Environmental pollutants and bad bugs work hand in glove.

'Bad bacteria' could alter the toxicokinetics of environmental pollutants, thereby exacerbating chemically induced tumorigenesis. Recently, Roje et al. reported that specific gut microbiota can metabolize nitrosamine compounds to a toxic oxidation product, aggravating bladder cancer development and progression. These findings have important implications for tumor intervention through the gut microbiota.

Microbially derived surfactants: an ecofriendly, innovative, and effective approach for managing environmental contaminants.

The natural environment is often contaminated with hydrophobic pollutants such as long-chain hydrocarbons, petrochemicals, oil spills, pesticides, and heavy metals. Hydrophobic pollutants with a toxic nature, slow degradation rates, and low solubility pose serious threats to the environment and human health. Decontamination based on conventional chemical surfactants has been found to be toxic, thereby limiting its application in pharmaceutical and cosmetic industries. In contrast, biosurfactants synthesized by various microbial species have been considered superior to chemical counterparts due to their non-toxic and economical nature. Some biosurfactants can withstand a wide range of fluctuations in temperature and pH. Recently, biosurfactants have emerged as innovative biomolecules not only for solubilization but also for the biodegradation of environmental pollutants such as heavy metals, pesticides, petroleum hydrocarbons, and oil spills. Biosurfactants have been well documented to function as emulsifiers, dispersion stabilizers, and wetting agents. The amphiphilic nature of biosurfactants has the potential to enhance the solubility of hydrophobic pollutants such as petroleum hydrocarbons and oil spills by reducing interfacial surface tension after distribution in two immiscible surfaces. However, the remediation of contaminants using biosurfactants is affected considerably by temperature, pH, media composition, stirring rate, and microorganisms selected for biosurfactant production. The present review has briefly discussed the current advancements in microbially synthesized biosurfactants, factors affecting production, and their application in the remediation of environmental contaminants of a hydrophobic nature. In addition, the latest aspect of the circular bioeconomy is discussed in terms of generating biosurfactants from waste and the global economic aspects of biosurfactant production.

Environmental pollutants as risk factors for autism spectrum disorders: a systematic review and meta-analysis of cohort studies.

BACKGROUND: Autism Spectrum Disorder (ASD) is a lifelong neurodevelopmental condition affecting communication, social interaction, and behavior. Evidence suggests that environmental pollutants are associated with ASD incidence. This review aimed to analyze the effect of environmental pollutants on ASD. METHODS: Systematic review and meta-analysis of cohort studies evaluated the association between exposure to environmental pollutants and ASD. We searched COCHRANE CENTRAL, MEDLINE, CINAHL, LILACS, EMBASE, PsycINFO, Web of Science, SciELO, and gray literature from inception to January 2023. The model used for meta-analysis was inverse variance heterogeneity (IVhet). The effect measures were the beta coefficient (ß) and the relative risk (RR) with their 95% confidence intervals (95% CI). Sensitivity analyses were carried out using an instrument to screen or diagnose autism. RESULTS: A total of 5,780 studies were identified; 27 were included in the systematic review, and 22 were included in the meta-analysis. These studies included 1,289,183 participants and 129 environmental pollutants. Individual meta-analyses found a significant association between nitrogen dioxide RR = 1.20 (95% CI: 1.03 to 1.38; I2: 91%), copper RR = 1.08 (95% CI: 1.03 to 1.13; I2: 0%), mono-3-carboxy propyl phthalate ß = 0.45 (95% CI: 0.20 to 0.70; I2: 0%), monobutyl phthalate ß = 0.43 (95% CI: 0.13 to 0.73; I2: 0%) and polychlorinated biphenyl (PCB) 138 RR = 1.84 (95% CI: 1.14 to 2.96; I2:0%) with ASD. Subgroup meta-analyses found a significant association with carbon monoxide RR = 1.57 (95% CI: 1.25 to 1.97; I2: 0%), nitrogen oxides RR = 1.09 (95% CI: 1.04 to 1.15; I2: 34%) and metals RR = 1.13 (95% CI: 1.01 to 1.27; I2:24%). CONCLUSION: This study found positive associations nitrogen dioxide, copper, mono-3-carboxypropyl phthalate, monobutyl phthalate, and PCB 138, and the development of ASD, likewise, with subgroups of pollutants carbon monoxide, nitrogen oxides, and metals. Therefore, it is important to identify these risk factors in children and adolescents to contribute to ASD and identify prevention strategies effectively.

