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Ambient air pollution has been reported to be a risk factor for hypertensive disorders of pregnancy (HDP). Past studies have reported supportive evidence, but evidence from China is scarce and does not integrate the different periods of the pregnancy course. In this study, 1945 pregnant women with HDP and healthy pregnancies between 2016 and 2022 from the Renmin Hospital of Wuhan University registry network database were analysed. The geographic information, biological information and demographic information of the case were fused in the analysis. Machine learning methods were used to obtain the weight of the variable. Then, we used the generalized linear mixed model to evaluate the relationship between increased exposure to each pollutant at different periods of HDP and examined it in different groups. The results showed that SO2 had the predominate impact (12.65 %) on HDP compared with other air pollutants. SO2 exposure was associated with an increased risk of HDP. Increased unit SO2 concentrations were accompanied by an increased risk of HDP (OR = 1.33, 95 % CI: 1.13, 1.566), and the susceptible window for this effect was mainly in the first trimester (OR = 1.242, 95 % CI: 1.092, 1.412). In addition, SO2 exposure was associated with an increased risk of HDP in urban maternity (OR = 1.356, 95 % CI: 1.112, 1.653), obese maternity (OR = 3.58, 95 % CI: 1.608, 7.971), no higher education maternity (OR = 1.348, 95 % CI: 1.065, 1.706), nonzero delivery maternity (OR = 1.981, 95 % CI: 1.439, 2.725), maternal with first time maternity (OR = 1.247, 95 % CI: 1.007, 1.544) and other groups. In summary, SO2 exposure in early pregnancy is one of the risk factors for HDP, and the increased risk of HDP due to increased SO2 exposure may be more pronounced in obese, urban, low-education, and nonzero delivery populations.

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Sulfur dioxide (SO2) derivatives are typically employed as antioxidants in food and pharmaceutical processing. However, excessive sulfite intake could trigger serious health problems. Hence, it is urgent to establish a rapid and effective system for monitoring SO2. This study adopted a one-step hydrothermal method to synthesize dual-emitting nitrogen-doped carbon quantum dots (CECDs) and developed a ratiometric sensor for sulfite using CECDs-Cr (VI) composites. The emission intensity ratio (I440/I500) of the CECDs-Cr (VI) composites increased considerably with the addition of HSO3-. A method based on the ratiometric sensor was established for SO2 derivatives with advanced efficiency and excellent linearity over a broad concentration range of 0-500 µM (R2 = 0.9946). Four medicine-food homology materials (MFHMs) fumigated with sulfur have been accurately detected using this approach. Furthermore, a portable test tube was prepared to achieve rapid and semi-quantitative detection of SO2 residues and applied to real samples. This work presents an effective approach to develop a rapid on-site detection platform for sulfite residues in food and pharmaceuticals.

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BACKGROUND: Coal-fired power plants are major contributors of ambient sulfur dioxide (SO2) air pollution. Epidemiological literature suggests an adverse association between SO2 exposure during gestation and preterm birth (PTB; <37 weeks completed gestation). PTB is strongly associated with infant mortality and increased risk for later life morbidities. OBJECTIVE: We investigated associations between SO2 and PTB in North Carolina and evaluated whether the associations were modified by race/ethnicity. METHODS: We assembled a retrospective, administrative cohort of singleton births in North Carolina from 2003-2015. We used US EPA EQUATES data to assign long-term SO2 gestational exposures to eligible births for the entire pregnancy and by trimester. We used multivariable generalized linear regression to estimate risk differences (RD (95%CI)) per 1-ppb increase in SO2, adjusted for gestational parent education, Medicaid status, marital status, and season of conception. Multi-pollutant models were additionally adjusted for other criteria air co-pollutants (O3, PM2.5, NO2). RESULTS: The median SO2 (24-hour average) across exposure windows was ~1.5 (IQR: 1.8) ppb. The overall baseline risk for PTB was 8,756 per 100,000 live births. When stratified by race/ethnicity, the baseline risk for PTB was 12215, 7824, and 7187 per 100,000 live births among non-Hispanic Black, non-Hispanic white, and Hispanic births, respectively. RDs per 1-ppb increase in SO2 averaged across the entire pregnancy were 317.0 (95%CI: 279.4, 354.5) and 568.2 (95%CI: 500.3, 636.1) per 100,000 live births for single- and multi-pollutant models, respectively. For the PTB multi-pollutant models, we observed similar RDs for non-Hispanic Black participants (669.6 [95%CI: 573.9, 765.2]) and non-Hispanic white participants (635.4 [95%CI: 557.2, 713.6]) with smaller RDs for Hispanic participants (336.8 [95%CI: 241.3, 432.2]). SIGNIFICANCE: The results for our adjusted single- and multi-pollutant models showed adverse associations between SO2 and PTB, with some evidence of effect measure modification by race/ethnicity within subcategories of PTB.

