While the association of PM2.5 exposure with premature deaths of lung cancer, chronic obstructive pulmonary disease, ischemic heart disease, and cerebrovascular disease are well documented, there are growing evidences that exposure to PM2.5 in ambient air could also lead to health effects on brain, reproduction, immune, and metabolism. However, the underlying mechanism for the health effect of PM2.5 is complicated, with various hypothetical pathways proposed. It is generally believed that oxidative stress and pulmonary inflammation are the direct effects caused by PM2.5 particles, which in turn lead to systematic inflammation and result in endothelial dysfunction, automatic nervous system imbalance. Substantial evidence from toxicological and epidemiological studies has been accumulated to reveal the mechanism of the health effects of PM2.5, however, many times these pieces of evidence are not consistent and sometimes even conflict with each other.
To address the complicated nature of the health effects of PM2.5, one needs to consider both health effects and PM characteristics at same time, e.g. time after exposure (lag effects), size and chemical composition of particles, and susceptible population. Here, we suggest these variables compose four dimensions which are necessary to describe the health effects of PM2.5 and the underlying mechanism of these effects: 1. Time after Exposure (Lag Effect); 2. Size Effect of Fine Particles; 3. Component Effect of Fine Particles; 4. Susceptible Population.
Using the four dimensions of the variables will not only help us to understand the complicated nature of the health effects of PM2.5 and to identify the main size fraction and chemical composition of PM2.5 that cause the effects, but also provide us with comprehensive evidence in a broad perspective for the air pollution control and public health prevention strategy.
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