Mechanisms insights into bisphenol S-induced oxidative stress, lipid metabolism disruption, and autophagy dysfunction in freshwater crayfish.

Bisphenol S (BPS) is widely used in plastic products, food packaging, electronic products, and other applications. In recent years, BPS emissions have increasingly impacted aquatic ecosystems. The effects of BPS exposure on aquatic animal health have been documented; however, our understanding of its toxicology remains limited. This study aimed to explore the mechanisms of lipid metabolism disorders, oxidative stress, and autophagy dysfunction induced in freshwater crayfish (Procambarus clarkii) by exposure to different concentrations of BPS (0 µg/L, 1 µg/L, 10 µg/L, and 100 µg/L) over 14 d. The results indicated that BPS exposure led to oxidative stress by inducing elevated levels of reactive oxygen species (ROS) and inhibiting the activity of antioxidant-related enzymes. Additionally, BPS exposure led to increased lipid content in the serum and hepatopancreas, which was associated with elevated lipid-related enzyme activity and increased expression of related genes. Furthermore, BPS exposure decreased levels of phosphatidylcholine (PC) and phosphatidylinositol (PI), disrupted glycerophospholipid (GPI) metabolism, and caused lipid deposition in the hepatopancreatic. These phenomena may have occurred because BPS exposure reduced the transport of fatty acids and led to hepatopancreatic lipid deposition by inhibiting the transport and synthesis of PC and PI in the hepatopancreas, thereby inhibiting the PI3K-AMPK pathway. In conclusion, BPS exposure induced oxidative stress, promoted lipid accumulation, and led to autophagy dysfunction in the hepatopancreas of freshwater crayfish. Collectively, our findings provide the first evidence that environmentally relevant levels of BPS exposure can induce hepatopancreatic lipid deposition through multiple pathways, raising concerns about the potential population-level harm of BPS and other bisphenol analogues.

Coke oven emissions exacerbate allergic asthma by promoting ferroptosis in airway epithelial cells.

Epidemiological studies have shown that coke oven emissions (COEs) affect the deterioration of asthma, but has not been proven by experimental results. In this study, we found for the first time that COEs exacerbate allergen house dust mite (HDM)-induced allergic asthma in the mouse model. The findings reveal that airway inflammation, airway remodeling and allergic reaction were aggravated in the COE + HDM combined exposure group compared with the individual exposure group. Mechanism studies indicated higher levels of iron and MDA in the COE + HDM combined exposure group, along with increased expression of Ptgs2 and reduced GPX4 expression. Iron chelator deferoxamine (DFO) effectively inhibited ferroptosis induced by COE synergistically with HDM in vitro. Further studies highlighted the role of ferritinophagy in the COE + HDM-induced ferroptosis. 3-methyladenine (3-MA) could inhibit ferroptosis in the COE + HDM exposure group. Interestingly, we injected DFO intraperitoneally into mice in the combined exposure group and found DFO could significantly inhibit the COE-exacerbated ferroptosis and allergic asthma. Our findings link ferroptosis with COE-exacerbated allergic asthma, implying that ferroptosis may have important therapeutic potential for asthma in patients with occupational exposure of COE.

Multi-omics integration analysis: Tools and applications in environmental toxicology.

