Mercury (Hg) and methylmercury (CH3Hg) bind strongly to micro and nano (NP) particles and this partitioning impacts their fate and bioaccumulation into food webs, and, as a result, potential human exposure. This partitioning has been shown to influence the bioavailability of inorganic Hg to methylating bacteria, with NP-bound Hg being more bioavailable than particulate HgS, or organic particulate-bound Hg. In this study we set out to investigate whether the potential interactions between dissolved ionic Hg (HgII) and CH3Hg and NPs was due to incorporation of Hg into the core of the cadmium selenide and sulfide (CdSe; CdS) nanoparticles (metal exchange or surface precipitation), or due purely to surface interactions. The interaction was assessed based on the quenching of the fluorescence intensity and lifetime observed during HgII or CH3Hg titration experiments of these NP solutions. Additional analysis using inductively coupled plasma mass spectrometry of CdSe NPs and the separated solution, obtained after HgII additions, showed that there was no metal exchange, and X-ray photoelectron spectroscopy confirmed this and further indicated that the Hg was bound to cysteine, the NP capping agent. Our study suggests that Hg and CH3Hg adsorbed to the surfaces of NPs would have different bioavailability for release into water or to (de)methylating organisms or for bioaccumulation, and provides insights into the behavior of Hg in the environment in the presence of natural or manufactured NPs.

Particulate matter (PM) is considered an atmospheric pollutant that mostly affects human health. The finest fractions of PM (PM2.5 or less) play a major role in causing chronic diseases.The aim of this study was to investigate the genotoxic effects of PM0.5 collected in five Italian towns using different bioassays. The role of chemical composition on the genotoxicity induced was also evaluated.The present study was included in the multicentre MAPEC_LIFE project, which aimed to evaluate the associations between air pollution exposure and early biological effects in Italian children.PM10 samples were collected in 2 seasons (winter and spring) using a high-volume multistage cascade impactor. The results showed that PM0.5 represents a very high proportion of PM10 (range 10–63%). PM0.5 organic extracts were chemically analysed (PAHs, nitro-PAHs) and tested by the comet assay (A549 and BEAS-2B cells), MN test (A549 cells) and Ames test on Salmonella strains (TA100, TA98, TA98NR and YG1021).The highest concentrations of PAHs and nitro-PAHs in PM0.5 were observed in the Torino, Brescia and Pisa samples in winter. The Ames test showed low mutagenic activity. The highest net revertants/m3 were observed in the Torino and Brescia samples (winter), and the mutagenic effect was associated with PM0.5 (p < 0.01), PAH and nitro-PAH (p < 0.05) concentrations. The YG1021 strain showed the highest sensitivity to PM0.5 samples. No genotoxic effect of PM0.5 extracts was observed using A549 cells except for some samples in winter (comet assay), while BEAS-2B cells showed light DNA damage in the Torino, Brescia and Pisa samples in winter, highlighting the higher sensitivity of BEAS-2B cells, which was consistent with the Ames test (p < 0.01).The results obtained showed that it is important to further investigate the finest fractions of PM, which represent a relevant percentage of PM10, taking into account the chemical composition and the biological effects induced.

PM2.5 is becoming a worldwide environmental problem, which profoundly endangers public health, thus progressively capturing public attention this decade. As a fragile target of PM2.5, the underlying mechanisms of endothelial cell damage are still obscure. According to the previous microarray data and signaling pathway analysis, a new form of cell death termed ferroptosis in the current study is proposed following PM2.5 exposure. In order to verify the vital role of ferroptosis in PM2.5-induced endothelial lesion and further understand the potential mechanism involved, intracellular iron content, ROS release and lipid peroxidation, as well as biomarkers of ferroptosis were detected, respectively. As a result, uptake of particles increases cellular iron content and ROS production. Meanwhile, GSH depletion, and the decrease of GSH-Px and NADPH play significant roles in PM2.5-induced endothelial cell ferroptosis. Moreover, significantly changed expression of TFRC, FTL and FTH1 hinted that dysfunction of iron uptake and storage is a major inducer of ferroptosis. Importantly, index monitored above can be partially rescued by lipid peroxidation inhibitor ferrostatin-1 and iron chelator deferoxamine mesylate, which mediated antiferroptosis activity mainly depends on the restoration of antioxidant activity and iron metabolism. In conclusion, our data basically show that PM2.5 enhances ferroptosis sensitivity with increased ferroptotic events in endothelial cells, in which iron overload, lipid peroxidation and redox imbalance act pivotal roles.

