Conclusions of the French Food Safety Agency on the toxicity of bisphenol A

Since more than 10 years, risk assessment of bisphenol A (BPA) is debated at the international level. In 2008, the U.S. National Toxicology Program (NTP) expressed some concern for adverse effects, at current level of exposure to BPA, on developmental toxicity. In this context, the French Food Safety Agency (AFSSA) decided to review the toxicity data on BPA with a special focus on this endpoint at doses below 5mg/kg bw/day (the no observed adverse effect level set by different regulatory bodies). This paper summarizes the conclusions of a collective assessment conducted by an expert Working Group from AFSSA. Studies were classified into 3 groups: (i) finding no toxicity, (ii) reporting results not considered to be of concern and (iii) indicating warning signals. The term "warning signal" means that no formal conclusion can be drawn regarding the establishment of a health based guidance value but the study raises some questions about the toxicity of BPA at low doses. It was concluded that studies are needed to ascertain the significance for human health of these warning signals and to be able to propose new methodologies for assessing the risks associated with low doses of BPA and more generally of endocrine disruptors

Immobilisation in vitro du plomb par l'apatite : Influence sur la biodisponibilité de ce métal chez le rat

Not availableL'apatie est apparue comme un composé interessant pour retenir le plomb présent dans l'eau de boisson (cartouche) ou dans les eaux résiduelles (épuration par filtrage), de par sa capacité à réagir avec le métal pour former de la pyromorphite. En solution diluée, l'hydroxyapatite synthétique (HA, CA10(PO4)6(OH)2) dissoute a fourni des phosphates, réagissant avec le plomb (rapport molaire HA/Pb=1/10) pour former des précipités, au pH voisin de 6, qui se solubilisent à pH plus acide (3)

Immobilisation in vitro du plomb par l'apatie. (Influence sur la biodisponibilité de ce métal chez le rat)

METZ-SCD (574632105) / SudocSudocFranceF

Dose-Response Modelling of Paralytic Shellfish Poisoning (PSP) in Humans

Paralytic shellfish poisoning (PSP) is caused by a group of marine toxins with saxitoxin (STX) as the reference compound. Symptoms in humans after consumption of contaminated shellfish vary from slight neurological and gastrointestinal effects to fatal respiratory paralysis. A systematic review was conducted to identify reported cases of human poisoning associated with the ingestion of shellfish contaminated with paralytic shellfish toxins (PSTs). Raw data were collected from 143 exposed individuals (113 with symptoms, 30 without symptoms) from 13 studies. Exposure estimates were based on mouse bioassays except in one study. A significant relationship between exposure to PSTs and severity of symptoms was established by ordinal modelling. The critical minimal dose with a probability higher than 10% of showing symptoms is 0.37 µg STX eq./kg b.w. This means that 10% of the individuals exposed to this dose would have symptoms (without considering the severity of the symptoms). This dose is four-fold lower than the lowest-observed-adverse-effect-level (LOAEL) established by the European Food Safety Authority (EFSA, 2009) in the region of 1.5 μg STX eq./kg b.w. This work provides critical doses that could be used as point of departure to update the acute reference dose for STX. This is the first time a dose-symptoms model could be built for marine toxins using epidemiological data

Vigilance, veille et surveillance des risques alimentaires phycotoxiniques

Official routine monitoring of phycotoxins and toxinproducing algae is regularly implemented in the marine environment through phytoplankton identification in water samples, as well as by official analysis in shellfish in order to verify compliance with the maximum limits set in regulation (EC) no.853/2004. These activities are conducted by the official REPHY network, coordinated by IFREMER (French Research Institute for Exploitation of the Sea). As for other food safety hazards, the issue of emerging and non-regulated hazards needs to be fully addressed in addition to the ongoing above-mentioned surveillance efforts. This issue was submitted to ANSES (French Agency for Food, Environmental and Occupational Health & Safety) in the surveillance framework set up to verify the relevance of chemical tests to replace the mouse bio-assays formerly used for lipophilic toxin detection. The global algae surveillance plan implemented by IFREMER should make it possible to reach the goal of controlling emerging risk.La surveillance officielle des phycotoxines et de la flore productrice de celles-ci est régulièrement assurée en routine dans le milieu marin, grâce à des prélèvements d’eau pour lecture de flore comme par la réalisation d’analyses de coquillages. Ces dernières permettent le jugement de conformité par rapport aux teneurs maximales en phycotoxines réglementées fixées dans le règlement CE 853/2004. Ces actions relèvent du réseau officiel REPHY, animé par l’Ifremer. Comme pour d’autres dangers des aliments, se pose la question d’une veille sanitaire complémentaire de la surveillance précitée, face aux dangers non réglementés ou émergents. L’Anses a été saisie de la question dans un contexte de révision du dispositif officiel de vigilance mis en place dans le cadre de la vérification de la pertinence des analyses chimiques des toxines lipophiles, suite au passage du bio-essai sur souris aux tests chimiques. La surveillance globale des flores par l’Ifremer doit permettre d’atteindre l’objectif de maîtrise des risques émergents

