Micro- and nanoplastics (MNPs) and their potential toxicological outcomes: State of science, knowledge gaps and research needs

Abstract

Plastic waste has been produced at a rapidly growing rate over the past several decades. The environmental impacts of plastic waste on marine and terrestrial ecosystems have been recognized for years. Recently, researchers found that micro- and nanoplastics (MNPs), micron (100 nm - 5 mm) and nanometer (1 - 100 nm) scale particles and fibers produced by degradation and fragmentation of plastic waste in the environment, have become an important emerging environmental and food chain contaminant with uncertain consequences for human health. This review provides a comprehensive summary of recent findings from studies of potential toxicity and adverse health impacts of MNPs in terrestrial mammals, including studies in both in vitro cellular and in vivo mammalian models. Also reviewed here are recently released biomonitoring studies that have characterized the bioaccumulation, biodistribution, and excretion of MNPs in humans. The majority MNPs in the environment to which humans are most likely to be exposed, are of irregular shapes, varied sizes, and mixed compositions, and are defined as secondary MNPs. However, the MNPs used in most toxicity studies to date were commercially available primary MNPs of polystyrene (PS), polyethylene (PE), polyvinyl chloride (PVC), polyethylene terephthalate (PET), and other polymers. The emerging in vitro and in vivo evidence reviewed here suggests that MNP toxicity and bioactivity are largely determined by MNP particle physico-chemical characteristics, including size, shape, polymer type, and surface properties. For human exposure, MNPs have been identified in human blood, urine, feces, and placenta, which pose potential health risks. The evidence to date suggests that the mechanisms underlying MNP toxicity at the cellular level are primarily driven by oxidative stress. Nonetheless, large knowledge gaps in our understanding of MNP toxicity and the potential health impacts of MNP exposures still exist and much further study is needed to bridge those gaps. This includes human population exposure studies to determine the environmentally relevant MNP polymers and exposure concentrations and durations for toxicity studies, as well as toxicity studies employing environmentally relevant MNPs, with surface chemistries and other physico-chemical properties consistent with MNP particles in the environment. It is especially important to obtain comprehensive toxicological data for these MNPs to understand the range and extent of potential adverse impacts of microplastic pollutants on humans and other organisms.

Keywords: Micro- and nanoplastics; Oxidative stress; Physico-chemical properties; Toxicity.

Figure 1.

A. The number of peer-reviewed publications of MNP toxicity studies from January 2015 to September 2022. B. Types of MNP toxicity studies.

Figure 2.. Types of MNP particles used in toxicity studies.

PS: polystyrene, PE: polyethylene, LDPE: low density polyethylene, PP: polypropylene, PVC: polyvinyl chloride, PET: polyethylene terephthalate, PA: polyamide, PU: polyurethanes, TW: tire wear.

Figure 3.. A schematic diagram of potential mechanisms underlying MNP toxicity proposed in in vitro and in vivo studies.

A. Systemic levels. MNPs can be exposed through three routes, including ingestion, inhalation and possible dermal contact. Ingested or inhaled MNPs with small sizes could reach the systemic or portal circulation, and further distribute and accumulate in different organs, leading to organ dysfunction. Moreover, MNP particles could translocate through physiological barriers, including blood-placenta barrier, blood-brain barrier and blood-testis barrier, posing a potential risk to neural, reproductive and developmental systems. B. Cellular and molecular levels. The internalized MNP particles can cause lysosomal damage or mitochondrial dysfunction, which induces reactive oxygen species (ROS) production. Oxidative stress caused by overproduced ROS leads to a cascade of cellular effects, including endoplasmic reticulum (ER) stress, cytoskeletal dysfunction, protein oxidation, lipid peroxidation, and DNA damage. Moreover, oxidative stress leads to activation of molecular signaling pathways, which could further activate inflammation and transcription factors. These interconnected intracellular events collectively contribute to cell injury and death.