Microplastics and Inflammation: How Tiny Particles Contribute to Gut Dysbiosis, Neuroinflammation, and Beyond, part 2

January 24, 2025. 
Contributing Authors: Team TRILITY / ACEND

Microplastics, defined as plastic fragments smaller than five millimeters, are drawing increasing scrutiny due to their widespread presence in the environment and the concern that they may adversely affect human health. These minuscule particles typically originate from the breakdown of larger plastics or from primary sources such as microbeads in personal care products. Studies now confirm that microplastics appear in various food items, water supplies, and even the air we breathe. With each discovery, questions about their impact on our bodies grow more pressing. Researchers are especially focused on the ways microplastics might drive inflammation in the gastrointestinal tract, central nervous system (CNS), and other bodily regions. Examining how these microscopic polymers disrupt the microbiome and trigger chronic inflammation can offer valuable insight into risks that may affect long-term health.

The first step in understanding the effects of microplastics is exploring how they enter and accumulate within the body. Research in Environmental Science & Technology suggests that humans may ingest tens of thousands of microplastic particles each year (Cox et al., 2019). These particles often come from a wide range of everyday sources, including seafood, bottled water, and various packaged goods. Such widespread exposure underscores the need to comprehend the long-term implications of ingesting these particles, especially their propensity to initiate or worsen chronic inflammatory conditions.

One factor heightening concerns about microplastics is their ability to carry and release harmful chemicals. For instance, many plastics are manufactured with additives like plasticizers, which can leach out once the plastic particles enter the body. Microplastics also readily absorb pollutants from their environment, serving as transport vessels for compounds such as heavy metals or pesticides. When these contaminants are released within human tissues, they can spark immune responses, raising levels of inflammation and oxidative stress. Some microplastics are tiny enough—referred to as nanoplastics when under 100 nanometers—to cross cellular barriers, enter the bloodstream, and possibly migrate into organs (Galloway, 2015). This phenomenon is significant because once they infiltrate tissues, they can activate localized immune cells and set off systemic inflammatory cascades.

One of the principal areas of research into microplastics and inflammation revolves around the gut microbiome. The human gastrointestinal tract contains trillions of microorganisms that perform crucial tasks, from aiding digestion to regulating immune function. However, prolonged exposure to microplastics may disturb this microbial community. Scientists note that microplastics can alter the gut’s balance of beneficial and harmful bacteria, a condition termed dysbiosis (Prata et al., 2020). Dysbiosis can weaken the intestinal barrier, enabling even more potential toxins to pass into the bloodstream. This heightened permeability, sometimes called “leaky gut,” may encourage the spread of inflammatory signals throughout the body and amplify the risk of chronic inflammatory disorders.

Moreover, inflammation originating in the gut doesn’t necessarily stay there. The concept of a “gut-brain axis” explains how the state of the gastrointestinal tract can influence the central nervous system. If microplastics and the associated dysbiosis cause an upregulation in pro-inflammatory cytokines, these chemical messengers can enter circulation and cross the blood-brain barrier, potentially triggering inflammatory responses in the brain itself. The blood-brain barrier is a safeguard that screens many substances from entering brain tissue, but smaller or specially shaped microplastics might bypass these defenses (Wright & Kelly, 2017). Once these particles or their associated chemicals accumulate in the CNS, the immune cells within the brain—called microglia—can become activated. Prolonged stimulation of microglia is of particular concern; chronic neuroinflammation can lead to issues such as cognitive decline and heightened vulnerability to neurodegenerative diseases.

Research also reveals that microplastics might impact other parts of the body. The liver and kidneys, critical organs for detoxification and waste removal, can become focal points for microplastic deposition. If these particles remain lodged in tissue, they could generate a persistent inflammatory response and oxidative stress, gradually eroding organ function (Danopoulos et al., 2022). Even inhalation of airborne microplastics may lead to inflammation in the respiratory system, particularly if fibers embed themselves in lung tissue and trigger immune reactions. Such persistent irritation may heighten the likelihood of respiratory conditions.

