In response to the growing worldwide plastic pollution problem, the field of nanoplastics research is attempting to determine the risk of exposure to nanoparticles amidst their ever-increasing presence in the environment. Since little is known about the attributes of environmental nanoplastics (concentration, composition, morphology, and size) due to fundamental limitations in detection and quantification of smaller plastic particles, researchers often improvise by engineering nanoplastic particles with various surface modifications as models for laboratory toxicological testing. Polystyrene and other commercially available or easily synthesized polymer materials functionalized with surfactants or fluorophores are typically used for these studies. How surfactants, additives, fluorophores, the addition of surface functional groups for conjugation, or other changes to surface attributes alter toxicological profiles remains unclear. Additionally, the limited polymers used in laboratory models do not mimic the vast range of polymer types comprising environmental pollutants. Nanomaterials are tricky materials to investigate due to their high surface area, high surface energies, and their propensity to interact with molecules, proteins, and biological probes. These unique properties can often invalidate common laboratory assays. Extreme care must be taken to ensure that results are not artefactual. We have gathered zeta potential values for various polystyrene nanoparticles with different functionalization, in different solvents, from the reported literature. We also discuss the effects of surface engineering and solvent properties on interparticle interactions, agglomeration, particle-protein interactions, corona formation, nano-bio interfaces, and contemplate how these parameters might confound results. Various toxicological exemplars are critically reviewed, and the relevance and shortfalls of the most popular models used in nanoplastics toxicity studies published in the current literature are considered.

Brominated flame retardants (BFRs) are an important group of additives in plastics that increase resistance to ignition and slow down the rate of burning. Because of concerns about their environmental and human health impacts, however, some of the most widely employed BFRs, including hexabromocyclododecane (HBCD) and commercial mixtures of penta-, octa- and deca- (poly)bromodiphenyl ethers (PBDEs), have been restricted or phased out. In this review, the oceanic sources and pathways of PBDEs, the most widely used BFRs, are evaluated and quantified, with particular focus on emissions due to migration from plastics into the atmosphere versus emissions associated with the input of retarded or contaminated plastics themselves. Calculations based on available measurements of PBDEs in the environment suggest that 3.5 and 135 tonnes of PBDEs are annually deposited in the ocean when scavenged by aerosols and through air-water gas exchange, respectively, with rivers contributing a further ∼40 tonnes. Calculations based on PBDE migration from plastic products in use or awaiting or undergoing disposal yield similar net inputs to the ocean but indicate a relatively rapid decline over the next two decades in association with the reduction in the production and recycling of these chemicals. Estimates associated with the input of PBDEs to the ocean when “bound” to marine plastics and microplastics range from about 360 to 950 tonnes per year based on the annual production of plastics and PBDEs over the past decade, and from about 20 to 50 tonnes per annum based on the abundance and distribution of PBDEs in marine plastic litter. Because of the persistence and pervasiveness of plastics in the ocean and diffusion coefficients for PBDEs on the order of 10⁻²⁰ to 10⁻²⁷ m² s⁻¹, microplastics are likely to act as a long-term source of these chemicals though gradual migration. Locally, however, and more important from an ecotoxicological perspective, PBDE migration may be significantly enhanced when physically and chemically weathered microplastics are exposed to the oily digestive fluids conditions of fish and seabirds.

Bisphenol A (BPA), an endocrine-disrupting chemical that is largely produced and used in the plastics industry, causes environmental pollution and is absorbed by humans through consumption of food and liquids in polycarbonate containers. BPA exerts developmental and genetic toxicities to embryos and offsprings, but the embryotoxicity mechanism of this chemical is unclear. This study aimed to explore the toxic effect of BPA on embryonic development and elucidate its toxicity mechanism. Embryos of Xenopus laevis as a model were treated with different concentrations (0.1, 1, 10, and 20 μM) of BPA at the two-cell stage to investigate the developmental toxicity of BPA. Embryonic development and behaviors were monitored 24 h–96 h of BPA exposure. BPA concentrations greater than 1 μM exerted significant teratogenic effects on the Xenopus embryos, which showed short tail axis, miscoiled guts, and bent notochord as the main malformations. The 20 μM BPA-treated embryos were seriously damaged in all aspects and exhibited deformity, impaired behavioral ability, and tissue damage. The DNA integrity and apoptosis of the Xenopus embryos were also investigated. Exposure to BPA concentrations higher than 0.1 μM significantly induced DNA damage (p < 0.05). The 10 and 20 μM BPA-treated embryos exhibited higher levels of cleaved caspase-3 protein than the control. The ratios of bax/bcl-2 mRNA were significantly higher in the 10 μM and 20 μM-treated embryos than the ratio in the control group. Overall, data indicated that BPA can delay the early development, induce DNA damage and apoptosis, and eventually cause multiple malformations in Xenopus embryos.

