peer reviewed | Previous studies described high concentrations of mercury (Hg) and selenium (Se) in the blood of harbour seals, Phoca vitulina from the North Sea. In the present study, we evaluated the in vitro potential protective effects of sodium selenite (Na2SeO3) and selenomethionine (SeMet) on cell proliferation of harbour seal lymphocytes exposed to MeHgCl 0.75 µM. In vitro exposure of ConA-stimulated T lymphocytes resulted in severe inhibition of DNA synthesis, likely linked to severe loss of mitochondrial membrane potential at 0.75 µM. Neither selenite nor SeMet showed a protective effect against MeHg toxicity expressed at the T lymphocyte proliferation level for harbour seals. Selenite and SeMet did not show negative effects regarding lymphocyte proliferation and mitochondrial membrane potential. To conclude, our results clearly demonstrated that MeHg affected in vitro immune cells exposure with no protective effects of selenium at a molar ratio Hg:Se of 1:10 in harbour seals from the North Sea.

International audience | Food additives are one major hallmark of ultra-processed food in the Western-diet, a food habit often associated with metabolic disorders. Among these additives, the whitener and opacifying agent titanium dioxide (TiO2) raises public health issues due to the ability of TiO2 nanoparticles (NPs) to cross biological barriers and accumulate in different systemic organs like spleen, liver and pancreas. However before their systemic passage, the biocidal properties of TiO2 NPs may alter the composition and activity of the gut microbiota, which play a crucial role for the development and maintenance of immune functions. Once absorbed, TiO2 NPs may further interact with immune intestinal cells involved in gut microbiota regulation. Since obesity-related metabolic diseases such as diabetes are associated with alterations in the microbiota-immune system axis, this raises questions about the possible involvement of long-term exposure to food-grade TiO2 in the development or worsening of these diseases. The current purpose is to review the dysregulations along the gut microbiota-immune system axis after oral TiO2 exposure compared to those reported in obese or diabetic patients, and to highlight potential mechanisms by which foodborne TiO2 NPs may increase the susceptibility to develop obesity-related metabolic disorders.

International audience | Food additives are one major hallmark of ultra-processed food in the Western-diet, a food habit often associated with metabolic disorders. Among these additives, the whitener and opacifying agent titanium dioxide (TiO2) raises public health issues due to the ability of TiO2 nanoparticles (NPs) to cross biological barriers and accumulate in different systemic organs like spleen, liver and pancreas. However before their systemic passage, the biocidal properties of TiO2 NPs may alter the composition and activity of the gut microbiota, which play a crucial role for the development and maintenance of immune functions. Once absorbed, TiO2 NPs may further interact with immune intestinal cells involved in gut microbiota regulation. Since obesity-related metabolic diseases such as diabetes are associated with alterations in the microbiota-immune system axis, this raises questions about the possible involvement of long-term exposure to food-grade TiO2 in the development or worsening of these diseases. The current purpose is to review the dysregulations along the gut microbiota-immune system axis after oral TiO2 exposure compared to those reported in obese or diabetic patients, and to highlight potential mechanisms by which foodborne TiO2 NPs may increase the susceptibility to develop obesity-related metabolic disorders.

The increased frequency and intensity of short-term extreme warming phenomena have been associated to harsh biological and ecosystem outcomes (i.e., mass mortalities in marine organisms). Marine heatwaves (MHWs), occurring when seasonal temperature threshold is exceeded for at least 5 consecutive days, may reduce the tolerance of coastal species toward additional pressures, but interactions between such multiple stressors are virtually unexplored. The present study aimed to characterize in Mytilus galloprovincialis the influence of a simulated MHW scenario on the toxicological effects of the pharmaceutical carbamazepine (CBZ), ubiquitously detected in the marine environment and chosen as model compound for this relevant class of emerging contaminants. The bioaccumulation of CBZ and responsiveness of various biological parameters, including immune system, antioxidant status, lipid metabolism and cellular integrity, were analyzed in exposed mussels both during and after the end of the heatwave. MHW appeared to strongly modulate accumulation of CBZ, paralleled by weakened immunocompetence and onset of oxidative disturbance that finally evolved to cellular damages and lipid metabolism disorders. Elaboration of the overall results through a quantitative Weight of Evidence model, revealed the highest hazard in organisms exposed to both the stressors 10 days after the end of the heatwave, suggesting that MHWs could leave a footprint on the capability of mussels to counteract CBZ toxicity, thus affecting their vulnerability and predisposition to adverse effects toward multiple stressors.

