Spatial interaction and risk zoning of compound pollutants in farmland soils: Insights from heavy metals and polycyclic aromatic hydrocarbons in Hezhang County, China.

The accurate identification and assessment of comprehensive risks associated with compound pollution in agricultural ecosystems remain significant challenges due to the complexity of pollution sources, soil heterogeneity, and spatial variability. In this study, bivariate local indicators of spatial association (LISA) were applied to analyze the spatial interaction between heavy metals (HMs) and polycyclic aromatic hydrocarbons (PAHs) in farmland soils in Hezhang County. The results revealed distinct clusters with elevated concentrations of both HMs and PAHs, predominantly in areas affected by long-standing lead-zinc mining and smelting activities. Positive matrix factorization (PMF) was utilized to identify mining and smelting activities, and associated coal consumption as common sources of both pollutants, contributing 53 % and 28 %, respectively. Ecological health risk assessment results indicated that the combined pollution in this area has led to particularly severe ecological and cancer risks, with the pollution coefficient (Pc) exceeding 3.0, and risk values for both adults and children surpassing the threshold of 10-4. Through the integration of advanced bivariate LISA mapping and thorough risk assessment, this study precisely delineated ecological risk zones (33.1 %) and more refined health risk zones (40.1 %) associated with combined pollution. The southwest of Hezhang was identified as a critical hotspot for combined pollution risks, primarily due to intensive mining and smelting activities in the region. Overall, this study underscores the utility of bivariate LISA as a robust approach for delineating spatial clustering patterns caused by combined pollutants. It provides crucial insights for identifying regions with heightened human health and ecological risks in rural settings.

Potential of Coffee Cherry Pulp Extract against Polycyclic Aromatic Hydrocarbons in Air Pollution Induced Inflammation and Oxidative Stress for Topical Applications.

Airborne particulate matter (PM) contains polycyclic aromatic hydrocarbons (PAHs) as primary toxic components, causing oxidative damage and being associated with various inflammatory skin pathologies such as premature aging, atopic dermatitis, and psoriasis. Coffee cherry pulp (CCS) extract, rich in chlorogenic acid, caffeine, and theophylline, has demonstrated strong antioxidant properties. However, its specific anti-inflammatory effects and ability to protect macrophages against PAH-induced inflammation remain unexplored. Thus, this study aimed to evaluate the anti-inflammatory properties of CCS extract on RAW 264.7 macrophage cells exposed to atmospheric PAHs, compared to chlorogenic acid (CGA), caffeine (CAF), and theophylline (THP) standards. The CCS extract was assessed for its impact on the production of nitric oxide (NO) and expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Results showed that CCS extract exhibited significant antioxidant activities and effectively inhibited protease and lipoxygenase (LOX) activities. The PAH induced the increase in intracellular reactive oxygen species, NO, TNF-α, IL-6, iNOS, and COX-2, which were markedly suppressed by CCS extract in a dose-dependent manner, comparable to the effects of chlorogenic acid, caffeine, and theophylline. In conclusion, CCS extract inhibits PAH-induced inflammation by reducing pro-inflammatory cytokines and reactive oxygen species (ROS) production in RAW 264.7 cells. This effect is likely due to the synergistic effects of its bioactive compounds. Chlorogenic acid showed strong antioxidant and anti-inflammatory activities, while caffeine and theophylline enhanced anti-inflammatory activity. CCS extract did not irritate the hen's egg chorioallantoic membrane. Therefore, CCS extract shows its potential as a promising cosmeceutical ingredient for safely alleviating inflammatory skin diseases caused by air pollution.

Metastatic effects of hydroxy-polycyclic aromatic hydrocarbons on liver cancer cells mediated by estrogen receptor α.

