Impact of cesarean section on metabolic syndrome components in offspring rats.

INTRODUCTION: Epidemiological evidence suggests an association between CS and offspring metabolic syndrome (MetS), but whether a causal relationship exists is unknown. METHODS: In this study, timed-mated Wistar rat dams were randomly assigned to cesarean section (CS), vaginal delivery (VD), and surrogate groups. The offspring from both CS and VD groups were reared by surrogate dams until weaning, and weaned male offspring from both groups were randomly assigned to receive normal diet (ND) or high-fat/high-fructose diet (HFF) ad libitum for 39 weeks. RESULTS: By the end of study, CS-ND offspring gained 17.8% more weight than VD-ND offspring, while CS-HFF offspring gained 36.4% more weight than VD-HFF offspring. Compared with VD-ND offspring, CS-ND offspring tended to have increased triglycerides (0.27 mmol/l, 95% CI, 0.05 to 0.50), total cholesterol (0.30 mmol/l, -0.08 to 0.68), and fasting plasma glucose (FPG) (0.30 mmol/l, -0.01 to 0.60); more pronounced differences were observed between CS-HFF and VD-HFF offspring in these indicators (triglyceride, 0.66 mmol/l, 0.35 to 0.97; total cholesterol, 0.46 mmol/l, 0.13 to 0.79; and FPG, 0.55 mmol/l, 0.13 to 0.98). CONCLUSIONS: CS offspring were more prone to adverse metabolic profile and HFF might exacerbate this condition, indicating the association between CS and MetS is likely to be causal. IMPACT: Whether the observed associations between CS and MetS in non-randomized human studies are causally relevant remains undetermined. Compared with vaginally born offspring rats, CS born offspring gained more body weight and tended to have compromised lipid profiles and abnormal insulin sensitivity, suggesting a causal relationship between CS and MetS that may be further amplified by a high-fat/high-fructose diet. Due to the high prevalence of CS births globally, greater clinical consideration must be given to the potential adverse effects of CS, and whether these risks should be made known to patients in clinical practice merits evaluation.

The modification effect of fasting blood glucose level on the associations between short-term ambient air pollution and blood lipids.

The association between short-term ambient air pollution (AAP) exposure and blood lipids is inconsistent across populations. This study aimed to investigate the modifying effects of fasting blood glucose (FBG) levels on the associations between short-term AAP exposure and blood lipids in 110,637 male participants from Beijing, China. The results showed that FBG modified the association between short-term AAP exposure and blood lipids, especially low-density lipoprotein cholesterol (LDL-C). In the hyperglycemia group, a 10-µg/m3 increase in particles with diameters ≤ 2.5 µm (PM2.5), particles with diameters ≤ 10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), or a 1-mg/m3 increase in carbon monoxide (CO) was associated with a 0.454%, 0.305%, 1.507%, 0.872%, or 3.961% increase in LDL-C, respectively. In the nonhyperglycemic group, short-term increases in air pollutants were even associated with small decreases in LDL-C. The findings demonstrate that lipids in hyperglycemic individuals are more vulnerable to short-term AAP exposure than those in normal populations.

Association between Air Pollution and Lipid Profiles.

Dyslipidemia is a critical factor in the development of atherosclerosis and consequent cardiovascular disease. Numerous pieces of evidence demonstrate the association between air pollution and abnormal blood lipids. Although the results of epidemiological studies on the link between air pollution and blood lipids are unsettled due to different research methods and conditions, most of them corroborate the harmful effects of air pollution on blood lipids. Mechanism studies have revealed that air pollution may affect blood lipids via oxidative stress, inflammation, insulin resistance, mitochondrial dysfunction, and hypothalamic hormone and epigenetic changes. Moreover, there is a risk of metabolic diseases associated with air pollution, including fatty liver disease, diabetes mellitus, and obesity, which are often accompanied by dyslipidemia. Therefore, it is biologically plausible that air pollution affects blood lipids. The overall evidence supports that air pollution has a deleterious effect on blood lipid health. However, further research into susceptibility, indoor air pollution, and gaseous pollutants is required, and the issue of assessing the effects of mixtures of air pollutants remains an obstacle for the future.

Titanium dioxide nanoparticles: revealing the mechanisms underlying hepatotoxicity and effects in the gut microbiota.

