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Titanium dioxide as a food additive (E171) has been demonstrated to facilitate growth of chemically induced colorectal tumours in vivo and induce transcriptomic changes suggestive of an immune system impairment and cancer development. The present study aimed to investigate the molecular mechanisms behind the tumour stimulatory effects of E171 in combination with azoxymethane (AOM)/dextran sodium sulphate (DSS) and compare these results to a recent study performed under the same conditions with E171 only. BALB/c mice underwent exposure to 5 mg/kgbw/day of E171 by gavage for 2, 7, 14, and 21 days. Whole genome mRNA microarray analyses on the distal colon were performed. The results show that E171 induced a downregulation of genes involved in the innate and adaptive immune system, suggesting impairment of this system. In addition, over time, signalling genes involved in colorectal cancer and other types of cancers were modulated. In relation to cancer development, effects potentially associated with oxidative stress were observed through modulation of genes related to antioxidant production. E171 affected genes involved in biotransformation of xenobiotics which can form reactive intermediates resulting in toxicological effects. These transcriptomics data reflect the early biological responses induced by E171 which precede tumour formation in an AOM/DSS mouse model.

Current evidence of engineered nanomaterials' (ENM) toxicity has led to a latent concern about hazards for both humans and the environment. For this reason, some efforts have been made to suggest frameworks or other guidance to regulate ENM handling; however, the real exposure risk to humans has not been well established. The aims of this work were to analyze the difficulties in establishing regulations for ENM and to discuss some considerations that may be helpful for policy makers involved in the regulation of ENM. Difficulties in establishing regulations are based on the novel properties of ENM associated with cytotoxic effects, the insufficiency of standardized methods to test those effects and the lack of epidemiological evidence of ENM toxicity, especially in occupational settings. Nevertheless, we offer some suggestions for establishing regulations, which include frameworks oriented towards protecting personnel exposed to ENM without decreasing production. In addition, we propose an ENM data sheet to offer available information of ENM. Finally, ethical aspects should also be considered in developing ENM regulations because every person who is working around or consuming ENM has the right to be informed about the potential risk.

We investigated gene expression responses in BALB/c mice exposed by gavage to 5 mg/kg bw/day of E171 for 2, 7, 14 and 21 days. Food additive E171 (titanium dioxide) has been shown to induce oxidative stress and DNA damage in vitro as well as facilitating growth of colorectal tumours in vivo. Full genome expression changes of the colon of mice were investigated by using Agilent SurePrint G3 mouse Gene exp 60kv2 microarrays slides. The data presented in this DiB include all differentially expressed for each time point with EntrezGeneID, gene symbols, gene names and Log2FC as well as genes included in pathways after over-representation analysis in ConsensusPathDataBase. The functions of these genes in relation to the colon were described in our associated article (Proquin et al., 2017 in press) [1]. Raw and normalized gene expression data are available through NCBI GEO (GEO accession: GSE92563).