Hydroxy-polycyclic aromatic hydrocarbons (OH-PAHs) are a growing worldwide concern because of their persistence, ubiquity, and toxicity. Nonetheless, research on the toxicological mechanisms of OH-PAHs remains sparse, particularly concerning the risk of liver cancer. This study evaluated the effects of OH-PAHs on disrupting estrogen receptor α (ERα) and subsequently facilitating hepatocellular invasion and metastasis. Results revealed that all six OH-PAHs exhibited ERα agonistic activities at noncytotoxic levels, which were partially validated using molecular docking (MD) and molecular dynamics simulations (MDS). Furthermore, OH-PAHs with ERα agonistic properties stimulated a concentration-dependent increase in the migration and invasion of HepG2 cells. In addition, they disturbed the expression of target genes associated with epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM), and the invasion effects were significantly reversed by adding an ERα antagonist. Our results suggest an essential role of ERα in the metastasis of liver cancer cells induced by OH-PAHs and emphasize their potential ecological and health hazards.

Relative genotoxicity of polycyclic aromatic hydrocarbons inferred from free energy perturbation approaches.

Utilizing molecular dynamics and free energy perturbation, we examine the relative binding affinity of several covalent polycyclic aromatic hydrocarbon - DNA (PAH-DNA) adducts at the central adenine of NRAS codon-61, a mutational hotspot implicated in cancer risk. Several PAHs classified by the International Agency for Research on Cancer as probable, possible, or unclassifiable as to carcinogenicity are found to have greater binding affinity than the known carcinogen, benzo[a]pyrene (B[a]P). van der Waals interactions between the intercalated PAH and neighboring nucleobases, and minimal disruption of the DNA duplex drive increases in binding affinity. PAH-DNA adducts may be repaired by global genomic nucleotide excision repair (GG-NER), hence we also compute relative free energies of complexation of PAH-DNA adducts with RAD4-RAD23 (the yeast ortholog of human XPC-RAD23) which constitutes the recognition step in GG-NER. PAH-DNA adducts exhibiting the greatest DNA binding affinity also exhibit the least RAD4-RAD23 complexation affinity and are thus predicted to resist the GG-NER machinery, contributing to their genotoxic potential. In particular, the fjord region PAHs dibenzo[a,l]pyrene, benzo[g]chrysene, and benzo[c]phenanthrene are found to have greater binding affinity while having weaker RAD4-RAD23 complexation affinity than their respective bay region analogs B[a]P, chrysene, and phenanthrene. We also find that the bay region PAHs dibenzo[a,j]anthracene, dibenzo[a,c]anthracene, and dibenzo[a,h]anthracene exhibit greater binding affinity and weaker RAD4-RAD23 complexation affinity than B[a]P. Thus, the study of PAH genotoxicity likely needs to be substantially broadened, with implications for public policy and the health sciences. This approach can be broadly applied to assess factors contributing to the genotoxicity of other unclassified compounds.

Association between plasma CC16 levels and lung function changes in coke oven workers: A cohort study from 2014 to 2023.

Club cell secretory protein (CC16) is considered a biological marker indicating lung epithelial and lung permeability. The joint effect of polycyclic aromatic hydrocarbons (PAHs) exposure on CC16 levels and the association between CC16 levels and long-term lung function changes lacks epidemiological evidence. To investigate the effect of PAHs exposure on plasma CC16 levels and the association between CC16 levels and long-term lung function changes, this study enrolled 307 coke oven workers in 2014, measured their baseline concentrations of urinary PAHs metabolites and plasma CC16, with follow-up after nine years. Bayesian kernel machine regression (BKMR) was employed to analyze the effect of mixed PAHs metabolites. The dose-effect association between baseline CC16 levels and lung function during 2014-2023 was explored using restricted cubic spline (RCS) models, and stratified analysis investigated the effect modification of PAHs exposure and smoking status on this association. The median age of the participants was 40 years, with 93.81 % male. The results showed that plasma CC16 levels decreased by 2.02 ng/mL (95 % CI: -3.77, -0.27) among all participants and FVC (% predicted) decreased by 2.87 % (95 % CI: -5.59, -0.14) in the low CC16 group with each unit increase in log-transformed 2-OHNAP. The BKMR model revealed a negative association between PAHs metabolites and both plasma CC16 levels and FVC (% predicted). Plasma CC16 decreased by 1.05 units when all PAHs metabolites at P65 compared to those at P50. After 9 years of follow-up, baseline CC16 levels were significantly associated with follow-up FVC (% predicted), FEV1 (% predicted), and small airway dysfunction risk. Furthermore, high PAHs exposure and smoking enhanced the association between CC16 and lung function. In conclusion, PAHs exposure decreases CC16 levels, and coking workers with low baseline CC16 levels may experience more severe future lung function decline.