Numerous studies in recent years have questioned the safety of oral exposure to titanium dioxide nanoparticles (TiO2 NPs). TiO2 NPs are not only likely to accumulate in the gastrointestinal tract, but they are also found to penetrate the body circulation and reach distant organs. The liver, which is considered to be a target organ for nanoparticles, is of particular concern. TiO2 NPs accumulate in the liver and cause oxidative stress and inflammatory reactions, resulting in pathological damage. The impact of TiO2 NPs on liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) was studied using a meta-analysis. According to the findings, TiO2 NPs exposure can cause an elevation in AST and ALT levels in the blood. Furthermore, TiO2 NPs are eliminated mostly through feces, and their lengthy residence in the gut exposes them to microbiota. The gut microbiota is also dysbiotic due to titanium dioxide's antibacterial capabilities. This further leads to changes in the amount of microbiota metabolites, which can reach the liver with blood circulation and trigger hepatotoxicity through the gut-liver axis. This review examines the gut-liver axis to assess the effects of gut microbiota dysbiosis on the liver to provide suggestions for assessing the gut-hepatotoxicity of TiO2 NPs.

Effect of Nanomaterials on Gut Microbiota.

Nanomaterials are widely employed in everyday life, including food and engineering. Food additives on a nanoscale can enter the body via the digestive tract. The human gut microbiota is a dynamically balanced ecosystem composed of a multitude of microorganisms that play a crucial role in maintaining the proper physiological function of the digestive tract and the body's endocrine coordination. While the antibacterial capabilities of nanomaterials have received much interest in recent years, their impacts on gut microbiota ought to be cautioned about and explored. Nanomaterials exhibit good antibacterial capabilities in vitro. Animal studies have revealed that oral exposure to nanomaterials inhibits probiotic reproduction, stimulates the inflammatory response of the gut immune system, increases opportunistic infections, and changes the composition and structure of the gut microbiota. This article provides an overview of the impacts of nanomaterials, particularly titanium dioxide nanoparticles (TiO2 NPs), on the gut microbiota. It advances nanomaterial safety research and offers a scientific foundation for the prevention, control, and treatment of illnesses associated with gut microbiota abnormalities.

Associations of ambient temperature with creatine kinase MB and creatine kinase: A large sample time series study of the Chinese male population.

Previous evidence has associated non-optimal ambient temperature with an increased risk of myocardial infarction. However, no studies have shown an association between ambient temperature and biomarkers in the myocardium. This study aimed to investigate the association of ambient temperature with creatine kinase MB (CK-MB) and creatine kinase (CK). A total of 94,784 men aged 20-50 years were included in this study. We performed blood biochemical tests on the participants and used the daily average temperature to represent ambient temperature. The daily average ambient temperature was calculated by hourly observational data from meteorological indicators in Beijing. Lag effects were observed within 0-7 days. General additive models were used to observe nonlinear associations of ambient temperature with CK-MB and CK. Linear models were used to fit the associations of cold or heat with CK-MB and CK, respectively, after confirming the inflection point of ambient temperature. The OR value of abnormal CK-MB (CK) for a 1 °C increase or decrease was calculated by logistic regression. In the results, a V-shaped relationship between CK-MB and ambient temperature and a linear relationship between CK and ambient temperature were observed. Cold exposure was associated with increased CK-MB and CK levels. For a 1 °C decrease, CK-MB increased by 0.044 U/L (95 % CI: 0.017, 0.070 U/L) at lag day 0, and CK increased by 1.44 U/L (0.44, 2.44 U/L) at lag day 4 (the lag day with the strongest effect). The OR of high CK-MB was 1.047 (1.017, 1.077) at lag day 0, and the OR of high CK was 1.066 (1.038, 1.095) at lag day 4 for a 1 °C decrease. No heat-related elevation of CK-MB or CK was observed. In general, cold exposure is associated with increased levels of CK-MB and CK in humans, which may be associated with myocardial injury. Our findings illustrate the possible adverse effects of cold exposure on the myocardium from a biomarker perspective.

Effects of short-term high-concentration exposure to PM2.5 on pulmonary tissue damage and repair ability as well as innate immune events.

