A study from scientists at the University of California, Riverside, has shown for the first time that a father’s exposure to microplastics (MPs) can trigger metabolic dysfunctions in his offspring. The research, conducted using mouse models, highlights a previously unknown pathway through which environmental pollutants impact the health of future generations.
For the study, published in the Journal of the Endocrine Society, the researchers fed mice offspring a high-fat diet to mimic common unhealthy eating patterns and amplify metabolic risks. The results showed that female offspring of male mice exposed to MPs were significantly more susceptible to metabolic disorders than offspring of unexposed fathers, despite all offspring being fed the same high-fat diet.
The team also found that while male offspring did not develop diabetes, they showed a slight yet significant decrease in fat mass. Female offspring showed decreased muscle mass alongside increased diabetes.
To understand how the trait was passed down, the researchers used a specialized sequencing technology called PANDORA-seq, developed at UCR. They found that MP exposure alters the “cargo” of the sperm, affecting small molecules that regulate how genes are turned on and off. Specifically, the MP exposure significantly altered the sperm’s small RNA profile, including tRNA-derived small RNAs (tsRNAs) and rRNA-derived small RNAs (rsRNAs).
The study is the first to bridge the gap between paternal exposure to MPs and the long-term health of the next generation. The team hopes the findings will guide future investigation into how MPs and even smaller nanoplastics affect human development.
“Our future studies will likely look at whether maternal exposure produces similar risks and how these metabolic changes might be mitigated,” said Changcheng Zhou, professor of biomedical sciences at UCR and lead author of the study.
Data from UCR