Nowadays, traditional single-omics study is not enough to explain the causality between molecular alterations and toxicity endpoints for environmental pollutants. With the development of high-throughput sequencing technology and high-resolution mass spectrometry technology, the integrative analysis of multi-omics has become an efficient strategy to understand holistic biological mechanisms and to uncover the regulation network in specific biological processes. This review summarized sample preparation methods, integration analysis tools and the application of multi-omics integration analyses in environmental toxicology field. Currently, omics methods have been widely applied being as the sensitivity of early biological response, especially for low-dose and long-term exposure to environmental pollutants. Integrative omics can reveal the overall changes of genes, proteins, and/or metabolites in the cells, tissues or organisms, which provide new insights into revealing the overall toxicity effects, screening the toxic targets, and exploring the underlying molecular mechanism of pollutants.

Impacts of Environmental Concentrations of Nanoplastics on Zebrafish Neurobehavior and Reproductive Toxicity.

Nanoplastics, as emerging environmental pollutants, can transport contaminants across marine environments, polluting pristine ecosystems and being ingested by marine organisms. This transfer poses a severe threat to global aquatic ecosystems and potentially impacts human health through the food chain. Neurobehavioral and reproductive toxicity are critical areas of concern because they directly affect the survival, health, and population dynamics of aquatic species, which can have cascading effects on the entire ecosystem. Using zebrafish as a model organism, we investigated the toxic effects of environmental concentrations of polystyrene nanoplastics (PS-NPs). Behavioral assessments, including the novel tank test and open field test, demonstrated significant neurobehavioral changes, indicating increased anxiety and depressive behaviors. A pathological analysis of brain and gonadal tissues, along with evaluations of neurobehavioral and reproductive toxicity biomarkers, revealed that exposure to PS-NPs leads to brain tissue lesions, inflammatory responses, oxidative stress activation, hormone level disruptions, and gonadal damage. Real-time quantitative PCR studies of reproductive gene expression further showed that PS-NPs disrupt the endocrine regulation pathways of the brain-pituitary-gonadal (BPG) axis, causing reproductive toxicity with sex-specific differences. These findings provide crucial insights into the impacts of nanoplastics on aquatic organisms and their ecological risks, offering theoretical support for future environmental protection and pollutant management efforts.

Pedestrian flow-environmental pollutants interactions and health risks to residents in high-occupancy public areas of apartment buildings.

The current interaction of pedestrian flow and environmental pollutants in high-occupancy public areas of apartment and the risks of residents being exposed to environmental pollutants are issues that are often overlooked but urgently need to be addressed. In this study, we provide a comprehensive of pedestrian flow-environmental pollutants interactions and health risks to residents in first-floor public areas of apartment with high-occupancy. The main findings indicate that under closed management conditions, there is a significant increase in TVOC and noise levels during the peak periods of nighttime pedestrian flow. In the correlation analysis, the significant impact of time granularity selection in clarifying the correlation between pedestrian flow and environmental pollutants has been highlighted, with larger time granularities generally showing stronger correlations, while finer time granularities may help identify specific risks in areas directly connected to the external environment. There is a significant correlation exists between pedestrian flow and environmental pollutants (TVOC, ozone, and noise), with higher concentrations of these pollutants observed during peak pedestrian flow periods, thereby increasing the risk of residents being exposed to adverse environmental conditions. To mitigate the risks associated with TVOC pollution and noise exposure, it is crucial to maintain proper ventilation, avoid conducting cleaning or maintenance activities during peak hours, and implement noise-reducing measures, such as distancing noise sources from residential areas or installing soundproofing barriers. Additionally, the study identifies total volatile organic compounds originating from property maintenance activities and clarifies their dispersion patterns, emphasizing the importance of developing robust, standardized maintenance protocols for indoor environmental quality assurance. This research can improve the environmental sustainability of apartment buildings and provide a theoretical basis for the development of environmental health strategies for high-occupancy public areas of apartment buildings.

Identification and characterization of microplastics in human nasal samples.

KEY POINTS: Human nasal cavity samples were collected, and presence of microplastics were evaluated. Microplastics were present, and major types were polyethylene, polyester, acrylic polymer, and polypropylene. Further research is needed regarding microplastics and its clinical impact on human nasal cavity.

High-quality models for assessing the effects of environmental pollutants on the nervous system: 3D brain organoids.

