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.

Mortality risk from United States coal electricity generation.

Policy-makers seeking to limit the impact of coal electricity-generating units (EGUs, also known as power plants) on air quality and climate justify regulations by quantifying the health burden attributable to exposure from these sources. We defined "coal PM2.5" as fine particulate matter associated with coal EGU sulfur dioxide emissions and estimated annual exposure to coal PM2.5 from 480 EGUs in the US. We estimated the number of deaths attributable to coal PM2.5 from 1999 to 2020 using individual-level Medicare death records representing 650 million person-years. Exposure to coal PM2.5 was associated with 2.1 times greater mortality risk than exposure to PM2.5 from all sources. A total of 460,000 deaths were attributable to coal PM2.5, representing 25% of all PM2.5-related Medicare deaths before 2009 and 7% after 2012. Here, we quantify and visualize the contribution of individual EGUs to mortality.

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.

Environmental influences on ophthalmic conditions: A scoping review.

BACKGROUND: Environmental factors have been implicated in various eye pathologies. The purpose of this review is to synthesise the published research on environmental effects on eye disease. METHODS: Four databases were searched for terms relating to environmental exposures and ophthalmic disease. Titles and abstracts were screened followed by full-text review. Data was extracted from 118 included studies. Quality assessment was conducted for each study. RESULTS: Air pollutants, including nitrogen dioxide, nitrites, sulphur dioxide, particulate matter, carbon monoxide, ozone and hydrocarbons are associated with ocular conditions ranging from corneal damage to various retinopathies, including central retinal artery occlusion. Certain chemicals and metals, such as cadmium, are associated with increased risk of age-related macular degeneration. Climate factors, such as sun exposure, have been associated with the development of cataracts. Living in rural areas was associated with various age-related eye diseases whereas people living in urban settings had higher risk for dry eye disease and uveitis. CONCLUSION: Environmental exposures in every domain are associated with various ophthalmic conditions. These findings underscore the importance of continued research on the interplay between the environment and eye health.

Fire and Brimstone: SO2 as a Chemical Weapon in History.

Sulfur dioxide (SO2), a chemical produced from the burning of sulfur-containing materials, has a long history in chemical warfare. While it was largely used during ancient sieges, there were numerous proposals to weaponize it for the open battlefield in the early modern age.

Sulfur dioxide derivatives aggravated ovalbumin-induced asthma through targeting TRPV1 and tight junctions.

This study aimed to investigate the effects of sulfur dioxide (SO2) derivatives on asthma induced by ovalbumin (OVA). Sprague Dawley rats were sensitized to and challenged with OVA and SO2 derivatives (NaHSO3 and Na2SO3, 1:3 M/M) to establish 28-day (short-term) and 42-day (long-term) asthma models. Exposure to SO2 derivatives aggravated asthma and hence, promoted lung injury in OVA-induced asthma. In addition, it upregulated the protein expression of TRPV1 and downregulated the expression of tight junctions (TJs). These changes were dose-dependent and were more pronounced in the presence of a high concentration of SO2 derivatives. In vitro, SO2 derivatives also increased the calcium influx and TRPV1 protein expression, and decreased TJ expression. Besides, no significant difference in the TJ expression was found between the WT and TRPV1-/- mice. The underlying mechanism might be related to regulating the effects of TRPV1 and TJs.

DNA methylation is associated with prenatal exposure to sulfur dioxide and childhood attention-deficit hyperactivity disorder symptoms.

Epigenetic influence plays a role in the association between exposure to air pollution and attention deficit hyperactivity disorder (ADHD); however, research regarding sulfur dioxide (SO2) is scarce. Herein, we investigate the associations between prenatal SO2 exposure and ADHD rating scale (ARS) at ages 4, 6 and 8 years repeatedly in a mother-child cohort (n = 329). Whole blood samples were obtained at ages 2 and 6 years, and genome-wide DNA methylation (DNAm) was analyzed for 51 children using the Illumina Infinium HumanMethylation BeadChip. We analyzed the associations between prenatal SO2 exposure and DNAm levels at ages 2 and 6, and further investigated the association between the DNAm and ARS at ages 4, 6 and 8. Prenatal SO2 exposure was associated with ADHD symptoms. From candidate gene analysis, DNAm levels at the 6 CpGs at age 2 were associated with prenatal SO2 exposure levels. Of the 6 CpGs, cg07583420 (INS-IGF2) was persistently linked with ARS at ages 4, 6 and 8. Epigenome-wide analysis showed that DNAm at 6733 CpG sites were associated with prenatal SO2 exposure, of which 58 CpGs involved in Notch signalling pathway were further associated with ARS at age 4, 6 and 8 years, persistently. DNAm at age 6 was not associated with prenatal SO2 exposure. Changes in DNAm levels associated with prenatal SO2 exposure during early childhood are associated with increases in ARS in later childhood.