Why do these tiny particles provoke such pronounced inflammatory responses? One explanation involves the body’s innate reaction to any foreign material. Plastic is not a naturally occurring substance within the human body, so immune cells recognize microplastics as invaders. The immune response to these foreign particles includes producing free radicals and pro-inflammatory molecules, both of which can disrupt normal cellular processes. Additionally, the distinct shapes and sizes of microplastics may further influence inflammatory potential. For instance, fibrous microplastics can embed in tissues more easily, causing irritation and inflammation that may be more difficult for immune cells to resolve (Wright & Kelly, 2017).

Crucially, the health risks posed by microplastics underscore our close bond with the environment. The less plastic litter in our oceans, soil, and atmosphere, the fewer microplastics humans are likely to ingest. Effectively addressing plastic pollution through smarter waste management, more robust recycling efforts, and limits on single-use plastics is essential to reducing the overall burden. In parallel, awareness campaigns and lifestyle changes can help individuals limit personal exposure. Using water filters, consuming fewer heavily packaged foods, and steering clear of disposable plastics are practical steps people can adopt.

Still, the question of microplastic toxicity isn’t fully settled. Ongoing investigations attempt to pinpoint the precise exposure levels at which negative effects become pronounced. Future research might reveal that genetic factors or specific underlying health conditions make certain people more vulnerable. Furthermore, the environmental complexity of microplastics—encompassing diverse shapes, sizes, and chemical loads—makes it challenging to generalize findings. Differences in exposure and susceptibility mean that not everyone who consumes microplastics will experience the same health risks.

What is clear, though, is that microplastics can incite inflammatory processes across multiple body systems. From the gut microbiome to the brain, evidence indicates that the chronic presence of these particles may accelerate or exacerbate inflammatory pathways. Given that chronic inflammation underlies numerous diseases—from metabolic disorders to autoimmune conditions—understanding how microplastics could shift the body toward an inflammatory state remains an urgent priority. As we develop more sophisticated analytical tools and pursue long-term human studies, science will likely shed more light on the precise mechanisms at play.

In the meantime, proactive measures can make a difference. Governments can impose stricter regulations on the manufacturing and disposal of plastics, while industries can invest in alternative materials and eco-friendly packaging solutions. Scientists can focus on research that quantifies microplastic intake and identifies critical thresholds for harm. Physicians and public health experts can educate patients about potential risks and encourage practices that minimize unnecessary plastic use. Each of these steps will help reduce microplastic proliferation in the environment and, by extension, minimize their infiltration into the human body.

In sum, microplastics appear to contribute to inflammation throughout the body, from gut dysbiosis to potential neuroinflammation in the CNS. Their unique ability to transport harmful chemicals and penetrate biological barriers raises valid concerns about their role in initiating or worsening chronic inflammatory states. While the science is still evolving, current findings underscore the necessity for swift, coordinated efforts in research, policy, and individual action. Reducing plastic pollution is more than just an ecological imperative; it’s a direct path to safeguarding human health and curtailing exposure to these microscopic invaders.

References: Cox KD, Covernton GA, Davies HL, Dower JF, Juanes F, Dudas SE (2019). Human Consumption of Microplastics. Environmental Science & Technology 53(12): 7068-7074. Galloway TS (2015). Micro- and Nano-plastics and Human Health. In Bergmann M, Gutow L, Klages M (Eds.), Marine Anthropogenic Litter (pp. 343–366). Springer, Cham. Prata JC, da Costa JP, Lopes I, Duarte AC, Rocha-Santos T (2020). Environmental Exposure to Microplastics: An Overview on Possible Human Health Effects. Science of The Total Environment 702: 134455. Wright SL, Kelly FJ (2017). Plastic and Human Health: A Micro Issue? Environmental Science & Technology 51(12): 6634–6647. Danopoulos E, Twiddy M, West R, Rotchell JM (2022). A Rapid Review and Meta-Regression Analyses of the Toxicological Impacts of Microplastic Exposure in Human Cells. Science of The Total Environment 806: 150356.

Note: Always consult with a healthcare professional before considering any treatment options or significant dietary changes.