Exploration of microRNAs from blood extracellular vesicles as biomarkers of exposure to polycyclic aromatic hydrocarbons.

Exposure to polycyclic aromatic hydrocarbons (PAHs), ubiquitously environmental contaminant, leads to the development of major toxic effects on human health, such as carcinogenic and immunosuppressive alterations reported for the most studied PAH, i.e., benzo(a)pyrene (B(a)P). In order to assess the risk associated with this exposure, it is necessary to have predictive biomarkers. Thus, extracellular vesicles (EVs) and their microRNA (miRNA) contents, have recently been proposed as potentially interesting biomarkers in Toxicology. Our study here explores the use of vesicles secreted and found in blood fluids, and their miRNAs, as biomarkers of exposure to B(a)P alone and within a realistic occupational mixture. We isolated EVs from primary human cultured blood mononuclear cells (PBMCs) and rat plasma after PAH exposure and reported an increased EV production by B(a)P, used either alone or in the mixture, in vitro and in vivo. We then investigated the association of this EV release with the blood concentration of the 7,8,9,10-hydroxy (tetrol)-B(a)P reactive metabolite, in rats. By performing RNA-sequencing (RNA-seq) of miRNAs in PBMC-derived EVs, we analyzed miRNA profiles and demonstrated the regulation of the expression of miR-342-3p upon B(a)P exposure. We then validated B(a)P-induced changes of miR-342-3p expression in vivo in rat plasma-derived EVs. Overall, our study highlights the feasibility of using EVs and their miRNA contents, as biomarkers of PAH exposure and discusses their potential in environmental Toxicology.

[The involvement and underlying mechanism of the aryl hydrocarbon receptor (AhR) in the impairment of male mammalian fertility induced by environmental pollutants].

In recent decades, there has been a consistent decline in semen quality across the globe, with environmental pollution emerging as the predominant factor. Persistent organic pollutants (POPs) have garnered considerable attention due to their potent biological toxicity and resistance to natural degradation. Within this class of pollutants, polycyclic aromatic hydrocarbons (PAHs) and halogenated aromatic hydrocarbons (HAHs) have been identified as detrimental agents that can disrupt cellular physiological functions by activating aryl hydrocarbon receptor (AhR). However, the precise role of AhR in the adverse effects of environmental pollutants on male mammalian fertility remains incompletely understood. This article provides a comprehensive review of the impact of various environmental pollutants, specifically PAHs such as benzo[a]pyrene, 3-methylcholanthrene, and 7,12-dimethylbenzo[a]anthracene, HAHs including 2,3,7,8-tetrachlorodibenzo-p-dioxins, polychlorinated biphenyls, polybrominated diphenyl ethers, and the pollutant complex PM2.5, as well as cigarette smoke condensates, on male mammalian reproductive function. Additionally, this review focuses on the role of the AhR in mediating these effects. The objective of this review is to elucidate the involvement of AhR in the regulation of male mammalian fertility, thereby offering insights for prospective investigations into the interplay between AhR and male reproductive function, as well as the etiology of idiopathic male infertility in clinic.

Chemical exposure from the Hebei spirit oil spill accident and its long-term effects on mental health.

