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Abstract Background There is a fundamental gap of knowledge on the health effects caused by the interaction of engineered nanomaterials (ENM) with the gastro-intestinal tract (GIT). This is partly due to the incomplete knowledge of the complex physical and chemical transformations that ENM undergo in the GIT, and partly to the widespread belief that GIT health effects of ENM are much less relevant than pulmonary effects. However, recent experimental findings, considering the role of new players in gut physiology (e.g. the microbiota), shed light on several outcomes of the interaction ENM/GIT. Along with this new information, there is growing direct and indirect evidence that not only ingested ENM, but also inhaled ENM may impact on the GIT. This fact, which may have relevant implications in occupational setting, has never been taken into consideration. This review paper summarizes the opinions and findings of a multidisciplinary team of experts, focusing on two main aspects of the issue: 1) ENM interactions within the GIT and their possible consequences, and 2) relevance of gastro-intestinal effects of inhaled ENMs. Under point 1, we analyzed how luminal gut-constituents, including mucus, may influence the adherence of ENM to cell surfaces in a size-dependent manner, and how intestinal permeability may be affected by different physico-chemical characteristics of ENM. Cytotoxic, oxidative, genotoxic and inflammatory effects on different GIT cells, as well as effects on microbiota, are also discussed. Concerning point 2, recent studies highlight the relevance of gastro-intestinal handling of inhaled ENM, showing significant excretion with feces of inhaled ENM and supporting the hypothesis that GIT should be considered an important target of extrapulmonary effects of inhaled ENM. Conclusions In spite of recent insights on the relevance of the GIT as a target for toxic effects of nanoparticles, there is still a major gap in knowledge regarding the impact of the direct versus indirect oral exposure. This fact probably applies also to larger particles and dictates careful consideration in workers, who carry the highest risk of exposure to particulate matter.

• Most of the aluminum contained in the body (95%) has food for origin. • The amount of aluminum contained in a vaccine is insufficient to increase the aluminum level in the organism. • Direct toxicity and then indirect toxicity have been suggested as a potential explanation of human macrophagic myofasciitis. • This article demonstrates that to date no link can be established between the presence of aluminum in vaccines and human macrophagic myofasciitis. French people have never been so wary about vaccines. The use of aluminum salts in vaccine adjuvants to enhance effectiveness is one of the major reasons for this lack of confidence. The direct toxicity of aluminum is often put forward. Direct toxicity of aluminum has long been known − especially with occupational exposure–to be associated with characteristic clinical manifestations and increased blood aluminum level. Intoxication related to the excessive amount of an element in the body, whether be it lead poisoning following exposure to lead or mercury poisoning for instance, is always associated with metal increase in biological media. To date no link has been established between the direct toxicity of aluminum and vaccines. Aluminum levels in biological media of vaccinated subjects are not different from those of unvaccinated subjects. This is consistent with the very small amount of aluminum contained in one dose of vaccine. Indirect toxicity of aluminum was suggested to explain macrophagic myofasciitis in humans in 2011, a disease that could be mediated by an autoimmune/autoinflammatory mechanism. This hypothesis has recently been refuted in a large pharmaco-epidemiological study proving that aluminum-containing adjuvants of vaccines are not responsible for this autoimmune/autoinflammatory syndrome. [ABSTRACT FROM AUTHOR]

Oil water-soluble fractions (WSFs) compounds have low persistence in water; evaporating in a matter of hours to days. Nonetheless, they pose high toxicity to exposed biota. Their effects may be instantaneous or delayed, affecting, respectively, mainly survival vs growth and reproduction. We investigated the effects of crude oil WSFs on freshwater meiobenthos, with a focus on nematode assemblages, in community microcosm experiments lasting 15 weeks. Treatments consisted of the application of different concentrations of oil WSFs, i.e. high (100%) medium (50%) and low (10%), and effects were assessed one, three, nine and 15 weeks after contamination, allowing us to detect both short-term and lasting effects of oil-WSF. Additionally, we compared the effects of a single contamination event with those of a so-called 'constant' oil-WSF contamination where we replenished evaporated water with water containing the medium concentration of oil WSF. Next to nematodes, the most abundant meiofaunal taxa were rotifers, gastrotrichs, oligochaetes and tardigrades. Total abundance, different diversity indices, the composition of feeding-types and the age structure were investigated in the assessment of direct oil effects on the structure of nematode assemblages. Limited immediate effects were observed, except for a significant decrease of the index of taxonomic distinctness, which already appeared in the first week. Significant impacts on total nematode abundance, diversity and species composition only became apparent after 9–15 weeks of incubation, indicating that delayed effects of a single exposure are far more pronounced than instantaneous effects. Moreover, for most response variables, the strongest impacts were not observed in the highest-concentration treatment, but in a medium-concentration treatment with regular replenishment of oil WSF, suggesting that internal exposure may be important in generating effects. Furthermore, the predictability of the sensitivity of individual species was sometimes poor, which may not only result from these species' sensitivities, but also from alterations in interspecific interactions in polluted communities. Further toxicity tests should be carried out in order to unravel the main modes of action of crude oil WSF which lead to the observed long-term sublethal effects on nematode communities. • Different endpoints were investigated to assess oil WSF on nematodes assemblages. • Assessed endpoints included abundance, diversity, age structure and feeding types. • Crude oil water-soluble fractions caused mostly long-term effects on nematodes. • After 15 weeks, the abundance and diversity of nematodes were severely reduced. • Dedicated experiments should unravel modes of (longer-term) action of crude oil WSF. [ABSTRACT FROM AUTHOR]

