Investigating the nature of PM₁₀ is crucial to differentiate sources and their relative contributions. In this study we compared the levels, and the chemical and mineralogical properties of PM₁₀ particles sampled in different seasons at monitoring stations representative of urban background, urban traffic and suburban traffic areas of Naples city. The aims were to relate the PM₁₀ load and characteristics to the location of the monitoring stations, to investigate the different sources contributing to PM₁₀ and to highlight PM₁₀ seasonal variability. Bulk analyses of chemical species in the PM₁₀ fraction included total carbon and nitrogen, δ¹³C and other 20 elements. Both natural and anthropogenic sources were found to contribute to the exceedances of the EU PM₁₀ limit values. The natural contribution was mainly related to marine aerosols and soil dust, as highlighted by X-ray diffractometry and SEM-EDS microscopy. The percentage of total carbon suggested a higher contribution of biogenic components to PM₁₀ in spring. However, this result was not supported by the δ¹³C values which were seasonally homogeneous and not sufficient to extract single emission sources. No significant differences, in terms of PM₁₀ load and chemistry, were observed between monitoring stations with different locations, suggesting a homogeneous distribution of PM₁₀ on the studied area in all seasons. The anthropogenic contribution to PM₁₀ seemed to dominate in all sites and seasons with vehicular traffic acting as a main source mostly by generation of non-exhaust emissions Our findings reinforce the need to focus more on the analysis of PM₁₀ in terms of quality than of load, to reconsider the criteria for the classification and the spatial distribution of the monitoring stations within urban and suburban areas, with a special attention to the background location, and to emphasize all the policies promoting sustainable mobility and reduction of both exhaust and not-exhaust traffic-related emissions.

Microplastics are widespread throughout aquatic environments. However, there is currently insufficient understanding of the factors influencing ingestion of microplastics by organisms, especially higher predators such as fish. In this study we link ingestion of microplastics by the roach Rutilus rutilus, within the non-tidal part of the River Thames, to exposure and physiological factors. Microplastics were found within the gut contents of roach from six out of seven sampling sites. Of sampled fish, 33% contained at least one microplastic particle. The majority of particles were fibres (75%), with fragments and films also seen (22.7% and 2.3% respectively). Polymers identified were polyethylene, polypropylene and polyester, in addition to a synthetic dye. The maximum number of ingested microplastic particles for individual fish was strongly correlated to exposure (based on distance from the source of the river). Additionally, at a given exposure, the size of fish correlated with the actual quantity of microplastics in the gut. Larger (mainly female) fish were more likely to ingest the maximum possible number of particles than smaller (mainly male) fish. This study is the first to show microplastic ingestion within freshwater fish in the UK and provides valuable new evidence of the factors influencing ingestion that can be used to inform future studies on exposure and hazard of microplastics to fish.

Genetic and epigenetic changes were investigated in chronically irradiated Scots pine (Pinus sylvestris L.) populations from territories that were heavily contaminated by radionuclides as result of the Chernobyl Nuclear Power Plant accident. In comparison to the reference site, the genetic diversity revealed by electrophoretic mobility of AFLPs was found to be significantly higher at the radioactively contaminated areas. In addition, the genome of pine trees was significantly hypermethylated at 4 of the 7 affected sites.

The concentration distributions, compositional profiles and seasonal variations of 17 perfluoroalkyl acids (PFAAs) in PM₁₀ (particles with aerodynamic diameters < 10 μm) were determined in seven coastal cities of the Bohai and Yellow Seas. The detection rates of perfluorooctanoic acid (PFOA) and short-chain components (perfluoroalkyl carboxylic acids (PFCAs) with ≤7 carbon atoms and perfluoroalkane sulfonic acids (PFSAs) with ≤5 carbon atoms) were much higher than those of other long-chain PFAA species. The annual average concentration of total PFAAs in PM₁₀ ranged from 23.6 pg/m³ to 94.5 pg/m³ for the sampling cities. The monthly mean concentrations of PFAAs in PM₁₀ in some sampling cities reached a peak value in winter, while no significant seasonal differences presented in other cities. High concentrations of PFAAs in the northern cities generally occurred during the local heating period (from November to March). Generally, the dominant components of PFAAs were PFOA and perfluorobutyric acid (PFBA). Some significantly positive correlations (p < 0.01) between the 10 dominant components were revealed in the sampling cities, which implied similar sources and fate behaviors. Based on the simulated 72-hr backward trajectory tracking of air masses, the clustering results demonstrated the sampling cities were affected mainly by the atmospheric transport in sequence from the northwest, the southwest and the open seas, and many transport trajectories of air masses passed by the local fluorine chemical manufacturers in Liaoning, Shandong, Jiangsu, and Hubei Provinces. The estimated average daily intake (ADI) corresponding to the residents in different age groups indicated insignificant contributions to PFOA and perfluorooctane sulfonate (PFOS) exposures by inhalation of PM₁₀ compared to ingestion by daily diet, while the higher ADI of PFOA than the reported levels for adults should be a concern. The calculated hazard ratios (HR) exhibited low noncancer risks by inhalation exposure to PFOA and PFOS in PM₁₀.

