Exposure and health risk assessment of volatile organic compounds among drivers and passengers in long-distance buses.

Exposure to volatile organic compounds (VOCs) such as benzene, toluene, ethylbenzene, xylene, and formaldehyde from long-distance buses has been reported to adversely affect human health. This study investigates the concentrations of these five VOCs and evaluates their health risks to drivers and passengers on board. Ten trips from Taipei to Taichung were performed during the warm and cold seasons of 2021-2022. Two locations inside the bus were established to collect air samples by a 6-liter canister for drivers and passengers. Exposure concentrations of benzene, toluene, ethylbenzene, and xylene were analyzed via gas chromatography with a flame ionization detector and the formaldehyde concentration was monitored using a formaldehyde meter. Subsequently, a Monte Carlo simulation was conducted to evaluate the carcinogenic and non-carcinogenic risks of the five VOCs. Formaldehyde emerged as the highest detected compound (9.06 ± 3.77 µg/m3), followed by toluene (median: 6.11 µg/m3; range: 3.86-14.69 µg/m3). In particular, formaldehyde was identified to have the significantly higher concentration during non-rush hours (10.67 ± 3.21 µg/m3) than that during rush hours (7.45 ± 3.41 µg/m3) and during the warm season (10.71 ± 2.97 µg/m3) compared with that during the cold season (7.41 ± 4.26 µg/m3). Regarding non-carcinogenic risks to drivers and passengers, the chronic hazard indices for these five VOCs were under 1 to indicate an acceptable risk. In terms of carcinogenic risk, the median risks of benzene and formaldehyde for drivers were 2.88 × 10-6 (95% confidence interval [CI]: 2.11 × 10-6 - 5.13 × 10-6) and 1.91 × 10-6 (95% CI: 4.54 × 10-7 - 3.44 × 10-6), respectively. In contrast, the median carcinogenic risks of benzene and formaldehyde for passengers were less than 1 × 10-6 to present an acceptable risk. This study suggests that benzene and formaldehyde may present carcinogenic risks for drivers. Moreover, the non-carcinogenic risk for drivers and passengers is deemed acceptable. We recommended that the ventilation frequency be increased to mitigate exposure to VOCs in long-distance buses.

Effects of occupational exposure to metal fume PM2.5 on lung function and biomarkers among shipyard workers: a 3-year prospective cohort study.

OBJECTIVE: This study investigates the associations of α1-antitrypsin, inter-α-trypsin inhibitor heavy chain (ITIH4), and 8-isoprostane with lung function in shipyard workers exposed to occupational metal fume fine particulate matter (PM2.5), which is known to be associated with adverse respiratory outcomes. METHODS: A 3-year follow-up study was conducted on 180 shipyard workers with 262 measurements. Personal exposure to welding fume PM2.5 was collected for an 8-h working day. Pre-exposure, post-exposure, and delta (∆) levels of α1-antitrypsin, ITIH4, and 8-isoprostane were determined in urine using enzyme-linked immunosorbent assays. Post-exposure urinary metals were sampled at the beginning of the next working day and analyzed by inductively coupled plasma-mass spectrometry. Lung function measurements were also conducted the next working day for post-exposure. RESULTS: An IQR increase in PM2.5 was associated with decreases of 2.157% in FEV1, 2.806% in PEF, 4.328% in FEF25%, 5.047% in FEF50%, and 7.205% in FEF75%. An IQR increase in PM2.5 led to increases of 42.155 µg/g in ∆α1-antitrypsin and 16.273 µg/g in ∆ITIH4. Notably, IQR increases in various urinary metals were associated with increases in specific biomarkers, such as post-urinary α1-antitrypsin and ITIH4. Moreover, increases in ∆ α1-antitrypsin and ∆ITIH4 were associated with decreases in FEV1/FVC by 0.008% and 0.020%, respectively, and an increase in ∆8-isoprostane resulted in a 1.538% decline in FVC. CONCLUSION: Our study suggests that urinary α1-antitrypsin and ITIH4 could indicate early lung function decline in shipyard workers exposed to metal fume PM2.5, underscoring the need for better safety and health monitoring to reduce respiratory risks.