Although soluble hydrocarbons persist for only hours to days in aquatic environments, they potentially pose a high toxicity to aquatic biota. Here we investigate effects of the water-soluble fraction (WSF) of crude oil on estuarine meiofauna, with special focus on nematodes. Copepods and amphipods were the most sensitive taxa, disappearing almost completely within 3 weeks after exposure. In nematodes, we observed mostly sublethal short-term effects of WSF, such as changes in feeding-type composition and age structure. In the longer term (months), total nematode density and species composition were significantly affected, whereas different diversity indices did not exhibit significant responses. Deposit-feeding and predatory nematodes were the most affected feeding types. Nevertheless, sensitivity was species-specific, with sometimes opposing responses between even congeneric species. Our results demonstrate the need to assess WSF effects on communities at the species level and over time periods well exceeding the residence time of the WSF in the environment. • Crude oil water-soluble fraction caused short- and long-term effects on meiobenthos. • Amphipods and harpacticoid copepods were strongly affected in the short term. • WSF affected nematode age distribution and feeding-type composition in the short term. • WSF affected nematode abundance and species composition only in the longer term. • This implies that WSF was not lethal to nematodes but impaired their reproduction. [ABSTRACT FROM AUTHOR]

Highlights • Childhood cancer patients and survivors seem at higher risk for tinnitus development compared to siblings. • Platinum agents, high dose cranial radiation and central nervous system tumors are risk factors for tinnitus development. • Regular screening for tinnitus and information providing before, during and after childhood cancer therapy is recommended. Abstract Background Tinnitus can occur during and after treatment for childhood cancer. Studies on the occurrence of, and risk factors for tinnitus during and after childhood cancer treatment are scarce. The aim of this study is to get insight into the frequency and risk factors of tinnitus during and after childhood cancer therapy, based on a review of all previously reported literature. Materials and methods Systematic electronic literature searches that combined childhood cancer with different treatments and tinnitus terms were performed in the databases EMBASE, Medline, Cochrane, Web of Science, and Google Scholar. Studies were included based on reporting the frequency of tinnitus during and/or after childhood cancer, with 75% of participants being under the age of 25 at time of diagnosis, diagnosed with any type of childhood malignancy and treated with any type of chemotherapy and/or radiotherapy. A risk of bias assessment per research question was performed. Results Tinnitus incidence rates were reported up to 15.9 (95% CI 11.8–21.4) during therapy and up to 5.4 (95% CI 4.3–6.9) more than 5 years after diagnosis. The relative risk of developing tinnitus as compared to siblings during and after childhood cancer therapy were reported up to 17.2 (95% CI 11.8–25.0) during therapy and up to 3.7 (95% CI 2.7–5.1) more than 5 years after diagnosis. Independent risk factors for tinnitus development included high dose cranial radiation and platinum based chemotherapy. Conclusion The frequency of and risk to develop tinnitus seems to be higher in childhood cancer patients and survivors as compared to the normal population. Regular tinnitus screening before, during and after therapy with standardized questionnaires for early detection seems therefore reasonable in order to identify high-risk patients and eventually develop successful clinical preventive, supportive and management strategies. [ABSTRACT FROM AUTHOR]