Vaccines are essential for children to defend against infection. Per- and polyfluoroalkyl substances (PFAS) are emerging contaminants with the characteristics of persistence and bioaccumulation. PFAS exposure can affect the function of the nervous, endocrine, and immune system of animals and humans. We aimed to conduct a systematic review and meta-analysis of the epidemiological studies investigating potential relationships between PFAS exposure and vaccine antibody levels, and assessed whether PFAS would affect vaccine response in healthy children. A literature search was conducted in PubMed, Web of Science, and Scopus databases up to February 2022. We chose studies that measured serum vaccines antibodies and PFAS concentrations of the participants. Essential information, including mean difference of percentage change, regression coefficient, odds ratio, Spearman correlation coefficient, and 95% confidence intervals, were extracted from the selected studies to conduct descriptive analysis and meta-analysis where appropriate. The qualities of these studies were evaluated as well. Finally, nine epidemiological studies about children met our inclusion criteria. A high degree of heterogeneity is observed in terms of breastfeeding time, confounder control, and detection method. Exposure to perfluorooctanoic acid and perfluorohexane sulfonic acid is negatively associated with tetanus antibody level in children without heterogeneity by Cochran's Q test (p = 0.26; p = 0.55), and exposure to perfluorohexane sulfonate is negatively associated with tetanus antibody level but with heterogeneity (p = 0.04). This comprehensive review suggests that PFAS can have adverse health effects on children by hindering the production of vaccine antibodies. There are some consistent and negative associations between children exposure to certain PFAS and tetanus antibody level. The association of the other four vaccines (measles, rubella, mumps, and influenza) with PFAS remains uncertain, because very few studies are available. Further studies are needed to validate the possible associations.

Growing evidence recommends that radiofrequency radiations might be a new type of environmental pollutant. The consequences of RFR on the human immune system have gained considerable interest in recent years, not only to examine probable negative effects on health but also to understand if RFR can modulate the immune response positively. Although several studies have been published on the immune effects of RFR but no satisfactory agreement has been reached. Hence this review aims to evaluate the RFR modulating impacts on particular immune cells contributing to various innate or adaptive immune responses. In view of existing pieces of evidence, we have suggested an intracellular signaling cascade responsible for RFR action. The bio-effects of RFR on immune cell morphology, viability, proliferation, genome integrity, and immune functions such as ROS, cytokine secretion, phagocytosis, apoptosis, etc. are discussed. The majority of existing evidence point toward the possible shifts in the activity, number, and/or function of immunocompetent cells, but the outcome of several studies is still contradictory and needs further studies to reach a conclusion. Also, the direct association of experimental studies to human risks might not be helpful as exposure parameters vary in real life. On the basis of recent available literature, we suggest that special experiments should be designed to test each particular signal utilized in communication technologies to rule out the hypothesis that longer exposure to RFR emitting devices would affect the immunity by inducing genotoxic effects in human immune cells.

Identifying the adverse impacts of pesticide exposure is essential to guide regulations that are protective of wildlife and human health. Within rice ecosystems, amphibians are valuable indicators because pesticide applications coincide with sensitive reproductive and developmental life stages. We conducted two experiments using wild cane toads (Rhinella marina) to test 1) whether environmentally relevant exposure to a commercial formulation of butachlor, an acetanilide herbicide used extensively in rice, affects amphibian development and 2) whether cane toad tadpoles are capable of acclimatizing to sub-lethal exposure. First, we exposed wild cane toads to 0.002, 0.02, or 0.2 mg/L of butachlor (Machete EC), during distinct development stages (as eggs and hatchlings, as tadpoles, or continuously) for 12 days. Next, we exposed a subset of animals from the first experiment to a second, lethal concentration and examined survivorship. We found that cane toads exposed to butachlor developed slower and weighed less than controls, and that development of the thyroid gland was affected: exposed individuals had smaller thyroid glands and thyrocyte cells, and more individual follicles. Analyses of the transcriptome revealed that butachlor exposure resulted in downregulation of transcripts related to metabolic processes, anatomic structure development, immune system function, and response to stress. Last, we observed evidence of acclimatization, where animals exposed to butachlor early in life performed better than naïve animals during a second exposure. Our findings indicate that the commercial formulation of butachlor, Machete EC, causes thyroid endocrine disruption in vertebrates, and suggest that exposure in lowland irrigated rice fields presents a concern for wildlife and human health. Furthermore, we establish that developmental assays with cane toads can be used to screen for adverse effects of pesticides in rice fields.

