Despite intensive ecotoxicological research, we still know relatively little about the ecological impacts of many environmental contaminants. Filling these knowledge gaps is particularly important regarding amphibians, because they play significant roles in freshwater and terrestrial ecosystems, and their populations are declining worldwide. In this study, we investigated two pollutants that have been poorly studied in ecotoxicology despite their widespread occurrence in surface waters: the herbicide terbuthylazine and the pharmaceutical drug carbamazepine. We exposed two anuran species throughout their larval development to each of two environmentally relevant concentrations of each pollutant, and recorded mortality and 17 sub-lethal endpoints up to several months after exposure. Mortality was low and unrelated to treatment. In agile frogs (Rana dalmatina), we found that treatment with 0.3 μg/L terbuthylazine decreased tadpole activity and reduced fat bodies in juveniles, whereas treatment with 50 μg/L carbamazepine decreased spleen size and increased spleen pigmentation. In common toads (Bufo bufo), treatment with 0.003 μg/L terbuthylazine increased body mass at metamorphosis, treatment with 0.3 μg/L terbuthylazine increased the size of optic tecta, and treatment with 0.5 μg/L carbamazepine decreased hypothalamus size. Treatment with 50 μg/L carbamazepine reduced the feeding activity of toad tadpoles, decreased their production of anti-predatory bufadienolide toxins, and increased their body mass at metamorphosis; juvenile toads in this treatment group had reduced spleen pigmentation. Neither treatments affected the time to metamorphosis, post-metamorphic body mass, or sex ratios significantly. These results show that environmental levels of both terbuthylazine and carbamazepine can have several sub-lethal effects on anurans, which may be detrimental to individual fitness and population persistence in natural conditions. Our findings further highlight that toxic effects cannot be generalized between chemicals of similar structure, because the terbuthylazine effects we found do not conform with previously reported effects of atrazine, a related and extensively studied herbicide.

Recently it has been shown that there are two types of magnetite particles in the human brain, some, which occur naturally and are jagged in appearance, and others that arise from industrial sources, such as coal fired power plants, and are spherical. In order to confirm the latter, the magnetic component of coal ash is first purified and characterized by XRD, showing that it is magnetite with an average particle size of 211 nm. Studies confirm the coal ash magnetic behavior, and that the magnetite is not bound to the other components of coal ash but exist as an isolatable component. SEM studies confirm that in the process of burning coal at very high temperatures for industrial uses, the magnetite formed is spherically shaped, as recent studies of brain tissues of highly exposed urban residents have found. As such, the use of coal for industrial applications such as coking in the production of steel and in power plants is indicated to be a major source of the spherical magnetic combustion-associated magnetite fine particle and nanoparticle environmental pollution. The capacity of these magnetic particles to penetrate and damage the blood-brain-barrier and the early development of Alzheimer's disease hallmarks in exposed populations calls for detail analysis of magnetic fine and nanoparticle distribution across the world.Summation: Industrial coal usage produces spherical magnetic particles and nanoparticles, identical to those associated with neurological disorders.

Metal exposure can produce oxidative stress by disrupting the prooxidant/antioxidant balance. It has been suggested that calcium (Ca) may provide protection against metal toxicity in the organism. The objective of this study is to explore the effects of Ca availability and metal pollution on oxidative stress biomarkers in pied flycatcher (Ficedula hypoleuca) nestlings. For this purpose, we performed a Ca-supplementation experiment with birds inhabiting a Ca-poor and metal-polluted area in SW Finland. An array of oxidative stress biomarkers (GSH, GSH:GSSG ratio, GPx, GST, CAT, SOD, lipid peroxidation and protein carbonylation) was measured in red blood cells. The effects of antioxidant molecules and oxidative damage on nestling size, growth, fledging success and fledgling number were evaluated. We observed an up-regulation of GST activity and increased protein carbonyl content in the polluted zone, probably related to a combination of higher metal exposure and reduced food quantity and quality in this area. As expected, birds from the unpolluted zone showed higher GSH:GSSG ratio but, unexpectedly, also showed signs of higher lipid peroxidation (not statistically significant, p = 0.056), both responses likely being related with the lower Ca availability. Our study suggests that different measures of oxidative damage are affected by different factors: while damage to proteins was the target of metal exposure/food limitation, poor Ca availability may enhance damage to lipids in growing birds. The intercorrelations found between Ca in plasma, metal exposure and the different oxidative stress biomarkers show that the antioxidant defense is finely regulated to cope with increased oxidative challenges. Finally, our results suggest that the antioxidant status during early development, conditioned by environmental pollution and Ca availability, is one factor affecting nestling survival and fledgling number.