Impact of occupational noise exposure on the hearing level in hospital staffs: a longitudinal study.

The study aimed to evaluate the impact of occupational noise on hearing loss among healthcare workers using audiometry. A longitudinal study was conducted with a six-month follow-up period in a hospital with 21 participants, divided into high-noise-exposure (HNE) and low-noise-exposure (LNE) groups. Mean noise levels were higher in the HNE group (70.4 ± 4.5 dBA), and hearing loss was measured using pure-tone audiometry at baseline and follow-up. The HNE group had significantly higher mean threshold levels at frequencies of 0.25 kHz, 0.5 kHz, 4.0 kHz, and an average of 0.5, 1, 2, and 4 kHz (all p-values < 0.05) after the follow-up period. After adjusting for confounding factors, the HNE group had significantly higher hearing loss levels at 0.25 kHz, 0.5 kHz, and average frequencies of 0.5, 1, 2, and 4 kHz compared to the LNE group at the second measurement. Occupational noise levels above 65 dBA over six months were found to cause significant threshold changes at frequencies of 0.25 kHz, 0.5 kHz, and an average of 0.5-4.0 kHz. This study highlights the risk of noise-induced hearing loss among healthcare workers and emphasizes the importance of implementing effective hearing conservation programs in the workplace. Regular monitoring and assessment of noise levels and hearing ability, along with proper use of personal protective equipment, are crucial steps in mitigating the impact of occupational noise exposure on the hearing health of healthcare workers.

Prevention of Work Absence Due to Back Pain: A Network Meta-Analysis.

This paper reviewed the most effective strategies for preventing work absence due to back pain (BP) and BP episodes (the number of people reporting back pain). We searched randomized controlled trials (RCTs) of prevention strategies for BP from previous meta-analyses, PubMed, CENTRAL, and Embase and conducted a network meta-analysis. Thirteen RCTs (2033 participants) were included. Low- to high-quality evidence showed that exercise combined with ergonomics, education, back belts, and education combined with ergonomics did not prevent sickness absenteeism or BP episodes. There was moderate-quality evidence that exercise, especially resistance exercise, was the best prevention strategy to reduce the number of people reporting absenteeism due to BP (risk ratio [RR] = 0.10; 95% CI: 0.01 to 0.69). Moderate-quality evidence suggested that resistance and stretching exercises combined with education was the best prevention strategy to reduce pain (RR = 0.80; 95% CI: 0.67 to 0.96) and the number of absenteeism days for BP (standardized mean difference [SMD] = -0.39; 95% CI: -0.77 to -0.02). In conclusion, exercise, especially resistance and stretching exercises, and exercise combined with education were ranked as the best interventions to prevent sickness absenteeism and BP episodes.

Role of DCLK1/Hippo pathway in type II alveolar epithelial cells differentiation in acute respiratory distress syndrome.

BACKGROUND: Delay in type II alveolar epithelial cell (AECII) regeneration has been linked to higher mortality in patients with acute respiratory distress syndrome (ARDS). However, the interaction between Doublecortin-like kinase 1 (DCLK1) and the Hippo signaling pathway in ARDS-associated AECII differentiation remains unclear. Therefore, the objective of this study was to understand the role of the DCLK1/Hippo pathway in mediating AECII differentiation in ARDS. MATERIALS AND METHODS: AECII MLE-12 cells were exposed to 0, 0.1, or 1 µg/mL of lipopolysaccharide (LPS) for 6 and 12 h. In the mouse model, C57BL/6JNarl mice were intratracheally (i.t.) injected with 0 (control) or 5 mg/kg LPS and were euthanized for lung collection on days 3 and 7. RESULTS: We found that LPS induced AECII markers of differentiation by reducing surfactant protein C (SPC) and p53 while increasing T1α (podoplanin) and E-cadherin at 12 h. Concurrently, nuclear YAP dynamic regulation and increased TAZ levels were observed in LPS-exposed AECII within 12 h. Inhibition of YAP consistently decreased cell levels of SPC, claudin 4 (CLDN-4), galectin 3 (LGALS-3), and p53 while increasing transepithelial electrical resistance (TEER) at 6 h. Furthermore, DCLK1 expression was reduced in isolated human AECII of ARDS, consistent with the results in LPS-exposed AECII at 6 h and mouse SPC-positive (SPC+) cells after 3-day LPS exposure. We observed that downregulated DCLK1 increased p-YAP/YAP, while DCLK1 overexpression slightly reduced p-YAP/YAP, indicating an association between DCLK1 and Hippo-YAP pathway. CONCLUSIONS: We conclude that DCLK1-mediated Hippo signaling components of YAP/TAZ regulated markers of AECII-to-AECI differentiation in an LPS-induced ARDS model.

