Changes in the Non-targeted Metabolomic Profile of Three-year-old Toddlers with Elevated Exposure to Polycyclic Aromatic Hydrocarbons.

Objective: To investigate changes in the urinary metabolite profiles of children exposed to polycyclic aromatic hydrocarbons (PAHs) during critical brain development and explore their potential link with the intestinal microbiota. Methods: Liquid chromatography-tandem mass spectrometry was used to determine ten hydroxyl metabolites of PAHs (OH-PAHs) in 36-month-old children. Subsequently, 37 children were categorized into low- and high-exposure groups based on the sum of the ten OH-PAHs. Ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry was used to identify non-targeted metabolites in the urine samples. Furthermore, fecal flora abundance was assessed by 16S rRNA gene sequencing using Illumina MiSeq. Results: The concentrations of 21 metabolites were significantly higher in the high exposure group than in the low exposure group (variable importance for projection > 1, P < 0.05). Most of these metabolites were positively correlated with the hydroxyl metabolites of naphthalene, fluorine, and phenanthrene ( r = 0.336-0.531). The identified differential metabolites primarily belonged to pathways associated with inflammation or proinflammatory states, including amino acid, lipid, and nucleotide metabolism. Additionally, these distinct metabolites were significantly associated with specific intestinal flora abundances ( r = 0.34-0.55), which were mainly involved in neurodevelopment. Conclusion: Higher PAH exposure in young children affected metabolic homeostasis, particularly that of certain gut microbiota-derived metabolites. Further investigation is needed to explore the potential influence of PAHs on the gut microbiota and their possible association with neurodevelopmental outcomes.

An extensive investigation on human risk associated with PAHs in fish and sediment in Bushehr, Northern of Persian Gulf.

Here, a comprehensive study was designed to estimate the human risk assessment attributed to exposure of polycyclic aromatic hydrocarbons (PAHs)in sediment and fish in most polluted shore area in north of Persian Gulf. To this end, a total of 20 sediment and inhabitual Fish, as one of most commercial fish, samples were randomly collected from 20 different stations along Bushehr Province coastline. The 16 different components of PAHs were extracted from sediment and edible parts of inhabitual fish and measured with high-performance liquid chromatography (HPLC) and gas chromatography (GC), respectively. In addition, dietary daily intake (DDI) values of PAHs via ingestion Indian halibut and the incremental lifetime cancer risk (ILCR) attributed to human exposure to sediments PAHs via (a) inhalation, (b) ingestion, and (c) dermal contact for two groups of ages: children (1-11 years) and adults (18-70 years) were estimated. The results indicated that all individual PAHs except for Benzo(b)flouranthene (BbF) and Benzo(ghi) perylene (BgP) were detected in different sediment sample throughout the study area with average concentration between 2.275 ± 4.993 mg.kg-1 dw. Furthermore, Naphthalene (Nap) with highest average concentration of 3.906 ± 3.039 mg.kg-1 dw was measured at the Indian halibut. In addition, the human risk analysis indicated that excess cancer risk (ECR) attributed to PAHs in sediment and fish in Asaluyeh with high industrial activities on oil and derivatives were higher the value recommended by USEPA (10-6). Therefore, a comprehensive analysis on spatial distribution and human risk assessment of PAHs in sediment and fish can improve the awareness on environmental threat in order to aid authorities and decision maker to find a sustainable solution.

Air pollution and skin diseases: A comprehensive evaluation of the associated mechanism.

Air pollutants deteriorate the survival environment and endanger human health around the world. A large number of studies have confirmed that air pollution jeopardizes multiple organs, such as the cardiovascular, respiratory, and central nervous systems. Skin is the largest organ and the first barrier that protects us from the outside world. Air pollutants such as particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs) will affect the structure and function of the skin and bring about the development of inflammatory skin diseases (atopic dermatitis (AD), psoriasis), skin accessory diseases (acne, alopecia), auto-immune skin diseases (cutaneous lupus erythematosus(CLE) scleroderma), and even skin tumors (melanoma, basal cell carcinoma (BCC), squamous-cell carcinoma (SCC)). Oxidative stress, skin barrier damage, microbiome dysbiosis, and skin inflammation are the pathogenesis of air pollution stimulation. In this review, we summarize the current evidence on the effects of air pollution on skin diseases and possible mechanisms to provide strategies for future research.

