Under the background of climate change, the escalating air pollution and extreme weather events have been identified as risk factors for chronic respiratory diseases (CRD), causing serious public health burden worldwide. This review aims to summarize the effects of changed atmospheric environment caused by climate change on CRD. Results indicated an increased risk of CRD (mainly COPD, asthma) associated with environmental factors, such as air pollutants, adverse meteorological conditions, extreme temperatures, sandstorms, wildfire, and atmospheric allergens. Furthermore, this association can be modified by factors such as socioeconomic status, adaptability, individual behavior, medical services. Potential pathophysiological mechanisms linking climate change and increased risk of CRD involved pulmonary inflammation, immune disorders, oxidative stress. Notably, the elderly, children, impoverished groups and people in regions with limited adaptability are more sensitive to respiratory health risks caused by climate change. This review provides a reference for understanding risk factors of CRD in the context of climate change, and calls for the necessity of adaptive strategies. Further interdisciplinary research and global collaboration are needed in the future to enhance adaptability and address climate health inequality.
Climate Change ; Humans ; Air Pollution/adverse effects* ; Risk Factors ; Respiratory Tract Diseases/etiology* ; Chronic Disease ; Air Pollutants/adverse effects* ; Environmental Exposure/adverse effects*

BACKGROUND: Lead is a persistent inorganic environmental pollutant with global implication for human health. Among the diseases associated with lead exposure, the damage to the central nervous system has received considerable attention. It has been reported that long-term lead exposure increases the risk of meningioma; however, the underlying mechanism remains poorly understood. Clinical studies have indicated that loss-of-function and mutations in the neurofibromin-2 (NF2) gene play a crucial role in promoting meningioma formation. METHODS: The effect of Pb on meningioma were tested in-vitro and in-vivo. Two human meningioma cell lines were used in this study, including NF2-wildtype IOMM-Lee cell and NF2-null CH157-MN cell. Cell viability, cell cycle and cell size were examined after Pb exposure. The expression of Merlin, mammalian sterile 20-like kinases 1 and 2 (MST1/2) and Yes-associated protein (YAP) from these two meningioma cells were analyzed by Western blot. A xenograft mouse model was constructed by subcutaneous injection of IOMM-Lee meningioma cells. RESULTS: This study demonstrated that treatment with lead induce dose-dependent proliferation in IOMM-Lee cell (with an EC₅₀ value of 19.6 µM). Moreover, IOMM-Lee cell exhibited augmented cell size in conjunction with elevated levels of phosphorylated histone H3, indicative of altered cell cycle progression resulting from lead exposure. However, no significant change was observed in the CH157-MN cell. Additionally, the Merlin-Hippo signaling pathway was inactivated with decreased Merlin and phosphorylation levels of MST1/2 and YAP, leading to increased YAP nuclear translocation in IOMM-Lee cells. However, there was no change in the Merlin-Hippo signaling pathway in CH157-MN cells after lead treatment. The administration of Pb resulted in an acceleration of the subcutaneous IOMM-Lee meningioma xenograft growth in mice. CONCLUSIONS Overall, the current study elucidates the potential mechanism by which lead exposure promotes the proliferation of meningioma with NF2 expression for the first time.
Meningioma/genetics* ; Neurofibromin 2/genetics* ; Humans ; Cell Proliferation/drug effects* ; Animals ; Signal Transduction/drug effects* ; Mice ; Hippo Signaling Pathway ; Lead/adverse effects* ; Cell Line, Tumor ; Protein Serine-Threonine Kinases/genetics* ; Meningeal Neoplasms ; Environmental Pollutants/adverse effects* ; Female