Joint Associations of Short-Term Exposure to Ambient Air Pollutants with Hospital Admission of Ischemic Stroke.

BACKGROUND: Studies have estimated the associations of short-term exposure to ambient air pollution with ischemic stroke. However, the joint associations of ischemic stroke with air pollution as a mixture remain unknown. METHODS: We employed a time-stratified case-crossover study to investigate 824,808 ischemic stroke patients across China. We calculated daily mean concentrations of particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5), maximum 8-h average for O3 (MDA8 O3), nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO) across all monitoring stations in the city where the IS patients resided. We conducted conditional logistic regression models to estimate the exposure-response associations. RESULTS: Results from single-pollutant models showed positive associations of hospital admission for ischemic stroke with PM2.5 (excess risk [ER] = 0.38%, 95% confidence interval [CI]: 0.29% to 0.47%, for 10 µg/m3), MDA8 O3 (ER = 0.29%, 95% CI: 0.18% to 0.40%, for 10 µg/m3), NO2 (ER = 1.15%, 95% CI: 0.92% to 1.39%, for 10 µg/m3), SO2 (ER = 0.82%, 95% CI: 0.53% to 1.11%, for 10 µg/m3) and CO (ER = 3.47%, 95% CI: 2.70% to 4.26%, for 1 mg/m3). The joint associations (ER) with all air pollutants (for interquartile range width increases in each pollutant) estimated by the single-pollutant model was 8.73% and was 4.27% by the multipollutant model. The joint attributable fraction of ischemic stroke attributable to air pollutants based on the multipollutant model was 7%. CONCLUSIONS: Short-term exposures to PM2.5, MDA8 O3, NO2, SO2, and CO were positively associated with increased risks of hospital admission for ischemic stroke. The joint associations of air pollutants with ischemic stroke might be overestimated using single-pollutant models. See video abstract at, http://links.lww.com/EDE/C8.

Short-Term Exposure to Sulfur Dioxide and Nitrogen Monoxide and Risk of Out-of-Hospital Cardiac Arrest.

BACKGROUND & AIMS: Over the past decades, particulate matter (PM), especially fine PM <2.5 µm in aerodynamic diameter (PM2.5) has been a major research focus. However, the air pollutant is a mixture of gases or vapour-phase compounds, such as carbon monoxide (C), nitrogen oxides (NOx), photochemical oxidants (Ox), and sulfur dioxide (SO2). Little is known about their cardiovascular effect, individually or in combination with PM. Thus, we aimed to determine the associations between the incidence of acute cardiac events and both gaseous and PM using a case-crossover design. METHODS: Cardiovascular cases were identified through the Gunma Prefectural Ambulance Activity Database in Japan in 2015 (1,512 out-of-hospital cardiac arrest [OHCA] and 1,002 heart failures from 53,006 ambulance cases). Air quality data from the nearest station was for day of the arrest (lag0) and 1-2 days before the arrest (lag1, lag2) and the moving average across days 0-1 (lag0-1). Conditional logistic regression was used for unadjusted and adjusted analysis for temperature and humidity. RESULTS: Independent associations of OHCA were daily concentrations of SO2 at lag1 (OR 1.173, 95%CI 1.004, 1.370; p=0.044) and lag0-1 (OR 1.203, 95%CI 1.015, 1.425; p=0.033); and daily NO concentrations at lag2 (OR 1.039, 95%CI 1.007, 1.072; p=0.016). The incidence of heart failure was significantly associated with daily concentrations of Ox on the day of the event in univariable model but not after adjustment for temperature and humidity. No associations were found for other pollutants. CONCLUSIONS: Short-term exposure to SO2 and NO are associated with an increased risk of OHCA.