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

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Sulfur dioxide (SO2) is one of the most used additives in wine industry for its antioxidant and antimicrobial activity. However, due to health concerns, consumers' demand of wines with either reduced or totally replaced SO2 has increased. This study aimed to assess the effect of partial and total replacement of SO2 with a vine-shoots extract rich in stilbenes in rosé (cv. Sangiovese) and red (cv. Negramaro) wines respectively. Color as well as phenolic, volatile, and sensory profiles of wines were evaluated at bottling and during storage. The results showed that the vine-shoots extract increased the levels of trans-resveratrol, catechin, and gallic acid in wines. Moreover, the positive correlation of procyanidin dimers in red wine suggested an increase of the polymerization reactions. The amount of added extract probably provided lower antimicrobial protection compared to SO2, as indicated by the higher levels of ethyl phenol. The decrease of individual anthocyanins and oxidation aldehydes observed in wines with SO2 replacement and the higher levels of caftaric acid in the rosé wine with the extract suggested a shift of the oxidative protection, with a lower protection towards anthocyanin degradation and higher protection towards carbonyl formation and oxidation of readily oxidizable phenolic acids.

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Background: Endogenous sulfur dioxide (SO2) plays a crucial role in protecting heart from myocardial fibrosis by inhibiting the excessive growth of cardiac fibroblasts. This study aimed to investigate potential mechanisms by which SO2 suppressed myocardial fibrosis. Methods and results: Mouse model of angiotensin II (Ang II)-induced cardiac fibrosis and cell model of Ang II-stimulated cardiac fibroblast proliferation were employed. Our findings discovered that SO2 mitigated the aberrant phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) induced by Ang II, leading to a reduction of fibroblast proliferation. Mechanistically, for the first time, we found that SO2 sulfenylated ERK1/2, and inhibited ERK1/2 phosphorylation and cardiac fibroblast proliferation, while a sulfhydryl reducing agent dithiothreitol (DTT) reversed the above effects of SO2. Furthermore, mutant ERK1C183S (cysteine 183 to serine) abolished the sulfenylation of ERK by SO2, thereby preventing the inhibitory effects of SO2 on ERK1 phosphorylation and cardiac fibroblast proliferation. Conclusion: Our study suggested that SO2 inhibited cardiac fibroblast proliferation by sulfenylating ERK1/2 and subsequently suppressing ERK1/2 phosphorylation. These new findings might enhance the understanding of the mechanisms underlying myocardial fibrosis and emphasize the potential of SO2 as a novel therapeutic target for myocardial fibrosis.

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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.

