Short-term exposure to sulfur dioxide and the occurrence of chronic obstructive pulmonary disease: An updated systematic review and meta-analysis based on risk of bias and certainty of evidence.

Several studies have documented a relationship between short-term exposure to atmospheric sulfur dioxide (SO2) and chronic obstructive pulmonary disease (COPD). However, findings vary across different regions. This meta-analysis employed a random-effects model to calculate the combined risk estimate for each 10-µg/m3 increase in ambient SO2 concentration. Subgroup analysis aimed to identify sources of heterogeneity. To assess potential bias, studies were evaluated using a domain-based assessment tool developed by the World Health Organization. Sensitivity analyses, based on bias risk, explored how model assumptions influenced associations. An evidence certainty framework was used to evaluate overall evidence quality. The study protocol was registered with PROSPERO (CRD42023446823). We thoroughly reviewed 191 full-text articles, ultimately including 15 in the meta-analysis. The pooled relative risk for COPD was 1.26 (95 % CI 0.94-1.70) per 10-µg/m3 increase in ambient SO2. Eleven studies were deemed high risk due to inadequate handling of missing data. Overall evidence certainty was rated as medium. Given SO2's significant public health implications, continuous monitoring is crucial. Future research should include countries in Africa and Oceania to enhance global understanding of atmospheric SO2-related health issues.

Air pollution disproportionately impairs beneficial invertebrates: a meta-analysis.

Air pollution has the potential to disrupt ecologically- and economically-beneficial services provided by invertebrates, including pollination and natural pest regulation. To effectively predict and mitigate this disruption requires an understanding of how the impacts of air pollution vary between invertebrate groups. Here we conduct a global meta-analysis of 120 publications comparing the performance of different invertebrate functional groups in unpolluted and polluted atmospheres. We focus on the pollutants ozone, nitrogen oxides, sulfur dioxide and particulate matter. We show that beneficial invertebrate performance is reduced by air pollution, whereas the performance of plant pest invertebrates is not significantly affected. Ozone pollution has the most detrimental impacts, and these occur at concentrations below national and international air quality standards. Changes in invertebrate performance are not dependent on air pollutant concentrations, indicating that even low levels of pollution are damaging. Predicted increases in tropospheric ozone could result in unintended consequences to global invertebrate populations and their valuable ecological services.

The effects of short-time air pollution, SO2, and ozone on biochemical, histo-pathological, oxidative stress, and carcinogenesis related genes expressions in the liver of the rats.

OBJECTIVE OF THE RESEARCH: Air pollution is a universal issue and has significant deleterious effects on both human health and also environment. The important indicators of air pollution include ozone (O3), particulate matter (PM), nitrogen dioxide (NO2), and sulfur dioxide (SO2). This research aims to investigate the impacts of ambient air pollution (AAP), SO2, and O3 on oxidative stress parameters, liver tissue histopathology, and expression of some carcinogenesis-related genes in the hepatic tissue of rats. MATERIALS AND METHODS: 32 Wistar rats were randomly allocated to four groups: the control group, the AAP group, the SO2 group (10 ppm), and the ozone group (0.6 ppm). Over a period of five consecutive weeks, the rats were exposed to the specified pollutants for 3 h daily; liver tissues were harvested and instantly fixed with formalin. Pathological changes were assessed in the tissue samples. Additionally, the RT-qPCR technique was utilized to investigate Expression alterations of BAX, p-53, BCL2, caspase-3, caspase-8 and caspase-9. Furthermore, 30 milligrams of hepatic tissues were extracted to assess the activities of oxidative stress enzymes. RESULTS: The liver catalase and MDA activity were elevated in the air pollution (p < .05). Also, liver GPx activity in air pollution and ozone groups was significant in comparison to the control group (p < .05). The SO2 group exhibited severe lesions in histopathology examinations. CONCLUSIONS: The findings revealed an alteration in liver histopathology, an induction of oxidative stress, and the expression of some apoptosis-related genes in hepatic tissues after exposure to AAP, SO2, and O3.

Cytosolic acidification and oxidation are the toxic mechanisms of SO2 in Arabidopsis guard cells.

