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.

The levels and spatial distribution of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) in freshwater products from Northeast China were investigated by gas chromatography coupled to isotope dilution high-resolution mass spectrometry. All samples were on-spot sampled from main production regions of freshwater products in Northeast China, and these samples were used to systematically assess the potential health risks of OCPs and PCBs associated with consumption of these fishery products. Dichlorodiphenyltrichloroethanes (DDTs), hexachlorocyclohexane (HCHs), hexachlorobenzene (HCB) and PCBs were the major pollutants with 100% detection rates, and their levels ranged from 0.086 to 58, 0.038–3.3, 0.093–4.5 and 0.032–1.4 ng g⁻¹ wet weight, respectively. The estimated dietary intakes of these contaminants were all below their corresponding acceptable daily intakes. Significant regional differences in the levels of OCPs and PCBs (P ≦ 0.001) were found in samples from Liaoning and Inner Mongolia. The results showed that the concentrations of targeted contaminants in aquatic products had species-specific characteristics, and the levels of targeted pollutants in Oncorhynchus mykiss and Eriocheir sienesis were significantly higher than those in other aquatic product species. Advisories on ten species of aquatic products suggested that consumption of Eriocheir sinensis, Oncorhynchus mykiss and Cyprinus carpio at a rate exceeding 15 meals per month would pose a cancer risk. A health risk assessment indicated that exposure to these pollutants through freshwater products consumption would cause a non-ignorable potential carcinogenic risk to humans.

Heavy metals in the topsoil affected adversely human health through inhalation, ingestion and dermal contact. The health risk assessment, which are quantified from soil heavy metals sources under different land use, can provide an important reference basis for preventing and controlling the soil heavy metals pollution from the source. In this study, simple statistical analysis and Positive Matrix Factorization (PMF) were used to quantify sources of soil heavy metals; then a health risk assessment (HRA) model combined with PMF was proposed to assess quantificationally the human health risk (including non-cancer risk and cancer risk) from sources under residential-land, forest-land and farm land. Xiang River New District (XRNQ) was chosen as the example and four significant sources were quantitatively analyzed in the study. For cancer risk, industrial discharge was the largest source and accounted for about 69.6%, 69.7%, 56.5% for adults under residential-land, forest-land and farm-land, respectively. For non-cancer risk, industrial discharge was still the largest significant source under residential-land and forest-land and accounted for about 41.7%, 39.2% for adult, respectively; while agricultural activities accounted for about 51.8% for adult under farm-land. The risk trend of children, including cancer risk and non-cancer risk, was similar with adults. However, the non-cancer risk areas of adults affected by industrial discharge was higher than that of children, while the cancer risk areas of adults were on the contrary. The new exploration was useful to assess health risk quantification from sources under different land use, thus providing certain reference in preventing and controlling the pollution from the source for local authorities effectively.

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.

Antifouling biocides in surface sediments and gastropod tissues were assessed for the first time along coastal areas of Panama under the influence of maritime activities, including one of the world's busiest shipping zones: the Panama Canal. Imposex incidence was also evaluated in five muricid species distributed along six coastal areas of Panama. This TBT-related biological alteration was detected in three species, including the first report in Purpura panama. Levels of organotins (TBT, DBT, and MBT) in gastropod tissues and surficial sediments ranged from <5 to 104 ng Sn g⁻¹ and <1–149 ng Sn g⁻¹, respectively. In addition, fresh TBT inputs were observed in areas considered as moderate to highly contaminated mainly by inputs from fishing and leisure boats. Regarding booster biocides, TCMTB and dichlofluanid were not detected in any sample, while irgarol 1051, diuron and DCOIT levels ranged from <0.08 to 2.8 ng g⁻¹, <0.75–14.1 ng g⁻¹, and <0.38–81.6 ng g⁻¹, respectively. The highest level of TBT (149 ng Sn g⁻¹) and irgarol 1051 (2.8 ng g⁻¹), as well as relevant level of DCOIT (5.7 ng g⁻¹), were detected in a marina used by recreational boats. Additionally, relatively high diuron values (14.1 ng g⁻¹) were also detected in the Panama Canal associate to a commercial port. DCOIT concentrations were associated with the presence of antifouling paint particles in sediments obtained nearby shipyard or boat maintenance sites. The highest levels of TBT, irgarol 1051, and diuron exceeded international sediment quality guidelines indicating that toxic effects could be expected in coastal areas of Panama. Thus, the simultaneous impacts produced by new and old generations of antifouling paints highlight a serious environmental issue in Panamanian coastal areas.

