Prenatal PFAS Exposure and Childhood Asthma: A Ronneby, Sweden Cohort Study

09 Apr 20265 min read0 viewsJournal Feed

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by Annelise J. Blomberg, Christel Nielsen, Beata Borgström Bolmsjö, Marie-Abèle Bind, Linda Hartman, Anna Saxne Jöud Background Early-life exposure to per- and polyfluoroalkyl substances (PFAS) may impact the developing lungs and immune system and increase the risk of childhood asthma, but no studies have been conducted in a high-exposed population.

The objective of this study was to estimate associations between prenatal PFAS exposure and childhood incidence of asthma and wheeze in Blekinge County, Sweden, where a subset of residents in the city of Ronneby was exposed to PFAS from drinking water contaminated by aqueous film-forming foam (AFFF). Methods and findings We constructed a register-based open cohort of 11,488 children born in Blekinge county between 2006 and 2013 and followed each individual from birth until age 12 or December 31, 2022.

Maternal address history was linked to water distribution records to create a categorical proxy variable for prenatal PFAS exposure from drinking water.

Clinical Editorial

Context and study aims

This register-based cohort study examined whether prenatal exposure to per- and polyfluoroalkyl substances (PFAS) from drinking water linked to AFFF contamination is associated with childhood asthma and wheeze in Blekinge County, Sweden, with a focus on a highly exposed subpopulation in Ronneby.

Design, population, and exposure assessment

The analysis used an open cohort of 11,488 children born in Blekinge County between 2006 and 2013, followed from birth until age 12 or December 31, 2022.
Prenatal PFAS exposure was inferred by linking maternal address history to water distribution records to construct a categorical proxy for exposure during gestation.
Outcomes were identified from administrative health records, capturing incident wheeze and asthma cases.

Analytical approach and secondary methods

Primary analyses employed Cox proportional hazards models to estimate hazard ratios for wheeze and asthma, adjusting for a range of individual-level confounders, including maternal smoking in early pregnancy, maternal age at delivery, parity, child sex, parental asthma, and socioeconomic factors.
A secondary analytic approach used Rubin Causal Model (RCM) methods to estimate average marginal effects within a very highly exposed subgroup, leveraging a matched dataset of very-high and background-exposed individuals balanced on measured confounders.

Key findings on incidence and exposure strata

During follow-up, 18% of children developed wheeze and 17% developed asthma.
Very high prenatal PFAS exposure was associated with asthma incidence (hazard ratio 1.44; 95% CI 1.08–1.92).
No observed associations were found for the high or intermediate exposure groups with either asthma or wheeze.
In the RCM framework, the estimated cumulative incidence of asthma was 16.1% in the background-exposed group versus 26.7% in the very highly exposed group, indicating a differential burden in the highly exposed population.

Interpretation and context

The study reports an association between very high prenatal PFAS exposure and increased incidence of childhood asthma, while associations with wheeze or with lower exposure levels were not evident in primary analyses.
The authors emphasize replication of findings and discuss potential public health relevance in the context of AFFF-related PFAS contamination.

Limitations and uncertainties

The exposure assessment relies on a proxy based on residential history and water distribution records, which may introduce misclassification of prenatal PFAS exposure.
The primary associations are observed for the very highly exposed group; estimates for other exposure levels show no significant associations.
While adjustments account for several confounders, residual confounding cannot be excluded, and causal interpretation remains cautious pending replication.