Table 5.

Impacts of microplastics on the development of pulmonary diseases and associated molecular mechanisms. Microplastics can induce various harmful effects on lung health, such as inflammation, disruption of lung surfactant integrity, antiproliferative activity against human alveolar cells, lung fibrosis, loss of elasticity, exacerbation of asthma, and pathological changes that may lead to chronic obstructive pulmonary disease

Biological effect on the lung	Mechanism	Reference
Inflammatory responses	More significant neutrophil influx into rat lung after instillation of 64 nm polystyrene Increased lactate dehydrogenase and protein in bronchoalveolar lavage Increased expression of interleukin-8 in adenocarcinoma human alveolar basal epithelial (A549) cells	Brown et al. (2001)
Altering lung surfactant properties	Microplastics modified the phase behaviour, surface tension, and membrane structure of the lung surfactant Microplastic adsorbs phospholipid components of lung surfactants better and promotes the production of free radicals	Shi et al. (2022b)
Inhibition of human alveolar cells proliferation Potential toxicity	Population-level decrease in metabolic activity parallel to the reduction in the proliferation rate Significant changes in the morphology of cells exposed to microplastics of 1 μm	Goodman et al. (2021)
Reduced cell viability, induced cell cycle S phase arrest, stimulated inflammatory gene transcriptions and modified the expression of proteins linked with cell cycle and pro-apoptosis	Induced up-regulation of pro-inflammatory cytokines such as interleukin-8, NFκB and tumour necrosis factor-α, as well as pro-apoptotic proteins such as caspase 3, caspase 8, caspase 9, death receptor 5, and cytochrome c	Xu et al. (2019)
Increased migration and epithelial-to-mesenchymal transition markers Membrane potential changes and impaired cellular energy metabolism	Upregulation of reactive oxygen species and NADPH oxidase 4 (NOX4) Causes mitochondrial dysfunction Activation endoplasmic reticulum stress	Halimu et al. (2022)
Pulmonary cytotoxicity and inflammation by inducing reactive oxygen species in human non-tumorigenic lung epithelial cell line (BEAS-2B)	Increase expression of interleukin-8 and interleukin-6, and induce reactive oxygen species Disruption of lung epithelial barrier through oxidative stress and inflammation	Dong et al. (2020)
Induces inflammation, deposition of microplastics, lung histological changes	Alveolar destruction and bronchial epithelium disarrangement Interleukin-6, tumour necrosis factor-α and interleukin-1β were upregulated Modulation of lncRNAs and circRNAs	Fan et al. (2022)
Worsens airway inflammation Increased phagocytosis Increased cellular stress responses and programmed cell death in the asthma model	Increased pulmonary inflammatory cells Increased macrophages accumulation and phagocytosis Increased production of mucus, immunoglobulin G1, and Immunoglobulin E Increased interleukin-4, interleukin-5, and Th1 type tumour necrosis factor-α	Lu et al. (2021b)

NFκB is the nuclear factor kappa-light-chain-enhancer of activated B cells and NADPH is the nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4).