While evidence indicates that exposure to oil spill incidents can affect mental health, it is unclear whether the mental health effects result from the incident itself or from exposure to associated chemicals. Oil contains chemicals that can impact mental health and these chemicals may have long-term effects due to their persistence in the environment. To address the gap in current knowledge, we conducted cross-sectional and prospective analyses of data from adults who participated in the Health Effects of the Hebei Spirit Oil Spill study. To assess chemical exposure from oil spills, we used indirect exposure indicators such as distance from the contaminated oil band to residences and duration of clean-up work, along with direct exposure indicators such as urine metabolite concentrations of volatile organic compounds and polycyclic aromatic hydrocarbons. Mental health assessments covered posttraumatic stress disorder (PTSD), depression, state anxiety, and trait anxiety. In the cross-sectional analyses, all four mental health issues were found to be associated with proximity to the oil band (p-value<0.05) and showed a positive association with clean-up work duration (p-value<0.05). Cox regression analysis revealed that higher urinary t, t-muconic acid levels were associated with an increased risk of depression (Hazard Ratio [HR] = 1.55, 95 % Confidence Interval [CI] = 1.05-2.28), and elevated 1-hydroxypyrene levels increased the risk of PTSD (HR = 1.60, 95 % CI = 1.03-2.48). Additionally, higher urinary 2-naphthol levels were associated with increased state anxiety (HR = 1.39, 95 % CI = 1.00-1.93) and trait anxiety (HR = 1.64, 95 % CI = 1.15-2.32). These associations persisted even after controlling for distance and duration variables related to psychosocial exposure. Our findings suggest that environmental disaster response plans should prioritize minimizing chemical exposure while also considering the duration and nature of the mental health impacts.

Toxicity of the oil spilled on the Brazilian coast at different degrees of natural weathering to early life stages of the zebrafish Danio rerio.

Toxicity of water accommodated fractions (WAF) from the oil spilled on the Brazilian coast at different stages of weathering were investigated using Danio rerio. Weathering stages included emulsified oil that reached the coast (OM) and oil collected 50 days later deposited on beach sand (OS) or adhered to shore rocks (OR). Parent and alkylated naphthalenes decreased whereas phenanthrenes increased from less weathered WAF-OM to more weathered WAF-OS and WAF-OR. More weathered WAF-OS and WAF-OR were more potent inducers of zebrafish developmental delay, suggesting that parent and alkylated phenanthrenes are involved. However, less weathered WAF-OM was a more potent inducer of failure in swim-bladder inflation than more weathered WAF-OS and WAF-OR, suggesting that parent and alkylated naphthalenes are involved. Decreases in heart rates and increased heart and skeletal deformities were observed in exposed larvae. Lowest observed effect concentrations for different developmental toxicity endpoints are within environmentally relevant polycyclic aromatic hydrocarbon concentrations.

Water-accommodated fractions of heavy and light oils impact DNA integrity, embryonic development, and immune system of Japanese medaka at early life stages.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants generally found in complex mixtures. PAHs are known to cause pleiotropic effects on living organisms, including developmental defects, mutagenicity, carcinogenicity and immunotoxicity, and endocrine disruptions. The main goal of this study is to evaluate the toxicity of water-accommodated fractions (WAFs) of oils in two life stages of the Japanese medaka, larvae and juveniles. The deleterious effects of an acute exposure of 48 h to two WAFs from Arabian light crude oil (LO) and refined oil from Erika (HO) were analyzed in both stages. Relevant endpoints, including ethoxy resorufin-O-deethylase (EROD) activity, DNA damage (Comet assay), photomotor response, and sensitivity to nervous necrosis virus (NNV) infection, were investigated. Larvae exposed to both oil WAFs displayed a significant induction of EROD activity, DNA damage, and developmental anomalies, but no behavioral changes. Deleterious effects were significantly increased following exposure to 1 and 10 µg/L of LO WAFs and 10 µg/L of HO WAFs. Larval infection to NNV induced fish mortality and sharply reduced reaction to light stimulation. Co-exposure to WAFs and NNV increased the mortality rate, suggesting an impact of WAFs on fish defense capacities. WAF toxicity on juveniles was only observed following the NNV challenge, with a higher sensitivity to HO WAFs than to LO WAFs. This study highlighted that environmentally realistic exposure to oil WAFs containing different compositions and concentrations of oil generated high adverse effects, especially in the larval stage. This kind of multi-marker approach is particularly relevant to characterize the toxicity fingerprint of environmental mixtures of hydrocarbons and PAHs.

