[Association between long-term exposure to ambient ozone and sperm quality in Shandong Province].

Objective: To evaluate the association between long-term exposure to ambient ozone (O3) and sperm quality. Methods: From January 1, 2014, to December 31, 2019, healthy sperm donors were recruited through the Human Sperm Bank of Shandong University Affiliated Reproductive Hospital. A total of 37 977 sperm donation data from 2 971 healthy volunteers were analyzed. The average annual O3 concentration (0.01°× 0.01°) was matched according to household address. A multivariate mixed-effect model was used to analyze the exposure-response relationship between the average O3 exposure concentration and sperm quality in the previous year, with each donor as a random intercept. All results were presented as % changes with 95% confidence intervals (CIs) for all sperm parameters associated with 10 µg/m3 increases in O3. The effects of individual characteristics on the association between O3 and sperm quality were evaluated by stratified analysis. Results: The average O3 concentration in the year before semen collection was (107.09±7.50) µg/m3. Each 10 µg/m3 increase in O3 was associated with declined sperm concentration (-3.12%, 95%CI:-4.55%, -1.67%), total sperm count (-5.21%, 95%CI:-7.28%, -3.09%), total sperm motility (-1.49%, 95%CI:-2.37%, -0.61%), progressive motility (-2.53%, 95%CI:-3.78%, -1.26%), total motile sperm count (-5.82%, 95%CI:-8.17%, -3.41%), and progressively motile sperm count (-6.22%, 95%CI:-8.73%, -3.64%). Men aged 30 and above, obese, and with lower education levels might be more susceptible to the influence of O3 on sperm quality, but the difference was not statistically significant (P>0.05). Conclusion: Long-term exposure to O3 in Shandong Province is associated with a decrease in sperm quality.

Research on the spatial and temporal patterns of ozone concentration and population health effects in the Central Plains Urban Agglomeration from 2017 to 2020.

Fine particulate matter (PM2.5) and near-surface ozone (O3) are the main atmospheric pollutants in China. Long-term exposure to high ozone concentrations adversely affects human health. It is of great significance to systematically analyze the spatiotemporal evolution mechanism and health effects of ozone pollution. Based on the ozone data of 91 monitoring stations in the Central Plains Urban Agglomeration from 2017 to 2020, the research used Kriging method and spatial autocorrelation analysis to investigate the spatiotemporal variations of ozone concentration. Additionally, the study assessed the health effects of ozone on the population using the population exposure risk model and exposure-response relationship model. The results indicated that: (1) The number of premature deaths caused by ozone pollution in the warm season were 37,053 at 95% confidence interval (95% CI: 28,190-45,930) in 2017, 37,685 (95% CI: 28,669-46,713) in 2018, and 37,655 (95% CI: 28,647-46,676) in 2019. (2) The ozone concentration of the Central Plains urban agglomeration showed a decreasing trend throughout the year and during the warm season from 2017 to 2020, there are two peaks monthly, one is June, and the other is September. (3) In the warm season, the high-risk areas of population exposure to ozone in the Central Plains Urban Agglomeration were mainly concentrated in urban areas. In general, the population exposure risk of the south is lower than that of the north. The number of premature deaths attributed to ozone concentration during the warm season has decreased, but some southern cities such as Xinyang and Zhumadian have also seen an increase in premature deaths. China has achieved significant results in air pollution control, but in areas with high ozone concentrations and high population density, the health burden caused by air pollution remains heavy, and stricter air pollution control policies need to be implemented.

Accumulation of Alpha-Synuclein and Increase in the Inflammatory Response in the substantia nigra, Jejunum, and Colon in a Model of O3 Pollution in Rats.

