Toxicity of Microplastics and Nanoplastics in Mammalian Systems

Cheryl Qian Ying Yong, Suresh Valiyaveettil, Bor Luen Tang, Cheryl Qian Ying Yong, Suresh Valiyaveettil, Bor Luen Tang

Abstract

Fragmented or otherwise miniaturized plastic materials in the form of micro- or nanoplastics have been of nagging environmental concern. Perturbation of organismal physiology and behavior by micro- and nanoplastics have been widely documented for marine invertebrates. Some of these effects are also manifested by larger marine vertebrates such as fishes. More recently, possible effects of micro- and nanoplastics on mammalian gut microbiota as well as host cellular and metabolic toxicity have been reported in mouse models. Human exposure to micro- and nanoplastics occurs largely through ingestion, as these are found in food or derived from food packaging, but also in a less well-defined manner though inhalation. The pathophysiological consequences of acute and chronic micro- and nanoplastics exposure in the mammalian system, particularly humans, are yet unclear. In this review, we focus on the recent findings related to the potential toxicity and detrimental effects of micro- and nanoplastics as demonstrated in mouse models as well as human cell lines. The prevailing data suggest that micro- and nanoplastics accumulation in mammalian and human tissues would likely have negative, yet unclear long-term consequences. There is a need for cellular and systemic toxicity due to micro- and nanoplastics to be better illuminated, and the underlying mechanisms defined by further work.

Keywords: human cells; microplastics; mouse cells; nanoplastics; oxidative stress; toxicants; toxicity.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
A schematic diagram illustrating potential (speculative at the moment) cellular mechanisms of MP/NP toxicity. MPs/NPs can be taken up through ingestion and inhalation. MPs/NPs could damage the plasma membrane and impair the gut barrier (left). These could also perturb signaling of cell surface receptors, and alter gene expression in the nucleus. Endocytosed MPs/NPs could also perturb the endocytic pathway function and compromise the endosomal membranes. Stresses arising from the above could activate the cellular innate immune system, with endogenous and secreted damage-associated molecular patterns (DAMP) inducing the innate immunity-mediating toll-like receptors (TLRs). Stresses could induce ROS production from the NADP oxidases (NOXs). Mitochondrial impairment, either by MPs/NPs from endosomes or in response to stresses, could also produce more ROS through impairment in the efficiency of electron transport chain (ETC) processes. MPs/NPs gain access into the circulation if the gut–vascular barrier is compromised or it may speculatively occur by transcytosis, thus reaching other organs. The lung probably has a more direct access to airborne MPs/NPs (right).

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