Assessment of parent and alkyl -PAHs in surface sediments of Iranian mangroves on the northern coast of the Persian Gulf: Spatial accumulation distribution, influence factors, and ecotoxicological risks.

Spatial patterns, potential origins, and ecotoxicological risk of alkylated (APAH) -and parent -(PPAH) polycyclic aromatic hydrocarbons (PAHs) were studied in mangrove surface sediments along the northern coasts of the Persian Gulf, Iran. The mean total concentrations (ngg-1dw) ∑32PAH, ∑PPAHs and ∑APAHs in sediments were 3482 (1689-61228), 2642 (1109-4849), and 840 (478-1273), respectively. The spatial variability was similar among these PAH groups, with the highest levels occurring in Nayband National Marine Park (NNMP). Physicochemical environmental factors, such as sediment grain size, and total organic carbon (TOC) contents, are significant factors of PAH distribution. These findings suggest that PAH pollution level is moderate-to-high, supporting the current view that mangrove ecosystems are under intensive anthropogenic impacts, such as petrochemical, oil and gas loads, port activities, and urbanization. Non-parametric multidimensional scaling (NPMDS) ordination demonstrated that NNMP mangrove is the critical site exhibiting high loading of PAH pollutants. Here, for the first time in this region, Soil quality guidelines (SQGs), Toxic equivalency quotient (TEQ), Mutagenic equivalency quotient (MEQ), and composition indices comprising Mean maximum permissible concentration quotient (m-MPC-Q), and Mean effect range median quotient (m-ERM-Q) methods were used to have a comprehensive risk assessment for PAH compounds and confirmed medium-to-high ecological risks of PAHs in the study area, particularly in the western part of the Gulf, highlighting the industrial impacts on the environment.

A multigenerational study can detect the evolutionary response to BaP exposure in the non-biting freshwater midge Chironomus riparius.

The release of polycyclic aromatic hydrocarbons (PAHs) into the environment is posing a threat to ecosystems and human health. Benzo(a)pyrene (BaP) is considered a biomarker of PAH exposure and is classified as a Group 1 carcinogen. However, it was not known whether BaP is mutagenic, i.e. induces inherited germline mutations. In this study, we used a recently established method, which combines short-term mutation accumulation lines (MAL) with whole genome sequencing (WGS) to assess mutagenicity in the non-biting midge Chironomus riparius. The mutagenicity analysis was supplemented by an evaluation of the development of population fitness in three successive generations in the case of chronic exposure to BaP at a high concentration (100 µg/L). In addition, the level of ROS-induced oxidative stress was examined in vivo. Exposure to the higher BaP concentration led to an increase in germline mutations relative to the control, while the lower concentration showed no mentionable effect. Against expectations, BaP exposure decreased ROS-level compared to the control and is thus probably not responsible for the increased mutation rate. Likewise, the higher BaP concentration decreased fitness measured as population growth rate per day (PGR) significantly over all generations, without signs of rapid evolutionary adaptations. Our results thus highlighted that high BaP exposure may influence the evolutionary trajectory of organisms.

A novel approach to assess the health risk of aryl hydrocarbon receptor-bound contaminants via inhalation exposure using CYP1A1 expression as a biomarker.

Polycyclic aromatic hydrocarbons (PAHs) and dioxins are potential causes of multiple diseases by activating the aryl hydrocarbon receptor (AhR) pathway. Health risk assessment of chemicals primarily relies on the relative potency factor (RPF), although its accuracy may be limited when solely using EC50 values. The induction of cytochrome P4501A1 (CYP1A1) serves as a biomarker for AhR activation and is an integrator of dioxin-like toxicity. Here, we present a method for evaluating the risks associated with AhR activation using mathematical models of dose-CYP1A1 induction. The dose-effect curves for certain PAHs and dioxins, including Ant, BghiP, 1,2,3,4,7,8-HxCDD, and others, exhibited a non-classical S-shaped form. The toxic equivalent factor (TEF) profiles revealed a broad range of toxic equivalent factor values. The TEFs for PAHs ranged from approximately 0.01 to 6, with higher values being observed when the concentration was less than 10-10 M, with the exceptions of Ace, Phe, and BghiP. Most congeners of dioxins got the lowest TEF value at around 10-10 M, ranging from 0.04 to 1.00. The binding affinity of AhR to ligands did not display a strong correlation with the EC50 of CYP1A1 expression, suggesting that the AhR-mediated effects of PAHs and dioxins are not fixed but instead fluctuate with the dose. Air samples acquired from a parking area were used to compare the proficiency of RPF and our current approach. In the current method, naphthalene and chrysene were the primary contributors of PAHs to AhR-mediated risks in parking lots air samples, respectively. However, the contributions of naphthalene and chrysene could be disregarded in the RPF approach.

