New research from the University of Leicester has confirmed thatchildren in the UK are reaching adulthood with permanently reduced lung capacitybecause of air pollution, placing them on a direct trajectory towardheart disease decades before their time.

The findings come from two interlinked studies produced by Leicester's Centre for Environmental Health and Sustainability, examining the effect of air pollutants at every stage from pregnancy through to early adulthood. The more recent,published in Environmental Research in 2026, tracked approximately 5,200 children from the UK's Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort, measuring their lung function at ages 8, 15, and 24 years.

A companion2024 paper in ERJ Open Research, using data from nearly 200,000 adults in the UK Biobank, then quantified exactly how much of that lung damage converts into cardiovascular disease and premature death.

The 2026 ALSPAC study, led by Katie Eminson and ProfessorAnna Hansellof Leicester's Centre for Environmental Health and Sustainability, is one of the first UK studies to follow lung function growth continuously from childhood to early adulthood. Its central finding: air pollution is associated with impaired lung growth throughout childhood, but the damage is most pronounced during adolescence, precisely when the lungs are growing at their fastest rate.

Lung function typically peaks in the late teens for girls and early twenties for boys. Any reduction in that growth trajectory, even a small one, sets an irreversibly lower ceiling on the total lung capacity a person will carry through adult life.

The study concluded that reducing air pollution exposure in childhood is essential to promoting lifelong lung health, a conclusion that carries urgent weight given that the UK continues toexceed World Health Organisation guidelines for particulate matter in numerous urban areas.

Exposure to primary road traffic particulate matter (PM10) during the first trimester of pregnancy was already shown by an earlier LeicesterALSPAC analysis published in the American Journal of Respiratory and Critical Care Medicineto be associated with significantly lower forced expiratory volume (FEV1) in children at age eight. The 2026 study extended that tracking to age 24, allowing researchers to capture not just snapshots of lung size but the full arc of lung development and to confirm that the adverse associations persist.

The second pillar of Leicester's research shifts from lungs to hearts. The2024 study by Anna Guyatt, Yutong Samuel Cai, Martin Tobin, and Anna Hansellused UK Biobank data on approximately 200,000 adults, followed for eight years, to ask a specific mechanistic question: how much of air pollution's lethal effect on the heart actually travels through damaged lungs?

The answer was stark. Reduced FEV1, the volume of air a person can forcibly exhale in one second, and the standard clinical measure of lung impairment, was found to mediate between 10% and 30% of the mortality and cardiovascular disease risk attributable to PM2.5 and nitrogen dioxide (NO2). Specifically, impaired lung function mediated 18% of PM2.5's effect and 27% of NO2's effect on all-cause mortality. For incident cardiovascular disease specifically, the mediated proportions were 9% for PM2.5 and 16% for NO2.

This matters because it reframes what polluted air actually does to a body over time. Pollution does not merely irritate airways. It erodes the mechanical efficiency of the lungs, and that degraded efficiency then independently raises the probability of a heart attack, a stroke, or early death. The study's authors used data from theUK Biobank cohort, with baseline lung function measurements taken between 2006 and 2010, making it one of the largest mediation analyses of this kind ever conducted in a UK population.

Source: International Business Times UK