The neurotoxicity of arsenic is a serious health problem, especially for children. DNA epigenetic change may be an important pathogenic mechanism, but the molecular pathway remains obscure. In this study, the weaned male Sprague-Dawly (SD) rats were treated with arsenic trioxide via drinking water for 6 months, simulating real developmental exposure situation of children. Arsenic exposure impaired the cognitive abilities, and altered the expression of neuronal activity-regulated genes. Total arsenic concentrations of cortex and hippocampus tissues were significantly increased in a dose-dependent manner. The reduction in 5-methylcytosine (5 mC) and 5-hydroxymethylcytosine (5hmC) levels as well as the down-regulation of DNA methyltransferases (DNMTs) and ten–eleven translocations (TETs) expression suggested that DNA methylation/demethylation processes were significantly suppressed in brain tissues. S-adenosylmethionine (SAM) level wasn't changed, but the expression of the important indicators of oxidative/anti-oxidative balance and tricarboxylic acid (TCA) cycle was significantly deregulated. Overall, arsenic can disrupt oxidative/anti-oxidative balance, further inhibit TETs expression through TCA cycle and alpha-ketoglutarate (α-KG) pathway, and consequently cause DNA methylation/demethylation disruption. The present study implies oxidative stress but not SAM depletion may lead to DNA epigenetic alteration and arsenic neurotoxicity.

We used replicated paddy microcosm systems to estimate the tropic transfer of citrate-coated silver nanoparticles (AgNP citrate), polyvinylpyrrolidone (PVP)-coated AgNP (AgNP PVP), and silver ions (AgNO₃) for 14 days under two exposure regimes (a single high-dose exposure; 60 μg L⁻¹ and a sequential low-dose exposure at 1 h, 4 days and 9 days; 20 μg L⁻¹ × 3 = 60 μg L⁻¹). Most Ag ions from AgNO₃ had dispersed in the water and precipitated partly on the sediment, whereas the two Ag NPs rapidly coagulated and precipitated on the sediment. The bioconcentration factors (BCFs) of Ag from AgNPs and AgNO₃ in Chinese muddy loaches and biofilms were higher than those of river snails in both exposure conditions. These BCFs were more prominent for 14 days exposure (7.30 for Chinese muddy loach; 4.48 for biofilm) in the low-dose group than in the single high-dose group. Their retention of AgNPs and Ag ions differed between the two exposure conditions, and uptake and elimination kinetics of Ag significantly differed between AgNP citrate and AgNP PVP in the sequential low-dose exposure. Stable isotopes analyses indicated that the trophic levels between Chinese muddy loaches and biofilms and between river snails and biofilms were 2.37 and 2.27, respectively. The biomagnification factors (BMFs) of AgNPs and AgNO₃ between Chinese muddy loaches and biofilms were significantly higher than those between river snails and biofilms under both exposure settings. The BMFs of AgNP citrate and AgNO₃ between Chinese muddy loaches and biofilms were greater than those of AgNP PVP for 14 days in the single high-dose group, whereas the BMFs of AgNP PVP were greater than those of AgNP citrate and AgNO₃ in the sequential low-dose group. These microcosm data suggest that AgNPs have the potential to impact on ecological receptors and food chains.