This work aimed to study the effect of repeated exposure to low doses of ozone on alpha-synuclein and the inflammatory response in the substantia nigra, jejunum, and colon. Seventy-two male Wistar rats were divided into six groups. Each group received one of the following treatments: The control group was exposed to air. The ozone groups were exposed for 7, 15, 30, 60, and 90 days for 0.25 ppm for four hours daily. Afterward, they were anesthetized, and their tissues were extracted and processed using Western blotting, immunohistochemistry, and qPCR. The results indicated a significant increase in alpha-synuclein in the substantia nigra and jejunum from 7 to 60 days of exposure and an increase in NFκB from 7 to 90 days in the substantia nigra, while in the jejunum, a significant increase was observed at 7 and 15 days and a decrease at 60 and 90 days for the colon. Interleukin IL-17 showed an increase at 90 days in the substantia nigra in the jejunum and increases at 30 days and in the colon at 15 and 90 days. Exposure to ozone increases the presence of alpha-synuclein and induces the loss of regulation of the inflammatory response, which contributes significantly to degenerative processes.

Maternal Exposure to Environmental Air Pollution and Premature Rupture of Membranes: Evidence from Southern China.

BACKGROUND Exposure to air pollution (AP) during pregnancy is associated with pre-labor rupture of membranes (PROM). However, there is limited research on this topic, and the sensitive exposure windows remain unclear. The present study assessed the association between AP exposure and the risk of PROM, as well as seeking to identify the sensitive time windows. MATERIAL AND METHODS This retrospective study analyzed 4276 pregnant women's data from Tongling Maternal and Child Health Hospital from 2020 to 2022. We obtained air pollution data, including particulate matter (PM) with an aerodynamic diameter of ≤2.5 µm (PM2․5), particulate matter with an aerodynamic diameter of ≤10 µm (PM10), nitrogen dioxide (NO2), and ozone (O3), from the Tongling Ecology and Environment Bureau. Demographic information was extracted from medical records. We employed a distributed lag model to identify the sensitive exposure windows of prenatal AP affecting the risk of PROM. We conducted a sensitivity analysis based on pre-pregnancy BMI. RESULTS We found a significant association between prenatal exposure to AP and increased PROM risk after adjusting for confounders, and the critical exposure windows of AP were the 6th to 7th months of pregnancy. In the underweight group, an increase of 10 µg/m³ in PM2․5 was associated with a risk of PROM, with an odds ratio (OR) of 1.48 (95% CI: 1.16, 1.89). Similarly, a 10 µg/m³ increase in PM10 was associated with a risk of PROM, with an OR of 1.45 (95% CI: 1.05, 1.77). CONCLUSIONS Prenatal exposure to AP, particularly during months 6-7 of pregnancy, is associated with an increased risk of PROM. This study extends and strengthens the evidence on the association between prenatal exposure to AP and the risk of PROM, specifically identifying the critical exposure windows.

Ozone pollution contributes to the yield gap for beans in Uganda, East Africa, and is co-located with other agricultural stresses.

Air quality negatively impacts agriculture, reducing the yield of staple food crops. While measured data on African ground-level ozone levels are scarce, experimental studies demonstrate the damaging impact of ozone on crops. Common beans (Phaseolus vulgaris), an ozone-sensitive crop, are widely grown in Uganda. Using modelled ozone flux, agricultural surveys, and a flux-effect relationship, this study estimates yield and production losses due to ozone for Ugandan beans in 2015. Analysis at this scale allows the use of localised data, and results can be presented at a sub-regional level. Soil nutrient stress, drought, flood risk, temperature and deprivation were also mapped to investigate where stresses may coincide. Average bean yield losses due to ozone were 17% and 14% (first and second growing season respectively), equating to 184 thousand tonnes production loss. However, for some sub-regions, losses were up to 27.5% and other crop stresses also coincided in these areas. This methodology could be applied widely, allowing estimates of ozone impact for countries lacking air quality and/or experimental data. As crop productivity is below its potential in many areas of the world, changing agricultural practices to mitigate against losses due to ozone could help to reduce the crop yield gap.

Inconsequential role for chemerin-like receptor 1 in the manifestation of ozone-induced lung pathophysiology in male mice.

