Pollution of marine environments with microplastic particles (i.e. plastic fragments <5 mm) has increased rapidly during the last decades. As these particles are mainly of terrestrial origin, coastal ecosystems such as coral reefs are particularly threatened. Recent studies revealed that microplastic ingestion can have adverse effects on marine invertebrates. However, little is known about its effects on small-polyp stony corals that are the main framework builders in coral reefs. The goal of this study is to characterise how different coral species I) respond to microplastic particles and whether the exposure might II) lead to health effects. Therefore, six small-polyp stony coral species belonging to the genera Acropora, Pocillopora, and Porites were exposed to microplastics (polyethylene, size 37–163 μm, concentration ca. 4000 particles L−1) over four weeks, and responses and effects on health were documented.The study showed that the corals responded differentially to microplastics. Cleaning mechanisms (direct interaction, mucus production) but also feeding interactions (i.e. interaction with mesenterial filaments, ingestion, and egestion) were observed. Additionally, passive contact through overgrowth was documented. In five of the six studied species, negative effects on health (i.e. bleaching and tissue necrosis) were reported.We here provide preliminary knowledge about coral-microplastic-interactions. The results call for further investigations of the effects of realistic microplastic concentrations on growth, reproduction, and survival of stony corals. This might lead to a better understanding of resilience capacities in coral reef ecosystems.

Microplastics are a widespread environmental pollutant in aquatic ecosystems and have the potential to eventually sink to the sediment, where they may pose a risk to sediment-dwelling organisms. While the impacts of exposure to microplastics have been widely reported for marine biota, the effects of microplastics on freshwater organisms at environmentally realistic concentrations are largely unknown, especially for benthic organisms. Here we examined the effects of a realistic concentration of polyethylene microplastics in sediment on the growth and emergence of a freshwater organism Chironomus tepperi. We also assessed the influence of microplastic size by exposing C. tepperi larvae to four different size ranges of polyethylene microplastics (1–4, 10–27, 43–54 and 100–126 μm). Exposure to an environmentally relevant concentration of microplastics, 500 particles/kgsediment, negatively affected the survival, growth (i.e. body length and head capsule) and emergence of C. tepperi. The observed effects were strongly dependent on microplastic size with exposure to particles in the size range of 10–27 μm inducing more pronounced effects. While growth and survival of C. tepperi were not affected by the larger microplastics (100–126 μm), a significant reduction in the number of emerged adults was observed after exposure to the largest microplastics, with the delayed emergence attributed to exposure to a stressor. While scanning electron microscopy showed a significant reduction in the size of the head capsule and antenna of C. tepperi exposed to microplastics in the 10–27 μm size range, no deformities to the external structure of the antenna and mouth parts in organisms exposed to the same size range of microplastics were observed. These results indicate that environmentally relevant concentrations of microplastics in sediment induce harmful effects on the development and emergence of C. tepperi, with effects greatly dependent on particle size.

Arsenic induced senescence (AIS) has been identified in the population of West Bengal, India very recently. Also there is a high incidence of arsenic induced peripheral neuropathy (PN) throughout India. However, the epigenetic regulation of AIS and its contribution in arsenic induced PN remains unexplored. We recruited seventy two arsenic exposed and forty unexposed individuals from West Bengal to evaluate the role of senescence associated miRNAs (SA-miRs) in AIS and their involvement if any, in PN. The downstream molecules of the miRNA associated with the disease outcome, was also checked by immuoblotting. In vitro studies were conducted with HEK 293 cells and sodium arsenite exposure. Our results show that all the SA-miRs were upregulated in comparison to unexposed controls. miR-29a was the most significantly altered, highest expression being in the arsenic exposed group with PN, suggesting its association with the occurrence of PN. We looked for the expression of peripheral myelin protein 22 (PMP22), a specific target of miR-29a associated with myelination and found that both in vitro and in vivo results showed over-expression of the protein. Since this was quite contrary to miRNA regulation, we checked for intermediate players β-catenin and GSK-3β upon arsenic exposure which affects PMP22 expression. We found that β-catenin was upregulated in vitro and was also highest in the arsenic exposed group with PN while GSK-3β followed the reverse pattern. Our findings suggest that arsenic exposure alters the expression of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible for arsenic induced PN.