BACKGROUND: There is growing evidence that the occurrence and severity of respiratory diseases in children are related to the concentration of air pollutants. Nonetheless, evidence regarding the association between short-term exposure to air pollution and outpatient visits for respiratory diseases in children remains limited. Outpatients cover a wide range of disease severity, including both severe and mild cases, some of which may need to be transferred to inpatient treatment. This study aimed to quantitatively evaluate the impact of short-term ambient air pollution exposure on outpatient visits for respiratory conditions in children. METHODS: This study employed data of the Second People's Hospital of Yichang from January 1, 2016 to December 31, 2023, to conduct a time series analysis. The DLNM approach was integrated with a generalized additive model to examine the daily outpatient visits of pediatric patients with respiratory illnesses in hospital, alongside air pollution data obtained from monitoring stations. Adjustments were made for long-term trends, meteorological variables, and other influencing factors. RESULTS: A nonlinear association was identified between PM_2.5, PM₁₀, O₃, NO₂, SO₂, CO levels and the daily outpatient visits for respiratory diseases among children. All six pollutants exhibit a hysteresis impact, with varying durations ranging from 4 to 6 days. The risks associated with air pollutants differ across various categories of children's respiratory diseases; notably, O₃ and CO do not show statistical significance concerning the risk of chronic respiratory conditions. Furthermore, the results of infectious respiratory diseases were similar with those of respiratory diseases. CONCLUSIONS Our results indicated that short-term exposure to air pollutants may contribute to an increased incidence of outpatient visits for respiratory illnesses among children, and controlling air pollution is important to protect children's health.
Humans ; China/epidemiology* ; Air Pollutants/analysis* ; Respiratory Tract Diseases/chemically induced* ; Child ; Child, Preschool ; Environmental Exposure/adverse effects* ; Air Pollution/analysis* ; Infant ; Male ; Particulate Matter/adverse effects* ; Female ; Ambulatory Care/statistics & numerical data* ; Outpatients/statistics & numerical data* ; Adolescent ; Infant, Newborn

BACKGROUND: Previous studies have demonstrated that short-term exposure to ambient particulate matter elevates the risk of ischemic stroke in major urban areas of various countries. However, there is a notable gap in research focusing on remote areas inhabited by ethnic minorities and the cumulative effects of air pollutants. Our study conducted in the area aims to explore the potential association between ischemic stroke and air pollutants and contribute to improving health outcomes among the community. METHODS: This retrospective observational study was conducted at the Xing'an League People's Hospital in Inner Mongolia. The medical records of 4,288 patients admitted for IS between November 1, 2019, and October 31, 2020, were reviewed. Data on demographics (age and sex), air pollutants (PM₁₀, PM_2.5, NO₂, NO, CO, and O₃), and meteorological factors (daily average temperature, daily average wind speed, and daily average atmosphere pressure) were collected and analyzed. The statistical analysis included descriptive statistics, Poisson distribution analysis to evaluate the adverse effects of atmospheric pollutants on daily hospitalizations, and subgroup analysis to determine whether gender and age could modify the impact on hospitalizations. RESULTS: A substantial correlation was revealed in single-day lags model. The peak delayed effects of PM₁₀, PM_2.5, SO₂, and NO₂ were observed at lag8 (PM₁₀ (OR = 1.016, 95%CI 1.002, 1.030), PM_2.5 (OR = 1.027, 95%CI 1.007, 1.048), SO₂ (OR = 1.153, 95%CI 1.040, 279) and NO₂ (OR = 1.054, 95%CI 1.005, 1.105)) while males exhibited a consistent trend from lag0 to lag8 (PM₁₀ (OR = 1.035, 95%CI 1.018, 1.053), PM_2.5 (OR = 1.056, 95%CI 1.030, 1.082), SO₂ (OR = 1.220, 95%CI 1.072, 1.389), NO₂ (OR = 1.126, 95%CI 1.061, 1.120), CO (OR = 10.059, 95%CI 1.697, 59.638) and O₃ (OR = 0.972, 95%CI 0.946, 0.999)). When gender and age were considered, a positive impact was also observed after three days cumulative effect in males. CONCLUSIONS There is a significant cumulative effect of exposure to air pollution on IS hospital admissions, especially the males and patients under the age of 65. Our results also suggested that a notable association between CO and NO₂ in two-pollutant models.
Humans ; Male ; Female ; Air Pollution/analysis* ; China/epidemiology* ; Retrospective Studies ; Middle Aged ; Air Pollutants/analysis* ; Aged ; Particulate Matter/analysis* ; Hospitalization/statistics & numerical data* ; Adult ; Ischemic Stroke/chemically induced* ; Environmental Exposure/adverse effects* ; Aged, 80 and over

