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.

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.

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.

Short-term exposure to air pollution and hospital admission after COVID-19 in Catalonia: the COVAIR-CAT study.

BACKGROUND: A growing body of evidence has reported positive associations between long-term exposure to air pollution and poor COVID-19 outcomes. Inconsistent findings have been reported for short-term air pollution, mostly from ecological study designs. Using individual-level data, we studied the association between short-term variation in air pollutants [nitrogen dioxide (NO2), particulate matter with a diameter of <2.5 µm (PM2.5) and a diameter of <10 µm (PM10) and ozone (O3)] and hospital admission among individuals diagnosed with COVID-19. METHODS: The COVAIR-CAT (Air pollution in relation to COVID-19 morbidity and mortality: a large population-based cohort study in Catalonia, Spain) cohort is a large population-based cohort in Catalonia, Spain including 240 902 individuals diagnosed with COVID-19 in the primary care system from 1 March until 31 December 2020. Our outcome was hospitalization within 30 days of COVID-19 diagnosis. We used individual residential address to assign daily air-pollution exposure, estimated using machine-learning methods for spatiotemporal prediction. For each pandemic wave, we fitted Cox proportional-hazards models accounting for non-linear-distributed lagged exposure over the previous 7 days. RESULTS: Results differed considerably by pandemic wave. During the second wave, an interquartile-range increase in cumulative weekly exposure to air pollution (lag0_7) was associated with a 12% increase (95% CI: 4% to 20%) in COVID-19 hospitalizations for NO2, 8% (95% CI: 1% to 16%) for PM2.5 and 9% (95% CI: 3% to 15%) for PM10. We observed consistent positive associations for same-day (lag0) exposure, whereas lag-specific associations beyond lag0 were generally not statistically significant. CONCLUSIONS: Our study suggests positive associations between NO2, PM2.5 and PM10 and hospitalization risk among individuals diagnosed with COVID-19 during the second wave. Cumulative hazard ratios were largely driven by exposure on the same day as hospitalization.

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.

Long-term tropospheric ozone pollution disrupts plant-microbe-soil interactions in the agroecosystem.

Tropospheric ozone (O3 ) threatens agroecosystems, yet its long-term effects on intricate plant-microbe-soil interactions remain overlooked. This study employed two soybean genotypes of contrasting O3 -sensitivity grown in field plots exposed elevated O3 (eO3 ) and evaluated cause-effect relationships with their associated soil microbiomes and soil quality. Results revealed long-term eO3 effects on belowground soil microbiomes and soil health surpass damage visible on plants. Elevated O3 significantly disrupted belowground bacteria-fungi interactions, reduced fungal diversity, and altered fungal community assembly by impacting soybean physiological properties. Particularly, eO3 impacts on plant performance were significantly associated with arbuscular mycorrhizal fungi, undermining their contribution to plants, whereas eO3 increased fungal saprotroph proliferation, accelerating soil organic matter decomposition and soil carbon pool depletion. Free-living diazotrophs exhibited remarkable acclimation under eO3 , improving plant performance by enhancing nitrogen fixation. However, overarching detrimental consequences of eO3 negated this benefit. Overall, this study demonstrated long-term eO3 profoundly governed negative impacts on plant-soil-microbiota interactions, pointing to a potential crisis for agroecosystems. These findings highlight urgent needs to develop adaptive strategies to navigate future eO3 scenarios.

Exploring the association between early-life air pollution exposure and autism spectrum disorders in children: A systematic review and meta-analysis.

The objective of this meta-analysis is to investigate the association between air pollution and the vulnerability of children to autism spectrum disorders (ASD). A thorough examination and analysis of data obtained from a compilation of 14 studies was undertaken, with a particular emphasis on investigating the effects of nitrogen dioxide (NO2), oxide of nitrogen (NOx), ozone (O3), and particulate matter (PM10 and PM2.5) on individuals diagnosed with ASD. The findings demonstrate a moderate association between exposure to nitrogen dioxide (NO2) and ASD, as indicated by a combined odds ratio (OR) of 1.13 and a 95% confidence interval (CI) spanning from 0.77 to 1.549. O3 shows a combined odds ratio (OR) of 0.82, along with a 95% confidence interval (CI) ranging from 0.49 to 1.14. NOx shows a moderate level of heterogeneity (I² = 75.9%, p = 0.002), suggesting that the impact of NOx on the risk of ASD. There is a statistically significant relationship between exposure to O3 and ASD, although the strength of this relationship is diminished. The findings demonstrated a noteworthy correlation between exposure to PM10 and PM2.5 and the occurrence of ASD. The study found a significant correlation, in relation to PM2.5, with a combined odds ratio (OR) of 1.22 and a 95% confidence interval (CI) ranging from 1.11 to 1.34. The findings have significant implications for the formulation of programs aimed at reducing exposure to harmful chemicals, especially among vulnerable groups such as children.