Salmonid smolt caudal fin and liver transcriptome responses to low sulfur marine diesel and high sulfur fuel oil water accommodated fractions for assessing oil spill effects in marine environments.

The environmental impact of oil spills is a critical concern, particularly pertaining to low sulfur marine diesel (LSMD) and high sulfur fuel oil (HSFO) that are commonly involved in coastal spills. Although transcriptomic biomonitoring of sentinel animals can be a powerful tool for assessing biological effects, conventional methods utilize lethal sampling to examine the liver. As a non-lethal alternative, we have previously shown salmonid caudal fin cyp1a1 is significantly responsive to LSMD-derived toxicants. The present study further investigated the transcriptomic biomonitoring potential of coho salmon smolt caudal fin in comparison to liver tissue in the context of LSMD and HSFO seawater accommodated fraction (seaWAF) exposure in cold-water marine environments. Assessing the toxicity of these seaWAFs involved quantifying polycyclic aromatic hydrocarbon (tPAH50) concentrations and generating gene expression profiles. Initial qPCR analyses revealed significant cyp1a1 response in both liver and caudal fin tissues of both genetic sexes to all seaWAF exposures. RNA-Seq analysis, focusing on the highest LSMD and HSFO seaWAF concentrations (28.4±1.8 and 645.08±146.3 µg/L tPAH50, respectively), revealed distinct tissue-specific and genetic sex-independent transcriptomic responses with an overall enrichment of oxidative stress, cell adhesion, and morphogenesis-related pathways. Remarkably, the caudal fin tissue exhibited transcriptomic response patterns comparable to liver tissue, particularly consistent differential expression of 33 gene transcripts in the liver (independent of sex and oil type) and 44 in the caudal fin. The present work underscores the viability of using the caudal fin as a non-lethal alternative to liver sampling for assessing and tracking oil spill exposure in marine environments.

Bioconcentration and lethal effects of gas-condensate and crude oil on nearshore copepod assemblages.

The progressive establishment of gas platforms and increasing petroleum accidents pose a threat to zooplankton communities and thus to pelagic ecosystems. This study is the first to compare the impacts of gas-condensate and crude oil on copepod assemblages. We conducted microcosm experiments simulating slick scenarios at five different concentrations of gas-condensate and crude oil to determine and compare their lethal effects and the bioconcentration of low molecular weight polycyclic aromatic hydrocarbons (LMW-PAHs) in eastern Mediterranean coastal copepod assemblages. We found that gas-condensate had a two-times higher toxic effect than crude oil, significantly reducing copepod survival with increased exposure levels. The LMW-PAHs bioconcentration factor was 1-2 orders of magnitude higher in copepods exposed to gas-condensate than in those exposed to crude oil. The median lethal concentration (LC50) was significantly lower in calanoids vs. cyclopoid copepods, suggesting that calanoids are more susceptible to gas-condensate and crude oil pollution, with potential trophic implications.

Large-scale soil application of hydrochar: Reducing its polycyclic aromatic hydrocarbon content and toxicity by heating.

The beneficial roles of hydrochar in carbon sequestration and soil improvement are widely accepted. Despite few available reports regarding polycyclic aromatic hydrocarbons (PAHs) generated during preparation, their potential negative impacts on ecosystems remain a concern. A heating treatment method was employed in this study for rapidly removing PAHs and reducing the toxicity of corn stover-based hydrochar (CHC). The result showed total PAHs content (∑PAH) decreased and then sharply increased within the temperature range from 150 °C to 400 °C. The ∑PAH and related toxicity in CHC decreased by more than 80% under 200 °C heating temperature, compared with those in the untreated sample, representing the lowest microbial toxicity. Benzo(a)pyrene produced a significant influence on the ecological toxicity of the hydrochar among the 16 types of PAHs. The impact of thermal treatment on the composition, content, and toxicity of PAHs was significantly influenced by the adsorption, migration, and desorption of PAHs within hydrochar pores, as well as the disintegration and aggregation of large molecular polymers. The combination of hydrochar with carbonized waste heat and exhaust gas collection could be a promising method to efficiently and affordably reduce hydrochar ecological toxicity.

