Several studies highlighted the ubiquitous presence of ibuprofen and aluminum in the aquatic environment around the world and demonstrated their potential to induce embryotoxic and teratogenic defects on aquatic species individually. Although studies that evaluate developmental alterations induced by mixtures of these pollutants are scarce; and, since environmental contamination presented in the form of a mixture of toxicants with different chemical properties and toxicity mechanisms capable of generating interactions; the objective of this study was to evaluate the developmental defects, teratogenic alterations, and oxidative stress induced by individual forms and the mixture of ibuprofen (IBU) and aluminum (Al) on zebrafish embryos. Oocytes exposed to environmentally relevant concentrations of IBU (0.1–20 μg L-1) and Al (0.01–8 mg L-1) and one binary mixture. The LC50 and EC50 were obtained to calculate the teratogenic index (TI). The IBU LC50, EC50, and TI were 8.06 μg L-1, 2.85 μg L-1 and 2.82. In contrast, Al LC50 was 5.0 mg L-1with an EC50 of 3.58 mg L-1 and TI of 1.39. The main alterations observed for individual compounds were hatching alterations, head malformation, skeletal deformities, hypopigmentation, pericardial edema, and heart rate impairment. The mixture also showed significant delays to embryonic development. Moreover, oxidative stress biomarkers of cellular oxidation and antioxidant defenses at 72 and 96 hpf significantly increased. Results show that environmentally relevant concentrations of ibuprofen (IBU), aluminum (Al), and their mixture promote a series of developmental defects, teratogenic effects, and oxidative disruption on D. rerio embryos, and the interaction of both substances altered the response. In conclusion, morphological and biochemical tests are suitable tools for assessing the health risk of aquatic wildlife by exposure to individual and mixed pollutants in freshwater bodies.

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.

To characterise the mass concentration, size-distribution, and respiratory deposition of selected trace metals (Cr, Mn, Fe, Ni, Cu, Zn, Ba, and Pb) in size-segregated PM₂.₅, a long-term monitoring campaign was undertaken at an urban background site in Como (Northern Italy). 96-h aerosol samples were collected weekly, from May 2015 to March 2016, using a 13-stage low pressure impactor and analysed via laser ablation-inductively coupled plasma-mass spectrometry. Significantly higher levels of trace metals were generally found during the heating season (two to more than four times) compared to the non-heating period at all size ranges, especially for concentrations in PM₀.₁–₁. Distinct distribution profiles characterised the different elements, even though the corresponding heating and non-heating shapes always exhibited similar features, with negligible seasonal shifts in the average mass median aerodynamic diameters. Fe, Ba, and Cu had >70% of their mass in PM₁–₂.₅, whereas Pb, Zn, and Ni showed higher contributions in the accumulation mode (>60%). Finally, broad size-distributions were found for Cr and Mn. The multiple-path particle dosimetry model estimated the overall deposition fractions in human airways varying between 27% (Pb) and 48% (Ba). The greatest deposition variability was always registered in the head region of the respiratory system, with the highest contributions for those metals predominantly accumulated in the PM₂.₅ coarse modes. In contrast, the deposition in the deepest respiratory tract maintained nearly constant proportions over time, becoming notably important for Pb, Ni, and Zn (∼13%) with respect to their total deposition. The comparison with national limits established for Pb and Ni suggested the absence of significant risks for the local population, as expected, with average concentrations two orders of magnitude lower than the corresponding annual limit and objective value. Similar findings were reported for all the other metals, for which the estimated hazard quotients were always well <1.

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.

