Polyaromatic hydrocarbons (PAHs), such as pyrene, benzo[a]pyrene, phenanthrene, and anthracene induce toxic, carcinogenic, and mutagenic effects on living organisms and are considered as primary pollutants. Traditional methods for their identification are often laborious and time-consuming and do not account for the heterogeneous nature of their distribution. Here we present confocal microscopy as a rapid and accurate technique for direct analysis of PAHs in soil samples without the complexity of sample pre-processing which might delay results for several days. The method uses the intrinsic fluorescence of PAHs for detection and their emission spectra for the identification of different PAHs. A clear difference was observed in the fluorescence spectral properties of phenanthrene, pyrene and naphthalene in real-time environmental samples. The post-processing of confocal scans obtained in the detection stage of PAHs was completed through the application of ImageJ software. Intrinsic fluorescence-based detections of PAHs may open new avenues in terms of rapid detection and identification of PAHs in heterogeneous complex soil samples.

This review synthesises information from published articles on the incorporation of pollutants by macroinvertebrates from sandy beaches, including both field samplings and bioassays. The hypothesis that macroinvertebrates quantitatively reflect the presence of pollutants in sediment, acting as biomonitors, was tested through a meta-analysis based on studies performed in situ. More than half of the studies were conducted in the Mediterranean. Of the 53 articles based on field samplings, less than half (40%) determined the concentration of pollutants in the sediment as well as in the organisms. Donacidae, Talitridae, and Hippidae were tested as biomonitors, mainly of trace elements. Donacidae and Talitridae reflected in their soft tissues the presence of most trace elements in the sediment, which was not the case with Hippidae. Few studies (≤2 articles) evaluated the response of these macroinvertebrates to persistent organic pollutants, hydrocarbons, or microplastic. A selection based on sampling of sediment and species not yet tested as biomonitors is necessary due to the scarcity of a baseline worldwide and because responses to pollutants may be species-specific.

Toxicological studies have demonstrated the associations between fine particle (PM₂.₅) components and various cytotoxic endpoints. However, few studies have investigated the toxicological effects of source-specific PM₂.₅ at the individual level. To investigate the potential impact of source-specific PM₂.₅ on cytotoxic effects, we performed repeated personal PM₂.₅ monitoring of 48 adult participants in Hong Kong during the winter and summer of 2014–2015. Quartz filters were analyzed for carbonaceous aerosols and water-soluble ions in PM₂.₅. Teflon filters were collected to determine personal PM₂.₅ mass and metal concentrations. The toxicological effects of personal PM₂.₅ exposure—including cytotoxicity, inflammatory response, and reactive oxygen species (ROS) production—were measured using A549 cells in vitro. Personal PM₂.₅ samples collected in winter were more effective than those collected in summer at inducing cytotoxicity and the expression of proinflammation cytokine IL-6. By contrast, summer personal PM₂.₅ samples induced high ROS production. We performed a series of statistical analyses, Spearman correlation and a source apportionment approach with a multiple linear regression (MLR) model, to explore the sources contributing most significantly to personal PM₂.₅ bioreactivity. Secondary inorganic species and transition metals were discovered to be weak-to-moderately associated with cytotoxicity (rₛ: 0.26–0.55; p < 0.01) and inflammatory response (rₛ: 0.26–0.44; p < 0.05), respectively. Carbonaceous aerosols (i.e., organic and elemental carbon; rₛ: 0.23–0.27; p < 0.05) and crustal material (Mg and Ca) was positively associated with ROS generation. The PMF–MLR models revealed that tailpipe exhaust and secondary sulfate contributed to ROS generation, whereas secondary nitrate was the major contributor to PM₂.₅ cytotoxicity and inflammation. These results improve and variate the arguments for practical policies designed to mitigate the risks posed by air pollution sources and to protect public health.

