What does smoking do to your biological age?

Smoking significantly accelerates the ageing of lung cells. In the lung tissue of smokers and COPD patients, damaged proteins accumulate in small cellular vesicles because a normal cellular clean-up system no longer functions properly. Notably, this pattern closely resembles what is seen in naturally ageing lung cells. The amount of these damaged-protein accumulations was associated with the severity of pulmonary emphysema. This holds true for both cell studies and human tissue.

Smoking also has a measurable effect on DNA, through so-called epigenetic changes. These are chemical marks on the DNA that regulate which genes are switched on or off, and they are used as a measure of biological ageing. Smoking exposure was associated with changes at more than a hundred gene loci in immune cells. This is an association, not a proven causal relationship, and the research did not involve tobacco smokers exclusively. However, it fits the broader picture that smoking accelerates the biological clock.

The consequences for the immune system are concretely noticeable. Smokers with the skin condition psoriasis respond demonstrably less well to modern immunotherapy than non-smokers: the likelihood of a good treatment outcome fell by approximately 20% in both current and former smokers. This suggests that smoking alters the immune system for a prolonged period, even after quitting.

The effects on fertility have been studied extensively. Smoking damages both egg and sperm quality, increases the risk of miscarriage and preterm birth, and reduces birth weight by 150 to 300 grams in children carried to full term. Quitting smoking substantially reduces these risks. The same applies to the risk of bacterial pneumonia: the risk rises sharply with the amount smoked, but after ten years of not smoking the risk is equivalent to that of people who have never smoked. Quitting is therefore worthwhile, even if you have smoked for a long time.