Neo-construction of a SO2-tunable near-infrared ratiometric fluorescent probe for high-fidelity diagnosis and evaluation hazards of Cd2+-induced liver injury.

Cadmium-contaminated water and food are seriously hazardous to the human health, especially liver injury. To understand the entanglement relationship between cadmium ion (Cd2+)-induced liver injury and the biomarker sulfur dioxide (SO2), a reliable bioanalytical tool is urgently needed, detecting SO2 to diagnose and evaluate the extent of liver injury in vivo. Herein, based on the Förster resonance energy transfer (FRET) mechanism, a novel SO2-tunable NIR ratiometric fluorescent probe (SMP) was developed, it was used to diagnose and treat liver injury induced by Cd2+ in biosystems. Specifically, it was constructed by conjugating a NIR dicyanoisophorone with a NIR benzopyranate as the donor and acceptor, respectively, and the ratiometric response of SO2- regulated by the Michael addition reaction. In addition, SMP exhibits rapid reaction time (<15 s), two well-resolved emission peaks (68 nm) with less cross-talk between channels for high imaging resolution, superior selectivity, and low limit of detection (LOD=80.3 nM) for SO2 detection. Impressively, SMP has been successfully used for intracellular ratiometric imaging of Cd2+-induced SO2 and diagnostic and therapeutic evaluation in liver injury mice models with satisfactory results. Therefore, SMP may provide a powerful molecular tool for revealing the occurrence and development relationship between SO2 and Cd2+-induced liver injury. ENVIRONMENTAL IMPLICATION: Cadmium ions are one of the well-known toxic environmental pollutants, which are enriched in the human body through inhalation of cadmium-contaminated air or from the food chain, leading to damage in various organs, especially liver injury. Therefore, we developed a novel fluorescent probe that can specifically detect SO2 in Cd2+-induced liver injury, which is critically important for the diagnosis and evaluation of Cd2+-induced liver injury diseases. The specific detection of SO2 of this probe has been successfully demonstrated in live HepG2 cells and Cd2+-induced liver injury mice.

Low-level ambient sulfur dioxide exposure and genetic susceptibility associated with incidence of idiopathic pulmonary fibrosis: A national prospective cohort study.

BACKGROUND: The association between long-term air pollution exposure and the development of idiopathic pulmonary fibrosis (IPF) has been established, but the evidence regarding the effect of low levels of air pollution, especially ambient sulfur dioxide (SO2), is limited. Besides, the combined effect and interaction between genetic susceptibility and ambient SO2 on IPF remain uncertain. METHODS: This study retrieved data from 402,042 participants who were free of IPF at baseline in the UK Biobank. The annual mean concentration of ambient SO2 was estimated for each participant based on their residential addresses using a bilinear interpolation method. Cox proportional hazard models were used to examine the relationship between ambient SO2 and incident IPF. We further generated a polygenic risk score (PRS) for IPF and estimated the combined effects of genetic susceptibility and ambient SO2 on incident IPF. RESULTS: After a median follow-up of 11.78 years, 2562 cases of IPF were identified. The results indicated that each 1 µg/m3 increase in ambient SO2 was associated with a hazard ratio (HR) (95% confidence interval [CI]) of 1.67 (1.58, 1.76) for incident IPF. The study found statistically significant synergistic additive interaction between genetic susceptibility and ambient SO2. Individuals with high genetic risk and high ambient SO2 exposure had a higher risk of developing IPF (HR = 7.48, 95% CI:5.66, 9.90). CONCLUSION: The study suggests that long-term exposure to ambient SO2, even at concentrations lower than current air quality guidelines set by the Word Health Organization and European Union, may be an important risk factor for IPF. This risk is more pronounced among people with a high genetic risk. Therefore, these findings emphasize the need to consider the potential health effects of SO2 exposure and the necessity for stricter air quality standards.

Short-Term Association between Sulfur Dioxide and Mortality: A Multicountry Analysis in 399 Cities.

