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Since long-term exposure to PM2.5 is a growing concern in Taiwan, therefore, our study aimed to investigate the association between different PM2.5 concentrations and cause-specific mortalities, as well as explore the influence of demographic, socio-economic, and geographic determinants on mortality. Utilizing a Distributed Lag Non-Linear Model (DLNM), we estimated the PM2.5-attributable mortality burden among the elderly population (above 65 years) in Taiwan from 2005 to 2018. Our analysis considered various thresholds defined by the World Health Organization (WHO) to assess the impact of PM2.5 concentrations, ranging from standard Air Quality Guidelines (AQG) levels (0–15 μg/m3) to higher interim targets (up to 80 μg/m3). Our study reveals that achieving AQG levels (< 15 μg/m3) in Taiwan could potentially prevent 5571 elderly deaths, including 889 deaths from CVDs, 934 deaths from RTIs, and 680 deaths from chronic diseases. We observed a rapid increase in attributable deaths at lower PM2.5 concentrations, with a subsequent marginal increase at higher levels of exposure. We also identified several factors that modify the effects of PM2.5 exposures among elderly. For example, we found that higher elderly population ratios and high-income households were associated with an elevated risk of PM2.5-related deaths. In contrast, higher social welfare expenditure, better availability of medical practitioners per square kilometer, and higher forest-to-land ratios were associated with positive effects, indicating their potential in reducing mortality risk. This study fills a knowledge gap by examining the health consequences of varying PM2.5 levels and explored the complex interplay between demographic, socio-economic, and geographic factors in relation to PM2.5-related mortality. [ABSTRACT FROM AUTHOR]

The measurements of temporal change to indoor contaminant concentrations are critical to understanding pollution characteristics. As commercial sensors are becoming increasingly commonplace, concentration accuracy is still a critical issue. The most common methods for measuring indoor particulate pollutants based on filter-based gravimetric methods. However, the gravimetric method is expensive, time-consuming, and often provides little temporal information. More and more commercial sensors are utilized to collect larger and temporal information about indoor air pollutants. Nevertheless, limited data support the accuracy of commercial sensors so far. Thus, this study aims to evaluate the performance of commercial sensors. PM2.5 were collected for 30 days by personal environmental monitors with an airflow of 2 L/min on 37-mm Teflon filters and commercial sensors, simultaneously in a three-story house. Moreover, the intra-sensor comparison was conducted for 24 hours by the resolution in 1 minute. Finally, the linear regression model was built to adjust commercial sensors. The intra-sensor comparison results revealed that 24 hours average coefficient of variation (CV value) of PM2.5 in this study were under 10% and the R2 of the adjusted equation was 0.9394. We provide an accurate concentration of commercial sensors to estimate the association between pollutants exposure and health.

Influenza remains one of the most serious infectious diseases. Gallic acid is one of the most common and representative phenolic acids found in various plants. This is an interesting subject to explore how gallic acid could inhibit H1N1 influenza virus infection by reducing the production of virulent proteins and interrupting autophagy machinery for influenza virus replication on the host cell. Cellular viability was assessed by XTT assay. The inhibitory effects on the H1N1 influenza virus were assessed by hemagglutination assay, plaque assay, and qRT‐PCR. Western blot analysis was used for detecting protein levels of M1, M2, NP, LC3B, and beclin‐1. Autophagy activity was demonstrated by acridine orange staining assay. The result demonstrated that there was no cytotoxic effect of gallic acid on A549 cells, and gallic acid could restore the cellular viability of H1N1 influenza virus‐infected A549 cells within the experimental concentration treatment. Moreover, gallic acid could effectively restrain viral activity of the H1N1 influenza virus. After the treatment of gallic acid, the production of virulent H1N1 influenza virus proteins, that is, M1, M2, and NP protein were reduced. As for autophagic mechanism, both of the LC3B II conversion and the level ratio of LC3B II to LC3B I were notably decreased. The acridine orange staining assay also revealed decreased accumulation of autophagosomes in H1N1 influenza virus‐infected cells. In conclusion, gallic acid suppresses H1N1 influenza viral infectivity through restoration of autophagy pathway and inhibition of virulent M1, M2, and NP protein production. [ABSTRACT FROM AUTHOR]