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A cohort study published in PLOS Medicine looks at prenatal exposure to PFAS and the incidence of asthma and wheeze in children.
Dr Erika Kennington, Head of Research & Innovation at Asthma + Lung UK, said:
“This is a large and rigorous study which demonstrates that massively high levels of water-borne PFAS exposure is associated with the development of lung conditions, adding to existing evidence that PFAS exposure is bad for the lungs.
“But the study does have limitations – the people included in the study would have been exposed to PFAS both before and after birth. This means we can’t be certain that this association of increased incidence of asthma in ‘very high PFAS exposed’ individuals is purely due to pre-birth exposure. Additionally, the study appears to only be indicating an association between asthma and water-borne PFAS exposure at massively high levels, so there is limited relevance to a wider population.
“To gain a better understanding of the causes of asthma in children, we need research to examine how PFAS alter the normal function of the lungs. Continued research into why asthma prevalence is increasing is vital, yet despite lung conditions being the third biggest cause of death in the UK, funding for respiratory research is on life-support. Urgent action is needed to boost research investment.”
Comments from our friends at the Aus SMC:
Associate Professor Peter Franklin is Director of Occupational Respiratory Epidemiology (ORE) and Deputy Head of School (Research) in the School of Population and Global Health at The University of Western Australia
“The adverse health effects of PFAS chemicals remain uncertain, particularly at the low levels of exposure that occur in the general community. The current study found that exposure to PFAS during pregnancy increased the risk of developing asthma in childhood. However, the risk was only observed in the study’s ‘very high’ exposure group. There was no increased risk in children born to mothers in either the ‘high’ or ‘intermediate’ exposure groups.
“The average potential PFAS concentrations in mothers in the ‘very high’ exposure group were many times greater than what has been found in the general population, and even much higher than what was found in high exposure risk groups in Australia, i.e. around airforce bases at Oakey, Williamtown and Katherine. Even the ‘high’ and ‘intermediate’ groups had much greater average PFAS concentrations than those high exposure risk groups in Australia.
“The study had limitations, not least that exposure was based on residential address in the years prior to, and the nine months of, pregnancy, rather than determined from personal blood samples. However, the study adds evidence of potential adverse health effects at high exposure to PFAS chemicals. The effects of low-level exposure, if any, are still unclear.”
Peter has not declared any conflicts of interest.
Professor Ian Rae is an expert on chemicals in the environment from the School of Chemistry at the University of Melbourne. He was also an advisor to the United Nations Environment Programme on chemicals in the environment and is former President of the Royal Australian Chemical Institute
“This Swedish study is the latest instalment of research results that suggest that the fluorinated chemicals (PFAS) to which we are all exposed, in one way or another, may be having harmful effects. Many other epidemiological (population-based) studies have shown correlations between exposure and a range of health effects. But taking the next step, establishing cause and effect beyond just correlation, is not really possible by population studies. Much more research would be needed for that, such as establishing the exact mechanism by which harm is caused. The authors acknowledge this, calling for repetition of their work, but also claiming that there is already a biologically plausible link between between exposure and the effects they have studied. That is, there is at least some notion of the likely biological mechanism.
“Because their study involved large number of children, over 11,000, extended over more than a decade, and was based in a region where drinking water was comparatively more contaminated by PFAS so inadvertent doses were higher than in other studies, the authors feel that their results are among the more significant.
“The exposure of fetuses to PFAS ingested with drinking water by pregnant mothers correlated well with the childhood incidence of respiratory symptoms, asthma and wheezing. The exposure was due to contamination of drinking water by industrial waste from film-forming industry. Among the contaminants detected in the study was the original ‘villain’ in the PFAS saga – the first one to be banned under the Stockholm Convention on Persistent Organic Pollutants (POPs) – perfluorooctane sulfonic acid (PFOS). The careful process of deciding which pollutants to ban takes a few years, but once banning of PFOS under the Convention seemed likely, manufacturers introduced fluorinated substances that were not-PFOS but were chemically similar, such as perfluorohexane sulfonic acid (PFHxS) and perfluooctanoic acid (PFOA). Both of these ‘lookalikes’ now come under the Stockholm Convention, too, and all three were present in the drinking water available to the mothers in this study.”
Ian has not declared any conflicts of interest.
Prof Asma Khalil, Professor of Obstetrics and Maternal Medicine and Consultant Obstetrician, City St George’s, University of London (CSGUL), said:
“This appears to be an important study because it examines a population with unusually high PFAS exposure from contaminated drinking water, which may help address one of the major limitations of earlier studies conducted mainly in background-exposed populations. Previous research on prenatal PFAS exposure and childhood asthma has been mixed, so a study in a highly exposed setting is potentially very informative.
“From the press release, the main message is fair: the study reports an association between very high prenatal PFAS exposure and higher rates of childhood asthma, rather than proving that PFAS definitely caused asthma. That distinction matters, because this is still observational research and residual confounding can never be fully excluded. Important alternative explanations include postnatal exposure, co-exposure to other environmental contaminants, and household factors such as smoking.