A Quantitative Adverse Outcome Pathway for Embryonic Activation of the Aryl Hydrocarbon Receptor of Fishes by Polycyclic Aromatic Hydrocarbons Leading to Decreased Fecundity at Adulthood.

Quantitative adverse outcome pathways (qAOPs) describe the response-response relationships that link the magnitude and/or duration of chemical interaction with a specific molecular target to the probability and/or severity of the resulting apical-level toxicity of regulatory relevance. The present study developed the first qAOP for latent toxicities showing that early life exposure adversely affects health at adulthood. Specifically, a qAOP for embryonic activation of the aryl hydrocarbon receptor 2 (AHR2) of fishes by polycyclic aromatic hydrocarbons (PAHs) leading to decreased fecundity of females at adulthood was developed by building on existing qAOPs for (1) activation of the AHR leading to early life mortality in birds and fishes, and (2) inhibition of cytochrome P450 aromatase activity leading to decreased fecundity in fishes. Using zebrafish (Danio rerio) as a model species and benzo[a]pyrene as a model PAH, three linked quantitative relationships were developed: (1) plasma estrogen in adult females as a function of embryonic exposure, (2) plasma vitellogenin in adult females as a function of plasma estrogen, and (3) fecundity of adult females as a function of plasma vitellogenin. A fourth quantitative relationship was developed for early life mortality as a function of sensitivity to activation of the AHR2 in a standardized in vitro AHR transactivation assay to integrate toxic equivalence calculations that would allow prediction of effects of exposure to untested PAHs. The accuracy of the predictions from the resulting qAOP were evaluated using experimental data from zebrafish exposed as embryos to another PAH, benzo[k]fluoranthene. The qAOP developed in the present study demonstrates the potential of the AOP framework in enabling consideration of latent toxicities in quantitative ecological risk assessments and regulatory decision-making. Environ Toxicol Chem 2024;43:2145-2156. © 2024 SETAC.

Polycyclic aromatic hydrocarbons exposure associated with increased risk of psoriasis.

Psoriasis is considered to be multifactorial, with both genetic and environmental factors contributing to its development. Polycyclic aromatic hydrocarbons (PAHs) are widespread in the environment, originating from sources such as cigarette smoke, exhaust emissions, grilled foods, smoked foods and urban air. Researchs have established a link between PAHs exposure and autoimmune disorders; however, specific effects of PAHs on psoriasis remain underexplored. This study aims to evaluate the correlation between PAHs exposure and susceptibility to psoriasis. We analysed eight monohydroxy PAHs (1-Hydroxynaphthalene (1-NAP), 2-Hydroxynaphthalene (2-NAP), 3-Hydroxyfluorene (3-FLU), 2-Hydroxyfluorene (2-FLU), 1-Hydroxyphenanthrene (1-PHE), 1-Hydroxypyrene (1-PYR), 2-Hydroxyphenanthrene (2-PHE) and 3-Hydroxyphenanthrene (3-PHE)) in 5996 participants from the National Health and Nutrition Examination Survey (NHANES). We employed multivariate logistic regression, trend analysis, weighted quantile sum (WQS) regression and restricted cubic spline (RCS) analysis to investigate the relationship between PAHs exposure and psoriasis risk. Multivariate logistic regression and trend analysis revealed that monohydroxy PAHs, including 2-NAP, 3-FLU, 2-FLU and the mixture of 2-PHE and 3-PHE, are associated with an increased risk of psoriasis. Additionally, WQS regression showed a significant positive correlation between combined exposure to monohydroxy PAHs and psoriasis risk, with the mixture of 2-PHE and 3-PHE (47.3%) being the most influential factor. RCS regression further corroborated these findings. Specifically, 2-FLU can increase the expression of psoriasis-related inflammatory factors in HaCaT cells. In conclusion, PAHs exposure increases the risk of developing psoriasis. Efforts to reduce PAHs levels in the environment and minimise exposure are crucial for public health strategies aimed at preventing psoriasis.

