Forever chemicals in children's blood are linked to weaker bones by age 12 - especially in girls

Adolescence is when the skeleton does most of its construction work. The bone mass accumulated during the teenage years forms the reserve that must last a lifetime - a reserve that determines fracture risk at age 70 as much as anything that happens in between. If something disrupts that accumulation, the consequences may not appear for decades, but they are essentially irreversible.

New research published in the Journal of the Endocrine Society suggests that per- and polyfluoroalkyl substances - the synthetic chemicals known as PFAS or 'forever chemicals' - may be doing exactly that. In a longitudinal study following 218 children from birth through age 12, researchers found that higher blood concentrations of one specific PFAS compound, perfluorooctanoic acid (PFOA), were associated with lower forearm bone density at age 12.

Tracking exposure across childhood

What distinguishes this study from earlier PFAS research is its temporal depth. Rather than measuring chemical exposure at a single time point, the researchers measured blood PFAS concentrations at four stages: at delivery, and at ages 3, 8, and 12 years. Bone density was assessed at age 12 using dual-energy X-ray absorptiometry (DXA), the standard clinical tool for measuring bone mineral density.

This design allowed the team to examine whether the timing of exposure mattered - whether PFAS levels during infancy, early childhood, or middle childhood were more strongly associated with bone outcomes than exposure at other ages. The answer appears to be yes: for different PFAS compounds, the associations with lower bone density varied depending on when the exposure occurred, suggesting that certain developmental stages may be especially vulnerable to chemical disruption.

Sex differences in vulnerability

The associations between PFAS exposure and lower bone density were stronger among females than males. This sex difference is consistent with what endocrinologists would predict, given the known interactions between PFAS and hormonal signaling. PFAS compounds have been shown to interfere with estrogen and thyroid hormone pathways, both of which play central roles in bone development. During puberty, when sex hormones drive the dramatic increase in bone mineral accretion that establishes peak bone mass, any disruption to hormonal signaling could have outsized effects - and those effects may be more pronounced in females, whose bone development is more estrogen-dependent.

The PFOA signal

Of the PFAS compounds measured, PFOA showed the clearest association with reduced bone density. PFOA is one of the most studied members of the PFAS family - a compound once widely used in nonstick cookware, food packaging, and water-repellent coatings. Although its production has been phased out in many countries, it persists in the environment and in the human body for years after exposure. Most people alive today carry measurable levels of PFOA in their blood.

The mechanism by which PFOA might affect bone is not fully established, but animal studies have shown that PFAS can interfere with osteoblast function (the cells that build bone), alter calcium metabolism, and disrupt the hormonal signals that coordinate bone remodeling. Whether the concentrations found in the study's participants are sufficient to produce clinically meaningful effects on bone strength - as opposed to statistically detectable differences in density measurements - remains an open question.

218 children, important limits

The study cohort of 218 children is small by epidemiological standards, and the findings should be interpreted with that in mind. Small sample sizes limit statistical power and make it harder to detect modest effects or to distinguish genuine associations from chance findings. The study was drawn from a prospective pregnancy and birth cohort, which provides valuable longitudinal data but may not represent the broader population.

The researchers also note that bone density at age 12 does not capture the full picture of skeletal health. Peak bone mass is typically achieved in the late teens or early twenties, and whether the density differences observed at age 12 persist, widen, or narrow during subsequent years is unknown. Longer follow-up will be needed to determine whether early PFAS exposure has lasting consequences for adult bone health.

Reducing exposure during key windows

Lead author Jessie P. Buckley of the UNC Gillings School of Global Public Health framed the findings in terms of prevention. If certain developmental windows are particularly sensitive to PFAS effects on bone, then reducing exposure during those periods could be a targeted public health strategy. Drinking water contamination remains the primary source of PFAS exposure for many communities, and efforts to reduce PFAS in water supplies and consumer products could yield benefits that extend beyond the more commonly studied endpoints of cancer and thyroid disease.

The study adds to a growing body of evidence that PFAS exposure during early life may carry long-term health consequences that are only now becoming visible as longitudinal cohorts reach the ages where effects can be measured. With thousands of PFAS compounds in commercial use and widespread environmental contamination, the full scope of their health impact is still being defined.

The research was funded by the National Institute of Environmental Health Sciences and involved collaborators from Johns Hopkins, Brown University, the CDC, the University of Cincinnati, the University of Pennsylvania, Simon Fraser University, and George Washington University.