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A recent study has provided some of the clearest evidence to date of how smoking physically damages the human lungs. For the first time, scientists directly measured how smoking alters the mechanical properties of actual human lung tissue, discovering that smoking makes the lungs significantly stiffer—similar to the damage observed in fibrosis, a serious lung disease characterized by scarring.
Led by researchers at the University of California, Riverside, the study was published in the Journal of the Royal Society Interface. The lungs are primarily composed of soft, sponge-like tissue called lung parenchyma, which expands and contracts with each breath. Maintaining this flexibility is crucial for efficient oxygen transfer into the bloodstream and the removal of carbon dioxide. When lung tissue becomes rigid, breathing becomes more difficult because the tissue resists expansion, reducing oxygen flow and making even simple activities tiring.
While smoking has long been associated with illnesses such as COPD, emphysema, lung cancer, and fibrosis, scientists previously lacked detailed knowledge of how smoking physically alters lung tissue itself. To explore this, researchers obtained lung samples from donors—either for transplantation or research purposes. They carefully cut small square sections of lung tissue and stretched them in various directions, measuring how much resistance the tissue offered against movement.
The findings highlighted significant differences between smokers and non-smokers. Lung tissue from smokers became markedly stiffer when stretched, resisting expansion more than healthy tissue from non-smokers. This behavior closely resembles fibrosis, where scar tissue gradually stiffens the lungs, making breathing more difficult over time.
Mona Eskandari, a mechanical engineer at UC Riverside and the study’s lead author, explained that earlier studies often used animal models or tested tissue stretched in only one direction. However, real lungs expand in multiple directions simultaneously during breathing. To better mimic this natural process, Eskandari’s team stretched the tissue across multiple directions at once, providing a more accurate understanding of lung mechanics in vivo.
The study also revealed an unexpected variation within the lungs: tissue from the upper regions was generally stiffer than tissue from lower areas, even within the same lung lobe. Researchers suggest gravity might influence this difference, as humans spend most of their lives upright, causing different long-term physical stresses on upper versus lower lung regions. This could explain why certain areas are more prone to injury or complications, especially in situations like ventilator use, where overstretching can cause damage—indicating some lung regions are inherently more vulnerable to mechanical stress.
Additionally, the study examined how lung tissue responds during repeated stretching cycles. Results showed that human lung tissue dissipates more energy during such cycles than lung tissue from mice, highlighting potential limitations in extrapolating animal data directly to humans. This finding is particularly relevant for the development of “digital twin” computer models that simulate breathing, disease progression, and treatment outcomes. Eskandari noted that reliance on animal data might lead to incomplete or inaccurate models of human lung behavior.
The team also observed early signs that lung stiffness may increase with age, though further research is needed to confirm this trend. One challenge faced was the limited availability of human donor lungs suitable for detailed testing, as such samples are rare. Nonetheless, the researchers believe their dataset represents one of the most comprehensive collections of mechanical data from human lung tissue to date.
Ultimately, these findings could influence the design of ventilators, surgical planning, and computational models that predict how diseased lungs respond to stress and therapy. Eskandari founded the biomechanics Experimental and Computational Health Laboratory (bMECH) at UC Riverside to explore how biological tissues behave mechanically.
This research importantly provides new, direct insights into the physical damage caused by smoking inside human lungs—strengthened by the fact that it examined actual human tissue rather than relying solely on animal models. However, due to the scarcity of donor lungs, larger-scale studies are necessary to better understand how smoking, aging, and disease influence lung stiffness over time.
For those interested in lung health, it’s also worth exploring studies about marijuana’s effects, as well as why some non-smokers develop lung disease while some heavy smokers do not. Recent research suggests that olive oil could promote longevity, and vitamin D may reduce the risk of autoimmune diseases.
Source: University of California, Riverside.
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