We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Tracing micro and nanoplastics toxicity in human pulmonary fibroblasts through integrated Raman and transcriptomic analyses
AI summary Read the abstract
Researchers used integrated Raman spectroscopy and transcriptomic analysis to trace the cellular effects of micro- and nanoplastic exposure on human pulmonary fibroblasts. They found that plastic particle exposure altered gene expression patterns related to inflammation, oxidative stress, and cellular structure. The study provides molecular-level evidence that inhaled microplastics can trigger measurable biological responses in lung cells, supporting concerns about respiratory health risks.
Inhaled micro- and nanoplastics can reach the distal regions of the lungs, where their elimination is limited due to the lack of efficient clearance mechanisms. Although polystyrene particles have been detected in human lung tissue, the molecular effects of such exposures remain poorly characterized. Understanding the cellular response to microplastics exposure, particularly at the transcriptional and structural levels, is essential for assessing potential health risks. The purpose of this study was to evaluate the impact of primary polystyrene micro- and nanoparticles on human pulmonary fibroblasts, a relevant in vitro model for investigating the molecular mechanisms underlying microplastics-induced pulmonary toxicity. Monodisperse polystyrene particles with diameters of 0.1, 1 and 5 μm were used to evaluate size-dependent internalization and cellular response in human pulmonary fibroblasts. Cells were cultured under standard conditions and exposed to particles in vitro. Internalization and fate of microplastics were tested using Raman microscopy, while transcriptomic alterations were assessed by RNA sequencing to identify early molecular responses associated with particle size. Raman microscopy confirmed the internalization of 0.1 μm polystyrene particles by human pulmonary fibroblasts. Particles sized 1 μm showed a high affinity for the fibroblast cell membrane, however, definitive confirmation or exclusion of their internalization into the cells was not possible due to the sample preparation protocol and measurement conditions used. In contrast, exposure to 5 μm particles resulted in pronounced cytotoxicity across tested concentrations, precluding RNA-seq analysis. Transcriptomic profiling assessed by principal component analysis revealed distinct gene expression patterns in cells following exposure to 0.1 and 1 μm particles. Exposure to 0.1 μm particles led to upregulation of genes involved in mitochondrial function and protein synthesis. In contrast, 1 μm particles caused downregulation of genes associated with oxidative phosphorylation and proteostasis. This study shows that particle size and concentration critically influence the molecular response of human pulmonary fibroblasts to polystyrene micro- and nanoparticles. Raman microscopy proved a valuable tool for detecting particle internalization and assessing size-related biochemical changes, including in the nanoscale range.
More Papers Like This
Integration of transcriptomics and metabolomics reveal cytotoxic mechanisms of Polyethylene terephthalate microplastics in BEAS-2B cells
AI summary Read the abstract
Researchers exposed human lung cells to PET microplastics and used combined gene and metabolite analysis to uncover the mechanisms of toxicity. They found that the microplastics disrupted lipid metabolism and activated cell death pathways, reducing cell viability over time. The study suggests that inhaled PET microplastics could pose risks to respiratory health by triggering harmful molecular changes in lung tissue.
Nanoplastic Pollution of Human Bronchoalveolar Lavage Probed Based on Tip-Enhanced Raman Scattering
AI summary Read the abstract
Scientists used a super-sensitive imaging technique to detect nanoplastics, plastic bits smaller than a human cell, in fluid taken from human lungs, finding roughly 50 billion tiny particles per liter, most of which were nanoplastics rather than the larger microplastics we usually hear about. This matters because it shows these ultra-small plastic fragments are already present deep in our airways, and this new detection method could help researchers better study how they might affect our health.
Detection of microplastics in human lung tissue using μFTIR spectroscopy
AI summary Read the abstract
Researchers analyzed lung tissue from 13 people and found microplastics in 11 of the samples, identifying 12 different plastic types including polypropylene and polyester. The particles were found in all regions of the lungs, with significantly higher concentrations in the lower lung. This is one of the first studies to directly confirm that microplastics from everyday environments can be inhaled and accumulate deep in human lung tissue.
A single-cell perspective on polyethylene microplastic toxicity: linking fibroblast reprogramming to immune microenvironment alterations in the lung
AI summary Read the abstract
Scientists exposed rats' lungs to polyethylene microplastics (a common plastic found in air pollution) over time and used advanced cell-tracking technology to see exactly what happens inside lung tissue. They found that these plastic particles trigger immune cells to release signals that push scar-tissue-forming cells into overdrive, leading to thickened, scarred lung tissue and disrupted immune function. Since microplastics are already known to accumulate in human lungs, this research helps explain a possible mechanism behind plastic-related lung damage and points to specific molecules that could one day be targeted to prevent or treat it.
Label-free stimulated Raman scattering imaging of intracellular microplastics in mammalian cells
AI summary Read the abstract
Researchers used label-free stimulated Raman scattering imaging to visualize microplastic uptake and distribution inside mammalian cells without fluorescent labels, finding that intracellular microplastics were associated with elevated reactive oxygen species, reduced cell viability, and altered lipid metabolism.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.