Emissions from burning of biomass in the Amazon region have adverse effects on the environment and human health. Herein, particulate matter (PM) emitted from biomass burning in the Amazon region during two different periods, namely intense and moderate, was investigated. This study focused on: i) organic characterization of nitro- and oxy-polycyclic aromatic hydrocarbons (PAHs); ii) assessment of the excess lifetime cancer risk (LCR); and iii) assessment of the in vitro mutagenic effects of extractable organic matter (EOM). Further, we compared the sensitivity of two mutagenicity tests: Salmonella/microsome test and cytokinesis-block micronucleus (CBMN) with human lung cells. Among the nitro-PAHs, 2-nitrofluoranthene, 7-nitrobenz[a]anthracene, 1-nitropyrene, and 3-nitrofluoranthene showed the highest concentrations, while among oxy-PAHs, 2-metylanthraquinone, benz[a]anthracene-7,12-dione, and 9,10-anthraquinone were the most abundant. The LCR calculated for nitro-PAH exposure during intense biomass burning period showed a major contribution of 6-nitrochrysene to human carcinogenic risk. The EOM from intense period was more mutagenic than that from moderate period for both TA98 and YG1041 Salmonella strains. The number of revertants for YG1041 was 5–50% higher than that for TA98, and the most intense responses were obtained in the absence of metabolic activation, suggesting that nitroaromatic compounds with direct-acting frameshift mutagenic activity are contributing to the DNA damage. Treatment of cells with non-cytotoxic doses of EOM resulted in an increase in micronuclei frequencies. The minimal effective dose showed that Salmonella/microsome test was considerably more sensitive in comparison with CBMN mainly for the intense burning period samples. This was the first study to assess the mutagenicity of EOM associated with PM collected in the Amazon region using Salmonella/microsome test. The presence of compounds with mutagenic effects, particularly nitro- and oxy-PAHs, and LCR values in the range of 10⁻⁵ indicate that the population is potentially exposed to an increased risk of DNA damage, mutation, and cancer.

Numerous studies on microplastics (MPs; Ø < 5 mm) in the aquatic environment have been published, but knowledge about the occurrence and ecological risks of MPs is limited. This is in part because current data on the distribution of MPs are comparable only to a limited extent, due to the many different methods of investigation. In addition, sample preparation is often difficult such that standard procedures are lacking. The aim of this work was to simplify the preparation of different kinds of MP samples. Our method makes use of the electrostatic behavior of plastic particles to facilitate their separation from sample matter, with up to 99% of the original sample mass removed without any loss of MPs. To determine the efficacy of this approach, four different materials (quartz sand, freshwater suspended particulate matter, freshwater sediment, and beach sand) were spiked with MPs (size: 0.063–5 mm from the seven most common types of plastics, one bioplastic type, polyethylene fibers, and tire wear. A modified electrostatic metal/plastic separator was used to reduce the sample mass and concentrate the plastics based on their physical separation. The recovery achieved with this method was as high as nearly 100% for each type of material. The method was then tested on plastic particles of different shapes and types isolated from the Rhine River. These were successfully electroseparated from the four materials, which demonstrated the utility of this method. Its advantages include the simplified handling and preparation of different field samples as well as a much shorter processing time, because after the last separation step there is hardly any biological material remaining in the sample fraction.