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.

Effect of ambient ozone pollution on disease burden globally: A systematic analysis for the global burden of disease study 2019.

BACKGROUND: Exposure to ambient ozone pollution causes health loss and even death, and both are the main risk factors for the disease burden worldwide. We comprehensively evaluated the ozone pollution-related disease burden. METHODS: First, numbers and age-standardized rates of deaths and disability-adjusted life years (DALYs) were assessed globally and by sub-types in 2019. Furthermore, the temporal trend of the disease burden was explored by the linear regression model from 1990 to 2019. The cluster analysis was used to evaluate the changing pattern of related disease burden across Global Burden of Disease Study (GBD) regions. Finally, the age-period-cohort (APC) model and the Bayesian age-period-cohort (BAPC) model were used to predict the future disease burden in the next 25 years. RESULT: Exposure to ozone pollution contributed to 365,222 deaths and 6,210,145 DALYs globally in 2019, which accounted for 0.65 % of deaths globally and 0.24 % of DALYs globally. The disease burden was consistently increasing with age. Males were high-risk populations and low-middle socio-demographic index (SDI) regions were high-risk areas. The disease burden of ozone pollution varied considerably across the GBD regions and the countries. In 2019, the number of deaths and DALYs cases increased by 76.11 % and 56.37 %, respectively compared to those in 1990. The predicted results showed that the number of deaths cases and DALYs cases for both genders would still increase from 2020 to 2044. CONCLUSION: In conclusion, ambient ozone pollution has threatened public health globally. More proactive and effective strategic measures should be developed after considering global-specific circumstances.

The association between ambient air pollution and migraine: a systematic review.

Some studies have shown the effect of air pollution on migraine. However, it needs to be confirmed in larger-scale studies, as scientific evidence is scarce regarding the association between air pollution and migraine. Therefore, this systematic review aims to determine whether there are associations between outdoor air pollution and migraine. A literature search was performed in Scopus, Medline (via PubMed), EMBASE, and Web of Science. A manual search for resources and related references was also conducted to complete the search. All observational studies investigating the association between ambient air pollution and migraine, with inclusion criteria, were entered into the review. Fourteen out of 1417 identified articles met the inclusion criteria and entered the study. Among the gaseous air pollutants, there was a correlation between exposure to nitrogen dioxide (NO2) (78.3% of detrimental relationships) and carbon monoxide (CO) (68.0% of detrimental relationships) and migraine, but no apparent correlation has been found for sulfur dioxide (SO2) (21.2% of detrimental relationships) and ozone (O3) (55.2% of detrimental relationships). In the case of particulate air pollutants, particulate matter with a diameter of 10 µm or less (PM10) (76.0% of detrimental relationships) and particulate matter with a diameter of 2.5 µm or less (PM2.5) (61.3% of detrimental relationships) had relationships with migraine. In conclusion, exposure to NO2, CO, PM10, and PM2.5 is associated with migraine headaches, while no conclusive evidence was found to confirm the correlation between O3 and SO2 with migraine. Further studies with precise methodology are recommended in different cities around the world for all pollutants with an emphasis on O3 and SO2.

Environmental pollutants PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) impair human cognitive functions.

