Polybrominated diphenyl ethers (PBDEs) are listed as persistent organic pollutants (POPs) in the Stockholm Convention. It has been established that PBDEs may be released into the environment during improper handling and disposal of e-waste and other products containing PBDEs that is prevalent in developing countries. This research work assessed the status of PBDE contamination at dumpsites in Nigeria. Soil and edible plant samples were collected from the dumpsites and control sites for analysis. The concentrations of ∑₇PBDE in the topsoils around the dumpsites at 0–15 cm depth ranged from 112 to 366 ng/g dry weight (dw) while that of the topsoil of the control site 500 m from the dumpsite ranged from 26.8 to 39.7 ng/g dw. These high concentrations stem likely from open burning of waste including electronic waste on the landfills. Plant samples (bentgrass, spinach, tomatoes, pumpkin and sweet potatoes) around the dumpsites were found to be contaminated by PBDEs with levels ranging from 25.0 to 60.5 ng/g dw in plant roots and from 8.45 to 32.2 ng/g dw in plant shoots for ∑₇PBDE. This suggests that consumption of vegetables by humans and ingestion of contaminated soils and feed by chickens and cows can transfer PBDEs into the human food chain around the dumpsites. The comparison of PBDE levels in soils and the PBDE levels in chicken eggs from the former study indicate that PBDE levels in the soils are sufficient to explain the levels in the chicken eggs with a reasonable carry-over rate for PBDEs of 0.28 on average. The PBDE contamination in the soil was sufficient to result in a relevant exposure of humans via accumulation in eggs. The study shows that a better management of end-of-life products containing PBDEs is needed to reduce PBDE exposure risk in Africa.

We investigated the tissue distribution, trophic transfer, and ecological risk of 13 trace elements in 26 East Asian finless porpoises (Neophocaena asiaeorientalis sunameri), an endangered species found in the Liaodong Bay and the north Yellow Sea. All the investigated trace elements were detected in the tissue and food web of the East Asian finless porpoises. The concentrations of the potentially toxic elements were 2.37 × 10⁻⁵ – 754 mg kg⁻¹ dry weight (dw) in stranded porpoises and 0.01–159 mg kg⁻¹ dw in their food web. Tissue-specific distribution of the trace elements generally ranked as: liver > kidney > heart > lung > muscle. Zn was the dominant contaminant in the five investigated tissues. Significant positive correlations were found between body length or age and some trace elements, especially Cd. Adults (≥2 years old) presented higher concentrations of most of the trace elements than juveniles (<2 years old). Sex-dependent distribution of the trace elements was insignificant except for Mn, Ni, and Zn in muscle and renal tissue. As, Cu, Mn, Ni, Pb, and V biodiluted across the East Asian finless porpoise food web while Zn biomagnified. However, Hg, Cd, Co, Cr, Se, and Sn did not exhibit apparent trophic transfer trends. Overall, ecological risk assessment of trace elements in East Asian finless porpoises suggested that greater attention should be given to Hg, As, Cd, and Se.

Individuals with metabolic disorders exhibit enhanced susceptibility to the cardiovascular health effects of particulate air pollution, but the underlying mechanisms are not yet understood. We aim to assess whether changes in proinflammatory lipid signals are associated with fine particulate matter (PM₂.₅) exposure in individuals with and without prediabetes. A longitudinal panel study was conducted in Beijing, China, and included 120 participants followed up over 589 clinical visits from August 2013 to February 2015. We measured 12 lipids derived from arachidonic acid pathways in blood samples of the participants via targeted lipidomic analyses. Ambient PM₂.₅ concentrations were continuously monitored at a station for associations with the lipids. Among the 120 participants, 110 (mean [SD] age at recruitment, 56.5 [4.2] years; 31 prediabetics) who visited the clinic at least twice over the follow-up period were assigned exposure values of the outdoor residential PM₂.₅ concentrations during the 1–14 days preceding each clinical visit. With an interquartile range increase in the 1-day-lag PM₂.₅ exposure (64.0 μg/m³), the prediabetic group had consistently greater increases in the concentration of arachidonate metabolites derived from the cytochrome P450 (CYP450) pathway (5,6-DHET, 15.8% [95% CI, 3.5–29.7%]; 8,9-DHET, 9.7% [95% CI, 0.6–19.6%]; 11,12-DHET, 8.3% [95% CI, 1.9–15.1%]; 14,15-DHET, 7.4% [95% CI, 0.9–14.4%]; and 20-HETE, 8.9% [95% CI, 1.0–17.5%]), compared with the healthy group. Among CYP450-derived lipids, 14,15-DHET and 20-HETE significantly mediated 8% and 8% of the PM₂.₅-associated increase in white blood cells, 10% and 13% of that in neutrophils, and 20% and 23% of that in monocytes, respectively, in the prediabetic group. In conclusion, proinflammatory lipid signals from CYP450 pathways triggered the health effects of particulate air pollution in individuals with prediabetes, suggesting that targeting lipid metabolism has therapeutic potential to attenuate or prevent the cardiovascular effects of air pollution in susceptible populations.