Climate change, air quality, and respiratory health: a focus on particle deposition in the lungs.

This review article delves into the multifaceted relationship between climate change, air quality, and respiratory health, placing a special focus on the process of particle deposition in the lungs. We discuss the capability of climate change to intensify air pollution and alter particulate matter physicochemical properties such as size, dispersion, and chemical composition. These alterations play a significant role in influencing the deposition of particles in the lungs, leading to consequential respiratory health effects. The review paper provides a broad exploration of climate change's direct and indirect role in modifying particulate air pollution features and its interaction with other air pollutants, which may change the ability of particle deposition in the lungs. In conclusion, climate change may play an important role in regulating particle deposition in the lungs by changing physicochemistry of particulate air pollution, therefore, increasing the risk of respiratory disease development.

Climate change influences particle deposition in the lungs by modifying the physicochemical properties of particulate air pollution, thereby escalating the risk of respiratory disease development.It is crucial for healthcare providers to educate patients about the relationship between climate change and respiratory health.People with conditions such as asthma, COPD, and allergies must understand how changes in weather, air pollution, and allergens can exacerbate their symptoms.Instruction on understanding air quality indices and pollen predictions, along with recommendations on adapting everyday activities and medication regimens in response, is essential.

N terminal prohormone of brain natriuretic peptide is associated with improved heart rate recovery after treadmill exercise test.

Background: Heart rate recovery (HRR) and N terminal-pro B type natriuretic peptide (NT-proBNP) are markers for survival and cardiac function; however, Little is known about their association. Method: We examined 2540 healthy subjects aged 12-49 years with data from National Health and Nutrition Examination Survey(NHANES) 1999-2002. HRR parameters 1-3 min after exercise were calculated from exercise test results. Baseline characteristics, anthropometric and NT-proBNP, and other risk covariates were obtained. Result: The results showed that NT-proBNP was positively correlated with HRR2(correlation coefficient (cc) = 0.042 [0.029-0.054], P < 0.001) and HRR3(cc = 0.046 [0.029-0.064], P = 0.001); with further adjustment, the associations remained significant between NT-proBNP and HRR2(cc = 0.030 [0.010-0.049], P = 0.004)/HRR3(cc = 0.029[0.004-0.054], P = 0.025). Our study also found significant correlations between NT-pro BNP and SBP(cc = -0.026 [-0.046∼-0.005], P = 0.017), DBP(cc = -0.037 [-0.062∼-0.012], P = 0.005), and total cholesterol(cc = -0.065 [-0.12∼-0.018], P = 0.009). Conclusions: Our results suggest that BNP might reduce heart rate after exercise by inhibiting the sympathetic nervous system (SNS), reducing HRR2 and HRR3, as these phases involve the reduction of heart rate through cardiac sympathetic withdrawal. Moreover, the interaction of BNP on the SNS might be related to the effect of BNP on cardiovascular risks.

Short-term mediating effects of PM2.5 on climate-associated COPD severity.