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Background Acute community-acquired pneumonia (CAP) is considered the leading cause of infectious death worldwide. Air pollution and prolonged exposure to airborne contaminants have been implicated in various respiratory conditions, including asthma and chronic obstructive pulmonary disease (COPD). However, the specific impact of air pollution on pneumonia, particularly CAP, remains underexplored. Given the rising levels of urban air pollution and its potential health ramifications, our study aimed to examine the association between exposure to outdoor air pollution and severity as well as the outcomes of pneumonia cases requiring hospitalization. Methodology A cohort analytical study with retrospective data collection was carried out in the pulmonology department of the Gabès University Hospital between January and October 2022. We compared levels of particulate matter less than or equal to 10µm in aerodynamic diameter (PM10), sulfur dioxide (SO2), ozone (O3), moisture and ambient temperature with severity and outcomes of pneumonia requiring hospitalization. The choice of these specific pollutants and environmental factors was based on their established impact on respiratory health and their prevalence in the study region. Results Increased sulfur dioxide (SO2) levels were associated with increased use of non-invasive ventilation (NIV) (r = 0.400). Higher levels of particulate matter (PM10) were significantly associated with the development of lung abscesses. Similarly, increased humidity and ambient temperature were strongly correlated with the development of lung abscesses. Increased air SO2 levels were correlated with a higher CURB65 score (r = 0.299). High outdoor SO2 levels and increasing moisture content were associated with increased Pneumonia Severity Index (PSI) score (r = 0.303 and = 0.310, respectively). Higher levels of PM10 were associated with an increased risk of pleural effusion, a serious complication of pneumonia. Finally, higher ambient temperatures were correlated with more extensive opacities on chest X-rays (r = 0.706), suggesting the severity of pneumonia. Conclusion This study highlights the significant associations between environmental factors and various clinical parameters in pneumonia patients. The findings underscore the importance of considering environmental exposures, such as air quality and weather conditions, in understanding and managing the severity of pneumonia.

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The removal of arsenic (As(III)) from acidic wastewater using neutralization or sulfide precipitation generates substantial arsenic-containing hazardous solid waste, posing significant environmental challenges. This study proposed an advanced ultraviolet (UV)/dithionite reduction method to recover As(III) in the form of valuable elemental arsenic (As(0)) from acidic wastewater, thereby avoiding hazardous waste production. The results showed that more than 99.9 % of As(III) was reduced to As(0) with the residual concentration of arsenic below 25.0 µg L-1 within several minutes when the dithionite/As(III) molar ratio exceeded 1.5:1 and the pH was below 4.0. The content of As(0) in precipitate reached 99.70 wt%, achieving the purity requirements for commercial As(0) products. Mechanistic investigations revealed that SO2·â€’ and H· radicals generated by dithionite photolysis under UV irradiation are responsible for reducing As(III) to As(0). Dissolved O2, Fe(III), Fe(II), Mn(II), dissolved organic matter (DOM), and turbidity slightly inhibited As(III) reduction via free radicals scavenging or light blocking effect, whereas other coexisting ions, such as Mg(II), Zn(II), Cd(II), Ni(II), F(-I), and Cl(-I), had limited influence on As(III) reduction. Moreover, the cost of treating real arsenic-containing (250.3 mg L-1) acidic wastewater was estimated to be as low as $0.668 m-3, demonstrating the practical applicability of this method. This work provides a novel method for the reductive recovery of As(III) from acidic wastewater.

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Sulfur dioxide (SO2) fumigation was studied in laboratory to determine its potential as an alternative treatment for postharvest control of stored product insects, confused flour beetle, Tribolium confusum Jacquelin du Val (Coleoptera: Tenebrionidae), and rice weevil, Sitophilus oryzae (L.) (Coleoptera: Curculionidae). Three-hour fumigations with 0.1%-2.0% SO2 were conducted against eggs, immature stages, and adults of the 2 insects at 20 °C. Effective control of both insects was achieved. However, there were considerable variations between the 2 insects and among different life stages. Confused flour beetle was more susceptible to SO2 fumigation than rice weevil. Complete control of adults and all life stages of confused flour beetle was achieved in 3-h fumigations with 0.5% and 2.0% SO2, respectively. For rice weevil, 3-h fumigation with 1.5% SO2 resulted in 96.5% adult mortality and the fumigation with 2.0% SO2 resulted in 99.27% mortality of adults and 87.5% mortality of immature stages. Three-hour fumigations with 1% SO2 resulted in <5% egg survival to adults. The study demonstrated high efficacy of SO2 fumigation against the insects and suggested that SO2 fumigation has good potential for postharvest pest control on stored products.