To investigate the toxic effect and mechanism of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) in aquatic plants, in vivo and in vitro exposure to BDE-47 were conducted. After 14-d exposure to 5–20 μg/L BDE-47, the growth of Lemna minor plants was significantly suppressed, and the chlorophyll and soluble protein contents in fronds markedly decreased. Accordingly, the photosynthetic efficiency (Fv/Fm, PI) decreased. When the thylakoid membranes isolated from healthy fronds was exposed to 5–20 mg/L BDE-47 directly in vitro for 1 h, the photosynthetic efficiency also decreased significantly. In both the in vitro (5–20 μg/L) and in vivo (5–20 mg/L) experiments, BDE-47 led to an increased plasma membrane permeability. Hence, we concluded that BDE-47 had a direct toxicity to photosynthetic membranes and plasma membranes. However, direct effects on the activities of peroxidase (POD), malate dehydrogenase (MDH) and nitroreductase (NR) were not observed by adding 5–20 mg/L BDE-47 into crude enzyme extracts. The malondialdehyde (MDA) and superoxide anion radical (O 2 − ) contents in the BDE-47 treated fronds were higher than those in the control fronds, suggesting that L . minor can not effectively relieve reactive oxygen species (ROS). The data above indicates that BDE-47 is toxic to L . minor through acting directly on biomembranes, which induces the production of ROS and thus causes remarkable oxidative damage to cells. [ABSTRACT FROM AUTHOR]

Background: There is a fundamental gap of knowledge on the health effects caused by the interaction of engineered nanomaterials (ENM) with the gastro-intestinal tract (GIT). This is partly due to the incomplete knowledge of the complex physical and chemical transformations that ENM undergo in the GIT and partly to the widespread belief that GIT health effects of ENM are much less relevant than pulmonary effects. However, recent experimental findings, considering the role of new players in gut physiology (e.g. the microbiota), shed light on several outcomes of the interaction ENM/GIT. Along with this new information, there is growing direct and indirect evidence that not only ingested ENM, but also inhaled ENM may impact on the GIT. This fact, which may have relevant implications in occupational setting, has never been taken into consideration. This review paper summarizes the opinions and findings of a multidisciplinary team of experts, focusing on two main aspects of the issue: 1) ENM interactions within the GIT and their possible consequences, and 2) relevance of gastro-intestinal effects of inhaled ENMs. Under point 1, we analyzed how luminal gut-constituents, including mucus, may influence the adherence of ENM to cell surfaces in a size-dependent manner, and how intestinal permeability may be affected by different physico-chemical characteristics of ENM. Cytotoxic, oxidative, genotoxic and inflammatory effects on different GIT cells, as well as effects on microbiota, are also discussed. Concerning point 2, recent studies highlight the relevance of gastro-intestinal handling of inhaled ENM, showing significant excretion with feces of inhaled ENM and supporting the hypothesis that GIT should be considered an important target of extrapulmonary effects of inhaled ENM. Conclusions: In spite of recent insights on the relevance of the GIT as a target for toxic effects of nanoparticles, there is still a major gap in knowledge regarding the impact of the direct versus indirect oral exposure. This fact probably applies also to larger particles and dictates careful consideration in workers, who carry the highest risk of exposure to particulate matter. [ABSTRACT FROM AUTHOR]

Fenthion (organophosphate) was used in Australia to target adults, eggs and larvae of Mediterranean fruit fly (Medfly), Ceratitis capitata Wiedmann (Diptera: Tephritidae) in deciduous fruits. With its removal from use in 2015, clothianidin and thiacloprid (neonicotinoids) were evaluated for any adulticide, ovicide or larvicide (eggs, larvae) activity against Medfly in a series of laboratory and field-cage experiments in peach and nectarine. We included fenthion in all experiments as a positive control. As an adulticide, fenthion had the greatest residual toxicity on fruit, with 7 d old residues killing 44% of adults within 48 h compared to thiacloprid (17%) and clothianidin (30%). When applied as a larvicide to naturally infested peaches, none of the insecticides was 100% effective, though fewest pupae (1.18 ± 0.19 pupae/fruit) (indirect measurement of larval survival) were produced when treated with fenthion, followed by clothianidin (3.40 ± 0.33 pupae/fruit) and thiacloprid (6.88 ± 0.34 pupae/fruit); with 11.35 ± 0.30 pupae/fruit in control (water). In peaches treated 48 h post-infestation, fenthion was most effective in reducing numbers of pupae and adult emergence and with higher percentage of deformed adults, with thiacloprid=clothianidin. In nectarines treated 48 h post-infestation, fenthion was most effective in reducing numbers of pupae and adult emergence as well as with higher percentage of deformed adults, followed by clothianidin. Insecticides were least effective when applied as a preventative 24 h or 7 d prior to infestation, with fenthion more effective than clothianidin. Whilst our study shows that neither clothianidin nor thiacloprid are equivalent to fenthion, they are acceptable substitutes to growers for use for Medfly in deciduous fruits given that fenthion is no longer available to growers in Australia. We recommend that growers incorporate other controls to target the adult stage rather than rely only on new insecticides. [ABSTRACT FROM AUTHOR]