Polycyclic aromatic hydrocarbons exposure and arterial stiffness-related plasma miRNAs: A panel study.

The underlying mechanisms between polycyclic aromatic hydrocarbons (PAHs) exposure and arterial stiffness are poorly understood. We carried out a panel study involving three repeated surveys to examine the associations of individual and mixture of PAHs exposure with arterial stiffness-related miRNAs among 123 community adults. In linear mixed-effect (LME) models, we found that urinary 9-hydroxyfluorene (9-OHFlu), 2-hydroxyphenanthrene (2-OHPh), 9-hydroxyphenanthrene (9-OHPh) at lag 0 day were positively linked to miR-146a and/or miR-222. The Bayesian kernel machine regression (BKMR) analyses revealed positive overall associations of PAHs mixture at lag 0 day with miR-146a and miR-222, and urinary 9-OHFlu contributed the most. In addition, an inter-quartile range (IQR) increase in urinary 9-OHFlu at lag 0 day was associated with elevated miR-146a and miR-222 by 0.16 (95% CI: 0.02, 0.30) to 0.34 (95% CI: 0.13, 0.54). Accordingly, exposure to PAHs, especially 9-OHFlu at lag 0 day, was related to elevated arterial stiffness-related plasma miRNAs.

Atmospheric occurrences and bioavailability health risk of PAHs and their derivatives surrounding a non-ferrous metal smelting plant.

Non-ferrous metal smelting emits large amounts of organic compounds into the atmosphere. Herein, 20 parent polycyclic aromatic hydrocarbons (PPAHs), 9 nitrated PAHs (NPAHs), 14 chlorinated PAHs (ClPAHs), and 6 alkylated PAHs (APAHs) in atmospheric samples from a typical non-ferrous metal smelting plant (NMSP) and residential areas were detected. In NMSP, benzo[a]pyrene, dibenz[a,h]anthracene, 6-nitrochrysene, 9-chlorofluorene, and 1-methylfluorene were the predominant compounds in the particulate phase, while phenanthrene constituted 57.3% in the gaseous phase. The concentration of PAHs in residential areas around NMSP was 1.8 times higher than that in the control area. Additionally, there was a significant negative correlation between the concentration and the distance from the NMSP. In terms of health risks, although the skin penetration coefficient of PM2.5 is smaller than that of the gaseous phase, dermal absorption of PM2.5 posed a greater threat to the population, the incremental lifetime cancer risk (ILCR) of NMSP was 1.8 × 10-4. After considering bioavailability, BILCR decreased by 1-2 orders of magnitude in different regions, and dermal absorption decreased more than inhalation intake. Nevertheless, the dermal absorption of PM2.5 in NMSP still presents a probable carcinogenic risk. This study provides a necessary reference for the subsequent control of NMSP contamination.

Prepubertal exposure to polycyclic aromatic hydrocarbons are associated with early pubertal development onset in boys: A longitudinal study.

OBJECTIVE: To investigate the effects of polycyclic aromatic hydrocarbons(PAHs) on puberty in boys. METHODS: 695 subjects were selected from four primary schools in Chongqing, China. 675 urine samples from these boys were collected four PAH metabolites: 1-hydroxypyrene, 2-hydroxynaphthoic, 2-hydroxyfluorene, and 9-hydroxyphenanthrene. Pubertal development of 695 boys was assessed at follow-up visits starting in December 2015 and occurring every six months thereafter until now, data used in this article ending in June 2021. A total of 12 follow-up visits were performed. Cox proportional hazards regression models were used to analyze the relationship between PAH metabolite concentrations and indicators of pubertal timing. RESULTS: The mean age at puberty onset of testicular volume, facial hair, pubic hair, first ejaculation, and axillary hair in boys was 11.66, 12.43, 12.51, 12.72 and 13.70 years, respectively. Cox proportional hazards regression models showed that boys with moderate level of 1-OHPyr exposure was associated with earlier testicular development (hazard ratio [HR] = 1.276, 95% confidence interval [CI]: 1.006-1.619), with moderate level of 2-OHNap were at higher risk of early testicular development (HR = 1.273, 95% CI: 1.002-1.617) and early axillary hair development (HR = 1.355, 95% CI: 1.040-1.764), with moderate level of 2-OHFlu was associated with earlier pubic hair development (HR = 1.256, 95% CI: 1.001-1.577), with high level of 9-OHPhe were at higher risk of early fisrt ejaculation (HR = 1.333, 95% CI: 1.005-1.767) and early facial hair development (HR = 1.393, 95% CI: 1.059-1.831). CONCLUSION: Prepubertal exposure to PAHs may be associated with earlier pubertal development in boys.