“A strength is the use of register-based clinical outcomes in a real-world population, which is generally more robust than relying only on self-reported symptoms. Another strength is that the Ronneby contamination incident created a wide exposure gradient, which is useful when exploring whether very high exposure levels may carry risks that are harder to detect in general populations.
“The main limitation is that prenatal exposure seems to have been estimated largely from maternal residential history and water distribution records rather than direct biomarker measurements for every pregnancy, so some exposure misclassification is possible. In addition, if the association was seen mainly at the very highest exposure levels, the findings may not be directly generalisable to populations with much lower everyday exposure.
“Overall, this sounds like a useful and policy-relevant study that adds to concerns about PFAS as potentially harmful developmental exposures, but it should be interpreted as evidence of association rather than proof of causation. Replication in other highly exposed populations will be important before making very strong claims about the magnitude of risk.“
Prof Oliver Jones, Professor of Chemistry, RMIT University, said:
“This is an interesting study, and it is not the first to suggest possible health effects from the exceedingly high PFAS exposure in this specific Swedish town. The story of Ronneby, which has some of the worst PFAS contamination anywhere in the world, could almost read like a new literary genre – Chemical Nordic Noir. However, there are some key points to keep in mind when looking at the results of this particular study.
“Firstly, the children’s exposure to PFAS was not directly measured, but estimated based on their addresses and how long they lived there. We don’t know how much PFAS they were actually exposed to.
“Secondly, what has been reported is an association, not a direct relationship. It does not prove causation. One might find a statistical association between asthma and any number of factors, but that does not automatically prove that one caused the other. It just gives you an idea of what might be worth exploring further.
“If PFAS did cause asthma, we might expect to see a dose-dependent effect – e.g., the more PFAS the child was exposed to, the higher their likelihood of developing asthma, but this was not observed. The alleged effect was seen except in those in the very highest PFAS exposure group, who were exposed to exceedingly high PFAS concentrations hundreds of times higher than usual, for several decades. Previous studies of possible links between PFAS and asthma also did not find a clear link.
“Finally, while the results suggest a possible health effect of certain types of PFAS at very, very high concentrations, they don’t prove anything directly. There are very few, if any, communities anywhere that have been exposed to a concentration of PFAS anywhere near that associated with asthma in this case.
“Thus, even if everything in this paper is correct, the results are likely to apply only to this specific town – so we do not have to worry about PFAS giving us asthma”.
Prof Seif Shaheen, Professor of Life Course Epidemiology, Queen Mary University of London (QMUL), said:
“The authors of this Swedish study report an increase in diagnosed asthma amongst a very small subgroup (2%) of cohort offspring, potentially exposed to very high concentrations of PFAS in utero. They rightly emphasise caution regarding a causal interpretation, for many reasons: prenatal PFAS exposure relied on a proxy estimate based on data from another cohort, but was not directly measured in cohort mothers in pregnancy; residual confounding by social circumstances cannot be ruled out, given that mothers who had very high exposure in pregnancy differed with respect to their education, compared to less exposed mothers; the association did not show a dose-response (higher exposure, higher risk) – whilst this weakens causal inference, it is possible that a threshold risk above a very high exposure level exists; the data could not distinguish prenatal from childhood exposure. Regarding potential mechanisms, it would have been informative if allergic versus non-allergic asthma could have been distinguished, but these data were not available. A reassuring conclusion, however, is that, even if the reported association between very high prenatal PFAS exposure and childhood asthma is causal, the majority of individuals in most general populations, who are exposed to much lower levels of PFAS, would not be at increased risk.”
Prof Kevin McConway, Emeritus Professor of Applied Statistics, Open University, said:
“The researchers found evidence of a correlation between children in a place in Sweden having had very high exposure to PFAS while they were still in the womb, and an increased risk of being diagnosed with childhood asthma. The findings of this research may seem alarming, but there are important questions to ask about how far they might apply. That’s for two sets of reasons.
“First, the researchers found evidence of the correlation only for those who had very high exposure, through their mother’s drinking water. Second, this is a correlation from an observational study and it’s not necessarily the case that the increased asthma risk was caused by the PFAS exposure.
“It’s true that, in some areas in the Swedish municipality of Ronneby, the water supply had extremely high levels of PFAS because of run-off from a fire-fighting foam used at a nearby military airfield. I’ve read that the level of PFAS detected in the water supply was extraordinarily high, possibly the highest ever measured anywhere. (This serious water issue has since been fixed).
“The researchers found statistically convincing evidence of a correlation with child asthma risk only for the very highest exposure levels they examined, where the mother had been registered at an address receiving the highly contaminated water for all five years preceding the date her child was delivered. The researchers did not find any clear evidence of an increased risk, compared to children whose mothers had not lived in the area affected by the contaminated water, for children whose mothers might have had some exposure to the contamination, but for shorter periods of time.
“Thus, it’s quite plausible that these results apply only to areas of drinking water very badly contaminated with PFAS, or even possibly only areas with very high contamination with PFAS from the same kind of fire-fighting foam. There are likely to be very few such areas. So even if we could be confident that it’s the PFAS causing the increased risk (and we can’t be confident of that), the public health risk is likely to be limited to a few places. Future research elsewhere might show the risk is more widespread, but on the basis of this research paper, we just can’t know that.
