In this study, we conducted a time-series study among 476 COVID-19 patients caused by the Delta SARS-CoV2 variant to explore the effects of short-term PM exposure on the risk of severe COVID-19. We observed that short-term exposure to PM was positively associated with the risk of severe COVID-19, and either sex or age did not alter the association. To our knowledge, this is the first individual-level study to evaluate the relationship between short-term PM exposure and the risk of severe COVID-19 in China.
A multicenter study in 33 European countries found that PM2.5 was positively related to the number of COVID-19 deaths . Although this study was qualitative and did not consider potential confounding factors, it provided evidence of PM exposure contributing to a poor prognosis of COVID-19. A global research based on satellite data showed that approximately 15% of the global COVID-19 mortality (27% in East Asia, 19% in Europe, and 17% in North America) were attributed to the long-term PM2.5 exposure . A study in California reported that a wildfire increased the PM2.5 concentration in ten counties by 220.71%, and subsequently, the number of deaths from COVID-19 in these areas increased by 148.2% . Another study in London showed that environmental PM2.5 was positively correlated with the mortality of COVID-19. For a unit increase in PM2.5, the number of deaths due to COVID-19 increased by 2.3% . Another study explored the relationships between long-term exposure to PM2.5 and the hospitalization of COVID-19 in Cincinnati and found that a unit increase in 10-year average PM2.5 concentration was correlated with an 18% higher hospitalization rate . Although most of the previous studies were ecological and focused on the COVID-19 mortality or hospitalization rate, their findings indirectly supported that PM exposure was related to the severity of COVID-19. Moreover, our results showed that the effect of PM2.5 seemed to be stronger than PM10. This may be attributed to the smaller particle size of PM2.5, which can penetrate deep into the alveoli and bronchioles, and thus has more potent biological toxicity .
The following reasons may explain the potential links between PM and severe COVID-19. Firstly, PM suspended in the air, especially for PM2.5, may not only carry the SARS-CoV-2, but also enhance the attachment and replication of the virus in the bronchus by damaging the integrity of bronchial epithelial cells . Secondly, as pointed by Domingo et al., SARS-CoV-2 attached to PM may survive longer and be more aggressive in the immune system, which was aggravated by exposure to high concentrations of air pollutants . Thirdly, as mentioned before, PM2.5 can reach the alveoli, thereby delivering the SARS-CoV-2 to the target type II alveolar cells . Previous studies have shown that PM, especially PM2.5, can stimulate activated alveolar macrophages and then induce pro-inflammatory cytokines production and release, thus aggravating the allergic inflammation in the lungs . Fourthly, the metals and polycyclic aromatic hydrocarbons that make up PM2.5 facilitate the production of free radicals, which may oxidize alveolar cells. Excessive free radicals would weaken cellular antioxidant capacity, leading to lipid peroxidation and increased intracellular calcium concentration, further inducing cellular damage . Finally, the SARS-CoV-2 entered the cell through binding to the angiotensin-converting enzyme 2 (ACE2) receptor, and this process can be enhanced by PM exposure . The binding of the SARS-CoV-2 and the ACE2 receptor resulted in the down-regulation of the latter. The ACE2 mediated the transformation of angiotensin II to angiotensin 1-7 through the G protein-coupled receptor pathway and worked with angiotensin 1-7 by anti-inflammatory and antioxidant to protect the body. The down-regulation of ACE2 decreased its protective effect and worsened the effect of angiotensin II .
Our study had several limitations. First, we estimated the PM exposure level of each patient based on the monitoring data from the fixed sites, which may not accurately reflect the individual exposure. Second, other factors related to the severity of COVID-19, which were not considered in the analysis, may affect the results. Third, since the epidemic was under control for a short time, the sample size of this study was relatively small, especially for the number of severe patients. The association between PM and severe COVID-19 needs to be further confirmed in future studies.