Impact of arsenic and PAHs compound contamination on microorganisms in coking sites: From a community to individual perspective.

Arsenic (As) and polycyclic aromatic hydrocarbons (PAHs) are highly toxic, carcinogenic and teratogenic, and are commonly found in soils of industrial sites such as coking plants. They exert environmental stresses on soil microorganisms, but their compounding effects have not been systematically studied. Exploring the effects of compound contamination on microbial communities, species and genes is important for revealing the ecological damage caused by compound contamination and offering scientific insights into soil remediation strategies. In this study, we selected soil samples from 0 to 100 cm depth of a coking site with As, PAHs and compound contamination. We investigated the compound effects of As and PAHs on microbial communities by combining high-throughput sequencing, metagenomic sequencing and genome assembly. Compared with single contamination, compound contamination reduced the microbial community diversity by 10.68%-12.07% and reduced the community richness by 8.39%-18.61%. The compound contamination decreased 32.41%-46.02% of microbial PAHs metabolic gene abundance, 11.36%-19.25% of cell membrane transport gene abundance and 12.62%-57.77% of cell motility gene abundance. Xanthobacteraceae, the biomarker for compound contaminated soils, harbors arsenic reduction genes and PAHs degradation pathways of naphthalene, benzo [a]pyrene, fluorene, anthracene, and phenanthrene. Its broad metabolic capabilities, encompassing sulfur metabolism and quorum sensing, facilitate the acquisition of energy and nutrients, thereby conferring ecological niche advantages in compound contaminated environments. This study underscores the significant impacts of As and PAHs on the composition and function of microbial communities, thereby enriching our understanding of their combined effects and providing insights for the remediation of compound contaminated sites.

Risk Factors Associated with Urothelial Bladder Cancer.

BACKGROUND: Urothelial bladder carcinoma (UBC) is the most frequent histologic form of bladder cancer, constituting 90% of the cases. It is important to know the risk factors of UBC to avoid them and to decrease its recurrence after treatment. The aim of this review was to provide an overview of the risk factors associated with UBC incidence. METHODS: A comprehensive literature search from 2012 to 2024 was carried out in databases such as PubMed, Google Scholar, and Medline with potential keywords such as "bladder cancer", "urothelial bladder cancer", "incidence of urothelial bladder cancer worldwide", "mortality rate of bladder cancer", "incidence according to gender", "treatment for bladder cancer", and "risk factors of bladder cancer". Smoking tobacco was comprehended to be the major risk factor for UBC. Smoke from tobacco products contains polycyclic aromatic hydrocarbons (PAHs) and aromatic amines such as 4-aminobiphenyl, which are known to cause UBC. Smoking-related bladder cancer mortality ranks just second to smoking-related lung cancer mortality. For non-smokers, pollution became a major risk factor associated with UBC. Polycyclic aromatic hydrocarbons (PAHs) are linked to many cancers, especially to UBC. Indoor and outdoor pollution generates VOCs (volatile organic compounds) and PAHs. Small-particle matter < 2.5 is linked to UBC and lung cancers. Drinking chlorinated water is linked to UBC. Also, swimming in chlorinated pools that produce trihalomethanes increases the risk of many cancers, and especially of bladder cancer. Occupational exposure to carcinogens, specifically aromatic amines, is a significant UBC risk factor. It has been estimated that approximately 20% of all UBCs may be linked to this type of exposure, primarily in industrial settings that treat dye, paint, petroleum chemicals, and metal. The other risk factors included genetics, diet, and medical conditions. Alcohol, consumption of processed meat and whole milk, and higher intakes of selenium and vitamins A and E also contribute to the development of UBC. Further, chemotherapeutic agents, oral hypoglycemic drugs, and radiation therapy are positively associated with UBC. CONCLUSIONS: The significance of the initial prevention of UBC must be emphasized, and especially programs for quitting cigarettes should be encouraged and supported. However, smoking is not the only risk factor for UBC. For non-smokers, other risk factors should be investigated. Air and water pollution are linked to UBC. Indoor and outdoor pollution should be more controlled. Patients and people should be informed of the risk of drinking chlorinated water and swimming in chlorinated pools.

