Air pollution's numerical, spatial, and temporal heterogeneous impacts on childhood hand, foot and mouth disease: a multi-model county-level study from China.

BACKGROUND: While stationary links between childhood hand, foot and mouth disease (HFMD) and air pollution are known, a comprehensive study on their heterogeneous relationships (nonstationarity), jointly considering numerical, temporal and spatial dimensions, has not been reported. METHODS: Monthly HFMD incidence and air pollution data were collected at the county level from Sichuan-Chongqing, China (2009-2011), alongside meteorological and social environmental covariates. Key influential factors were identified using random forest (RF) under the stationary assumption. Factors' numerically, temporally, and spatially heterogeneous relationships with HFMD were assessed using generalized additive model (GAM) and geographically and temporally weighted regression (GTWR). RESULTS: Our findings highlighted the relatively higher stationary contributions of fine particulate matter (PM2.5) and ozone (O3) to HFMD incidence across Sichuan-Chongqing counties. We further uncovered heterogeneous impacts of PM2.5 and O3 from three nonstationary perspectives. Numerically, PM2.5 showed an inverse 'V'-shaped relationship with HFMD incidence, while O3 exhibited a complex pattern, with increased HFMD incidence at low PM2.5 and moderate O3 concentrations. Temporally, PM2.5's impact peaked in autumn and was weakest in spring, whereas O3's effect was strongest in summer. Spatially, hotspot mapping revealed high-risk clusters for PM2.5 impact across all seasons, with notable geographical variations, and for O3 in spring, summer, and autumn, concentrated in specific regions of Sichuan-Chongqing. CONCLUSIONS: This study underscores the nuanced and three-perspective heterogeneous influences of air pollution on HFMD in small areas, emphasizing the need for differentiated, localized, and time-sensitive prevention and control strategies to enhance the precision of dynamic early warnings and predictive models for HFMD and other infectious diseases, particularly in the fields of environmental and spatial epidemiology.

Estimating future climate change impacts on human mortality and crop yields via air pollution.

Future climate change may bring local benefits or penalties to surface air pollution, resulting from changing temperature, precipitation, and transport patterns, as well as changes in climate-sensitive natural precursor emissions. Here, we estimate the climate penalties and benefits at the end of this century with regard to surface ozone and fine particulate matter (PM[Formula: see text]; excluding dust and smoke) using a one-way offline coupling between a general circulation model and a global 3-D chemical-transport model. We archive meteorology for the present day (2005 to 2014) and end of this century (2090 to 2099) for seven future scenarios developed for Phase 6 of the Coupled Model Intercomparison Project. The model isolates the impact of forecasted anthropogenic precursor emission changes versus that of climate-only driven changes on surface ozone and PM[Formula: see text] for scenarios ranging from extreme mitigation to extreme warming. We then relate these changes to impacts on human mortality and crop production. We find ozone penalties over nearly all land areas with increasing warming. We find net benefits due to climate-driven changes in PM[Formula: see text] in the Northern Extratropics, but net penalties in the Tropics and Southern Hemisphere, where most population growth is forecast for the coming century.

Association of ambient air pollution and Air Quality Index with risk of sudden sensorineural hearing loss: a cross-sectional study.

OBJECTIVES: To explore the associations of air pollutants and Air Quality Index (AQI) with risk of sudden sensorineural hearing loss (SSNHL) DESIGN: Cross-sectional study SETTING: Medical record data and local population data collected between 2014 and 2022 in Changshu, China were retrospectively reviewed. PARTICIPANTS: Adults aged 18 years and above who were diagnosed with SSNHL in Changshu No. 1 People's Hospital or Changshu No. 2 People's Hospital from the spring of 2014 to the fall of 2022 were included in the study. OUTCOME MEASURE: SSNHL was diagnosed by clinicians using the Chinese diagnostic criteria for SSNHL. RESULTS: Compared with those exposed to the lowest tertile of carbon monoxide (CO), the prevalence ratio for those exposed to middle and high tertiles of CO were 1.113 (95% CI 1.022 to 1.213) and 1.230 (95% CI 1.105 to 1.369), respectively. The risk of SSNHL was increased by 30.6% (95% CI 9.9% to 55.4%) per doubling increment of CO. No categorical association was found between ozone (O3) exposure and risk of SSNHL, however, an increased risk of 22.2% (0.8%-48.2%) was identified for each doubling of O3. No association was identified between other pollutants and AQI and risk of SSNHL. CONCLUSIONS: In this study, CO and O3 were associated with an increased risk of SSNHL in Changshu, China. Further studies are warranted to confirm our findings.