SO2/H2SO3 can damage plants. However, its toxic mechanism has still been controversial. Two models have been proposed, cytosolic acidification model and cellular oxidation model. Here, we assessed the toxic mechanism of H2SO3 in three cell types of Arabidopsis thaliana, mesophyll cells, guard cells (GCs), and petal cells. The sensitivity of GCs of Chloride channel a (CLCa)-knockout mutants to H2SO3 was significantly lower than those of wildtype plants. Expression of other CLC genes in mesophyll cells and petal cells were different from GCs. Treatment with antioxidant, disodium 4,5-dihydroxy-1,3-benzenedisulfonate (tiron), increased the median lethal concentration (LC50) of H2SO3 in GCs indicating the involvement of cellular oxidation, while the effect was negligible in mesophyll cells and petal cells. These results indicate that there are two toxic mechanisms of SO2 to Arabidopsis cells: cytosolic acidification and cellular oxidation, and the toxic mechanism may vary among cell types.

Release of ATP in the lung evoked by inhalation of irritant gases in rats.

Adenosine triphosphate (ATP) can be released into the extracellular milieu from various types of cells in response to a wide range of physical or chemical stresses. In the respiratory tract, extracellular ATP is recognized as an important signal molecule and trigger of airway inflammation. Chlorine (Cl2), sulfur dioxide (SO2), and ammonia (NH3) are potent irritant gases and common industrial air pollutants due to their widespread uses as chemical agents. This study was carried out to determine if acute inhalation challenges of these irritant gases, at the concentration and duration simulating the accidental exposures to these chemical gases in industrial operations, triggered the release of ATP in the rat respiratory tract; and if so, whether the level of ATP in bronchoalveolar lavage fluid (BALF) evoked by inhalation challenge of a given irritant gas was elevated by chronic allergic airway inflammation. Our results showed: 1) inhalation of these irritant gases caused significant increases in the ATP level in BALF, and the magnitude of evoked ATP release was in the order of Cl2 > SO2 > NH3. 2) Chronic airway inflammation induced by ovalbumin-sensitization markedly elevated the ATP level in BALF during baseline (breathing room air) but did not potentiate the release of ATP in the lung triggered by inhalation challenges of these irritant gases. These findings suggested a possible involvement of the ATP release in the lung in the regulation of overall airway responses to acute inhalation of irritant gases and the pathogenesis of chronic allergic airway inflammation.NEW & NOTEWORTHY Extracellular adenosine triphosphate (ATP) is a contributing factor and signaling molecule of airway inflammation. This study demonstrated for the first time that the ATP release in the lung was markedly elevated after acute inhalation challenges of three common industrial air pollutants; the order of the response magnitude was chlorine > sulfur dioxide > ammonia. These findings provided new information and improved our understanding of the adverse pulmonary effects caused by accidental inhalation exposures to these irritant gases.

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.

Co-exposure to fluoride and sulfur dioxide induces abnormal enamel mineralization in rats via the FGF9-mediated MAPK signaling pathway.

Fluoride (F) and sulfur dioxide (SO2) contamination is recognized as a public health concern worldwide. Our previous research has shown that Co-exposure to F and SO2 can cause abnormal enamel mineralization. Ameloblastin (AMBN) plays a crucial role in the process of enamel mineralization. However, the process by which simultaneous exposure to F and SO2 influences enamel formation by regulating AMBN expression still needs to be understood. This study aimed to establish in vivo and in vitro models of F-SO2 Co-exposure and investigate the relationship between AMBN and abnormal enamel mineralization. By overexpressing/knocking out the Fibroblast Growth Factor 9 (FGF9) gene, we investigated the impact of FGF9-mediated Mitogen-Activated Protein Kinase (MAPK) signaling on AMBN synthesis to elucidate the mechanism underlying the induction of abnormal enamel mineralization by F-SO2 Co-exposure in rats. The results showed that F-SO2 exposure damaged the structure of rat enamel and ameloblasts. When exposed to F or SO2, gradual increases in the protein expression of FGF9 and phosphorylated p38 mitogen-activated protein kinase (p-P38) were observed. Conversely, the protein levels of AMBN, phosphorylated extracellular signal-regulated kinase (p-ERK), and phosphorylated c-Jun N-terminal kinase (p-JNK) were decreased. AMBN expression was significantly correlated with FGF9, p-ERK, and p-JNK expression in ameloblasts. Interestingly, FGF9 overexpression reduced the levels of p-ERK and p-JNK, worsening the inhibitory effect of F-SO2 on AMBN. Conversely, FGF9 knockout increased the phosphorylation of ERK and JNK, partially reversing the F-SO2-induced downregulation of AMBN. Taken together, these findings strongly demonstrate that FGF9 plays a critical role in F-SO2-induced abnormal enamel mineralization by regulating AMBN synthesis through the JNK and ERK pathways.

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.

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.

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.

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.

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.

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.

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.

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.

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.