We executed this study to determine if chemerin-like receptor 1 (CMKLR1), a Gi/o protein-coupled receptor expressed by leukocytes and non-leukocytes, contributes to the development of phenotypic features of non-atopic asthma, including airway hyperresponsiveness (AHR) to acetyl-ß-methylcholine chloride, lung hyperpermeability, airway epithelial cell desquamation, and lung inflammation. Accordingly, we quantified sequelae of non-atopic asthma in wild-type mice and mice incapable of expressing CMKLR1 (CMKLR1-deficient mice) following cessation of acute inhalation exposure to either filtered room air (air) or ozone (O3), a criteria pollutant and non-atopic asthma stimulus. Following exposure to air, lung elastic recoil and airway responsiveness were greater while the quantity of adiponectin, a multi-functional adipocytokine, in bronchoalveolar lavage (BAL) fluid was lower in CMKLR1-deficient as compared to wild-type mice. Regardless of genotype, exposure to O3 caused AHR, lung hyperpermeability, airway epithelial cell desquamation, and lung inflammation. Nevertheless, except for minimal genotype-related effects on lung hyperpermeability and BAL adiponectin, we observed no other genotype-related differences following O3 exposure. In summary, we demonstrate that CMKLR1 limits the severity of innate airway responsiveness and lung elastic recoil but has a nominal effect on lung pathophysiology induced by acute exposure to O3.

Exposure to Concurrent Heatwaves and Ozone Pollution and Associations with Mortality Risk: A Nationwide Study in China.

BACKGROUND: Concurrent extreme events are projected to occur more frequently under a changing climate. Understanding the mortality risk and burden of the concurrent heatwaves and ozone (O3) pollution may support the formulation of adaptation strategies and early warning systems for concurrent events in the context of climate change. OBJECTIVES: We aimed to estimate the mortality risk and excess deaths of concurrent heatwaves and O3 pollution across 250 counties in China. METHODS: We collected daily mortality, meteorological, and air pollution data for the summer (1 June to 30 September) during 2013-2018. We defined heatwaves and high O3 pollution days, then we divided the identified days into three categories: a) days with only heatwaves (heatwave-only event), b) days with only high O3 pollution (high O3 pollution-only event), and c) days with concurrent heatwaves and high O3 pollution (concurrent event). A generalized linear model with a quasi-Poisson regression was used to estimate the risk of mortality associated with extreme events for each county. Then we conducted a random-effects meta-analysis to pool the county-specific estimates to derive the overall effect estimates. We used mixed-effects meta-regression to identify the drivers of the heterogeneity. Finally, we estimated the excess death attributable to extreme events (heatwave-only, high O3 pollution-only, and concurrent events) from 2013 to 2020. RESULTS: A higher all-cause mortality risk was associated with exposure to the concurrent heatwaves and high O3 pollution than exposure to a heatwave-only or a high O3 pollution-only event. The effects of a concurrent event on circulatory and respiratory mortality were higher than all-cause and nonaccidental mortality. Sex and age significantly impacted the association of concurrent events and heatwave-only events with all-cause mortality. We estimated that annual average excess deaths attributed to the concurrent events were 6,249 in China from 2017 to 2020, 5.7 times higher than the annual average excess deaths attributed to the concurrent events from 2013 to 2016. The annual average proportion of excess deaths attributed to the concurrent events in the total excess deaths caused by three types of events (heatwave-only events, high O3 pollution-only events, and concurrent events) increased significantly in 2017-2020 (31.50%; 95% CI: 26.73%, 35.53%) compared with 2013-2016 (9.65%; 95% CI: 5.67%, 10.81%). Relative excess risk due to interaction revealed positive additive interaction considering the concurrent effect of heatwaves and high O3 pollution. DISCUSSION: Our findings may provide scientific basis for establishing a concurrent event early warning system to reduce the adverse health impact of the concurrent heatwaves and high O3 pollution. https://doi.org/10.1289/EHP13790.

Associations between long-term exposure to air pollution and kidney function utilizing electronic healthcare records: a cross-sectional study.