The potential leakage from marine CO2 storage sites is of increasing concern, but few studies have evaluated the probable adverse effects on marine organisms. Fish, one of the top predators in marine environments, should be an essential representative species used for water column toxicity testing in response to waterborne CO2 exposure. In the present study, we conducted fish life cycle toxicity tests to fully elucidate CO2 toxicity mechanism effects. We tested sub-lethal and lethal toxicities of elevated CO2 concentrations on marine medaka (Oryzias melastigma) at different developmental stages. At each developmental stage, the test species was exposed to varying concentrations of gaseous CO2 (control air, 5%, 10%, 20%, and 30%), with 96 h of exposure at 0–4 d (early stage), 4–8 d (middle stage), and 8–12 d (late stage). Sub-lethal and lethal effects, including early developmental delays, cardiac edema, tail abnormalities, abnormal pigmentation, and mortality were monitored daily during the 14 d exposure period. At the embryonic stage, significant sub-lethal and lethal effects were observed at pH < 6.30. Hypercapnia can cause long-term and/or delayed developmental embryonic problems, even after transfer back to clean seawater. At fish juvenile and adult stages, significant mortality was observed at pH < 5.70, indicating elevated CO2 exposure might cause various adverse effects, even during short-term exposure periods. It should be noted the early embryonic stage was found more sensitive to CO2 exposure than other developmental stages of the fish life cycle. Overall, the present study provided baseline information for potential adverse effects of high CO2 concentration exposure on fish developmental processes at different life cycle stages in marine ecosystems.

Dust emissions from copper smelters processing arsenic-bearing ores represent a risk to soil environments due to the high levels of As and other inorganic contaminants. Using an in situ experiment in four different forest and grassland soils (pH 3.2–8.0) we studied the transformation of As-rich (>50 wt% As) copper smelter dust over 24 months. Double polyamide bags with 1 g of flue dust were buried at different depths in soil pits and in 6-month intervals; then those bags, surrounding soil columns, and soil pore waters were collected and analysed. Dust dissolution was relatively fast during the first 6 months (5-34%), and mass losses attained 52% after 24 months. The key driving forces affecting dust dissolution were not only pH, but also the water percolation/retention in individual soils. Primary arsenolite (As2O3) dissolution was responsible for high As release from the dust (to 72%) and substantial increase of As in the soil (to a 56 × increase; to 1500 mg kg−1). Despite high arsenolite solubility, this phase persisted in the dust after 2 years of exposure. Mineralogical investigation indicated that mimetite [Pb5(AsO4)3(Cl,OH)], unidentified complex Ca-Pb-Fe-Zn arsenates, and Fe oxyhydroxides partly controlled the mobility of As and other metal(loid)s. Compared to As, other less abundant contaminants (Bi, Cu, Pb, Sb, Zn) were released into the soil to a lesser extent (8-40% of total). The relatively high mobility of As in the soil can be seen from decreases of bulk As concentrations after spring snowmelt, high water-extractable fractions with up to ∼50% of As(III) in extracts, and high As concentrations in soil pore waters. Results indicate that efficient controls of emissions from copper smelters and flue dust disposal sites are needed to prevent extensive contamination of nearby soils by persistent As.

It is critical to estimate the exposure to indoor air pollution of residents spending most of their time in such microenvironments. However, the understanding regarding PM2.5 exposure in residential indoor environments is very limited. In this study, we collected participants' basic information and time–activity patterns, as well as details of other factors related to indoor air pollution exposure, through questionnaires presented to a large population in 37 counties of China. Continuous monitoring of ambient PM2.5 concentrations was performed using an environmental fixed-site monitoring network. Residential indoor PM2.5 concentrations were predicted using a mass balance model based on the data obtained. Evaluation of continuous daily average residential indoor PM2.5 exposure doses for large populations during winter revealed concentrations ranged from 67 to 195 μg/m3. Finally, differences in residential indoor PM2.5 exposure between northern and southern China were investigated. The results suggested that residential indoor PM2.5 concentrations in northern China, associated with heating, were higher than in the south. The established model could be important for improved understanding of human exposure to indoor PM2.5 air pollution.

Food intake is one of the main pathways of human exposure to chlorinated paraffins (CPs). This study assessed the dietary exposure for the general Chinese population to short-chain chlorinated paraffin (SCCPs) and medium-chain chlorinated paraffins (MCCPs) through meat and meat products. Twenty samples of meat and meat products from 20 Chinese provinces were collected in 2011. As the sampling sites covered about two-thirds of the Chinese population, the meat samples were considered to be representative of the true characteristics of CPs contamination in Chinese meat products. The concentrations of SCCPs and MCCPs in the meat samples were measured using the comprehensive two-dimensional gas chromatography electron capture negative ionization high-resolution time-of-flight mass spectrometry method. Forty-eight SCCP and MCCP homolog groups were detected in the meat samples. The mean SCCP and MCCP concentrations in all meat samples were 129 ± 4.1 ng g⁻¹ wet weight and 5.7 ± 0.59 ng g⁻¹ wet weight, respectively. The concentrations of SCCPs and MCCPs varied in samples from different provinces. The geographical distribution of CP concentrations was similar to the distribution of CPs manufacturing plants in China. The most abundant groups of SCCPs in all samples were C₁₀₋₁₁ Cl₆₋₇, and the most abundant groups of MCCPs in most samples were C₁₄ Cl₇₋₈. The possible sources of SCCPs and MCCPs in meat and meat products might be CP-42 and CP-52. The 50th percentile estimated daily intakes of SCCPs and MCCPs through meat consumption for a “standard” Chinese adult male were 0.13 and 0.0047 μg kg⁻¹ bw d⁻¹, respectively, both much lower than the tolerable daily intakes (TDIs) for SCCPs and MCCPs. This preliminary risk assessment has indicated that the indirect exposure of SCCPs and MCCPs through meat consumption does not pose significant risk to human health in China.