The impact of short-term exposure to environmental factors such as temperature, relative humidity (RH), and fine particulate matter (PM2.5) on chronic obstructive pulmonary disease (COPD) remains unclear. The objective of this study is to investigate PM2.5 as a mediator in the relationship between short-term variations in RH and temperature and COPD severity. A cross-sectional study was conducted on 930 COPD patients in Taiwan from 2017 to 2022. Lung function, COPD Assessment Test (CAT) score, and modified Medical Research Council (mMRC) dyspnea scale were assessed. The mean and differences in 1-day, 7-day, and 30-day individual-level exposure to ambient RH, temperature, and PM2.5 were estimated. The associations between these factors and clinical outcomes were analyzed using linear regression models and generalized additive mixed models, adjusting for age, sex, smoking, and body mass index. In the total season, increases in RH difference were associated with increases in forced expiratory volume in 1 s (FEV1) / forced vital capacity (FVC), while increases in temperature difference were associated with decreases in FEV1 and FEV1/FVC. Increases in PM2.5 mean were associated with declines in FEV1. In the cold season, increases in temperature mean were associated with decreases in CAT and mMRC scores, while increases in PM2.5 mean were associated with declines in FEV1, FVC, and FEV1/FVC. In the warm season, increases in temperature difference were associated with decreases in FEV1 and FEV1/FVC, while increases in RH difference and PM2.5 mean were associated with decreases in CAT score. PM2.5 fully mediated the associations of temperature mean with FEV1/FVC in the cold season. In conclusion, PM2.5 mediates the effects of temperature and RH on clinical outcomes. Monitoring patients during low RH, extreme temperature, and high PM2.5 levels is crucial. Capsule of findings The significance of this study is that an increase in ambient RH and temperature, as well as PM2.5 exposure, were significantly associated with changes in lung function, and clinical symptoms in these patients. The novelty of this study is that PM2.5 plays a mediating role in the association of RH and temperature with COPD clinical outcomes in the short term.

The impact of air pollution on respiratory diseases in an era of climate change: A review of the current evidence.

The impacts of climate change and air pollution on respiratory diseases present significant global health challenges. This review aims to investigate the effects of the interactions between these challenges focusing on respiratory diseases. Climate change is predicted to increase the frequency and intensity of extreme weather events amplifying air pollution levels and exacerbating respiratory diseases. Air pollution levels are projected to rise due to ongoing economic growth and population expansion in many areas worldwide, resulting in a greater burden of respiratory diseases. This is especially true among vulnerable populations like children, older adults, and those with pre-existing respiratory disorders. These challenges induce inflammation, create oxidative stress, and impair the immune system function of the lungs. Consequently, public health measures are required to mitigate the effects of climate change and air pollution on respiratory health. The review proposes that reducing greenhouse gas emissions contribute to slowing down climate change and lessening the severity of extreme weather events. Enhancing air quality through regulatory and technological innovations also helps reduce the morbidity of respiratory diseases. Moreover, policies and interventions aimed at improving healthcare access and social support can assist in decreasing the vulnerability of populations to the adverse health effects of air pollution and climate change. In conclusion, there is an urgent need for continuous research, establishment of policies, and public health efforts to tackle the complex and multi-dimensional challenges of climate change, air pollution, and respiratory health. Practical and comprehensive interventions can protect respiratory health and enhance public health outcomes for all.

Associations of particulate matter, gaseous pollutants, and road traffic noise with the prevalence of asthma in children.

