Children exposed to extreme levels of “permanent chemicals” before birth were significantly more likely to develop asthma. This provides rare real-world evidence from a highly contaminated community and raises urgent questions about childhood exposure risks.
Study: Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and the incidence of childhood asthma and wheezing: a register-based cohort study in Ronneby, Sweden. Image credit: PeopleImages/Shutterstock.com
Per- and polyfluoroalkyl substances (PFAS), also known as “forever chemicals,” have been widely studied for their potential effects on human health and development. In recent research, PLOS medicine reported that very high prenatal PFAS exposure is associated with higher incidence of childhood asthma.
Increase in childhood asthma linked to environmental exposures
Asthma is the leading cause of noncommunicable childhood disease and has increased in prevalence over the past 50 years. Environmental exposures, including air pollutants and infectious agents, have been repeatedly associated with increased risk of asthma.
PFAS cross the placenta, so exposure can occur before birth. Such early-life exposures are associated with immunosuppression, including increased risk of childhood infections and decreased antibody responses to vaccination. However, despite its biological plausibility, the association between PFAS exposure and childhood asthma remains inconclusive, and the results of epidemiological studies based on background PFAS exposure are contradictory.
To address this question, the current study includes a very high exposure group, unlike previous studies that primarily focused on low exposure populations.
The study included 11,488 children born in Blekinge County, Sweden. Blekinge County includes the town of Ronneby, where approximately one-third of households were exposed to drinking water contaminated with PFAS from aqueous film-forming foam (AFFF) for more than 30 years.
The PFAS concentration in the contaminated water was 10,380 ng/L, compared to 48 ng/L in Ronneby’s second water project and 5 ng/L in the neighboring town. Two years after the contamination was discovered, approximately 3,400 residents were found to have extremely high serum PFAS levels.
Using water distribution records, we created a surrogate variable for prenatal PFAS exposure, stratified into very high, high, intermediate, and background exposure.
- Very high exposure: Mother lived in an address with contaminated water supply for more than 5 years before giving birth
- High exposure: Mother lived at such an address for at least 1 out of 5 years, but not all 5 years
- Intermediate exposure: Mother lived in Ronneby but not within the contaminated supply area
- Background disclosure: Mother did not live in Ronneby.
To test these categories, the authors compared serum PFAS levels in mothers of children in this cohort to mothers in another group of women who had lived at addresses within contaminated water supplies for 5 years prior to measurements.
Most of the children in the study had older siblings, nonsmoking mothers, and two Swedish-born parents. Median maternal age at delivery was 30 years. Approximately 17% of children had asthma in one or both parents.
Very high exposure is associated with increased asthma incidence
Approximately 2% of children had very high prenatal exposure, compared to 4% with high exposure and 14% with moderate exposure. The remaining children lived outside Ronneby. During the follow-up period, approximately 18% of children had registry-based wheeze-related outcomes (based on diagnosis and prescription) and 17% had asthma.
Very high PFAS exposure was associated with a 44% higher risk of developing childhood asthma. Other exposure categories showed no association, and despite biological plausibility, no association was observed for wheezing. Results were adjusted for maternal smoking and age. Child gender, parental asthma, socio-economic factors, and other factors Equality and maternal education.
In absolute terms, 26.7% of very highly exposed children developed asthma, compared with 16.1% of the group with comparable background exposure. This difference of more than 10 percentage points was repeated after restricting diagnoses to children aged 3 years and older with clinically diagnosed asthma. We use a more strict definition of “asthma (3+)”.
Chemical exposure is associated with inflammation and airway hyperresponsiveness
Lung development begins early before birth and is easily disrupted by environmental pollutants. Preclinical studies have demonstrated that PFAS can concentrate in lung tissue. These can disrupt immune processes, increase inflammation in the lungs, and alter gene expression profiles. These effects may make the lungs more susceptible to hypersensitivity reactions and increase susceptibility to asthma.
Previous epidemiological studies provided mixed evidence, likely because they were relatively small, used parent-reported outcomes, and were limited to background PFAS exposure. The current findings may suggest a threshold effect, with an association emerging only at very high exposure levels.
strengths and limitations
This study covered the full range of PFAS exposures, including a subset of atypical very high exposures. Detailed long-term follow-up information was available; And the results were based on clinical diagnosis and prescription records.
Using residential address to determine prenatal exposure is less accurate than direct measurement of biomarkers and may introduce misclassification bias. It does not distinguish between prenatal and early childhood exposures, and many highly exposed children continued to live in contaminated areas after birth, making it difficult to separate out prenatal effects. Parental smoking after birth may be a source of unmeasured confounding.
Extreme PFAS exposure may increase risk of childhood asthma
Study results suggest that very high PFAS exposure may be associated with increased risk of childhood asthma. These findings are likely not to apply at low levels of prenatal exposure; and may reflect a combination of prenatal and childhood exposures rather than prenatal exposure alone. Further studies using direct measurements are required to confirm these results.
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