Early-life ozone exposure and childhood otitis media: Unveiling critical windows of risk.

BACKGROUND: Despite increasing evidence of a strong correlation between air pollution and otitis media (OM), the impact of early-life ozone (O3) exposure on the development of OM in children remains uncertain. OBJECTIVES: To explore the connection between early-life O3 exposure and OM, and to identify the critical time period(s) during which O3 exposure significantly influences the development of OM in children. METHODS: We conducted a study involving 8689 children living in Changsha, China. Information regarding personal factors, health conditions, and the indoor environment was gathered using questionnaires. Personal exposure to outdoor O3 and other major pollutants at the place of residence during the periods before conception, prenatal periods, and after birth was calculated by applying the inverse distance weighted (IDW) method with data gathered from ten air quality monitoring stations. Multiple logistic regression analyses were employed to investigate the associations between O3 exposure and children's OM. RESULTS: After controlling for covariates and ambient temperature, exposure to O3 during the year preceding pregnancy was correlated with childhood lifetime OM, showing ORs (95 % CI) of 1.28 (1.01-1.64). O3 exposures in the 10th-12th, 7th-9th, and 4th-6th months before pregnancy were all linked to children's lifetime OM. Within the multi-window model, we detected that O3 exposure in the 10th to 12th month prior to pregnancy was significantly related to lifetime OM, showing ORs (95 % CI) of 1.28 (1.05-1.55). A significant link was discovered between childhood OM and O3 exposure after controlling for six other pollutants (SO2, PM2.5, NO2, PM2.5-10, CO, and PM10) during the 10th to 12th month prior to conception. Exposure to O3 during the 36th gestational week significantly raised the likelihood of childhood lifetime OM. There is a significant interaction between O3 and temperature exposure during the first trimester of pregnancy and one year before pregnancy on childhood lifetime OM. CONCLUSIONS: Preconceptional O3 exposure and its interaction with low temperature played critical roles in children's OM development, backing the hypothesis of "(pre) fetal origins of childhood OM".

Childhood Helicobacter pylori infection: Impacts of environmental exposures and parental stress.

BACKGROUND: Helicobacter pylori infection (HPI) is extremely common in the world, particularly in less developed areas, but the primary causes of childhood HPI are unspecified. OBJECTIVES: To determine the influences of exposure to home environmental factors (HEFs), outdoor air pollutants (OAPs), and parental stress (PS), as well as their interactions on children's HPI. METHODS: We implemented a retrospective cohort study with 8689 preschoolers from nine districts at Changsha, China, was conducted using questionnaires to collect data of health and HEFs. Temperature and OAPs data were collected from ten and eight monitoring stations, individually. Temperature and OAPs exposures were calculated for all home addresses using the inversed distance weighted (IDW) model. Multiple logistic regression analysis was carried out to determine the separate and combined impacts of HEFs, OAPs, and PS on HPI. RESULTS: Children's HPI was significantly associated with exposure to moisture-specific indoor allergens in one-year preceding conception, gestation, and first year, smoke-specific air pollution throughout life, and plant-specific allergens in previous year. Outdoor exposures to CO in the 7th-9th month before conception, as well as PM2.5 in the second trimester and previous year, were associated with HPI, with ORs (95 % CIs) of 1.22 (1.05-1.41), 1.23 (1.03-1.46), and 1.33 (1.14-1.55). Parents' socioeconomic and psychological stress indicators were positively related to HPI. High socioeconomic indicators and psychological stresses increased the roles of indoor renovation and moisture indicators as well as outdoor SO2, PM2.5 and O3 on children's HPI over their entire lives. Parental psychological stress interacts with indoor renovation-specific air pollution, moisture- and plant-specific allergens, as well as outdoor traffic-related air pollution on HPI, during a critical time window in early life. CONCLUSIONS: Indoor and outdoor air pollutants, as well as allergens, separately and interactively exert important effects on childhood HPI, lending support to the "(pre-) fetal origin of HPI" hypothesis.

Combined exposure of polystyrene microplastics and benzo[a]pyrene in rat: Study of the oxidative stress effects in the liver.