Effects of Air Pollution on Chemosensory Dysfunction in COVID-19 Patients.

BACKGROUND: In some patients, coronavirus disease 2019 (COVID-19) is accompanied by loss of smell and taste, and this has been reportedly associated with exposure to air pollutants. This study investigated the relationship between the occurrence of chemosensory dysfunction in COVID-19 patients and air pollutant concentrations in Korea. METHODS: Information on the clinical symptom of chemosensory dysfunction, the date of diagnosis, residential area, age, and sex of 60,194 confirmed COVID-19 cases reported to the Korea Disease Control and Prevention Agency from January 20 to December 31, 2020 was collected. In addition, the daily average concentration of air pollutants for a week in the patients' residential area was collected from the Ministry of Environment based on the date of diagnosis of COVID-19. A binomial logistic regression model, using age and gender, standardized smoking rate, number of outpatient visits, 24-hour mean temperature and relative humidity at the regional level as covariates, was used to determine the effect of air pollution on chemosensory dysfunction. RESULTS: Symptoms of chemosensory dysfunction were most frequent among patients in their 20s and 30s, and occurred more frequently in large cities. The logistic analysis showed that the concentration of particulate matter 10 (PM10) and 2.5 (PM2.5) up to 2 days before the diagnosis of COVID-19 and the concentration of sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) at least 7 days before the diagnosis of COVID-19 affected the development of chemosensory dysfunction. In the logistic regression model adjusted for age, sex, standardized smoking rate, number of outpatient visits, and daily average temperature and relative humidity, it was found that an increase in the interquartile range of PM10, PM2.5, SO2, NO2, and CO on the day of diagnosis increased the incidence of chemosensory dysfunction 1.10, 1.10, 1.17, 1.31, and 1.19-fold, respectively. In contrast, the O3 concentration had a negative association with chemosensory dysfunction. CONCLUSION: High concentrations of air pollutants such as PM10, PM2.5, SO2, NO2, and CO on the day of diagnosis increased the risk of developing chemosensory dysfunction from COVID-19 infection. This result underscores the need to actively prevent exposure to air pollution and prevent COVID-19 infection. In addition, policies that regulate activities and products that create high amounts of harmful environmental wastes may help in promoting better health for all during COVID-19 pandemic.

Residential greenness attenuated association of long-term air pollution exposure with elevated blood pressure: Findings from polluted areas in Northern China.

Background: Evidence on the hypertensive effects of long-term air pollutants exposure are mixed, and the joint hypertensive effects of air pollutants are also unclear. Sparse evidence exists regarding the modifying role of residential greenness in such effects. Methods: A cross-sectional study was conducted in typically air-polluted areas in northern China. Particulate matter with diameter < 1 µm (PM1), particulate matter with diameter < 2.5 µm (PM2.5), particulate matter with diameter < 10 µm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) were predicted by space-time extremely randomized trees model. We used the Normalized Difference Vegetation Index (NDVI) to reflect residential green space. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were examined. We also calculated the pulse pressure (PP) and mean arterial pressure (MAP). Generalized additive model and quantile g-computation were, respectively, conducted to investigate individual and joint effects of air pollutants on blood pressure. Furthermore, beneficial effect of NDVI and its modification effect were explored. Results: Long-term air pollutants exposure was associated with elevated DBP and MAP. Specifically, we found a 10-µg/m3 increase in PM2.5, PM10, and SO2 were associated with 2.36% (95% CI: 0.97, 3.76), 1.51% (95% CI: 0.70, 2.34), and 3.54% (95% CI: 1.55, 5.56) increase in DBP; a 10-µg/m3 increase in PM2.5, PM10, and SO2 were associated with 1.84% (95% CI: 0.74, 2.96), 1.17% (95% CI: 0.52, 1.83), and 2.43% (95% CI: 0.71, 4.18) increase in MAP. Air pollutants mixture (one quantile increase) was positively associated with increased values of DBP (8.22%, 95% CI: 5.49, 11.02) and MAP (4.15%, 95% CI: 2.05, 6.30), respectively. These identified harmful effect of air pollutants mainly occurred among these lived with low NDVI values. And participants aged ≥50 years were more susceptible to the harmful effect of PM2.5 and PM10 compared to younger adults. Conclusions: Our study indicated the harmful effect of long-term exposure to air pollutants and these effects may be modified by living within higher green space place. These evidence suggest increasing residential greenness and air pollution control may have simultaneous effect on decreasing the risk of hypertension.

