Conclusions from a Swiss official control of the safety assessment for food contact polyolefins through the compliance documentation of the producers.

Swiss control authorities checked the safety assessment of nine major producers of polyolefin granulates for making food contact materials. It was a pilot project to gain experience on the procedure of collecting and evaluating compliance documentation, but also to obtain insight into the quality of compliance work performed by the main plastic producers. It revealed that there are fundamental problems in performing such control. These are reported with proposals for improvement. For most products, the safety assessment made available did not correspond to the requirements, as confirmed by a group of internationally recognised experts, who were asked for their opinion on whether the safety of the migrates was assessed in accordance to 'internationally accepted scientific methods on risk assessment', as required by Art. 19 of Regulation (EU) 10/2011 and specified by EFSA.

Toxicological Assessment of Mineral Hydrocarbons in Foods: State of Present Discussions.

The evaluation of mineral oils by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) provided high acceptable daily intakes for classes largely falling into the mass range strongly accumulated by humans. Because they are roughly 2 orders of magnitude above the present exposure, they authorize strongly increased exposure. An approach based on accumulation seems more adequate. Increased organ weights might be more critical than granulomas. Aromatic hydrocarbons with 1-2 aromatic rings should be distinguished from those with at least 3 aromatic rings. If mineral oil saturated hydrocarbon limits were low, no limit might be needed for the 1-2 ring aromatics. It should be considered to phase out substantial use of mineral oils in food application.

Mineral oil saturated hydrocarbons (MOSH) in female Fischer 344 rats; accumulation of wax components; implications for risk assessment.

Female Fischer 344 rats were exposed to three MOSH mixtures: oils largely below and above C25 (S-C25 and L-C25) and a 1:1 mixture of L-C25 with a wax; doses of 400, 1000 and 4000mg/kg feed were administered during 120days. MOSH were determined by on-line HPLC-GC-FID in liver, spleen, adipose tissue and the carcass. The composition of the hydrocarbons accumulated in the tissues was further analyzed by comprehensive two-dimensional GC (GC×GC). MOSH in the mass range of C26-30 were more strongly accumulated than those between C20-25, which does not support the present classification of MOSH differentiating at n-C25 for risk assessment. Compared to the total of the MOSH, n-alkanes and n-alkyl monocyclic naphthenes were generally enriched in adipose tissue. In liver and spleen, n-alkanes up to C25 were eliminated, but strongly accumulated at around C30. Based on this profile, poor solubility and the melting points, it is hypothesized that crystallization protects these wax components against metabolism and elimination. In the liver, relative retention of n-alkanes decreased again beyond C30, accentuated at high exposure, suggesting reduced absorption. Compared to the animal data, accumulation of n-alkanes from food sources, such as apples, into human tissues seems low, perhaps because of low absorption due to their presence in crystalline form. A series of dominant isoalkanes, accumulated in all tissues analyzed, was characterized, though without proposing a structure. Implications on present regulation of white mineral oil products are discussed.

Accumulation of mineral oil saturated hydrocarbons (MOSH) in female Fischer 344 rats: Comparison with human data and consequences for risk assessment.

Female Fischer 344 rats were orally exposed to a mixture of mineral oil saturated hydrocarbons (MOSH) of broad molecular mass range at doses of 40, 400 and 4000mg/kg feed. Amounts and compositions of the MOSH were analyzed in liver, spleen, adipose tissue and the carcass after exposure during 30, 60, 90 and 120d as well as after 90d exposure followed by 30d depuration. At 40mg/kg in the feed, after 30d of exposure, 10.9% of the ingested MOSH were recovered from the animal body; after 90d plus 30d depuration it was 3.9%. In liver and spleen, the maximum retention in terms of molecular mass (simulated distillation) was at n-C29; in adipose tissue and carcass it was at n-C15/16. The differentiation between MOSH below and above n-C25 (Class I versus Class II and III oils), used for present regulation, is not supported by the present data on accumulation; structural characteristics seem more pertinent than molecular mass. Concentrations in the tissues increased far less than proportionally with the dose, rendering linear extrapolation to low doses questionable. No steady state was reached after 120d. In fact, comparing with the concentrations in human tissues at the estimated exposure, extrapolation from animal experiments seems to grossly underestimate human internal exposure. Comprehensive two-dimensional gas chromatography (GCxGC) was used to characterize the MOSH residues in the tissues with the aim of identifying the most strongly accumulated types. In the liver and spleen, the highly branched hydrocarbons dominated, whereas in the adipose tissue it was the n-alkanes and species with main n-alkyl moieties. Strong MOSH accumulation is not of concern per se, but the safety at the high concentrations in human tissues needs to be re-evaluated, possibly taking into account also end points other than granuloma formation.

Compliance work for food contact materials: feasibility of the legally required safety assessment of an epoxy/amine-based coating for domestic water pipe restoration.

Options were explored for fulfilling the legally required safety assessment for a widely applied epoxy/amine coating used for restoring corroded domestic drinking water supply systems. The coating was made up of two components mixed shortly before application, the first mainly consisting of bisphenol A diglycidyl ether (BADGE), the second of various amines. The analytically identified starting substances were all authorised, but only constituted a small proportion of the low molecular mass material left after curing and potentially migrating into water. Reaction products synthesised from constituents of the starting components (expected oligomers) could not be eluted from GC even after derivatisation, indicating that standard GC-MS screening would miss most potential migrants. They were detectable by size exclusion chromatography (SEC) after acetylation. HPLC with MS or fluorescence detection was possible for constituents including a BADGE moiety, but phenalkamines could not be detected with adequate sensitivity. Possibilities for determining long-term migration relevant for chronic toxicity are discussed. Analysis in water shortly after application of the coating overestimates migration if migration decreases over time and requires detection limits far out of reach. Analysis of a solvent extract of the coating is easier and provides an upper estimate of what could migrate into the drinking water over the years. However, to satisfy the regulatory requirements, components of the complex mixture need to be identified at lower proportions than those accessible. In vitro testing of the whole mixture for genotoxicity is expected to fail because of the required sensitivity and the glycidyl functions probably wrongly resulting in positive tests. The difficulties in dealing with this situation are discussed.

Assessment of epoxidized soy bean oil (ESBO) migrating into foods: comparison with ESBO-like epoxy fatty acids in our normal diet.

Epoxidized soy bean oil (ESBO) was found to be toxic for rats, but the toxic constituent is unknown. It became an issue as the migration from the gaskets in the lids for jars into oily foods regularly far exceeds the European legal limit (overall migration limit and specific migration limit derived from the tolerable daily intake (TDI)). In the context of risk management it was of interest to determine the epoxidized fatty acids of ESBO in those foods of our normal diet which are expected to contain the highest concentrations, i.e., oxidized edible oils (including degraded frying oils), fried foods, bakery ware and roasted meat. The contribution of epoxy oleic acid from ESBO to our diet turned out to be negligible. If this acid were the toxic component in ESBO, the toxicological assessment would primarily be a warning regarding oxidized fats and oils. The contribution of diepoxy linoleic acid from ESBO might be similar to the exposure from oxidized fats and oils of our diet, whereas the intake of triepoxy linolenic acid from ESBO exceeds that from normal food by around two orders of magnitude. Hence use of an epoxidized edible oil virtually free of linolenic acid would be inconspicuous in our diet.