Cadmium (Cd) is a harmful heavy metal that can cause many health problems, while selenium (Se) is an essential nutrient for organisms that can protect them from heavy metal-induced damage. To explore the effects of Se on Cd-induced mitophagy in the liver, forty 3-month-old New Zealand white rabbits (2–2.5 kg), half male and half female, were randomly divided into four groups: the Control group, the Se (0.5 mg/kg body weight (BW)) group, the Cd (1 mg/kg BW) group and the Se+Cd group. After 30 days, the toxicity from Cd in the liver was assessed in terms of the nuclear xenobiotic receptor (NXR) response, oxidative stress and mitophagy. It was found that Cd decreased the activities of CYP450 enzymes and antioxidant enzymes and increased the contents of malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) and also increased the consumption of reduced glutathione (GSH). Moreover, the mRNA levels of NXRs (CAR, PXR, AHR and Nrf2), some mitochondrial function factors (PGC-1α, Sirt1, Sirt3, Nrf1 and TFAM) and mitochondrial fusion factors (Mfn1, Mfn2 and OPA1) were downregulated, but the mRNA levels of other mitochondrial function factors (VDAC1, Cyt C and PRDX3), mitochondrial fission factors (Fis1 and MFF) and those in the PINK1/Parkin-mediated mitophagy pathway (p62, Bnip3 and LC3) were upregulated under Cd exposure. The protein expression levels of Nrf2, SOD2, PGC-1α, PINK1 and Parkin were consistent with the mRNA expression levels in the Cd group. Se alleviated the changes in the abovementioned factors induced by Cd. In conclusion, the results indicate that Cd can cause oxidative stress in rabbit livers by inhibiting NXRs and the antioxidation response leading to mitophagy, and these harmful changes caused by Cd can be alleviated by Se.

Chlorine-based compounds are typical persistent organic pollutants (POPs) that are widely generated in industrial production. This paper reports an effective and rapid pulsed laser irradiation technique for the dechlorination of hexachlorobenzene (HCB), a model pollutant, without additional catalysts or supports. The effects of the laser parameters, including the laser wavelength and power, on the dechlorination efficiency, were also investigated. The optimized results showed that a lower laser wavelength of 266 nm with 10 mJ/pulse power exhibited the highest dechlorination efficiency with 95% within 15 min. In addition, the laser beam effect was examined by designing the direct-pulsed laser single and multipath irradiation system. The results showed that improving the laser beam profile resulted in more than 95% dechlorination efficiency within 5 min. Thus, the dechlorination reaction proceeded much faster as the surface area that the laser beam came in contact with increased due to the multipath system than the single pathway. Gas chromatography identified benzene as the final product of HCB with pentachlorobenzene (PCB), tetrachlorobenzene (TeCB), trichlorobenzene (TCB), dichlorobenzene (DCB), and chlorobenzene (CB) as intermediate products. The mechanism of HCB dechlorination was explained by a comparison of theoretical calculations with the experimental results. The present study reports an advanced technique for the complete dechlorination of chlorobenzenes, which holds great application potential in environmental remediation.

Little is known about the association between ambient temperature and DNA methylation, which is a potential biological process through which ambient temperature affects health. This study aimed to evaluate the association between ambient temperature and DNA methylation across human genome. We included 479 Australian women, including 132 twin pairs and 215 sisters of these twins. Blood-derived DNA methylation was measured using the HumanMethylation450 BeadChip array. Data on average ambient temperature during eight different exposure windows [lag0d (the blood draw day), lag0-7d (the current day and previous seven days prior to blood draw), lag0-14d, lag0-21d, lag0-28d, lag0-90d, lag0-180d, and lag0-365d)] was linked to each participant's home address. For each cytosine-guanine dinucleotide (CpG), we evaluated the association between its methylation level and temperature using generalized estimating equations (GEE), adjusting for important covariates. We used comb-p and DMRcate to identify differentially methylated regions (DMRs). We identified 31 CpGs at which blood DNA methylation were significantly associated with ambient temperature with false discovery rate [FDR] < 0.05. There were 82 significant DMRs identified by both comb-p (Sidak p-value < 0.01) and DMRcate (FDR < 0.01). Most of these CpGs and DMRs only showed association with temperature during one specific exposure window. These CpGs and DMRs were mapped to 85 genes. These related genes have been related to many human chronic diseases or phenotypes (e.g., diabetes, arthritis, breast cancer, depression, asthma, body height) in previous studies. The signals of short-term windows (lag0d and lag0-21d) showed enrichment in biological processes related to cell adhesion. In conclusion, short-, medium-, and long-term exposures to ambient temperature were all associated with blood DNA methylation, but the target genomic loci varied by exposure window. These differential methylation signals may serve as potential biomarkers to understand the health impacts of temperature.

Incubation under controlled laboratory conditions were performed to assess the toxic effects of two plastic derived chemicals, bisphenol A (BPA) and di-(2-ethylhexyl) phthalate (DEHP), on the growth, photosynthetic efficiency and photosynthetic activity of the cosmopolitan diatom Chaetoceros decipiens-lorenzianus. Non-axenic diatom cells were exposed to concentrations of BPA and DEHP (separately and in mixture), mimicking concentrations observed in contaminated marine ecosystems, for seven days. Upon short-term exposure (i.e., during the first 48 h), BPA and DEHP induced a slight but significant stimulation of biomass and photosynthetic activity relative to the control, whereas, no significant impact was observed on the photosynthetic efficiency. Nevertheless, this pattern was transient. The stimulation was followed by a return to control conditions for all treatments at the end of incubation. These results showed that the cosmopolitan diatom Chaetoceros was not impacted by representative in situ concentrations of plastic derivatives, thus confirming its ability to thrive in coastal anthropogenic environments.