One of the fundamentals in the ecotoxicological studies is the need of data comparison, which can be easily reached with the help of a standardized biological model. In this context, any biological model has been still proposed for the biomonitoring and risk evaluation of freshwaters until now. The aim of this review is to illustrate the ecotoxicological studies carried out with the zebra mussel Dreissena polymorpha in order to suggest this bivalve species as possible reference organism for inland waters. In detail, we showed its application in biomonitoring, as well as for the evaluation of adverse effects induced by several pollutants, using both in vitro and in vivo experiments. We discussed the advantages by the use of D. polymorpha for ecotoxicological studies, but also the possible limitations due to its invasive nature.

A pot experiment was conducted to investigate the solubility and redox species of antimony (Sb) in a relocated shooting range soil and its uptake by Lolium perenne L. and Holcus lanatus L. under different water regimes. After 1-week waterlogging, the total Sb concentration in soil solution decreased from ∼110 μg L−1 to <20 μg L−1, and slowly increased over the following 4 weeks, with the dissolution of Fe and Mn (hydr)oxides. In this process, half of the Sb in soil solution was reduced to Sb(III), which greatly affected the plant uptake of Sb. Waterlogging increased shoot Sb concentrations of L. perenne by ∼10 fold but decreased uptake in H. lanatus by 80%. Results indicate that Sb might primarily be taken up as Sb(III) by L. perenne and as Sb(V) by H. lanatus. Temporary waterlogging of soil may increase the risk of trace elements entering the food chain.

Assessments of antimony (Sb) and arsenic (As) contamination in sediments are reported on a wide range of different particle size fractions, including <63 μm, < 180 μm and <2 mm. Guidelines vary between jurisdictions which limits comparative assessment between contamination events and complicates ecotoxicity assessment, and almost no information exists on Sb size distribution in contaminated sediments. This study quantified and compared the size distribution of Sb and As in 11 sediments (and 2 floodplain soils) collected along 320 km of waterway contaminated by historic mining activity. Sediment particle size distribution was the primary determinant of total metalloid load in size fractions across the varying substrates of the waterway. Minerals and sorption complexes influenced metalloid particle distribution but relative importance depended on location. Arsenic concentrations were greatest in the fine <63 μm fraction across all the different river environments (7.3–189 mg kg⁻¹, or 1–26% of total sample As), attributed to fine-grained primary arsenopyrite and/or sorption of As(V) to fine solid-phases. The Sb particle size concentrations were greatest in mid-size fractions (205–903 mg kg⁻¹) in the upper catchment and up to 100 km downstream to the mid-catchment as a result of remnant Sb minerals. Antimony concentrations in the lower catchment were greatest in the <63 μm fraction (8.8–12.1 mg kg⁻¹), reflecting the increasing importance of sorption for Sb particle associations. This work demonstrates the importance of particle size analysed for assessment of sediment quality, and provides support for analysis of at least the <250 μm fraction for Sb and As when comparing pollutant distribution in events impacted by primary contamination. Analysis of the <63 μm fraction, however, provides good representation in well-dispersed contaminated sediments.

Ambient fine particulate matter (PM2.5) pollution has been implicated in the development of hypertensive disorders of pregnancy. However, evidence on the effects of PM2.5-derived chemical constituents on gestational blood pressure (BP) is limited, and the potential mechanisms underlying the association remain unclear. In this study, we repeated three consecutive 72-h personal air sampling and BP measurements in 215 pregnant women for 590 visits during pregnancy. Individual PM2.5 exposure level was assessed by gravimetric method and 28 PM2.5 chemical constituents were analyzed by ED-XRF method. Plasma biomarkers of endothelial function and inflammation were measured using multiplexed immunoassays. Robust multiple linear regression models were used to estimate the associations among personal PM2.5 exposure and chemical constituents, BP changes (compared with pre-pregnancy BP) and plasma biomarkers. Mediation analyses were performed to evaluate underlying potential pathways. Result showed that exposure to PM2.5 was significantly associated with increases in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the early second trimester. Meanwhile, elevated concentration of lead (Pb) constituent in PM2.5 was significant associated with increases in DBP and MAP after adjusting for PM2.5 total mass. PM2.5 and Pb constituent also presented positive associations with plasma biomarkers of endothelial function (ET-1, E-selectin, ICAM-1) and inflammation (IL-1β, IL-6, TNFα) significantly. After multiple adjustment, elevated ET-1 and IL-6 were significantly correlated with increased gestational BP, and respectively mediated 1.24%–25.06% and 7.01%–10.69% of the increased BP due to PM2.5 and Pb constituent exposure. In conclusion, our results suggested that personal exposure to PM2.5 and Pb constituent were significantly associated with increased BP during pregnancy, and the early second trimester might be the sensitive window of PM2.5 exposure. The endothelial dysfunction and elevated inflammation partially mediated the effect of PM2.5 and Pb constituent on BP during pregnancy.