OBJECTIVE: Environmental pollution is an emerging global public health problem across the world and causes serious threats to ecosystems, human health, and the planet. This study is designed to explore the impact of environmental pollution particulate matter PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) on cognitive functions in students from schools located in or away from air-polluted areas. SUBJECTS AND METHODS: In this study, two schools were selected: one was located near a traffic-polluted area (school #1), and the second was in an area away from the traffic-polluted area (school #2). In this study, a total of 300 students were recruited: 150 (75 male and 75 female) students from school #1 located in a traffic-polluted area, and 150 students (75 male and 75 female) from school #2 located away from a traffic polluted area. The overall average age of students was 13.53±1.20 years. The students were selected based on age, gender, health status, height, weight, BMI, ethnicity, and homogenous socio-economic and educational status. The pollutants PM2.5, PM10, CO, NO2, O3, and SO2 were recorded in the surrounding environment. The overall mean concentration of environmental pollutants in school #1 was 35.00±0.65 and in school #2 was 29.95±0.32. The levels of airborne particles were measured, and the cognitive functions were recorded using the Cambridge Neuropsychological Test Automated Battery (CANTAB). The students performed the cognitive functions tasks, including the attention switching task (AST), choice reaction time (CRT), and motor screening task (MOT). RESULTS: The results revealed that the AST-Mean 928.34±182.23 vs. 483.79±146.73 (p=0.001), AST-mean congruent 889.12±197.12 vs. 473.30±120.11 (p=0.001), AST-mean in-congruent 988.98±201.27  vs. 483.87±144.57 (p=0.001), CRT-Mean 721.36±251.72  vs. 418.17±89.71 (p=0.001), and MOT-Mean 995.07±394.37 vs. 526.03±57.83 (p=0.001) were significantly delayed among the students who studied in school located in the traffic polluted area compared to students who studied in school which was located away from the traffic-polluted area. CONCLUSIONS: Environmental pollution was significantly higher in motor vehicle-congested areas. Cognitive functions were impaired among the students who were studying in a school located in a polluted area. The results further revealed that the students studying in schools located in environmentally polluted areas have attention, thinking, and decision-making abilities related to cognitive function impairment.

Long-term ozone exposure and mortality in patients with chronic kidney disease: a large cohort study.

BACKGROUND: Epidemiologic studies on the effects of long-term exposure to ozone (O3) have shown inconclusive results. It is unclear whether to O3 has an effect on chronic kidney disease (CKD). We investigated the effects of O3 on mortality and renal outcome in CKD. METHODS: We included 61,073 participants and applied Cox proportional hazards models to examine the effects of ozone on the risk of end-stage renal disease (ESRD) and mortality in a two-pollutants model adjusted for socioeconomic status. We calculated the concentration of ozone exposure one year before enrollment and used inverse distance weighting (IDW) for interpolation, where the exposure was evenly distributed. RESULTS: In the single pollutant model, O3 was significantly associated with an increased risk of ESRD and all-cause mortality. Based on the O3 concentration from IDW interpolation, this moving O3 average was significantly associated with an increased risk of ESRD and all-cause mortality. In a two-pollutants model, even after we adjusted for other measured pollutants, nitrogen dioxide did not attenuate the result for O3. The hazard ratio (HR) value for the district-level assessment is 1.025 with a 95% confidence interval (CI) of 1.014-1.035, while for the point-level assessment, the HR value is 1.04 with a 95% CI of 1.035-1.045. The impact of ozone on ESRD, hazard ratio (HR) values are, 1.049(95%CI: 1.044-1.054) at the district unit and 1.04 (95%CI: 1.031-1.05) at the individual address of the exposure assessment. The ozone hazard ratio for all-cause mortality was 1.012 (95% confidence interval: 1.008-1.017) for administrative districts and 1.04 (95% confidence interval: 1.031-1.05) for individual addresses. CONCLUSIONS: This study suggests that long-term ambient O3 increases the risk of ESRD and mortality in CKD. The strategy to decrease O3 emissions will substantially benefit health and the environment.

Exposure to ambient air pollution and metabolic dysfunction-associated fatty liver disease: Findings from over 2.7 million adults in Northwestern China.