Modeling PAH Mixture Interactions in a Human In Vitro Organotypic Respiratory Model.

One of the most significant challenges in human health risk assessment is to evaluate hazards from exposure to environmental chemical mixtures. Polycyclic aromatic hydrocarbons (PAHs) are a class of ubiquitous contaminants typically found as mixtures in gaseous and particulate phases in ambient air pollution associated with petrochemicals from Superfund sites and the burning of fossil fuels. However, little is understood about how PAHs in mixtures contribute to toxicity in lung cells. To investigate mixture interactions and component additivity from environmentally relevant PAHs, two synthetic mixtures were created from PAHs identified in passive air samplers at a legacy creosote site impacted by wildfires. The primary human bronchial epithelial cells differentiated at the air-liquid interface were treated with PAH mixtures at environmentally relevant proportions and evaluated for the differential expression of transcriptional biomarkers related to xenobiotic metabolism, oxidative stress response, barrier integrity, and DNA damage response. Component additivity was evaluated across all endpoints using two independent action (IA) models with and without the scaling of components by toxic equivalence factors. Both IA models exhibited trends that were unlike the observed mixture response and generally underestimated the toxicity across dose suggesting the potential for non-additive interactions of components. Overall, this study provides an example of the usefulness of mixture toxicity assessment with the currently available methods while demonstrating the need for more complex yet interpretable mixture response evaluation methods for environmental samples.

3-Methyl-phenanthrene (3-MP) disrupts the electrical and contractile activity of the heart of the polar fish, navaga cod (Eleginus nawaga).

Alkylated polycyclic aromatic hydrocarbons are abundant in crude oil and are enriched during petroleum refinement but knowledge of their cardiotoxicity remains limited. Polycyclic aromatic hydrocarbons (PAHs) are considered the main hazardous components in crude oil and the tricyclic PAH phenanthrene has been singled out for its direct effects on cardiac tissue in mammals and fish. Here we test the impact of the monomethylated phenanthrene, 3-methylphenanthrene (3-MP), on the contractile and electrical function of the atrium and ventricle of a polar fish, the navaga cod (Eleginus nawaga). Using patch-clamp electrophysiology in atrial and ventricular cardiomyocytes we show that 3-MP is a potent inhibitor of the delayed rectifier current IKr (IC50 = 0.25 µM) and prolongs ventricular action potential duration. Unlike the parent compound phenanthrene, 3-MP did not reduce the amplitude of the L-type Ca2+ current (ICa) but it accelerated current inactivation thus reducing charge transfer across the myocyte membrane and compromising pressure development of the whole heart. 3-MP was a potent inhibitor (IC50 = 4.7 µM) of the sodium current (INa), slowing the upstroke of the action potential in isolated cells, slowing conduction velocity across the atrium measured with optical mapping, and increasing atrio-ventricular delay in a working whole heart preparation. Together, these findings reveal the strong cardiotoxic potential of this phenanthrene derivative on the fish heart. As 3-MP and other alkylated phenanthrenes comprise a large fraction of the PAHs in crude oil mixtures, these findings are worrisome for Arctic species facing increasing incidence of spills and leaks from the petroleum industry. 3-MP is also a major component of polluted air but is not routinely measured. This is also of concern if the hearts of humans and other terrestrial animals respond to this PAH in a similar manner to fish.

A systematic toxicologic study of polycyclic aromatic hydrocarbons on aquatic organisms via food-web bioaccumulation.

