. BaP (4μM, 24h) induced inflammation in the cells. Metabolomics analysis revealed that BaP (4μM, 6h) treatment altered the cellular lipid metabolic profile with increased phospholipid metabolites and reduced sphingolipid metabolites and free fatty acids (FFAs). The proportion of ω-3 polyunsaturated fatty acid (PUFA) was also decreased. Mechanically, BaP (4μM) increased the phospholipase A2 (PLA2) activity at 4h as well as the mRNA level of Pla2g2a at 12h. The pro-inflammatory effect of BaP was reversed by the cytosolic PLA2 (cPLA2) inhibitor and chelator of intracellular Ca²⁺. This study revealed that BaP, as a component of PM_2.5, induces pulmonary injury by activating PLA2 and elevating lysophosphatidylcholine (LPC) in a Ca²⁺-dependent manner in the alveolar type II cells.