Traffic-related air pollution (TRAP) contains a plethora of hazardous pollutants, and is associated with a multitude of adverse health effects. However, up to now, no early biomarkers that can quickly reflect the health damage induced by TRAP. We conducted a randomized crossover trial in 35 healthy adults. Each subject was exposed to high- and low- levels of TRAP by walking in the park and along the side road leading to the freeway (road). The cardiopulmonary function parameters were measured before and after each walk session, and blood was collected 2 h after the two sessions. The present study revealed an intriguing phenomenon: the cardiac function was preferentially damaged by acute TRAP exposure. Then, we investigated the extent of damage to various human cells from exposure to TRAP by the technology of cell-of-origin of plasma cell-free DNA. Consequently, we found that only the cell-specific DNA methylation level of endothelial cells (EC) was elevated after exposure to TRAP (road) in comparison with the control (park), indicating that TRAP exposure primarily damages the EC. EC is an integral part of the cardiovascular system. This evidence indicated that TRAP exposure primarily damaged the cardiac function, compared with the other functions. Based on the cell-specific gene database of EC, we found higher levels of DNA methylation in the exon region after exposure to the TRAP session compared with the control session. Meanwhile, we also found that TRAP exposure could induce an elevated level of NACC2 in plasma, suggesting that plasma NACC2 could serve as a potential biomarker for damage of EC induced by TRAP exposure. This study suggests that the first target cell type damaged by TRAP is EC, and that the expression of NACC2 and its DNA methylation level in plasma may be a useful biomarker reflecting TRAP exposure-induced EC damage.
Keywords: Biomarker; Cell-of-origin; Human health; Plasma cell-free DNA; Traffic-related air pollution.
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