The present opinion deals with an updated safety assessment of the food additive titanium dioxide (E 171) based on new relevant scientific evidence considered by the Panel to be reliable, including data obtained with TiO 2 nanoparticles ( NP s) and data from an extended one‐generation reproductive toxicity ( EOGRT ) study. Less than 50% of constituent particles by number in E 171 have a minimum external dimension < 100 nm. In addition, the Panel noted that constituent particles < 30 nm amounted to less than 1% of particles by number. The Panel therefore considered that studies with TiO 2 NP s < 30 nm were of limited relevance to the safety assessment of E 171. The Panel concluded that although gastrointestinal absorption of TiO 2 particles is low, they may accumulate in the body. Studies on general and organ toxicity did not indicate adverse effects with either E 171 up to a dose of 1,000 mg/kg body weight (bw) per day or with TiO 2 NP s (> 30 nm) up to the highest dose tested of 100 mg/kg bw per day. No effects on reproductive and developmental toxicity were observed up to a dose of 1,000 mg E 171/kg bw per day, the highest dose tested in the EOGRT study. However, observations of potential immunotoxicity and inflammation with E 171 and potential neurotoxicity with TiO 2 NP s, together with the potential induction of aberrant crypt foci with E 171, may indicate adverse effects. With respect to genotoxicity, the Panel concluded that TiO 2 particles have the potential to induce DNA strand breaks and chromosomal damage, but not gene mutations. No clear correlation was observed between the physico‐chemical properties of TiO 2 particles and the outcome of either in vitro or in vivo genotoxicity assays. A concern for genotoxicity of TiO 2 particles that may be present in E 171 could therefore not be ruled out. Several modes of action for the genotoxicity may operate in parallel and the relative contributions of different molecular mechanisms elicited by TiO 2 particles are not known. There was uncertainty as to whether a threshold mode of action could be assumed. In addition, a cut‐off value for TiO 2 particle size with respect to genotoxicity could not be identified. No appropriately designed study was available to investigate the potential carcinogenic effects of TiO 2 NP s. Based on all the evidence available, a concern for genotoxicity could not be ruled out, and given the many uncertainties, the Panel concluded that E 171 can no longer be considered as safe when used as a food additive.

The synthesis of some noncommercial racemic 1,2-diaryl-2-hydroxyethanones (benzoins) is described, optimizing the previously reported methodologies. In a further step, the kinetic resolution of these substrates is reported, obtaining conversions of around 50% and ee(p) higher than 99% in very short reaction times. As enzymatic catalyst, after screening of several enzymes, the lipase TL (from Pseudomonas stutzeri) was the most efficient, working in an organic solvent with a very low log P value, such as THF. Finally, the dynamic-kinetic resolution of different benzoins using a lipase-ruthenium-catalyzed transesterification in organic solvents is described for the first time, obtaining conversions up to 90% maintaining the excellent enantioselectivity in all cases.

The Panel on Food Additives and Flavourings added to Food (FAF) provided a scientific opinion re-evaluating the safety of phosphates (E 338-341, E 343, E 450-452) as food additives. The Panel considered that adequate exposure and toxicity data were available. Phosphates are authorised food additives in the EU in accordance with Annex II and III to Regulation (EC) No 1333/2008. Exposure to phosphates from the whole diet was estimated using mainly analytical data. The values ranged from 251 mg P/person per day in infants to 1,625 mg P/person per day for adults, and the high exposure (95th percentile) from 331 mg P/person per day in infants to 2,728 mg P/person per day for adults. Phosphate is essential for all living organisms, is absorbed at 80-90% as free orthophosphate excreted via the kidney. The Panel considered phosphates to be of low acute oral toxicity and there is no concern with respect to genotoxicity and carcinogenicity. No effects were reported in developmental toxicity studies. The Panel derived a group acceptable daily intake (ADI) for phosphates expressed as phosphorus of 40 mg/kg body weight (bw) per day and concluded that this ADI is protective for the human population. The Panel noted that in the estimated exposure scenario based on analytical data exposure estimates exceeded the proposed ADI for infants, toddlers and other children at the mean level, and for infants, toddlers, children and adolescents at the 95th percentile. The Panel also noted that phosphates exposure by food supplements exceeds the proposed ADI. The Panel concluded that the available data did not give rise to safety concerns in infants below 16 weeks of age consuming formula and food for medical purposes.

The substitution of water in the half-sandwich complexes Cp*Rh(H2O)3 2+ and Cp*Ir(H2O)3 2+ (Cp* = η5-pentamethylcyclopentadienyl anion) by Cl-, Br-, I-, SCN-, py-CN (4-cyanopyridine), py-nia (nicotinamide), py (pyridine), TU (thiourea), and DMS (dimethylsulfide) was studied by stopped-flow spectroscopy at variable concentration, temperature, and pressure. The proton dissociation constants of the triaqua complexes, pK a = 6.47 (for rhodium) and pK a = 3.86 (for iridium), as well as the equilibrium constants for the formation of the dinuclear species (Cp*M)2(μ-OH)3 + were obtained by spectrophotometric titrations. The equilibrium constants K 1 for the formation of the monosubstituted complexes Cp*M(H2O)2L+/2+, as determined for anionic and neutral ligands L, lie in the range 102−105 M-1 and follow the sequences K(Cl-) < K(Br-) < K(I-) and K(py-CN) < K(py-nia) < K(py) < K(TU,DMS). Assuming the Eigen−Wilkins mechanism for the formation of the monosubstituted complexes, second-order rate constants k f,1 were corrected for outer sphere complex formation and for statistical factors to obtain rate constant k i‘ for the interchange step. The interchange rates k i‘ are nearly independent of the nature of L and very close to the rate of water exchange (k ex(Rh) = (1.6 ± 0.3) × 105 s-1 and k ex(Ir) = (2.5 ± 0.08) × 104 s-1). In all cases, i.e., for M = Rh and Ir and for L = anionic or neutral, the volume of the transition state is larger than that of the triaqua species. These findings support the operation of an I d mechanism without excluding a D mechanism. For a given ligand L, the substitution of another water molecule in the complexes Cp*M(H2O)2L+/2+ is by 1 order of magnitude slower than the substitution of the first water molecule in the triaqua species Cp*M(H2O)3 2+, as verified, for example, by k f,1 = 2.61 × 103 and k f,2 = 3.09 × 102 M-1 s-1 for M = Ir and L = py.