Short-term heavy air pollution still occurs frequently worldwide, especially during the winter heating period in some developing countries, which is usually accompanied by the temporary explosive growth of PM2.5. The pulmonary damage caused by PM2.5 exposure has been determined, but there have been few studies on the repair ability after the cessation of exposure and the important role of innate immune events. This study established a short-term (30 days) high-concentration (15 mg/kg body weight) PM2.5 exposure and recovery (15 days of exposure cessation) model by intratracheal instillation. The results showed that short-term PM2.5 exposure increased the content of collagen fiber in rat lung tissue, which was significantly repaired after recovery by 15 days of exposure cessation. Meanwhile, exposure to PM2.5 also caused changes in lung epithelial function, macrophage polarization and cell autophagy function. Most of these changes could be restored or reversed to a certain extent after recovery. However, there were also some biomarkers, including CLDN18.1, SP-A, SP-D, iNOS, CD206, Beclin1, p62 and LC3B, that were still significantly different between the exposure and control groups after recovery, suggesting that some toxic effects, especially epithelial function damage, were not completely repaired. In addition, there was a significant correlation between pulmonary fibrosis and innate immunity. The present study demonstrated that short-term high-concentration exposure to PM2.5 could cause temporary lung tissue damage and related innate immune events in rats, and the repair ability existed after the cessation of exposure, but part of the damage that required special attention still persisted.

Titanium Dioxide Nanoparticles Altered the lncRNA Expression Profile in Human Lung Cells.

Respiration is considered to be the main occupational or environmental exposure pathway of titanium dioxide nanoparticles (TiO2 NPs), and the lung is considered to be the target organ of respiratory exposure; however, the mechanism of respiratory toxicity is not fully understood. In this study, the effect of TiO2 NPs on the expression profile of long non-coding RNA (lncRNA) in bronchial epithelial cells (BEAS-2B) was investigated to understand their potential toxic mechanism. BEAS-2B cells were treated with 100 µg/mL TiO2 NPs for 48 h, then RNA sequencing was performed to screen the differential lncRNAs compared with the control group, and the enrichment pathways of the differentially expressed lncRNAs were further analyzed using the Kyoto Encyclopedia of Genes and Genomes (KEGG). The results identified a total of 45,769 lncRNAs, and 277 different lncRNAs were screened. KEGG pathway analysis showed that the targeted mRNAs of these different lncRNAs were enriched in the pyrimidine metabolism pathway. This work demonstrates that TiO2 NPs could alter the lncRNA expression profile in BEAS-2B cells, and epigenetics may play a role in the mechanism of respiratory toxicity induced by TiO2 NPs.

Long Non-Coding RNA Expression Profile Alteration Induced by Titanium Dioxide Nanoparticles in HepG2 Cells.

The liver is considered the major target organ affected by oral exposure to titanium dioxide nanoparticles (TiO2 NPs), but the mechanism of hepatotoxicity is not fully understood. This study investigated the effect of TiO2 NPs on the expression profile of long non-coding RNA (lncRNA) in hepatocytes and tried to understand the potential mechanism of hepatotoxicity through bioinformatics analysis. The human hepatocellular carcinoma cells (HepG2) were treated with TiO2 NPs at doses of 0-200 µg/mL for 48 h and then RNA sequencing was implemented. The differential lncRNAs between the control and TiO2 NPs-treated groups were screened, then the lncRNA-mRNA network and enrichment pathways were analyzed via multivariate statistics. As a result, 46,759 lncRNAs were identified and 129 differential lncRNAs were screened out. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the targeted mRNAs of those differential lncRNAs were enriched in the Hedgehog signaling pathway, Vasopressin-regulated water reabsorption, and Glutamatergic synapse. Moreover, two lncRNA-mRNA networks, including lncRNA NONHSAT256380.1-JRK and lncRNA NONHSAT173563.1-SMIM22, were verified by mRNA detection. This study demonstrated that an alteration in the lncRNA expression profile could be induced by TiO2 NPs and epigenetics may play an important role in the mechanism of hepatotoxicity.

Genetic damage and potential mechanism exploration under different air pollution patterns by multi-omics.

