Fathers’ microplastic exposure tied to their children’s metabolic problems

(Press-News.org) RIVERSIDE, Calif. -- A study led by biomedical 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.

While MPs have already been detected in human reproductive systems, the study, published in the Journal of the Endocrine Society, is the first to bridge the gap between paternal exposure to MPs and the long-term health of the next generation (the “F1 offspring”).

MPs are tiny plastic particles (less than 5 millimeters) resulting from the breakdown of consumer products and industrial waste. Metabolic disorders refer to a cluster of conditions — including increased blood pressure, high blood sugar, and excess body fat — that increase the risk of heart disease and diabetes.

To induce metabolic disorders in F1 offspring, the researchers fed them a high-fat diet. This approach helps reveal the effects of paternal exposure that might otherwise remain mild or hidden under normal diet conditions. The high-fat diet mimics common unhealthy eating patterns, such as the Western diet, and amplifies metabolic risks. Because the fathers themselves were fed a regular diet, the obesity seen in F1 offspring is diet-induced.

The research team found 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 exact reasons for this sex-specific effect are still unclear,” said Changcheng Zhou, a professor of biomedical sciences in the UCR School of Medicine and the lead author of the study. “In our study, female offspring developed diabetic phenotypes. We observed upregulation of pro-inflammatory and pro-diabetic genes in their livers — genes previously linked to diabetes. These changes were not seen in male offspring.” 

The research team 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) — types of small non-coding RNAs. Unlike DNA, which provides the “blueprint” for life, these RNA molecules may act like “dimmer switches” for genes, controlling how much or how little a gene is expressed during development.

“To our knowledge, ours is the first study to show that paternal exposure to microplastics can affect sperm small non-coding RNA profiles and induce metabolic disorders in offspring,” Zhou said.

Zhou emphasized that the study suggests the impact of plastic pollution is not limited to the individual exposed; it may leave a biological imprint that predisposes children to chronic diseases. 

“Our discovery opens a new frontier in environmental health, shifting the focus toward how both parents’ environments contribute to the health of their children,” he said. “These findings from a mouse study likely have implications for humans. Men planning to have children should consider reducing their exposure to harmful substances like microplastics to protect both their health and that of their future children.”

The research 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,” Zhou said.

Zhou was joined in the study by Seung Hyun Park, Jianfei Pan, Ting-An Lin, Sijie Tang, and Sihem Cheloufi at UCR; Xudong Zhang and Qi Chen at the University of Utah School of Medicine; and Tong Zhou at the University of Nevada, Reno School of Medicine.

The study was partially supported by grants from the National Institutes of Health.

The title of the paper is “Paternal microplastic exposure alters sperm small non-coding RNAs and affects offspring metabolic health in mice.”

The University of California, Riverside is a doctoral research university, a living laboratory for groundbreaking exploration of issues critical to Inland Southern California, the state and communities around the world. Reflecting California's diverse culture, UCR's enrollment is more than 26,000 students. The campus opened a medical school in 2013 and has reached the heart of the Coachella Valley by way of the UCR Palm Desert Center. The campus has an annual impact of more than $2.7 billion on the U.S. economy. To learn more, visit www.ucr.edu.

END