Chia-Pin Chio

Researchers and transnational public health organizations have recognized aerosol transmission as an essential route of COVID‐19 transmission. Therefore, improving ventilation systems is now adopted as a core preventive measure. As young children aged 2–6 in kindergartens generally lack vaccine protection and multiple infection clusters have been identified during the pandemic, we aimed to quantify the risk of aerosol transmission in kindergartens in Taipei, Taiwan. From August to November 2021, we conducted on‐site visits and continuously monitored indoor air quality indicators including carbon dioxide (CO₂) in a kindergarten located in northern Taiwan. We utilized the Wells–Riley model to estimate the basic reproduction number (R₀) of each classroom and staff office, with input parameters including the number of occupants, duration of their stay, and indoor/outdoor CO₂ concentration. Contagious settings were defined as those where the R₀ estimate exceeded 1. We conducted a scenario/sensitivity analysis to assess the effect of simulated improvement measures. During school hours, the average concentration of CO₂ in each classroom and the staff office was often more than 400 ppm higher than the outdoor levels. The R₀ estimates gradually increased from Monday to Friday and throughout school hours, corresponding to the hourly and daily distribution of the CO₂ concentration, which could not dissipate completely during off‐duty time. The R₀ estimates during school hours ranged from 3.01 to 3.12 in classrooms with a maximum of 30 occupants. To lower the R₀ estimate, it is imperative to substantially reduce the number of occupants, the duration of their stay, and indoor CO₂ concentration. The risk of outbreaks of cluster infections in kindergartens should not be underestimated. Feasible strategies to mitigate this risk should include improving ventilation systems through engineering control and limiting the number of indoor occupants and their time staying indoor through administrative control.

Over one-third of energy is generated from coal consumption in Taiwan. In order to estimate the health impact assessment attributable to PM_2.5 concentrations emitted from coal consumption in Taiwan. We applied a Gaussian trajectory transfer-coefficient model to obtain county-wide PM_2.5 exposures from coal consumption, which includes coal-fired power plants and combined heat and power plants. Next, we calculated the mortality burden attributable to PM_2.5 emitted by coal consumption using the comparative risk assessment framework developed by the Global Burden of Disease study. Based on county-level data, the average PM_2.5 emissions from coal-fired plants in Taiwan was estimated at 2.03 ± 1.29 (range: 0.32–5.64) μg/m³. With PM_2.5 increments greater than 0.1 μg/m³, there were as many as 16 counties and 66 air quality monitoring stations affected by coal-fired plants and 6 counties and 18 monitoring stations affected by combined heat and power plants. The maximum distances affected by coal-fired and combined heat and power plants were 272 km and 157 km, respectively. Our findings show that more counties were affected by coal-fired plants than by combined heat and power plants with significant increments of PM_2.5 emissions. We estimated that 359.6 (95% CI: 334.8–384.9) annual adult deaths and 124.4 (95% CI: 116.4–132.3) annual premature deaths were attributable to PM_2.5 emitted by coal-fired plants in Taiwan. Even in six counties without power plants, there were 75.8 (95% CI: 60.1–91.5) deaths and 25.8 (95%CI: 20.7–30.9) premature deaths annually attributable to PM_2.5 emitted from neighboring coal-fired plants. This study presents a precise and effective integrated approach for assessing air pollution and the health impacts of coal-fired and combined heat and power plants.