Microplastics (MPs) and benzo[a]pyrene (B[a]P) are prevalent environmental pollutants. Numerous studies have extensively reported their individual adverse effects on organisms. However, the combined effects and mechanisms of exposure in mammals remain unknown. Thus, this study aims to investigate the potential effects of oral administration of 0.5µm polystyrene (PS) MPs (1 mg/mL or 5 mg/mL), B[a]P (1 mg/mL or 5 mg/mL) and combined (1 mg/mL or 5 mg/mL) on 64 male SD rats by gavage method over 6-weeks. The results demonstrate that the liver histopathological examination showed that the liver lobules in the combined (5 mg/kg) group had blurred and loose boundaries, liver cord morphological disorders, and significant steatosis. The levels of AST, ALT, TC, and TG in the combined dose groups were significantly higher than those in the other groups, the combined (5 mg/kg) group had the lowest levels of antioxidant enzymes and the highest levels of oxidants. The expression of Nrf2 was lowest and the expression of P38, NF-κB, and TNF-α was highest in the combined (5 mg/kg) group. In conclusion, these findings indicate that the combination of PSMPs and B[a]P can cause the highest levels of oxidative stress and elicit markedly enhanced toxic effects, which cause severe liver damage.

High humidity and NO2 co-exposure exacerbates allergic asthma by increasing oxidative stress, inflammatory and TRP protein expressions in lung tissue.

Allergic asthma is a chronic inflammatory airway disease with a high mortality rate and a rapidly increasing prevalence in recent decades that is closely linked to environmental change. Previous research found that high humidity (HH) and the traffic-related air pollutant NO2 both aggregated allergic asthma. Their combined effect and mechanisms on asthma exacerbation, however, are unknown. Our study aims to toxicologically clarify the role of HH (90%) and NO2 (5 ppm) on allergic asthma. Ninety male Balb/c mice were randomly assigned to one of six groups (n = 15 in each): saline control, ovalbumin (OVA)-sensitized, OVA + HH, OVA + NO2, OVA + HH + NO2, and OVA + HH + NO2+Capsazepine (CZP). After 38 days of treatment, the airway function, pathological changes in lung tissue, blood inflammatory cells, and oxidative stress and inflammatory biomarkers were comprehensively assessed. Co-exposure to HH and NO2 exacerbated histopathological changes and airway hyperresponsiveness, increased IgE, oxidative stress markers malonaldehyde (MDA) and allergic asthma-related inflammation markers (IL-1ß, TNF-α and IL-17), and upregulated the expressions of the transient receptor potential (TRP) ion channels (TRPA1, TRPV1 and TRPV4). Our findings show that co-exposure to HH and NO2 disrupted the Th1/Th2 immune balance, promoting allergic airway inflammation and asthma susceptibility, and increasing TRPV1 expression, whereas CZP reduced TRPV1 expression and alleviated allergic asthma symptoms. Thus, therapeutic treatments that target the TRPV1 ion channel have the potential to effectively manage allergic asthma.

Serum-based ATR-FTIR spectroscopy combined with multivariate analysis for the diagnosis of pre-diabetes and diabetes.

Diabetes mellitus (DM) is a metabolic disease with an increasing prevalence that is causing worldwide concern. The pre-diabetes stage is the only reversible stage in the patho-physiological process towards DM. Due to the limitations of traditional methods, the diagnosis and detection of DM and pre-diabetes are complicated, expensive, and time-consuming. Therefore, it would be of great benefit to develop a simple, rapid and inexpensive diagnostic test. Herein, the infrared (IR) spectra of serum samples from 111 DM patients, 111 pre-diabetes patients and 333 healthy volunteers were collected using attenuated total reflection Fourier-transform IR (ATR-FTIR) spectroscopy and this was combined with the multivariate analysis of principal component analysis linear discriminant analysis (PCA-LDA) to develop a discriminant model to verify the diagnostic potential of this approach. The study found that the accuracy of the test model established by ATR-FTIR spectroscopy combined with PCA-LDA was 97%, and the sensitivity and specificity were 100% and 100% in the control group, 94% and 98% in the pre-diabetes group, and 91% and 98% in the DM group, respectively. This indicates that this method can effectively diagnose DM and pre-diabetes, which has far-reaching clinical significance.