BACKGROUND: Spinosad is a biopesticide widely used for control of Frankliniella occidentalis (Pergande). It is reported to be non-toxic toseveral predatorymite speciesusedfor thebiological controlof thrips. PredatorymitesTyphlodromipsmontdorensis (Schicha), Neoseiulus cucumeris (Oudemans) and Hypoaspis miles (Berlese) have been used for control of F. occidentalis. This study investigated the impact of direct and residual toxicity of spinosad on F. occidentalis and predatory mites. The repellency of spinosad residues to these predatory mites was also investigated. RESULTS: Direct contact tospinosad effectively reducedthenumber of F. occidentalis adultsandlarvae, causing>96%mortality. Spinosad residues aged 2-96 h were also toxic to F. occidentalis. Direct exposure to spinosad resulted in >90% mortality of all three mite species. Thresholds for the residual toxicity (contact) of spinosad (LT25) were estimated as 4.2, 3.2 and 5.8 days for T. montdorensis, N. cucumeris and H. miles respectively.Whenmites were simultaneously exposed to spinosad residues and fed spinosad-intoxicated thrips larvae, toxicity increased. Residual thresholds were re-estimated as 5.4, 3.9 and 6.1 days for T. montdorensis, N. cucumeris and H. miles respectively. Residues aged 2-48 h repelled T. montdorensis and H. miles, and residues aged 2-24 h repelled N. cucumeris. CONCLUSION: Predatory mites can be safely released 6 days after spinosad is applied for themanagement of F. occidentalis. [ABSTRACT FROM AUTHOR]

Abstract: The aim of the study was to evaluate the antiproliferative and cytotoxic properties of triamcinolone acetonide (TA) on human retinal pigment epithelium cells (ARPE19) and the role of epicellular crystalline deposits. Monolayer cultures of ARPE19 cells were used. Purified or unpurified crystalline TA suspension (0.01–1.0mg/ml) or the vehicle alone (benzyl alcohol, 0.025%–0.00025%), diluted in culture medium, were added to the cells that were either grown on cell culture dishes covered by a protecting membrane filter insert or without a filter. After 1, 3, 5 and 7days mitochondrial activity was measured using the MTT assay and the morphology assessed microscopically. Cellular proliferative activity was monitored by BrdU-incorporation into cellular DNA. For cytotoxicity assays ARPE19 cells were grown to confluence and then cultured in a serum-deficient medium to ensure a static milieu. Annexin V-FITC and propidium iodide co-staining was performed and analyzed by flow cytometry. Exposure to TA without direct cellular contact showed a moderate antiproliferative activity resulting in a dose-dependent suppression of DNA synthesis (maximum 42.7%), but not a cytotoxic effect. In contrast, adherent deposits of crystalline TA particles on top of the cell layer caused a rapid-progressive and dose-dependent cell death preceded by an early phosphatidylserine externalization to the outer leaflet of the plasma membrane. Within a healthy, confluent cell layer the number of viable cells decreased by 14.2, 20.8 and 68.8%, respectively, after one day of direct exposure. Exposure to the vehicle alone caused only a slight growth inhibitory effect in a proliferating cell layer, but early signs of cell death were detected even at the lowest concentration tested. In conclusion, the effect of the vehicle is less pronounced than formerly assumed, but not negligible, thus indicating a beneficial effect of purification. While non-adherent TA, if purified, appears to be safe in clinically used concentrations, direct physical contact with crystalline particles might cause a local, rapid-progressive cytotoxicity that involves the induction of the apoptotic cascade. Therefore, epiretinal deposits after intravitreal TA administration might be critical in terms of long-term biocompatibility. [Copyright &y& Elsevier]

Current understanding of the health risks and adverse effects upon exposure to fine particles is premised on the direct association of particles with target organs, particularly the lung; however, fine-particle exposure has also been found to have detrimental effects on sealed cavities distant to the portal-of-entry, such as joints. Moreover, the fundamental toxicological issues have been ascribed to the direct toxic mechanisms, in particular, oxidative stress and proinflammatory responses, without exploring the indirect mechanisms, such as compensated, adaptive, and secondary effects. In this Review, we recapitulate the current findings regarding the detrimental effects of fine-particle exposure on joints, the surrounding cells, and microenvironment, as well as their deteriorating impact on the progression of arthritis. We also elaborate the likely molecular mechanisms underlying the particle-induced detrimental influence on joints, not limited to direct toxicity, but also considering the other indirect mechanisms. Because of the similarities between fine air particles and engineered nanomaterials, we compare the toxicities of engineered nanomaterials to those of fine air particles. Arthritis and joint injuries are prevalent, particularly in the elderly population. Considering the severity of global exposure to fine particles and limited studies assessing the detrimental effects of fine-particle exposure on joints and arthritis, this Review aims to appeal to a broad interest and to promote more research efforts in this field.