Plastic ingestion has been widely investigated to understand its adverse harms on fauna, but the role of fauna itself in plastic fragmentation has been rarely addressed. Here, we review and discuss the available experimental results on the role of terrestrial and aquatic macrofauna in plastic biofragmentation and degradation. Recent studies have shown how biting, chewing, and stomach contractions of organisms shatter ingested plastic along their digestive tracts. Gut microbial communities can play a role in biodegradation and their composition can shift according to the type of plastic ingested. Shifts in molecular weights, chemical bond forming and breaking, and changes in thermal modification detected in the plastic debris present in the faeces also suggest active biodegradation. A few studies have also shown interactions other than ingestion, such as burrowing, may actively or passively promote physical plastic fragmentation by fauna. We suggest that further investigations into the role of fauna in physical fragmentation and chemical degradation linked to active ingestion and gut associated microbiota metabolism, respectively, should be conducted to better evaluate the impact of these mechanisms on the release of micro- and nano-plastic in the environment. Knowledge on macrofauna other than marine invertebrates and terrestrial soil dwelling invertebrates is particularly lacking, as well as focus on broader types of plastic polymers.

Bisphenol A diglycidyl ether (BADGE), bisphenol F diglycidyl ether (BFDGE), and their derivatives are frequently used in food packaging materials. Some toxicological studies have shown that the endocrine-disrupting activities of these compounds are similar to or higher than those of bisphenol A (BPA), which may also adversely affect the growth and development of children and adolescents. Here, we investigated nine bisphenol-diglycidyl ethers (BDGEs) in 181 paired urine and serum samples from children and adolescents from Beijing to determine their partitioning, clearance and exposure levels. The results showed that nine BDGEs were detected in 181 urine and serum samples from children and adolescents from Beijing. Bisphenol A bis(2,3-dihydroxypropyl) glycidyl ether (BADGE·2H₂O) was the primary pollutant. The daily intake of ∑BDGEs was 15.217 ng/kg bw/day among children and adolescents in Beijing. The ranking of BDGEs in terms of renal clearance rate (CLᵣₑₙₐₗ) in this study population was BADGE > BADGE·2H₂O > BFDGE > bisphenol F bis(3-chloro-2-hydroxypropyl) glycidyl ether (BFDGE·2HCl) > bisphenol A (3-chloro-2-hydroxypropyl) (2,3-dihydroxypropyl) glycidyl ether (BADGE·HCl·H₂O). In addition, the serum and urine ratios (S/U ratios) of BFDGE·2HCl, BADGE·2H₂O, BFDGE, BADGE, and BADGE·HCl·H₂O were higher than 1, indicating that these contaminants have a higher enrichment capacity in human blood. To our knowledge, this is the first study on the partitioning and renal clearance rate of BDGEs in paired urine and serum samples from children and adolescents.

Whether propylene oxide (PO) exposure is associated with hyperglycemia were rarely explored. We aimed to determine the relationship between PO exposure and glucose metabolism, and potential role of oxidative stress. Among 3294 Chinese urban adults, urinary PO metabolite (N-Acetyl-S-(2-hydroxypropyl)-L-cysteine, 2HPMA), biomarkers of oxidative DNA damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) and lipid peroxidation (8-isoprostane, 8-iso-PGF₂α) in urine were determined. The associations of 2HPMA with 8-OHdG, 8-iso-PGF₂α, fasting plasma glucose (FPG), and risk of diabetes were explored. The roles of 8-OHdG and 8-iso-PGF₂α on association of 2HPMA with FPG and risk of diabetes were detected. After adjusted for potential confounders, each 1-unit increase in log-transformed concentration of 2HPMA was associated with a 0.15-mmol/L increase in FPG level, and the adjusted OR (95% CI) of diabetes by the associations of log-transformed urinary 2HPMA concentrations was 1.47 (95% CI: 1.03–2.11). Combination effects of 2HPMA with 8-OHdG or 8-iso-PGF₂α on risk of diabetes were detected, and elevated 8-iso-PGF₂α significantly mediated 34.5% of the urinary 2HPMA-associated FPG elevation. PO exposure was positively associated with FPG levels and risk of diabetes. PO exposure combined with DNA oxidative damage or lipid peroxidation may increase the risk of diabetes, and lipid peroxidation may partially mediate the PO exposure-induced FPG elevation.

