Inhaling Microplastics, a Pollutant, Linked to Higher PF Risk in Mice
The inhalation of tiny plastic particles called polystyrene microplastics — an emerging pollutant that affects both terrestrial and aquatic ecosystems — was associated with the development of pulmonary fibrosis (PF) in healthy mice, a study shows.
Notably, these microplastics were found to promote oxidative stress and damage to lung cells, resulting in tissue scarring, or fibrosis.
Treatment with melatonin, a common antioxidant, eased lung fibrosis in mice exposed to microplastics.
These findings further support the potential hazards of microplastics in health, and highlight that inhaling polystyrene microplastics may be a potential risk factor for PF, the researchers noted.
“Overall, our findings provide new insights on the potential risks of [polystyrene microplastics] inhalation to terrestrial mammals,” the team wrote.
The study, “Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice,” was published in the journal Ecotoxicology and Environmental Safety.
According to the researchers, a number of studies have investigated the impact of microplastic pollution on the environment. However, little research has been done on the toxicological effects of such pollutants on mammals — and on their respiratory systems.
Given their non-degradable properties, plastic materials are broken down into tiny particles, called microplastics, that are scattered in the air and water, becoming a major pollutant in the world.
“Synthetic textile, weathered rubber and municipal waste are the most common objects that produce MPs [microplastics] in daily life, which are inhaled by people,” the researchers wrote, adding that “MPs have also been found in human lung tissue samples.”
A previous study estimated the number of microplastics in the human body via inhalation could reach several millions per year, and increasing evidence suggests that they can cause lung micro-injuries, oxidative stress, and inflammation — all factors implicated in PF.
Oxidative stress is a type of cellular damage resulting from an imbalance between the production of potentially harmful oxidant molecules and the cells’ ability to clear them with antioxidants.
Idiopathic pulmonary fibrosis (IPF), or PF of unknown cause, is thought to be caused by a combination of genetic and occupational and environmental factors. Occupational exposure to airborne microplastics in synthetic textile and vinyl, or PVC, industries previously has been associated with lung damage and IPF-like disease.
However, whether microplastic pollution is a risk factor of IPF remains largely unclear.
Now, a team of researchers in China investigated whether and how inhalation of polystyrene microplastics promoted PF in mice.
Polystyrene microplastics were chosen because this type of plastic is used as a bulk plastic for consumer use and is rapidly broken down when exposed to direct sunlight. Moreover, its microparticles can be found in a wide range of industries.
Researchers first found that inhalation of polystyrene microplastics three times a week for three weeks triggered PF in mice, and in a dose-dependent manner. Inhaled exposure to these microplastics promoted lung fibrosis, as well as a significant increase in the levels of fibrotic markers.
Further analyses in the lungs of these mice showed significant changes in the levels of several molecules that suggested alveolar epithelial damage and increased oxidative stress. Alveolar epithelial cells are those that line the small air sacs responsible for gas exchange in the lungs.
In addition, the levels of pro-inflammatory molecules, as well as the activation of the Wnt/β-catenin signaling pathway — central to the fibrotic activity observed in many fibrotic diseases — were significantly increased with increasing doses of inhaled polystyrene microplastics.
Notably, simultaneous treatment with melatonin, a common antioxidant often used as a supplement to promote sleep, partially prevented the microplastic-induced lung fibrosis and increases in pro-fibrotic and oxidative stress markers in these mice.
The team also found that lab-grown human alveolar cells exposed to these microplastics promoted the activation of neighboring lung fibroblasts — a type of cell implicated in PF — characterized by an increase in the levels of pro-fibrotic molecules.
However, fibroblasts directly exposed to microplastics did not show signs of activation, suggesting that “injuries to lung epithelial cells play an important role in the development of lung fibrosis,” the researchers wrote.
These results suggest that inhalation of polystyrene microplastics “induces pulmonary fibrosis via activation of oxidative stress and Wnt/β-catenin signaling pathway in mice,” and that “antioxidants could ameliorate the PS-MPs [polystyrene microplastic] related pulmonary fibrosis,” the team wrote.
The scientists said their findings give new insight into the potential risks of these pollutants to land-based mammals.
Given that researchers used pure spherical polystyrene microplastics of one size, further studies using other sizes and shapes, closer to what is found in the air, are needed to better understand the role of these pollutants in the risk of PF.
Also, microplastics can attach other pollutants and microorganisms in nature, which may add another layer of complexity to the role these particles play in lung diseases, the researchers noted.