BACKGROUND: Epidemiological evidence on the health risks of sulfur dioxide (SO2) is more limited compared with other pollutants, and doubts remain on several aspects, such as the form of the exposure-response relationship, the potential role of copollutants, as well as the actual risk at low concentrations and possible temporal variation in risks. OBJECTIVES: Our aim was to assess the short-term association between exposure to SO2 and daily mortality in a large multilocation data set, using advanced study designs and statistical techniques. METHODS: The analysis included 43,729,018 deaths that occurred in 399 cities within 23 countries between 1980 and 2018. A two-stage design was applied to assess the association between the daily concentration of SO2 and mortality counts, including first-stage time-series regressions and second-stage multilevel random-effect meta-analyses. Secondary analyses assessed the exposure-response shape and the lag structure using spline terms and distributed lag models, respectively, and temporal variations in risk using a longitudinal meta-regression. Bi-pollutant models were applied to examine confounding effects of particulate matter with an aerodynamic diameter of ≤10µm (PM10) and 2.5µm (PM2.5), ozone, nitrogen dioxide, and carbon monoxide. Associations were reported as relative risks (RRs) and fractions of excess deaths. RESULTS: The average daily concentration of SO2 across the 399 cities was 11.7 µg/m3, with 4.7% of days above the World Health Organization (WHO) guideline limit (40 µg/m3, 24-h average), although the exceedances occurred predominantly in specific locations. Exposure levels decreased considerably during the study period, from an average concentration of 19.0 µg/m3 in 1980-1989 to 6.3 µg/m3 in 2010-2018. For all locations combined, a 10-µg/m3 increase in daily SO2 was associated with an RR of mortality of 1.0045 [95% confidence interval (CI): 1.0019, 1.0070], with the risk being stable over time but with substantial between-country heterogeneity. Short-term exposure to SO2 was associated with an excess mortality fraction of 0.50% [95% empirical CI (eCI): 0.42%, 0.57%] in the 399 cities, although decreasing from 0.74% (0.61%, 0.85%) in 1980-1989 to 0.37% (0.27%, 0.47%) in 2010-2018. There was some evidence of nonlinearity, with a steep exposure-response relationship at low concentrations and the risk attenuating at higher levels. The relevant lag window was 0-3 d. Significant positive associations remained after controlling for other pollutants. DISCUSSION: The analysis revealed independent mortality risks associated with short-term exposure to SO2, with no evidence of a threshold. Levels below the current WHO guidelines for 24-h averages were still associated with substantial excess mortality, indicating the potential benefits of stricter air quality standards. https://doi.org/10.1289/EHP11112.

Sulphur dioxide and fluoride co-exposure cause enamel damage by disrupting the Cl-/HCO3- ion transport.

OBJECTIVE: Although there is growing evidence linking the exposure to sulphur dioxide (SO2) and fluoride to human diseases, there is little data on the co-exposure of SO2 and fluoride. Moreover, literature on SO2 and fluoride co-exposure to enamel damage is insufficient. In this work, we concentrate on the concurrent environmental issues of excessive SO2 and fluoride in several coal-consuming regions. METHOD: To identify the toxicity of SO2 and fluoride exposure either separately or together, we used both ICR mice and LS8 cells, and factorial design was employed to assess the type of potential combined action. RESULT: In this study, co-exposure to SO2 and fluoride exacerbated enamel damage, resulting in more severe enamel defects of incisor and the damage occurred earlier. Cl-/HCO3- exchanger expression is increased by SO2 and fluoride in mouse incisor. Consistent with in vivo results, co-exposure of SO2 and fluoride decreased pHi and increased [Cl-]i level by increasing the expression of the Cl-/HCO3- exchanger in LS8 cells. Furthermore, SO2 and F may increase merlin protein expression, and merlin deficiency causes AE2 expression to decrease in vitro. CONCLUSION: Overall, these results indicate that co-exposure to SO2 and fluoride may result in more toxicity both in vitro and in vivo than a single exposure to SO2 and fluoride, suggesting that residents in areas contaminated with SO2 and fluoride may be more likely to suffer enamel damage.

Sulfur dioxide may predominate in the adverse effects of ambient air pollutants on semen quality among the general population in Hefei, China.

Previous studies have reported potential adverse effects of exposure to ambient air pollutants on semen quality in infertile men, but studies on the general population have been limited and inconsistent, and the pollutants that play a major role remain unclear. This study aimed to explore the potential association between exposure to six air pollutants (PM2.5, PM10, NO2, SO2, O3 and CO) during different sperm development periods and semen quality among the general population, and to explore the interaction between different air pollutant exposures. We included 1515 semen samples collected from the Human Sperm Bank. We improved individuals' exposure level estimation by combining inverse distance weighting (IDW) interpolation with satellite remote sensing data. Multivariate linear regression models, restricted cubic spline functions and double-pollutant models were used to assess the relationship between exposure to six air pollutants and sperm volume, concentration, total sperm number and sperm motility. A negative association was found between SO2 exposure and progressive motility and total motility during 0-90 lag days and 70-90 lag days, and SO2 exposure during 10-14 lag days adversely affected sperm concentration and total sperm number. Sensitive analyses for qualified sperm donors and the double-pollutant models obtained similar results. Additionally, there were nonlinear relationships between exposure to PM, NO2, O3, CO and a few semen parameters, with NO2 and O3 exposure above the threshold showing negative correlations with total motility and progressive motility, respectively. Our study suggested that SO2 may play a dominant role in the adverse effects of ambient air pollutants on semen quality in the general population by decreasing sperm motility, sperm concentration and total sperm number. Also, even SO2 exposure lower than the recommended standards of the World Health Organization (WHO) could still cause male reproductive toxicity, which deserves attention.

