PFAS exposure in early life linked to lower bone density in teenage girls

A new study has found that children exposed to PFAS chemicals in early life show measurably lower bone density by the time they reach their teenage years, with girls showing a stronger effect than boys. PFAS, or per- and polyfluoroalkyl substances, are a class of synthetic chemicals used in nonstick cookware, food packaging, firefighting foam, and waterproof textiles. They accumulate in the body over time and do not break down in the environment, which is why they are commonly called forever chemicals. Their presence in drinking water and food is now effectively universal in industrialized countries.

The bone density finding matters because adolescence is the period when humans accumulate the majority of their lifetime bone mass. Peak bone mass, reached in the late teens and early twenties, determines fracture risk decades later. A person who enters adulthood with lower peak bone density faces a steeper trajectory toward osteoporosis and fractures in middle age and beyond. If PFAS exposure during early childhood is reducing the ceiling on that accumulation, the health consequences will not be visible as broken bones in childhood. They will appear as osteoporosis in women in their fifties and sixties.

What the study measured and who was included

The research drew on data from Project Viva, a long-running birth cohort study based in Massachusetts that has tracked participants since the late 1990s. Researchers measured PFAS blood levels in mothers during pregnancy and in children at multiple time points through early childhood. Bone density was assessed using dual-energy X-ray absorptiometry, the standard clinical tool for measuring bone mineral density, when participants reached early adolescence. The analysis controlled for calcium intake, physical activity, dairy consumption, and other dietary variables to isolate the PFAS association.

The PFAS compounds most strongly associated with reduced bone density were PFOA (perfluorooctanoic acid) and PFOS (perfluorooctane sulfonic acid), the two compounds with the longest history of commercial use and the most extensive human exposure data. Both have been phased out of production in the United States under EPA agreements, but they persist in the environment and in human bodies for years. Children born in the 1990s and early 2000s, when manufacturing use of these compounds was still widespread, were exposed to them through contaminated water, food, and household products.

Why girls appear more vulnerable than boys

The sex difference in PFAS impact on bone density likely relates to how PFAS chemicals interact with estrogen signaling. PFAS compounds have been identified as endocrine disruptors, meaning they interfere with hormone activity in the body. Estrogen plays a central role in regulating bone metabolism in females, promoting bone formation during puberty and maintaining bone density in adulthood. Disruption of estrogen signaling during the critical window of puberty, when bone accrual accelerates sharply, could explain why the effect on bone density is more pronounced in girls than in boys.

A 2020 study published in Environmental Health Perspectives examined PFAS exposure and bone density in a separate cohort of adolescent girls in Denmark and found a similar pattern, with higher PFOA and PFOS blood levels associated with lower lumbar spine and femoral neck bone density. The Danish finding and the Project Viva findings together strengthen the case that this is a real biological effect rather than a statistical artifact of a single study.

The timing of exposure and its role in severity

One of the more specific findings in the new study is that the timing of PFAS exposure within early childhood matters, not just the total accumulated dose. Exposure in the first two years of life showed a stronger association with later bone density reduction than exposure measured at ages five or six. This points to developmental windows during which bone-forming cells, called osteoblasts, may be particularly sensitive to disruption. It also suggests that efforts to reduce PFAS exposure in pregnant women and infants could have disproportionate benefits compared to reducing exposure at later ages.

The mechanism by which PFAS affects osteoblast function is still being investigated. Laboratory studies have shown that PFOA and PFOS suppress osteoblast differentiation and proliferation in cell cultures, and that they promote the activity of osteoclasts, which are the cells that break bone down. The net effect is a shift in bone turnover away from formation and toward resorption. Whether that shift during early childhood has permanent effects on peak bone mass, or whether it is partially reversible if exposure is reduced, is not yet established in human data.

How widespread PFAS contamination actually is

The Environmental Working Group, a nonprofit research organization, has mapped PFAS contamination in US drinking water systems using data from utility testing and EPA monitoring programs. Their database identifies PFAS contamination in water systems serving over 200 million Americans. Military bases, industrial sites, and areas near airports that used PFAS-containing firefighting foam are the most heavily contaminated locations, but the chemicals have migrated broadly into groundwater supplies far from those original sources.

The EPA finalized maximum contaminant levels for six PFAS compounds in April 2024, setting enforceable limits for PFOA and PFOS at 4 parts per trillion each, the lowest level that can be reliably measured. Water utilities have until 2027 to comply with the new limits. In the meantime, PFAS exposure through drinking water continues in communities where filtration systems have not yet been installed. Activated carbon filters and reverse osmosis systems both remove PFAS effectively, but they are not standard equipment in most US homes.