The purposes of this study were to elucidate the associations between exposure to particulate matter, gaseous pollutants, and road traffic noise and asthma prevalence and to determine the interaction between exposure to multiple pollutants and asthma in children. A total of 3,246 children were recruited from 11 kindergartens in New Taipei City, Taiwan. Land use regression (LUR) was used to establish predictive models for estimating individual exposure levels of particulate matter, gaseous pollutants, and the 24 h A-weighted equivalent sound pressure level (LAeq,24). Multiple logistic regression was performed to test the associations between exposure to these environmental factors and asthma prevalence in children. Multiple-exposure models revealed that an interquartile-range (IQR) increase in PM2.5 (1.17 µg/m3) and PM10 (10.69 µg/m3) caused a 1.34-fold (95% confidence interval [CI] = 1.05-1.70) and 1.17-fold (95% CI = 1.01-1.36) increase in risk of asthma prevalence in children after adjusting for LAeq,24 and NO2. Co-exposure to PM2.5, LAeq,24, and O3, SO2, or CO, as well as co-exposure to PM10, LAeq,24, and CO produced similar findings. Only exposure to one IQR of SO2 (0.15 ppb) was observed a significant association (odds ratio = 1.16, 95% CI = 1.00-1.34) with the asthma prevalence in children after adjusting for PM10 and LAeq,24. Exposure to PM2.5, PM10, and SO2 may be associated with a higher asthma prevalence in children, while other gaseous pollutants and road traffic noise did not demonstrate significant associations. The interaction of exposure to air pollutants and road traffic noise on asthma prevalence in children was not observed in this study.

Association between ambient BTEX mixture and neurological hospitalizations: A multicity time-series study in Taiwan.

BACKGROUND: Benzene, toluene, ethylbenzene, and xylenes, collectively known as BTEX, are hazardous chemical mixtures, and their neurological health effects have not been thoroughly evaluated. We examined the association between BTEX exposure and neurological hospital admissions. METHODS: This was a multicity time-series study conducted in five major Taiwanese cities. Daily hospital admission records for diseases of the nervous system from January 1, 2016, to December 31, 2017, were collected from the National Health Insurance Research Database. Ambient BTEX and criteria pollutant concentrations and weather factors were collected from Photochemical Assessment Monitoring Stations. We applied a Poisson generalized additive model (GAM) and weighted quantile sum regression to calculate city-specific effect estimates for BTEX and conducted a random-effects meta-analysis to pool estimates. RESULTS: We recorded 68 neurological hospitalizations per day during the study period. The daily mean BTEX mixture concentrations were 22.5 µg/m3, ranging from 18.3 µg/m3 in Kaohsiung to 27.0 µg/m3 in Taichung, and toluene (13.6 µg/m3) and xylene (5.8 µg/m3) were the dominant chemicals. Neurological hospitalizations increased by an average of 1.6 % (95 % CI: 0.6-2.6 %) for every interquartile range (15.8 µg/m3) increase in BTEX at lag 0 estimated using a GAM model. A quartile increase in the weighted sum of BTEX exposure was associated with a 1.7 % (95 % CI: 0.6-2.8 %) increase in daily neurological hospitalizations. CONCLUSION: We found consistent acute adverse effects of BTEX on neurological hospitalizations in Taiwan, with toluene and xylene as the dominant chemicals. These findings aid the development of more targeted public health interventions.

Critical air pollutant assessments and health effects attributed to PM2.5 during and after COVID-19 lockdowns in Iran: application of AirQ+ models.

Objectives: The aim of this study was to evaluate changes in air quality index (AQI) values before, during, and after lockdown, as well as to evaluate the number of hospitalizations due to respiratory and cardiovascular diseases attributed to atmospheric PM2.5 pollution in Semnan, Iran in the period from 2019 to 2021 during the COVID-19 pandemic. Methods: Daily air quality records were obtained from the global air quality index project and the US Environmental Protection Administration (EPA). In this research, the AirQ+ model was used to quantify health consequences attributed to particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5). Results: The results of this study showed positive correlations between air pollution levels and reductions in pollutant levels during and after the lockdown. PM2.5 was the critical pollutant for most days of the year, as its AQI was the highest among the four investigated pollutants on most days. Mortality rates from chronic obstructive pulmonary disease (COPD) attributed to PM2.5 in 2019-2021 were 25.18% in 2019, 22.55% in 2020, and 22.12% in 2021. Mortality rates and hospital admissions due to cardiovascular and respiratory diseases decreased during the lockdown. The results showed a significant decrease in the percentage of days with unhealthy air quality in short-term lockdowns in Semnan, Iran with moderate air pollution. Natural mortality (due to all-natural causes) and other mortalities related to COPD, ischemic heart disease (IHD), lung cancer (LC), and stroke attributed to PM2.5 in 2019-2021 decreased. Conclusion: Our results support the general finding that anthropogenic activities cause significant health threats, which were paradoxically revealed during a global health crisis/challenge.

