Papers

Low-dose polystyrene microplastics exposure increases susceptibility to obesity-induced MASLD via disrupting intestinal barrier integrity and gut microbiota homeostasis

A mouse study found that even low doses of polystyrene microplastics made fatty liver disease significantly worse when combined with a high-fat diet, creating a "double hit" effect. The microplastics damaged the gut lining, disrupted beneficial gut bacteria, and triggered inflammation that spread to the liver, and these harmful effects were difficult to reverse even after two weeks of stopping exposure.

Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study

Researchers tested UV-aged polypropylene microplastics from everyday plastic cup lids on mice and lab-grown liver tissue, finding that more heavily aged particles caused greater liver damage. The aged microplastics disrupted energy production in liver cells and caused a harmful buildup of antioxidant molecules, suggesting that the weathered microplastics people encounter in daily life may be more toxic than pristine ones.

Single-cell RNA-seq analysis decodes the kidney microenvironment induced by polystyrene microplastics in mice receiving a high-fat diet

Using advanced single-cell gene analysis, researchers found that mice fed both polystyrene microplastics and a high-fat diet suffered significantly worse kidney damage than either exposure alone. The combination reshaped the kidney's cellular environment, promoting scarring, triggering cancer-related pathways, and altering immune cell populations. This is particularly relevant to human health because many people are simultaneously exposed to microplastics through food and drink while also consuming high-fat diets.

Low-dose polystyrene microplastics exposure impairs fertility in male mice with high-fat diet-induced obesity by affecting prostate function

Male mice exposed to low doses of microplastics had lower sperm quality and fewer offspring, and these effects were significantly worse when combined with a high-fat diet. The combination triggered inflammation and cell death in the prostate gland, reducing key nutrients in seminal fluid needed for sperm health. This suggests that microplastic exposure may be an overlooked factor in declining male fertility, especially for those with metabolic conditions like obesity.

Low-dose of polystyrene microplastics induce cardiotoxicity in mice and human-originated cardiac organoids

Researchers found that even low doses of polystyrene microplastics can damage heart tissue in both mice and lab-grown human heart organoids. The microplastics triggered oxidative stress and disrupted energy production in heart cells, leading to inflammation and cell death. This is one of the first studies to show heart-specific toxicity from microplastics at doses meant to reflect realistic human exposure levels.

Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids

Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.

Integrated transcriptomics and metabolomics to explore the varied hepatic toxicity induced by aged- and pristine-microplastics: in vivo and human-originated liver organoids-based in vitro study

Using human liver organoids (miniature lab-grown livers), researchers found that sun-aged microplastics caused more damage to liver cells than fresh microplastics, even at concentrations matching what is found inside human bodies. The aged particles specifically disrupted energy production in mitochondria and altered an amino acid metabolism pathway linked to cardiovascular disease. This is significant because most microplastics in the environment have been weathered by sunlight, meaning the real health risk may be greater than studies using pristine plastics suggest.

Inhalable microplastics prevails in air: Exploring the size detection limit

Researchers developed a method using Raman microscopy to detect airborne microplastics as small as 1 micrometer, significantly improving upon previous detection limits. They found that the number of microplastics in air samples increased dramatically when smaller particles were counted, with inhalable-sized particles being the most prevalent. The findings suggest that current estimates of human microplastic exposure through breathing may substantially undercount the actual amount.

Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver

Using advanced single-cell analysis, researchers showed that microplastics worsened non-alcoholic fatty liver disease in mice fed a high-fat diet by changing how immune cells behaved in the liver. Microplastic exposure amplified inflammatory responses and altered the communication between different liver cell types. This study is important because it reveals specific immune mechanisms by which microplastics could worsen liver disease, a condition already affecting roughly one in four adults worldwide.

Lung microbiota participated in fibrous microplastics (MPs) aggravating OVA-induced asthma disease in mice

In a mouse study, inhaling fiber-shaped microplastics significantly worsened asthma symptoms, including airway inflammation, mucus buildup, and lung tissue scarring. The microplastic fibers also disrupted the balance of bacteria living in the lungs and activated inflammatory pathways. Since fibrous microplastics are the most common airborne shape and have been found in human lungs, this research suggests they could worsen respiratory conditions like asthma in people.

Combined effect of polystyrene microplastics and bisphenol A on the human embryonic stem cells-derived liver organoids: The hepatotoxicity and lipid accumulation

Researchers used human stem cell-derived liver organoids to study the combined toxic effects of polystyrene microplastics and the plasticizer bisphenol A. The study found that co-exposure produced enhanced hepatotoxicity and lipid accumulation compared to individual exposures, with changes in markers related to oxidative stress, inflammation, and energy metabolism in the liver tissue model.

The iron matters: Aged microplastics disrupted the iron homeostasis in the liver organoids

Researchers compared the effects of fresh versus aged polystyrene microplastics on lab-grown human liver tissue and found that aged particles caused significantly more damage. The aged microplastics disrupted iron balance in liver cells, leading to a form of cell death called ferroptosis, and triggered inflammatory responses. The study suggests that weathered microplastics encountered in everyday life may pose greater risks to liver health than the pristine particles typically used in laboratory studies.

Microplastic Exposure in COPD Alters the Immune Microenvironment: Implications for Tumor-Promoting Inflammation

Researchers used single-cell RNA sequencing to analyze how microplastic exposure affects the lung immune environment in mice with COPD. They found that microplastics worsened inflammation, increased immune cell exhaustion, and reduced the population of cells critical for lung repair, creating conditions that may be more favorable for tumor development. The study suggests that microplastic exposure may intensify the already elevated cancer risk associated with COPD by promoting a tumor-permissive immune environment.

Aged microplastics disrupted copper homeostasis to induce vascular toxicity: in vivo and human vascular organoids-based in vitro study

Researchers evaluated the vascular toxicity of aged polypropylene microplastics using both human vascular organoids and in vivo models, finding that aged microplastics disrupted copper homeostasis in blood vessel cells. This copper imbalance led to oxidative stress and damage to the vascular endothelium. The study suggests that the aging process microplastics undergo in the environment may make them more harmful to the cardiovascular system than fresh particles.

Polystyrene microplastics exposure increases the disruption of intestinal barrier integrity and gut microbiota homeostasis during obesity and aging

Researchers found that polystyrene microplastic exposure worsened intestinal barrier dysfunction in mice on high-fat diets, with the combination of obesity and microplastic exposure producing greater gut permeability and inflammation than either factor alone, suggesting compounding risks in metabolically vulnerable individuals.

Corrigendum to “Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids” [Sci. Total Environ. 806 (2022) 150328]

Safety analysis of immediate breast reconstruction with a deep inferior epigastric perforator (DIEP) flap in the post-COVID-19 era: a comparison between pre- and post-pandemic cohorts

Not relevant to microplastics — this surgical study evaluates the safety of resuming DIEP flap breast reconstruction surgery following the COVID-19 pandemic, comparing patient outcomes between pre- and post-pandemic cohorts.

Independent and combined associations of multiple heavy metal exposure with lung function: A population-based study in US children

This population-based study of over 1,200 US children found that combined exposure to 12 urinary metals significantly reduced lung function across all measured parameters, with lead identified as the largest individual contributor to respiratory harm.