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Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), are pulmonary conditions that cause significant morbidity and mortality. The common etiologies of these conditions include pneumonia, pulmonary contusion, fat embolism, smoke inhalation, sepsis, shock, and acute pancreatitis. Inflammation, oxidative stress, apoptosis, and autophagy are key pathophysiological mechanisms underlying ALI. Hydrogen sulfide (H2S) and sulfur dioxide (SO2) are sulfur-containing gas signaling molecules that can mitigate these pathogenic processes by modulating various signaling pathways, such as toll-like receptor 4 (TLR4)/nod-like receptor protein 3 (NLRP3), extracellular signal-regulating protein kinase 1/2 (ERK1/2), mitogen-activated protein kinase (MAPK), phosphatidyl inositol 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), and nuclear factor kappa B (NF-κB), thereby conferring protection against ALI. Given the limited clinical effectiveness of prevailing ALI treatments, investigation of the modulation of sulfur-containing gas signaling molecules (H2S and SO2) in ALI is imperative. This article presents an overview of the regulatory pathways of sulfur-containing gas signaling molecules in ALI animal models induced by various stimuli, such as lipopolysaccharide, gas inhalation, oleic acid, and ischemia-reperfusion. Furthermore, this study explored the therapeutic prospects of diverse H2S and SO2 donors for ALI, stemming from diverse etiologies. The aim of the present study was to establish a theoretical framework, in order to promote the new treatment of ALI.

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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.

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Objectives: Mast cell (MC) degranulation is a key process in allergic reactions and inflammatory responses. Aspartate aminotransferase 1 (AAT1)-derived endogenous sulfur dioxide (SO2) is an important regulator of MC function. However, the mechanism underlying its role in MC degranulation remains unclear. This study aimed to investigate the mechanism by which endogenous SO2 controlled MC degranulation. Methods: HMC-1 and Rat basophilic leukemia cell MC line (RBL-2H3) were used in the cell experiments. SO2 content was detected by in situ fluorescent probe. MC degranulation represented by the release rate of MC ß-hexosaminidase was determined using a colorimetric assay. Sulfenylation of galectin-9 (Gal-9) in MCs and purified protein was detected using a biotin switch assay. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to determine the exact sulfenylation sites of Gal-9 by SO2. Animal models of passive cutaneous anaphylaxis (PCA) and hypoxia-driven pulmonary vascular remodeling were used to investigate the effect of SO2 on mast cell activation in vivo. Site-directed mutation of Gal-9 was conducted to confirm the exact site of SO2 and support the significance of SO2/Gal-9 signal axis in the regulation of MC degranulation. Results: Degranulation was increased in AAT1-knockdowned MCs, and SO2 supplementation reversed the increase in MC degranulation. Furthermore, deficiency of endogenous SO2 contributed to IgE-mediated degranulation in vitro. Besides, SO2 inhibited IgE-mediated and hypoxia-driven MC degranulation in vivo. Mechanistically, LC-MS/MS analysis and site-directed mutation results showed that SO2 sulfenylated Gal-9 at cysteine 74. Sulfenylation of the 74th cysteine of Gal-9 protein was required in the SO2-inhibited MC degranulation under both physiological and pathophysiological conditions. Conclusion: These findings elucidated that SO2 inhibited MC degranulation via sulfenylating Gal-9 under both physiological and pathophysiological conditions, which might provide a novel treatment approach for MC activation-related diseases.

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Mitochondria, central organelles pivotal for eukaryotic cell function, extend their influence beyond ATP production, encompassing roles in apoptosis, calcium signaling, and biosynthesis. Recent studies spotlight two emerging determinants of mitochondrial functionality: intramitochondrial viscosity and sulfur dioxide (SO2) levels. While optimal mitochondrial viscosity governs molecular diffusion and vital processes like oxidative phosphorylation, aberrations are linked with neurodegenerative conditions, diabetes, and cancer. Similarly, SO2, a gaseous signaling molecule, modulates energy pathways and oxidative stress responses; however, imbalances lead to cytotoxic sulfite and bisulfite accumulation, triggering disorders such as cancer and cardiovascular anomalies. Our research focused on development of a dual-channel fluorescent probe, applying electron-withdrawing acceptors within a coumarin dye matrix, facilitating monitoring of mitochondrial viscosity and SO2 in live cells. This probe distinguishes fluorescence peaks at 650 nm and 558 nm, allowing ratiometric quantification of SO2 without interference from other sulfur species. Moreover, it enables near-infrared viscosity determination, particularly within mitochondria. The investigation employed theoretical calculations utilizing Density Functional Theory (DFT) methods to ascertain molecular geometries and calculate rotational energies. Notably, the indolium segment of the probe exhibited the lowest rotational energy, quantified at 7.38 kcals/mol. The probe featured heightened mitochondrial viscosity dynamics when contained within HeLa cells subjected to agents like nystatin, monensin, and bacterial lipopolysaccharide (LPS). Overall, our innovative methodology elucidates intricate mitochondrial factors, presenting transformative insights into cellular energetics, redox homeostasis, and therapeutic avenues for mitochondrial-related disorders.