BACKGROUND: Chronic kidney disease (CKD) affects more than 38 million people in the United States, predominantly those over 65 years of age. While CKD etiology is complex, recent research suggests associations with environmental exposures. METHODS: Our primary objective is to examine creatinine-based estimated glomerular filtration rate (eGFRcr) and diagnosis of CKD and potential associations with fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) using a random sample of North Carolina electronic healthcare records (EHRs) from 2004 to 2016. We estimated eGFRcr using the serum creatinine-based 2021 CKD-EPI equation. PM2.5 and NO2 data come from a hybrid model using 1 km2 grids and O3 data from 12 km2 CMAQ grids. Exposure concentrations were 1-year averages. We used linear mixed models to estimate eGFRcr per IQR increase of pollutants. We used multiple logistic regression to estimate associations between pollutants and first appearance of CKD. We adjusted for patient sex, race, age, comorbidities, temporality, and 2010 census block group variables. RESULTS: We found 44,872 serum creatinine measurements among 7,722 patients. An IQR increase in PM2.5 was associated with a 1.63 mL/min/1.73m2 (95% CI: -1.96, -1.31) reduction in eGFRcr, with O3 and NO2 showing positive associations. There were 1,015 patients identified with CKD through e-phenotyping and ICD codes. None of the environmental exposures were positively associated with a first-time measure of eGFRcr < 60 mL/min/1.73m2. NO2 was inversely associated with a first-time diagnosis of CKD with aOR of 0.77 (95% CI: 0.66, 0.90). CONCLUSIONS: One-year average PM2.5 was associated with reduced eGFRcr, while O3 and NO2 were inversely associated. Neither PM2.5 or O3 were associated with a first-time identification of CKD, NO2 was inversely associated. We recommend future research examining the relationship between air pollution and impaired renal function.

Association of ambient ozone exposure and greenness exposure with hemorrhagic stroke mortality at different times: A cohort study in Shandong Province, China.

Evidence on the association between long-term ozone exposure and greenness exposure and hemorrhagic stroke (HS) is limited, with mixed results. One potential source of this inconsistency is the difference in exposure time metrics. This study aimed to investigate the association between long-term exposure to ambient ozone, greenness, and mortality from HS using exposure metrics at different times. We also examined whether greenness exposure modified the relationship between ozone exposure and mortality due to HS. The study population consisted of 45771 participants aged ≥40 y residing in 20 counties in Shandong Province who were followed up from 2013 to 2019. Ozone exposure metrics (annual mean and warm season) and the normalized difference a measure of greenness exposure, were calculated. The relationship between environmental exposures (ozone and greenness exposures) and mortality from HS was assessed using time-dependent Cox proportional hazards models, and the modification of greenness exposure was examined using stratified analysis with interaction terms. The person-years at the end of follow-up were 90,663. With full adjustments, the risk of death from hemorrhagic stroke increased by 5% per interquartile range increase in warm season ozone [hazard ratio =1.05; 95 % confidence interval: 1.01-1.08]. No clear association was observed between annual ozone and mortality HS. Both the annual and summer NDVI were found to reduce the risk of HS mortality. The relationships were influenced by age, sex, and residence (urban or rural). Furthermore, greenness exposure was shown to have a modifying effect on the relationship between ozone exposure and the occurrence of HS mortality (P for interaction = 0.001). Long-term exposure to warm season O3 was positively associated with HS mortality, while greenness exposure was inversely associated with HS mortality. Greenness exposure may mitigate the negative effects of warm season ozone exposure on HS mortality.

Sex differences and dietary patterns in the association of air pollutants and hypertension.

BACKGROUND: Hypertension is one of the major public health problems in China. Limited evidence exists regarding sex differences in the association between hypertension and air pollutants, as well as the impact of dietary factors on the relationship between air pollutants and hypertension. The aim of this study was to investigate the sex-specific effects of dietary patterns on the association between fine particulate matter (PM2.5), ozone(O3) and hypertension in adults residing in Jiangsu Province of China. METHODS: A total of 3189 adults from the 2015 China Adult Chronic Disease and Nutrition Surveillance in Jiangsu Province were included in this study. PM2.5 and O3 concentrations were estimated using satellite space-time models and assigned to each participant. Dietary patterns were determined by reduced rank regression (RRR), and multivariate logistic regression was used to assess the associations of the obtained dietary patterns with air pollutants and hypertension risk. RESULTS: After adjusting for confounding variables, we found that males were more sensitive to long-term exposure to PM2.5 (Odds ratio (OR) = 1.42 95%CI:1.08,1.87), and females were more sensitive to long-term exposure to O3 (OR = 1.61 95%CI:1.15,2.23). Traditional southern pattern identified through RRR exhibited a protective effect against hypertension in males (OR = 0.73 95%CI: 0.56,1.00). The results of the interaction between dietary pattern score and PM2.5 revealed that adherence to traditional southern pattern was significantly associated with a decreased risk of hypertension in males (P < 0.05), while no significant association was observed among females. CONCLUSIONS: Our findings suggested that sex differences existed in the association between dietary patterns, air pollutants and hypertension. Furthermore, we found that adherence to traditional southern pattern may mitigate the risk of long-term PM2.5 exposure-induced hypertension in males.

