The seasonal variation, spatial distribution, and ecological risks of thirteen organophosphate pesticides (OPPs) were studied in the Sundays and Swartkops estuaries in South Africa. Ten pesticides were detected in surface water samples from both estuaries, while all OPPs were detected in sediments. The highest concentration of OPPs (18.8 μg pyrazophos L⁻¹) was detected in surface water samples from Swartkops Estuary, while 48.7 μg phosalone kg⁻¹ dw was the highest in sediments collected from Sundays Estuary. There was no clear seasonal pattern in OPPs occurrence in surface water from both systems. However, their occurrence in sediments was in the following order: winter > autumn > summer > spring, perhaps indicating major pesticide input in the winter seasons. Results from ecological risk assessment showed that pyraclofos and chlorpyrifos (CHL) in surface water from both systems are respectively likely to cause high acute and chronic toxicity to fish (risk quotient – RQ > 1). For sediments of both estuaries, the highest acute and chronic RQs for fish were calculated for isazophos and CHL respectively. The majority of the detected OPPs in sediments posed potential high risks to Daphnia magna from both systems. These results suggest that these aquatic organisms (fish, and Daphnia), if present in the studied estuaries, can develop certain forms of abnormalities due to OPP exposure. To this end, proper measures should be taken to reduce OPP input into the estuarine systems.

Ciprofloxacin (CFX) and ofloxacin (OFX) are two of the most often used fluoroquinolone antibiotics, and their residues are found in large amounts in various aquatic settings. However, the toxicity tests of CFX using eukaryotic organisms such as Daphnia magna are inadequate, and the test result of OFX is currently unknown. Therefore, the chronic toxicity test for D. magna was performed during 42 days under exposure to CFX and OFX concentrations of 50, 500, and 5000 μg L⁻¹. All exposure conditions did not cause mortality for D. magna. CFX exposure at 500 μg L⁻¹ resulted in an earlier oogenesis date and increased brood size in the second birth. The Poisson-based generalized linear mixed-effects model revealed that the reduction of fertility was statistically significant for the CFX and OFX exposures at 5000 μg L⁻¹. On the other hand, the production of dead eggs as offspring degradation was also found significantly as maternal D. magna exposed to antibiotics at 5000 μg L⁻¹. In addition, following long-term exposure to antibiotics, maternal adaptation to antibiotics was established for offspring deterioration and fertility. However, the OFX exposure showed that the fertility-suppressed effects continued for a longer period than the CFX exposure. Although no rational explanation has yet been given for the more substantial effect of OFX on reducing fertility than CFX, molecular cell biology and symbiotic microbial flora derived from previous studies could explain our ecotoxicological results. This study is the first report for the OFX chronic toxicities on D. magna by comparing it to the toxicity of CFX. Our study contributes to guiding the future impact assessment of fluoroquinolone antibiotic pollution on ecosystems, including the need for new statistical methods in ecotoxicological studies.

There is limited information regarding the toxicity of the trace element thallium (Tl) to aquatic biota, most of which assesses acute toxicity and bioaccumulation. The relative lack of chronic Tl toxicity data compromises the establishment of water quality criteria for this trace metal. In the presented work, chronic toxicity endpoints (final body weight (a proxy measure of growth), survival, and reproduction) and Tl body burden were measured in the freshwater crustacean Daphnia magna during a 21-day exposure to dissolved Tl. Thallium caused complete mortality in daphnids between exposure concentrations of 424 and 702 μg L⁻¹. In contrast with previously published work examining acute Tl toxicity, exposure to Tl for 21 days was not associated with changes in whole-body potassium concentration. This was despite a 710-fold increase in Tl body burden in animals exposed to 424 μg L⁻¹ relative to the control. Median effect concentrations (EC₅₀’s) for growth and reproduction (total neonates produced), were 1.6 (95% confidence interval: 1.0–3.1) and 11.1 (95% confidence interval: 5.5–21.8) μg Tl L⁻¹, respectively. A no observable effect concentration (NOEC) of 0.9 μg Tl L⁻¹ for growth, and a NOEC range of 0.9–83 μg Tl L⁻¹ for a variety of reproductive metrics, was measured. A lowest observable effect concentration (LOEC) of 8.8 μg Tl L⁻¹ was determined for the effects of Tl on growth and most of the reproductive endpoints examined. These data indicate that under controlled laboratory conditions D. magna is significantly less sensitive to Tl than the species on which the current Canadian Council of Ministers of the Environment regulatory guideline value of 0.8 μg L⁻¹ is based.