The interrelationships among long-term ambient air pollution exposure, emotional distress and cognitive decline in older adulthood remain unclear. Long-term exposure may impact cognitive performance and subsequently impact emotional health. Conversely, exposure may initially be associated with emotional distress followed by declines in cognitive performance. Here we tested the inter-relationship between global cognitive ability, emotional distress, and exposure to PM₂.₅ (particulate matter with aerodynamic diameter <2.5 μm) and NO₂ (nitrogen dioxide) in 6118 older women (aged 70.6 ± 3.8 years) from the Women’s Health Initiative Memory Study. Annual exposure to PM₂.₅ (interquartile range [IQR] = 3.37 μg/m³) and NO₂ (IQR = 9.00 ppb) was estimated at the participant’s residence using regionalized national universal kriging models and averaged over the 3-year period before the baseline assessment. Using structural equation mediation models, a latent factor capturing emotional distress was constructed using item-level data from the 6-item Center for Epidemiological Studies Depression Scale and the Short Form Health Survey Emotional Well-Being scale at baseline and one-year follow-up. Trajectories of global cognitive performance, assessed by the Modified-Mini Mental State Examination (3MS) annually up to 12 years, were estimated. All effects reported were adjusted for important confounders. Increases in PM₂.₅ (β = -0.144 per IQR; 95% CI = −0.261; −0.028) and NO₂ (β = −0.157 per IQR; 95% CI = −0.291; −0.022) were associated with lower initial 3MS performance. Lower 3MS performance was associated with increased emotional distress (β = −0.008; 95% CI = −0.015; −0.002) over the subsequent year. Significant indirect effect of both exposures on increases in emotional distress mediated by exposure effects on worse global cognitive performance were present. No statistically significant indirect associations were found between exposures and 3MS trajectories putatively mediated by baseline emotional distress. Our study findings support cognitive aging processes as a mediator of the association between PM₂.₅ and NO₂ exposure and emotional distress in later-life.

This study aims to investigate the adsorption behavior of cationic and anionic dyes of methylene blue (MB) and Congo red (CR) onto wet-torrefied Chlorella sp. microalgal biochar respectively, as an approach to generate a waste-derived and low-cost adsorbent. The wet-torrefied microalgal biochar possessed microporous properties with pore diameter less than 2 nm. The optimum adsorbent dosage of wet-torrefied microalgal biochar for MB and CR dyes removal were determined at 1 g/L and 2 g/L, respectively, with their natural pHs as the optimum adsorption pHs. The determined equilibrium contact times for MB and CR were 120 h and 4 h, respectively. Based on the equilibrium modeling, the results revealed that Langmuir isotherm showed the best model fit, based on the highest R² coefficient, for both the adsorption processes of MB and CR using the wet-torrefied microalgal biochar, indicating that the monolayer adsorption was the dominant process. From the modeling, the maximum adsorption capacities for MB and CR were 113.00 mg/g and 164.35 mg/g, respectively. The kinetic modeling indicated the adsorption rate and mechanism of the dyes adsorption processes, which could be crucial for future modeling and application of wet-torrefied microalgal biochar. From the results, it suggests that the valorization of microalgae by utilizing wet-torrefied microalgal biochar as the effective adsorbent for the removal of toxic dyes with an approach of microalgal biorefinery and value-added application to the environment is feasible.

