Titanium dioxide (TiO2) nanoparticles added to foods can worsen intestinal inflammation in persons with inflammatory bowel disease such as ulcerative colitis.
- Inflammatory bowel disease (IBD) namely ulcerative colitis and Crohn’s disease is on the rise worldwide and several factors are believed to play a role, especially a Western lifestyle and diet.
- Current study suggests titanium dioxide, a food grade additive in several foods could increase intestinal inflammation associated with IBD and exacerbate the condition.
As mentioned earlier, IBD incidence is on the increase and in addition to genetic factors, a Western diet is thought to play a major role in its pathogenesis.
Not much is known about the effects of TiO2 in the intestine and existing research is mostly about its effects on the respiratory tract following inhalation where it is known to cause airway inflammation and asthma. However, earlier studies have shown TiO2 can cause production of reactive oxygen species and trigger inflammation and tissue damage both in culture cells (in vitro) as well as inside the body (in vivo).
The research team of Gerhard Rogler, professor of gastroenterology and hepatology at the
University of Zurich proceeded to investigate the effects of TiO2 on the intestinal tract and its possible role in the pathogenesis of inflammatory bowel disease.
Titanium dioxide Effects On Intestinal Cells – Findings Of The Study
- To study the effects of TiO2 the team initially analyzed its effect in cell cultures. It was observed that titanium dioxide nanoparticles could penetrate human intestinal epithelial cells and macrophages and accumulate within them.
- The nanoparticles triggered an inflammatory reaction in the intestinal cells by activating the NLRP3 (nod like receptor P3) inflammasome, a part of the non-specific immune response that perceived the inorganic nanoparticles as danger signals.
- Additionally, in mice models of inflammatory bowel disease, it was observed that oral administration of TiO2 worsened the intestinal inflammation and destruction of the epithelial cells by activating the NLRP3 pathway.
- The TiO2 particles were shown to accumulate in the spleen of mice indicating that the particles were absorbed from the intestine into the blood circulation and reached the spleen.
- When the blood of patients with ulcerative colitis was tested, they were noted to have an increased of TiO2, again strongly suggesting that these particles were absorbed into the blood stream through the diseased intestinal cells in ulcerative colitis where the normal protective barrier of the intestinal epithelium is lost.
Inflammatory Bowel Disease
Among the environmental factors, a predominantly Western lifestyle and diet have been shown to be associated with an increased risk of developing IBD.
Interestingly alterations in the Nlrp3 gene have been identified in Crohn’s disease patients lending credence to the observation that TiO2 particles mediated damage to the intestinal mucosa in mice models of IBD was through activation of this pathway.
Takeaway From The Study
- Based on the observations of the study team, the Nlrp3 pathway could be studied as a target for possible therapeutic interventions in inflammatory bowel disease in future research.
- Importantly, the findings of the study suggest that persons diagnosed with inflammatory bowel disease should avoid consuming foods containing titanium dioxide and pay careful attention to food labels before purchasing. Instead, they should switch to a diet low in inorganic components including inorganic nanoparticles to keep their disease under check.
These studies would help in gaining more insight into the biological effects of these particles and help in formulating and fine tuning guidelines for use of inorganic nanoparticles by the food industry with strict regulations.
References:
- Titanium Dioxide Nanoparticles in Food and Personal Care Products - (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3288463/)
- What You Should Know about Titanium Dioxide - (https://www.bestfoodfacts.org/titanium-dioxide-maynard/)