Persistent Organic Pollutants and Type 1 Diabetes in Youth
Author Information
Author(s): Bresson Sophie E., Isom Scott, Jensen Elizabeth T., Huber Sandra, Oulhote Youssef, Rigdon Joseph, Lovato James, Liese Angela D., Pihoker Catherine, Dabelea Dana, Ehrlich Shelley, Ruzzin Jérôme
Primary Institution: University of Oslo
Hypothesis
POPs are associated with T1D and directly cause pancreatic β-cell dysfunction and/or destruction.
Conclusion
The study suggests that certain persistent organic pollutants may play a role in the etiology of type 1 diabetes in youth and negatively affect pancreatic β-cell function.
Supporting Evidence
- Participants with higher levels of p,p’-DDE, trans-nonachlor, and PCB-153 had increased odds of type 1 diabetes with normal insulin sensitivity.
- PCB-153 and p,p’-DDE impaired insulin production and secretion in pancreatic β-cells in vitro.
- Long-term exposure to PCB-153 and p,p’-DDE progressively decreased β-cell viability.
Takeaway
Some chemicals in the environment can make it harder for kids to produce insulin, which is important for controlling blood sugar.
Methodology
The study analyzed plasma samples from participants in the SEARCH for Diabetes in Youth Case Control Study and conducted in vitro experiments on pancreatic β-cells.
Limitations
The study relied on fasting human samples, which may miss manifestations of dysglycemia.
Participant Demographics
Participants were aged 10–22 years, including controls and those with type 1 diabetes categorized by insulin sensitivity.
Statistical Information
P-Value
p<0.05
Confidence Interval
95% CI 1.0, 3.8 for p,p’-DDE
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website