A new study shows that exposure to per- and polyfluoroalkyl substances (PFAS) during pregnancy can reduce lung function among young people, leaving measurable traces as they age well into their twenties. The findings suggest that these widespread chemicals may disrupt the delicate early programming of the lungs and immune system – a change that could have long-term consequences at the population level, says a researcher.
In recent years, attention has increasingly turned to PFAS: chemicals that virtually all people carry in their bodies. Because many PFAS are suspected endocrine disruptors, concern is growing that they may affect health, even very early in life.
Now, a new study in Denmark suggests that exposure to PFAS during fetal development can influence lung function well into adulthood.
For each individual, the effect may be difficult to disentangle from all the other factors that shape lung function, such as smoking or physical activity. But for the population as a whole, the implications could be substantial.
“The differences are small for the individual, but at the population level, even small shifts in maximum lung function matter. If you enter adulthood with slightly lower lung capacity, your risk of crossing the threshold into chronic obstructive pulmonary disease earlier in life increases,” says a researcher behind the study, Sandra Søgaard Tøttenborg, Head of Environmental Research and Associate Professor at Copenhagen University Hospital – Bispebjerg and Frederiksberg.
The research has been published in Environmental Research.
Why PFAS can affect the lungs already in fetal life
According to Sandra Søgaard Tøttenborg, we still do not fully understand what PFAS mean for human health. Because the substances can cross the placenta, researchers are concerned that they may interfere with the hormone-regulated processes that shape the lungs and immune system in the womb. Disrupting this early programming may leave lasting traces in how these systems function later in life.
Previous studies have pointed in this direction. However, the studies that have examined lung outcomes have typically followed children only until around the age of 12 years. That, Sandra Søgaard Tøttenborg explains, is not sufficient, because the lungs continue to mature well into adolescence.
“If you want to assess whether maximum lung potential is affected, you need to follow individuals until they are young adults – when lung function peaks. Another important point is that most previous studies have examined one PFAS substance at a time. In reality, we are exposed to many different chemicals simultaneously, and they can affect the body differently when they occur together – cocktail effects. That is why we decided to conduct a study that examined both lung function at age 19–20 years and the impact of an entire mixture of PFAS at the same time,” she says.
Why the researchers had to follow participants into young adulthood
The researchers used data from the Fetal Programming of Sperm Quality (FEPOS) cohort, which consists of young Danish men whose mothers participated in Danish National Birth Cohort, a large-scale womb-to-tomb cohort.
As the name suggests, the original purpose of FEPOS was to investigate how influences during fetal life affect men’s sperm quality. But because Sandra Søgaard Tøttenborg completed her PhD under the supervision of a lung specialist, she knew that there are very few high-quality data on lung function in otherwise healthy young men.
She therefore saw an opportunity to include spirometry in the study.
The researchers measured 15 different PFAS in blood samples taken from the mothers during the first trimester. The samples had been stored in the Danish National Biobank since pregnancy.
Information on the sons’ childhood asthma, hay fever and eczema came from questionnaires completed by the mothers when the children were 7 and 11 years old, and data on asthma in adolescence came from questionnaires completed by the participants themselves at age 18 years.
In total, 866 individuals were included in the analysis used to estimate the effect of the entire PFAS mixture.
“The Danish National Birth Cohort is a gold mine for research, because the children have been followed from fetal life through childhood and adolescence – first via their mothers and later through contact with the young people themselves. Now many of them are on the verge of having children of their own, so the story can continue,” says Sandra Søgaard Tøttenborg.
PFAS exposure resulted in measurably lower lung function among young men
The study showed that higher exposure to the PFAS mixture during foetal life was associated with lower forced expiratory volume in one second (FEV₁) and forced vital capacity (FVC) in young adulthood.
FEV₁ describes how much air a person can exhale in the first second of a forced breath, and FVC reflects the total volume of air that can be emptied from the lungs after a deep inhalation.
On average, the analysis showed about 85 mL lower FEV₁ and 88 mL lower FVC for each increase in the PFAS mixture – roughly equivalent to the volume of a small sip of water. This may not sound like much, but at the population level, even small shifts affect overall lung capacity.
By contrast, the ratio between the two measurements remained unchanged, suggesting that PFAS exposure primarily affects lung volume rather than airway resistance itself.
The associations were statistically significant and correspond to approximately a 2% reduction in both FEV₁ and FVC for a 19-year-old man 183 cm tall.
The researchers found no clear association between PFAS exposure and asthma, either in childhood or at age 18.
They did, however, observe a lower incidence of hay fever in childhood – an unexpected finding that will require further investigation.
A biological explanation: what PFAS does to lung development
According to Sandra Søgaard Tøttenborg, there are plausible biological explanations for why PFAS exposure during fetal development can influence lung capacity for the rest of a person’s life.
Animal studies have shown changes in alveolar maturation and inflammatory responses following prenatal exposure to perfluorooctanesulfonic acid (PFOS), indicating a more immature lung at birth.
At the molecular level, PFAS can potentially interfere with signalling pathways that help the lungs mature before birth, including the peroxisome proliferator–activated receptor system and glucocorticoid pathways. These pathways normally regulate how lung tissue develops and becomes ready to function after birth.
“Our findings – lower FEV₁ and FVC without changes in the FEV₁/FVC ratio – are consistent with a small, persistent effect on lung volume development rather than obstructive lung disease,” says Sandra Søgaard Tøttenborg.
PFAS must be stopped at the source
According to Sandra Søgaard Tøttenborg, the results underline the importance of regulating and reducing PFAS exposure in the population – particularly among pregnant women.
They also highlight the need to think in terms of chemical mixtures rather than individual substances. In real life, exposure involves a complex chemical cocktail, and interactions between substances may affect public health.
In her view, the study supports a longstanding suspicion among researchers: that PFAS exposure during fetal life can interfere with the developmental processes that shape the lungs and immune system.
The study design is also among the strongest of its kind to date.
“If all the research that already exists on PFAS has not been enough to stop emissions at the source, I hope our results can provide an additional incentive. All PFAS should be banned. We measured 15, but there are more than 10,000 variants, and regulating them one by one makes no sense. As a society, we must be able to demand action when we again and again see these substances linked to shifts in health parameters. When the entire population is exposed, even small changes become a matter of public concern,” says Sandra Søgaard Tøttenborg.
