Prenatal Exposure to Microplastics Impacts Microbiome, Increases Asthma Risk

Prenatal exposure to different microplastic particles may impact the neonatal gut microbiome in a manner that increases individuals’ risk of asthma, new findings suggest, and this impact is transmissible through live microbiota.

These results were presented at the American Thoracic Society (ATS) 2025 International Conference, with the poster being titled ‘Urban Air, Diesel Exhaust and Microplastic Particles Predispose to Asthma Origin Via Gut Microbiome Alteration.’ The findings were the result of research conducted by such investigators as Alexey V. Fedulov, MD, PhD, of Brown University School of Medicine.

“Among the particles microplastics are a ‘new’ type and are increasingly found in the organism of humans; accumulating evidence implies health risks, but often no link to disease is seen making causality hard to establish,” Fedulov and colleagues wrote.1

The investigators pointed to growing evidence indicating a link between disruptions in the gut microbiome and the development of asthma and allergies in general, although they further noted that direct causality remained difficult to confirm. The underlying mechanisms, they expressed, related to exposure to airborne environmental particles triggering asthma have not been sufficiently explored.

The team further highlighted that such exposures have also been shown to impact gut microbial composition. Microplastics are a relatively novel class of particles that have been detected in human tissues and connected to several health concerns. Disease outcomes’ connection to such exposures, however, had complicated efforts to prove a causal connection as well.

Fedulov at al decided to explore such interactions using a mouse model that was developed to simulate prenatal exposure to 3 forms of airborne particles—concentrated ambient particles (CAP), diesel exhaust particles (DEP), and microplastic particles. Through their model, they sought to explore how these exposures impact asthma susceptibility among offspring and whether the gut microbiome plays a mediating role.

In their study design, they exposed pregnant mice via inhalation to CAP, DEP, or microplastic particles. The offspring of these mice showed a predisposition to asthma, developing airway inflammation following their exposure to an otherwise sub-threshold dose of allergen—1 known not to induce disease in the control animals.

They evaluated whether gut microbiota were responsible for this susceptibility through the use of gut microbiome transplants (GMT) that were performed during their analysis. Microbiota from neonates with a lack of exposure to any allergen were transferred to microbiota-depleted recipient pups.

Later, Fedulov and coauthors evaluated the subjects for asthma-related features, including eosinophilic infiltration in bronchoalveolar lavage fluid, airway hyperresponsiveness, lung tissue inflammation, and elevated levels of Th2 cytokines interleukin (IL)-4, IL-5, and IL-13.

Among the most notable findings the investigators uncovered were that the GMT from all 3 exposure groups, including the microplastic exposure group, was found to have been sufficient to transfer asthma predisposition to naïve recipients.

After their GMT material was sterilized using radiation, the investigative team determined that it no longer induced asthma-like symptoms, which they determined would suggest that live microbes are necessary for such impacts. Antibiotic administration alongside the GMT also prevented the onset of symptoms related to asthma, which the team determined further supported the role of viable bacterial species.

Fedulov et al’s metagenomic analysis identified a higher abundance of Butyribacter, Acetatifactor, Coproplasma, Kineothrix, and members of the Lachnospiraceae family in the CAP and DEP cohorts, though their analyses for microplastic samples are ongoing. In their functional analyses, results pointed to these taxa as producers of short-chain fatty acids (SCFAs), especially acetate and butyrate.

These fatty acids are known to affect the function of dendritic cells (DCs). Further evaluations by the investigators confirmed altered SCFA levels and a shift in DC activity toward a pro-allergic phenotype in the exposed offspring.

These results, overall, provide mechanistic insight into the manner in which environmental particle exposure during an animal’s pregnancy may contribute to allergic airway disease in offspring. The findings therefore suggest specific microbial targets for future analyses.

For any additional information on new data presented at ATS, view updates in the latest conference coverage.

References

1. Fedulov A, Yano N, et al. (Poster Board # 204) Urban Air, Diesel Exhaust and Microplastic Particles Predispose to Asthma Origin Via Gut Microbiome Alteration. Abstract presented at the American Thoracic Society (ATS) International Conference 2025 in San Francisco, CA, from May 18 - May 21, 2025.