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Microplastics featured article

Introduction

Microplastics are everywhere: in the food we eat, the water we drink, and even the air we breathe. Imagine consuming the equivalent of a credit card’s worth of plastic every week—just by going about your daily routine. As startling as it may seem, this is the reality we face, exposing our bodies to a hidden threat that’s growing by the day.

What are microplastics? They're tiny pieces of plastic or other polymer-based materials, ranging from 5 millimeters (~0.2 inches) to as small as 100 nanometers, often called nanoplastics. These tiny particles contain a variety of chemicals that are harmful to humans, including polyethylene terephthalate (commonly called PET), polyethylene, polypropylene, polyvinyl chloride, polystyrene, polyester, polyurethane, polyamide, styrene acrylate, and polymethyl-methacrylate.

Roughly 70% to 80% of micro- and nanoplastics come from the breakdown of larger plastic pieces, either through oxidation or other degradation...

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  • Microplastics

    Environmental physicochemical and biological processes drive microplastic generation, dispersal, chemical aging, pollutant sorption, and trophic transfer.

News & Publications

  • Chemical additives in plastics are associated with more than 350,000 cardiovascular deaths worldwide in a single year, with the Middle East, South Asia, and Africa bearing the greatest burden. www.thelancet.com
    Cardiovascular Environment

    Plastics may be a hidden contributor to heart disease: chemical additives that disrupt hormone function and damage blood vessels. Evidence indicates that di-2-ethylhexylphthalate (DEHP)—a phthalate used to soften plastics—drives oxidative stress, metabolic dysfunction, and cardiovascular disease. A recent study found that this plastic additive may have contributed to more than 350,000 cardiovascular deaths worldwide in 2018.

    To estimate the global burden of cardiovascular disease linked to DEHP exposure, researchers combined country-level cardiovascular death rates with regional exposure estimates. They calculated the number of deaths and years of life lost that were likely due to the chemical, drawing on published hazard ratios and biomonitoring data.

    They found that DEHP exposure contributed to 356,000 cardiovascular deaths in 2018—around 13% of heart-related deaths among adults aged 55 to 64. Exposure varied widely by region. The Middle East and South Asia had the highest levels of several DEHP metabolites, including mono (2-ethylhexyl) phthalate at 19.460 micromoles per liter—six times higher than levels in Europe. Africa also showed high concentrations, including the highest recorded level of mono (2-ethyl-5-carboxypentyl) phthalate at 65.452 micromoles per liter. The Middle East, South Asia, and Africa bore the greatest exposure burden, while Europe had the lowest.

    These findings suggest that chemical additives in plastics pose a serious threat to cardiovascular health, especially in regions with growing plastic production or weaker environmental protections. As plastic products break down, they shed tiny fragments known as microplastics, which carry considerable health risks. Learn more in this episode featuring Dr. Rhonda Patrick.

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  • Lifestyle and environmental exposures—termed the 'exposome'—may substantially outpace genetic factors in driving premature death and age-related disease. www.nature.com
    Epigenetics Aging Genetics Environment

    While genes play a role in aging, lifestyle and environmental exposures—collectively called the exposome—may have a more robust effect on aging and longevity. A recent study found that the exposome contributes far more to premature death and age-related diseases than genetic risk alone.

    Researchers analyzed data from nearly 500,000 people enrolled in the UK Biobank to measure the exposome’s role in aging. They identified environmental exposures linked to early death and biological aging, then used a proteomic age clock—a tool that tracks molecular signs of aging—to confirm which exposures accelerate the aging process. Finally, they compared the exposome’s influence on disease risk to that of genetic predisposition.

    The exposome explained 17 percentage points more of the variation in mortality than genetic risk, which accounted for less than two percentage points. It was more strongly connected to lung, heart, and liver diseases, while genetic factors were more closely associated with certain cancers and dementias. The analysis identified three disease states and 22 biomarkers related to liver and kidney function, cardiovascular and metabolic health, inflammation, longevity, genetics, and vitamin and mineral status that independently drive biological aging and disease risk.

    These findings suggest that the exposome is critical in shaping health and longevity. While genes contribute to some diseases, environmental exposures throughout life greatly influence aging and survival. Air pollution is an exposome element contributing to disease and early death. Learn how wearable devices measure the air pollution exposome in this episode featuring Dr. Michael Snyder.

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  • Data from nearly 80,000 twin pairs suggest that brain aneurysm ruptures are more commonly caused by environmental factors than by genes. (2010) www.sciencedaily.com
    Genetics Environment Tobacco Blood Pressure Aneurysm

    From the article:

    During the past few decades, the genetic makeup has been regarded as playing a significant role in the development of SAH [subarachnoid haemorrhage]. Contrary to this belief, however, a twin study recently published in the journal Stroke showed that environmental factors account for most of the susceptibility to develop SAH Conducted in Finland, Sweden and Denmark, the study is the largest population level twin study in the world.

    This means that instead of screening the close family members of SAH patients, the focus of preventive treatment may now be increasingly shifted to the efficient management of hypertension and smoking cessation intervention. This is what we do with other cardiovascular diseases as well."

    The Nordic study combined data on almost 80,000 pairs of twins over several decades. All in all, the follow-up time of all of the twin pairs corresponds to a staggering 6 million person-years.

    The researchers nevertheless emphasize that there are rare cases of families among whose members SAH is significantly more common than in the overall population. In these cases genetic factors are the principal cause underlying the development of the disease.

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