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In light of the broad spectrum of products containing nanosilver, the harmfulness of nanosilver to human health and the environment was intensively discussed at a conference held in February 2012 at the BfR. The conference agenda covered the aspects of analytics of nanosilver materials, human exposure and toxicology as well as effects on microorganisms and the environment. The discussion recovered major gaps related to commonly agreed guidelines for sample preparation and central analytical techniques. In particular, the characterization of the nanoparticles in complex matrices was regarded as a challenge which might become a pitfall for further innovation and application. Historical and anecdotal records of colloidal silver have been sometimes taken as empirical proof for the general low toxicity of nanosilver. Yet as reported herein, a growing number of animal studies following modern performance standards of toxicity testing have been carried out recently revealing well-characterized adverse effects on different routes of exposure in addition to argyria. Furthermore, recent approaches in exposure assessment were reported. However, consumer exposure scenarios are only starting to be developed and reliable exposure data are still rare. It was further widely agreed on the workshop that the use of silver may lead to the selection of silver resistant bacteria. With respect to its environmental behavior, it was suggested that nanosilver released to wastewater may have negligible ecotoxicological effects. Finally, the presentations and discussion on risk assessment and regulation of nanosilver applications gave insights into different approaches of risk assessment of nanomaterials to be performed under the various regulatory frameworks.

5-Hydroxymethylfurfural (HMF) and furfuryl alcohol (FFA) are moderately potent rodent carcinogens that are present in thermally processed foodstuffs. The carcinogenic effects were hypothesized to originate from sulfotransferase (SULT)-mediated bioactivation yielding DNA-reactive and mutagenic sulfate esters, a confirmed metabolic pathway of HMF and FFA in mice. It is known that orthologous SULT forms substantially differ in substrate specificity and tissue distribution. This could influence HMF- and FFA-induced carcinogenic effects. Here, we studied HMF and FFA sulfoconjugation by 30 individual SULT forms of humans, mice and rats. The catalytic efficiencies (kcat/KM) of HMF sulfoconjugation of human SULT1A1 (13.7 s−1 M−1), mouse Sult1a1 (15.8 s−1 M−1) and 1d1 (4.8 s−1 M−1) and rat Sult1a1 (5.3 s−1 M−1) were considerably higher than those of all other SULT forms investigated (≤0.73 s−1 M−1). FFA sulfoconjugation was monitored using adenosine as a nucleophilic scavenger for the reactive 2-sulfoxymethylfuran (t1/2 = 20 s at 37 °C). The resulting adduct N6-((furan-2-yl)methyl)-adenosine (N6-MF-A) was quantified by isotope-dilution UPLC-MS/MS. The rates of N6-MF-A formation showed that hSULT1A1 and its orthologues in mice and rats were also the most important contributors to FFA sulfoconjugation in each of the species. Taken together, the catalytic capacity of hSULT1A1 is comparable to that of mSult1a1 in mice, the species in which carcinogenic effects of HMF and FFA were detected. This is of primary concern due to the expression of hSULT1A1 in many different tissues.Electronic supplementary materialThe online version of this article (doi:10.1007/s00204-014-1392-6) contains supplementary material, which is available to authorized users.