Microplastic pollution has become ubiquitous, affecting a wide variety of biota. Although microplastics are known to alter the development of a range of marine invertebrates, no studies provide a detailed morphological characterisation of the developmental defects. Likewise, the developmental toxicity of chemicals leached from plastic particles is understudied. The consequences of these developmental effects are likely underestimated, and the effects on ecosystems are unknown. Using the sea urchin Paracentrotus lividus as a model, we studied the effects of leachates of three forms of plastic pellet: new industrial pre-production plastic nurdles, beached pre-production nurdles, and floating filters, known as biobeads, also retrieved from the environment. Our chemical analyses show that leachates from beached pellets (biobead and nurdle pellets) and highly plasticised industrial pellets (PVC) contain polycyclic aromatic hydrocarbons and polychlorinated biphenyls, which are known to be detrimental to development and other life stages of animals. We also demonstrate that these microplastic leachates elicit severe, consistent and treatment-specific developmental abnormalities in P. lividus at embryonic and larval stages. Those embryos exposed to virgin polyethylene leachates with no additives nor environmental contaminants developed normally, suggesting that the abnormalities observed are the result of exposure to either environmentally adsorbed contaminants or pre-existing industrial additives within the polymer matrix. In the light of the chemical contents of the leachates and other characteristics of the plastic particles used, we discuss the phenotypes observed during our study, which include abnormal gastrulation, impaired skeletogenesis, abnormal neurogenesis, redistribution of pigmented cells and embryo radialisation.

The Yangtze River Delta (YRD) is one of the fastest developing areas in eastern China and contains many chemical industry parks. The profiles and sources of polycyclic aromatic hydrocarbons (PAHs) in soil in chemical industry parks and surrounding areas in the YRD were investigated by analyzing soil samples (n = 64) were collected in the YRD and Rudong chemical park (RD), a typical chemical park in the Yangtze River Delta. The total concentrations of 19 PAHs in the YRD soil samples were 16.3–4694 ng g⁻¹ (mean 688 ng g⁻¹), and the total concentrations of PAHs in RD were 21.6–246 ng g⁻¹ (mean 75.4 ng g⁻¹). The PAHs in soil in YRD were dominated by four-ring and five-ring PAHs, and the PAHs in RD were dominated by two-ring and three-ring PAHs. It suggested that PAHs may have been supplied to soil in YRD predominantly through coal combustion and vehicle emissions, PAHs in the soil of RD may be due to the volatilization and leakage of chemical raw material. According to the different distribution characteristics of PAHs, the ratio (1.5) of (2 + 3) rings/4 rings was proposed to identify the chemical source of PAHs. The PAH isomer ratios and principal component analysis/multiple linear regression (PCA/MLRA) results indicated that PAHs concentrations in soil in the YRD and RD are mainly supplied by industrial and traffic emissions. Incremental lifetime cancer risks (ILCRs) indicated that PAHs in soil pose negligible cancer risks to children and adults, but much stronger risks to children than adults.

Nitrated aromatic compounds, the ubiquitous nitrogen-containing organic pollutants, impact the environment and organisms adversely. As industrial raw materials and intermediates, nitrated aromatic compounds and their aromatic precursors are widely employed in the industrial production activities. Nevertheless, their emission from industrial waste gases has so far not been studied extensively. In this study, the concentrations of 12 nitrated aromatic compounds in the particle and gas phases downwind of 16 factories encompassing eight industries (i.e., pharmaceutical, weaving and dyeing, herbicide, explosive, painting, phenolic resin, paper pulp and polystyrene foam industries), were determined by ultra-high-performance liquid chromatography-mass spectrometry. Their concentrations in the particle and gas phases from different factories ranged from 114.7 ± 63.5 to 296.6 ± 62.5 ng m⁻³ and 148.7 ± 7.4 to 309.8 ± 26.2 ng m⁻³, respectively, thus, exhibiting significantly high concentrations as compared to the background sites. Among the 12 detected species, 4-nitrophenol, 5-nitrosalicylic acid, 3-nitrosalicylic acid and 4-methyl-2,6-dinitrophenol were observed to be the predominant species, with total fractions up to 47.9–72.3% and 63.1–70.3% in the particle and gas phases, respectively. Their emission profiles with respect to the industrial activities exhibited large discrepancies as compared to the combustion sources, thus, indicating different formation mechanisms. The emission ratios of particulate nitrated aromatic compounds owing to the industrial activities were estimated between 0.5 ± 0.2 and 4.3 ± 1.5 ng μg⁻¹, which were higher than or comparable to those from various combustion sources. The findings from this study confirm the industrial emission to be an important source of nitrated aromatic compounds in the atmosphere. The substantial emissions of nitrated aromatic compounds from various industries reported in this study provide the fundamental basis for further emission estimation and pollution control.

