Paternal exposure to microplastics alters the metabolic health of offspring

Paternal exposure to microplastics alters the metabolic health of offspring

A study conducted 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 disorders in his offspring. Research using mouse models reveals a previously unknown pathway through which environmental pollutants influence the health of future generations.

While MPs have already been detected in human reproductive systems, says the study published in theJournal of the Endocrine Societyis the first to close 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) that are formed when consumer goods and industrial waste decompose. Metabolic disorders refer to a range of conditions – including elevated 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 remain mild or hidden under normal nutritional conditions. The high-fat diet mimics common unhealthy eating habits like the Western diet and increases metabolic risks. Since the fathers themselves were fed regularly, the obesity observed in F1 offspring is nutritionally related.

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, even though all offspring received the same high-fat diet.

The exact reasons for this gender-specific effect are still unclear. In our study, female offspring developed diabetic phenotypes. We observed upregulation of pro-inflammatory and pro-diabetic genes in their liver - genes that have previously been linked to diabetes. These changes were not observed in male offspring.”

Changcheng Zhou, professor of biomedical sciences at the UCR School of Medicine and lead author of the study

The research team found that although male offspring did not develop diabetes, they did show a slight but significant decrease in fat mass. Female offspring showed reduced muscle mass and increased diabetes.

To understand how the trait was passed down, researchers used a special sequencing technology called PANDORA-seq, developed at UCR. They found that MP exposure changes sperm “cargo,” affecting small molecules that regulate how genes are turned on and off.

In particular, MP exposure significantly altered sperm 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 can act like “dimmer switches” for genes, controlling how much or how little a gene is expressed during development.

"To our knowledge, our study is the first to show that paternal exposure to microplastics can affect sperm small noncoding RNA profiles and cause metabolic disorders in offspring," Zhou said.

Zhou emphasized that the study suggests that the effects of plastic pollution are not limited to those exposed; It can leave a biological impression that predisposes children to chronic illness.

"Our discovery opens new frontiers in environmental health and shifts the focus to 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 pollutants such as microplastics to protect both their health and that of their future children."

The research team hopes the findings will guide future research into how MPs and even smaller nanoplastics impact human development.

"Our future studies will likely examine whether maternal exposure poses 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 from 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 supported in part by grants from the National Institutes of Health.

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