Association between ambient air pollution and age-related macular degeneration: a meta-analysis.

BACKGROUND: Several epidemiological studies have investigated the association between ambient air pollution and age-related macular degeneration (AMD). However, a consensus has not yet been reached. Our meta-analysis aimed to clarify this association. METHODS: Databases, including PubMed, EMBASE, and Web of Science, were searched for relevant studies from 01 January 2000 to 30 January 2024. English-language, peer-reviewed studies using cross-sectional, prospective, or retrospective cohorts and case-control studies exploring this relationship were included. Two authors independently extracted data and assessed study quality. A random-effects model was used to calculate pooled covariate-adjusted odds ratios. Heterogeneity across studies was also tested. RESULTS: We identified 358 relevant studies, of which eight were included in the meta-analysis. Four studies evaluated the association between particulate matter less than 2.5 µm in diameter (PM2.5) and AMD, and three studies explored the relationship between nitrogen dioxide (NO2) or ozone (O3) and AMD. The pooled odds ratios were 1.16 (95% confidence interval [CI]: 1.11-1.21), 1.17 (95% CI: 1.09-1.25), and 1.06 (95% CI: 1.05-1.07), respectively. CONCLUSION: Current evidence suggests a concomitant positive but not causal relationship between PM2.5, NO2, or O3 and AMD risk.

Pre-pregnancy ozone and ultrafine particulate matter exposure during second year of life associated with decreased cognitive and adaptive functioning at aged 2-5 years.

BACKGROUND: This study sought to investigate the association of prenatal and early life exposure to a mixture of air pollutants on cognitive and adaptive outcomes separately in children with or without autism spectrum disorder (ASD). METHODS: Utilizing data from the CHARGE case-control study (birth years: 2000-2016), we predicted daily air concentrations of NO2, O3, and particulate matter <0.1 µm (PM0.1), between 0.1 and 2.5 µm (PM0.1-2.5), and between 2.5 and 10 µm (PM2.5-10) using chemical transport models with ground-based monitor adjustments. Exposures were evaluated for pre-pregnancy, each trimester, and the first two years of life. Individual and combined effects of pollutants were assessed with Vineland Adaptive Behavior Scales (VABS) and Mullen Scales of Early Learning (MSEL), separately for children with ASD (n = 660) and children without ASD (typically developing (TD) and developmentally delayed (DD) combined; n = 753) using hierarchical Bayesian Kernel Machine Regression (BKMR) models with three groups: PM size fractions (PM0.1, PM0.1-2.5, PM2.5-10), NO2, and O3. RESULTS: Pre-pregnancy Ozone was strongly negatively associated with all scores in the non-ASD group (group posterior inclusion probability (gPIP) = 0.83-1.00). The PM group during year 2 was also strongly negatively associated with all scores in the non-ASD group (gPIP = 0.59-0.93), with PM0.1 driving the group association (conditional PIP (cPIP) = 0.73-0.96). Weaker and less consistent associations were observed between PM0.1-2.5 during pre-pregnancy and ozone during year 1 and VABS scores in the ASD group. CONCLUSIONS: These findings prompt further investigation into ozone and ultrafine PM as potential environmental risk factors for neurodevelopment.

Long-term exposure to air pollution and precocious puberty in South Korea.