First Record of Malformation in Seahorses Attributed to the Oil Spill off the Brazilian Coast in 2019.

In 2019, there was an environmental catastrophe in Brazil, when more than 5000 tons of unknown origin crude oil invaded beaches and mangroves. Two years later, two monitoring areas were selected to study seahorses' offspring: Massangana River estuary (apparently healthy area) and Cocaia Island (affected area). Thirty-six reproductive events of Hippocampus reidi (Syngnathidae) couples from these two areas were monitored to analyze the offspring. At the apparently healthy area, no newborns with malformations were found. However, the offspring from Cocaia Island showed a mean of 19.73% (±5.23) malformations in newborns. It is argued that the toxic/teratogenic effects of polycyclic aromatic hydrocarbons have affected the population in two ways: directly through the induction of mutations in the germ cells of the species and through a drastic reduction of the population (bottleneck effect) whose density observed today recovered through consanguineous couplings, potentiating deleterious genotypes in the offspring. Environ Toxicol Chem 2024;43:1996-2004. © 2024 SETAC.

PAHs as environmental pollutants and their neurotoxic effects.

Polycyclic aromatic hydrocarbons (PAHs), which are widely present in incompletely combusted air particulate matter <2.5 µm (PM2.5), tobacco and other organic materials, can enter the human body through various routes and are a class of environmental pollutants with neurotoxic effects. PAHs exposure can lead to abnormal development of the nervous system and neurobehavioral abnormalities in animals, including adverse effects on the nervous system of children and adults, such as a reduced learning ability, intellectual decline, and neural tube defects. After PAHs enter cells of the nervous system, they eventually lead to nervous system damage through mechanisms such as oxidative stress, DNA methylation and demethylation, and mitochondrial autophagy, potentially leading to a series of nervous system diseases, such as Alzheimer's disease. Therefore, preventing and treating neurological diseases caused by PAHs exposure are particularly important. From the perspective of the in vitro and in vivo effects of PAHs exposure, as well as its effects on human neurodevelopment, this paper reviews the toxic mechanisms of action of PAHs and the corresponding prevention and treatment methods to provide a relevant theoretical basis for preventing the neurotoxicity caused by PAHs, thereby reducing the incidence of diseases related to the nervous system and protecting human health.

Associations between fine particulate matter, gene expression, and promoter methylation in human bronchial epithelial cells exposed within a classroom under air-liquid interface.

Associations between indoor air pollution from fine particulate matter (PM with aerodynamic diameter dp < 2.5 µm) and human health are poorly understood. Here, we analyse the concentration-response curves for fine and ultrafine PM, the gene expression, and the methylation patterns in human bronchial epithelial cells (BEAS-2B) exposed at the air-liquid interface (ALI) within a classroom in downtown Rome. Our results document the upregulation of aryl hydrocarbon receptor (AhR) and genes associated with xenobiotic metabolism (CYP1A1 and CYP1B1) in response to single exposure of cells to fresh urban aerosols at low fine PM mass concentrations within the classroom. This is evidenced by concentrations of ultrafine particles (UFPs, dp < 0.1 µm), polycyclic aromatic hydrocarbons (PAH), and ratios of black carbon (BC) to organic aerosol (OA). Additionally, an interleukin 18 (IL-18) down-regulation was found during periods of high human occupancy. Despite the observed gene expression dysregulation, no changes were detected in the methylation levels of the promoter regions of these genes, indicating that the altered gene expression is not linked to changes in DNA methylation and suggesting the involvement of another epigenetic mechanism in the gene regulation. Gene expression changes at low exposure doses have been previously reported. Here, we add the possibility that lung epithelial cells, when singly exposed to real environmental concentrations of fine PM that translate into ultra-low doses of treatment, may undergo epigenetic alteration in the expression of genes related to xenobiotic metabolism. Our findings provide a perspective for future indoor air quality regulations. We underscore the potential role of indoor UFPs as carriers of toxic molecules with low-pressure weather conditions, when rainfall and strong winds may favour low levels of fine PM.