Associations between congenital heart disease and air pollutants at different gestational weeks: a time-series analysis.

Exposure to air pollution during pregnancy has been linked to birth defects. But the directions of studies on the associations between air pollutants exposure and effect on the incidence of congenital heart disease (CHDs) were inconsistent. To date, few studies were concentrated on the effects of both particulate matter and gaseous air pollutant exposure on CHDs across the full gestational week simultaneously. Our study aimed to investigate the critical exposure windows for each air pollutant throughout 40 gestational weeks. Data on CHDs, air pollution, and meteorological factors from 2013 to 2019 were collected in Lanzhou, China. A distributed lag nonlinear model combined with a quasi-Poisson regression model was applied to evaluate the weekly exposure-lag-response association between air pollutants levels and CHDs, and the subgroup analyses were conducted by gender (baby boy and baby girl). The study included 1607 mother-infant pairs. The results demonstrated that exposure of pregnant women to particulate matter ≤ 5 µm (PM2.5) at lag 1-4 weeks was significantly associated with the risk of CHDs, and the strongest effects were observed in the lag 1 week (1.150, 95%CI 1.059-1.248). For exposure to particulate matter ≤ 10 µm (PM10) at lag 1-3 weeks, the strongest effects were observed in the lag 1 week (1.075, 95% CI 1.026-1.128). For exposure to sulfur dioxide (SO2) at lag 1-4 weeks, the strongest effects were observed in the lag 1 week (1.154, 95% CI 1.025-1.299). For exposure to carbon monoxide (CO) at lag 1-3 weeks, the strongest effects were observed in the lag 1 week (1.089, 95% CI 1.002-1.183). For exposure to ozone (O3) concentration at lag 9-15 weeks, the strongest effects were observed in the lag 15 weeks (1.628, 95% CI 1.001-2.649). The cumulative effects of PM2.5, PM10, SO2, and CO along weeks with a maximum of 1.609 (95%CI 1.000-2.589), 1.286 (95%CI 1.007-1.641), 1.648 (95%CI 1.018-2.668), and 1.368 (95%CI 1.003, 1.865), respectively. The effects were obvious in the initial gestational weeks too. Through the gender stratification analysis, the air pollutants with significant effects were PM2.5 for baby boys and PM2.5, PM10, SO2, CO, NO2, and O3 for baby girl. For the relationship between CHDs and air pollution in Lanzhou, PM2.5, PM10, SO2, CO, and O3 played an important role in the initial gestational weeks, especially for baby girl.

Linear and non-linear relationships between sulfur dioxide and semen quality: A longitudinal study in Anhui, China.

Existing evidence indicates that ambient air pollutants pose a threat to human semen quality; however, these findings are sparse and controversial. Besides, their non-linear dose-response relationship has not yet been well investigated. This study aimed to explore the linear and non-linear associations of gaseous air pollutants exposure with semen quality based on a large longitudinal cohort. A total of 15,112 males (with 28,267 semen tests) from the Anhui prospective assisted reproduction cohort were analyzed. Individual air pollutants exposure before semen tests in four exposure windows (i.e., 0-9, 10-14, 70-90, and 0-90 days) were estimated by inverse distance weighting interpolation. Linear mixed-effects models, cubic spline analysis and piecewise regression were used to test the potential linear and non-linear dose-response relationships. Ambient SO2 exposure was negatively associated with all semen quality parameters (all p values < 0.05), except for the progressive motility in the 0-90 and 70-90 days exposure windows. There were 'J' or 'U' shaped dose-response relationships of ambient SO2 exposure with total sperm count, progressive motility, total motility, progressively motile sperm count, and total motile sperm count (p values for non-linearity < 0.05), but not sperm concentration. Piecewise regression analysis also indicated a negative association of SO2 exposure with semen quality only when SO2 exposure was below the cut-off points identified by cubic spline analyses, which were all smaller than 40 µg/m3, the 2021 updated WHO air quality guideline level for SO2 exposure. Overall, we found that SO2 exposure was negatively associated with semen quality. Ambient SO2 exposure could reach the maximum hazardous dose even below the WHO air quality guideline level for SO2 exposure, suggesting a refinement to the current guideline.