In Japan, during the high economic growth period (1950-1960s), air pollution due to sulfur dioxide (SO₂) and dust derived from large-scale factories and power plants was apparent in many industrial districts, and it caused serious health problems such as the so-called "Yokkaichi Asthma." Many epidemiological studies have revealed the relationship between air pollution and respiratory diseases, and have provided scientific evidence for the regulatory control of air pollution. The concentration of SO₂ has markedly decreased since the 1970s, and its adverse health effects have improved. In contrast, increased automobile traffic has caused considerable traffic-related air pollution, including nitrogen oxides (NOx) and particulate matter (PM). Epidemiological studies in Chiba and Tokyo revealed that the prevalence and incidence of asthma were significantly higher among individuals living in roadside areas than among those living in other areas. Large-scale epidemiological studies conducted in urban districts have revealed an association between traffic-related air pollution and the onset of asthma in schoolchildren and persistence of asthmatic symptoms in preschool children. Thereafter, the concentrations of NOx and PM gradually decreased due to the control measures based on the Automobile NOx/PM Law enforced in 2001. Thus, epidemiological studies have contributed to a reduction in air pollution caused by automobile exhaust emissions. Recently, the adverse health effects of ambient fine PM (PM_2.5) and ozone (O₃) at ground level have become an international concern. Our epidemiological studies showed that short-term exposure to considerably low concentrations of PM_2.5 and O₃ was associated with a decrease in pulmonary function among asthmatic children and increased airway inflammation in healthy adolescents. The effects of exposure to PM_2.5 during pregnancy and early childhood on children's development have also been reported. These air pollutants consist of not only emissions from primary sources but also secondary formations in the atmosphere. They are affected by climate change and spread worldwide. Air quality control measures and climate change adaptation and mitigation strategies are synergistic, and will have co-benefits on human health. Therefore, global efforts are required to protect populations from the health risks posed by these air pollutants.
Japan/epidemiology* ; Humans ; Air Pollution/analysis* ; Air Pollutants/adverse effects* ; Particulate Matter/adverse effects* ; Asthma/chemically induced* ; Vehicle Emissions ; Epidemiologic Studies ; Environmental Exposure/adverse effects* ; Sulfur Dioxide/analysis*

BACKGROUND: Evidence on the combined effects of air pollutants and greenspace exposure on pulmonary tuberculosis (PTB) treatment is limited, particularly in developing countries with high levels of air pollution. OBJECTIVE: We aimed to examine the individual and combined effects of long-term exposure to air pollutants on PTB treatment outcomes while also investigating the potential modifying effect of greenspace. METHODS: This population-based study included 82,784 PTB cases notified in Zhejiang Province, China, from 2015 to 2019. The 24-month average concentrations of particulate matter with an aerodynamic diameter ≤2.5 µm (PM_2.5), ozone (O₃), nitrogen dioxide (NO₂), and sulfur dioxide (SO₂) before PTB diagnosis were estimated using a dataset derived from satellite-based machine learning models and monitoring stations. Greenspace exposure was assessed using the annual China Land Cover Dataset. We conducted analyses using time-varying Cox proportional hazards models and cumulative risk indices. RESULTS: In individual effect models, each 10 µg/m³ increase in PM_2.5, NO₂, O₃, and SO₂ concentrations was associated with hazard ratios for PTB treatment success of 0.95 (95% confidence interval (CI): 0.93-0.97), 0.92 (95% CI: 0.91-0.94), 0.98 (95% CI: 0.97-0.99), and 1.52 (95% CI: 1.49-1.56), respectively. In combined effect models, long-term exposure to the combination of air pollutants was negatively associated with PTB treatment success, with a joint hazard ratio (JHR) of 0.79 (95% CI: 0.63-0.96). Among the pollutants examined, O₃ contributed the most to the increased risks, followed by PM_2.5 and NO₂. Additionally, areas with moderate levels of greenspace showed a reduced risk (JHR = 0.81, 95% CI: 0.62-0.98) compared with the estimate from the third quantile model (JHR = 0.68, 95% CI: 0.52-0.83). CONCLUSIONS Combined air pollutants significantly impede successful PTB treatment outcomes, with O₃ and PM_2.5 accounting for nearly 75% of this detrimental effect. Moderate levels of greenspace can mitigate the adverse effects associated with combined air pollutants, leading to improved treatment success for patients with PTB.
Humans ; China/epidemiology* ; Air Pollutants/analysis* ; Tuberculosis, Pulmonary/drug therapy* ; Particulate Matter/adverse effects* ; Male ; Female ; Middle Aged ; Environmental Exposure/analysis* ; Ozone/adverse effects* ; Adult ; Sulfur Dioxide/adverse effects* ; Treatment Outcome ; Air Pollution/adverse effects* ; Aged ; Nitrogen Dioxide/adverse effects* ; Young Adult ; Adolescent