A 28-day, 2-year study reveals that adolescents are more fatigued and distressed on days with greater NO2 and CO air pollution.

This 2-year, 28-day study examined whether adolescents felt greater fatigue and emotional distress the same day and the day after air quality was worse. We linked objective daily air quality measurements to daily self-reports from 422 Mexican-American adolescents in Los Angeles County, California from 2009 to 2011 (50% girls, MAge = 15 years). A robust, within-subject analysis of 9696 observations revealed that adolescents with ongoing physical complaints reported greater fatigue and emotional distress on days that the air contained higher levels of nitrogen dioxide (NO2) and carbon monoxide (CO). Regardless of physical complaints, adolescents on average also reported greater fatigue the day after NO2 levels were higher. The same-day and next-day associations between air pollution and distress were mediated via daily increases in fatigue. Results were robust when controlling for day of the week, and daily temperature and humidity. Sulfur dioxide (SO2), ozone (O3), PM2.5 and PM10 were not related to daily fatigue or distress.

Association between air pollution and the prevalence of allergic rhinitis in Chinese children: A systematic review and meta-analysis.

Background: Allergic rhinitis (AR) is a common chronic inflammatory disease with bothersome symptoms. However, the effect of air pollution on the prevalence of AR in children is controversial. Objective: This study aimed to investigate the association between air pollution and the prevalence of AR in Chinese children. Methods: This study, in China, included 160,356 students ages 0-18 years who completed a questionnaire about the accuracy of the International Study of Asthma and Allergies in Childhood (ISAAC). The effect of different air pollutants on the prevalence rate were evaluated by meta-analysis. Also, it evaluated the effect of different air pollutants on the prevalence rate. Results: The differences in the effects of sulfur dioxide (SO2) exposure (combined odds ratio [ORcombined] 1.03 [95% confidence interval {CI}, 1.01-1.05]; p = 0.010) and nitrogen dioxide (NO2) exposure (ORcombined 1.11 [95% CI, 1.05-1.18]; p = 0.0006) on the risk of childhood AR was statistically significant. The effect of particulate matter with aerodynamic diameter of <10 µm (PM10) exposure on the risk of childhood AR was statistically significant (ORcombined 1.02 [95% CI, 1.01-1.03]; p < 0.001), the effect of particulate matter with aerodynamic diameter of <2.5 µm (PM2.5) exposure on the risk of childhood AR was statistically significant (ORcombined 1.15 [95% CI, 1.03-1.29]; p = 0.02), and the effect of ozone exposure on the risk of childhood AR was not statistically significant (ORcombined 0.98 [95% CI, 0.67-1.41]; p = 0.13). Conclusion: NO2, SO2, PM2.5, and PM10 were associated with the prevalence of AR in Chinese children. PM2.5 had the highest correlation with AR prevalence.

The relationship between air pollutant levels and aneurysmal subarachnoid hemorrhage.

BACKGROUND: The relationship between air pollutants, including fine particles (particulate matter [PM] < 10 µm and < 2.5 µm), and aneurysmal subarachnoid hemorrhage (SAH) has been inadequately studied, and the results remain inconclusive. In this study, we attempted to investigate the relationship between air pollutant levels and aneurysmal SAH. METHODS: Ninety-two patients diagnosed with aneurysmal SAH were retrospectively included in the study. Medical records were reviewed, and levels of pollutants, including those of sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and PM with an aerodynamic diameter < 10 and 2.5 µm (PM10 and PM2.5), were collected from the open-source Air Korea website for a period of 4 days. Independent t-tests were conducted to identify the difference in the pollutant levels between the data obtained on the day of aneurysm rupture (D-0) and the other 3 days (D-7, D-2, and D-1). RESULTS: A majority (40.2%) of the patients experienced aneurysm rupture during the fall season when the mean daily pollutant levels were 0.004 ± 0.001 (ppm, SO2), 0.517 ± 0.218 (ppm, CO), 0.02056 ± 0.012 (ppm, O3), 0.02628 ± 0.015 (ppm, NO2), 36.36957 ± 24.538 (µg/m3, PM10), and 19.75581 ± 13.494 (µg/m3, PM2.5), respectively. The level of NO2 was significantly higher on the day of aneurysm rupture (P = .035) than on the other days, while the levels of CO and O3 were nonsignificantly higher (P = .081, P = .055, respectively) on the day of aneurysm rupture than on the other days. There was no significant differences in the PM levels between the 4 days. CONCLUSION: A relationship between PM levels and aneurysm rupture was not identified. Only the levels of classic air pollutant (CO, O3, and NO2) were higher on the aneurysm rupture day than on the other days.

