Metal pollution is a growing concern that affects the health of humans and animals globally. Copper is an essential insect micronutrient required for respiration, pigmentation and oxidative stress protection but can also act as a potentially toxic trace element. While several studies have focused on the negative fitness effects of copper on the aquatic larvae of mosquitoes, the effects of larval copper exposure on adult mosquito fitness (i.e., survival and fecundity) and their ability to transmit parasites (i.e., vector competence) remains unclear. Here, using a well-studied model vector-parasite system, the mosquito Aedes aegypti and parasite Dirofilaria immitis, we show that sublethal copper exposure in larval mosquitoes alters adult female fecundity and vector competence. Specifically, mosquitoes exposed to copper had a hormetic fecundity response and mosquitoes exposed to 600 μg/L of copper had significantly fewer infective parasite larvae than control mosquitoes not exposed to copper. Thus, exposure of mosquito larvae to copper levels far below EPA-mandated safe drinking water limits (1300 μg/L) can impact vector-borne disease dynamics not only by reducing mosquito abundance (through increased larval mortality), but also by reducing parasite transmission risk. Our results also demonstrated that larval copper is retained through metamorphosis to adulthood in mosquitoes, indicating that these insects could transfer copper from aquatic to terrestrial foodwebs, especially in urban areas where they are abundant. To our knowledge this is the first study to directly link metal exposure with vector competence (i.e., ability to transmit parasites) in any vector-parasite system. Additionally, it also demonstrates unequivocally that mosquitoes can transfer contaminants from aquatic to terrestrial ecosystems. These results have broad implications for public health because they directly linking contaminants and vector-borne disease dynamics, as well as linking mosquitoes and contaminant dynamics.

The Antarctic continent is among the most pristine regions; yet various organic contaminants have been measured there routinely. Air and snow samples were collected during the austral spring (October–November, 2010) along the western Antarctic Peninsula and analyzed for organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) to assess the relative importance of long-range transport versus local primary or secondary emissions. Highest concentrations of PCBs, PBDEs and DDTs were observed in the glacier’s snow sample, highlighting the importance of melting glaciers as a possible secondary source of legacy pollutants to the Antarctic. In the atmosphere, contaminants were mainly found in the vapor phase (>65%). Hexachlorobenzene (33.6 pg/m3), PCBs (11.6 pg/m3), heptachlor (5.64 pg/m3), PBDEs (4.22 pg/m3) and cis-chlordane (2.43 pg/m3) were the most abundant contaminants. In contrast to other compounds, PBDEs seem to have originated from local sources, possibly the research station itself. Gas-particle partitioning for analytes were better predicted using the adsorption partitioning model than an octanol-based absorption approach. Diffusive flux calculations indicated that net deposition is the dominant pathway for PBDEs and chlordanes, whereas re-volatilization from snow (during melting or metamorphosis) was observed for PCBs and some OCPs.

Both amphibian metamorphosis assay (AMA) and larval amphibian growth and development assay (LAGDA) can detect thyroid-mediated modality and adversity on the basis of morphological changes during the thyroid hormone-dependent metamorphosis. They are used for identification of thyroid hormone system disrupting chemicals (TDCs) for non-target organisms or the environment. The EU Guidance recommends that the AMA and the LAGDA should be used to address sufficient investigation of the thyroid-mediated modality and adversity, respectively. In the EU discussions over identification of TDCs, the necessity of using LAGDA as a follow-up of positive results of the AMA has been questioned because of the overlap between the endpoints and the exposure of both tests. This study analyzed similarities, differences, and sensitivity of these two assays in detection of TDCs. For agonists and most of antagonists of the hypothalamic-pituitary-thyroid (HPT) axis, both AMA and LAGDA can detect the thyroid-mediated modality and adversity. The LAGDA, as a follow-up of the positive results of the AMA, may not be needed because the results of AMA are considered enough for identification of TDCs. For chemicals like inhibitors of iodotyrosine deiodinase, the LAGDA is considered necessary for identification of TDCs because the thyroid-mediated adversity cannot be detected until Nieuwkoop and Faber (NF) stage 62. Incorporation of mechanistic endpoints into existing test guidelines and the use of Xenopus Eleutheroembryo Thyroid Assay (XETA), extended amphibian metamorphosis assay (EAMA) and adverse outcome pathways (AOPs) for testing and identification of TDCs are further discussed.