Analyse critique des résultats d’une étude de toxicité sur le développement du système nerveux ainsi que d’autres données publiées récemment sur les effets toxiques du bisphénol A

Analyse critique des résultats d’une étude de toxicité sur le développement du système nerveux ainsi que d’autres données publiées récemment sur les effets toxiques du bisphénol

Occurrence of β-N-methylamino-l-alanine (BMAA) and Isomers in Aquatic Environments and Aquatic Food Sources for Humans

The neurotoxin β-N-methylamino-l-alanine (BMAA), a non-protein amino acid produced by terrestrial and aquatic cyanobacteria and by micro-algae, has been suggested to play a role as an environmental factor in the neurodegenerative disease Amyotrophic Lateral Sclerosis-Parkinsonism-Dementia complex (ALS-PDC). The ubiquitous presence of BMAA in aquatic environments and organisms along the food chain potentially makes it public health concerns. However, the BMAA-associated human health risk remains difficult to rigorously assess due to analytical challenges associated with the detection and quantification of BMAA and its natural isomers, 2,4-diamino butyric acid (DAB), β-amino-N-methyl-alanine (BAMA) and N-(2-aminoethyl) glycine (AEG). This systematic review, reporting the current knowledge on the presence of BMAA and isomers in aquatic environments and human food sources, was based on a selection and a score numbering of the scientific literature according to various qualitative and quantitative criteria concerning the chemical analytical methods used. Results from the best-graded studies show that marine bivalves are to date the matrix containing the higher amount of BMAA, far more than most fish muscles, but with an exception for shark cartilage. This review discusses the available data in terms of their use for human health risk assessment and identifies knowledge gaps requiring further investigations

Correction: Occurrence of β-N-methylamino-l-alanine (BMAA) and Isomers in Aquatic Environments and Aquatic Food Sources for Humans. Toxins 2018, 10, 83

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Shellfish monitoring for lipophilic phycotoxins in France, recommendation for an updated sampling strategy

In France, the sampling strategy for the official monitoring of lipophilic phycotoxins in bivalve shellfish relies on the definition of risk areas and high risk periods, during which a systematic weekly analysis of toxins in shellfish is performed. Since 2010, high risk periods are defined as follows: the occurrence of one result above the European regulatory limit (160 μg equivalent okadaic acid/kg shellfish) over the last 3 years leads to that month being considered a high risk period. This definition was established according to a statistical analysis of the official monitoring results for the period 2003-2008, based on the mouse bioassay (MBA) as the official analytical method. As of the 1st January 2010, the MBA has been replaced by LC-MS/MS. In 2014, a new statistical analysis was performed, based this time on results for the period 2010-2013 for which quantitative LC-MS/MS data are available. We tested the robustness of the definition set in 2010 and identified a new methodology to improve our sampling strategy for lipophilic toxins in bivalve shellfish, based on Bayesian inference

Cellular and Molecular Aspects of the β-N-Methylamino-l-alanine (BMAA) Mode of Action within the Neurodegenerative Pathway: Facts and Controversy

The implication of the cyanotoxin β-N-methylamino-l-alanine (BMAA) in long-lasting neurodegenerative disorders is still a matter of controversy. It has been alleged that chronic ingestion of BMAA through the food chain could be a causative agent of amyotrophic lateral sclerosis (ALS) and several related pathologies including Parkinson syndrome. Both in vitro and in vivo studies of the BMAA mode of action have focused on different molecular targets, demonstrating its toxicity to neuronal cells, especially motoneurons, and linking it to human neurodegenerative diseases. Historically, the hypothesis of BMAA-induced excitotoxicity following the stimulation of glutamate receptors has been established. However, in this paradigm, most studies have shown acute, rather than chronic effects of BMAA. More recently, the interaction of this toxin with neuromelanin, a pigment present in the nervous system, has opened a new research perspective. The issues raised by this toxin are related to its kinetics of action, and its possible incorporation into cellular proteins. It appears that BMAA neurotoxic activity involves different targets through several mechanisms known to favour the development of neurodegenerative processes