Adverse health effects have been observed in nearby residents due to exposure to petrochemical-derived chemicals. The objective of this study was to examine associations of soluble metals with lung and liver toxicity in fine particulate matter (PM_2.5) in the vicinity of a petrochemical complex. PM_2.5 was collected in the vicinity of a petrochemical complex of Mailiao Township (Yunlin County, Taiwan) to investigate lung and liver toxicity in BALB/c mice. The PM_2.5 concentration was 30.2 ± 11.2 μg/m³, and the PM_2.5 was clustered in major local emissions (19.1 μg/m³) and minor local emissions (14.1 μg/m³) using a k-means clustering model. The PM_2.5 (50 and 150 μg/kg) and PM_2.5-equivalent soluble nickel (Ni), vanadium (V), and lead (Pb) concentrations were intratracheally instilled into BALB/c mice. PM_2.5 and V significantly decreased the tidal volume after exposure (p < 0.05). The peak expiratory flow (PEF) and peak inspiratory flow (PIF)/PEF ratio were significantly altered by 150 μg/kg V (p < 0.05). V and Pb significantly increased total protein and lactate dehydrogenase (LDH) levels in bronchoalveolar lavage fluid (BALF) (p < 0.05). Interleukin (IL)-6 in BALF significantly increased after exposure to Pb (p < 0.05) accompanied by lung inflammatory infiltration. PM_2.5 and Pb significantly increased levels of 8-isoprostane (p < 0.05). The level of caspase-3 activity significantly increased after exposure to Pb (p < 0.05). LDH in the liver was significantly increased by PM_2.5 (p < 0.05). 8-Isoprostane in the liver was significantly increased by PM_2.5 and Pb (p < 0.05). IL-6 in the liver was significantly increased by PM_2.5, Ni, V, and Pb after exposure (p < 0.05), accompanied by liver inflammatory infiltration. Our results demonstrated that V in PM_2.5 was associated with an increase in 8-isoprostane for all emissions and major local petrochemical emissions. In conclusion, V contributes to in vivo liver toxicity induced by PM_2.5 in the vicinity of a petrochemical complex.

Environmental bisphenol A (BPA) exposure has been linked to a variety of adverse health effects such as developmental and reproductive issues. However, establishing a clear association between BPA and the likelihood of human health is complex yet fundamentally uncertain. The purpose of this study was to assess the potential exposure risks from environmental BPA among Chinese population based on five human health outcomes, namely immune response, uterotrophic assay, cardiovascular disease (CVD), diabetes, and behavior change. We addressed these health concerns by using a stochastic integrated risk assessment approach. The BPA dose-dependent likelihood of effects was reconstructed by a series of Hill models based on animal models or epidemiological data. We developed a physiologically based pharmacokinetic (PBPK) model that allows estimation of urinary BPA concentration from external exposures. Here we showed that the daily average exposure concentrations of BPA and urinary BPA estimates were consistent with the published data. We found that BPA exposures were less likely to pose significant risks for infants (0–1 year) and adults (male and female >20 years) with −6-fold increase in uterus weight and immune response outcomes, respectively. Moreover, our results indicated that there was 50 % risk probability that the response outcomes of CVD, diabetes, and behavior change with or without skin absorption would increase 10⁻⁴–10⁻²-fold. We conclude that our approach provides a powerful tool for tracking and managing human long-term BPA susceptibility in relation to multiple exposure pathways, and for informing the public of the negligible magnitude of environmental BPA pollution impacts on human health.

SUMMARY: Indoor transmission of respiratory droplets bearing influenza within humans poses high risks to respiratory function deterioration and death. Therefore, we aimed to develop a framework for quantifying the influenza infection risk based on the relationships between inhaled/exhaled respiratory droplets and airborne transmission dynamics in a ventilated airspace. An experiment was conducted to measure the size distribution of influenza-containing droplets produced by coughing for a better understanding of potential influenza spread. Here we integrated influenza population transmission dynamics, a human respiratory tract model, and a control measure approach to examine the indoor environment–virus–host interactions. A probabilistic risk model was implemented to assess size-specific infection risk for potentially transmissible influenza droplets indoors. Our results found that there was a 50% probability of the basic reproduction number (R₀) exceeding 1 for small-size influenza droplets of 0·3–0·4µm, implicating a potentially high indoor infection risk to humans. However, a combination of public health interventions with enhanced ventilation could substantially contain indoor influenza infection. Moreover, the present dynamic simulation and control measure assessment provide insights into why indoor transmissible influenza droplet-induced infection is occurring not only in upper lung regions but also in the lower respiratory tract, not normally considered at infection risk.