Colorimetric Detection of Acenaphthene and Naphthalene Using Functionalized Gold Nanoparticles.

Polycyclic aromatic hydrocarbons are a class of chemicals that occur naturally. They generally demonstrate a high degree of critical toxicity towards humans. Acenaphthene and naphthalene contain compounds that are commonly found in the environment as compared to other PAHs. Consequently, a reliable method of detecting PAHs is crucial for the monitoring of water quality. A colorimetric method based on sodium nitrite-functionalized gold nanoparticles was developed in this study for acenaphthene and naphthalene detection. Different functionalized parameters are determined for the optimization of assay conditions. A linear relationship was found in the analyte concentration range of 0.1-10 ppm with the limit of detection for acenaphthene and naphthalene being 0.046 ppm and 0.0015 ppm, respectively, under the optimized assay conditions. The method's recovery rate for actual samples falls within the range of 98.4-103.0%. In selective and anti-interference tests, the presence of cations and anions has minimal impact on the detection of the analyte. The colorimetric detection method proposed in this study effectively determines the presence of the analyte in real water samples and has a high recovery rate.

Data on lung and intestinal microbiome after air pollution exposure in ageing rats.

Air pollution has been linked to respiratory diseases, and urban air pollution can be attributed to a number of emission sources. The emitted particles and gases are the primary components of air pollution that enter the lungs during respiration. Particulate matter with an aerodynamic diameter of ≤ 2.5 µm (PM2.5) can deposit deep into the respiratory tract via inhalation and has been proposed as a causative agent for adverse respiratory health. In addition, the lung contains a diverse microbial community (microbiome) that maintains normal homeostasis and is significantly altered in a variety of pulmonary disorders. Air pollution, specifically PM2.5, has previously been shown to significantly alter the composition of the lower airway microbiome, which has been linked to decreased lung function in chronic obstructive pulmonary disease (COPD) patients. Surprisingly, the intestinal microbiome has also been implicated in the modulation of pulmonary inflammatory diseases. Therefore, dysbiosis of the lung and intestinal microbiomes pose significant negative effects on human health. This dataset describes the microbial community profiles of the lungs and intestines of ageing rats exposed to ambient unconcentrated traffic-related air pollution for three months. The whole-body exposure system was equipped with and without high efficiency particulate air (HEPA) filtration (gaseous vs. PM2.5 pollution). The data can provide valuable information on lung and intestinal microbiome changes, including that which was only found after traffic-related air pollution exposure.

Diesel exhaust particles inhibit lung branching morphogenesis via the YAP/TAZ pathway.

Prenatal exposure to air pollution may associated with inhibition of lung development in the child, however the possible mechanism is unclear. We investigated the effects of traffic-related diesel exhaust particle (DEP) exposure on fetal lung branching morphogenesis and elucidate the possible mechanism. Ex vivo fetal lungs collected from ICR mice at an age of 11.5 embryonic (E) days were exposed to DEPs at 0 (control), 10, and 50 µg/mL and branching morphogenesis was measured for 3 days. Normal IMR-90 human fetal lung fibroblast cells were exposed to DEPs at 0 (control), 10, and 50 µg/mL for 24 h. We observed that DEP exposure significantly inhibited lung branching morphogenesis with reduced lung branching ratios and surface areas on day 3. RNA sequencing (RNA-Seq) showed that DEP increased the inflammatory response and impaired lung development-related gene expressions. DEPs significantly decreased Yes-associated protein (YAP), phosphorylated (p)-YAP, transcriptional coactivator with a PDZ-binding motif (TAZ), and p-TAZ in IMR-90 cells at 10 and 50 µg/mL. Treatment of fetal lungs with the YAP inhibitor, PFI-2, also demonstrated restricted lung branching development similar to that of DEP exposure, with a significantly decreased lung branching ratio on day 3. DEP exposure significantly decreased the lung branching modulators fibroblast growth factor receptor 2 (FGFR2), sex-determining region Y-box 2 (SOX2), and SOX9 in IMR-90 cells at 10 and 50 µg/mL. Fetal lung immunofluorescence staining showed that DEP decreased SOX2 expression in fibronectin+ fibroblasts. DEP exposure decreased the cellular senescence regulator, p-sirtuin 1 (SIRT1)/SIRT1 in IMR-90 cells, with RNA-Seq showing impaired telomere maintenance. DEP exposure impaired fetal lung growth during the pseudoglandular stage through dysregulating the Hippo signaling pathway, causing fibroblast lung branching restriction and early senescence. Prenatal exposure to traffic-related air pollution has adverse effects on fetal lung development.

