Microplastics, airway inflammation, and chronic respiratory disease: A mechanistic links to COPD and Asthma

Maryam Alsadat Baniaghil; Atoosa  Ryahi; Niloofar Keikhaei; Mohsen Farrokhpour

doi:10.66224/jcbior.7.2.365

Authors

Maryam Alsadat Baniaghil Department of Internal Medicine, School of Medicine, Qom University of Medical Sciences, Qom, Iran https://orcid.org/0000-0001-8948-9313
Atoosa Ryahi Student Research Committee, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Niloofar Keikhaei Sayad Shirazi Hospital, Department of Internal Medicine, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
Mohsen Farrokhpour Firouzgar Hospital, Department of Internal Medicine, School of Medicine, Iran University of Medical Sciences, Tehran, Iran https://orcid.org/0000-0001-6057-5437

DOI:

https://doi.org/10.66224/jcbior.7.2.365

Keywords:

Microplastics, Nanoplastics, Airway inflammation, Asthma, Chronic obstructive pulmonary disease

Abstract

Microplastics (MPs) and nanoplastics (NPs) are increasingly recognized as ubiquitous environmental contaminants with potential implications for respiratory health. Inhalation represents an important route of exposure, and the detection of plastic particles in human lung tissue has provided direct evidence that these particles can reach the respiratory system. This narrative review summarizes current evidence on the potential mechanisms linking inhaled MPs and NPs to chronic airway inflammation, with particular emphasis on asthma and chronic obstructive pulmonary disease (COPD). Recent studies indicate that plastic particles can induce oxidative stress, mitochondrial dysfunction, epithelial barrier disruption, altered macrophage responses, and persistent inflammatory signaling. In experimental models of asthma, MPs and NPs may enhance allergen-induced airway inflammation through epithelial injury, alarmin release, T helper 2 (Th2)-associated responses, eosinophilic inflammation, airway hyperresponsiveness, and airway remodeling. Emerging COPD-related evidence suggests that MPs may interact with pathways involved in mitochondrial injury, ferroptosis, epithelial dysfunction, and chronic pulmonary inflammation. Moreover, the potential for MPs to adsorb or transport environmental contaminants, allergens, and other particulate pollutants raises the possibility that their respiratory effects may be amplified under realistic co-exposure conditions. Despite increasing mechanistic evidence, substantial uncertainty remains regarding environmentally relevant exposure levels, chronic human exposure, individual susceptibility, and causal relationships with asthma or COPD. Future research should therefore prioritize standardized exposure assessment, longitudinal epidemiological studies, and multi-pollutant experimental models to determine whether MPs represent independent disease-causing agents or clinically relevant modifiers of chronic airway disease.

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