The prenatal and postnatal effects of air pollution on asthma in children with atopic dermatitis.

OBJECTIVES: Air pollution is strongly associated with asthma, but has not been determined to induce new-onset asthma development in children with atopic dermatitis (AD). WORKING HYPOTHESIS: To assess whether prenatal/postnatal exposure to air pollutants triggers new-onset asthma development in children with AD. STUDY DESIGN: Retrospective cohort study. PATIENT-SUBJECT SELECTION: Data of patients 3% were significantly influenced by prenatal exposure to PM2.5 , especially SO2 , NO, and NO2 . CONCLUSIONS: Prenatal and postnatal exposure to air pollution have an association with asthma development in AD patients.

Association Between Maternal Exposure to SO2 and Congenital Ear Malformations in Offspring: A Population-Based Case-Control Study in Liaoning Province, China.

Objectives: To examine associations between maternal sulfur dioxide (SO2) exposure and congenital ear malformations risk in offspring. Methods: We surveyed 1676 cases with congenital ear malformations and 7950 controls from the Maternal and Child Health Certificate Registry of Liaoning Province between 2010 and 2015. SO2 concentrations were obtained from the Municipal Environment Protection Bureau of Liaoning Province. Multivariable logistic regression models and Restricted cubic splines (RCS) model were used to assess the aforementioned association. Results: There were significant associations between maternal SO2 exposure and congenital ear malformations risk during the 3 months before conception (OR Q4 vs. Q1 = 1.93, 95% CI = 1.43-2.59) and the 3 months after conception (OR Q4 vs. Q1 = 1.63, 95% CI = 1.22-2.18). Similar results were obtained in the analysis of single-month exposure windows, except for the third month before conception and the third month after conception. Moreover, these findings were broadly consistent across subgroups and robust in sensitivity analyses. There were non-linear dose-response associations between SO2 exposure and congenital ear malformations based on restricted cubic spline model analysis. Conclusion: Maternal SO2 exposure is associated with increased congenital ear malformations risk in offspring.

Long-term exposure to ambient air pollution and serum liver enzymes in older adults: A population-based longitudinal study.

PURPOSE: To investigate the association of long-term exposure to ambient air pollution with serum liver enzymes in older adults. METHODS: In this longitudinal study, we investigated 318,911 adults aged 65 years or older and assessed their long-term residential exposure to particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5), particulate matter with an aerodynamic diameter ≤10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). Linear mixed models and generalized linear mixed models were implemented for exposure-response analyses. RESULTS: Each interquartile range (IQR) increase of PM2.5, PM10, SO2, NO2, CO, and O3 exposures was significantly associated with a 4.6%, 4.6%, 5.6%, 4.6%, 6.2%, and 3.6% increase in alanine aminotransferase (ALT), and a 4.6%, 5.2%, 3.6%, 3.3%, 6.1%, and 4.0% increase in aspartate aminotransferase (AST), respectively. Each IQR increase of PM2.5, PM10, SO2, NO2, CO, and O3 exposures was significantly associated with a 23%, 24%, 28%, 17%, 31%, and 19% increase in odds of elevated ALT (>40 U/L), and a 32%, 39%, 40%, 32%, 57%, and 25% increase in odds of elevated AST (>40 U/L), respectively. CONCLUSIONS: Long-term exposure to ambient air pollution was significantly associated with increased serum liver enzyme levels in older adults, suggesting that air pollution exposures may induce hepatocellular injury.

Maternal Exposure to Sulfur Dioxide and Risk of Omphalocele in Liaoning Province, China: A Population-Based Case-Control Study.