Ambient relative humidity-dependent obstructive sleep apnea severity in cold season: A case-control study.

BACKGROUND: The objective of this study was to examine associations of daily averages and daily variations in ambient relative humidity (RH), temperature, and PM2.5 on the obstructive sleep apnea (OSA) severity. METHODS: A case-control study was conducted to retrospectively recruit 8628 subjects in a sleep center between January 2015 and December 2021, including 1307 control (apnea-hypopnea index (AHI) < 5 events/h), 3661 mild-to-moderate OSA (AHI of 5-30 events/h), and 3597 severe OSA subjects (AHI > 30 events/h). A logistic regression was used to examine the odds ratio (OR) of outcome variables (daily mean or difference in RH, temperature, and PM2.5 for 1, 7, and 30 days) with OSA severity (by the groups). Two-factor logistic regression models were conducted to examine the OR of RH with the daily mean or difference in temperature or PM2.5 with OSA severity. An exposure-response relationship analysis was conducted to examine the outcome variables with OSA severity in all, cold and warm seasons. RESULTS: We observed associations of mean PM2.5 and RH with respective increases of 0.04-0.08 and 0.01-0.03 events/h for the AHI in OSA patients. An increase in the daily difference of 1 % RH increased the AHI by 0.02-0.03 events/h in OSA patients. A daily PM2.5 decrease of 1 µg/m3 reduced the AHI by 0.03 events/h, whereas a daily decrease in the RH of 1 % reduced the AHI by 0.03-0.04 events/h. The two-factor model confirmed the most robust associations of ambient RH with AHI in OSA patients. The exposure-response relationship in temperature and RH showed obviously seasonal patterns with OSA severity. CONCLUSION: Short-term ambient variations in RH and PM2.5 were associated with changes in the AHI in OSA patients, especially RH in cold season. Reducing exposure to high ambient RH and PM2.5 levels may have protective effects on the AHI in OSA patients.

Health risk assessment of exposure to ambient formaldehyde in carpet manufacturing industries.

Formaldehyde is categorized as a definitive carcinogen by the International Agency for Research on Cancer. To the best of our knowledge, no study has assessed the health risks of occupational exposure of workers in carpet manufacturing plants to formaldehyde. Therefore, this study assesses the health risks of the occupational exposure to formaldehyde of 67 male workers in carpet manufacturing plants in Iran in 2022. Exposure to formaldehyde was quantitatively determined after collecting personal exposure samples from the workers' respiratory zone and spectrophotometric analysis based on method number 3500 of the National Institute of Occupational Safety and Health. In the next step, the carcinogenic and noncarcinogenic risks based on personal exposure to formaldehyde were evaluated. Sensitivity analyses were employed using the Monte Carlo simulation method. The mean inhalation exposure of workers to formaldehyde was 0.636 mg m-3. The inhalation cancer risk value based on the integrated risk information system for formaldehyde was 4.06×10-4 ± 3.17×10-5 (mean ± standard deviation), which exceeded the value reported by the US Environmental Protection Agency. An unacceptable carcinogenic risk level was found in 75.6% of workers. The highest mean inhalation cancer risk was 6.74×10-4 (i.e., 6.74 additional cases per 10,000 employees exposed) was found in sizing post employees. The hazard quotient of formaldehyde was 0.311±0.024. The formaldehyde concentration had a considerable effect on the health risk. The findings of this study provide valuable scientific information that supports the development of future policies to enhance the health status of employees in carpet manufacturing plants.