BACKGROUND AND AIM: The increasing prevalence of precocious puberty (PP) has emerged as a significant medical and social problem worldwide. However, research on the relationship between long-term air pollution exposure and PP has been relatively limited. We thus investigated the association between long-term air pollution exposure and the onset of PP in South Korea. METHODS: We investigated a retrospective cohort using the Korea National Health Insurance Database. Six-year-old children born from 2007 to 2009 were examined (2013-2015). We included boys ≤10 years and girls aged ≤9 years who visited hospitals for early pubertal development, were diagnosed with PP per the ICD-10 (E228, E301, and E309), and received gonadotropin-releasing hormone agonist treatment. We analyzed data for boys up until 10 years old (60-month follow-up) and for girls up to 9 years old (48-month follow-up). We assessed the association between long-term air pollution exposure and the onset of PP using a Cox proportional hazard model. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) per 1 µg/m3 increase in fine particulate matter (PM2.5) and particulate matter (PM10) and per 1 ppb increase in sulfur dioxide (SO2), nitrogen dioxide (NO2), and ozone (O3). RESULTS: This study included 1,205,784 children aged six years old between 2013 and 2015. A positive association was found between the 48-month moving average PM2.5 (HR: 1.019; 95% CI: 1.012, 1.027), PM10 (HR: 1.009; 95% CI: 1.006, 1.013), SO2 (HR: 1.037; 95% CI: 1.018, 1.055), and O3 (HR: 1.006; 95% CI: 1.001, 1.010) exposure and PP in girls but not boys. CONCLUSIONS: This study provides valuable insights into the harmful effects of air pollution during childhood and adolescence, emphasizing that air pollution is a risk factor that should be managed and reduced.

Long-term exposure to ambient ozone and adult-onset asthma: A prospective cohort study.

BACKGROUND: The association between long-term exposure to ozone (O3) and adult-onset asthma (AOA) remains inconclusive, and analysis of causality is lacking. OBJECTIVES: To examine the causal association between long-term O3 exposure and AOA. METHODS: A prospective cohort study of 362,098 participants was conducted using the UK Biobank study. Incident cases of AOA were identified using health administrative data of the National Health Services. O3 exposure at participants' residential addresses was estimated by a spatio-temporal model. Instrumental variable (IV) modelling was used to analyze the causal association between O3 exposure and AOA, by incorporating wind speed and planetary boundary layer height as IVs into time-dependent Cox model. Negative control outcome (accidental injury) was also used to additionally evaluate unmeasured confounding. RESULTS: During a mean follow-up of 11.38 years, a total of 10,973 incident AOA cases were identified. A U-shaped concentration-response relationship was observed between O3 exposure and AOA in the traditional Cox models with HR of 0.916 (95% CI: 0.888, 0.945) for O3 at low levels (<38.17 ppb), and 1.204 (95% CI: 1.168, 1.242) for O3 at high levels (≥38.17 ppb). However, in the IV analysis we only found a statistically significant association between high-level O3 exposure and AOA risk, but not for low-level O3 exposure. No significant associations between O3 exposure and accidental injury were observed. CONCLUSION: Our findings suggest a potential causal relationship between long-term exposure to high-level ambient O3 and increased risks of AOA.

Warm season ambient ozone and children's health in the USA.

BACKGROUND: Over 120 million people in the USA live in areas with unsafe ozone (O3) levels. Studies among adults have linked exposure to worse lung function and higher risk of asthma and chronic obstructive pulmonary disease (COPD). However, few studies have examined the effects of O3 in children, and existing studies are limited in terms of their geographic scope or outcomes considered. METHODS: We leveraged a dataset of encounters at 42 US children's hospitals from 2004-2015. We used a one-stage case-crossover design to quantify the association between daily maximum 8-hour O3 in the county in which the hospital is located and risk of emergency department (ED) visits for any cause and for respiratory disorders, asthma, respiratory infections, allergies and ear disorders. RESULTS: Approximately 28 million visits were available during this period. Per 10 ppb increase, warm-season (May through September) O3 levels over the past three days were associated with higher risk of ED visits for all causes (risk ratio [RR]: 0.3% [95% confidence interval (CI): 0.2%, 0.4%]), allergies (4.1% [2.5%, 5.7%]), ear disorders (0.8% [0.3%, 1.3%]) and asthma (1.3% [0.8%, 1.9%]). When restricting to levels below the current regulatory standard (70 ppb), O3 was still associated with risk of ED visits for all-cause, allergies, ear disorders and asthma. Stratified analyses suggest that the risk of O3-related all-cause ED visits may be higher in older children. CONCLUSIONS: Results from this national study extend prior research on the impacts of daily O3 on children's health and reinforce the presence of important adverse health impacts even at levels below the current regulatory standard in the USA.