BACKGROUND: Recent studies have provided compelling evidence that exposure to brominated flame retardants (BFRs) can adversely affect human health. We aim to explore the potential impact of BFRs on adiposity and central obesity. METHODS: Data from the National Health and Nutrition Examination Surveys (NHANES) cycles conducted between 2009 and 2014 was used to study the connections between variables. After filtering, we analyzed a sample of 4,110 adults aged 20 years and above. Our goal was to examine the potential association between BFRs and consequences and investigate the part played by oxidative stress and inflammatory markers as intermediaries. To achieve this, we used advanced statistical methods such as weighted quantile sum (WQS) regression, quantile-based g-computation (QGC), and the Bayesian kernel machine regression (BKMR). RESULTS: The findings showed that among the examined chemicals, exposure to PBDE85 (weight: 41%), PBDE100 (24%), and PBB153 (23%) may be the dominant contributors to general obesity risk. Upon controlling for all variables that could impact the results, it was found that the QGC outcomes indicated a positive correlation between exposure to mixtures of brominated flame retardants and the occurrence of abdominal obesity (OR = 1.187, 95% CI: 1.056-1.334, p = 0.004). Significant contributions were made by PBDE85 (52%), PBB153 (27%), and PBDE100 (21%). Mediation analysis shows that lymphatic cells (LC) and albumin (ALB) partially mediate the link between brominated flame retardants and obesity. The results of BKMR are generally consistent with those of WQS and QGC. CONCLUSION At a population level, our research has revealed a noteworthy correlation between BFRs and obesity. However, further investigation is required through prospective cohort studies and in-depth mechanistic exploratory studies.
Humans ; Flame Retardants/adverse effects* ; Oxidative Stress/drug effects* ; Adult ; Male ; Female ; Middle Aged ; Inflammation/epidemiology* ; Obesity/chemically induced* ; Biomarkers/blood* ; Nutrition Surveys ; Mediation Analysis ; Young Adult ; United States/epidemiology* ; Environmental Exposure/adverse effects* ; Aged ; Environmental Pollutants/adverse effects* ; Halogenated Diphenyl Ethers/adverse effects*

BACKGROUND: Previous evidence showed that ambient air pollution and cardiovascular mortality are related. However, there is a lack of evidence towards the modification effect of long-term lifestyle on the association between short-term ambient air pollution and death from cardiovascular events. METHOD: A total of 14,609 death from major adverse cardiovascular events (MACE) were identified among the China Kadoorie Biobank participants from 2013 to 2018. Ambient air pollution exposure including particulate matter 2.5 (PM_2.5), SO₂, NO₂, CO, and O₃ from the same period were obtained from space-time model reconstructions based on remote sensing data. Case-crossover design and conditional logistic regression was applied to estimate the effect of short-term exposure to air pollutants on MACE mortality. RESULTS: We found MACE mortality was significantly associated with PM_2.5 (relative percent increase 2.91% per 10 µg/m³ increase, 95% CI 1.32-4.53), NO₂ (5.37% per 10 µg/m³ increase, 95% CI 1.56-9.33), SO₂ (6.82% per 10 µg/m³ increase, 95% CI 2.99-10.80), and CO (2.24% per 0.1 mg/m³ increase, 95% CI 1.02-3.48). Stratified analyses indicated that drinking was associated with elevated risk of MACE mortality with NO₂ and SO₂ exposure; physical inactivity was associated with higher risk of death from MACE when exposed to PM_2.5; and people who had balanced diet had lower risk of MACE mortality when exposed to CO and NO₂. CONCLUSIONS The study results showed that short-term exposure to ambient PM_2.5, NO₂, SO₂, and CO would aggravate the risk of cardiovascular mortality, yet healthy lifestyle conduct might mitigate such negative impact to some extent.
Humans ; Cardiovascular Diseases/epidemiology* ; China/epidemiology* ; Male ; Female ; Air Pollution/adverse effects* ; Middle Aged ; Air Pollutants/analysis* ; Particulate Matter/analysis* ; Environmental Exposure/adverse effects* ; Life Style ; Aged ; Adult ; Risk Factors ; Cross-Over Studies ; East Asian People

