Can Exposure to Environmental Chemicals Increase the Risk of Diabetes Type 1 Development?

Figure 1

Mechanisms suggested to be involved in pathways of T1DM development after exposure to environmental chemicals via food/gut, air/lungs, and skin. Chemicals can act directly on beta or immune cells, by binding to receptors (X and Y-receptors could, for instance, be adrenergic-, purinergic-, or scavenger receptors) or after uptake in the cells by pinocytosis, endocytosis, or diffusion. Chemicals can also affect factors like mucosal permeability, the microbiome, or the hormone balance, all shown to interact with the immune system. Several chemicals have been shown to induce epigenetic changes. Chemical exposures can further lead to apoptosis or cell death, increased oxidative stress, impaired insulin response, altered immune function or immunosuppression, molecular mimicry, and posttranslational modifications.