Long-term trends in mortality risk associated with short-term exposure to air pollution in 10 Japanese cities between 1977 and 2015.

BACKGROUND AND AIM: Short-term associations between air pollution and mortality have been well reported in Japan, but the historical changes in mortality risk remain unknown. We examined temporal changes in the mortality risks associated with short-term exposure to four criteria air pollutants in selected Japanese cities. METHODS: We collected daily mortality data for non-accidental causes (n = 5,748,206), cardiovascular (n = 1,938,743) and respiratory diseases (n = 777,266), and air pollutants (sulfur dioxide [SO2], nitrogen dioxide [NO2], suspended particulate matter [SPM], and oxidants [Ox]) in 10 cities from 1977 to 2015. We performed two-stage analysis with 5-year stratification to estimate the relative risk (RR) of mortality per 10-unit increase in the 2-day moving average of air pollutant concentrations. In the first stage, city-specific associations were assessed using a quasi-Poisson generalized linear regression model. In the second stage, city-specific estimates were pooled using a random-effects meta-analysis. Linear trend and ratio of relative risks (RRR) were computed to examine temporal changes. RESULTS: When stratifying the analysis by every 5 years, average concentrations in each sub-period decreased for SO2, NO2, and SPM (14.2-2.3 ppb, 29.4-17.5 ppb, 52.1-20.6 µg/m3, respectively) but increased for Ox (29.1-39.1 ppb) over the study period. We found evidence of a negative linear trend in the risk of cardiovascular mortality associated with SPM across sub-periods. However, the risks of non-accidental and respiratory mortality per 10-unit increase in SPM concentration were significantly higher in the most recent period than in the earliest period. Other gaseous pollutants did not show such temporal risk change. The risks posed by these pollutants were slightly to moderately heterogeneous in the different cities. CONCLUSIONS: The mortality risks associated with short-term exposure to SPM changed, with different trends by cause of death, in 10 cities over 39 years whereas the risks for other gaseous pollutants were relatively stable.

Sulphur dioxide and fluoride co-exposure induce incisor hypomineralization and amelogenin upregulation via YAP/RUNX2 signaling pathway.

Sulphur dioxide (SO2) and fluoride are among the most common environmental pollutants affecting human health, and both co-exist in areas predominantly consuming coal. It is vital to analyse the combined toxicity of SO2 and fluoride, and their effects on health and the underlying mechanisms of their co-exposure have not yet been adequately assessed. In the present study, we used ICR mice and LS8 cells to investigate the toxicity of SO2 and fluoride exposure to the enamel, alone or in combination. Factorial design analysis was used to reveal the combined toxicity in vitro and in vivo. Co-exposure to SO2 and fluoride exacerbated enamel injury, resulting in more severe hypomineralization of incisor, and enamel structure disorders in mice, and could induce the accumulation of protein residue in the matrix of the enamel. Amelogenin expression was increased upon exposure to SO2 and fluoride, but enamel matrix proteases were not affected. Consistent with our in vivo results, co-exposure of SO2 and fluoride aggravated amelogenin expression in LS8 cells, and increased the YAP and RUNX2 levels. Co-exposure to SO2 and fluoride resulted in greater toxicity than individual exposure, both in vitro and in vivo, indicating that residents of areas exposed to SO2 and fluoride may have an increased risk of developing enamel damage.

Sulfur dioxide-enhanced asthma susceptibility is involved with inhibition of bitter taste transduction in mouse lung.