Effects of polycyclic aromatic hydrocarbons on the gut-testis axis.

Polycyclic aromatic hydrocarbons (PAHs) are a large group of organic compounds which are comprised of two or more fused benzene rings. As a typical environmental pollutant, PAHs are widely distributed in water, soil, atmosphere and food. Despite extensive researches on the mechanisms of health damage caused by PAHs, especially their carcinogenic and mutagenic toxicity, there is still a lack of comprehensive summarization and synthesis regarding the mechanisms of PAHs on the gut-testis axis, which represents an intricate interplay between the gastrointestinal and reproductive systems. Thus, this review primarily focuses on the potential forms of interaction between PAHs and the gut microbiota and summarizes their adverse outcomes that may lead to gut microbiota dysbiosis, then compiles the possible mechanistic pathways on dysbiosis of the gut microbiota impairing the male reproductive function, in order to provide valuable insights for future research and guide further exploration into the intricate mechanisms underlying the impact of gut microbiota dysbiosis caused by PAHs on male reproductive function.

A single and short exposure to heated tobacco vapor or cigarette smoke affects macrophage activation and polarization.

The toxicity of heated tobacco products (HTP) on the immune cells remains unclear. Here, U937-differentiated macrophages were exposed to a single and short-term exposure (30 minutes) of HTP vapor or cigarette smoke (CS) in an air-liquid interface (ALI) system to evaluate the effects on macrophages' early activation and polarization. In our system, HTP released lower amounts of polycyclic aromatic hydrocarbons (PAHs), but higher nicotine levels than CS into the cell culture supernatant. Both tobacco products triggered the expression of the α-7 nicotinic receptor (α7 nAChR) and reactive oxygen species (ROS) production. When challenged with a bacterial product, lipopolysaccharide (LPS), cells exposed to HTP or CS failed to respond properly and enhance ROS production upon LPS stimuli. Furthermore, both tobacco products also impaired bacterial phagocytosis and the exposures triggered higher IL-1ß secretion. The α7 nAChR antagonist treatment rescued the effects caused only by HTP exposure. The CS-exposed group switched macrophage to the pro-inflammatory M1, while HTP polarized to the suppressive M2 profile. Associated, data highlight that HTP and CS exposures similarly activate macrophages; nonetheless, the α7 nAChR pathway is only involved in HTP actions, and the distinct subsequent polarization caused by HTP or CS may influence the outcome of host defense.

Ecotoxicological risk of asphalt pavements to aquatic animals associated with pollutant leaching.

Contaminants such as heavy metals and polycyclic aromatic hydrocarbons (PAHs) can be released from asphalt pavement and transported through stormwater runoff to nearby water bodies, leading to water pollution and potential harm to living aquatic animals. This study characterizes the heavy metal and PAH leaching from various asphalt paving materials and their potential ecotoxicological effects on zebrafish Danio rerio. Artificial runoffs were prepared in the laboratory concerning the effects of water, temperature, and traffic. The concentrations of heavy metals and PAHs in the leachates were quantified, while the toxicity assessment encompassed mortality, metal stress, PAH toxicity, inflammation, carcinogenicity, and oxidative damage. Gene expressions of related proteins or transcription factors were assessed, including metallothionines, aryl hydrocarbon receptors, interleukin-1ß, interleukin-10, nuclear factor-κB, tumor necrosis factor-α, tumor suppressor p53, heat shock protein 70, and reactive oxygen species (ROS). The findings demonstrate that leachates from asphalt pavements containing waste bottom ash, crumb rubber, or specific chemicals could induce notable stress and inflammation responses in zebrafish. In addition, potential carcinogenic effects and the elevation of ROS were identified within certain treatment groups. This study represents the first attempt to assess the ecotoxicity of pavement leachates employing a live fish model, thereby improving the current understanding of the environmental impact of asphalt pavements.