Pollution damages ecosystems around the globe and some forms of pollution, like oil pollution, can be either man-made or derived from natural sources. Despite the pervasiveness of oil pollution, certain organisms are able to colonise polluted or toxic environments, yet we only have a limited understanding of how they are affected by it. Here, we analysed phenotypic responses to oil pollution in guppies (Poecilia reticulata) living in oil-polluted habitats across southern Trinidad. We analysed body-shape and life-history traits for 352 individuals from 11 independent populations, six living in oil-polluted environments (including the naturally oil-polluted Pitch Lake), and five stemming from non-polluted habitats. Based on theory of, and previous studies on, responses to environmental stressors, we predicted guppies from oil-polluted waters to have larger heads and shallower bodies, to be smaller, to invest more into reproduction, and to produce more but smaller offspring compared to guppies from non-polluted habitats. Contrary to most of our predictions, we uncovered strong population-specific variation regardless of the presence of oil pollution. Moreover, guppies from oil-polluted habitats were characterised by increased body size; rounder, deeper bodies with increased head size; and increased offspring size, when compared to their counterparts from non-polluted sites. This suggests that guppies in oil-polluted environments are not only subject to the direct negative effects of oil pollution, but might gain some (indirect) benefits from other concomitant environmental factors, such as reduced predation and reduced parasite load. Our results extend our knowledge of organismal responses to oil pollution and highlight the importance of anthropogenic pollution as a source of environmental variation. They also emphasise the understudied ecological heterogeneity of extreme environments.

Moxidectin is an antiparasitic drug belonging to the class of the macrocyclic lactones, subgroup mylbemicins. It is used worldwide in veterinary practice, but little is known about its potential environmental risks. Thus, we used the zebrafish embryo as a model system to study the potential effects of moxidectin on aquatic non-target organisms. The analyses were performed in two experimental sets: (1) acute toxicity and apical endpoints were characterized, with biomarker assays providing information on the activity levels of catalase (CAT), glutathione S-transferase (GST), lactate dehydrogenase (LDH), and acetylcholinesterase (AChE); and (2) internal concentration and spatial distribution of moxidectin were determined using ultraperformance liquid chromatography quadrupole-time-of-flight mass spectrometry (UPLC-QToF-MS) and matrix-assisted laser desorption/ionization-MS imaging (MALDI-MSi). The acute toxicity to zebrafish embryos (96 hpf) appeared mainly as a decrease in hatching rates (EC₅₀ = 20.75 μg/L). It also altered the enzymatic activity of biomarker enzymes related to xenobiotic processing, anaerobic metabolism, and oxidative stress (GST, LDH, and CAT, respectively) and strongly accumulated in the embryos, as internal concentrations were 4 orders of magnitude higher than those detected in exposure solutions. MALDI-MSi revealed accumulations of the drug mainly in the head and eyes of the embryos (72 and 96 hpf). Thus, our results show that exposure to moxidectin decreases hatching success by 96 h and alters biochemical parameters in the early life stages of zebrafish while accumulating in the head and eye regions of the animals, demonstrating the need to prioritize this compound for environmental studies.

To evaluate pesticide regulatory standards in agricultural crops, we introduced a regulatory modeling framework that can flexibly evaluate a population’s aggregate exposure risk via maximum residue levels (MRLs) under good agricultural practice (GAP). Based on the structure of the aggregate exposure model and the nature of variable distributions, we optimized the framework to achieve a simplified mathematical expression based on lognormal variables including the lognormal sum approximation and lognormal product theorem. The proposed model was validated using Monte Carlo simulation, which demonstrates a good match for both head and tail ends of the distribution (e.g., the maximum error = 2.01% at the 99th percentile). In comparison with the point estimate approach (i.e., theoretical maximum daily intake, TMDI), the proposed model produced higher simulated daily intake (SDI) values based on empirical and precautionary assumptions. For example, the values at the 75th percentile of the SDI distributions simulated from the European Union (EU) MRLs of 13 common pesticides in 12 common crops were equal to the estimated TMDI values, and the SDI values at the 99th percentile were over 1.6-times the corresponding TMDI values. Furthermore, the model was refined by incorporating the lognormal distributions of biometric variables (i.e., food intake rate, processing factor, and body weight) and varying the unit-to-unit variability factor (VF) of the pesticide residues in crops. This ensures that our proposed model is flexible across a broad spectrum of pesticide residues. Overall, our results show that the SDI is significantly reduced, which may better reflect reality. In addition, using a point estimate or lognormal PF distribution is effective as risk assessments typically focus on the upper end of the distribution.

