Microplastics and nanoplastics (MNPs) are ubiquitous environmental contaminants. Their prevalence, persistence, and increasing industrial production have led to questions about their long-term impact on human and animal health. This narrative review describes the effects of MNPs on oxidative stress, inflammation, and aging. Exposure to MNPs leads to increased production of reactive oxygen species (ROS) across multiple experimental models, including cell lines, organoids, and animal systems. ROS can cause damage to cellular macromolecules such as DNA, proteins, and lipids. Direct interaction between MNPs and immune cells or an indirect result of oxidative stress-mediated cellular damage may lead to increased production of pro-inflammatory cytokines throughout different MNP-exposure conditions. This inflammatory response is a common feature in the pathogenesis of neurodegenerative, cardiovascular, and other age-related diseases. MNPs also act as cell senescence inducers by promoting mitochondrial dysfunction, impairing autophagy, and activating DNA damage responses, exacerbating cellular aging altogether. Increased senescence of reproductive cells and transfer of MNPs/induced damages from parents to offspring in animals further corroborates the transgenerational health risks of the tiny particles. This review aims to provoke a deeper investigation into the notorious effects these pervasive particles may have on human well-being and longevity.

Microplastics have gained much attention due to their prevalence and abundance in our everyday lives. They have been detected in household items such as sugar, salt, honey, seafood, tap water, water bottles, and food items wrapped in plastic. Once ingested, these tiny particles can travel to internal organs such as the kidney and liver and cause adverse effects on the cellular level. Here, human embryonic kidney (HEK 293) cells and human hepatocellular (Hep G2) liver cells were used to examine the potential toxicological effects of 1 μm polystyrene microplastics (PS-MPs). Exposing cells to PS-MPs caused a major reduction in cellular proliferation but no significant decrease in cell viability as determined by the trypan blue assay in both cell lines. Cell viability remained at least 94% for both cell lines even at the highest concentration of 100 μg/mL of PS-MPs. Phase-contrast imaging of both kidney and liver cells exposed to PS-MPs at 72 h showed significant morphological changes and uptake of PS-MP particles. Confocal fluorescent microscopy confirmed the uptake of 1 μm PS-MPs at 72 h for both cell lines. Additionally, flow cytometry experiments verified that more than 70% of cells internalized 1 μm PS-MPs after 48 h of exposure for both kidney and liver cells. Reactive oxygen species (ROS) studies revealed kidney and liver cells exposed to PS-MPs had increased levels of ROS at each concentration and for every time point tested. Furthermore, quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis at 24 and 72 h revealed that both HEK 293 and Hep G2 cells exposed to PS-MPs lowered the gene expression levels of the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and antioxidant enzymes superoxide dismutase 2 (SOD2) and catalase (CAT), thus reducing the potential of SOD2 and CAT to detoxify ROS. These adverse effects of PS-MPs on human kidney and liver cells suggest that ingesting microplastics may lead to toxicological problems on cell metabolism and cell-cell interactions. Because exposing human kidney and liver cells to microplastics results in morphological, metabolic, proliferative changes and cellular stress, these results indicate the potential undesirable effects of microplastics on human health.

African Americans (AAs) have higher mortality rate from breast cancer than that of Caucasian Americans (CAs) even when socioeconomic factors are accounted for. To better understand the driving biological factors of this health disparity, we performed a comprehensive differential gene expression analysis, including subtype- and stage-specific analysis, using the breast cancer data in the Cancer Genome Atlas (TCGA). In total, 674 unique genes and other transcripts were found differentially expressed between these two populations. The numbers of differentially expressed genes between AA and CA patients increased in each stage of tumor progression: there were 26 in stage I, 161 in stage II, and 223 in stage III. Resistin, a gene that is linked to obesity, insulin resistance, and breast cancer, was expressed more than four times higher in AA tumors. An uncharacterized, long, non-coding RNA, LOC90784, was down-regulated in AA tumors, and its expression was inversely related to cancer stage and was the lowest in triple negative AA breast tumors. Network analysis showed increased expression of a majority of components in p53 and BRCA1 subnetworks in AA breast tumor samples, and members of the aurora B and polo-like kinase signaling pathways were also highly expressed. Higher gene expression diversity was observed in more advanced stage breast tumors suggesting increased genomic instability during tumor progression. Amplified resistin expression may indicate insulin-resistant type II diabetes and obesity are associated with AA breast cancer. Expression of LOC90784 may have a protective effect on breast cancer patients, and its loss, particularly in triple negative breast cancer, could be having detrimental effects. This work helps elucidate molecular mechanisms of breast cancer health disparity and identifies putative biomarkers and therapeutic targets such as resistin, and the aurora B and polo-like kinase signaling pathways for treating AA breast cancer patients.