Pollution-induced declines in fishery resources restrict the sustainable development of fishery. As a kind of typical environmental pollutant, the mechanism of polycyclic aromatic hydrocarbons (PAHs) facilitating fishery resources declines needs to be fully illustrated. To determine how PAHs have led to declines in fishery resources, a systematic toxicologic analysis of the effects of PAHs on aquatic organisms via food-web bioaccumulation was performed in the Pearl River and its estuary. Overall, PAH bioaccumulation in aquatic organisms was correlated with the trophic levels along food-web, exhibiting as significant positive correlations were observed between PAHs concentration and the trophic levels of fishes in the Pearl River Estuary. Additionally, waterborne PAHs exerted significant direct effects on dietary organisms (P < 0.05), and diet-borne PAHs subsequently exhibited significant direct effects on fish (P < 0.05). However, an apparent block effect was found in dietary organisms (e.g., zooplankton) where 33.49 % of the total system throughput (TST) was retained at trophic level II, exhibiting as the highest PAHs concentration, bioaccumulation factor (BAF), and biomagnification factor (BMF) of ∑15PAHs in zooplankton were at least eight-fold greater than those in fishes in both the Pearl River and its estuary, thereby waterborne PAHs exerted either direct or indirect effects on fishes that ultimately led to food-web simplification. Regardless of the block effect of dietary organisms, a general toxic effect of PAHs on aquatic organisms was observed, e.g., Phe and BaP exerted lethal effects on phytoplankton Chlorella pyrenoidosa and zooplankton Daphnia magna, and decreased reproduction in fishes Danio rerio and Megalobrama hoffmanni via activating the NOD-like receptors (NLRs) signaling pathway. Consequently, an assembled aggregate exposure pathway for PAHs revealed that increases in waterborne PAHs led to bioaccumulation of PAHs in aquatic organisms along food-web, and this in turn decreased the reproductive ability of fishes, thus causing decline in fishery resources.

A meta-analysis of the carcinogenic effects of particulate matter and polycyclic aromatic hydrocarbons.

Urbanization has numerous benefits to human society, but some aspects of urban environments, such as air pollution, can negatively affect human health. Two major air pollutants, particulate matter (PM) and polycyclic aromatic hydrocarbons (PAH), have been classified as carcinogens by the International Agency for Research on Cancer. Here, we answer two questions: (1) What are the carcinogenic effects of PM and PAH exposure? (2) How does carcinogenic risk vary across geographical regions? We performed a comprehensive literature search of peer-reviewed published studies examining the link between air pollution and human cancer rates. Focusing on studies published since 2014 when the last IARC monograph on air pollution was published, we converted the extracted data into relative risks and performed subgroup analyses. Exposure to PM2.5 (per 10 µg/m3) resulted in an 8.5% increase in cancer incidence when all cancer types were combined, and risk for individual cancer types (i.e. lung cancer and adenocarcinoma) was also elevated. PM2.5 was also associated with 2.5% higher mortality due to cancer when all types of cancer were combined, and for individual cancer types (i.e., lung and breast cancer). Exposure to PM2.5 and PM10 posed the greatest risk to lung cancer incidence and mortality in Europe (PM2.5 RR 2.15; PM10 RR 1.26); the risk in Asia and the Americas was also elevated. Exposure to PAH and benzo[a]pyrene significantly increased the pooled risk of cancer incidence (10.8% and 8.0% respectively) at the highest percentile of exposure concentration. Our meta-analyses of studies over the past decade shows that urban air pollution in the form of PM2.5, PM10, and PAH all elevate the incidence and mortality of cancer. We discuss the possible mechanisms of carcinogenesis of PM and PAH. These results support World Health Organization's conclusion that air pollution poses among the greatest health risks to humans living in cities.

AhR agonists screening and identification in indoor dust based on non-target chemical analysis by GC-Q-TOFMS and biological effect evaluation referring to ToxCast/Tox21 database.

Numerous studies reported the concentration of agonists of aryl hydrocarbon receptor (AhR) in indoor dust by target chemical analysis or the biological effects of activating the AhR by indoor extracts, but the major AhR agonists identification in indoor dust were rarely researched. In the present study, the indoor dust samples were collected for 7-ethoxyresorufin O-deethylase (EROD) assay and both non-targeted and targeted chemical analysis for AhR agonists by gas chromatography quadrupole time-of-flight mass spectrometry and gas chromatography-mass spectrometry analysis. Coupled with non-targeted analysis and toxicity Forecaster (ToxCast)/Tox21 database, 104 ToxCast chemicals were screened to be able to induce EROD response. The combination of targeted chemical analyses and biological effects evaluation indicated that PAHs, dibutyl phthalate (DBP) and Cypermethrin might be the important AhR-agonists in different indoor dust and mainly contributed in 1.84%-97.56 % (median: 26.62%) of total observed biological effects through comparing toxic equivalency quotient derived from chemical analysis with biological equivalences derived from bioassay. DBP and cypermethrin seldom reported in the analysis of AhR agonists should raise great concern. In addition, the present results in experiment of synthetic solution of 4 selected AhR-agonists pointed out that some unidentified AhR agonists existed in indoor dust.

