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.

Prediction value of neutrophil and eosinophil count at risk of COPD exacerbation.

INTRODUCTION: Predicting acute exacerbations (AEs) in chronic obstructive pulmonary disease (COPD) is crucial. This study aimed to identify blood biomarkers for predicting COPD exacerbations by inflammatory phenotypes. MATERIALS AND METHODS: We analyzed blood cell counts and clinical outcomes in 340 COPD patients aged 20-90 years. Patients were categorized into eosinophilic inflammation (EOCOPD) and non-eosinophilic inflammation (N-EOCOPD) groups. Blood cell counts, eosinophil-to-lymphocyte ratio (ELR), neutrophil-to-lymphocyte ratio (NLR) and neutrophil-to-eosinophil ratio (NER) were calculated. Linear and logistic regression models assessed relationships between health outcomes and blood cell counts. RESULTS: EOCOPD patients had distinct characteristics compared to N-EOCOPD patients. Increased neutrophil % and decreased lymphocyte % were associated with reduced pulmonary function, worse quality of life and more exacerbations, but they did not show statistical significance after adjusting by age, sex, BMI, smoking status, FEV1% and patient's medication. Subgroup analysis revealed a 1.372-fold increase in the OR of AE for every 1 unit increase in NLR in EOCOPD patients (p < .05). In N-EOCOPD patients, every 1% increase in blood eosinophil decreased the risk of exacerbation by 59.6%. CONCLUSIONS: Our study indicates that distinct white blood cell profiles in COPD patients, with or without eosinophilic inflammation, can help assess the risk of AE in clinical settings.

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.

Climate change and mortality rates of COPD and asthma: A global analysis from 2000 to 2018.

BACKGROUND: Climate change plays a significant role in global health threats, particularly with respiratory diseases such as chronic obstructive pulmonary disease (COPD) and asthma, but the long-term global-scale impact of climate change on these diseases' mortality remains unclear. OBJECTIVE: This study aims to investigate the impact of climate change on the age-standardized mortality rates (ASMR) of COPD and asthma at national levels. METHODS: We used Global Burden of Disease (GBD) data of ASMR of COPD and asthma from 2000 to 2018. The climate change index was represented as the deviance percentage of temperature (DPT) and relative humidity (DPRH), calculated based on 19-year temperature and humidity averages. Annual temperature, RH, and fine particulate matter (PM2.5) levels in 185 countries/regions were obtained from ERA5 and the OECD's environmental statistics database. General linear mixed-effect regression models were used to examine the associations between climate change with the log of ASMR (LASMR) of COPD and asthma. RESULTS: After adjusting for annual PM2.5, SDI level, smoking prevalence, and geographical regions, a 0.26% increase in DPT was associated with decreases of 0.016, 0.017, and 0.014 per 100,000 people in LASMR of COPD and 0.042, 0.046, and 0.040 per 100,000 people in LASMR of asthma for both genders, males, and females. A 2.68% increase in DPRH was associated with increases of 0.009 and 0.011 per 100,000 people in LASMR of COPD. We observed a negative association of DPT with LASMR for COPD in countries/regions with temperatures ranging from 3.8 to 29.9 °C and with LASMR for asthma ranging from -5.3-29.9 °C. However, we observed a positive association of DPRH with LASMR for both COPD and asthma in the RH range of 41.2-67.2%. CONCLUSION: Climate change adaptation and mitigation could be crucial in reducing the associated COPD and asthma mortality rates, particularly in regions most vulnerable to temperature and humidity fluctuations.

Climate-mediated air pollution associated with COPD severity.

Air pollution has been reported to be associated with chronic obstructive pulmonary disease (COPD). Our study aim was to examine the mediating effects of air pollution on climate-associated health outcomes of COPD patients. A cross-sectional study of 117 COPD patients was conducted in a hospital in Taiwan. We measured the lung function, 6-min walking distance, oxygen desaturation, white blood cell count, and percent emphysema (low attenuation area, LAA) and linked these to 0-1-, 0-3-, and 0-5-year lags of individual-level exposure to relative humidity (RH), temperature, and air pollution. Linear regression models were conducted to examine associations of temperature, RH, and air pollution with severity of health outcomes. A mediation analysis was conducted to examine the mediating effects of air pollution on the associations of RH and temperature with health outcomes. We observed that a 1 % increase in the RH was associated with increases in forced expiratory volume in 1 s (FEV1), eosinophils, and lymphocytes, and a decrease in the total-lobe LAA. A 1 °C increase in temperature was associated with decreases in oxygen desaturation, and right-, left-, and upper-lobe LAA values. Also, a 1 µg/m3 increase in PM2.5 was associated with a decrease in the FEV1 and an increase in oxygen desaturation. A 1 µg/m3 increases in PM10 and PM2.5 was associated with increases in the total-, right-, left, upper-, and lower-lobe (PM2.5 only) LAA. A one part per billion increase in NO2 was associated with a decrease in the FEV1 and an increase in the upper-lobe LAA. Next, we found that NO2 fully mediated the association between RH and FEV1. We found PM2.5 fully mediated associations of temperature with oxygen saturation and total-, right-, left-, and upper-lobe LAA. In conclusion, climate-mediated air pollution increased the risk of decreasing FEV1 and oxygen saturation and increasing emphysema severity among COPD patients. Climate change-related air pollution is an important public health issue, especially with regards to respiratory disease.