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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.

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Inflammation is a complex physiological response involving various cellular and molecular events. Sulfur dioxide (SO2), recognized as both an endogenous signaling molecule and anti-inflammatory agent, plays a crucial role in modulating inflammation and maintaining cellular homeostasis. To gain deeper insights into the dynamics of inflammation-related processes, real-time monitoring of SO2 concentrations within cellular organelles is imperative. Here, we developed a near-infrared fluorescent probe, R2, equipped with lysosomal targeting features. R2 effectively monitors dynamic SO2 concentration changes during inflammation. The fluorescence intensity at 703 nm of R2 shows a strong linear correlation with the concentration of SO2, displaying a rapid response time to SO2 within 10 s and maintaining excellent photostability. The successful application of R2 in elucidating dynamic SO2 concentration changes in lysosomal during cellular and rat inflammatory processes underscores its significant potential as a tool for understanding the pathogenesis of inflammation-related diseases.

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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.

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The study aimed to elucidate the mechanisms by which sulfur dioxide (SO2) alleviates organ damage during sepsis using RNA-Seq technology. A cecal ligation and puncture (CLP) sepsis model was established in rats, and the effects of SO2 treatment on organ damage were assessed through histopathological examinations. RNA-Seq was performed to analyze differentially expressed genes (DEGs), and subsequent functional annotations and enrichment analyses were conducted. The CLP model successfully induced sepsis symptoms in rats. Histopathological evaluation revealed that SO2 treatment considerably reduced tissue damage across the heart, kidney, liver, and lungs. RNA-Seq identified 950 DEGs between treated and untreated groups, with significant enrichment in genes associated with ribosomal and translational activities, amino acid metabolism, and PI3K-Akt signaling. Furthermore, gene set enrichment analysis (GSEA) showcased enrichments in pathways related to transcriptional regulation, cellular migration, proliferation, and calcium-ion binding. In conclusion, SO2 effectively mitigates multi-organ damage induced by CLP sepsis, potentially through modulating gene expression patterns related to critical biological processes and signaling pathways. These findings highlight the therapeutic promise of SO2 in managing sepsis-induced organ damage.

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Current evidence suggests that airborne pollutants have a detrimental effect on fetal growth through the emergence of small for gestational age (SGA) or term low birth weight (TLBW). The study's objective was to critically evaluate the available literature on the association between environmental pollution and the incidence of SGA or TLBW occurrence. A comprehensive literature search was conducted across Pubmed/MEDLINE, Web of Science, Cochrane Library, EMBASE, and Google Scholar using predefined inclusion and exclusion criteria. The methodology adhered to the PRISMA guidelines. The systematic review protocol was registered in PROSPERO with ID number: CRD42022329624. As a result, 69 selected papers described the influence of environmental pollutants on SGA and TLBW occurrence with an Odds Ratios (ORs) of 1.138 for particulate matter ≤ 10 µm (PM10), 1.338 for particulate matter ≤ 2.5 µm (PM2.5), 1.173 for ozone (O3), 1.287 for sulfur dioxide (SO2), and 1.226 for carbon monoxide (CO). All eight studies analyzed validated that exposure to volatile organic compounds (VOCs) is a risk factor for SGA or TLBW. Pregnant women in the high-risk group of SGA occurrence, i.e., those living in urban areas or close to sources of pollution, are at an increased risk of complications. Understanding the exact exposure time of pregnant women could help improve prenatal care and timely intervention for fetuses with SGA. Nevertheless, the pervasive air pollution underscored in our findings suggests a pressing need for adaptive measures in everyday life to mitigate worldwide environmental pollution.