Chemicals in consumer products have become the focus of recent regulatory developments including California's Safer Consumer Products Act. However, quantifying the amount of chemicals released during the use and post-use phases of consumer products is challenging, limiting the ability to understand their impacts. Here we present a comprehensive framework, OrganoRelease, for estimating the release of organic chemicals from the use and post-use of consumer products given limited information. First, a novel Chemical Functional Use Classifier estimates functional uses based on chemical structure. Second, the quantity of chemicals entering different product streams is estimated based on market share data of the chemical functional uses. Third, chemical releases are estimated based on either chemical product categories or functional uses by using the Specific Environmental Release Categories and EU Technological Guidance Documents. OrganoRelease connects 19 unique functional uses and 14 product categories across 4 data sources and provides multiple pathways for chemical release estimation. Available user information can be incorporated in the framework at various stages. The Chemical Functional Use Classifier achieved an average accuracy above 84% for nine functional uses, which enables the OrganoRelease to provide release estimates for the chemical, mostly using only the molecular structure. The results can be can be used as input for methods estimating environmental fate and exposure.

Organophosphate flame retardants (OPFRs) have been commonly observed in indoor dust, food, and drinking water in China, but little is known about their exposure levels or factors leading to exposure in Chinese children. In this study, we measured eight metabolites of OPFRs (mOPFRs) in 227 urine samples collected from 0- to 5-year-old children in China. The high detection rates of mOPFRs (60%–100%) in the collected urine samples demonstrated the widespread exposure of this population to OPFRs. The median concentrations indicated that bis(2-chloroethyl)phosphate (BCEP, 0.85 ng/mL) and diphenyl phosphate (DPHP, 0.27 ng/mL) were the dominant chlorinated mOPFRs and nonchlorinated mOPFRs, respectively. Interestingly, the median urinary levels of bis(1-chloro-2-propyl)phosphate (BCIPP, 6.48 ng/mL) and bis(2-butoxyethyl)phosphate (BBOEP, 0.31 ng/mL) in inpatient infants were one order of magnitude higher (p < 0.01) than those observed in outpatient infants. For home-stay participants, furthermore, infants (0–1 year) had the highest median levels of BCIPP (0.72 ng/mL) and dibutyl phosphate (DBP, 0.14 ng/mL) among the three age groups (i.e., 0–1, >1–3, and >3–5 years), and significantly (p < 0.05) negative age-related relationships were found for both urinary mOPFRs. Two set of data on estimated daily intakes (EDIs) were calculated based on the fraction of OPFR excreted as the corresponding mOPFR (FUE) in human liver microsomes (EDIHLM) and S9 fraction (EDIS₉) system, respectively. In general, children have relatively high EDIs of tris(2-chloroethyl)phosphate (TCEP: EDIHLM = 485 ng/kg bw/day, EDIS₉ = 261 ng/kg bw/day). Furthermore, 17% or 21% of inpatient infants had EDIs that exceeded the reference dose, whereas this value was reduced to 13% in outpatient infants; and this value decreased with age among all home-stay children (0–5 years). Our results indicated that inpatient and home-stay infants had a higher potential risk of OPFR exposure. To our knowledge, this is the first study to identify the elevated urinary levels of mOPFRs in inpatients.

Decabromodiphenyl Ethane (DBDPE), a kind of new brominated flame retardants (NBFRs) used to replace DecaBDE, has been frequently detected in the environment and human samples. In this study, we explored its toxic effects on male mouse offspring after perinatal exposure to DBDPE. During the perinatal period, pregnant ICR mice were exposed to DBDPE (100 μg/kg body weight) via oral gavage. After weaning, male offspring were fed on a low-fat diet and a high-fat diet, respectively. We measured and recorded body weight, liver weight, and epididymis fat mass, blood biochemical markers, metabolites changes in liver, and gene expression involved in lipid and glucose homeostasis. The results showed that perinatal exposure to DBDPE increased the risk of obesity in mouse offspring and affected triglyceride synthesis, bile secretion, purine synthesis, mitochondrial function and glucose metabolism, furthermore, the use of HFD feeding may further exacerbate these effects. All of these results show that early-life exposure to low doses of DBDPE can promote the development of metabolic dysfunction, which in turn induces obesity.