Microbial communities play vital roles in the biogeochemistry of nutrients in coastal saltmarshes, ultimately controlling water quality, nutrient cycling, and detoxification. We determined the structure of microbial populations inhabiting coastal saltmarsh sediments from northern Barataria Bay, Louisiana, USA to gain insight into impacts on the biogeochemical cycles affected by Macondo oil from the 2010 Deepwater Horizon well blowout two years after the accident. Quantitative PCR directed toward specific functional genes revealed that oiled marshes were greatly diminished in the population sizes of diazotrophs, denitrifiers, nitrate-reducers to ammonia, methanogens, sulfate-reducers and anaerobic aromatic degraders, and harbored elevated numbers of alkane-degraders. Illumina 16S rRNA gene sequencing indicated that oiling greatly changed the structure of the microbial communities, including significant decreases in diversity. Oil-driven changes were also demonstrated in the structure of two functional populations, denitrifying and sulfate reducing prokaryotes, using nirS and dsrB as biomarkers, respectively. Collectively, the results from 16S rRNA and functional genes indicated that oiling not only markedly altered the microbial community structures, but also the sizes and structures of populations involved in (or regulating) a number of important nutrient biogeochemical cycles in the saltmarshes. Alterations such as these are associated with potential deterioration of ecological services, and further studies are necessary to assess the trajectory of recovery of microbial-mediated ecosystem functions over time in oiled saltmarsh sediment.

Moss (as a reference material) and camphor (Cinnamomum Camphora) leaf, branch bark and bark samples were systematically collected across an urban-rural gradient in Guiyang (SW China) to determine the efficacy of using these bio-indicators to evaluate nitrogen (N) pollution. The tissue N concentrations (0.13%–2.70%) and δ¹⁵N values (−7.5‰ to +9.3‰) of all of these bio-indicators exhibited large spatial variations, as they recorded higher values in urban areas that quickly decreased with distance from the city center; moreover, both soil N concentrations and soil δ¹⁵N values were found no significant differences within each 6 km from the urban to the rural area. This not only suggests that the different N uptake strategies and variety of N responses of these bio-indicators can be reflected by their different susceptibilities to variations in N deposition but also reveals that they are able to indicate that urban N deposition is mostly from traffic and industry (NOₓ-N), whereas rural N deposition is mainly from agriculture (NHₓ-N). Compared to previously collected urban moss and camphor leaf samples, the significantly increased δ¹⁵N values in current urban moss and camphor leaf samples further indicate a greater contribution of NOₓ-N than NHₓ-N to urban N deposition. The feasibility of using the N concentrations and δ¹⁵N values of branch bark and bark as biomarkers of N deposition thus was further confirmed through the comparative use of these bio-indicators. It can be concluded that vascular plant leaves, branch bark and bark can be used as useful biomonitoring tools for evaluating atmospheric N pollution. For further study, quantitative criteria for the practical use of these bio-indicators in response to N deposition should be developed and the differences in the δ¹⁵N values of different plant parts should also be considered, particularly in urban environments that are severely disrupted by atmospheric pollution.

Venlafaxine is an antidepressant and anti-anxiety drug that has been detected in municipal wastewater at low μg/L concentrations. In this study, the nest-defense behavior of adult male fathead minnows (Pimephales promelas) was observed in fish exposed for a full lifecycle to venlafaxine nominal concentrations of 0.88, 8.8, and 88 μg/L (i.e. 1, 9.3, 75 μg/L mean measured concentrations). Nest-defense behaviors quantified were the time taken to contact a dummy intruder fish (on a flexible stick, held near each nest) and the number of contacts made during a 1 min period. In male fathead minnows exposed to venlafaxine over a full lifecycle at environmentally relevant nominal concentrations (i.e. 0.88 and 8.8 μg/L) no significant effects were observed in behavior. However, in males exposed over a full lifecycle to the highest concentration of venlafaxine (i.e. 88 μg/L), nest-defense behaviors were increased in males with empty nests, as shown by the significantly elevated percentage of empty-nest males that made contact with the dummy intruder fish (89%) relative to the lower percentage of contacts (65%) among the Control males (p = 0.046). Lifecycle exposure to high venlafaxine (88 μg/L) caused males to over-protect their empty nests. Environmental venlafaxine concentrations are approximately 70 x lower than this, so it is unlikely that behavioral changes from venlafaxine exposure would occur in the environment. Normal nest defense behaviours in control males varied, depending on whether they were protecting empty nests or nests with eggs. Compared to Control males with empty nests, more Control males with eggs in their nests made contact with the dummy intruder fish (p = 0.014), contact was faster (i.e. <10 s, p = 0.011), and they hit the dummy intruder fish more times in 1 min (p = 0.031) This study is the first to assess reproductive behaviors in fish exposed to an antidepressant over a full lifecycle.