Sulfur dioxide (SO2) may induce asthma-like symptoms or worsen existing asthma, but the underlying mechanism is still unclear. In this study, the relationship between SO2 exposure, asthma development, and bitter taste transduction was analyzed using ovalbumin (OVA)-induced and SO2-aggravated asthma models. The results showed that twenty-seven and twelve bitter taste receptors (Tas2rs) were detectable in mouse trachea and lung, respectively, and that all of them were nearly down-regulated in OVA-induced BALB/c and C57BL/6 asthmatic mice. SO2 exposure alone did not trigger a distinct asthma-like phenotype, but the combination of SO2 and OVA allergen caused more severe asthma symptoms in mice including enhanced inflammatory cells infiltration, thickened airway walls, increased mucus secretion, and elevated expression of proinflammatory and Th2 cytokines (TNF-α, IL-4, IL-5, IL-13). Furthermore, SO2 enhanced the transcriptional repression of Tas2rs in OVA-induced asthmatic mice. These results indicated that the occurrence of mice asthma was correlated with the inhibition of bitter taste transduction, and more severe airway inflammation and injury were accompanied with an enhanced inhibition of bitter taste transduction. Our findings suggest that SO2 inhalation may amplify Th2 inflammatory responses in the lung of asthmatic mice by inhibiting bitter taste transduction, and thereby exacerbate asthma symptoms.

Effects of meteorological factors and air pollutants on the incidence of COVID-19 in South Korea.

Air pollution and meteorological factors can exacerbate susceptibility to respiratory viral infections. To establish appropriate prevention and intervention strategies, it is important to determine whether these factors affect the transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Therefore, this study examined the effects of sunshine, temperature, wind, and air pollutants including sulfur dioxide (SO2), carbon monoxide (CO), ozone (O3), nitrogen dioxide (NO2), particulate matter ≤2.5 µm (PM2.5), and particulate matter ≤10 µm (PM10) on the age-standardized incidence ratio of coronavirus disease (COVID-19) in South Korea between January 2020 and April 2020. Propensity score weighting was used to randomly select observations into groups according to whether the case was cluster-related, to reduce selection bias. Multivariable logistic regression analyses were used to identify factors associated with COVID-19 incidence. Age 60 years or over (odds ratio [OR], 1.29; 95% CI, 1.24-1.35), exposure to ambient air pollutants, especially SO2 (OR, 5.19; 95% CI, 1.13-23.9) and CO (OR, 1.17; 95% CI, 1.07-1.27), and non-cluster infection (OR, 1.28; 95% CI, 1.24-1.32) were associated with SARS-CoV-2 infection. To manage and control COVID-19 effectively, further studies are warranted to confirm these findings and to develop appropriate guidelines to minimize SARS-CoV-2 transmission.

Sulfur dioxide improves drought tolerance through activating Ca2+ signaling pathways in wheat seedlings.

Sulfur dioxide (SO2) and drought are two important co-occurring abiotic stresses affecting the growth and productivity of plants. Here, we will investigate the role of Ca2+ in regulating antioxidant defense during drought or SO2/drought stress, and the effect of SO2 pretreatment on the physiological response of wheat seedlings to drought stress. The results showed that exogenous Ca2+ increased the activities of SOD, CAT and POD, and reduced the contents of H2O2 and MDA in drought-treated wheat seedlings, suggesting Ca2+ could improve drought tolerance by promoting antioxidant defense in plants. Moreover, exogenous Ca2+ up-regulated the expression of two stress-responsive transcription factor (TF) genes, ERF1 and MYB30, to cope with drought stress. Exposure of wheat seedlings to 10 mg m-3 SO2 significantly enhanced the activities of SOD, CAT and POD. The contents of H2O2 and MDA remained at control levels, showing that SO2 at this concentration led to an activation of the antioxidant defense system and did not cause oxidative damage to the seedlings. Furthermore, 10 mg m-3 SO2 pretreatment increased the expression of CCaMK and CPK10, enhanced the activities of SOD and POD, and reduced the accumulation of H2O2 and MDA in drought-treated wheat seedlings, showing a role of SO2 in protection of plants against drought stress. However, with removal of Ca2+ by spraying EGTA on the SO2-pretreated wheat seedlings, the expression of transcription factor genes and activities of antioxidant enzymes were decreased, and the contents of H2O2 and MDA enhanced to the level of drought treatment alone, suggesting a role of Ca2+ in the SO2-induced alleviation of drought stress. Together, these results indicated that exogenous Ca2+ increased defense-related gene expression and enzyme activity in response to drought stress, and that pre-exposure to appropriate levels of SO2 could improve drought tolerance through activation of Ca2+ signaling pathways in plants. This study would provide new strategy for enhancing plant resistance to environmental stress.

Effects of sulfur dioxide, ozone, and ambient air pollution on lung histopathology, oxidative-stress biomarkers, and apoptosis-related gene expressions in rats.