BACKGROUND: Depression among older adults is an important public health issue, and air and noise pollution have been found to contribute to exacerbation of depressive symptoms. This study examined the association of exposure to air and noise pollutants with clinically-newly-diagnosed depressive disorder. The mediating role of individual pro-inflammatory markers was explored. METHODS: We linked National Health Insurance claim data with 2998 healthy community-dwellers aged 55 and above who participated in the Healthy Aging Longitudinal Study between 2009 and 2013. Newly diagnosed depressive disorder was identified using diagnostic codes from the medical claim data. Pollutants were estimated using nationwide land use regression, including PM_2.5 and PM₁₀, carbon monoxide, ozone, nitrogen dioxide, sulfur dioxide, and road traffic noise. Cox proportional hazard models were employed to examine the association between pollutants and newly developed depressive disorders. The mediating effect of serum pro-inflammatory biomarkers on the relationship was examined. RESULTS: Among the 2998 participants, 209 had newly diagnosed depressive disorders. In adjusted Cox proportional hazard models, one interquartile range increase in PM_2.5 (8.53 µg/m³) was associated with a 17.5% increased hazard of developing depressive disorders. Other air pollutants and road traffic noise were not linearly associated with depressive disorder incidence. Levels of serum tumor necrosis factor receptor 1 mediated the relationship between PM_2.5 and survival time to newly onset depressive disorder. CONCLUSION PM_2.5 is related to an increased risk of newly developed depressive disorder among middle-aged and older adults, and the association is partially mediated by the pro-inflammatory marker TNF-R1.
Humans ; Particulate Matter/analysis* ; Male ; Female ; Middle Aged ; Longitudinal Studies ; Aged ; Incidence ; Air Pollutants/analysis* ; Environmental Exposure/adverse effects* ; Taiwan/epidemiology* ; Receptors, Tumor Necrosis Factor, Type I/blood* ; Proportional Hazards Models ; Biomarkers/blood* ; Depression/epidemiology* ; Aged, 80 and over ; Depressive Disorder/chemically induced* ; Risk Factors ; Air Pollution/adverse effects*

BACKGROUND: The objective of this study was to investigate the potential link between myopia in adolescents and exposure to per- and polyfluoroalkyl substances (PFASs). METHODS: This investigation included 1971 subjects with accessible PFAS level data, myopia status, and associated variables from four cycles of the National Health and Nutritional Examination Survey (NHANES). The investigation focused on specific PFAS compounds found in the serum, including perfluorohexane sulfonate (PFHxS), perfluorononanoic acid (PFNA), perfluorooctanoic acid (PFOA), and perfluorooctane sulfonic acid (PFOS), chosen for their frequent detection. Owing to the skewed nature of the PFAS level data, the PFAS levels were log-transformed (Ln-PFAS) prior to analysis. Logistic regression, restricted cubic spline modeling, subgroup analysis, and sensitivity analysis were used to examine the associations between exposure to PFASs and the onset of myopia. RESULTS: PFOA levels were significantly associated with myopia risk (OR: 1.33; 95% CI: 1.05-1.69; P = 0.019). More specifically, with respect to the first quartile, the second quartile (OR_Q2: 1.69; 95% CI: 1.16-2.46; P = 0.007), third quartile (OR_Q3: 1.45; 95% CI: 1.03-2.03; P = 0.035), and highest quartile (OR_Q4: 1.58; 95% CI: 1.12-2.21; P = 0.010) of participants presented with increased myopia risk. Mediation analysis revealed that PFOA and myopia risk were partially mediated by serum albumin (ALB), with a mediation percentage of 22.48% (P = 0.008). A nonlinear inverted U-shaped relationship was identified between the level of PFOA and myopia risk (P for nonlinearity = 0.005). CONCLUSION Our findings suggest a potential link between exposure to PFOA and the likelihood of myopia development in young individuals and a mediating effect of serum ALB on this relationship. Notably, PFOA was identified as a key PFAS significantly contributing to the observed link between PFAS exposure and myopia risk. The potential threat of PFOA to myopia should be examined further.
Humans ; Fluorocarbons/adverse effects* ; Myopia/blood* ; Adolescent ; Male ; Female ; Prevalence ; Environmental Exposure/adverse effects* ; Nutrition Surveys ; Environmental Pollutants/adverse effects* ; United States/epidemiology* ; Alkanesulfonic Acids/blood* ; Caprylates/blood* ; Serum Albumin/metabolism* ; Child ; Sulfonic Acids