Dear Editor
I read the article of Sun et al. with great interest, and I would like to suggest a possible mechanism that can contribute to higher hospital admissions and death rates for cardiovascular and cardiac diseases following exposure to short-term high ambient air pollution concentrations.
A recent study has identified an association between short-term exposure to particulate matter (PM10/PM2.5) and mortality from nervous diseases, as well as short-term exposure to nitrogen oxides (NO2) and metabolic mortality (1). Furthermore, the research has confirmed associations of particulate matter with natural, cardiovascular, cardiac, and respiratory causes of death and NO2 with respiratory mortality. The study has also hypothesized biological mechanisms through which air pollution could increase the risk of short-term death from metabolic and nervous diseases. The authors suggested that the adverse effects of PM and NO2 on the nervous and metabolic systems may be attributed to inflammatory pathways and oxidative stress. These, along with other unknown factors, could also contribute to short-term death from cardiovascular and cardiac disease by acting through a mechanism mediated by an increase in blood pressure during acute exposure to high-level air pollution.
Indeed, short-term exposure to high-level ambient PM2.5 has been associated with a significant increase in central systolic blood pressure (cSBP) in a Chinese community-based population (2). This observation is important because cSBP is a key determinant of cardiovascular risk and has been associated with adverse cardiovascular outcomes. The study found that an interquartile range change (80.25 μg/m3) in PM2.5 at high exposure level on the day of central aortic BP measurement was associated with a 2.54 mm Hg increase in cSBP. This association suggests that short-term exposure to high levels of PM2.5 can have immediate effects on central blood pressure.
The study findings are consistent with previous research in different populations, which reported associations between particulate matter exposure and central aortic pulse pressure in hypertensive patients and increased central systolic blood pressure in older women. The study also introduced the exposure-response curve model and found that there may be threshold effects between air pollution exposure and central hemodynamics. This effect suggests that the impact of particulate matter exposure on central blood pressure may not be linear and that there may be a threshold beyond which exposure leads to significant increases in cSBP. The study results also indicate that the effects of PM2.5 on cSBP were observed at high concentration exposures of PM2.5.
If further research confirms this hypothesis, tight blood pressure control is advisable for individuals with high blood pressure during exposure to high-level air pollution, and it would have significant implications for clinical practice.
1. Fan, F., Wang, S., Zhang, Y., Xu, D., Jia, J., Li, J., … & Huo, Y. (2019). Acute effects of high-level PM2.5 exposure on central blood pressure. Hypertension, 74(6), 1349-1356. doi:10.1161/HYPERTENSIONAHA.119.13408
2. Fan, F., Wang, S., Zhang, Y., Xu, D., Jia, J., Li, J., … & Huo, Y. (2019). Acute effects of high-level PM2.5 exposure on central blood pressure. Hypertension, 74(6), 1349-1356. doi:10.1161/HYPERTENSIONAHA.119.13408
Increase in blood pressure could mediate cardiovascular and cardiac diseases following short-term exposure to high ambient air pollution concentrations