Air pollution below US regulatory standards and cardiovascular diseases using a double negative control approach.

Growing evidence suggests that long-term air pollution exposure is a risk factor for cardiovascular mortality and morbidity. However, few studies have investigated air pollution below current regulatory limits, and causal evidence is limited. We use a double negative control approach to examine the association between long-term exposure to air pollution at low concentration and cardiovascular hospitalizations among US Medicare beneficiaries aged ≥65 years between 2000 and 2016. The expected values of the negative outcome control (preceding-year hospitalizations) regressed on exposure and negative exposure control (subsequent-year exposure) are treated as a surrogate for omitted confounders. With analyses separately restricted to low-pollution areas (PM2.5 < 9 µg/m³, NO2 < 75.2 µg/m3 [40 ppb], warm-season O3 < 88.2 µg/m3 [45 ppb]), we observed positive associations of the three pollutants with hospitalization rates of stroke, heart failure, and atrial fibrillation and flutter. The associations generally persisted in demographic subgroups. Stricter national air quality standards should be considered.

Intermittent ozone inhalation during house dust mite-induced sensitization primes for adverse asthma phenotype.

The ability of air pollution to induce acute exacerbation of asthma is well documented. However, the ability of ozone (O3), the most reactive gaseous component of air pollution, to function as a modulator during sensitization is not well established. C57BL/6 J male mice were intranasally sensitized to house dust mite (HDM) (40 µg/kg) for 3 weeks on alternate days in parallel with once-a-week O3 exposure (1 ppm). Mice were euthanized 24 h following the last HDM challenge. Lung lavage, histology, lung function (both forced oscillation and forced expiration-based), immune cell profiling, inflammation (pulmonary and systemic), and immunoglobulin production were assessed. Compared to HDM alone, HDM + O3 leads to a significant increase in peribronchial inflammation (p < 0.01), perivascular inflammation (p < 0.001) and methacholine-provoked large airway hyperreactivity (p < 0.05). Serum total IgG and IgE and HDM-specific IgG1 were 3-5 times greater in HDM + O3 co-exposure compared to PBS and O3-exposed groups. An increase in activated/mature lung total and monocyte-derived dendritic cells (p < 0.05) as well as T-activated, and T memory lymphocyte subset numbers (p < 0.05) were noted in the HDM + O3 group compared to HDM alone group. Concurrent O3 inhalation and HDM sensitization also caused significantly greater (p < 0.05) lung tissue interleukin-17 pathway gene expression and mediator levels in the serum. Redox imbalance was manifested by impaired lung antioxidant defense and increased oxidants. O3 inhalation during allergic sensitization coalesces in generating a significantly worse TH17 asthmatic phenotype.

The Lag -Effects of Air Pollutants and Meteorological Factors on COVID-19 Infection Transmission and Severity: Using Machine Learning Techniques.

BACKGROUND: Exposure to air pollution is a major health problem worldwide. This study aimed to investigate the effect of the level of air pollutants and meteorological parameters with their related lag time on the transmission and severity of coronavirus disease 19 (COVID-19) using machine learning (ML) techniques in Shiraz, Iran. Study Design: An ecological study. METHODS: In this ecological research, three main ML techniques, including decision trees, random forest, and extreme gradient boosting (XGBoost), have been applied to correlate meteorological parameters and air pollutants with infection transmission, hospitalization, and death due to COVID-19 from 1 October 2020 to 1 March 2022. These parameters and pollutants included particulate matter (PM2), sulfur dioxide (SO2 ), nitrogen dioxide (NO2 ), nitric oxide (NO), ozone (O3 ), carbon monoxide (CO), temperature (T), relative humidity (RH), dew point (DP), air pressure (AP), and wind speed (WS). RESULTS: Based on the three ML techniques, NO2 (lag 5 day), CO (lag 4), and T (lag 25) were the most important environmental features affecting the spread of COVID-19 infection. In addition, the most important features contributing to hospitalization due to COVID-19 included RH (lag 28), T (lag 11), and O3 (lag 10). After adjusting for the number of infections, the most important features affecting the number of deaths caused by COVID-19 were NO2 (lag 20), O3 (lag 22), and NO (lag 23). CONCLUSION: Our findings suggested that epidemics caused by COVID-19 and (possibly) similarly viral transmitted infections, including flu, air pollutants, and meteorological parameters, can be used to predict their burden on the community and health system. In addition, meteorological and air quality data should be included in preventive measures.

