Age-Accelerating Poison in the Air and Food: Microplastics

Highlights

• Microplastics accumulate in the fatty tissue—known as adipose tissue—of mice following microplastic exposure.
• The buildup of microplastics in adipose tissue is associated with increased markers of aging, such as those linked to DNA damage and inflammation.

Microplastics pervade the air we breathe, the soil beneath our feet, our water supply, and have even made their way into our food. It seems that avoiding exposure to these small particles—less than five millimeters in size—is virtually impossible, so figuring out how they affect our physiology has become paramount.

Now, published in Scientific Reports, Kim and colleagues from Catholic Kwandong University in South Korea have found an association between microplastics exposure and adipose tissue aging in mice. Along those lines, microplastics exposure was linked to increased protein markers for inflammation, DNA damage, and cellular senescence—an age-associated, dysfunctional cellular state. If these findings from mice translate to humans, environmental microplastics exposure could be speeding up the pace at which we age, increasing the likelihood of meeting the grim reaper earlier on.

Microplastics More than Double Protein Markers Associated with Aging

Aged, dysfunctional adipose tissue releases inflammatory factors and has been linked to insulin resistance, diabetes, and obesity, possibly even contributing to aging itself. For this reason, Kim and colleagues proposed that adipose tissue aging may be intricately linked to the general processes of aging. Along those lines, they sought to pinpoint whether microplastics accumulate in adipose tissue following exposure and whether this buildup is associated with an upsurge of proteins linked to aging.

To start their experiment, the Korean researchers fed mice a suspension of microplastics for two weeks and then measured levels of microplastics in adipose tissue. Their imaging data confirmed that microplastics accumulate in adipose tissue after 14 days of exposure.

Kim and colleagues also found that a key indicator of senescence—SA-ꞵ-galactosidase—was elevated in the adipose tissue of mice exposed to microplastics. Other protein markers that increased with microplastics exposure included the protein HMGB1, an inflammation indicator, and H2A.X, a marker of DNA damage. For each of these proteins, microplastics exposure more than doubled their levels in adipose tissue. These findings show that microplastics exposure dramatically increases levels of protein markers associated with aging, suggesting that microplastics accelerate adipose tissue aging.

Urgent Public Action Required to Reduce Microplastics in the Environment

The findings from Kim and colleagues suggest that microplastic exposure through oral ingestion may accelerate aging in the adipose tissue of mice. While speeding up the aging of adipose tissue may contribute to age-related metabolic problems as well as general aging, the effects of microplastics on other organ systems still need to be explored.

For example, our body’s largest organ, the skin, receives exposure to microplastics from the air, yet microplastics’ effects on skin aging need examination. Furthermore, since microplastics have been documented in food and water supplies, researchers must also check to see how they may affect gut, urinary, and kidney system aging—all systems that filter ingested food and water. Finally, even if microplastics are found to accelerate aging throughout our bodies, the only way to mitigate their effects would be some public service effort to rid our environment of them. All the same, since they were first documented in the stomachs of albatrosses in the 1960s, one can only fathom the prevalence of environmental microplastics now. Thus, minimizing and reversing our environment’s accumulation of microplastics could take centuries, maybe even presenting an impossible challenge.