Ambient air pollutants exposures may lead to aggravated Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD). However, there is still a scarcity of empirical studies that have rigorously estimated this association, especially in regions where air pollution is severe. To fill in the literature gap, we conducted a cross-sectional study involving 2711,207 adults living in five regions of southern Xinjiang Uyghur Autonomous Region in 2021. Using a Space-Time Extra-Trees model, we assessed the four-year (2017-2020) average concentrations of particulate matter with aerodynamic diameter ≤1 µm (PM1), particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), particulate matter with aerodynamic diameter ≤10 µm (PM10), ozone (O3), sulfur dioxide (SO2), and carbon monoxide (CO), and then assigned these values to the participants. Generalized linear mixed models were employed to examine the relationships between air pollutants and the prevalence of MAFLD, with adjustment for multiple confounding factors. The odds ratios and 95% confidence intervals of MAFLD were 2.002 (1.826-2.195), 1.133 (1.108-1.157), 1.034 (1.027-1.040), 1.077 (1.023-1.134), 2.703 (2.322-3.146) and 1.033 (1.029-1.036) per 10 µg/m3 increase in the 4-year average PM1, PM2.5, PM10, O3, SO2 and CO exposures, respectively. The robustness of the findings was confirmed by a series of sensitivities. In summary, long-term exposure to ambient air pollutants was associated with increased odds of MAFLD, particularly in males and individuals with unhealthy lifestyles.

Modification of heat-related effects on mortality by air pollution concentration, at small-area level, in the Attica prefecture, Greece.

BACKGROUND: The independent effects of short-term exposure to increased air temperature and air pollution on mortality are well-documented. There is some evidence indicating that elevated concentrations of air pollutants may lead to increased heat-related mortality, but this evidence is not consistent. Most of these effects have been documented through time-series studies using city-wide data, rather than at a finer spatial level. In our study, we examined the possible modification of the heat effects on total and cause-specific mortality by air pollution at municipality level in the Attica region, Greece, during the warm period of the years 2000 to 2016. METHODS: A municipality-specific over-dispersed Poisson regression model during the warm season (May-September) was used to investigate the heat effects on mortality and their modification by air pollution. We used the two-day average of the daily mean temperature and daily mean PM10, NO2 and 8 hour-max ozone (O3), derived from models, in each municipality as exposures. A bivariate tensor smoother was applied for temperature and each pollutant alternatively, by municipality. Α random-effects meta-analysis was used to obtain pooled estimates of the heat effects at different pollution levels. Heterogeneity of the between-levels differences of the heat effects was evaluated with a Q-test. RESULTS: A rise in mean temperature from the 75th to the 99th percentile of the municipality-specific temperature distribution resulted in an increase in total mortality of 12.4% (95% Confidence Interval (CI):7.76-17.24) on low PM10 days, and 21.25% (95% CI: 17.83-24.76) on high PM10 days. The increase on mortality was 10.09% (95% CI: - 5.62- 28.41) on low ozone days, and 14.95% (95% CI: 10.79-19.27) on high ozone days. For cause-specific mortality an increasing trend of the heat effects with increasing PM10 and ozone levels was also observed. An inconsistent pattern was observed for the modification of the heat effects by NO2, with higher heat effects estimated in the lower level of the pollutant. CONCLUSIONS: Our results support the evidence of elevated heat effects on mortality at higher levels of PM10 and 8 h max O3. Under climate change, any policy targeted at lowering air pollution levels will yield significant public health benefits.

Severer air pollution, poorer cognitive function: Findings from 176,345 elders in Northwestern China.

BACKGROUND: Limited evidence exists regarding the link between air pollution exposure and cognitive function in developing countries, particularly in areas with abundant natural sources of particulate matter. OBJECTIVES: To investigate this association in a large representative sample of the elderly in northwestern China. METHODS: We performed a cross-sectional study among 176,345 participants aged 60-100 years in northwestern China in 2020. A satellite-based spatiotemporal model was applied to assess three-year annual averages of particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5), ≤ 10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) at residential address. Poor cognitive function was assessed using the Mini-Mental State Examination (MMSE). Generalized linear mixed models were used to assess associations. RESULTS: Compared with participants with the lowest quartiles of PM2.5, PM10, and O3 levels, those with the second, third, and highest quartiles of air pollutants consistently showed increased odds of poor cognitive function and decreased MMSE scores. The odds ratios of poor cognitive function associated with a 10 µg/m3 increment in PM2.5, PM10, and O3 were 1.26 (95 % confidence interval [CI]: 1.17, 1.36), 1.06 (95 %CI: 1.04, 1.08), and 2.76 (95 %CI: 2.11, 3.62), respectively. Subgroup analyses suggested stronger associations between air pollution exposures and poor cognitive function among participants who were younger, were non-Uyghur and were physically active. CONCLUSION: Long-term exposures to PM2.5, PM10 and O3 were associated with poor cognitive function in elders. Our results suggest that reducing air pollution may alleviate the burden of poor cognitive function in the elderly.

