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Micro- and Nanoplastics as Potential Drivers of Dilated Cardiomyopathy
Summary
This review paper looks at growing lab evidence that tiny plastic particles (microplastics and nanoplastics) — which have already been found in human heart tissue — may damage heart cells by causing stress and dysfunction inside them, potentially contributing to a serious heart condition called dilated cardiomyopathy, especially in people who are already genetically at risk. It's important to note this is based on animal and cell studies, not proof that plastics cause heart disease in humans yet, but it highlights why researchers want to study this connection further and why reducing plastic exposure might be a reasonable precaution.
Dilated cardiomyopathy (DCM) is a leading cause of heart failure, but up to 50% of cases have no definitive etiology. Genetic susceptibility alone does not account for phenotypic inconsistency, so a 'two-hit' model has been proposed to explore the spectrum of gene-environment interactions. Certain triggers, such as alcohol, chemotherapy agents, and viral myocarditis, are well-established second hits in the pathogenesis of DCM. The exposome, which encompasses environmental and social exposures across the lifespan, provides a more comprehensive framework to understand these interactions. In patients with DCM, air pollution and heavy metals have already been associated with higher rates of mortality and heart failure hospitalization. Microplastics and nanoplastics (MNPs) are novel components of the exposome. They form from the degradation of plastics and enter the circulatory system primarily through ingestion and inhalation. They have recently been found in human cardiovascular tissue, including atherosclerotic plaques and the myocardium. In vivo and in vitro models consistently demonstrate that MNPs induce oxidative stress, mitochondrial dysfunction, and calcium dysregulation. These pathways are shared with established cardiotoxins and converge on cardiomyocyte death, fibrosis, and eccentric ventricular remodeling, which is consistent with the pathogenesis and phenotype of DCM. In genetically susceptible individuals, MNP exposure may therefore contribute to the progression from subclinical myocardial injury to overt systolic dysfunction. This narrative review synthesizes preclinical mechanistic evidence linking MNP exposure to myocardial injury, compares the underlying mechanisms with those of other environmental pollutants and cardiovascular toxins, and integrates these findings within the proposed 'two-hit' model of DCM. Whether MNP exposure contributes to DCM in humans remains to be established, but understanding the potential consequences of MNPs has important implications for prevention, therapeutic development and health policy. Standardization of detection methods, chronic low-dose exposure models, and prospective human studies using functional cardiac assessment are needed before translating these experimental findings into clinical practice.