Impacts of COVID-19's restriction measures on personal exposure to VOCs and aldehydes in Taipei City.

The Coronavirus Disease 2019 (COVID-19) pandemic provided an unprecedented natural experiment, that allowed us to investigate the impacts of different restrictive measures on personal exposure to specific volatile organic compounds (VOCs) and aldehydes and resulting health risks in the city. Ambient concentrations of the criteria air pollutants were also evaluated. Passive sampling for VOCs and aldehydes was conducted for graduate students and ambient air in Taipei, Taiwan, during the Level 3 warning (strict control measures) and Level 2 alert (loosened control measures) of the COVID-19 pandemic in 2021-2022. Information on the daily activities of participants and on-road vehicle counts nearby the stationary sampling site during the sampling campaigns were recorded. Generalized estimating equations (GEE) with adjusted meteorological and seasonal variables were used to estimate the effects of control measures on average personal exposures to the selected air pollutants. Our results showed that ambient CO and NO2 concentrations in relation to on-road transportation emissions were significantly reduced, which led to an increase in ambient O3 concentrations. Exposure to specific VOCs (benzene, methyl tert-butyl ether (MTBE), xylene, ethylbenzene, and 1,3-butadiene) associated with automobile emissions were remarkably decreased by ~40-80 % during the Level 3 warning, resulting in 42 % and 50 % reductions of total incremental lifetime cancer risk (ILCR) and hazard index (HI), respectively, compared with the Level 2 alert. In contrast, the exposure concentration and calculated health risks in the selected population for formaldehyde increased by ~25 % on average during the Level 3 warning. Our study improves knowledge of the influence of a series of anti-COVID-19 measures on personal exposure to specific VOCs and aldehydes and its mitigations.

Interactions of chemical components in ambient PM2.5 with influenza viruses.

The significance of this work is that ambient PM2.5 is a direct transmission mode for influenza virus infection to the human alveolar epithelium. The concentration of PM2.5 was 11.7 ± 5.5 µg/m3 in Taipei during 24 December 2019-13 January 2020. Approximately 79% of inhaled PM2.5 is able to reach the upper-to-lower airway, and 47% of PM2.5 is able to reach the alveolar epithelium for influenza virus infection. Influenza A and B viruses were detected in PM2.5 on 9 days, and the influenza A/H5 virus was detected on 15 days during the study period. FL and Pyr were negatively correlated with the influenza A virus. D(ah)P and Acp were positively correlated with the influenza B and A/H5 viruses, respectively. Cd, V, and Zn were positively correlated with the influenza A, B, and A/H5 viruses, respectively. Next, influenza A, B, and A/H5 viral plasmids interacted with carbon black, H2O2, DEPs, and UD. We observed that H2O2 significantly decreased levels of complementary DNA of the three influenza viruses. DEPs and UD significantly decreased influenza A and A/H5 viral levels. In conclusion, chemicals in PM2.5 may play vital roles in terms of viable influenza virus in the atmosphere.

Particulate matter and SARS-CoV-2: A possible model of COVID-19 transmission.

Coronavirus disease 2019 (COVID-19), an acute respiratory disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly developed into a pandemic throughout the world. This disease is a highly infectious novel coronavirus and can affect people of all ages. Previous reports observed that particulate matter (PM) provided a platform for intermixing with viruses (i.e., influenza). However, the role of PM in SARS-CoV-2 transmission remains unclear. In this paper, we propose that PM plays a direct role as a "carrier" of SARS-CoV-2. SARS-CoV-2 is reported to have a high affinity for the angiotensin-converting enzyme 2 (ACE2) receptor. Indirectly, exposure to PM increases ACE2 expression in the lungs which facilitates SARS-CoV-2 viral adhesion. Thus, the high risk of SARS-CoV-2 in heavily polluted regions can be explained by upregulation of ACE2 caused by PM. PM could be both a direct and indirect transmission model for SARS-CoV-2 infection.