The prevalence of environmental problems and the increasing risk of human exposure to environmental pollutants have become a global concern. The increasing environmental pollution is one of the main reasons for the rising incidence of most neurological-related diseases in recent years. However, the ethical constraints of direct human research and the racial limitations of animal models have slowed the progress of research in this area. The purpose of this study is to review the neurotoxicity of different environmental pollutants on the brain using brain organoids as a new model and to conclude that brain organoids may play a key role in assessing the mechanisms by which environmental pollutants affect neurogenesis and cause neurological pathogenesis. To accurately determine the negative effects of environmental pollutants on the nervous system, self-organizing brain organoids that are highly similar to the developing brain have become a new model system for studying the effects of environmental pollutants on human brain development and disease. This study uses brain organoids as a model to summarize the neurotoxicity of different environmental pollutants on the nervous system, including structural changes in brain organoids, inhibition of neuronal differentiation and migration, impairment of mitochondrial function, damage to cellular cilia, and influence on signaling pathways. In conclusion, exposure to environmental pollutants may cause different neurotoxicity to the nervous system. Therefore, it is crucial to understand how to use brain organoids to ameliorate neurological disorders caused by environmental pollution.

Anthropogenic gadolinium contaminations in the marine environment and its ecological implications.

Due to the widespread application in medicine and industry of anthropogenic gadolinium (Gdanth), the widespread of Gd anomaly in surface water has leading to disruption of the natural Gd geochemical cycle. However, challenges related to the identification and quantification of Gdanth, assessment of its impacts on marine ecosystems, and exploration of strategies for mitigating its adverse effects still exist. Meanwhile, as the major source of the Gdanth, the environmental geochemical behavior of Gd-based contrast agents (GBCAs), which are used in medical diagnostics in magnetic resonance imaging (MRI), are still poorly understood. In this review, we 1) analyzed Gd anomalies in samples from published literature worldwide, confirmed their prevalence (81.25% for sea and lake water, 72.73% for river water), 2) demonstrated that the third-order polynomial method is the preferred approach for the detection of Gdanth in surface seawater, 3) outlined the species and applications of Gdanth and its impacts on marine environment, 4) explored the process of GBCAs influx into the ocean and demonstrated the concentration of Gdanth in coral samples was mainly affected by terrestrial input GBCAs (63.75%) through Pearson correlation analysis and principle component analysis, 5) proposed effective management strategies for GBCAs at all stages from production to release into the ocean, 6) formulated an expectation for future research on marine Gdanth.

Structural and Electronic Factors Controlling the Efficiency and Rate of Intersystem Crossing to the Triplet State in Thiophene Polycyclic Derivatives.

Thiophene polycyclic derivatives are widely used in organic light-emitting diodes, photovoltaics, and medicinal chemistry applications. Understanding the electronic and structural factors controlling their intersystem crossing rates is paramount for these applications to be successful. This study investigates the photophysical, electronic structure, and excited state dynamics of 1,2-benzodiphenylene sulfide, benzo[b]naphtho[1,2-d]thiophene, and benzo[b]naphtho[2,3-d]thiophene in polar aprotic and non-polar solvents. Steady-state absorption and emission spectroscopy, femtosecond transient absorption spectroscopy, and DFT and TD-DFT calculations are employed. Low fluorescence quantum yields of 1.2 to 2.7% are measured in acetonitrile and cyclohexene, evidencing that the primary relaxation pathways in these thiophene derivatives are nonradiative. Linear interpolation of internal coordinates calculations predict that an S-C bond elongation reaction coordinate facilitates the efficient intersystem crossing to the T1 state. Excitation of 1,2-benzodiphenylene sulfide and benzo[b]naphtho[1,2-d]thiophene at 350 nm or benzo[b]naphtho[2,3-d]thiophene at 365 nm, populates the lowest-energy 1ππ* state, which relaxes to the 1ππ* minimum in tens of picoseconds or intersystem crosses to the triplet manifold in ca. 500 ps to 1.1 ns depending on the position at which the benzene rings are added. Excitation at 266 nm does not affect the intersystem crossing rates. Laser photodegradation experiments demonstrate that the thiophene polycyclic derivatives are highly photostable.