Benzo(a)pyren-7,8-dihydrodiol-9,10-epoxide (BPDE) is an endocrine disrupter and ultimate carcinogenic product of benzo(a)pyrene (BaP). Numerous studies have shown that BPDE causes trophoblast-related diseases, such as preeclampsia, growth restriction or miscarriages. However, the underlying mechanism, especially the mitochondria-related BPDE-induced trophoblast dysfunction remains unknown. In this study, we examined mitochondrial functions in BPDE-induced human trophoblast cell line Swan 71. BPDE decreased cell ability, attenuated cell invasion and HCG secretion, induced cell apoptosis, decreased mitochondrial membrane potential, increased reactive oxygen species (ROS) and MDA, and decreased SOD activity in a dose-dependent manner. In the mechanism, BPDE significantly increased pro-apoptosis protein (P53 and Bak1) and decreased anti-apoptosis protein (Bcl-2). Furthermore, the protein expression levels of mitochondrial fusion genes (Mfn1, Mfn2, and OPA1) were decreased and those of fission genes (Fis1 and Drp1) were increased with increasing concentrations of BPDE and incubation time, resulting in the release of Cyt c and activation of Caspase 3, which irreversibly induced trophoblast cell apoptosis. This study reveals the mechanism of dysfunction of trophoblast cells through cell apoptosis due to the disorder of mitochondrial fission/fusion after exposure to BPDE, providing a further experimental understanding the adverse effects of BaP on trophoblast cells in early pregnancy.

Lead poisoning is considered a public health threat, particularly in developing countries. Health problems from Pb exposure occur in many parts of the world, especially near Pb mines, Pb smelters, and used lead–acid battery (ULAB) recycling plants. In this study, we analyzed the urine metabolome of residents in a village located near a ULAB recycling facility to investigate the biological effects of Pb exposure (ULAB: n = 44, Reference: n = 51). Lasso linear regression models were moderately predictive of blood Pb levels, as evaluated by a training set (R² = 0.813) and against an external test set (R²EXT = 0.647). In lasso logistic regression models, areas under receiver operating characteristic curves, as measured by 5-fold cross-validation (AUCCV = 0.871) and against an external test set (AUCEXT = 0.917), indicated accurate classification of urine samples from the affected village and from a reference site. Ten candidate biomarkers identified at false discovery rates of <0.05 were associated with ATP-binding cassette (ABC) transporters, possibly related to the disruption of small-molecule transport in the kidney; amino acid, porphyrin, and chlorophyll metabolism; and the heme biosynthetic pathway. Collectively, the results suggest that lead Pb is related to the health effects in individuals residing in ULAB site by alteration of these biological pathways.

Temperature has been associated with population health, but few studies have projected the future temperature-related years of life lost attributable to climate change. To project future temperature-related disease burden in Tianjin, we selected years of life lost (YLL) as the dependent variable to explore YLL attributable to climate change. A generalized linear model (GLM) and distributed lag non-linear model were combined to assess the non-linear and delayed effects of temperature on the YLL of non-accidental mortality. Then, we calculated the YLL changes attributable to future climate scenarios in 2055 and 2090. The relationships of daily mean temperature with the YLL of non-accident mortality were basically U-shaped. Both the daily mean temperature increase on high-temperature days and its drop on low-temperature days caused an increase of YLL and non-accidental deaths. The temperature-related YLL will worsen if future climate change exceeds 2 °C. In addition, the adverse effects of extreme temperature on YLL occurred more quickly than that of the overall temperature. The impact of low temperature was greater than that of high temperature. Men were vulnerable to high temperature compared with women. This analysis highlights that the government should formulate environmental policies to reach the Paris Agreement goal.

A mesocosm case study was conducted to gain understanding and practical knowledge on biofilm emerging contaminants biodegradation capacity under stressor and multiple stressor conditions. Two real life scenarios: I) biodegradation in a pristine intermittent stream experiencing acute pollution and II) biodegradation in a chronically polluted intermittent stream, were examined via a multifactorial experiment using an artificial stream facility. Stream biofilms were exposed to different water flow conditions i.e. permanent and intermittent water flow. Venlafaxine, a readily biodegradable pharmaceutical was used as a measure of biodegradation capacity while pollution was simulated by a mixture of four emerging contaminants (erythromycin, sulfisoxazole, diclofenac and imidacloprid in addition to venlafaxine) in environmentally relevant concentrations. Biodegradation kinetics monitored via LC-MS/MS was established, statistically evaluated, and used to link biodegradation with stress events. The results suggest that the effects of intermittent flow do not hinder and may even stimulate pristine biofilm biodegradation capacity. Chronic pollution completely reduced biodegradation in permanent water flow experimental treatments while no change in intermittent streams was observed. A combined effect of water flow conditions and emerging contaminants exposure on biodegradation was found. The decrease in biodegradation due to exposure to emerging contaminants is significantly greater in streams with permanent water flow suggesting that the short and medium term biodegradation capacity in intermittent systems may be preserved or even greater than in perennial streams.