Organisms that rely on aquatic habitats in roaded landscapes face a growing array of consequences from pollution, especially due to freshwater salinization. Critically, these consequences can vary from population to population depending on exposure histories and evolutionary responses. Prior studies using transplant and common garden experiments have found that aquatic-stage wood frogs (Rana sylvatica) from roadside populations are less fit in the wild and more sensitive to road salt than their counterparts from woodland populations away from roads. While this pattern is consistent with local maladaptation, unresolved insights into the timing and duration of these effects leave open the possibility that negative outcomes are countered during development. Here, we asked whether the survival disadvantage of roadside wood frogs is stage-specific, and whether this disadvantage reverses before metamorphosis. We used a common garden road salt exposure experiment and a field-based reciprocal transplant experiment to examine differences in survival across life-history stage and with respect to population type. In each experimental context, roadside embryos showed a survival disadvantage relative to woodland embryos, and this disadvantage was not reversed prior to metamorphosis. We also found that salt exposure delayed metamorphosis more strongly for roadside than woodland populations. Together, these results suggest that local maladaptation in aquatic-stage wood frogs is driven by embryonic sensitivity to salt and that roadside populations are further compromised by delayed developmental rates. Future studies should consider which embryonic traits fail to adapt to salt toxicity, and how those traits might correlate with terrestrial trait variation.

There is growing evidence of widespread contamination of freshwater ecosystems with microplastics. However, the effects of chronic microplastic ingestion and its interaction with other pollutants and stress factors on the life-history traits and the host-microbiome of aquatic invertebrates are not well understood. This study investigates the effects of exposure to sediment spiked with 1 μm polystyrene-based latex microplastic spheres, an environmentally realistic concentration of a pyrethroid pesticide (esfenvalerate), and a combination of both treatments on the life-history traits of the benthic-dwelling invertebrate, Chironomus riparius and its microbial community. The chironomid larvae were also exposed to two food conditions: abundant or limited food in the sediment, monitored for 28 and 34 days respectively. The microplastics and esfenvalerate had negative effects on adult emergence and survival, and these effects differed between the food level treatments. The microbiome diversity was negatively affected by the exposure to microplastics, while the relative abundances of the four top phyla were significantly affected only in the high food level treatment. Although the combined exposure to microplastics and esfenvalerate showed some negative effects on survival and emergence, there was little evidence for synergistic effects when compared to the single exposure. The food level affected all life-history traits and the microbiota, and lower food levels intensified the negative effects of the exposure to microplastics, esfenvalerate and their combination. We argue that these pollutants can affect crucial life-history traits such as successful metamorphosis and the host-microbiome. Therefore, it should be taken into consideration for toxicological assessment of pollutant acceptability. Our study highlights the importance of investigating possible additive and synergic activities between stressors to understand the effects of pollutants in the life story traits and host-microbiome.

Metabolic disorders induced by endocrine disruptors (ED) may contribute to amphibian population declines but no transgenerational studies have evaluated this hypothesis. Here we show that Xenopus tropicalis, exposed from the tadpole stage, to the ED benzo[a]pyrene (BaP, 50 ng.L⁻¹) produced F2 progeny with delayed metamorphosis and sexual maturity. At the adult stage, F2–BaP females displayed fatty liver with inflammation, tissue disorganization and metabolomic and transcriptomic signatures typical of nonalcoholic steato-hepatitis (NASH). This phenotype, similar to that observed in F0 and F1 females, was accompanied by a pancreatic insulin secretory defect. Metabolic disrupted F2–BaP females laid eggs with metabolite contents significantly different from the control and these eggs did not produce viable progeny. This study demonstrated that an ED can induce transgenerational disruption of metabolism and population collapse in amphibians under laboratory conditions. These results show that ED benzo[a]pyrene can impact metabolism over multiple generations and support epidemiological studies implicating environmental EDs in metabolic diseases in humans.

Changing light conditions due to human activities represents an important emerging environmental concern. Although changes to natural light conditions can be independently detrimental, in nature, organisms commonly face multiple stressors. To understand the consequences of altered light conditions, we exposed a model amphibian (wood frog; Lithobates sylvaticus) to a control and two anthropogenic light conditions: intensified daytime illuminance and artificial light at night - ALAN (intensified daytime illuminance + extended photoperiod). We measured (1) metrics of fitness (hatching success as well as survival to, size at, and time to metamorphosis) (2) susceptibility (time to death) to a commonly co-occurring anthropogenic stressor, road salt (NaCl) and (3) susceptibility (infection load) to a common parasite (trematode). We also explored behavioral (swimming activity) and physiological (baseline corticosterone (CORT) release rates) changes induced by these light conditions, which may mediate changes in the other measured parameters. We found that both intensified daytime illuminance and ALAN reduced hatching success. In contrast, for amphibians that successfully hatched, neither treatment affected amphibian survival or time to metamorphosis but individuals exposed to ALAN were larger at metamorphosis. The light treatments also had marginal effects; individuals in ALAN treatments were more susceptible to NaCl and trematodes. Finally, tadpoles exposed to ALAN moved significantly less than tadpoles in the control and intensified daytime illuminance treatments, while light had no effect on CORT release rate. Overall, changes in light conditions, in particular ALAN, significantly impacted an amphibian model in laboratory conditions. This work underscores the importance of considering not only the direct effects of light on fitness metrics but also the indirect effects of light with other abiotic and biotic stressors. Anthropogenic-induced changes to light conditions are expected to continue increasing over time so understanding the diverse consequences of shifting light conditions will be paramount to protecting wildlife populations.