PURPOSE OF THE STUDY: Ambient air pollution (AAP) has become an important health problem globally. Besides, several pieces of evidence indicate that air pollutants such as sulfur dioxide (SO2) and ozone (O3) are major contributors to a wide range of non-communicable diseases. The present study investigated the effects of AAP, sulfur dioxide, and ozone on oxidative stress, histopathology, and some apoptosis-related genes expressions of lung tissue in a rat model. MATERIALS AND METHODS: Thirty-two Wistar rats were randomly divided into the control, AAP, sulfur dioxide (10 ppm), and ozone (0.6 ppm) groups. After five consecutive weeks' exposure to the selected pollutants (3 h/day), lung tissues were harvested and immediately fixed with formalin. The samples were routinely processed, sectioned, stained with hematoxylin and eosin (H&E), and finally assessed for presence of pathological changes. Expression changes of BAX, p-53, EGFR, caspase-3, caspase-8 and caspase-9 were assayed using the RT-qPCR method. One hundred milligrams of lung tissues were extracted and the supernatants were used for assaying malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase activities. RESULTS: GPx activity was increased in the ozone (P = 0.05) and AAP (P < 0.001) groups and also MDA level in sulfur dioxide group (P = 0.008). Pathological lesions were mild, moderate, and severe in the sulfur dioxide, ozone, and AAP groups, respectively, as compared to control group (P ˂ 0.05). Exposure to AAP and sulfur dioxide enhanced BAX (P = 0.002) and caspase-8 (P < 0.001) mRNA expression, respectively. Caspases-3 and -8 mRNA expressions were elevated in ozone group (P < 0.001). CONCLUSIONS: The results indicated induction of oxidative stress. Our results suggest the apoptosis stimuli effect of AAP and also the extrinsic apoptotic pathway trigger effect of sulfur dioxide and ozone in the lung tissue in the concentrations used in the present study. The histopathological and the genes expression changes may be a result of the induced oxidative stress in the lung tissues.

Relationship between ambient air pollution and preterm birth: a retrospective birth cohort study in Yan'an, China.

Preterm birth (PTB) has been associated with exposure to air pollution, but it is unclear whether effects might vary among air pollution sources in a valley city, and yet few studies have investigated refined susceptible windows for PTB. We performed a retrospective birth cohort study in Yan'an city, a typical valley city in the west of China, and analyze the effects of air pollutants on premature delivery, identify critical windows for maternal air pollutants exposure and PTB. The pregnant women who gave birth in the Affiliated Hospital of Yan'an University and Yan'an people's Hospital from January 1, 2018 to December 31, 2019 were selected as the research objects. A questionnaire survey and medical records were conducted. The daily average concentrations of particulate matter with aerodynamic diameters of ≤ 2.5 µm (PM2.5) and ≤ 10 µm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2) and ozone (O3) in Yan'an City from January 1, 2017 to December 31, 2019 were collected. After controlling the confounding factors of PTB by logistic regression model, the effect of air pollutants on preterm birth was analyzed. After controlling the confounding factors such as maternal age, gestational times and gestational hypertension syndrome, PTB was associated with exposure to third trimester PM10 (adjusted odds ratio [aOR] = 1.019, 95% confidence interval [95%CI] = 1.004-1.035). PTB risk increased with second trimester exposure to SO2 (aOR = 1.039, CI = 1.011-1.068), also with third trimester (aOR = 1.031, CI = 1.010-1.053). PTB was also associated with third trimester O3 (aOR = 1.023, CI = 1.005-1.041). This study indicates that maternal exposure to PM10, SO2 and O3 might lead to increased risk of PTB, and critical exposure windows were inconsistent.

Hourly Air Pollutants and Acute Coronary Syndrome Onset in 1.29 Million Patients.

