This study strengthens the evidence that PFAS exposure is influenced by product use and varies by race. In our cohort of middle-aged women, non-Hispanic white women had higher blood levels of PFOA and PFHxS compared with African Americans. These findings are consistent with previous reports of differences by race [9, 12, 13]. Consumer product sources of PFASs are difficult to untangle, and this study extends work identifying consumer product pathways for exposure to these chemicals and draws attention to food packaging and dental floss as modifiable sources. Although information about behavior was collected several years after the blood sample, this may not be a grave limitation because serum PFAS levels reflect long-term behavioral averages and people’s habits are likely consistent.

Among African Americans, but not other participants, eating prepared food from coated cardboard containers was associated with higher levels of four of the six PFAS chemicals evaluated (PFOA, PFNA, PFDeA, and PFOS). The differences in associations observed among African American and non-Hispanic white participants may be mediated by differences in the types of prepared food consumed most frequently: In this study, African Americans ate French fries more often than non-Hispanic whites, so we infer that they may also consume more fast food such as hamburgers, which are sold in paper wrappers. Recent data on fast food packaging show that fluorinated chemicals are detected more frequently in paper wrappers than in paperboard containers [21], so if French fries are a proxy for some exposure from food in paper wrappers, this could contribute to the differences in associations observed among African American and non-Hispanic white participants. Our questionnaire did not directly assess exposure to paper food wrappers. Harris et al. asked more generally about fast food consumption and found that eating fast food at least twice a week contributed to somewhat higher levels of PFOA, PFNA, and Me-PFOSA-AcOH in children in a model mutually adjusted for race [13].

Flossing with Oral-B Glide was associated with higher levels of PFHxS. All three Glide products that we tested contained fluorine, consistent with available information that Oral-B Glide is made with PTFE and supporting our hypothesis that Oral-B Glide is a potential exposure source for PFASs. In addition, three other flosses also tested positive for fluorine, including two of three store-brand products advertised as “compare to Oral-B Glide” on the package, and one described online as “single strand Teflon® fiber” [51]. Our question did not distinguish non-flossers from people who floss with products other than Oral-B Glide, so the availability of PTFE-based flosses other than Oral-B Glide likely weakened the associations in our study, since these participants are categorized as “never” despite having a similar exposure source as the “ever” group. Our product testing results suggest that PTFE-based flosses are widely available, but that consumers can use advertising claims to help identify them. Although most of the PFAS content is expected to be polymerized in the filament, previous product testing has shown that carboxylic PFASs are detected in PTFE-based dental floss [27, 31]; no testing has been performed for the sulfonic PFASs. We were surprised to find the strongest association with PFHxS rather than the carboxylic PFASs, but proprietary production practices and formulations limit our ability to predict possible exposures. This is the first evidence that flossing with PTFE-based dental floss could contribute to an individual’s body burden of PFASs, but additional data are required to verify this finding, for example, demonstrating the potential for PFASs in floss to migrate into saliva or onto hands.

As expected, living in a city with a PFAS-contaminated water supply was associated with higher serum concentrations of PFAS chemicals. We found a significant association with three of the six PFAS chemicals evaluated (PFOA, PFNA, and PFHxS). Despite the potential for UCMR3 data to misclassify some participants—for example, those served by a small water supply not monitored under UCMR3 or by a private well, or who live in a city served by multiple public water supplies—the positive associations that we observed are consistent with findings from Hurley et al. [14] and emphasize that contaminated drinking water can be a substantial contributor to PFAS exposure. Having stain-resistant treated furniture and carpets were associated with higher levels of PFNA in all participants and PFDeA in non-Hispanic whites. Treated furniture and carpets are known sources of PFASs including PFNA and PFDeA [31], although previous studies of exposure have detected links with sulfonic, rather than carboxylic, PFASs [13, 52].

While our analysis did not identify specific behavioral pathways contributing to racial disparities in exposure, the difference in PFHxS could be mediated by factors associated with education. More education was associated with higher PFHxS among non-Hispanic whites, and a greater proportion of non-Hispanic whites had at least a Bachelor’s degree in our study. While education may partially reflect socioeconomic status, Nelson et al. found that racial differences in exposure persisted after controlling for family income [12]. More likely, there are PFAS-related behaviors not included in our model that vary by education in non-Hispanic whites. Neither education nor any other variables measured in this study were explanatory for the observed race difference in PFOA.

Consuming microwave popcorn and eating food prepared with nonstick cookware had no significant association with PFAS levels, consistent with findings from Wu et al. [35]. In contrast to previous studies, we did not detect an association between PFAS levels and consumption of seafood in the past month [17]. Although we did not account for seafood consumption at restaurants, we observed similar rates of seafood consumption in this study. However, our power may have been limited by the smaller subsample of participants asked this question.

Our study is limited by the number and location of participants, nearly all of whom lived in California. However, exposures in our study were largely comparable with those of similar-aged women in NHANES, which is designed to collect a nationally representative sample. This suggests that our smaller population—which was half African American—was typical in its PFAS exposure. Future work should include persons of Hispanic ethnicity, who often have lower exposures in NHANES analyses [9,10,11,12], and Asian Americans, whose exposures have not been characterized. Investigating the reasons for differences in exposure by race or ethnicity can help identify major exposure pathways.

A strength of this study was the opportunity to collect detailed behavioral information related to exposure from consumer products. While NHANES collects comprehensive information about diet, the few questions it includes about consumer product behaviors have well-established links to health (e.g., using sunscreen) and are not likely related to PFAS exposure. Our survey allowed consideration of a wider range of behaviors, including exploratory exposure routes, and could also target specific product types. For example, NHANES did not distinguish between different floss products when it asked about frequency of dental flossing. Our results can inform priorities for future studies that require a short questionnaire or are not designed to uncover new pathways of exposure.

Our understanding of sources of PFAS exposure remains incomplete, however. The R2 values for our mutually adjusted models are comparable with those obtained by Harris et al. [13], who used a similar analytical approach to assess predictors of PFAS exposure in children. Behaviors that may contribute to exposure but were not measured in this study are one source of unexplained variation, such as consuming food sold in paper wrappers. Occupational exposure to PFAS can be a major source for workers who manufacture these chemicals or frequently use PFAS-containing products, such as firefighters or ski technicians [53,54,55], although we expect few of our participants to have such occupational histories. Other unexplained variation can be attributed to the use of binary predictor variables, and the noise associated with self-reported behavioral data. The semi-structured interviews gave insight into the reliability of the self-report: for example, we learned that participants had difficulty identifying “nonstick cookware” but could easily check the brand of floss that they use. Because this study leveraged already-collected biomonitoring data, the behavioral predictors report on participant activity several years after the blood draws. However, with half-lives roughly between 3 and 8 years (for PFOA, PFOS, and PFHxS) [56], blood levels of PFASs are representative of long-term behavioral averages. In addition, we expect that participants’ behaviors are generally similar over time, especially at the coarse level of categorization used in this study. Changes in behavior over time would introduce some measurement error to our results, but we cannot evaluate the magnitude of the error since we did not collect information about changes in behavior over time.

While this study did not capture all the potentially important sources of PFASs, our results strengthen the evidence for exposure to PFASs from food packaging and implicate exposure from PTFE-based dental floss for the first time—a finding that warrants prompt follow-up in a future study. Environmental contamination by PFASs, for example in drinking water, remains a major public health threat, but our results also support removing PFASs from products as a way to reduce human exposure. For now, altering consumer product behaviors is one way for individuals to lower their personal exposure to these harmful chemicals.