The controversy about the impacts of the tiny particles of plastic that are ubiquitous in the environment on human health has given rise to a plethora of studies, all attempting to answer the question of what really happens when people ingest or inhale these particles.
Now, a team of scientists from Hong Kong and China recently published the results of their investigation into the health risks for humans of nanoplastics - particles 1,000 times smaller than an algal cell - in ACS’ latest issue of Environmental Science & Technology.
Researchers recently showed that particles less than 100 nm-wide can enter animals’ blood and organs, causing inflammation, toxicity and neurological changes. Zongwei Cai, Chunmiao Zheng and colleagues wanted to examine the molecular-level and metabolic impacts when human lung and liver cells are exposed to similarly sized nanoplastics. To that end, they cultured human liver and lung cells separately in laboratory plates and treated them with different amounts of 80 nm-wide plastic particles. After two days, electron microscopy images showed that nanoplastics had entered both types of cells without killing them. However, the scientists did find that the cells’ normal processes were disrupted.
The researchers looked at the compounds released by mitochondria — energy-producing organelles that are thought to be sensitive to nanoplastics — during metabolism. They saw that the more nanoplastics the liver and lung cells were exposed to, the more reactive oxygen species and different amounts of nucleotides, nucleosides, amino acids, peptides and carboxylic acids the cells produced. This indicates that multiple metabolic processes were disturbed, with in some cases, the mitochondrial pathways appearing to be dysfunctional. These observations demonstrate that while nanoplastics exposure doesn’t kill human lung and liver cells, it could disrupt critical processes, potentially causing negative impacts on organs, the researchers say.
This study is the first to show how nanoplastics impact mitochondrial cells in humans. The finding that nanoplastics can enter cells and induce mitochondrial damage without causing mass cell death is of particular interest. According to the authors of the study, the effects observed at the molecular and cellular levels could be considered ‘predisease events to predict nanoplastic exposure outcomes at the tissue and organ levels’.
As they write: “Thus, the mitochondrial damage observed in this study might cause cells and eventually organ tissues to malfunction.” Observing that pure commercial nanoplastics without additional chemicals were used in this study, and that nanoplastics pollution can vary in shape, age, and length of coexistence with other toxic chemicals in the environment, they conclude that the actual adverse impacts of nanoplastics on environmental and human health are likely to be greater than those measured in this study, and that a better understanding of the potential adverse effects of nanoplastics exposure in humans is needed.
Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells
Siyi Lin, Hongna Zhang, Chen Wang, Xiu-Li Su, Yuanyuan Song, Pengfei Wu, Zhu Yang, Ming-Hung Wong, Zongwei Cai, and Chunmiao Zheng
Environmental Science & Technology 2022 56 (17), 12483-12493
DOI: 10.1021/acs.est.2c03980