Effects of pre-natal and post-natal exposures to air pollution on onset and recurrence of childhood otitis media.

BACKGROUND: Despite mounting evidence linking outdoor air pollution with otitis media (OM), the role of air pollutant(s) exposure during which critical window(s) on childhood OM remains unknown. OBJECTIVES: We sought to identify the key air pollutant(s) and critical window(s) associated with the onset and recurrent attacks of OM in kindergarten children. METHODS: A combined cross-sectional and retrospective cohort study involving 8689 preschoolers aged 3-6 years was performed in Changsha, China. From 2013-2020, data on air pollutants were collected from ambient air quality monitoring stations in Changsha, and the exposure concentration to each child at their home address was calculated using the inverse distance weighted (IDW) method. The relationship between air pollution and OM in kindergarten children was studied using multiple logistic regression models. RESULTS: Childhood lifetime OM was associated with PM2.5, SO2 and NO2, with ORs (95% CI) of 1.43 (1.19-1.71), 1.18 (1.01-1.37) and 1.18 (1.00-1.39) by per IQR increase in utero exposure and with PM2.5, PM2.5-10 and PM10, with ORs = 1.15 (1.00-1.32), 1.25 (1.13-1.40) and 1.49 (1.28-1.74) for entire post-natal exposure, respectively. The 2nd trimester in utero and the post-natal period, especially the 1st year, were key exposure time windows to PM2.5 and PM10 associated with lifetime OM and the onset of OM. Similarly, the 4th gestational month was a critical window for all pollutants except CO exposure in relation to lifetime OM and OM onset, but not recurrent OM attacks. PM2.5 exposure during the nine gestational months and PM10 exposure during the first three years had cumulative effects on OM development. Our subgroup analysis revealed that certain children were more susceptible to the OM risk posed by air pollution. CONCLUSIONS: Early-life exposure to air pollution, particularly PM2.5 during the middle of gestation and PM10 during the early post-natal period, was associated with childhood OM.

Evaluation of acute toxicity response to the algae Chlorella pyrenoidosa of biosynthetic silver nanoparticles catalysts.

Biosynthetic of silver nanoparticles (AgNPs) by using fungi has attracted much attention due to its high catalytic efficiency and environmentally friendly characteristic. However, a few studies have focused on the ecological toxicity effects of biogenic AgNPs on algae. Here, we first investigated the catalytic reduction of 4-nitrophenol (4-NP) by WZ07-AgNPs biosynthesized by Letendraea sp. WZ07. WZ07-AgNPs had significant catalytic activity with 97.08% degradation of 4-NP in 3.5 min. Then, the toxic effects of WZ07-AgNPs and commercial-AgNPs were compared by Chlorella pyrenoidosa growth, chlorophyll content, protein content, physiological, and biochemical indexes. The results demonstrated that the algal cell biomass of C. pyrenoidosa was differentially inhibited after exposure to different concentrations of AgNPs, which showed concentration dependence and time dependence. The 96h-EC50 values of WZ07-AgNPs and commercial-AgNPs on C. pyrenoidosa were 15.99 mg/mL and 12.69 mg/mL, respectively. With the increase concentration of AgNPs, the chlorophyll content was gradually decreased, the protein content was first increased and then decreased, the activities of superoxide dismutase (SOD) and catalase (CAT) were decreased, and the level of malondialdehyde (MDA) was increased significantly of C. pyrenoidosa. In general, AgNPs affect the growth of algae to some extent. However, compared with commercial-AgNPs, WZ07-AgNPs is less toxic to C. pyrenoidosa, which could be used as a potential and an eco-friendly catalyst. This study provides a basis for the safe application of biosynthetic AgNPs.

Whole transcriptome sequencing and competitive endogenous RNA regulation network construction analysis in benzo[a]pyrene-treated breast cancer cells.

