The setting is Ronneby, a municipality of roughly 28,000 inhabitants in southern Sweden. For decades, aqueous film-forming foam, or AFFF, used in firefighting training at a nearby military airbase seeped into the groundwater that fed one of the town’s two water treatment plants. When the contamination was finally discovered in 2013, total PFAS concentrations in the water exceeded 10,000 nanograms per liter, dominated by perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS), with perfluorooctanoic acid (PFOA) also present. Retrospective analyses of archived newborn blood spots suggest the exposure began as early as 1985 and climbed steadily until around 2005 to 2007. The contaminated supply was shut off on December 16, 2013, but by then, some residents carried serum PFAS concentrations up to a hundred times higher than those seen in the general Swedish population.

That unusual exposure gradient is precisely what made Ronneby valuable to researchers. Most previous studies of PFAS and reproductive hormones have been conducted in populations with only background exposure, and their findings have been inconsistent. Regulatory bodies, including the European Food Safety Authority and the US National Academies of Sciences, have judged the evidence linking PFAS to reproductive hormone alterations insufficient. By studying children whose bodies span a range of exposures from background levels to extreme contamination, the Swedish team could probe exposure-response relationships that background-level studies simply cannot resolve.

The researchers drew on biobanked serum samples collected between 2014 and 2016 from participants in the Ronneby PFAS Biomarker Cohort, aged 5 to 20 years. The final study group comprised 87 girls and 84 boys aged 5 to 11, and 117 boys aged 12 to 20; girls aged 12 and older were excluded because menstrual cyclicity and contraceptive use would have introduced unmanageable variability. About 23 percent of participants came from nearby Karlshamn, where drinking water PFAS levels were below 5 nanograms per liter, providing a reference group. Serum concentrations of PFOS, PFHxS, and PFOA were measured by liquid chromatography-tandem mass spectrometry, and the sum of these three compounds served as the primary exposure measure. Hormones, including follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, sex hormone-binding globulin (SHBG), and total testosterone, were quantified with electrochemiluminescence immunoassays at an accredited clinical laboratory.

The exposure levels were striking. Among the younger children from Ronneby, median combined serum concentrations of the three PFAS exceeded 90 nanograms per milliliter, and among adolescent boys the median reached 173 nanograms per milliliter, with some individuals above 600. For context, the European Food Safety Authority considers a serum level of about 6 nanograms per milliliter to be the threshold below which the tolerable weekly intake of PFAS is assumed to be maintained. PFOS and PFHxS were strongly correlated with one another, reflecting their shared source in the contaminated water, and roughly one quarter of participants were classified as prenatally exposed based on residential records from the year of their birth.

The hormone findings split cleanly along developmental lines. Among children aged 5 to 11, higher PFAS concentrations were associated with elevated prolactin in both sexes, an association that held in the continuous models for girls and boys alike. Boys in this younger group also showed lower FSH as exposure increased, while boys in the medium exposure category had higher SHBG. When the researchers formally tested for sex differences, however, the interaction terms were not statistically significant, meaning they could not conclude that boys and girls responded differently. Among adolescent boys aged 12 to 20, the pattern shifted: higher PFAS levels were associated with lower LH, lower total testosterone, and a lower free androgen index, a calculated measure of bioavailable testosterone that combines testosterone and SHBG. In the categorical analysis, the reduction in LH was most evident in the medium-high exposure group, while testosterone and the androgen index declined across the higher exposure categories.

These results align closely with findings from other highly exposed populations. In the C8 Health Project in the Mid-Ohio Valley, where drinking water was contaminated by PFAS production facilities, higher PFOA and PFOS concentrations were linked to delayed puberty and lower testosterone in both boys and girls. More recently, adolescents living near a 3M chemical plant in Belgium showed similar patterns, with higher PFHxS and PFOA associated with lower LH and testosterone and higher SHBG in teenage boys. The convergence of evidence across three independent contamination hotspots on two continents strengthens the case that the associations are not statistical artifacts, though the observational design still cannot prove causation.

The prolactin finding is particularly intriguing because it is comparatively rare in the PFAS literature. Positive relationships between fluorochemical exposure and prolactin were reported in occupational studies in the 1990s, but few modern studies have examined the question. Prolactin is best known for its role in lactation, but it also feeds back on the hypothalamic-pituitary-gonadal axis, and pathological hyperprolactinemia in adults can suppress gonadotropin release and reduce sex steroid production. The Ronneby team is careful to note that their data do not demonstrate a prolactin-mediated suppression of the hormonal axis, since prolactin was elevated in young children but not in adolescent boys, in whom LH and testosterone were instead reduced. The hormone-specific associations may reflect other mechanisms or differing susceptibility across developmental stages, and experimental studies suggest PFAS may impair testosterone production by disrupting steroidogenesis in the Leydig cells of the testes, though exact mechanisms remain uncertain.

The study has limitations worth weighing. Blood samples were drawn at varying times of day, and hormones such as testosterone and LH follow circadian rhythms that peak in the early morning, introducing variability that likely attenuated the observed effect estimates rather than creating spurious ones. Immunoassay-based sex steroid measurements are less sensitive than mass spectrometry, particularly at the low concentrations typical of children, and most estradiol values fell below the laboratory’s reporting limit and could not be analyzed. The researchers also could not disentangle prenatal from postnatal exposure, because the contamination was already pervasive by the mid-1980s and the two exposure routes are highly correlated in this cohort. Sensitivity analyses adjusting for body mass index produced similar estimates for most hormones.

The clinical significance of the hormonal differences remains uncertain. Testosterone concentrations in the exposed adolescents were still within age-appropriate reference ranges, and pediatric reference intervals for prolactin are lacking, making interpretation difficult. What the study does establish is that real-world, AFFF-driven PFAS contamination, the same scenario now unfolding around airports, military bases, and industrial sites worldwide, is associated with detectable alterations in the hormonal regulation of children at multiple levels of the endocrine system. With legacy PFAS persisting in the environment despite regulatory restrictions and being replaced by newer compounds whose health effects are poorly characterized, the researchers call for longitudinal follow-up of highly exposed populations, more sensitive hormone measurement methods, and standardized sampling to determine whether these early hormonal shifts translate into delayed puberty or long-term reproductive consequences.

Subject of Research: Associations between serum PFAS concentrations and reproductive hormone levels in highly exposed children and adolescents

Article Title: Serum PFAS Concentrations and Reproductive Hormones in Highly Exposed Children and Adolescents

Article References: Hammarstrand, S., Andersson, E., Colldén, H., Lindh, C., Nielsen, C., Jakobsson, K., & Andersson, E. M. (2026). Serum PFAS Concentrations and Reproductive Hormones in Highly Exposed Children and Adolescents. Environmental Advances, Article 100764. https://doi.org/10.1016/j.envadv.2026.100764

Image Credits: AI Generated

DOI: 10.1016/j.envadv.2026.100764

Keywords: PFAS, endocrine disruption, puberty, reproductive hormones, testosterone, prolactin, drinking water contamination, firefighting foam, Ronneby, children's health, HPG axis, environmental epidemiology