Several environmental pollutants, including pesticides, herbicides and persistent organic pollutants play an important role in the development of chronic diseases. However, most studies have examined environmental pollutants toxicity in target organisms or using a specific toxicological test, losing the real effect throughout the ecosystem. In this sense an integrative environmental risk of pollutants assessment, using different model organisms is necessary to predict the real impact in the ecosystem and implications for target and non-target organisms.The objective of this study was to use alachlor, a chloroacetanilide herbicide responsible for chronic toxicity, to understand its impact in target and non-target organisms and at different levels of biological organization by using several model organisms, including membranes of dipalmitoylphosphatidylcholine (DPPC), rat liver mitochondria, bacterial (Bacillus stearothermophilus), plant (Lemna gibba) and mammalian cell lines (HeLa and neuro2a).Our results demonstrated that alachlor strongly interacted with membranes of DPPC and interfered with mitochondrial bioenergetics by reducing the respiratory control ratio and the transmembrane potential. Moreover, alachlor also decreased the growth of B. stearothermophilus and its respiratory activity, as well as decreased the viability of both mammalian cell lines. The values of TC₅₀ increased in the following order: Lemna gibba < neuro2a < HeLa cells < Bacillus stearothermophilus. Together, the results suggest that biological membranes constitute a putative target for the toxic action of this lipophilic herbicide and point out the risks of its dissemination on environment, compromising ecosystem equilibrium and human health.

Some of the older Swedish roads contain road tar underneath a surface layer of bituminous asphalt. This road tar, also known as tar asphalt, contains large amounts of polycyclic aromatic hydrocarbons (PAHs). There is concern about PAHs spreading from the bottom layers of these older roads to the surrounding environment, and that because of this spreading road tar asphalt should not be recycled but rather placed in landfills. However, a risk assessment of PAH spreading below roads has not yet been conducted. The first aim of this study was to assess this potential spreading of PAHs from underlying tar asphalt to the sand beneath, the soil next to the roads, as well as nearby groundwater. The second aim was to measure the bioavailability and estimate the toxicity of PAHs in all relevant media using polyoxymethylene (POM) passive samplers. Four road sections and nearby groundwater in northern Sweden were investigated, including a control road without tar asphalt. PAHs were detected in all analysed solid media at varying concentrations: in asphalt from 2.3 to 4800 mg kg⁻¹, in underlying sand from <1.5 to 460 mg kg⁻¹ and in slope soil from <1.5 to 36 mg kg⁻¹. However, the spread of PAHs from the asphalt to roadside soil and groundwater was very limited. Groundwater at most of the road sections contained very low or non-detectable levels of PAHs (<0.08–0.53 μg L⁻¹, excluding one site where fuel contamination is hypothesized). The PAHs generally showed low bioavailability. Only asphalt with PAH content >1200 mg kg⁻¹ exhibited bioavailable concentrations that exceeded threshold concentrations for serious risk. The most PAH contaminated sand and soil samples exhibited low toxicity when considering bioavailability, only in some cases exceeding chronic toxicity threshold concentrations. These results were compared with the Swedish EPA's guideline values for PAH in contaminated soil, which is shown to overpredict toxicity for these sites. Further research on the leaching and transportation processes of PAHs from subsurface tar asphalt is recommended for developing risk analysis approaches.