Comprehensive analysis of classroom microclimate in context to health-related national and international indoor air quality standards.

Indoor air quality (IAQ) and indoor air pollution are critical issues impacting urban environments, significantly affecting the quality of life. Nowadays, poor IAQ is linked to respiratory and cardiovascular diseases, allergic reactions, and cognitive impairments, particularly in settings like classrooms. Thus, this study investigates the impact of indoor environmental quality on student health in a university classroom over a year, using various sensors to measure 19 environmental parameters, including temperature, relative humidity, CO2, CO, volatile organic compounds (VOCs), particulate matter (PM), and other pollutants. Thus, the aim of the study is to analyze the implications of the indoor microclimate for the health of individuals working in the classroom, as well as its implications for educational outcomes. The data revealed frequent exceedances of international standards for formaldehyde (HCHO), VOC, PM2.5, NO, and NO2. HCHO and VOCs levels, often originating from building materials and classroom activities, were notably high. PM2.5 levels exceeded both annual and daily standards, while NO and NO2 levels, possibly influenced by inadequate ventilation, also surpassed recommended limits. Even though there were numerous exceedances of current international standards, the indoor microclimate quality index (IMQI) score indicated a generally good indoor environment, remaining mostly between 0 and 50 for this indicator. Additionally, analyses indicate a high probability that some indicators will exceed the current standards, and their values are expected to trend upwards in the future. The study highlighted the need for better ventilation and pollutant control in classrooms to ensure a healthy learning environment. Frequent exceedances of pollutant standards can suggest a significant impact on student health and academic performance. Thus, the present study underscored the importance of continuous monitoring and proactive measures to maintain optimal indoor air quality.

Embryonic Zebrafish as a Model for Investigating the Interaction between Environmental Pollutants and Neurodegenerative Disorders.

Environmental pollutants have been linked to neurotoxicity and are proposed to contribute to neurodegenerative disorders. The zebrafish model provides a high-throughput platform for large-scale chemical screening and toxicity assessment and is widely accepted as an important animal model for the investigation of neurodegenerative disorders. Although recent studies explore the roles of environmental pollutants in neurodegenerative disorders in zebrafish models, current knowledge of the mechanisms of environmentally induced neurodegenerative disorders is relatively complex and overlapping. This review primarily discusses utilizing embryonic zebrafish as the model to investigate environmental pollutants-related neurodegenerative disease. We also review current applicable approaches and important biomarkers to unravel the underlying mechanism of environmentally related neurodegenerative disorders. We found embryonic zebrafish to be a powerful tool that provides a platform for evaluating neurotoxicity triggered by environmentally relevant concentrations of neurotoxic compounds. Additionally, using variable approaches to assess neurotoxicity in the embryonic zebrafish allows researchers to have insights into the complex interaction between environmental pollutants and neurodegenerative disorders and, ultimately, an understanding of the underlying mechanisms related to environmental toxicants.

Perfluorooctane Sulfonate Exposure Induces Cardiovascular Dysfunction in Female Rats: Role of Ovaries.

Per- and polyfluoroalkyl substances (PFAS) are pervasive environmental pollutants frequently detected in drinking water worldwide. Reports linking PFAS exposure to cardiovascular disease have increased significantly in recent years. Furthermore, women appear to be more susceptible to the adverse effects of PFAS. However, the potential role of ovaries in the increased vulnerability of females to PFAS-related health effects remains unknown. In this study, we investigated the impact of perfluorooctane sulfonate (PFOS), a prominent PFAS, on the cardiovascular function in female rats with intact ovaries and ovariectomized (OVX) females. Bilateral OVX or sham surgeries were performed in 8-week-old female SD rats. Following recovery from surgeries, the rats were given drinking water containing 50 µg/mL of PFOS for 3 weeks. Control groups received PFOS-free water. PFOS exposure significantly reduced body weight but increased blood pressure similarly in both intact and OVX rats. Echocardiography analysis revealed that PFOS exposure decreased cardiac output, end-systolic volume, and end-diastolic volume in intact but not OVX rats. Vascular function studies demonstrated that PFOS equally reduced endothelium-dependent and -independent relaxation responses in intact and OVX rats. The endothelium-independent contractile responses were more pronounced in both intact and OVX rats. eNOS protein levels were similarly decreased in both intact and OVX rats. In conclusion, PFOS affects cardiac function through hormone-dependent mechanisms, while vascular function is impaired independent of ovarian status, indicating an intricate interplay between PFOS exposure, ovarian status, and cardiovascular function.