Multiple exposure pathways and health risk assessment of PAHs in Lanzhou city, a semi-arid region in northwest China.

In the sparse studies for multiple pathway exposure, attention has predominantly been directed towards developed regions, thereby overlooking the exposure level and health outcome for the inhabitants of the semi-arid regions in northwest China. However, cities within these regions grapple with myriad challenges, encompassing insufficient sanitation infrastructure and outdated heating. In this study, we analyzed the characteristics and sources of polycyclic aromatic hydrocarbons (PAHs) pollution in PM2.5, water, diet, and dust during different periods in Lanzhou, and estimated corresponding carcinogenic health risk through inhalation, ingestion, and dermal absorption. Our observations revealed the concentrations of PAHs in PM2.5, food, soil, and water are 200.11 ng m-3, 8.67 mg kg-1, 3.91 mg kg-1, and 14.5 ng L-1, respectively, indicating that the Lanzhou area was seriously polluted. Lifetime incremental cancer risk (ILCR) showed a heightened cancer risk to men compared to women, to the younger than the elderly, and during heating period as opposed to non-heating period. Notably, the inhalation was the primary route of PAHs exposure and the risk of exposure by inhalation cannot be ignored. The total environmental exposure assessment of PAHs can achieve accurate prevention and control of PAHs environmental exposure according to local conditions and targets.

Breath of Danger: Unveiling PM2.5's Stealthy Impact on Cancer Risks.

This article explores the intricate relationship between airborne particulate matter (PM), specifically PM2.5, and its profound impact on human health, emphasising the heightened risks of cancer. Examining the composition and characteristics of PM2.5, such as particle size and surface area, reveals its ability to induce inflammatory injury and oxidative damage. The carcinogenic potential extends beyond respiratory implications, affecting various organs, including the digestive tract, breast, and prostate. In addition to the genotoxic effects of PM2.5, attached polycyclic aromatic hydrocarbons are recognized to be endocrine-disrupting chemicals with specific implications for breast and prostate cancer. Long-term exposure to PM2.5 is associated with increased cancer mortality, with specific risks identified for different cancer types. The linear correlation between cancer risk and PM2.5 concentration calls for a re-evaluation of permissible emission levels. The article concludes by proposing specific mitigating strategies for individuals exposed to elevated PM2.5. It suggests antioxidant-rich diets and supplements, and exploring inhalation-based antioxidant administration as potential protective measures.

Interference of two typical polycyclic aromatic hydrocarbons on the induced anti-grazing defense of Tetradesmus obliquus.

Anthropogenic emissions of polycyclic aromatic hydrocarbons (PAHs) cause severe ecological impacts by contaminating natural water bodies, affecting various biological groups, and altering interspecies relationships and ecological functions. This study examined the effects of two typical PAHs, phenanthrene (Phe) and naphthalene (Nap), on the anti-grazing defense mechanisms of Tetradesmus obliquus, a primary producer in freshwater food chains. Four non-lethal concentrations (0.01, 0.1, 1, and 10 mg L-1) of Phe and Nap were tested and the population growth, photosynthetic capacity, pigment content, and morphological defense of T. obliquus were analyzed. The results indicated that Phe and Nap inhibited both the growth rate and formation of defensive colonies of T. obliquus induced by Daphnia grazing cues, and the inhibition ratio increased with concentration. Phe and Nap significantly shortened the defense colony formation time of T. obliquus. Phe and Nap significantly suppressed photosynthesis in the early stages; however, the photosynthetic efficiency recovered over time. These findings highlight the high sensitivity of grazing-induced colony formation in T. obliquus to Phe and Nap at non-lethal concentrations, which could affect the interactions between phytoplankton and zooplankton in aquatic ecosystems. Our study underscores the influence of Phe and Nap on the defense mechanisms of phytoplankton and the consequential effects on ecological interactions within freshwater ecosystems, providing insight into the complex impacts of pollutants on phytoplankton-zooplankton relationships. Therefore, it is necessary to consider interspecific interactions when assessing the potential negative effects of environmental pollutants on aquatic ecosystems.