Diluted bitumen (dilbit) from Alberta oil sands (Canada) is transported across major continental watersheds, yet little is known about its toxicity to fish if spilled into aquatic environments. The toxicity of Cold Lake (CLB) dilbit was assessed for medaka embryos (Oryzias latipes) exposed to water accommodated fractions (WAF) and chemically-enhanced WAF (CEWAF) using Corexit®EC9500A as dispersant. The effects of CLB toxicity were similar to conventional crude oils and Access Western Blend (AWB) dilbit. The prevalence of malformations and cyp1a mRNA synthesis in hatched fish increased monotonically with concentration during WAF and CEWAF treatments and provided a novel indicator of dilbit PAH toxicity. Apart from nfe2 (an antioxidant transcription factor), there were no statistically significant monotonic exposure-responses of ahr, arnt2, cat, sod, gpx, gst, gsr, g6pdh, p53, and hsp70 transcripts at total polycyclic aromatic hydrocarbons (TPAH) concentrations bracketing EC50s for embryotoxicity (WAF ≅ 3 μg/L; CEWAF ≅ 0.1 μg/L TPAH). Based on measured TPAH concentrations in exposure test solutions, CLB dilbit was 6–10 fold more toxic to medaka than AWB during chronic exposures. Lack of direct monotonic gene transcription responses to increasing oil concentrations during exposures that were embryotoxic suggests that the capacity of the oxidative stress response is limited in earlier lifestages or that differences exist among species in mechanisms of toxicity. This study provides a comparative framework for identifying suitable biomarkers and toxicity methods for those fish species in sensitive lifestages at highest risk of Canadian oil sands dilbit exposure following a spill in the freshwater environment.

Here we proposed a battery of non-invasive biomarkers and a histological survey to examine physiological/anatomical features in embryos, eleutheroembryos (13 days post-fertilization, dpf), and larvae (28–42 dpf) of medaka to investigate the effects of embryonic exposure to propylparaben (PrP). Concentrations <1000 μg PrP/L didn't exert early or late toxic effects. However, survivorship was affected at 4000 μg/L in eleutheroembryos and at ≥1000 μg/L in larvae. Histological alterations were found in 37.5% of eleutheroembryos exposed to 4000 μg PrP/L. Morphometric analysis of the gallbladder revealed significant dilation at ≥400 μg/L throughout embryo development. Ethoxyresorufin-O-deethylase (EROD), as indicator of cytochrome P4501A activity, didn't reveal induction/inhibition although its combination with a P4501A agonist (i.e. β-naphthoflavone) resulted in a synergic EROD response. Results suggest a low toxicity of PrP for fish and support the use of fish embryos and eleutheroembryos as alternatives of in vivo biomarkers indicative of exposure/toxicity.

The morphological anomalies of the early development stages of the sea urchin Paracentrotus lividus, caused by exposure to environmental stressors, are used as biomarker in ecotoxicological and ecological investigations. Here, we reviewed the available literature and classified the embryo and larval anomalies identified so far, to highlight potential commonalities or differences related to the biological action of the different stressors and their ecological impact. Morphological anomalies are influenced by a) the developmental stage of exposure to stressors; b) the intensity of the stress; c) the intra- and inter-cellular mechanisms affected by the exposure to environmental agents. The classification and analysis of embryo and larvae anomalies, either observed by the authors of this review and reported in literature, indicate that sea urchin abnormalities, caused by exposure to different stressors, can be very similar among them and classified into 18 main types, which can occur individually or mixed. All anomalies can be used to calculate an Index of Contaminant Impact to assess the impact of multiple stressors and to identify relationships between morphological anomalies and compromised biological mechanisms. This approach could be useful for a first screening of the presence of potential stressors impairing the growth and development of the early life stages of marine organisms, thus providing a relevant advancement for in future monitoring activities devoted to assess the health status in coastal marine ecosystems.

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.

Light pollution or artificial light at night (ALAN) is increasingly recognised to be an important anthropogenic environmental pressure on wildlife, affecting animal behaviour and physiology. Early life experiences are extremely important for the development, physiological status and health of organisms, and as such, early exposure to artificial light may have detrimental consequences for organism fitness. We experimentally manipulated the light environment of free-living great tit nestlings (Parus major), an important model species in evolutionary and environmental research. Haptoglobin (Hp) and nitric oxide (NOx), as important indicators of immunity, health, and physiological condition, were quantified in nestlings at baseline (13 days after hatching) and after a two night exposure to ALAN. We found that ALAN increased Hp and decreased NOx. ALAN may increase stress and oxidative stress and reduce melatonin which could subsequently lead to increased Hp and decreased NOx. Haptoglobin is part of the immune response and mounting an immune response is costly in energy and resources and, trade-offs are likely to occur with other energetically demanding tasks, such as survival or reproduction. Acute inhibition of NOx may have a cascading effect as it also affects other physiological aspects and may negatively affect immunocompetence. The consequences of the observed effects on Hp and NOx remain to be examined. Our study provides experimental field evidence that ALAN affects nestlings' physiology during development and early life exposure to ALAN could therefore have long lasting effects throughout adulthood.