Effects of 7-day polyphenol powder supplementation on cycling performance and lung function in an ozone-polluted environment.

PURPOSE: Polluted environments can adversely affect lung function and exercise performance. Evidence suggests that some nutrient supplements may offset pollution's detrimental effects. This study examined the effect of polyphenol supplementation on lung function and exercise performance in an ozone-polluted environment. METHODS: Ten male cyclists (mean ± SD: age, 43.8 ± 12.4 years; height, 177.8 ± 7.1 cm; weight, 76.03 ± 7.88 kg; VO2max 4.12 ± 0.72 L min-1) initially completed a baseline maximal incremental test and maximal effort 4 km time trial in ambient air. Thereafter cyclists completed two trials in an ozone-polluted environment (0.25 ppm) following seven days of supplementation with either polyphenol (PB) or placebo (PL). Experimental trials consisted of a three-stage submaximal test (50%, 60% and 70% incremental peak power) followed by a 4 km time trial. Lung function was measured pre- and post-exercise via spirometry and adverse respiratory symptoms with a Likert scale. RESULTS: Ozone exposure significantly reduced (p < 0.05) lung function relative to ambient air. There were no significant differences (p > 0.05) in measured variables across the three submaximal intensities. There was a small (d = 0.31) non-significant difference (p = 0.09) in 4 km performance in PB (406.43 ± 50.29 s) vs. PL (426.20 ± 75.06 s). Oxygen consumption during the time trial was greater in PB (3.49 ± 0.71 L min-1) vs PL (3.32 ± 0.71 L min-1, p = 0.01, d = 0.24). Cough severity (SOC) was lower (p = 0.03) with PB relative to PL. CONCLUSION: PB supplementation may provide small benefits to performance and reduce cough symptoms during high-intensity exercise in ozone-polluted environments.

Exploring the relationship between air quality index and lung cancer mortality in India: predictive modeling and impact assessment.

The Air Quality Index (AQI) in India is steadily deteriorating, leading to a rise in the mortality rate due to Lung Cancer. This decline in air quality can be attributed to various factors such as PM 2.5, PM 10, and Ozone (O3). To establish a relationship between AQI and Lung Cancer, several predictive models including Linear Regression, KNN, Decision Tree, ANN, Random Forest Regression, and XGBoost Regression were employed to estimate pollutant levels and Air Quality Index in India. The models relied on publicly available state-wise Air Pollution Dataset. Among all the models, the XGBoost Regression displayed the highest accuracy, with pollutant level estimations reaching an accuracy range of 81% to 98% during training and testing. The second-highest accuracy range was achieved by Random Forest. The paper also explores the impact of increasing pollution levels on the rising mortality rate among lung cancer patients in India.

Air pollution deaths attributable to fossil fuels: observational and modelling study.