The Sars-CoV-2 disease (known as COVID-19) has become a global public health emergency. Researchers have been unveiling the transmission mechanisms and disclosing possible contributing factors. Studies have theorized plausible linkage mechanisms between air pollution exposure and COVID-19 infection and have divided the air pollution exposure into two types: long-term exposure and short-term exposure. However, present studies on impacts of short-term exposure have not reached a conclusive result and are mostly focusing on Asian and European countries. In this study, we conduct a nationwide analysis to examine the association between short-term air pollution exposure and COVID-19 infection in the United States. Daily confirmed cases, air pollution information, and meteorological factors at the county level were collected between March 1st and June 30th, 2020. A total of 806 (out of 3143) counties were included in this study, with 554 counties for PM₂.₅ and 670 counties for ozone (O₃), which account for around 2.1 million cumulative confirmed cases, i.e., about 80% of all confirmed cases in the U.S. over the study period. A generalized additive model was applied to investigate the relationship between short-term exposure to PM₂.₅/O₃ and COVID-19 confirmed cases. The statistically significant results indicate that, with every 10 μg/m3 increase in mean pollutant concentration, the number of daily confirmed cases increases by 9.41% (CI: 8.77%–10.04%) for PM₂.₅ and by 2.42% (CI: 1.56%–3.28%) for O₃. The relative risks associated with short-term PM₂.₅ exposure remain positive after isolating the impacts of long-term exposure. The results of this study suggest that short-term exposure to air pollution, especially to PM₂.₅, may contribute to the spread and course of the pandemic. This finding has important implications for policymakers and the public to take preventive measures such as staying at home on polluted days while improving ventilation indoors to lower the probability of infection.

Pontardawe in South Wales, United Kingdom (UK), consistently has the highest concentrations of nickel (Ni) in PM₁₀ in the UK and repeatedly breaches the 20 ng m⁻³ annual mean EU target value. Several local industries use Ni in their processes. To assist policy makers and regulators in quantifying the relative Ni contributions of these industries and developing appropriate emission reduction approaches, the hourly concentrations of 23 elements were measured using X-ray fluorescence alongside meteorological variables and black carbon during a four-week campaign in November–December 2015. Concentrations of Ni ranged between 0 and 2480 ng m⁻³ as hourly means. Positive Matrix Factorization (PMF) was used to identify sources contributing to measured elements. Cluster analysis of bivariate polar plots of those factors containing Ni in their profile was further used to quantify the industrial processes contributing to ambient PM₁₀ concentrations. Two sources were identified to contribute to Ni concentrations, stainless-steel (which contributed to 10% of the Ni burden) and the Ni refinery (contributing 90%). From the stainless-steel process, melting activities were responsible for 66% of the stainless-steel factor contribution.

This study focused on the short-term whole organism bioassays (WOBs) on fish (Danio rerio) and crustaceans (Gammarus fossarum and Daphnia magna) to assess the negative biological effects of water from the major European River Sava and the comparison of the obtained results with in vitro toxicity data (ToxCast database) and Risk Quotient (RQ) methodology. Pollution profiles of five sampling sites along the River Sava were assessed by simultaneous chemical analysis of 562 organic contaminants (OCs) of which 476 were detected. At each sampling site, pharmaceuticals/illicit drugs category was mostly represented by their cumulative concentration, followed by categories industrial chemicals, pesticides and hormones. An exposure-activity ratio (EAR) approach based on ToxCast data highlighted steroidal anti-inflammatory drugs, antibiotics, antiepileptics/neuroleptics, industrial chemicals and hormones as compounds with the highest biological potential. Summed EAR-based prediction of toxicity showed a good correlation with the estimated toxicity of assessed sampling sites using WOBs. WOBs did not exhibit increased mortality but caused various sub-lethal biological responses that were dependant relative to the sampling site pollution intensity as well as species sensitivity. Exposure of G. fossarum and D. magna to river water-induced lower feeding rates increased GST activity and TBARS levels. Zebrafish D. rerio embryo exhibited a significant decrease in heartbeat rate, failure in pigmentation formation, as well as inhibition of ABC transporters. Nuclear receptor activation was indicated as the biological target of greatest concern based on the EAR approach. A combined approach of short-term WOBs, with a special emphasis on sub-lethal endpoints, and chemical characterization of water samples compared against in vitro toxicity data from the ToxCast database and RQs can provide a comprehensive insight into the negative effect of pollutants on aquatic organisms.

Particulate matter with a diameter of less than 2.5 μm or PM2.5 is recognized worldwide as a cause of public health problems, mainly associated with respiratory and cardiovascular diseases. There is accumulating evidence to show that exposure to PM2.5 has a crucial causative role in various neurological disorders, the main ones being dementia and Alzheimer's disease (AD). PM2.5 can activate glial and microglial activity, resulting in neuroinflammation, increased intracellular ROS production, and ultimately neuronal apoptosis. PM2.5 also causes the alteration of neuronal morphology and synaptic changes and increases AD biomarkers, including amyloid-beta and hyperphosphorylated-tau, as well as raising the levels of enzymes involved in the amyloidogenic pathway. Clinical trials have highlighted the correlation between exposure to PM2.5, dementia, and AD diagnosis. This correlation is also displayed by concordant evidence from animal models, as indicated by increased AD biomarkers in cerebrospinal fluid and markers of vascular injury. Blood-brain barrier disruption is another aggravated phenomenon demonstrated in people at risk who are exposed to PM2.5. This review summarizes and discusses studies from in vitro, in vivo, and clinical studies on causative relationships of PM2.5 exposure to AD-related neuropathology. Conflicting data are also examined in order to determine the actual association between ambient air pollution and neurodegenerative diseases.