Air pollution and risk of 32 health conditions: outcome-wide analyses in a population-based prospective cohort in Southwest China.

BACKGROUND: Uncertainty remains about the long-term effects of air pollutants (AP) on multiple diseases, especially subtypes of cardiovascular disease (CVD). We aimed to assess the individual and joint associations of fine particulate matter (PM2.5), along with its chemical components, nitrogen dioxide (NO2) and ozone (O3), with risks of 32 health conditions. METHODS: A total of 17,566 participants in Sichuan Province, China, were included in 2018 and followed until 2022, with an average follow-up period of 4.2 years. The concentrations of AP were measured using a machine-learning approach. The Cox proportional hazards model and quantile g-computation were applied to assess the associations between AP and CVD. RESULTS: Per interquartile range (IQR) increase in PM2.5 mass, NO2, O3, nitrate, ammonium, organic matter (OM), black carbon (BC), chloride, and sulfate were significantly associated with increased risks of various conditions, with hazard ratios (HRs) ranging from 1.06 to 2.48. Exposure to multiple air pollutants was associated with total cardiovascular disease (HR 1.75, 95% confidence intervals (CIs) 1.62-1.89), hypertensive diseases (1.49, 1.38-1.62), cardiac arrests (1.52, 1.30-1.77), arrhythmia (1.76, 1.44-2.15), cerebrovascular diseases (1.86, 1.65-2.10), stroke (1.77, 1.54-2.03), ischemic stroke (1.85, 1.61-2.12), atherosclerosis (1.77, 1.57-1.99), diseases of veins, lymphatic vessels, and lymph nodes (1.32, 1.15-1.51), pneumonia (1.37, 1.16-1.61), inflammatory bowel diseases (1.34, 1.16-1.55), liver diseases (1.59, 1.43-1.77), type 2 diabetes (1.48, 1.26-1.73), lipoprotein metabolism disorders (2.20, 1.96-2.47), purine metabolism disorders (1.61, 1.38-1.88), anemia (1.29, 1.15-1.45), sleep disorders (1.54, 1.33-1.78), renal failure (1.44, 1.21-1.72), kidney stone (1.27, 1.13-1.43), osteoarthritis (2.18, 2.00-2.39), osteoporosis (1.36, 1.14-1.61). OM had max weights for joint effects of AP on many conditions. CONCLUSIONS: Long-term exposure to increased levels of multiple air pollutants was associated with risks of multiple health conditions. OM accounted for substantial weight for these increased risks, suggesting it may play an important role in these associations.

Attributable deaths in Austria due to ozone under different climate scenarios.

Tropospheric ozone is an air pollutant that poses a public health problem in Europe. Climate change could increase the formation of ozone. Applying past and predicted annual total (all-cause) mortality data and modeled daily ozone concentrations, we performed a nationwide health impact assessment estimating annual ozone-related (attributable) deaths in Austria. Different approaches were compared. Estimates were based on maximal 1-h averages of ozone. Until the decade from 2045 till 2055, more people will die in Austria because of the demographic trends. Therefore, more deaths will also be attributable to ozone. Higher greenhouse gas emission scenarios (e.g. Representative Concentration Pathway RCP8.5 compared to RCP2.6) will lead to more ozone-related deaths, mostly due to the national emission of ozone precursors (a difference of 250-340 cases per year, depending on the model), but to a lesser extent because of global climate change. Increases in attributable deaths will be affected mostly by national, not global mitigation measures. National emission reduction will certainly have a strong and beneficial effect on local atmospheric chemistry, air quality, and public health.

Maternal ozone exposure lowers infant's birthweight: A nationwide cohort of over 4 million livebirths in Iran.

