Data from: High food grade titanium dioxide exposure is related to gut dysbiosis in healthy, young adults

This study aimed to test the hypothesis that chronic dietary exposure of TiO2 (titanium dioxide) in humans induces mucosal inflammation and oxidative stress, and causes gut dysbiosis, conditions that favor development of a broad range of chronic diseases. This hypothesis was tested for the first time via these specific aims: Aim 1: Define dietary TiO2 exposure by measuring fecal TiO2 content among 80 adults. Hypothesis 1a: Median fecal TiO2 content among adult participants (estimated at 0.2g/kgbw/d, range 0.01-3.4, based on preliminary data) will be used to stratify two distinct groups of high and low dietary TiO2 exposure. Hypothesis 1b: Estimation of dietary TiO2 from three standardized 24h recalls will be significantly related to fecal TiO2 content (r>0.5; p<0.05). Aim 2: Establish how dietary TiO2 exposure is related to the gut microbiome (phyla diversity and mechanism of action). Hypothesis 2a: Distinct 16s rRNA profiles, lower phylogenic diversity and lower fecal SCFA content (butyrate, propionate and acetate) will be identified among the high human TiO2 exposure group compared to the low exposure group. Hypothesis 2b: Significant differences in metabolomic pathway regulation (e.g. lipid metabolism, cellular community [tight junction] and oxidative stress [p53 signaling]) will be identified using iPATH3 and Pathview, and differences identified with PLS-DA modeling between high TiO2 and low TiO2 exposure groups. Aim 3: Establish how dietary TiO2 exposure is related to gut inflammation, permeability, oxidative stress and general homeostasis. Hypothesis 3: Intestinal biomarkers of inflammation [fecal calprotectin, lactoferrin, myeloperoxidase], permeability [A-1-antitrypsin], and gut homeostasis [intestinal alkaline phosphatase] will be significantly higher in the high human TiO2 exposure group compared to the low exposure group.