EFSA Panel on Biological Hazards (BIOHAZ); Scientific Opinion on VTEC-seropathotype and scientific criteria regarding pathogenicity assessment

During 2007-2010, 13 545 confirmed human VTEC infections and 777 haemolytic uraemic syndrome (HUS) cases were reported in the EU; isolates from 85 % of cases were not fully serotyped and therefore could not be classified using the Karmali seropathotype concept. Seropathotype group D covered 5 % of isolates from fully serotyped cases; 14 cases (0.7 %) belonged to seropathotype group E, defined by Karmali et al. (2003) as non-human only. Isolates from around 27 % of cases could not be assigned. There were no HUS cases reported for the serotypes in groups D and E but 17 HUS cases could not be assigned. The health outcome was reported for only a fraction of confirmed cases. About 64 % of patients presented with only diarrhoea; VTEC infection resulted in HUS in around 10 % of cases. The new ISO/TS 13136:2012 standard improves the detection of VTEC in food. An alternative concept based on the detection of verocytotoxins alone or genes encoding such verocytotoxins does not provide a sound scientific basis on which to assess risk to the consumer because there is no single or combination of marker(s) that fully define a ‘pathogenic’ VTEC. Strains positive for verocytotoxin 2 gene(vtx2)- and eae (intimin production)- or [aaiC (secreted protein of EAEC) plus aggR (plasmid-encoded regulator)] genes are associated with higher risk of more severe illness than other virulence gene combinations. The 2011 O104:H4 outbreak demonstrated the difficulty of predicting the emergence of ‘new’ pathogenic VTEC types by screening only for the eae gene or by focusing on a restricted panel of serogroups. A molecular approach utilising genes encoding virulence characteristics additional to the presence of vtx genes has been proposed

Should the scope of human mixture risk assessment span legislative/regulatory silos for chemicals?

Current chemicals regulation operates almost exclusively on a chemical-by-chemical basis, however there is concern that this approach may not be sufficiently protective if two or more chemicals have the same toxic effect. Humans are indisputably exposed to more than one chemical at a time, for example to the multiple chemicals found in food, air and drinking water, and in household and consumer products, and in cosmetics. Assessment of cumulative risk to human health and/or the environment from multiple chemicals and routes can be done in amixture risk assessment (MRA).Whilst there is a broad consensus on the basic science ofmixture toxicology, the path to regulatory implementation of MRA within chemical risk assessment is less clear. In this discussion piece we pose an open question: should the scope of human MRA cross legislative remits or ‘silos’?We define silos as, for instance, legislation that defines risk assessment practice for a subset of chemicals, usually on the basis of substance/product, media or process orientation. Currently any form of legal mandate for human MRA in the EU is limited to only a few pieces of legislation. We describe two lines of evidence, illustrated with selected examples, that are particularly pertinent to this question: 1) evidence that mixture effects have been shown for chemicals regulated in different silos and 2) evidence that humans are co-exposed to chemicals from different silos. We substantiate the position that, because there is no reason why chemicals allocated to specific regulatory silos would have non-overlapping risk profiles, then there is also no reason to expect that MRA limited only to chemicals within one silo can fully capture the risk that may be present to human consumers. Finally,we discuss possible options for implementation of MRA and we hope to prompt wider discussion of this issue.OAK Foundation (Grant number OCAY-13-391), European Food Safety Authority (Contract CFT/ EFSA/PPR/2010/04) and Norwegian Environment Agency (Contract 3013043