BACKGROUND: Nationwide evidence linking maternal ozone exposure with fetal growth restriction (FGR) was extensively scarce, especially in the Middle East with dry climate and distinct religious culture. METHODS: We carried out a national retrospective birth cohort study using registry-based records from 749 hospitals across 31 provinces in Iran from 2013 to 2018. Monthly concentrations of maximum daily average 8-hour (MDA8) ozone at 0.125° × 0.125° resolution were extracted from well-validated spatiotemporal grid dataset. Linear and logistic regression models were employed to evaluate associations of maternal MDA8 ozone exposure with birthweight outcomes. Assuming causality, the comparative risk assessment framework was utilized to estimate the burden of low birthweight (LBW), small for gestational age (SGA), and birthweight loss per livebirth (BLL) attributable to ambient ozone pollution. RESULTS: Of 4030383 livebirths included in the study, 264304 (6.6%) were LBW and 484405 (12.0%) were SGA. Each 10-ppb increase in MDA8 ozone exposure was associated with an odds ratio of 1.123 (95% confidence interval [CI]: 1.104 to 1.142) for LBW and 1.210 (95% CI: 1.197 to 1.223) for SGA, and a 30.5-g (95% CI: 29.0 to 32.0) reduction in birthweight. We observed approximately linear exposure-response relationships of maternal MDA8 ozone exposure with LBW (Pnonlinear= 0.786), SGA (Pnonlinear= 0.156), and birthweight reduction (Pnonlinear= 0.104). Under the premise of causal association, we estimated 6.6% (95% CI: 5.7 to 7.5) of LBW, 10.1% (95% CI: 9.6 to 10.6) of SGA, and 18.8 g (95% CI: 17.9 to 19.7) of BLL could be attributable to maternal ozone exposure in Iran. Considerably greater risk and burden of ozone-related FGR were observed among younger, less-educated, and rural-dwelling mothers. CONCLUSIONS: Our study provided compelling evidence that maternal ozone exposure was associated with heightened FGR risk and burden, particularly among socioeconomically disadvantaged mothers. These findings underscored the urgent need for government to incorporate socioeconomic factors into future ozone-related health policies, not only to mitigate pollution, but also minimize inequality.

Effect of air pollutants particulate matter (PM2.5, PM10), sulfur dioxide (SO2) and ozone (O3) on cognitive health.

Impaired cognitive health is the leading cause of various disabilities and disorders. Air pollution has been dramatically increasing over the last few decades and has been identified as a potential risk factor for impaired cognitive health. This study investigates the effect of air pollutants, particulate matter (PM2.5, PM10), sulfur dioxide (SO2), and ground-level ozone, on global cognitive health. The data on environmental pollutants and cognitive health were recorded from PubMed, Web of Science, Scopus, and Google Scholar. Initially, 790 articles were identified after screening for duplicates and applying the inclusion and exclusion criteria, 21 studies were included, and data was synthesized to get a pooled result. The overall results revealed that increased exposure to PM2.5 was positively and significantly associated with cognitive decline (OR 1.49; 95% CI 1.11, 1.99; p = 0.01). The risk of cognitive impairment due to PM10 (OR 1.30; 95% CI 1.00-1.70, p = 0.05), and SO2 (OR 1.39; 95% CI 1.27-1.51; p < 0.01) exposure were also significantly heightened. The study findings show that overall exposure to particulate matter PM2.5, PM10, and SO2 was associated with an increased risk of a decrease in global cognitive functions. The findings suggest that reducing levels of air pollutants could be a strategic approach to mitigate cognitive health risks in populations worldwide.

Sex Differences in Impacts of Early Gestational and Peri-Adolescent Ozone Exposure on Lung Development in Rats: Implications for Later Life Disease in Humans.

Air pollution exposure during pregnancy may affect fetal growth. Fetal growth restriction (FGR) is associated with reduced lung function in children that can persist into adulthood. Using an established model of asymmetrical FGR in Long-Evans rats, this study investigated sex differences in effects of early life ozone exposure on lung development and maturation. Adverse health effects for i) gestational exposure (with impacts on primary alveolarization), ii) peri-adolescent exposure (with impacts on secondary alveolarization), and iii) cumulative exposure across both periods were evaluated. Notably, female offspring were most affected by gestational ozone exposure, likely because of impaired angiogenesis and corresponding decreases in primary alveolarization. Females had diminished lung capacity, fewer mature alveoli, and medial hypertrophy of small and large pulmonary arteries. Males, especially FGR-prone offspring, were more affected by peri-adolescent ozone exposure. Males had increased ductal areas, likely due to disrupted secondary alveolarization. Altered lung development may increase risk of developing diseases, such as pulmonary arterial hypertension or chronic obstructive pulmonary disease. Pulmonary arterial hypertension disproportionately affects women. In the United States, chronic obstructive pulmonary disease prevalence is increasing, especially in women; and prevalence for both men and women is highest in urbanized areas. This investigation underlines the importance of evaluating results separately by sex, and provides biologic plausibility for later consequences of early-life exposure to ozone, a ubiquitous urban air pollutant.