BACKGROUND: Short-term exposure to ambient air pollution has been linked with daily hospitalization and mortality from acute coronary syndrome (ACS); however, the associations of subdaily (hourly) levels of criteria air pollutants with the onset of ACS and its subtypes have rarely been evaluated. METHODS: We conducted a time-stratified case-crossover study among 1 292 880 patients with ACS from 2239 hospitals in 318 Chinese cities between January 1, 2015, and September 30, 2020. Hourly concentrations of fine particulate matter (PM2.5), coarse particulate matter (PM2.5-10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3) were collected. Hourly onset data of ACS and its subtypes, including ST-segment-elevation myocardial infarction, non-ST-segment-elevation myocardial infarction, and unstable angina, were also obtained. Conditional logistic regressions combined with polynomial distributed lag models were applied. RESULTS: Acute exposures to PM2.5, NO2, SO2, and CO were each associated with the onset of ACS and its subtypes. These associations were strongest in the concurrent hour of exposure and were attenuated thereafter, with the weakest effects observed after 15 to 29 hours. There were no apparent thresholds in the concentration-response curves. An interquartile range increase in concentrations of PM2.5 (36.0 µg/m3), NO2 (29.0 µg/m3), SO2 (9.0 µg/m3), and CO (0.6 mg/m3) over the 0 to 24 hours before onset was significantly associated with 1.32%, 3.89%, 0.67%, and 1.55% higher risks of ACS onset, respectively. For a given pollutant, the associations were comparable in magnitude across different subtypes of ACS. NO2 showed the strongest associations with all 3 subtypes, followed by PM2.5, CO, and SO2. Greater magnitude of associations was observed among patients older than 65 years and in the cold season. Null associations of exposure to either PM2.5-10 or O3 with ACS onset were observed. CONCLUSIONS: The results suggest that transient exposure to the air pollutants PM2.5, NO2, SO2, or CO, but not PM2.5-10 or O3, may trigger the onset of ACS, even at concentrations below the World Health Organization air quality guidelines.

Enhancement of drought tolerance in Arabidopsis plants induced by sulfur dioxide.

Sulfur dioxide (SO2) is a common air pollutant that has multiple effects on plants. In the present study, the improvement of drought tolerance in Arabidopsis plants by SO2 fumigation was investigated. The results showed that pre-exposure to 30 mg/m3 SO2 for 72 h could reduce water loss, stomatal conductance (Gs) and the transpiration rate (Tr) but increased the net photosynthetic rate (Pn), water use efficiency (iWUE) and photosynthetic pigment contents under drought conditions. The activities of superoxide dismutase (SOD) and peroxidase (POD) were significantly increased, while the contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) were decreased in SO2-pretreated Arabidopsis plants under drought stress. Additionally, the activity of o-acetylserine(thio)lyase (OASTL) and the content of cysteine (Cys), the rate-limiting enzyme and the first organic product of sulfur assimilation, were significantly increased in drought-stressed plants after SO2 pretreatment, along with increases in other thiol-containing compounds, such as glutathione (GSH) and nonprotein thiol (NPT). Meanwhile, SO2 pre-exposure induced a higher level of proline accumulation, with increased activity of proline synthase P5CS and decreased activity of proline dehydrogenase ProDH. Consistent with the changes in enzyme activity, their corresponding gene expression patterns were different after SO2 treatment. Overall, the enhanced drought tolerance afforded by SO2 might be related to the improvement of plant photosynthesis, antioxidant defense, sulfur assimilation and osmotic adjustment. These findings provide new insights into the role of SO2 in plant adaptation to environmental stress.

Associations between Long-Term Air Pollution Exposure and Risk of Osteoporosis-Related Fracture in a Nationwide Cohort Study in South Korea.

Bone health is a major concern for aging populations globally. Osteoporosis and bone mineral density are associated with air pollution, but less is known about the impacts of air pollution on osteoporotic fracture. We aimed to assess the associations between long-term air pollution exposure and risk of osteoporotic fracture in seven large Korean cities. We used Cox proportional hazard models to estimate hazard rations (HRs) of time-varying moving window of past exposures of particulate matter (PM10), sulfur dioxide (SO2), carbon monoxide (CO), nitrogen dioxide (NO2), and ozone (O3) for osteoporotic fracture in Korean adults (age ≥ 50 years) in the National Health Insurance Service-National Sample Cohort data, followed 2002 to 2015. HRs were calculated for an interquartile range (IQR) increase. Comorbidity and prescription associated with osteoporosis, age, sex, body mass index, health behaviors, and income were adjusted in the models. Effect modification by age, sex, exercise, and income was examined. We assessed 56,467 participants over 535,481 person-years of follow up. Linear and positive exposure-response associations were found for SO2, while PM10 and NO2 showed nonlinear associations. SO2 was associated with osteoporosis-related fracture with marginal significance (HR for an IQR [2 ppb] increase = 1.04, 95% CI: 1.00, 1.09). The SO2 HR estimates were robust in analyses applying various moving windows of exposure (from one to three years of past exposure) and two-pollutant models. The central HR estimate of O3 implied positive associations but was not significant (HR for 0.007 ppm increase = 1.01, 95% CI: 0.97, 1.06). PM10, CO, and NO2 did not show associations. Vulnerable groups by sex, age, exercise, and income varied across air pollutants and there was no evidence of effect modifications. Long-term exposure to SO2, but not PM10, CO, NO2 and O3, was associated with increased osteoporotic fracture risks in Korean adults.