The molecular mechanism of evaluating 17β-estradiol (E₂)-induced toxicity in female Daphnia magna has not been determined. In this study, the transcriptome of D. magna was analyzed after exposure to three different concentrations (0, 10, and 100 ng L⁻¹) of E₂ at 3, 6, and 12 h. The results showed 351–17,221 significantly up-regulated and 505–10,282 significantly down-regulated genes (P < 0.05). Overall, the selected largest 10,282 (10 ng L⁻¹vs control at 12 h) down-regulated and 17,221 (100 vs 10 ng L⁻¹) up-regulated genes were identified; following annotation, pathways in cancer and RNA transport were found to be enriched according to the interaction network. Among all completed comparisons, KEGG pathways related to the immune system, cancer, disease infection, and active compound metabolism were identified by short time series expression miner analysis. A different set of genes fluctuated in a “U”-shaped pattern over time and at different concentrations of E₂, whereas some genes associated with disintoxication showed a reverse “U”-shaped response as E₂ administration was increased. These results suggest that E₂ exposure caused transcriptional changes in the immune system, disintoxication, disease prevention, and the protein degradation pathway.

In the previous publication “Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?” Conticini et al. hypothesized that the surplus of lethality of the novel SARS-CoV-2 in Northern Italy may be at least in part explained by the evidence of highest pollution reported in this area, as both severe COVID-19 and smog exposure are correlated to an innate immune system hyper-activation with subsequent lung inflammation and injury. Since this hypothesis alone does not fully explain why specific subgroups of patients are at major risk, we hypothesized that obesity may be one of the links between COVID-19 severity and high level of air pollution. First, obesity is a predisposing factor for SARS-Cov-2 infection and worse COVID-19 outcomes, and unequivocal evidence demonstrated that fat mass excess is independently associated with several pulmonary diseases and lung inflammation. Moreover, it has been shown that obesity may intensify the detrimental effects of air pollution on the lungs, and this is not surprising if we consider that these conditions share an excessive activation of the immune system and a lung inflammatory infiltrate. Finally, fat mass excess has also been speculated to be itself a consequence of air pollutants exposure, which has been proved to induce metabolic disruption and weight gain in murine models. In conclusion, although many variables must be taken into account in the analysis of the pandemic, our observations suggest that obesity may act as effect modifier of smog-induced lung-injury, and the concomitant presence of these two factors could better explain the higher virulence, faster spread and greater mortality of SARS-CoV-2 in Northern Italy compared to the rest of the country.

Perfluorobutanesulfonate (PFBS), an aquatic pollutant of emerging concern, is found to disturb the neural signaling along gut-brain axis, whereas probiotic additives have been applied to improve neuroendocrine function of teleosts. Both PFBS and probiotics can commonly target nervous system. However, whether and how probiotic bacteria can modulate the neurotoxicities of PFBS remain not explored. It is thus necessary to elucidate the probiotic modulation of PFBS neurotoxicity, which can provide implications to the application of probiotic bacteria in aquaculture industry. In the present study, adult zebrafish were exposed to 0, 10 and 100 μg/L PFBS with or without dietary administration of probiotic Lactobacillus rhamnosus. Interaction between PFBS and probiotic along gut-brain axis was examined, covering three dominant pathways (i.e., neurotransmission, immune response and hypothalamic-pituitary-adrenal (HPA) axis). The results showed that, compared to the single effects, PFBS and probiotic coexposure significantly altered the acetylcholinesterase activity and neurotransmitter profiles in gut and brain of zebrafish, with mild effects on neuronal integrity. Neurotransmitters closely correlated reciprocally in intestines, which, however, was distinct from the correlation profile in brains. In addition, PFBS and probiotic were combined to impact brain health through absorption of bacterial lipopolysaccharides and production of inflammatory cytokines. Relative to neurotransmission and immune signaling, HPA axis was not involved in the neurotoxicological interaction between PFBS and probiotic. Furthermore, it needs to point out that interactive modes between PFBS and probiotic varied a lot, depending on exposure concentrations, sex and toxic indices. Overall, the present study provided the first evidence that probiotic supplement could dynamically modulate the neurotoxicities of PFBS in teleost.