The influence of environmental factors related to Juvenile Dermatomyositis (JDM), its course and refractoriness to treatment.

OBJECTIVE: To evaluate the influence of environmental factors and prematurity relating to juvenile dermatomyositis (JDM), its course and refractoriness to treatment. METHODS: A case-control study with 35 patients followed up at a tertiary hospital and 124 healthy controls, all residents of São Paulo. Patients were classified according to monocyclic, polycyclic or chronic disease courses and refractoriness to treatment. The daily concentrations of pollutants (inhalable particulate matter-PM10, sulfur dioxide-SO2, nitrogen dioxide-NO2, ozone-O3 and carbon monoxide-CO) were provided by the Environmental Company of São Paulo. Data from the population were obtained through a questionnaire. RESULTS: Fifteen patients had monocyclic courses, and 19 polycyclic/chronic courses. Eighteen patients were refractory to treatment. Maternal occupational exposure to inhalable agents (OR = 17.88; IC 95% 2.15-148.16, p = 0.01) and exposure to O3 in the fifth year of life (third tertile > 86.28µg/m3; OR = 6.53, IC95% 1.60-26.77, p = 0.01) were risk factors for JDM in the multivariate logistic regression model. The presence of a factory/quarry at a distance farther than 200 meters from daycare/school (OR = 0.22; IC 95% 0.06-0.77; p = 0.02) was a protective factor in the same analysis. Prematurity, exposure to air pollutants/cigarette smoke/sources of inhalable pollutants in the mother's places of residence and work during the gestational period were not associated with JDM. Prematurity, maternal exposure to occupational pollutants during pregnancy as well as patient's exposure to ground-level pollutants up to the fifth year of life were not associated with disease course and treatment refractoriness. CONCLUSION: Risk factors for JDM were maternal occupational exposure and exposure to O3 in the fifth year of life.

Relationship between short-term ozone exposure, cause-specific mortality, and high-risk populations: A nationwide, time-stratified, case-crossover study.

BACKGROUND: Previous studies reported that short-term exposure to ground-level ozone is associated with mortality risk. However, due to the limited monitored areas, existing studies were limited in assessing the nationwide risk and suggesting specific vulnerable populations to the ozone-mortality risk. METHODS: We performed a nationwide time-stratified case-crossover study to evaluate the association between short-term ozone and cause-specific mortality in South Korea (2015-2019). A machine learning-ensemble prediction model (a test R2 > 0.96) was used to assess the short-term ozone exposure. Stratification analysis was conducted to examine the high-risk populations, and the excess mortality due to non-compliance with the WHO guideline was also assessed. RESULTS: For all-cause mortality (1,343,077 cases), the risk associated with ozone (lag0- 1) was weakly identified (odd ratio: 1.005 with 95% CI: 0.997-1.014), and the risk was prominent in mortality with circulatory system diseases. In addition, based on the point estimates, the ozone-mortality risk was higher in people aged less than 65y, and this pattern was also observed in circulatory system disease deaths and urban areas. CONCLUSIONS: This study provides national estimates of mortality risks associated with short-term ozone. Results showed that the benefits of stricter air quality standards could be greater in vulnerable populations.

Preconception mitochondrial DNA copy number plays a crucial role in linking prenatal air pollution with the risk of preterm birth.