The role of liver enzymes in the association between ozone exposure and diabetes risk: a cross-sectional study of Zhuang adults in China.

Background: Growing evidence has demonstrated the role of ambient air pollutants in driving diabetes incidence. However, epidemiological evidence linking ozone (O3) exposure to diabetes risk has been scarcely studied in Zhuang adults in China. We aimed to investigate the associations of long-term exposure to O3 with diabetes prevalence and fasting plasma glucose (FPG) and estimate the mediating role of liver enzymes in Zhuang adults. Methods: We recruited 13 843 ethnic minority adults during 2018-2019 based on a cross-sectional study covering nine districts/counties in Guangxi. Generalized linear mixed models were implemented to estimate the relationships between O3 exposure and diabetes prevalence and FPG. Mediation effect models were constructed to investigate the roles of liver enzymes in the associations of O3 exposure with diabetes prevalence and FPG. Subgroup analyses were conducted to identify potential effect modifications. Results: Long-term exposure to O3 was positively associated with diabetes prevalence and FPG levels in Zhuang adults, with an excess risk of 7.32% (95% confidence interval [CI]: 2.56%, 12.30%) and an increase of 0.047 mmol L-1 (95% CI: 0.032, 0.063) for diabetes prevalence and FPG levels, respectively, for each interquartile range (IQR, 1.18 µg m-3) increment in O3 concentrations. Alanine aminotransferase (ALT) significantly mediated 8.10% and 29.89% of the associations of O3 with FPG and diabetes prevalence, respectively, and the corresponding mediation proportions of alkaline phosphatase (ALP) were 8.48% and 30.00%. Greater adverse effects were observed in females, obese subjects, people with a low education level, rural residents, non-clean fuel users, and people with a history of stroke and hypertension in the associations of O3 exposure with diabetes prevalence and/or FPG levels (all P values for interaction < 0.05). Conclusion: Long-term exposure to O3 is related to an increased risk of diabetes, which is partially mediated by liver enzymes in Chinese Zhuang adults. Promoting clean air policies and reducing exposure to environmental pollutants should be a priority for public health policies geared toward preventing diabetes.

Associations of ambient ozone exposure and CD4+ T cell levels with mortality among people living with HIV: An eight-year longitudinal study.

There has been a consistent upward trend in ground-level ozone (O3) concentration in China. People living with HIV (PLWH) may be more vulnerable to the health impacts of O3 exposure due to their immunosuppressed state. This study aims to investigate the association between ambient O3 exposure and mortality among PLWH, as well as the potential exacerbating effects of a decreased CD4+ T cell level. Daily maximum 8-hour O3 concentrations were assigned to 7270 PLWH at a county level in Guangxi, China. Every 10-unit increase in ambient O3 concentration was associated with a significant rise in all-cause mortality ranging from 7.3 % to 28.7 % and a significant rise in AIDS-related mortality ranging from 8.4 % to 14.5 %. When PLWH had a higher CD4+ count (≥350 cells/µL), elevated O3 concentration was associated with increased blood CD4+ count at lag0 [percent change with 95 % confidence interval, 0.20(0.00, 0.40)], lag1 [0.26(0.06, 0.47)], and lag2 [0.23(0.03, 0.44)]; however, an opposite association was observed when CD4+ count was <350 cells/µL for half-year average [-2.45(-4.71, -0.14)] and yearly average [-3.42(-5.51, -1.29)] of O3 exposure. The association of O3 exposure with all-cause and AIDS-related mortality was more prominent among those with higher CD4+ count. Exploratory analysis revealed possible associations between O3 exposure and respiratory infections and clinical symptoms. These findings suggest potential synergistic effects between a compromised immune status and elevated O3 exposure levels on mortality risk among PLWH. Ambient O3 exposure should be considered as an emerging mortality risk factor for PLWH in the era of antiretroviral therapy, requiring further attention from researchers and healthcare professionals.

