Microplastics May Play Role in Idiopathic Pulmonary Fibrosis

Polyethylene terephthalate microplastics (PET-MPs) may initiate and exacerbate the progression of idiopathic pulmonary fibrosis (IPF), a new study found.

The findings come as public health officials have raised concerns about the potential health implications of microplastics. The report was published in the journal Ecotoxicology and Environmental Safety.¹

Defined as plastic particles smaller than 5 mm, microplastics enter the environment via industrial emissions, plastic degradation, and household products. | Image credit: yrabota - stock.adobe.com

While the underlying mechanisms behind the development of IPF are not yet fully understood, previous research has shown that environmental factors, including cigarette smoke and airborne particles, can contribute to the disease’s initiation and development, explained corresponding author Bing Bai, PhD, of the Fifth Affiliated Hospital of Zhengzhou University in China, and colleagues.²

The potential role of environmental factors is an important research topic, Bai and colleagues said, because the incidence of IPF is rising swiftly. A 2015 study, for instance, found that the global incidence of IPF was rising by approximately 11% per year.³

Bai and colleagues explored the potential role of microplastics in the rising rates of IPF.¹ Defined as plastic particles smaller than 5 mm, microplastics enter the environment via industrial emissions, plastic degradation, and household products. From there, ingestion, inhalation, and dermal contact can all lead to the microplastics entering the human body.

PET-MPs are the most common microplastics encountered in daily life, the authors explained, and there are several reasons why they may play a role in lung diseases like IPF.

“PET-MPs can induce oxidative stress, mitochondrial damage, and inflammatory responses in pulmonary cells, contributing to chronic lung injury,” the authors wrote, adding that PET-MP particles smaller than 10 μm can penetrate the alveolar barrier and accumulate in lung tissue, leading to a fibrosis-like pathology.

Yet, there is “scarce” research examining potential links between PET-MPs and the onset or exacerbation of IPF, the investigators noted. Bai and colleagues said they suspected that PET-MPs might contribute to IPF by modulating certain key molecular targets and signaling pathways.

To test the hypothesis, the investigators used public databases and a toxicity-prediction tool called ProTox 3.0 to identify potential targets and analyze their potential roles in IPF. They used network toxicology, molecular docking, Mendelian randomization, and single-cell sequencing analysis.

In the end, they identified 3 core targets through which they believe PET-MPs might aggravate IPF: AKT1, PIM1, and PIK3CD. The microplastics appear to affect metabolic, lipid, atherosclerosis, and C-type selection receptor signaling pathways, the authors said. They added that the binding affinity of PET-MPs to these core targets was “potent.”

The lung toxicity of PET-MPs may be associated with the proteins AKT1, PIK3CD, and PIM1, the authors said, and they said AT2 and CD8+ T cells are susceptible to the fibrotic effects induced by PET-MPs.

Bai and colleagues said the data show that prolonged exposure to microplastics is linked with the development of pulmonary interstitial fibrosis, and therefore they said it is urgent that regulators adopt better ways to track and restrict microplastics in the environment.

“Furthermore, establishing long-term exposure databases and conducting multi-regional cohort studies will be key to assessing population-level health impacts,” they wrote.

It will also be important to raise public awareness of the dangers of microplastics so that individuals—and their employers—can take steps to mitigate exposure.

The authors cautioned that their work was based on modeling toxicity using publicly available databases, adding that it is very difficult to adequately replicate long-term, low-dose exposure to microplastics. They concluded their hypotheses will require validation through both in vitro and in vivo experiments.

References

1. Zhao W, Yang S, Hu S, Feng Y, Bai B. Polyethylene terephthalate microplastics promote pulmonary fibrosis via AKT1, PIK3CD, and PIM1: A network toxicology and multi-omics analysis. Ecotoxicol Environ Saf. Published online August 27, 2025. doi:10.1016/j.ecoenv.2025.118954

2. Raghu G, Remy-Jardin M, Richeldi L, et al. Idiopathic pulmonary fibrosis (an update) and progressive pulmonary fibrosis in adults: an official ATS/ERS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med. 2022;205(9):e18-e47. doi:10.1164/rccm.202202-0399ST

3. Hutchinson J, Fogarty A, Hubbard R, McKeever T. Global incidence and mortality of idiopathic pulmonary fibrosis: a systematic review. Eur Respir J. 2015;46(3):795-806. doi:10.1183/09031936.00185114