Suchergebnisse

In risk assessment, no observed exposure level (NOAEL) and benchmark dose (BMD) are usually derived either from epidemiological studies in humans or from animal experiments. In many in vitro studies, concentration‐effect/response curves have been analyzed using different mathematical models finalized to the identification of EC50. In the present article, we propose a model to fit dose‐response curves in vitro. The BMD approach has been used to compare the cell viability (MTT assay) of different rat (C6 and PC12, glial and neuronal, respectively) and human cell lines (D384 and SK‐N‐MC, glial and neuronal, respectively) after 24‐hour exposure to the following neurotoxic substances: manganese chloride (MnCl2), methyl‐mercury (Me‐Hg), and the enantiomers of styrene oxide (SO). For all rat and human cell lines, the potency of the examined compounds was: MnCl2 < S‐SO < R‐SO < Me‐Hg. A preliminary comparison with in vivo toxicity data for these substances gave rise to consistent results. Whereas a reasonable agreement between in vitro and in vivo data has been found for Mn and styrene oxide, a wide scatter of LOAEL has been reported for Me‐Hg and these appear to be either much higher or lower than the BMD for the MTT assay we observed invitro.

Following a request from the German Federal Institute for Risk Assessment (BfR), the EFSA Panel for Contaminants in the Food Chain was asked to deliver a statement on the presence of microplastics and nanoplastics in food, with particular focus on seafood. Primary microplastics are plastics originally manufactured to be that size, while secondary microplastics originate from fragmentation. Nanoplastics can originate from engineered material or can be produced during fragmentation of microplastic debris. Microplastics range from 0.1 to 5,000 μm and nanoplastics from approximately 1 to 100 nm (0.001–0.1 μm). There is no legislation for microplastics and nanoplastics as contaminants in food. Methods are available for identification and quantification of microplastics in food, including seafood. Occurrence data are limited. In contrast to microplastics no methods or occurrence data in food are available for nanoplastics. Microplastics can contain on average 4% of additives and the plastics can adsorb contaminants. Both additives and contaminants can be of organic as well of inorganic nature. Based on a conservative estimate the presence of microplastics in seafood would have a small effect on the overall exposure to additives or contaminants. Toxicity and toxicokinetic data are lacking for both microplastics and nanoplastics for a human risk assessment. It is recommended that analytical methods should be further developed for microplastics and developed for nanoplastics and standardised, in order to assess their presence, identity and to quantify their amount in food. Furthermore, quality assurance should be in place and demonstrated. For microplastics and nanoplastics, occurrence data in food, including effects of food processing, in particular, for the smaller sized particles (< 150 μm) should be generated. Research on the toxicokinetics and toxicity, including studies on local effects in the gastrointestinal (GI) tract, are needed as is research on the degradation of microplastics and potential formation of nanoplastics in the human GI tract.