OBJECTIVES: To estimate all cause and cause specific deaths that are attributable to fossil fuel related air pollution and to assess potential health benefits from policies that replace fossil fuels with clean, renewable energy sources. DESIGN: Observational and modelling study. METHODS: An updated atmospheric composition model, a newly developed relative risk model, and satellite based data were used to determine exposure to ambient air pollution, estimate all cause and disease specific mortality, and attribute them to emission categories. DATA SOURCES: Data from the global burden of disease 2019 study, observational fine particulate matter and population data from National Aeronautics and Space Administration (NASA) satellites, and atmospheric chemistry, aerosol, and relative risk modelling for 2019. RESULTS: Globally, all cause excess deaths due to fine particulate and ozone air pollution are estimated at 8.34 million (95% confidence interval 5.63 to 11.19) deaths per year. Most (52%) of the mortality burden is related to cardiometabolic conditions, particularly ischaemic heart disease (30%). Stroke and chronic obstructive pulmonary disease both account for 16% of mortality burden. About 20% of all cause mortality is undefined, with arterial hypertension and neurodegenerative diseases possibly implicated. An estimated 5.13 million (3.63 to 6.32) excess deaths per year globally are attributable to ambient air pollution from fossil fuel use and therefore could potentially be avoided by phasing out fossil fuels. This figure corresponds to 82% of the maximum number of air pollution deaths that could be averted by controlling all anthropogenic emissions. Smaller reductions, rather than a complete phase-out, indicate that the responses are not strongly non-linear. Reductions in emission related to fossil fuels at all levels of air pollution can decrease the number of attributable deaths substantially. Estimates of avoidable excess deaths are markedly higher in this study than most previous studies for these reasons: the new relative risk model has implications for high income (largely fossil fuel intensive) countries and for low and middle income countries where the use of fossil fuels is increasing; this study accounts for all cause mortality in addition to disease specific mortality; and the large reduction in air pollution from a fossil fuel phase-out can greatly reduce exposure. CONCLUSION: Phasing out fossil fuels is deemed to be an effective intervention to improve health and save lives as part the United Nations' goal of climate neutrality by 2050. Ambient air pollution would no longer be a leading, environmental health risk factor if the use of fossil fuels were superseded by equitable access to clean sources of renewable energy.

Hourly Air Pollution Exposure and Emergency Hospital Admissions for Stroke: A Multicenter Case-Crossover Study.

BACKGROUND: Daily exposure to ambient air pollution is associated with stroke morbidity and mortality; however, the association between hourly exposure to air pollutants and risk of emergency hospital admissions for stroke and its subtypes remains relatively unexplored. METHODS: We obtained hourly concentrations of fine particulate matter (PM2.5), respirable particulate matter (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO) from the China National Environmental Monitoring Center. We conducted a time-stratified case-crossover study among 86 635 emergency hospital admissions for stroke across 10 hospitals in 3 cities (Jinhua, Hangzhou, and Zhoushan) in Zhejiang province, China, between January 1, 2016 and December 31, 2021. Using a conditional logistic regression combined with a distributed lag linear model, we estimated the association between hourly exposure to multiple air pollutants and risk of emergency hospital admissions for total stroke, ischemic stroke, hemorrhagic stroke, and undetermined type. RESULTS: Hourly exposure to PM2.5, PM10, NO2, and SO2 was associated with an increased risk of hospital admissions for total stroke and ischemic stroke. The associations were most pronounced during the concurrent hour of exposure and lasted for ≈2 hours. We found that the risk was more pronounced among male patients or those aged <65 years old. CONCLUSIONS: Our findings suggest that exposure to PM2.5, PM10, NO2, and SO2, but not CO and O3, is associated with emergency hospital admissions for total stroke or ischemic stroke shortly after exposure. Implementing targeted pollution emission reduction measures may have significant public health implications in controlling and reducing the burden of stroke.

Estimation of health risk and economic loss attributable to PM2.5 and O3 pollution in Jilin Province, China.

Ambient pollutants, particularly fine particulate matter (PM2.5) and ozone (O3), pose significant risks to both public health and economic development. In recent years, PM2.5 concentration in China has decreased significantly, whereas that of O3 has increased rapidly, leading to considerable health risks. In this study, a generalized additive model was employed to establish the relationship of PM2.5 and O3 exposure with non-accidental mortality across 17 districts and counties in Jilin Province, China, over 2015-2016. The health burden and economic losses attributable to PM2.5 and O3 were assessed using high-resolution satellite and population data. According to the results, per 10 µg/m3 increase in PM2.5 and O3 concentrations related to an overall relative risk (95% confidence interval) of 1.004 (1.001-1.007) and 1.009 (1.005-1.012), respectively. In general, the spatial distribution of mortality and economic losses was uneven. Throughout the study period, a total of 23,051.274 mortalities and 27,825.015 million Chinese Yuan (CNY) in economic losses were attributed to O3 exposure, which considerably surpassing the 5,450.716 mortalities and 6,553,780 million CNY in economic losses attributed to PM2.5 exposure. The O3-related health risks and economic losses increased by 3.75% and 9.3% from 2015 to 2016, while those linked to PM2.5 decreased by 23.33% and 18.7%. Sensitivity analysis results indicated that changes in pollutant concentrations were the major factors affecting mortality rather than baseline mortality and population.