RIVERSIDE, Calif. — A groundbreaking study by biomedical scientists at the University of California, Riverside, has revealed that a father’s exposure to microplastics (MPs) can lead to metabolic dysfunctions in his offspring. This research, conducted using mouse models, uncovers a previously unknown pathway through which environmental pollutants affect the health of future generations.
Published in the Journal of the Endocrine Society, the study is the first to establish a connection between paternal exposure to MPs and the long-term health of the next generation, termed the “F1 offspring.” Microplastics, tiny plastic particles less than 5 millimeters in size, result from the breakdown of consumer products and industrial waste. Metabolic disorders, which include conditions like high blood pressure, high blood sugar, and excess body fat, increase the risk of heart disease and diabetes.
Research Findings and Methodology
The research team induced metabolic disorders in F1 offspring by feeding them a high-fat diet, a method that reveals the effects of paternal exposure that might otherwise remain unnoticed under normal diet conditions. This approach mimics common unhealthy eating patterns, such as the Western diet, and amplifies metabolic risks. Notably, the fathers were fed a regular diet, indicating that the obesity observed in F1 offspring was diet-induced.
The study found that female offspring of male mice exposed to MPs were significantly more susceptible to metabolic disorders compared to offspring of unexposed fathers, despite all offspring consuming the same high-fat diet.
“The exact reasons for this sex-specific effect are still unclear,” said Changcheng Zhou, a professor of biomedical sciences at 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.”
While male offspring did not develop diabetes, they showed a slight yet significant decrease in fat mass. Female offspring, on the other hand, exhibited decreased muscle mass alongside increased diabetes.
Mechanisms of Inheritance
To understand how these traits were passed down, the researchers employed a specialized sequencing technology called PANDORA-seq, developed at UCR. They discovered that MP exposure alters the “cargo” of the sperm, affecting small molecules that regulate gene expression.
Specifically, 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 gene expression 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.
Implications and Future Research
Zhou emphasized that the study suggests the impact of plastic pollution extends beyond 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 investigations 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 added.
Joining Zhou in the study were 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 received partial support from grants from the National Institutes of Health.
The University of California, Riverside, a doctoral research university, serves as a living laboratory for groundbreaking exploration of issues critical to Inland Southern California, the state, and communities worldwide. Reflecting California’s diverse culture, UCR enrolls more than 26,000 students and has an annual impact of over $2.7 billion on the U.S. economy.