Nitrate and Nitrite Exposure Induces Visual Impairments in Adult Zebrafish.

Nitrate and nitrite have emerged as increasingly common environmental pollutants, posing significant risks to various forms of life within ecosystems. To understand their impact on the visual system of zebrafish, adult zebrafish were exposed to environmentally relevant concentrations of nitrate (10 mg/L) and nitrite (1 mg/L) for 7 days. Visual behaviors were examined using optomotor and avoidance response. The eyeballs of the zebrafish were collected for H&E staining, IHC, and qPCR. Exposure decreased visual behavior and the thickness of most retinal layers. Exposure decreased expression of pax6a, pax6b, gpx1a, and bcl2a. Exposure increased expression of esr1, esr1a, esr2b, cyp19a1b, sod1a, nos2a, casps3, and tp53, and increased retinal brain aromatase expression by IHC. Collectively, our findings demonstrate that nitrate and nitrite exposure negatively impacted the visual system of adult zebrafish, highlighting the potential hazards of these environmental pollutants on aquatic organisms.

The contribution of environmental pollutants to the risk of autism and other neurodevelopmental disorders: A systematic review of case-control studies.

Exposure to environmental pollutants, such as metals, pesticides, and air pollutants during early life, is a risk factor for neurodevelopmental disorders (NDDs), including Autism Spectrum Disorder (ASD). Our systematic review aimed to select and summarize more recent case-control studies that examined the association between prenatal and early postnatal exposure to environmental pollutants and NDDs. We searched five databases (Web of Science, PubMed, Embase, Scopus, Ovid), screened 2261 records, and included 24 eligible case-control studies. Meta-analyses were conducted on subgroups of at least three studies that shared both the outcome and the exposure. A noteworthy discovery from this literature review is the existence of non-linear or non-monotonic dose-response relationships between the exposure to certain metals and the risk of ASD. The meta-analysis revealed a significant association between exposure to particular matter (PM)10 during the first year of life and the risk of ASD. Overall, studies included in our systematic review indicate that exposure to several pollutants within the first three years of life was significantly associated with the risk of NDDs.

Perfluorooctanesulfonic acid (PFOS) induced cancer related DNA methylation alterations in human breast cells: A whole genome methylome study.

DNA methylation plays a pivotal role in cancer. The ubiquitous contaminant perfluorooctanesulfonic acid (PFOS) has been epidemiologically associated with breast cancer, and can induce proliferation and malignant transformation of normal human breast epithelial cells (MCF-10A), but the information about its effect on DNA methylation is sparse. The aim of this study was to characterize the whole-genome methylome effects of PFOS in our breast cell model and compare the findings with previously demonstrated DNA methylation alterations in breast tumor tissues. The DNA methylation profile was assessed at single CpG resolution in MCF-10A cells treated with 1 µM PFOS for 72 h by using Enzymatic Methyl sequencing (EM-seq). We found 12,591 differentially methylated CpG-sites and 13,360 differentially methylated 100 bp tiles in the PFOS exposed breast cells. These differentially methylated regions (DMRs) overlapped with 2406 genes of which 494 were long non-coding RNA and 1841 protein coding genes. We identified 339 affected genes that have been shown to display altered DNA methylation in breast cancer tissue and several other genes related to cancer development. This includes hypermethylation of GACAT3, DELEC1, CASC2, LCIIAR, MUC16, SYNE1 and hypomethylation of TTN and KMT2C. DMRs were also found in estrogen receptor genes (ESR1, ESR2, ESRRG, ESRRB, GREB1) and estrogen responsive genes (GPER1, EEIG1, RERG). The gene ontology analysis revealed pathways related to cancer phenotypes such as cell adhesion and growth. These findings improve the understanding of PFOS's potential role in breast cancer and illustrate the value of whole-genome methylome analysis in uncovering mechanisms of chemical effects, identifying biomarker candidates, and strengthening epidemiological associations, potentially impacting risk assessment.