The relationship between maternal peripheral blood mitochondrial DNA and adverse pregnancy outcomes, specifically preterm birth (PTB), remains uncertain. To investigate the effects of preconception mitochondrial DNA copy number (mtDNAcn) on the association between prenatal air pollutants exposure and PTB risk, a total of 1871 expectant mothers from six regions in Henan Province were recruited. Information regarding air pollutants was obtained from 151 environmental monitoring sites, and relative mtDNAcn was evaluated using real-time PCR analysis. After adjusting for potential confounding variables, it was determined that the risk of PTB increased with elevated levels of inhalable particulate matter (PM10), fine particulate matter (PM2.5), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (O3) exposure (P < 0.05) but decreased with higher nitrogen dioxide (NO2) exposure (0.05 < P < 0.10) during the entire pregnancy. Additionally, the preconception relative mtDNAcn was lower in the PTB group (0.82 ± 0.23) compared to the term group (0.92 ± 0.29). Furthermore, for each 0.1-unit increase in preconception mtDNAcn, the risk of PTB decreased by 14.8%. Stratified analyses revealed that the risk of PTB rose with increasing O3 concentrations, regardless of the relative mtDNAcn. Moreover, the study found a significant association between PTB risk and prenatal exposure to elevated PM10, PM2.5, SO2, and CO, particularly in mothers with low mtDNAcn (≤0.88) (P < 0.05). Conversely, a decrease in the PTB risk was observed with elevated NO2 exposure in mothers with high mtDNAcn (>0.88). Interaction analysis revealed that exposure to PM10, PM2.5, SO2, NO2, and CO interacted with mtDNAcn, respectively, affecting PTB risk (P-interaction<0.05). These findings indicate a noteworthy association between PTB risk and prenatal air pollutants exposure, which is influenced by the preconception mtDNAcn.

Association between ambient air pollution a week prior to delivery and preterm birth using a nationwide study in Sweden.

BACKGROUND: Air pollution exposure has been linked with increased risk of preterm birth, which is one of the leading causes of infant mortality. Limited studies have attempted to explore these associations in low-polluted areas. In this study, we aimed to assess the association between short-term exposure to ambient air pollution and preterm birth in Sweden. METHOD: In this population-based study we included preterm births between 2014 and 2019 from the Swedish Pregnancy Register. We applied a spatiotemporal model to estimate daily levels of particulate matter <2.5 µm (PM2.5), PM < 10 µm (PM10), nitrogen dioxide (NO2), and ozone (O3) at the residential address of each participant. We applied a time-stratified case-crossover design with conditional logistic regression analysis to estimate odds ratios (OR) of preterm birth per 10 µg/m3 (PM10, NO2, O3) and 5 µg/m3 (PM2.5) increase in air pollution exposure at 0-6-day lag. Two-pollutant models were applied to evaluate the independent association of each exposure on preterm birth. We also stratified by maternal characteristics to identify potential effect modifiers. RESULTS: 28,216 (4.5%) preterm births were included. An increase in O3 exposure was associated with increased odds of preterm birth [OR = 1.06 per 10 µg/m3 (95% CI, 1.02; 1.10]. PM2.5 and PM10 were not significantly associated with preterm birth, and NO2 displayed a negative nonlinear association with preterm birth. We did not observe any notable effect modification, but we found suggestive larger associations between O3 and preterm birth when stratifying by male sex, spontaneous delivery, and spring season. CONCLUSIONS: Increased O3 exposure one week before delivery was associated with an increased risk of preterm birth in Sweden, a country with levels of air pollution below the current World Health Organization air quality guidelines. Increases in O3 levels with climate change make these findings especially concerning.

Adverse effects of meteorological factors and air pollutants on dry eye disease: a hospital-based retrospective cohort study.

Although previous studies have suggested that meteorological factors and air pollutants can cause dry eye disease (DED), few clinical cohort studies have determined the individual and combined effects of these factors on DED. We investigated the effects of meteorological factors (humidity and temperature) and air pollutants [particles with a diameter ≤ 2.5 µ m (PM2.5), ozone (O3), nitrogen dioxide (NO2), and carbon monoxide (CO)] on DED. A retrospective cohort study was conducted on 53 DED patients. DED was evaluated by Symptom Assessment in Dry Eye (SANDE), tear secretion, tear film break-up time (TBUT), ocular staining score (OSS), and tear osmolarity. To explore the individual, non-linear, and joint associations between meteorological factors, air pollutants, and DED parameters, we used generalized linear mixed model (GLMM) and Bayesian kernel machine regression (BKMR). After adjusting for all covariates, lower relative humidity or temperature was associated with a higher SANDE (p < 0.05). Higher PM2.5, O3, and NO2 levels were associated with higher SANDE and tear osmolarity (p < 0.05). Higher O3 levels were associated with lower tear secretion and TBUT, whereas higher NO2 levels were associated with higher OSS (p < 0.05). BKMR analyses indicated that a mixture of meteorological factors and air pollutants was significantly associated with increased SANDE, OSS, tear osmolarity, and decreased tear secretion.

Air pollution and children's mental health in rural areas: compositional spatio-temporal model.