We investigated the profiles and levels of perfluoroalkyl carboxylic acid (PFCA) contamination in Pacific cod (Gadus macrocephalus) from the North Pacific Ocean. The mean concentrations of PFCAs containing 8 to 14 carbon atoms (C8–C14) in edible Pacific cod muscle ranged from 216 to 670 pg g⁻¹ wet weight in the Northeast Pacific Ocean (Seattle, Vancouver, Alaska, and Russia), from 819 to 1710 pg g⁻¹ wet weight in Japanese coastal waters (Hokkaido, Aomori, Iwate, Miyagi, Tottori, and Shimane), and from 288 to 892 pg g⁻¹ wet weight in Korean waters (Sokcho, Busan, and Yeosu). These results indicate there are geographical differences in the distribution of PFCAs. The long-chain PFCAs (C9–C14) contributed 96% of the total PFCA concentration across Japan, whereas they contributed only 33% of the total PFCA concentration in the USA and Canada. Long-chain PFCA concentrations in cod samples collected in Japanese and Korean waters were about three to four times those in samples from the USA, Canada, and Russia. Because seafood is considered an important dietary source of PFCAs, high concentrations of long-chain PFCAs in Pacific cod from Japanese and Korean waters may affect human dietary exposure and blood concentrations of long-chain PFCAs.

Crude oil and its constituents can have adverse effects on ecological and human health when released into the environment. The Canadian Council of Ministers of the Environment (CCME) has developed remedial guidelines and a risk assessment framework for both ecological and human exposure to PHC. One of the assumptions used in the derivation of these guidelines is that plants are unable to take up PHC from contaminated soil and therefore subsequent exposure at higher trophic levels is not a concern. However, various studies suggest that plants are indeed able to take up PHC into their tissues. Consumption of plants is a potential exposure pathway in both ecological (e.g., herbivorous and omnivorous birds, and mammals) and human health risk assessments. If plants can uptake PHC, then the current approach for risk assessment of PHC may underestimate exposures to ecological and human receptors. The present review aims to assess whether or not plants are capable of PHC uptake and accumulation. Twenty-one articles were deemed relevant to the study objective and form the basis of this review. Of the 21 primary research articles, 19 reported detectable PHC and/or its constituents in plant tissues. All but five of the 21 articles were published after the publication of the CCME Canada-Wide Standards. Overall, the present literature review provides some evidence of uptake of PHC and its constituents into plant tissues. Various plant species, including some edible plants, were shown to take up PHC from contaminated soil and aqueous media in both laboratory and field studies. Based on the findings of this review, it is recommended that the soil-plant-wildlife/human pathway should be considered in risk assessments to avoid underestimating exposure and subsequent toxicological risks to humans and wildlife.

Densely populated cities with a compact urban built environment have concerns over health risks derived from high levels of airborne particulate matter (PM) exposure. Understanding the association between PM and reactive oxygen species (ROS) is an important step towards unravelling the mechanisms behind. This study investigated the role of time-integrated PM sampling on cellular toxicity mechanism on a diurnal scale. The sampling took place in a highly urbanized part of Hong Kong at two contrast roadside and background sites, with simultaneous solid-PM and semi-volatile-PM (SV-PM) collection in both summer and winter seasons. A sampling day consisted three sampling intervals of 6 h each – 04:00–10:00, 12:00–18:00 and 20:00–02:00 h, representing morning rush hours, afternoon and night periods, respectively. Water and organic extracts of PM were prepared, with and without filtration, and exposed to RAW264.7 and A549 cell lines on a dose and time-dependent manner. Solid-PM and SV-PM contribution to total PM₂.₅ mass concentration was 9:1, with much higher SV-PM fraction at roadside over urban background (p < 0.001, n = 36). Also, the SV-PM mass concentration increased by 10–20% during 20:00–02:00 h compared to morning and afternoon sampling periods. Organic PM extract was observed to cause 23–29% higher cell death compared to water-soluble PM, which is complemented with increased ROS production in both cell lines. The cellular damage caused by oxidative stress, determined from increased HO-1 and TNF-α expression in RAW264.7 was higher compared to the A549, which demonstrated the greater induction of toxicity from organic PM extract over soluble PM. Similarly, the SV-PM induced greater than 2-fold cellular ROS generation on PM mass basis compared to solid-PM. Lack of phagocytic action in A549 compared to RAW264.7 suggested novel toxicity routes for water-soluble and organic PM that can be expected to occur during human PM inhalation-bronchi-alveolar exposure.