Evidence of the association between maternal sulfur dioxide (SO2) exposure and the risk of omphalocele is limited and equivocal. We aimed to assess the aforementioned topic during the first trimester of pregnancy. A population-based case-control study was carried out in infants consisting of 292 cases of omphalocele and 7,950 healthy infant controls. Exposure to SO2, particulate matter with aerodynamic diameters ≤ 10 µm, and nitrogen dioxide was assessed by averaging the concentration from all stations in the mother's residential city. SO2 exposure was categorized into three groups, with the lowest tertile defined as the reference category. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multivariable logistic regression models. Higher SO2 exposure during the first trimester was significantly associated with omphalocele risk [per standard deviation (42 ug/m3) increment: OR = 1.39, 95% CI = 1.22-1.65]. When focusing on shorter exposure windows, similar positive associations were observed for SO2 exposure in the first and third months of pregnancy. In addition, compared with the lowest tertile, high SO2 exposure in the second month of pregnancy increased the risk of omphalocele (OR = 2.80, 95% CI = 1.61-4.97). Maternal exposure to SO2 during the first trimester may increase the risk of omphalocele in offspring.

Association between gaseous air pollutants and idiopathic nephrotic syndrome in children: a 12-year population-based cohort study.

BACKGROUND: To date, there is insufficient knowledge about the association of air pollution and childhood nephrotic syndrome in the real world. This study aimed to evaluate the effects of the three common gaseous air pollutants, including sulfur dioxide, total hydrocarbon, and methane, on the risk of idiopathic nephrotic syndrome (INS) in children. METHODS: We collected data from the Taiwan National Health Insurance Research Database and Taiwan Air Quality-Monitoring Database. Children younger than 18 years old, identified from January 1, 2000, were followed up until the first diagnosis of INS was established or until December 31, 2012. We measured the incidence rates and hazard ratios for INS stratified based on the quartiles (Q1-Q4) of air pollutant concentration. Multivariate Cox proportional hazards models were also applied by adjusting age, sex, monthly income, and urbanization. RESULTS: Compared with participants exposed to Q1 concentrations, the adjusted hazard ratios (aHRs) for INS increased progressively along the four quartiles of sulfur dioxide, total hydrocarbon, and methane, from 1 (Q1) to 1.78 (Q4), 1 (Q1) to 3.49 (Q4), 1 (Q1) to 7.83 (Q4), respectively. CONCLUSIONS: Our study revealed that children with exposure to higher concentrations of sulfur dioxide, total hydrocarbon, and methane was associated with an increased risk of INS.

Ambient Air Pollution and Kawasaki Disease in Korean Children: A Study of the National Health Insurance Claim Data.

Background Kawasaki disease (KD) is a systemic vasculitis of unknown etiology that primarily affects children under 5 years of age. Some researchers suggested a potential triggering effect of air pollution on KD, but the findings are inconsistent and limited by small sample size. We investigated the association between ambient air pollution and KD among the population of South Korea younger than 5 years using the National Health Insurance claim data between 2007 and 2019. Methods and Results We obtained the data regarding particulate matter ≤10 or 2.5 µm in diameter, nitrogen dioxide, sulfur dioxide, carbon monoxide, and ozone from 235 regulatory monitoring stations. Using a time-stratified case-crossover design, we performed conditional logistic regression to estimate odds ratios (OR) of KD according to interquartile range increases in each air pollutant concentration on the day of fever onset after adjusting for temperature and relative humidity. We identified 51 486 children treated for KD during the study period. An interquartile range increase (14.67 µg/m3) of particulate matter ≤2.5 µm was positively associated with KD at lag 1 (OR, 1.016; 95% CI, 1.004-1.029). An interquartile range increase (2.79 ppb) of sulfur dioxide concentration was associated with KD at all lag days (OR, 1.018; 95% CI, 1.002-1.034 at lag 0; OR, 1.022; 95% CI, 1.005-1.038 at lag 1; OR, 1.017; 95% CI, 1.001-1.033 at lag 2). Results were qualitatively similar in the second scenario of different fever onset, 2-pollutant model and sensitivity analyses. Conclusions In a KD-focused national cohort of children, exposure to particulate matter ≤2.5 µm and sulfur dioxide was positively associated with the risk of KD. This finding supports the triggering role of ambient air pollution in the development of KD.