Air pollution stands as an environmental risk to child mental health, with proven relationships hitherto observed only in urban areas. Understanding the impact of pollution in rural settings is equally crucial. The novelty of this article lies in the study of the relationship between air pollution and behavioural and developmental disorders, attention deficit hyperactivity disorder (ADHD), anxiety, and eating disorders in children below 15 living in a rural area. The methodology combines spatio-temporal models, Bayesian inference and Compositional Data (CoDa), that make it possible to study areas with few pollution monitoring stations. Exposure to nitrogen dioxide (NO2), ozone (O3), and sulphur dioxide (SO2) is related to behavioural and development disorders, anxiety is related to particulate matter (PM10), O3 and SO2, and overall pollution is associated to ADHD and eating disorders. To sum up, like their urban counterparts, rural children are also subject to mental health risks related to air pollution, and the combination of spatio-temporal models, Bayesian inference and CoDa make it possible to relate mental health problems to pollutant concentrations in rural settings with few monitoring stations. Certain limitations persist related to misclassification of exposure to air pollutants and to the covariables available in the data sources used.

[The role of ozone in the pathogenesis of allergic rhinitis].

Allergic rhinitis （AR） is a nasal hypersensitivity disease that is influenced by environmental factors, genetic factors, and various inflammatory factors. The role and mechanisms of ozone, as a component of air pollution, in the pathogenesis of AR are not yet fully understood. This article provides a review of the impact of ozone on the epidemiology and pathology of AR, as well as its possible mechanisms, to provide new insights into the prevention and treatment of AR.

Potential Drivers for the Spatiotemporal Patterns of the Global Burden of Chronic Obstructive Pulmonary Disease Attributable to Ambient Ozone, 1990-2019.

Objectives: To identify the long-term spatiotemporal trend of ozone-related chronic obstructive pulmonary disease (COPD) burden by sex and country and to explore potential drivers. Methods: We retrieved data of ozone-related COPD death and disability adjusted life year (DALY) from the Global Burden of Disease 2019. We used a linear regression of natural logarithms of age-standardized rates (ASRs) with calendar year to examine the trends in ASRs and a panel regression to identify country-level factors associated with the trends. Results: Global ozone-attributable COPD deaths increased from 117,114 to 208,342 among men and from 90,265 to 156,880 among women between 1990 and 2019. Although ASRs of ozone-related COPD death and DALY declined globally, they increased in low and low-middle Socio-demographic Index (SDI) regions, with faster rise in women. Elevated average maximum temperature was associated with higher ozone-attributable COPD burden, while more green space was associated with lower burden. Conclusion: More efforts are needed in low and low-middle SDI regions, particularly for women, to diminish inter-country inequality in ozone-attributable COPD. Global warming may exacerbate the burden. Expanding green space may mitigate the burden.

Paris air quality monitoring for the 2024 Olympics and Paralympics: focus on air pollutants and pollen.

BACKGROUND: Exposure to air pollution can affect the health of individuals with respiratory disease, but may also impede the health and performance of athletes. This is potentially relevant for people travelling to and competing in the Olympic and Paralympic Games (OPG) in Paris. We describe anticipated air quality in Paris based on historical monitoring data and describe the impact of the process on the development of monitoring strategies for future international sporting events. METHODS: Air pollutant data for July to September 2020-2023 and pollen data for 2015-2022 were provided by Airparif (particulate matter (PM2.5), nitrogen dioxide (NO2) and ozone (O3)) and RNSA stations in the Paris region. Airparif's street-level numerical modelling provided spatial data for the OPG venues. RESULTS: The maximum daily mean PM2.5 was 11±6 µg/m3 at traffic stations, below the WHO recommended daily air quality threshold (AQT). Daily NO2 concentrations ranged from 5±3 µg/m3 in rural areas to 17±14 µgm3 in urban areas. Near traffic stations, this rose to 40±24 µg/m3 exceeding the WHO AQT. Both peaked around 06:00 and 20:00 UTC (coordinated universal time). The ambient O3 level exceeded the AQT on 20 days per month and peaked at 14:00 UTC. The main allergenic taxa from June to September was Poaceae (ie, grass pollen variety). CONCLUSION: Air pollutant levels are expected to be within accepted air quality thresholds at the Paris OPG. However, O3 concentrations may be significantly raised in very hot and clear conditions and grass pollen levels will be high, prompting a need to consider and manage this risk in susceptible individuals.