Psychometric Properties of the Traditional Chinese Version of the Stanford Presenteeism Scale (SPS-6) among Taiwanese Employees in Technology Companies.

Little attention has been paid by employers to reduced productivity at work due to illness (presenteeism) because valid instruments to measure presenteeism are lacking. We assessed psychometric properties of the traditional Chinese version of the six-item Stanford Presenteeism Scale (CSPS-6) among Taiwanese employees in technology companies. We carried out a cross-cultural adaptation study on 196 employees. Factor analyses were used to evaluate the construct validity of the CSPS-6. Cronbach's alpha was 0.74. The content validity of the CSPS-6 was good. Results of factor analyses confirmed the two-factor model of the CSPS-6. CSPS-6 scores were correlated with job stress (rs = −0.22, p = 0.002), the health status SF-36 (rs = 0.28 to 0.52, p < 0.0001), job satisfaction (rs = 0.41, p < 0.0001), and the presenteeism score of the Work Productivity and Activity Impairment Questionnaire: General Health (rs = −0.46, p < 0.0001). No correlations were found between presenteeism and the disability status (p = 0.19, F-value = 1.67, degrees of freedom = 2). The CSPS-6 was found to be reliable and valid in evaluating presenteeism of Taiwanese employees. Further studies should be undertaken to validate the CSPS-6 in other working populations and assess long-term effects of health problems associated with presenteeism.

Effects of antibiotics and metals on lung and intestinal microbiome dysbiosis after sub-chronic lower-level exposure of air pollution in ageing rats.

We investigated the effects of antibiotics, drugs, and metals on lung and intestinal microbiomes after sub-chronic exposure of low-level air pollution in ageing rats. Male 1.5-year-old Fischer 344 ageing rats were exposed to low-level traffic-related air pollution via whole-body exposure system for 3 months with/without high-efficiency particulate air (HEPA) filtration (gaseous vs. particulate matter with aerodynamic diameter of ≤2.5 µm (PM2.5) pollution). Lung functions, antibiotics, drugs, and metals in lungs were examined and linked to lung and fecal microbiome analyses by high-throughput sequencing analysis of 16 s ribosomal (r)DNA. Rats were exposed to 8.7 µg/m3 PM2.5, 10.1 ppb NO2, 1.6 ppb SO2, and 23.9 ppb O3 in average during the study period. Air pollution exposure decreased forced vital capacity (FVC), peak expiratory flow (PEF), forced expiratory volume in 20 ms (FEV20), and FEF at 25∼75% of FVC (FEF25-75). Air pollution exposure increased antibiotics and drugs (benzotriazole, methamphetamine, methyl-1 H-benzotriazole, ketamine, ampicillin, ciprofloxacin, pentoxifylline, erythromycin, clarithromycin, ceftriaxone, penicillin G, and penicillin V) and altered metals (V, Cr, Cu, Zn, and Ba) levels in lungs. Fusobacteria and Verrucomicrobia at phylum level were increased in lung microbiome by air pollution, whereas increased alpha diversity, Bacteroidetes and Proteobacteria and decreased Firmicutes at phylum level were occurred in intestinal microbiome. Lung function decline was correlated with increasing antibiotics, drugs, and metals in lungs as well as lung and intestinal microbiome dysbiosis. The antibiotics, drugs, and Cr, Co, Ca, and Cu levels in lung were correlated with lung and intestinal microbiome dysbiosis. The lung microbiome was correlated with intestinal microbiome at several phylum and family levels after air pollution exposure. Our results revealed that antibiotics, drugs, and metals in the lung caused lung and intestinal microbiome dysbiosis in ageing rats exposed to air pollution, which may lead to lung function decline.