Possible associations between prenatal exposure to environmental pollutants and neurodevelopmental outcome in children.

This study aimed to evaluate associations between prenatal and childhood exposure to phthalates and prenatal exposure to polychlorinated biphenyls (PCBs) and the development of 4-year-old children. Urinary metabolites of five phthalates were measured in women upon delivery, as well as serum concentrations of four PCB congeners. Postnatal phthalate metabolites were measured from children's urine obtained at the time of developmental assessment. The primary outcome was cognitive function as evaluated by the Wechsler Preschool and Primary Scale of Intelligence (WPPSI-III) administered at 4 years. Secondary outcomes were motor function and response to sensory stimuli as evaluated by the Developmental Coordination Disorder Questionnaire (DCDQ) and Short Sensory Profile (SSP) that the mothers filled out, respectively. The study included 57 mother-child pairs. Higher maternal phthalate metabolite concentrations were inversely associated with WPPSI-III scores among boys and not among girls. After using linear regression models and controlling for confounding variables, we found that higher levels of monobenzyl phthalate (MBzP) were the ones associated with lower WPPSI-III scores (p=0.004, 95 %CI [-14.18; -3.16]), lower DCDQ scores (p=0.007, 95 %CI [-6.08; -1.17] and lower SSP scores (p=0.004, 95 %CI [-7.47; -1.79]). No association was found between child urinary phthalate metabolite concentrations or maternal PCB blood concentrations and developmental function. These findings indicate that higher prenatal phthalate metabolite levels may be associated with deficits in neurologic development of young boys.

Effects of nasal allergens and environmental particulate matter on brainstem metabolites and the consequence of brain-spleen axis in allergic rhinitis.

BACKGROUND: The growing consensus links exposure to fine particulate matter (PM2.5) with an increased risk of respiratory diseases. However, little is known about the additional effects of particulate matter on brainstem function in allergic rhinitis (AR). Furthermore, it is unknown to what extent the PM2.5-induced effects in the brainstem affect the inflammatory response in AR. This study aimed to determine the effects, mechanisms and consequences of brainstem neural activity altered by allergenic stimulation and PM2.5 exposure. METHODS: Using an AR model of ovalbumin (OVA) elicitation and whole-body PM2.5 exposure, the metabolic profile of the brainstem post-allergen stimulation was characterized through in vivo proton magnetic resonance imaging (1H-MRS). Then, the transient receptor potential vanilloid-1 (TRPV1) neuronal expression and sensitivity in the trigeminal nerve in AR were investigated. The link between TRPV1 expression and brainstem differential metabolites was also determined. Finally, we evaluated the mediating effects of brainstem metabolites and the consequences in the brain-spleen axis in the inflammatory response of AR. RESULTS: Exposure to allergens and PM2.5 led to changes in the metabolic profiles of the brainstem, particularly affecting levels of glutamine (Gln) and glutamate (Glu). This exposure also increased the expression and sensitivity of TRPV1+ neurons in the trigeminal nerve, with the levels of TRPV1 expression closely linked to the brainstem metabolism of Glu and Gln. Moreover, allergens increased the activity of p38, while PM2.5 led to the phosphorylation of p38 and ERK, resulting in the upregulation of TRPV1 expression. The brainstem metabolites Glu and Gln were found to partially mediate the impact of TRPV1 on AR inflammation, which was supported by the presence of pro-inflammatory changes in the brain-spleen axis. CONCLUSION: Brainstem metabolites are altered under allergen stimulation and additional PM2.5 exposure in AR via sensitization of the trigeminal nerve, which exacerbates the inflammatory response via the brain-splenic axis.