Ambient air pollution was classified as carcinogenic to humans (Group 1) for lung cancer. DNA damage was an important first step in the process of carcinogenesis, and could also be induced by air pollution. In this study, intratracheal instillation and real-time air exposure system were combined to establish SHP (short-term high-level PM2.5) and LLPO (long-term low-level PM2.5 and O3) exposure patterns, respectively. Hierarchical levels of genetic biomarkers were analyzed to explore DNA damage effects in rats. Representative DNA repair genes from different repair pathways were selected to explore the relative expression levels. The methylation level of differentially expressed repair genes were also determined. Besides, miRNA sequencing and non-targeted metabolomic analysis were performed in rat lungs. KEGG and multi-omics analysis were used to explore the potential mechanism of genetic damage under different air pollution patterns. We found that LLPO exposure induced DSBs and chromosome damage. SHP exposure could induce DSBs and DNA oxidative damage, and the effects of genetic damage under this pollution pattern could be repaired by natural repair. Repair genes involved in two pattern were different. SHP exposure could induce higher methylation levels of RAD51, which might be a potential epigenetic mechanism for high-level PM2.5 induced down-regulated expression of RAD51 and DSBs. Besides, 29 overlapped alterations in metabolic pathways were identified by metabolomic and miRNA sequencing, including purine metabolism and pyrimidine metabolism after LLPO exposure. Differential miRNAs expression in lung tissue were associated with apoptosis, DNA damage and damage repair. We concluded that under different air pollution patterns, DNA damage biomarkers and activated targets of DNA damage repair network were both different. The genetic damage effects caused by high-level short-term PM2.5 can be alleviated by natural repair. We provided possible mechanisms by multi-omics which could explain the increased carcinogenic risk caused by air pollution.

Lipidomics Profiles and Lipid Metabolite Biomarkers in Serum of Coal Workers' Pneumoconiosis.

As a serious occupational pulmonary fibrosis disease, pneumoconiosis still lacks effective biomarkers. Previous studies suggest that pneumoconiosis may affect the body's lipid metabolism. The purpose of this study was to explore lipidomics profiles and lipid metabolite biomarkers in the serum of coal workers' pneumoconiosis (CWP) by a population case-control study. A total of 150 CWP cases and 120 healthy controls from Beijing, China were included. Blood lipids were detected in serum biochemistry. Lipidomics was performed in serum samples for high-throughput detection of lipophilic metabolites. Serum high density lipoprotein cholesterol (HDL-C) decreased significantly in CWP cases. Lipidomics data found 131 differential lipid metabolites between the CWP case and control groups. Further, the top eight most important differential lipid metabolites were screened. They all belonged to differential metabolites of CWP at different stages. However, adjusting for potential confounding factors, only three of them were significantly related to CWP, including acylhexosylceramide (AHEXCER 43:5), diacylglycerol (DG 34:8) and dimethyl-phosphatidylethanolamine (DMPE 36:0|DMPE 18:0_18:0), of which good sensitivity and specificity were proven. The present study demonstrated that lipidomics profiles could change significantly in the serum of CWP patients and that the lipid metabolites represented by AHEXCER, DG and DMPE may be good biomarkers of CWP.

DNA Oxidative Damage as a Sensitive Genetic Endpoint to Detect the Genotoxicity Induced by Titanium Dioxide Nanoparticles.

The genotoxicity of nanomaterials has attracted great attention in recent years. As a possible occupational carcinogen, the genotoxic effects and underlying mechanisms of titanium dioxide nanoparticles (TiO2 NPs) have been of particular concern. In this study, the effect of TiO2 NPs (0, 25, 50 and 100 µg/mL) on DNA damage and the role of oxidative stress were investigated using human bronchial epithelial cells (BEAS-2B) as an in vitro model. After detailed characterization, the cytotoxicity of TiO2 NPs was detected. Through transmission electron microscopy (TEM), we found that TiO2 NPs entered the cytoplasm but did not penetrate deep into the nucleus of cells. The intracellular levels of reactive oxygen species (ROS) significantly increased in a dose-dependent manner and the ratios of GSH/GSSG also significantly decreased. The results of the normal comet assay were negative, while the Fpg-modified comet assay that specifically detected DNA oxidative damage was positive. Meanwhile, N-acetyl-L-cysteine (NAC) intervention inhibited the oxidative stress and genotoxicity induced by TiO2 NPs. Therefore, it was suggested that TiO2 NPs could induce cytotoxicity, oxidative stress and DNA oxidative damage in BEAS-2B cells. DNA oxidative damage may be a more sensitive genetic endpoint to detect the genotoxicity of TiO2 NPs.