Perfluoroalkyl substances (PFASs) are a family of synthetic, fluorinated organic compounds. They have been widely used in industrial applications and consumer products and widespread in the environment, wildlife and human. Experimental and epidemiologic evidence suggested that PFASs are capable of interfering with endocrine processes and have potential reproductive and developmental toxicities. Polycystic ovarian syndrome (PCOS), one of the main reasons of female infertility, is a common endocrine disorder in reproductive age women. We performed a case-control study to evaluate associations between PCOS-related infertility and PFASs concentrations in plasma. A total of 180 infertile PCOS-cases and 187 healthy controls were recruited from the Center for Reproductive Medicine of Shandong University. Blood specimens were collected at enrollment and analyzed for ten PFASs using liquid chromatography-tandem mass spectrometry. Multivariable logistic regression procedure was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for each PFAS. Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) were the dominant PFASs in the plasma of participants, with the median concentration of 5.07 ng/mL and 4.05 ng/mL, respectively. The median levels of individual PFAS were not significantly different between PCOS-cases and controls. While adjusted for the potential confounders (age, BMI, household income, education level, employment status, age at menarche, menstrual volume), the plasma concentration of perfluorododecanoic acid (PFDoA), a 12 carbons lengths of perfluorocarboxylic acids, was associated with a significantly increased risk of PCOS-related infertility (medium vs low tertile: OR = 2.36, 95% CI: 1.12, 4.99, P = 0.02; high vs low tertile: OR = 3.04, 95% CI: 1.19, 7.67, P = 0.02), with the P trend 0.01. No significant relationship was observed between PCOS-related infertility and other PFAS analytes in the adjusted model, despite perfluoroundecanoic acid showed a negative association (P trend 0.03). The potential reproductive health effects of PFASs and the underlying mechanisms merit further investigation in the future.

In the study, the effects of dimethyl phthalate (DMP) on the antioxidant defense capacity and immune functions of human erythrocytes were experimentally explored. DMP affected the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) and the contents of glutathione (GSH) and malondialdehyde (MDA) in erythrocytes, thus impairing the function of antioxidant defense system of erythrocytes. When DMP concentration increased from 0 to 28 μmol L⁻¹, the SOD and GPX activities were increased firstly and then gradually decreased. When DMP concentration was below 20 μmol L⁻¹, the relative activity of SOD was enhanced by DMP and the effect was known as hormesis. The relative activity of GPX was also increased when the concentration of DMP was below 12 μmol L⁻¹. The CAT activity was more significantly inhibited by DMP than the activities of SOD and GPX, whereas the relative GSH content was increased by DMP. MDA levels were significantly changed after the exposure to DMP (0–24 μmol L⁻¹). The experimental results of the activity of SOD and CAT, and the content of MDA also suggested that DMP could inhibit the immune functions of red blood cells (RBCs), which were further proved by the decrease of two indicators (RBC-C₃b and RBC-IC) due to the destruction of C₃b receptor with immune adherence function on erythrocyte membrane. The study provides a deep understanding of the toxicity of DMP on erythrocytes.

Fish-associated antibiotic resistance genes (ARGs) have attracted increasing attention due to their potential risks to human beings via the food chain. However, data are scarce regarding the antibiotic resistance in fish themselves. Herein, the antibiotic resistance genes (ARGs) were assessed in the gut of four major Chinese freshwater carp (i.e., silver carp, grass carp, bighead carp, and crucian carp) from food retail markets. Results show that the abundances of target ARGs (e.g., tetA, tetO, tetQ, tetW, sulI, sulII, and blaTEM₋₁) and class 1 integrase (intI1) were in the range 9.4 × 10⁻⁶ - 1.6 × 10⁻¹ and 6.7 × 10⁻⁵ - 5.2 × 10⁻² gene copies per 16S rRNA gene, respectively. The sulI, sulII, and tetQ strongly correlated with silver and mercury resistance genes (e.g., silE and merR). The microbial taxa of fish gut could be partly separated among retail markets based on the PCA analysis. About 15.0% of the OTUs in fish gut were shared and 74.5% of the shared OTUs were identified as Acidobacteria, Bacteroidetes, Chloroflexi, Cyanobacteria, Firmicutes, and Proteobacteria. These phyla may constitute the core microbiota in the guts of the four Chinese freshwater carp. The possible ARG hosts were revealed based on the network analysis, and the presence of pathogen-associated resistant genera in fish gut highlights the need to fully understand their potential human health risks.

Parabens, broad-spectrum antimicrobial preservatives widely used in various consumer products and food, are suspected to be linked with several adverse health effects in humans, especially newborn babies, infants, and young children. While human exposure to parabens has been frequently reported by measuring the concentration of parabens in urine, similar measurements in breast milk have rarely been made. To determine paraben concentrations in breast milk and possible sources of exposure, four major parabens, including methylparaben (MP), ethylparaben (EP), propylparaben (PP), and butylparaben (BP) were measured in breast milk samples collected from 260 lactating women in South Korea. Demographic, socioeconomic, and behavioral factors associated with the presence of parabens in breast milk were determined. EP concentrations were detected at the highest levels in breast milk samples, followed by MP, PP, and BP. Pre-pregnancy BMI, parity, use of basic skin care products, use of cosmetics, canned beverage, and type of milk consumption were associated with higher frequencies of paraben detection. In addition, type of milk, parity, and drinking status were significantly associated with the concentration of EP. Multiple regression analyses showed that colostrum and transitional milk samples had higher levels of EP than mature milk samples. The estimated daily intake of parabens in infants via breastfeeding appears to be negligible when compared to the acceptable daily intake values set forth by the European Food Safety Authority (EFSA); however, considering the vulnerability of breastfed infants and ubiquitous sources of exposure from daily use of household and personal toiletries, efforts to identify sources and mitigate exposure are warranted.