“The issue about cause and effect is because the study is observational. Families who were exposed to the highest levels of drinking water contamination differed in terms of many factors from those who never lived in the affected areas. So, it’s possible that the observed differences between those family groups in childhood asthma risk could be caused by one or more of those other factors, and not by the PFAS contamination at all. But this doesn’t remove the possibility that the PFAS contamination is the cause – we just can’t be sure.
“To allow for this as far as they could, the researchers in the new study made statistical adjustments for several of the other factors on which they had data. They did this for the sex of the child, whether the mother smoked in early pregnancy, the mother’s age, how many previous children she had had, whether she had asthma, and some socioeconomic factors like the mother’s education level and family income. All these are known to be associated with child asthma risk. If some of those associations are ones of cause and effect, they could potentially be the cause of the observed association between very high exposure to PFAS in drinking water and child asthma risk, rather than the PFAS exposure being the cause. In this study, even after taking all these factors into account, the observed association still remains.
“The snag is that one can never be sure that all the relevant factors have been adjusted for in this way. And no statistical adjustment can be made for factors on which the researchers do not have data. So, as the researchers acknowledge in their paper, they cannot rule out other routes of cause and effect. For instance, they mention parental smoking after the child’s birth, as something that is associated with childhood asthma risk, but for which they didn’t have data and so couldn’t adjust.
“I also wondered about whether other environmental differences might be important. There’s a lot of evidence of correlation between air pollution levels and child asthma risk, and some evidence that this is a cause-and-effect relationship. Ambient noise levels, perhaps from traffic or industry, might come into it too. Both air pollution and noise levels can vary between places that are physically very close to one another. Distance from main roads might make big differences, for instance.
“But the researchers dismiss this, saying, “Other sources of environmental contamination, including air pollution and noise, are similar across all study participants and are unlikely to confound the observed PFAS-asthma association.” They give no evidence for this – I’d expect a little more to have been said, including about variation between places very close to one another.
“On the other hand, Ronneby municipality is fairly small (population about 29,000, and under 13,000 fort Ronneby town) and appears to have pleasant parks and open spaces (according to Wikipedia), so maybe the researchers’ statement is true. (I’ve never been to Ronneby and don’t know it personally, so can’t judge.). Nevertheless, doubt about cause and effect remain.
“These doubts spill over into the so-called Rubin Causal Model analysis that the researchers also performed. This would make sense in terms of establishing the strength of a cause-and-effect relationship if one could be sure that there are no factors that might come into the causal pattern and weren’t used in the statistical modelling. But we can’t know that – even if there’s no issue about air pollution or noise, the parental smoking after the child’s birth remains a concern, and there may be other relevant factors. So, in my view, this further analysis also doesn’t establish what’s causing what.
“The association between very high PFAS exposure (in the mother’s drinking water) and childhood asthma is really quite marked, though, whatever is actually causing it. I’ll give some figures on the risk of an asthma diagnosis above the age of 3 years – before that age, as the researchers explain, there can be some difficulties of diagnosis.
“Out of 100 children whose mothers lived in the same county as Ronneby, but in a different municipality, in the five years before the child’s birth, and so would probably have had very little (if any) exposure to the contaminated water, about 13 would have been diagnosed with asthma after the age of 3 years.
“Now imagine another 100 children, whose mothers were recorded as living in the area with the highly contaminated water supply for the five years before the child was born, but matched to the first 100 in terms of the factors that were used for statistical adjustment. According to the statistical modelling in the new research, 20 of those 100 would have been diagnosed with asthma after the age of 3 years. That’s a lot of extra asthma diagnoses. (As always in statistical modelling, there’s a margin of uncertainty, and a fairly substantial one – the number of diagnoses could plausibly be between about 15 and about 27).
“We still don’t know to what extent these extra diagnoses are actually caused by the water very polluted with PFAS affecting the children before birth – maybe other factors are involved, or as the researchers point out, many families would still have been drinking the polluted water for some time after the child’s birth, so maybe pollution during the child’s life outside the womb plays a role.
“All these considerations are part of the reasons why the researchers call for more research to see if their findings are replicated in other populations that are highly exposed to PFAS.”
‘Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and incidence of asthma and wheeze in childhood: A register-based cohort study in Ronneby, Sweden’ by Annelise J. Blomberg et al. was published in PLOS Medicine at 19:00 UK Time Thursday the 9th of April 2026.
DOI: https:// doi.org/10.1371/journal.pmed.1004659
Declared interests
Dr Erika Kennington: “As an employee of A+LUK, Erika oversees a service to facilitate lived experience insight for a number of pharmaceutical companies who are developing and launching new respiratory products, for which the charity receives payment.”
Prof Asma Khalil: “I have no relevant competing interests to declare.”
Prof Oliver Jones: “I am a Professor of Chemistry at RMIT University in Melbourne. My group is active in PFAS research. I have previously received funds from the Environment Protection Authority Victoria and various Australian Water utilities for research into environmental pollution, including PFAS.”
Prof Seif Shaheen: “no COI”
Prof Kevin McConway: “no relevant interests to declare”