Find out how old your lungs are — based on your smoking history or a spirometry FEV1 reading. See the effect of smoking on lung function and how much quitting can recover.
Lung age is the age at which a healthy non-smoker would typically have the same lung function as you — expressed in years, just like metabolic age or heart age. It provides an immediately intuitive way to understand the state of your respiratory health. A 45-year-old with a lung age of 60 has lungs that function like those of an average 60-year-old non-smoker.
The concept was developed largely to make spirometry results more meaningful to patients. Clinical spirometry reports typically express results as "FEV1 80% of predicted" — technically accurate but abstract. "Your lungs are 15 years older than you are" conveys the same information in a way that motivates action.
FEV1 — Forced Expiratory Volume in one second — is the volume of air a person can forcefully exhale in the first second of a maximal exhalation effort. It is the primary measure used in spirometry testing to assess lung function. Predicted FEV1 values are based on population norms derived from age, sex and height — taller people have larger lungs; FEV1 declines naturally with age.
The foundational science of smoking and lung decline comes from the landmark Fletcher-Peto study, which tracked lung function over 8 years in a cohort of London workers. The findings established what is now known as the Fletcher-Peto curve: non-smokers lose approximately 25-30 ml of FEV1 per year as a natural consequence of ageing — a slow, gradual decline that does not produce symptoms or disability in most people.
Smokers who are "susceptible" to smoking-induced lung damage — roughly one in six — lose 40-60 ml of FEV1 per year, accelerating their rate of decline by approximately double. Over 20 years, this difference compounds dramatically: a 40-year pack-a-day smoker who started at 20 may have lung function equivalent to a 55-65 year old non-smoker, depending on their individual susceptibility.
Lung function must decline to approximately 50% of predicted before most people experience breathlessness at rest. Smokers who feel fine may already have significant, irreversible lung damage accumulating silently for years. This is why spirometry at midlife — particularly for smokers — is so valuable: it reveals decline that the individual cannot feel.
Quitting smoking does not restore lost FEV1 — the structural damage from alveolar destruction and airway remodelling is largely permanent. However, quitting achieves something profoundly important: it stops the accelerated decline and returns the rate of lung function loss to the normal non-smoker rate.
This means a 50-year-old who quits smoking today will still have worse lung function than a never-smoker of the same age — but 20 years from now, the gap will be smaller than if they had continued, because further decline will proceed at only the normal rate. The earlier quitting happens, the more future decline is prevented.
Beyond lung function, quitting produces other respiratory benefits within weeks. Cilia — the tiny hair-like structures in airways that sweep mucus and pathogens toward the throat — begin regrowing within days. Airway inflammation reduces significantly within months. Frequency of respiratory infections falls.
A randomised trial by Parkes and colleagues published in the BMJ demonstrated that telling smokers their lung age significantly increased quit rates compared to giving standard spirometry results. Smokers who heard "your lungs are 15 years older than you" were measurably more likely to attempt quitting than those who received the same data expressed as percentages of predicted. This calculator applies that finding directly.
Excess abdominal fat reduces diaphragm excursion and restricts lung volume, particularly in supine positions. Obesity is associated with reduced FVC (total lung capacity measure) and a distinct restrictive pattern on spirometry. Weight loss produces measurable improvements in lung volumes.
Long-term exposure to particulate matter (PM2.5), nitrogen dioxide and occupational dusts produces lung damage mechanistically similar to smoking. People with careers in construction, mining, welding or agriculture — or who have lived for decades in high-pollution environments — may have lung ages older than their smoking history alone would suggest.
Well-controlled asthma does not typically accelerate long-term FEV1 decline. Poorly controlled asthma, however, drives chronic airway inflammation that, over decades, can produce fixed airflow limitation and an older lung age.
High cardiorespiratory fitness is associated with better lung function, maintained through stronger respiratory muscles and better lung efficiency. Non-smokers with high aerobic fitness often have lung ages several years younger than their chronological age. Regular aerobic exercise maintains respiratory muscle strength and helps prevent the diaphragm weakness seen in very sedentary older adults.
The most powerful single action is not smoking — or quitting if you currently smoke. Beyond that, the evidence supports regular aerobic exercise (at least 150 minutes of moderate-intensity activity per week), maintaining a healthy weight to avoid the restrictive effects of central obesity, and where possible reducing exposure to indoor and outdoor air pollution. Occupational exposures to dust, fumes and chemicals warrant appropriate respiratory protection.