Cardiorespiratory effects of indoor ozone exposure during sleep and the influencing factors: A prospective study among adults in China.

Ambient ozone (O3) is recognized as a significant air pollutant with implications for cardiorespiratory health, yet the effects of indoor O3 exposure have received less consideration. Furthermore, while sleep occupies one-third of life, research on the health consequences of O3 exposure during this crucial period is scarce. This study aimed to investigate associations of indoor O3 during sleep with cardiorespiratory function and potential predisposing factors. A prospective study among 81 adults was conducted in Beijing, China. Repeated measurements of cardiorespiratory indices reflecting lung function, airway inflammation, cardiac autonomic function, blood pressure, systemic inflammation, platelet and glucose were performed on each subject. Real-time concentrations of indoor O3 during sleep were monitored. Associations of O3 with cardiorespiratory indices were evaluated using linear mixed-effect model. Effect modification by baseline lifestyles (diet, physical activity, sleep-related factors) and psychological status (stress and depression) were investigated through interaction analysis. The average indoor O3 concentration during sleep was 20.3 µg/m3, which was well below current Chinese indoor air quality standard of 160 µg/m3. O3 was associated with most respiratory indicators of decreased airway function except airway inflammation; whereas the cardiovascular effects were only manifested in autonomic dysfunction and not in others. An interquartile range increases in O3 at 6-h average was associated with changes of -3.60 % (95 % CI: -6.19 %, -0.93 %) and -9.60 % (95 % CI: -14.53 %, -4.39 %) in FVC and FEF25-75, respectively. Further, stronger effects were noted among participants with specific dietary patterns, poorer sleep and higher level of depression. This study provides the first general population-based evidence that low-level exposure to indoor O3 during sleep has greater effects on the respiratory system than on the cardiovascular system. Our findings identify the respiratory system as an important target for indoor O3 exposure, and particularly highlight the need for greater awareness of indoor air quality, especially during sleep.

Recent Insights into the Environmental Determinants of Childhood Asthma.

PURPOSE OF REVIEW: Ubiquitous environmental exposures, including ambient air pollutants, are linked to the development and severity of childhood asthma. Advances in our understanding of these links have increasingly led to clinical interventions to reduce asthma morbidity. RECENT FINDINGS: We review recent work untangling the complex relationship between air pollutants, including particulate matter, nitrogen dioxide, and ozone and asthma, such as vulnerable windows of pediatric exposure and their interaction with other factors influencing asthma development and severity. These have led to interventions to reduce air pollutant levels in children's homes and schools. We also highlight emerging environmental exposures increasingly associated with childhood asthma. Growing evidence supports the present threat of climate change to children with asthma. Environmental factors play a large role in the pathogenesis and persistence of pediatric asthma; in turn, this poses an opportunity to intervene to change the course of disease early in life.

Air pollution and upper respiratory diseases: an examination among medically insured populations in Wuhan, China.

Multiple evidence has supported that air pollution exposure has detrimental effects on the cardiovascular and respiratory systems. However, most investigations focus on the general population, with limited research conducted on medically insured populations. To address this gap, the current research was designed to examine the acute effects of inhalable particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), ground-level ozone (O3), and sulfur dioxide (SO2) on the incidence of upper respiratory tract infections (URTI), utilizing medical insurance data in Wuhan, China. Data on URTI were collected from the China Medical Insurance Basic Database for Wuhan covering the period from 2014 to 2018, while air pollutant data was gathered from ten national monitoring stations situated in Wuhan city. Statistical analysis was performed using generalized additive models for quasi-Poisson distribution with a log link function. The analysis indicated that except for ozone, higher exposure to four other pollutants (NO2, SO2, PM2.5, and PM10) were significantly linked to an elevated risk of URTI, particularly during the previous 0-3 days and previous 0-4 days. Additionally, NO2 and SO2 were found to be positively linked with laryngitis. Furthermore, the effects of air pollutants on the risk of URTI were more pronounced during cold seasons than hot seasons. Notably, females and the employed population were more susceptible to infection than males and non-employed individuals. Our findings gave solid proof of the link between ambient air pollution exposure and the risk of URTI in medically insured populations.