Breast cancer is the most common malignant tumor in women worldwide, and environmental pollutants are considered to be risk factors. Currently, most studies into benzo[a]pyrene (B[a]P)-induced breast cancer focus on biological effects such as proliferation, invasion, and metastasis, DNA damage, estrogen receptor (ER)-related molecular mechanisms, oxidative damage, and other metabolic pathways. This study aims to provide insights into the role of B[a]P in breast cancer development through RNA-seq and bioinformatics analysis and construction of a competing endogenous RNA (ceRNA) regulatory network. By analyzing RNA-seq results, we identified 144 differentially-expressed circRNAs, 69 differentially-expressed lncRNAs, 20 differentially-expressed miRNAs, and 212 differentially-expressed mRNAs. Following on, we analyzed the gene ontology (GO) and KEGG enrichment functions of the differentially-expressed RNAs. In addition, the protein-protein interaction (PPI) network was mapped for differentially-expressed mRNAs. Subsequently, we constructed ceRNA networks, one of which consisted of 45 dysregulated circRNAs, 11 miRNAs, and 9 mRNAs, and a second consisted of 40 lncRNAs, 11 miRNAs, and 9 mRNAs. Finally, 6 circRNAs, 4 lncRNAs, 1 miRNA, and 4 mRNAs were randomly selected for quantitative real-time PCR verification. PCR results were further verified by Western blotting assays. These results show that the expression level of differentially-expressed RNA was consistent with the sequencing data, and the Western blotting results were highly consistent with the PCR results, confirming that the sequencing result was very reliable. This study systematically explores the ceRNA atlas of differentially-expressed genes related to B[a]P exposure in breast cancer cells, providing new insights into mechanisms of environmental pollutants in breast cancer.

Tamoxifen resistance-related ceRNA network for breast cancer.

Background: Tamoxifen (TMX) is one of the most widely used drugs to treat breast cancer (BC). However, acquired drug resistance is still a major obstacle to its application, rendering it crucial to explore the mechanisms of TMX resistance in BC. This aims of this study were to identify the mechanisms of TMX resistance and construct ceRNA regulatory networks in breast cancer. Methods: GEO2R was used to screen for differentially expressed mRNAs (DEmRNAs) leading to drug resistance in BC cells. MiRTarbase and miRNet were used to predict miRNAs and lncRNAs upstream, and the competing endogenous RNA (ceRNA) regulatory network of BC cell resistance was constructed by starBase. We used the Kaplan-Meier plotter and Gene Expression Profiling Interactive Analysis (GEPIA) to analyze the expression and prognostic differences of genes in the ceRNA network with core axis, and qRT-PCR was used to further verify the above conclusions. Results: We found that 21 DEmRNAs were upregulated and 43 DEmRNA downregulated in drug-resistant BC cells. DEmRNAs were noticeably enriched in pathways relevant to cancer. We then constructed a protein-protein interaction (PPI) network based on the STRING database and defined 10 top-ranked hub genes among the upregulated and downregulated DEmRNAs. The 20 DEmRNAs were predicted to obtain 113 upstream miRNAs and 501 lncRNAs. Among them, 7 mRNAs, 22 lncRNAs, and 11 miRNAs were used to structure the ceRNA regulatory network of drug resistance in BC cells. 4 mRNAs, 4 lncRNAs, and 3 miRNAs were detected by GEPIA and the Kaplan-Meier plotter to be significantly associated with BC expression and prognosis. The differential expression of the genes in BC cells was confirmed by qRT-PCR. Conclusion: The ceRNA regulatory network of TMX-resistant BC was successfully constructed and confirmed. This will provide an important resource for finding therapeutic targets for TMX resistance, where the discovery of candidate conventional mechanisms can aid clinical decision-making. In addition, this resource will help discover the mechanisms behind this type of resistance.

The complete chloroplast genome of Ageratum conyzoides (Asteraceae).

Ageratum conyzoides L. is an important Chinese medicinal plant. In this study, we reported the complete chloroplast genome of A. conyzoides. The chloroplast genome sequence is 151,309 bp in length and consisted of a large single copy (LSC) region (83,884 bp), a small single copy (SSC) region (17,771 bp), and two inverted repeats (IRs) (24,827 bp). It was composed of 126 genes and they were 81 protein-coding genes, 30 tRNA genes, 8 rRNA genes, and 7 pseudogene. Phylogenetic analysis with reported chloroplast genomes can not only show that A. conyzoides has a close genetic relationship with Centaurea diffusa and Carthamus tinctorius, but also provide new evidence for the identification of Praxelis clematidea and A. conyzoides.