Landscape of lipidomic metabolites in gut-liver axis of Sprague-Dawley rats after oral exposure to titanium dioxide nanoparticles.

BACKGROUND: The application of titanium dioxide nanoparticles (TiO2 NPs) as food additives poses a risk of oral exposure that may lead to adverse health effects. Even though the substantial evidence supported liver as the target organ of TiO2 NPs via oral exposure, the mechanism of liver toxicity remains largely unknown. Since the liver is a key organ for lipid metabolism, this study focused on the landscape of lipidomic metabolites in gut-liver axis of Sprague Dawley (SD) rats exposed to TiO2 NPs at 0, 2, 10, 50 mg/kg body weight per day for 90 days. RESULTS: TiO2 NPs (50 mg/kg) caused slight hepatotoxicity and changed lipidomic signatures of main organs or systems in the gut-liver axis including liver, serum and gut. The cluster profile from the above biological samples all pointed to the same key metabolic pathway and metabolites, which was glycerophospholipid metabolism and Phosphatidylcholines (PCs), respectively. In addition, absolute quantitative lipidomics verified the changes of three PCs concentrations, including PC (16:0/20:1), PC (18:0/18:0) and PC (18:2/20:2) in the serum samples after treatment of TiO2 NPs (50 mg/kg). The contents of malondialdehyde (MDA) in serum and liver increased significantly, which were positively correlated with most differential lipophilic metabolites. CONCLUSIONS: The gut was presumed to be the original site of oxidative stress and disorder of lipid metabolism, which resulted in hepatotoxicity through the gut-liver axis. Lipid peroxidation may be the initial step of lipid metabolism disorder induced by TiO2 NPs. Most nanomaterials (NMs) have oxidation induction and antibacterial properties, so the toxic pathway revealed in the present study may be primary and universal.

Screening of Serum Biomarkers of Coal Workers' Pneumoconiosis by Metabolomics Combined with Machine Learning Strategy.

Pneumoconiosis remains one of the most serious global occupational diseases. However, effective treatments are lacking, and early detection is crucial for disease prevention. This study aimed to explore serum biomarkers of occupational coal workers' pneumoconiosis (CWP) by high-throughput metabolomics, combining with machine learning strategy for precision screening. A case-control study was conducted in Beijing, China, involving 150 pneumoconiosis patients with different stages and 120 healthy controls. Metabolomics found a total of 68 differential metabolites between the CWP group and the control group. Then, potential biomarkers of CWP were screened from these differential metabolites by three machine learning methods. The four most important differential metabolites were identified as benzamide, terazosin, propylparaben and N-methyl-2-pyrrolidone. However, after adjusting for the influence of confounding factors, including age, smoking, drinking and chronic diseases, only one metabolite, propylparaben, was significantly correlated with CWP. The more severe CWP was, the higher the content of propylparaben in serum. Moreover, the receiver operating characteristic curve (ROC) of propylparaben showed good sensitivity and specificity as a biomarker of CWP. Therefore, it was demonstrated that the serum metabolite profiles in CWP patients changed significantly and that the serum metabolites represented by propylparaben were good biomarkers of CWP.

Advances in genotoxicity of titanium dioxide nanoparticles in vivo and in vitro.

Titanium dioxide nanoparticles (TiO2 NPs) are currently one of the most widely used nanomaterials. Due to an increasing scope of applications, the exposure of humans to TiO2 NP is inevitable, such as entering the body through the mouth with food additives or drugs, invading the damaged skin with cosmetics, and entering the body through the respiratory tract during the process of production and handling. Compared with TiO2 coarse particles, TiO2 NPs have stronger conductivity, reaction activity, photocatalysis, and permeability, which may lead to greater toxicity to organisms. Given that TiO2 was classified as a category 2B carcinogen (possibly carcinogenic to humans), the genotoxicity of TiO2 NPs has become the focus of attention. There have been a series of previous studies investigating the potential genotoxicity of TiO2 NPs, but the existing research results are still controversial and difficult to conclude. More than half of studies have shown that TiO2 NPs can cause genotoxicity, suggesting that TiO2 NPs are likely to be genotoxic to humans. And the genotoxicity of TiO2 NPs is closely related to the exposure concentration, mode and time, and experimental cells/animals as well as its physicochemical properties (crystal type, size, and shape). This review summarized the latest research progress of related genotoxic effects through in vivo studies and in vitro cell tests, hoping to provide ideas for the evaluation of TiO2 NPs genotoxicity.