Bisphenol A (BPA) is a classical chemical contaminant in food, and the mode of action (MOA) of BPA remains unclear, constraining the progress of risk assessment. This study aims to assess the potential MOAs of BPA regarding reproductive/developmental toxicity, neurological toxicity, and proliferative effects on the mammary gland and the prostate potentially related to carcinogenesis by using the Comparative Toxicogenomics Database (CTD)-based bioinformatics analysis and the quantitative weight of evidence (QWOE) approach on the basis of the principles of Toxicity Testing in the 21st Century. The CTD-based bioinformatics analysis results showed that estrogen receptor 1, estrogen receptor 2, mitogen-activated protein kinase (MAPK) 1, MAPK3, BCL2 apoptosis regulator, caspase 3, BAX, androgen receptor, and AKT serine/threonine kinase 1 could be the common target genes, and the apoptotic process, cell proliferation, testosterone biosynthetic process, and estrogen biosynthetic process might be the shared phenotypes for different target organs. In addition, the KEGG pathways of the BPA-induced action might involve the estrogen signaling pathway and pathways in cancer. After the QWOE evaluation, two potential estrogen receptor-related MOAs of BPA-induced testis dysfunction and learning-memory deficit were proposed. However, the confidence and the human relevance of the two MOAs were moderate, prompting studies to improve the MOA-based risk assessment of BPA.

Microplastics (MPs; <5 mm) released into freshwaters from anthropogenic sources accumulate in sediments, where they may pose an environmental threat to benthic organisms, such as nematodes. Several studies have examined the effects of nano- and microplastics on the nematode Caenorhabditis elegans, whereas reduced food availability was suggested as a possible explanation for the observed inhibitory effects. Therefore, this study should clarify whether micro-beads of different sizes (1.0 and 6.0 μm in diameter) and materials (polystyrene PS, silica) are able to interfere with the feeding of C. elegans on its bacterial diet (Escherichia coli), and, by this, lowering its consumption rate within 7 h of exposure. Moreover, it was examined whether an inhibited bacterial consumption was caused by a reduction of the nematode’s pumping rate, as a primary indicator of food ingestion. Bacterial consumption by C. elegans was significantly decreased in the presence of 1.0- and 6.0-μm PS beads (49–67% lower bacterial consumption compared to control), whereas in the presence of 1.0-μm silica beads feeding was not impeded. Interestingly, the pumping rate was significantly lower in the presence of non-ingestible 6.0-μm PS beads with 161 ± 16 pumps min⁻¹, while it was largely unchanged for nematodes exposed to ingestible 1.0-μm PS beads with 205 ± 12 pumps min⁻¹, compared to control conditions with 210 ± 18 pumps min⁻¹, respectively. As reduced bacterial consumption leads to generally lower energy reserves in C. elegans, these results allow to link observed inhibitory effects of MPs on the nematodes to a lower food availability. Such indirect, food-web related, effects of MPs should raise concern of ecological consequences in natural habitats, where temporal food deficiencies can occur. Consequently, disturbances in food availability and feeding efficiency should be regarded as important parameters in environmental risk assessments focusing on MPs.

Contamination of waters and soils with microplastics (MPs) is an emerging environmental issue worldwide. MPs constitute a cocktail of various additives and polymers besides adsorbing toxic heavy metals from the environment. This co-occurrence of MPs with heavy metals poses a threat to the health of organisms and is poorly understood. Ingestion of MPs contaminated with heavy metals may also result in subsequent transfer of heavy metals up in the food chain. MPs surfaces play a crucial role in the adsorption of heavy metals. Aged/biofouled MPs facilitate greater adsorption of metals and certain microplastic (MP) polymers adsorb some metals more specifically. External factors involved in the process of adsorption/accumulation of heavy metals are the solution pH, salinity, and the concentration of relevant heavy metals in the media. Desorption greatly depends upon pH of the external solution. This is more concerning as the guts/digestive systems of organisms have low pH which could enhance the desorption of toxic metals and making them accumulate in their bodies. The aim of this article is to discuss the abundance, distribution, adsorption, and desorption behavior of MPs for heavy metals, and their combined toxic effects on flora and fauna based on the limited research on this topic in the literature. There is an overarching need to understand the interactions of MPs with heavy metals in different ecosystems so that the extent of ecotoxic effects they pose could be assessed which would help in the environmental regulation of these pollutants.