Rare earth elements (REEs) concentrated in soils have attracted increasing attention about their impact on soil health as emerging contaminants. However, the sources of REEs enriched in soils are diverse and need to be further investigated. Here, surface soil samples were collected from southern Jiangxi Province, China. REEs contents and soil physicochemical properties were determined, and cerium (Ce) and europium (Eu) anomalies were calculated. Moreover, we established a model to further identify the main sources of REEs accumulation in the studied soils. Results show that the abundance of soil REEs reveals larger spatial variation, suggesting spatially heterogeneous distribution of REEs. The median content of light REEs in soils (154.5 mg kg⁻¹) of the study area was higher than that of heavy REEs and yttrium (35.8 mg kg⁻¹). In addition, most of the soil samples present negative Ce anomalies and all the soil samples present negative Eu anomalies implying the combined effect of weathering and potential exogenous inputs on soil REEs. Positive matrix factorization modeling reveals that soil REEs content is primarily influenced by soil parent materials. Potential anthropogenic sources include mining-related leachate, traffic exhaust, and industrial dust. These results demonstrate that the identification of sources of soil REEs is an important starting point for targeted REEs sources management and regulation of excessive and potentially harmful REEs levels in the soil.

Combined chemical oxidation and bioremediation is a promising method of treating polycyclic aromatic hydrocarbon (PAH) contaminated soil, wherein indigenous soil bacteria play a critical role in the subsequent biodegradation of PAHs after the depletion of the oxidant. In this study, different Fenton conditions were applied by varying either the oxidation mode (conventional Fenton (CF), Fenton-like (LF), modified Fenton (MF), and graded modified Fenton (GMF)) or the H₂O₂ dosage (0%, 3%, 6%, and 10% (v/v)) to treat PAH contaminated soil. The results revealed that when equal dosages of H₂O₂ are applied, PAHs are significantly removed following oxidation treatment, and the removal percentages obeyed the following sequence: CF > GMF > MF > LF. In addition, higher dosages of H₂O₂ improved the PAH removal from soil treated with the same oxidation mode. The ranges of total PAHs removal efficiencies in the soil added 3%, 6%, and 10% of H₂O₂ (v/v) were 18.04%∼59.48%, 31.88%∼71.83%, and 47.56%∼78.16%, respectively. The PAH removal efficiency decreased with increasing ring numbers for the same oxidation treatment. However, the negative influences on soil bacterial abundance, community composition, and function were observed after Fenton treatment. After Fenton oxidation, the bacterial abundance in the soil received 3%, 6%, and 10% of H₂O₂ (v/v) decreased 1.96–2.69, 2.44–3.22, and 3.09–3.42 orders of magnitude compared to the untreated soil. The soil bacterial abundance tended to be impacted by the oxidation mode and H₂O₂ dosage simultaneously. While the main factor influencing the soil bacterial community composition was the H₂O₂ dosages. The results of this study showed that different oxidation mode and H₂O₂ dosage exhibited different effects on PAHs removal and soil bacteria (including abundance, community composition, and function), and there was a trade-off between the removal of PAHs and the adverse impact on soil bacteria.

The coexistence of per- and polyfluoroalkyl substances (PFASs) and heavy metals have been found in soils. However, the interaction between the combined pollutants in soils remains unclear. In this study, the adsorption processes of single and combined Cr(VI) and chlorinated polyfluoroalkyl ether potassium sulfonate (F–53 B) in red, yellow and black soils were simulated. When compared with the single F–53 B and Cr(VI), the adsorption amount of the combined F–53 B and Cr(VI) on soils changed with the types of soils. The interactions between F–53 B and Cr(VI) in soils affected their adsorption behavior. The adsorption of the combined F–53 B and Cr(VI) best fit second-order kinetics and the Freundlich equation. Moreover, aluminum and iron oxides are highly correlated with adsorption of F–53 B and Cr(VI). Both F–53 B and Cr(VI) can form complexes with aluminum and iron oxides through electrostatic interactions, but PFOS could be bridged with iron oxides to form an inner sphere complex and with aluminum oxides to form an outer sphere complex. The coexistence of F–53 B and Cr(VI) could change the fluorescent group of dissolved organic matter (DOM) in soils due to the complexation between F–53 B and DOM. In addition, F–53 B increased the acid-soluble portion of Cr and decreased its residual form, which promoted the environmental risk of Cr in soils.