ZnO nanoparticles (ZnO-NPs) are emerging contaminants that raise the concerns of potential risk in the aquatic environment. It has been estimated that the environmental ZnO-NPs concentration is 76 μg/l in the aquatic environment. Our aim was to determine the aquatic toxicity of ZnO-NPs with chronic exposure at environmentally relevant concentrations using the nematode Caenorhabditis elegans. Two simulated environmentally relevant mediums—moderately hard reconstituted water (EPA water) and simulated soil pore water (SSPW)—were used to represent surface water and pore water in sediment, respectively. The results showed that the ZnO-NPs in EPA water has a much smaller hydrodynamic diameter than that in SSPW. Although the ionic release of Zn ions increased time-dependently in both mediums, the Zn ions concentrations in EPA water increased two-fold more than that in SSPW at 48 h and 72 h. The ZnO-NPs did not induce growth defects or decrease head thrashes in C. elegans in either media. However, chronic exposure to ZnO-NPs caused a significant reduction in C. elegans body bends in EPA water even with a relatively low concentration (0.05 μg/l); similar results were not observed in SSPW. Moreover, at the same concentrations (50 and 500 μg/l), body bends in C. elegans were reduced more severely in ZnO-NPs than in ZnCl2 in EPA water. The ATP levels were consistently and significantly decreased, and ROS was induced after ZnO-NPs exposure (50 and 500 μg/l) in EPA water. Our results provide evidences that chronic exposure to ZnO-NPs under environmentally relevant concentrations causes metabolic and locomotive toxicities implicating the potential ecotoxicity of ZnO-NPs at low concentrations in aquatic environments.

Data concerning the effects of prenatal exposures to nonylphenol (NP) and oxidative stress on neonatal birth outcomes from human studies are limited. A total of 146 pregnant women were studied (1) to investigate the association between prenatal NP exposure and maternal oxidative/nitrative stress biomarkers of DNA damage (8-hydroxy-2’-deoxyguanosine (8-OHdG), 8-nitroguanine (8-NO2Gua)) and lipid peroxidation (8-iso-prostaglandin F2α (8-isoPF2α), 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)) and (2) to explore the associations among oxidative stress biomarkers, NP exposure, and neonatal birth outcomes, including gestational age, birth weight, length, Ponderal index, and head and chest circumferences. NP significantly increased the 8-OHdG and 8-NO2Gua levels. All infants born to mothers with urinary 8-OHdG levels above the median exhibited a significantly shorter gestational duration (Badjusted = −4.72 days; 95% CI: −8.08 to −1.36 days). No clear association was found between NP levels and birth outcomes. Prenatal 8-OHdG levels might be a novel biomarker for monitoring fetal health related to NP exposure.

Next to imposing direct lethal effects, pollutants may also indirectly impose mortality by making prey organisms more vulnerable to predation. We report that four water boatmen species differed strongly in direct endosulfan-imposed mortality, and only the species that suffered highest mortality, Sigara iactans, also showed a reduction in escape swimming speed. While head AChE activity was inhibited in all four species, body ChE was only inhibited in S. iactans where it covaried with escape swimming speed, indicating a mechanistic link between body ChE and swimming speed. Our study underscores the need for risk assessment to consider sublethal pollutant effects, which may considerably affect survival rates under natural conditions, also when testing concentrations of a pesticide that cause direct mortality. Such sublethal effects may generate discrepancies between laboratory and field studies and should be considered when designing safety factors for toxicants where the risk assessment is solely based on LC50 values.

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.

It is important to evaluate how ambient particles are deposited in the human respiratory system in view of the adverse effects they pose to human health. Traditional methods of investigating human exposure to ambient particles suffer from drawbacks related either to the lack of chemical information from particle number-based measurements or to the poor time resolution of mass-based measurements. To address these issues, in this study, human exposure to ambient particulate matter was investigated using single particle analysis, which provided chemical information with a high time resolution. Based on single particle measurements conducted in the Pearl River Delta, China, nine particle types were identified, and EC (elemental carbon) particles were determined to be the most dominant type of particle. In general, the submicron size mode was dominant in terms of the number concentration for all of the particle types, except for Na-rich and dust particles. On average, around 34% of particles were deposited in the human respiratory system with 13.9%, 7.9%, and 12.6% being distributed in the head, tracheobronchial, and pulmonary regions, respectively. The amount of Na-rich particles deposited was the highest, followed by EC. The overall deposition efficiencies of the Na-rich and dust particles were higher than those of the other particle types due to their higher efficiencies in the head region, which could be caused by the greater sedimentation and impaction rates of larger particles. In the head region, the Na-rich particles made the largest contribution (30.5%) due to their high deposition efficiency, whereas in the tracheobronchial and pulmonary regions, EC made the largest contribution due to its high concentration. In summary, the findings of this initial trial demonstrate the applicability of single particle analysis to the assessment of human exposure to ambient particles and its potential to support traditional methods of analysis.

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.