Triclosan (TCS) is an organic compound with a wide range of antibiotic activity and has been widely used in items ranging from hygiene products to cosmetics; however, recent studies suggest that it has several adverse effects. In particular, TCS can be passed to both fetus and infants, and while some evidence suggests in vitro neurotoxicity, there are currently few studies concerning the mechanisms of TCS-induced developmental neurotoxicity. Therefore, this study aimed to clarify the effect of TCS on neural development using zebrafish models, by analyzing the morphological changes, the alterations observed in fluorescence using HuC-GFP and Olig2-dsRED transgenic zebrafish models, and neurodevelopmental gene expression. TCS exposure decreased the body length, head size, and eye size in a concentration-dependent manner in zebrafish embryos. It increased apoptosis in the central nervous system (CNS) and particularly affected the structure of the CNS, resulting in decreased synaptic density and shortened axon length. In addition, it significantly up-regulated the expression of genes related to axon extension and synapse formation such as α1-Tubulin and Gap43, while decreasing Gfap and Mbp related to axon guidance, myelination and maintenance. Collectively, these changes indicate that exposure to TCS during neurodevelopment, especially during axonogenesis, is toxic. This is the first study to demonstrate the toxicity of TCS during neurogenesis, and suggests a possible mechanism underlying the neurotoxic effects of TCS in developing vertebrates.

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.

It is well-known that the health effects of PM increase as particle size decreases: particularly, great concern has risen on the role of UltraFine Particles (UFPs). Starting from the knowledge that the main fraction of atmospheric aerosol in Rome is characterized by significant levels of PM2.5 (almost 75% of PM10 fraction is PM2.5), the paper is focused on submicron particles in such great urban area. The daytime/nighttime, work-/weekdays and cold/hot seasonal trends of submicron particles will be investigated and discussed along with NOx and total PAH drifts demonstrating the primary origin of UFPs from combustion processes. Furthermore, moving from these data, the total dose of submicron particles deposited in the respiratory system (i.e., head, tracheobronchial and alveolar regions in different lung lobes) has been estimated. Dosimeter estimates were performed with the Multiple-Path Particle Dosimetry model (MPPD v.2.1). The paper discusses the aerosol doses deposited in the respiratory system of individuals exposed in proximity of traffic. During traffic peak hours, about 6.6 × 1010 particles are deposited into the respiratory system. Such dose is almost entirely made of UFPs. According to the greater dose estimated, right lung lobes are expected to be more susceptible to respiratory pathologies than left lobes.

Insufficient evidence exists regarding the effects of microplastics (MPs) on the neuronal toxicity of heavy metals in the early stages of organisms. Herein, the effects of micro-polystyrene (μ-PS; 157 μm) and nano-polystyrene (n-PS; 100 nm) particles on the neurodevelopmental toxicity of mercury (Hg) in zebrafish embryos were compared. Zebrafish embryos exposed to Hg at the concentration of 0.1 mg L⁻¹ revealed blood disorders, delayed hatching, and malformations such as pericardial oedema and tail deformity. The length of the larval head was significantly reduced (P < 0.01) and in vivo expression of atoh1a in the cerebellum of neuron-specific transgenic zebrafish Tg(atoh1a:dTomato) larvae was inhibited by 29.46% under the Hg treatment. Most of the toxic effects were inhibited by the combined exposure to μ-PS or n-PS with Hg, and n-PS decreased the neurodevelopmental toxicity of Hg more significantly than μ-PS. Metabolomic analysis revealed that in addition to inhibiting the amino acid metabolism pathway as in the μ-PS+Hg treatment, the n-PS+Hg treatment inhibited unsaturated fatty acid metabolism in zebrafish larvae, likely because of a greater reduction in Hg bioavailability, thus reducing the oxidative damage caused by Hg in the larvae. The combined effects of MPs and heavy metals differ greatly among different species and their targeted effects. We conclude that the combined toxicity mechanisms of MPs and heavy metals require further clarification.

Fumonisin B1 (FB1) is a neurodegenerative mycotoxin synthesized by Fusarium spp., but the potential neurobehavioral toxicity effects in organisms have not been characterized clearly. Caenorhabditis elegans (C. elegans) has emerged as a promising model organism for neurotoxicological studies due to characteristics such as well-functioning nervous system and rich behavioral phenotypes. To investigate whether FB1 has neurobehavioral toxicity effects on C. elegans, the motor behavior, neuronal structure, neurotransmitter content, and gene expression related with neurotransmission of C. elegans were determined after exposed to 20–200 μg/mL FB1 for 24 h and 48 h, respectively. Results showed that FB1 caused behavioral defects, including body bends, head thrashes, crawling distance, mean speed, mean amplitude, mean wavelength, foraging behavior, and chemotaxis learning ability in a dose-, and time-dependent manner. In addition, when C. elegans was exposed to FB1 at a concentration of 200 μg/mL for 24 h and above 100 μg/mL for 48 h, the GABAergic and serotonergic neurons were damaged, but no effect on dopaminergic, glutamatergic, and cholinergic neurons. The relative content of GABA and serotonin decreased significantly. Furthermore, abnormal expression of mRNA levels associated with GABA and serotonin were found in nematodes treated with FB1, such as unc-30, unc-47, unc-49, exp-1, mod-5, cat-1, and tph-1. The neurobehavioral toxicity effect of FB1 may be mediated by abnormal neurotransmission of GABA and serotonin. This study provides useful information for understanding the neurotoxicity of FB1.