The use of insecticides based on metabolites found in live organisms, such as the insecticide spinosad, has been an option for the control of agricultural pests because of the allegedly low toxicological risk for nontarget arthropods, such as stingless bees. In the current study, we evaluate the effects of chronic oral exposure to spinosad during the larval phase on survival, developmental time, body mass, midgut epithelial remodeling, and the peritrophic matrix (PM) of Partamona helleri stingless bee workers. Worker larvae that were raised in the laboratory were orally exposed to different concentrations (0, 6.53, 13.06, 32.64, and 3,264 ng. a.i. bee⁻¹) of spinosad (formulation), and the resulting survival, developmental time, and body mass were studied. The concentration of spinosad recommended for use in the field (3,264 ng. a.i. bee⁻¹) reduced the survival of workers during development. Also, sublethal concentrations of spinosad delayed the development and caused morphological changes in the midgut epithelium. Finally, the chronic exposure of larvae to 32.64 ng. a.i. bee⁻¹ spinosad also altered the remodeling of the midgut during metamorphosis and affected the organization of the PM of larvae, pupae, and adults. Our data suggest possible environmental risks for using spinosad in cultures that are naturally pollinated by stingless bees.

In the marine environment, most bivalve species base their reproduction on external fertilization. Hence, gametes and young stages face many threats, including exposure to plastic wastes which represent more than 80% of the debris in the oceans. Recently, evidence has been produced on the presence of nanoplastics in oceans, thus motivating new studies of their impacts on marine life. Because no information is available about their environmental concentrations, we performed dose-response exposure experiments with polystyrene particles to assess the extent of micro/nanoplastic toxicity. Effects of polystyrene with different sizes and functionalizations (plain 2-μm, 500-nm and 50-nm; COOH-50 nm and NH₂-50 nm) were assessed on three key reproductive steps (fertilization, embryogenesis and metamorphosis) of Pacific oysters (Crassostrea gigas). Nanoplastics induced a significant decrease in fertilization success and in embryo-larval development with numerous malformations up to total developmental arrest. The NH₂-50 beads had the strongest toxicity to both gametes (EC₅₀ = 4.9 μg/mL) and embryos (EC₅₀ = 0.15 μg/mL), showing functionalization-dependent toxicity. No effects of plain microplastics were recorded. These results highlight that exposures to nanoplastics may have deleterious effects on planktonic stages of oysters, presumably interacting with biological membranes and causing cyto/genotoxicity with potentially drastic consequences for their reproductive success.

How exposure to contaminants may interfere with the widespread poleward range expansions under global warming is largely unknown. Pesticide exposure may negatively affect traits shaping the speed of range expansion, including traits related to population growth rate and dispersal-related traits. Moreover, rapid evolution of growth rates during poleward range expansions may come at a cost of a reduced investment in detoxification and repair thereby increasing the vulnerability to contaminants at expanding range fronts. We tested effects of a sublethal concentration of the widespread pesticide chlorpyrifos on traits related to range expansion in replicated edge and core populations of the poleward moving damselfly Coenagrion scitulum reared at low and high food levels in a common garden experiment. Food limitation in the larval stage had strong negative effects both in the larval stage and across metamorphosis in the adult stage. Exposure to chlorpyrifos during the larval stage did not affect larval traits but caused delayed effects across metamorphosis by increasing the incidence of wing malformations during metamorphosis and by reducing a key component of the adult immune response. There was some support for an evolutionary trade-off scenario as the faster growing edge larvae suffered a higher mortality during metamorphosis. Instead, there was no clear support for the faster growing edge larvae being more vulnerable to chlorpyrifos. Our data indicate that sublethal delayed effects of pesticide exposure, partly in association with the rapid evolution of faster growth rates, may slow down range expansions.