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P756 Assessment of metal exposures in deciduous teeth of patients with inflammatory bowel disease

N. Nair*1, C. Austin2, M. Rocha3, C. Gouveia3, P. Curtin2, C. Eisele1, J-f. Colombel4, J. Torres3,4, I. Peter1, M. Arora2

1Icahn School of Medicine at Mount Sinai Hospital, Department of Genetics and Genomic Sciences, New York, USA, 2Icahn School of Medicine at Mount Sinai Hospital, Department of Environmental Medicine and Public Health, New York, USA, 3Hospital Beatriz Ângelo, Surgical Department, Gastroenterology Division, Loures, Portugal, 4Icahn School of Medicine at Mount Sinai Hospital, Division of Gastroenterology, Department of Medicine, New York, USA

Background

Environmental factors are thought to play a major role in the pathogenesis of inflammatory bowel disease (IBD). Importantly, increasing epidemiological evidence suggests that exposures occurring during early life may be determinant of disease development. However, studying exposures occurring during this window of susceptibility is challenging, and very little has been elucidated about environmental exposures preceding disease onset. Teeth develop in an incremental manner, storing environmental information on compounds such as metals and organics as we age. The study of deciduous (baby) teeth-matrix biomarkers allows assessment of cumulative exposures, starting as early as the second trimester of prenatal development, and continuing into early childhood until teeth shedding. Herein, by studying deciduous teeth, we aimed to identify whether critical exposures during early development may be associated with IBD diagnosis later in life.

Methods

Adult IBD patients and healthy controls from a single-centre in Portugal were asked to donate their baby teeth; it is traditional for Portuguese families to keep naturally-shed deciduous teeth for years. Thirty teeth were obtained from 14 IBD patients (8 CD, 6 UC) and 16 from unaffected controls (3 from unaffected siblings of IBD patients). Laser ablation-inductively coupled mass spectrometry analysis was used to create temporal metal exposure profiles from the second trimester of pregnancy through the first 6 months of life. Data were analysed using distributed lag models by estimating the time-lagged association of exposures with IBD diagnosis while accounting for the correlated exposures.

Results

We found divergences in metal uptake in the teeth of individuals who eventually developed IBD when compared with controls in a time-dependent manner. Lead exposure, a known inflammatory toxicant that has been shown to predispose to murine colitis, as well as alter the gut microbiome and affect metabolic functions, was significantly higher during intra-uterine and the first 6 months of life (p < 0.05). Likewise, in IBD patients, copper (Cu) levels were significantly higher up to 15 weeks postnatally, and chromium (Cr) levels were also significantly elevated from 10 to 15 weeks before birth (both p < 0.05). While elevated copper levels have been shown in patients with UC, no link between chromium and IBD in humans has been previously established.

Conclusion

These data suggest that a deregulation in metal uptake during a critical window in early-life is a feature of IBD, prior to the emergence of any clinical symptoms.