Titanium dioxide nanoparticles induced reactive oxygen species (ROS) related changes of metabolomics signatures in human normal bronchial epithelial (BEAS-2B) cells.

Titanium dioxide often enters the respiratory tract in the form of nano-dust in occupational sites. Metabolomics may be a promising method for studying the toxicology of nano titanium dioxide. The intention of this study was to explore the possible impact of titanium dioxide nanoparticles (TiO2 NPs) on the metabolomics signatures of human normal bronchial epithelial (BEAS-2B) cells and to search for investigate the role of reactive oxygen species (ROS). In this study, BEAS-2B cells were treated by TiO2 NPs (0, 25, 50 and 100 µg/mL) for 48 h. The metabolites extracted from BEAS-2B cells were determined by untargeted metabolomics technique, and the differential metabolites and metabolic pathways were discovered by using multivariate analysis. Intracellular ROS was detected by DCFH-DA probe and flow cytometry method. Machine learning was used to explore the relationship between ROS and metabolomics changes. Totally, seventy-six differential metabolites and the steroid biosynthesis pathway of BEAS-2B cells were observed after treatment of TiO2 NPs. Lipid and lipid-like metabolites were the most significant classes among the metabolite products induced by TiO2 NPs. TiO2 NPs resulted in a dose-dependent increase in intracellular ROS levels, and correlated with most of the differential metabolites. In conclusion, TiO2 NPs increased the level of the oxidative stress, which could contribute to the altered signature represented by lipid metabolism in BEAS-2B cells.

Association between ambient air pollution and blood sex hormones levels in men.

Concerns are growing over time on the adverse health effects of air pollution. However, the association between ambient air pollution and blood sex hormones in men is poorly understood. We included 72,917 men aged 20-55 years from February 2014 to December 2019 in Beijing, China in this study. Blood testosterone, follicle stimulating hormone, luteinizing hormone, estradiol, and prolactin levels of each participant were measured. We collected exposure data of daily ambient levels of particulate matter ≤10 µm (PM10) and ≤2.5 µm (PM2.5), nitrogen dioxide, sulfur dioxide (SO2), carbon monoxide, and ozone. Generalized linear mixed models were used to analyze the potential association between ambient air pollution exposure and blood sex hormone levels. The results showed that both immediate and short-term cumulative PM2.5, PM10, and SO2 exposure was related to altered serum sex hormone levels in men, especially testosterone. An increase of 10 µg/m3 in PM2.5 and PM10 in the current day was related to a 1.6% (95% confidence interval [CI]: 0.9%-2.3%) and 1.1% (95% CI: 0.5%-1.6%) decrease in testosterone, respectively, and a decreasing tendency of accumulated effects persisted within lag 0-30 days. The present study demonstrated that it is important to control ambient air pollution exposure to reduce effects on the reproductive health of men.

Iodine in household cooking salt no longer plays a crucial role in iodine status of residents in Tianjin, China.

PURPOSE: The contribution of household cooking salt to population iodine status is decreasing in China, the applicability of the coverage rate of iodized salt (IS), proportion of adequately iodized salt (AIS), and salt iodine concentration (SIC) of household cooking salt used for iodine status assessment of residents requires further investigation. METHODS: Through the IDD control project, 16,445 children and 4848 pregnant women were recruited from Tianjin, China and the relationship between the coverage rate of IS, proportion of AIS, SIC, and population iodine status was analyzed. Additionally, through the thyroid health survey project, 856 children with IS or noniodized salt were recruited. The effects of different household cooking salts on individual iodine status and thyroid health were analyzed. RESULTS: After adjusting for confounding factors, no relationship was found between the coverage rate of IS, proportion of AIS, SIC of household cooking salt, and iodine status of children and pregnant women (all P > 0.05). No differences in levels of thyroid function and structural indicators were found in children with different household cooking salts (all P > 0.05). Additionally, no relationship was found between noniodized salt exposure and goiter, overt hyperthyroidism, overt hypothyroidism, thyroid nodules, antibody single positivity, or subclinical hypothyroidism (all P > 0.05). CONCLUSION: Iodine in household cooking salt no longer plays a crucial role in iodine status in Tianjin, China. Other indicators must be identified as beneficial supplements for precise iodine status evaluation not only in Tianjin but also in other large cities in China.

