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Deposition of microplastics associated with bioaccumulation of heavy metals in human lungs of smokers: Implications of adsorption and mobilization of metals via microplastics
Summary
Researchers compared lung tissue from smokers and non-smokers and found that smokers accumulated more microplastics alongside elevated levels of heavy metals in lung tissue, suggesting that tobacco smoke enhances chelation of heavy metals to airborne microplastics, increasing lung bioaccumulation.
Abstract Background Airborne micro- and nano plastics (MNPs), generated from synthetic textiles, vehicle tires and plastic wastes, are omnipresent in the environment and known to deposit in human lungs. Bioaccumulation of MNPs in lung tissues has been studied, but effect of tobacco smoking on deposition is not well understood. Tobacco smoke is known to contain heavy metals which can get adsorbed to the MNP surface, leading to increased environmental bioavailability. We hypothesized that smoking leads to enhanced chelation of heavy metals with airborne MNPs leading to accentuated lung bioaccumulation, thereby leading to lung pathologies. Methods Age (20-75 years) and sex-matched archival lung tissue samples from smokers (n = 9) and non-smokers (n = 10) were procured and quantified to assess: (a) the levels of MNPs by pyro-GC/MS and (b) heavy metals by ICP-MS. Furthermore, to establish if there exists a correlation between MNP deposition and disease occurrence in current smokers, tissue samples from age-matched patients with COPD (n = 4) and IPF (n = 4) underwent pyro-GC/MS analyses. Results A relatively higher level of MNPs were found in the lungs of smokers (43.67 mcg/gm) as compared to non-smoker (34.53 mcg/gm) upon pyro-GC/MS analyses. We observed a marked increase in the levels of polyethylene (PE; p< 0.0076), polycarbonate (PC; p< 0.0947) and nylon6 (N6; p < 0.0653) polymers in the lungs of smokers as compared to non-smokers. Metal analyses showed a significant (p <0.0001) increase in the levels of cadmium (Cd) in the lungs of smokers with the levels of deposited Cd being more pronounced for female smokers. Importantly, we observed a strong correlation (p < 0.05) between the amounts of accumulated PE and levels of Cd in the lungs. Pyro-GC/MS analyses did not reveal any relation between MNP deposition and disease occurrence in our study. Furthermore, little to no change in the level of deposited MNPs was observed in the lungs of current versus ex-smokers in disease cohorts. Conclusions Overall, our results show that smoking promotes bioaccumulation of certain MNPs (PE) with heavy metals (Cd) which may lead to adverse lung effects in smokers.