Research from the University of Porto and the University of Barcelona confirms that smoking accelerates aging across all tissues, not just the lungs, primarily through immune and inflammatory dysregulation.

Smoking causes a causal acceleration of tissue aging via DNA methylation, especially at sites associated with healthy longevity, with lung tissues showing significant overlap between smoking and aging methylation patterns.

Overall, smoking acts as an aging accelerator, with some molecular signatures of smoking remaining long-term even after cessation.

Smoking influences alternative splicing in tissues such as the lung, thyroid, and heart, leading to protein modifications, loss of function, and structural cellular changes, particularly in the thyroid gland.

Most gene expression changes due to smoking are tissue-specific, affecting organs like the lungs, pancreas, thyroid, and esophagus, with some genes upregulated across multiple tissues in response to toxic compounds like PAHs.

Quitting smoking can partially reverse gene expression and methylation changes, with gene expression being more reversible than methylation, although some epigenetic marks persist, especially in the lungs.

These irreversible molecular alterations are linked to aging mechanisms and contribute to the overall aging process.