1-Nitropyrene (1-NP) is one component of atmospheric fine particles. Previous report revealed that acute 1-NP exposure induced respiratory inflammation. This study aimed to investigate whether chronic 1-NP exposure induces pulmonary fibrosis. Male C57BL6/J mice were intratracheally instilled to 1-NP (20 μg/mouse/week) for 6 weeks. Diffuse interstitial inflammation, a-smooth muscle actin (a-SMA)-positive cells, a marker of epithelial-mesenchymal transition (EMT), and an extensive collagen deposition, measured by Masson staining, were observed in 1-NP-exposed mouse lungs. Pulmonary function showed that lung dynamic compliance (Cydn-min) was reduced in 1-NP-exposed mice. Conversely, inspiratory resistance (Ri) and expiratory resistance (Re) were elevated in 1-NP-exposed mice. Mechanistically, cell migration and invasion were accelerated in 1-NP-exposed pulmonary epithelial cells. In addition, E-cadherin, an epithelial marker, was downregulated, and vimentin, a-SMA and N-cadherin, three mesenchymal markers, were upregulated in 1-NP-exposed pulmonary epithelial cells. Although TGF-β wasn’t altered, phosphorylated Smad2/3 were enhanced in 1-NP-exposed pulmonary epithelial cells. Moreover, reactive oxygen species (ROS) were increased and endoplasmic reticulum (ER) stress was activated in 1-NP-exposed pulmonary epithelial cells. N-Acetylcysteine (NAC), an antioxidant, attenuated 1-NP-evoked excess ROS, ER stress and EMT in pulmonary epithelial cells. Similarly, pretreatment with NAC alleviated 1-NP-caused pulmonary EMT and lung fibrosis in mice. These results demonstrate that ROS-evoked ER stress contributes, at least partially, to 1-NP-induced EMT and pulmonary fibrosis.

The thyroperoxidase (TPO) enzyme is expressed by the thyroid follicular cells and is required for thyroid hormone synthesis. In turn, thyroid hormones are essential for brain development, thus inhibition of TPO in early life can have life-long consequences for brain function. If environmental chemicals with the capacity to inhibit TPO in vitro can also alter brain development in vivo through thyroid hormone dependent mechanisms, however, remains unknown. In this study we show that the in vitro TPO inhibiting pesticide amitrole alters neuronal migration and induces periventricular heterotopia; a thyroid hormone dependent brain malformation. Perinatal exposure to amitrole reduced pup serum thyroxine (T4) concentrations to less than 50% of control animals and this insufficiency led to heterotopia formation in the 16-day old pup’s brain. Two other in vitro TPO inhibitors, 2-mercaptobenzimidazole and cyanamide, caused reproductive toxicity and had only minor sporadic effects on the thyroid hormone system; consequently, they did not cause heterotopia. This is the first demonstration of an environmental chemical causing heterotopia, a brain malformation until now only reported for rodent studies with the anti-thyroid drugs propylthiouracil and methimazole. Our results highlight that certain TPO-inhibiting environmental chemicals can alter brain development through thyroid hormone dependent mechanisms. Improved understanding of the effects on the brain as well as the conditions under which chemicals can perturb brain development will be key to protect human health.