Short-term exposure to ambient air pollution and risk of daily hospital admissions for anxiety in China: A multicity study.

The potential impact of short-term exposure to ambient air pollution on risk of anxiety remains uncertain. We performed a detailed evaluation based on data from national insurance databases in China. Daily hospital admissions for anxiety disorders were identified in 2013-2017 from the national insurance databases covering up to 261 million urban residents in 56 cities in China. A two-stage time-series study was conducted to evaluate the associations between short-term exposure to major ambient air pollutants, including fine particles, inhalable particles, nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone, and carbon monoxide, and risk of daily hospital admissions for anxiety. Significant associations between short-term exposures to ambient NO2 and SO2 and risk of daily hospital admissions for anxiety were found in the overall analysis. Per 10 µg/m3 increases in NO2 at lag0 and SO2 at lag6 were associated with significant increases of 1.37% (95% CI: 0.14%, 2.62%) and 1.53% (95% CI: 0.59%, 2.48%) in anxiety admissions, respectively. Stronger associations were found in the southern region and patients <65 years for SO2. Short-term exposure to ambient air pollution is associated with increased risk of anxiety admissions, which may provide important implications for promotion of mental health in the public.

A ratiometric water-soluble fluorescent probe for the detection of sulfur dioxide derivative in sinusitis mice model.

Sulfur dioxide (SO2) plays an extremely important role in the basic processes of physiology and pathology. As an antioxidant, SO2 can maintain the redox homeostasis in the cell. Excessive inhalation of SO2 would lead to irreparable respiratory damage, resulting in respiratory diseases, neurological disorders, and even cardiovascular disease. Thus, it is urgent to exploit an excellent way to monitor SO2 derivatives in biological system. Herein, we design a water-soluble ratiometric fluorescent probe to fast detect the level of SO2 derivatives in living cells in vivo. The probe displays obvious fluorescence signal at long wavelength, which is helpful for imaging of biological system. After respond to SO2 derivatives, the fluorescence signal at 465 nm increases rapidly due to the Michael addition reaction is triggered, further causing the disruption of large conjugated system. The probe exhibits high selectivity and fast respond to SO2 derivatives, which can be able to sensitive and real-time monitoring of SO2 derivatives level in living cells. Moreover, the probe reveals a low detection limit and a great linear relationship to SO2 derivatives. Based on the negligible cytotoxicity and good biocompatibility of the probe, which is employed to detect exogenous and endogenous SO2 derivatives in living cells. In addition, it is also served as a potential chemical tool to detect SO2 derivatives in mice model of sinusitis.

The effect window for sulfur dioxide exposure in pregnancy on childhood asthma and wheezing: A case-control study.

BACKGROUND: The relationship between prenatal exposure to sulfur dioxide (SO2) and childhood wheezing and asthma is unclear. OBJECTIVE: To explore the association between prenatal exposure to SO2 and childhood wheeze and asthma. To investigate the effects for the exposure during different pregnancy trimesters. METHODS: We conducted a cross-sectional study firstly in Jinan City to get the prevalence of wheeze and asthma on children aged 18 months to 3 years. And then, we designed a case-control study based on population to evaluate the association between prenatal SO2 exposure and childhood asthma and wheezing. Based on the starting and ending date of pregnancy and specific residential addresses, the individual concentrations of SO2 during pregnancy was evaluated using an inverse distance weighted model. RESULTS: The prevalence of wheeze and asthma on children aged 18 months to 3 years was 2.07% in our cross-sectional study. 236 cases and 1445 controls were available for exposure estimates. The OR (95% CI) of 1.296 (1.130-1.491) was significant after adjusting for the covariates. In the first and third trimesters, the effects were enhanced to 1.602 (1.275-2.022) and 1.448 (1.179-1.783) in the multi-pollutant model with adjusting the effects of other trimesters. Coincidentally, the SO2 exposure level of the case in the first trimester was higher than that in the second and third trimesters (P < 0.001); however, there was no significant difference in exposure levels of the case between the second and third trimesters of pregnancy (P = 0.381). CONCLUSION: Prenatal exposure to higher concentration of SO2 could increase the risk of asthma and wheezing in younger children. The first trimester might be just the window for the toxic effect, while the third trimester was the sensitive window for the effect of SO2 exposure during pregnancy on childhood asthma.