A chemical contaminant of growing concern to freshwater aquatic organisms, including many amphibians, is chloride ion. The salinization of freshwater ecosystems is likely caused, in part, by the application of massive amounts of road de-icing salts to roadways during winter months. The issue of freshwater salinization has become the subject of many toxicity studies and is often investigated in conjunction with other chemical stressors. However, few published studies attempt to investigate the interactions of elevated chloride concentration and increased temperature. Further, no studies have investigated the gap between the recommended feeding conditions typically used in standard toxicity tests and those that may exist in natural amphibian habitats. This study addressed the critical issues of elevated chloride, increased temperature, and variation in food quality. We conducted a 96-h acute toxicity test to investigate acute chloride toxicity as impacted by different diets, as well as a chronic toxicity test to investigate the impacts of chloride, temperature, and resource quality on the survival and development of larval Lithobates sylvaticus (wood frogs). Chloride LC₅₀s ± 1 SE were 3769.22 ± 589.05, 2133.00 ± 185.95, and 2644.69 ± 209.73 mg Cl⁻/L were for non-fed, low-protein diet, and high-protein diet, respectively. For the chronic toxicity study, elevated chloride decreased tadpole survival. Increased temperature, and lower resource quality, were found negatively impacted survival of tadpoles and altered time-to-metamorphosis. This study shows that environmentally relevant concentrations of chloride, temperatures, and the protein content of the diet all exert critical effects on larval wood frogs.

This study aimed to investigate the effect of mono-(2-ethylhexyl) phthalate (MEHP), one of the major phthalate metabolites that are widespread in aquatic environments, on reproductive dysfunction, particularly on endocrine activity in adult male and female zebrafish. For 21 days, the zebrafish were exposed to test concentrations of MEHP (0, 2, 10, and 50 μg/mL) that were determined based on the effective concentrations (ECx) for zebrafish embryos. Exposure to 50 μg/mL MEHP in female zebrafish significantly decreased the number of ovulated eggs as well as the hepatic VTG mRNA abundance when those of the control group. Meanwhile, in female zebrafish, the biosynthetic concentrations of 17β-estradiol (E2) and the metabolic ratio of androgen to estrogen were remarkably increased in all MEHP exposed group compared with those in the control group, along with the elevated levels of cortisol. However, no significant difference was observed between these parameters in male zebrafishes. Therefore, exposure to MEHP causes reproductive dysfunction in female zebrafishes and this phenomenon can be attributed to the alteration in endocrine activities. Moreover, the reproductive dysfunction in MEHP-exposed female zebrafishes may be closely associated with stress responses, such as elevated cortisol levels. To further understand the effect of MEHP on the reproductive activities of fish, follow-up studies are required to determine the interactions between endocrine activities and stress responses. Overall, this study provides a response biomarker for assessing reproductive toxicity of endocrine disruptors that can serve as a methodological approach for an alternative to chronic toxicity testing.

Nickel and cobalt are essential elements that become toxic at high concentrations. Little is known about nickel and cobalt toxicity in aquatic animals. This study aimed to investigate acute and chronic toxicity of nickel and cobalt in Japanese flounder (Paralichthys olivaceous), with emphasis on oxidative stress reactions, histopathological changes, and differences in gene expression. The lethal concentration for 50% mortality (LC₅₀) in 3 and 8 cm Japanese flounder exposed to nickel for 96 h was found to be 86.2 ± 0.018 and 151.3 ± 0.039 mg/L; for cobalt exposure, LC₅₀ was 47.5 ± 0.015 and 180.4 ± 0.034 mg/L, respectively. Chronic nickel and cobalt exposure caused different degrees of oxidative enzyme activity changes in gill, liver, and muscle tissues. Erythrocyte deformations were detected after acute or chronic exposure to nickel and cobalt. the nickel and cobalt exposure also caused pathological changes such as spherical swelling over other gill patches, rod-like proliferations in the gill patch epithelial cell layer, and disorder in hepatocyte arrangement, cell swelling, and cytoplasm loosening. RNA-Seq indicated that there were 184 upregulated and 185 downregulated genes in the liver of Japanese flounder exposed to 15 mg/L nickel for 28 d. For cobalt, 920 upregulated and 457 downregulated genes were detected. Among these differentially expressed genes, 162 were shared by both nickel and cobalt exposure. In both nickel and cobalt, pathways including fatty acid elongation, steroid biosynthesis, unsaturated fatty acid biosynthesis, fatty acid metabolism, PPAR signaling, and ferroptosis were significantly enriched. Taken together, these results aided our understanding of the toxicity of nickel and cobalt in aquatic animals.