DNA damage, serum metabolomic alteration and carcinogenic risk associated with low-level air pollution.

Outdoor air pollution has been classified as carcinogenic to humans (Group 1) for lung cancer, but the underlying mechanism and key toxic components remain incompletely understood. Since DNA damage and metabolite alterations are associated with cancer progression, exploring potential mechanisms linking air pollution and cancer might be meaningful. In this study, a real-time ambient air exposure system was established to simulate the real-world environment of adult male SD rats in Beijing from June 13th, 2018, to October 8th, 2018. 8-OHdG in the urine, γ-H2AX in the lungs and mtDNA copy number in the peripheral blood were analyzed to explore DNA damage at different levels. Serum non-targeted metabolomics analysis was performed. Pair-wise spearman was used to explore the correlation between DNA damage biomarkers and serum differential metabolites. Carcinogenic risks of heavy metals and PAHs via inhalation were assessed according to US EPA guidelines. Results showed that PM2.5 and O3 were the major air pollutants in the exposure group and not detected in the control group. Compared with control group, higher levels of 8-OHdG, mtDNA copy number, γ-H2AX and PCNA-positive nuclei cells were observed in the exposure group. Histopathological evaluation suggested ambient air induced alveolar wall thickening and inflammatory cell infiltration in lungs. Perturbed metabolic pathways identified included glycolysis/gluconeogenesis metabolism, purine and pyrimidine metabolism, etc. γ-H2AX was positively correlated with serum ADP, 3-phospho-D-glyceroyl phosphate and N-acetyl-D-glucosamine. The BaPeq was 0.120 ng/m3. Risks of Cr(VI), As, V, BaP, BaA and BbF were above 1 × 10-6. We concluded that low-level air pollution was associated with DNA damage and serum metabolomic alterations in rats. Cr(VI) and BaP were identified as key carcinogenic components in PM2.5. Our results provided experimental evidence for hazard identification and risk assessment of low-level air pollution.

Exposure to the real ambient air pollutants alters the composition of nasal mucosa bacteria in the rat model.

Studies have indicated that ambient pollutant exposure correlates with nasal disease, in which nasal mucosa microbiota play a crucial role. However, the association between exposure to real-ambient air pollutants and the composition of nasal mucosa microbiota has not been well studied. This study aimed to explore the composition of nasal mucosa microbiota after exposure to real-ambient air pollutants with a special system. We monitored PM2.5, O3, etc. in the system and confirmed PM2.5 and O3 were the main pollutants. SD rats were exposed to the system for 16 weeks in summer or 22 weeks in autumn-winter. The concentrations of PM2.5 were 24.00 µg/m3 in the Summer stage and 22.21 µg/m3 in the autumn-winter stage. The O3 concentrations were 25.46 and 13.55 µg/m3, respectively. Exposure altered bacterial beta diversity in the summer stage. There were 4 and 3 different bacteria at the king, order, family and genus levels between the two groups at the two stages, respectively. The abundance of opportunistic pathogens changed, Pseudomonas decreased in summer stage, and Bifidobacterium increased in the autumn-winter stage. The influence of the season on the nasal mucosa microbiota was analyzed. The alpha diversity of the autumn-winter stage was higher than that of the summer stage. LEfSe analysis revealed 34 differential bacterial taxa at the king, order, family and genus level in the two control groups and 31 of the two exposure groups, which were not the same as the bacteria between the control groups and exposure groups. We found that PM2.5 combined with O3 exposure was associated with the composition of the nasal mucosa microbiota and the abundance of opportunistic pathogens, in which season likely impacted the microbiota.