Background Per- and polyfluoroalkyl substances (PFASs) are a class of artificially synthesized fluorinated organic compounds. Recent studies have found that PFASs have endocrine disrupting effects and can affect the homeostasis of sex hormones, but there are few relevant epidemiological studies on puberty.
Objective This study is conducted to explore the associations between serum PFASs and serum sex hormones among adolescents aged 12 to 20 years.
Methods This study was based on the public online data of the National Health and Nutrition Examination Survey (NHANES) (2013-2016). A subset (n=682) of populations aged 12-20 years that had data on demographic information, linear PFOA (n-PFOA), sum of branched isomers of PFOA (Sb-PFOA, branched PFOA isomers), linear PFOS, (n-PFOS), sum of PFOS isomers, (Sm-PFOS, monomethyl branched PFOS isomers), pefluorodecanoic acid (PFDeA), perfluorohexane sulfonic acid (PFHxS), perfluorononanoic acid (PFNA), 2-(N-methyl-perfluoroctanesulfonamido)acetic acid (Me-PFOSA-AcOH), perfluoroundecanoic acid (PFUA), perfluorododecanoic acid (PFDoA), estradiol (E2), testosterone (T), and sex hormone binding globulin (SHBG) was used. Serum PFASs and sex hormones were measured using high performance liquid chromatography coupled with tandem mass spectrometry, liquid chromatography-tandem mass spectrometry, and enzyme-linked immunosorbent assay respectively. Associations between PFASs and sex hormones were assessed using multiple linear regression models stratified by sex, age, and race.
Results Among the 628 participants aged 12-20 years, 359 were males (52.6%) averaged (15.83±2.44) years old, and 323 were females (47.4%) averaged (15.74±2.49) years old. The detection rates of five PFASs (n-PFOS, n-PFOA, PFNA, PFHxS, and Sm-PFOS) approached 100% (99.7%-99.9%), followed by PFDeA (62.0%), and the other four PFASs were all below 50%. The median exposure level of n-PFOS was the highest (2.20 μg·L-1), followed by n-PFOA (1.30 μg·L-1), and the remaining PFASs varied from 0.07-0.90 μg·L-1. After adjustments for potential confounders, in males, exposure to n-PFOA was negatively associated with E2 (b=-0.13, 95% CI:-0.26--0.003); when stratified by age, PFHxS was negatively associated with E2 (b=-0.09, 95% CI:-0.17--0.01) in the group of 16 to 20 years old, and negatively associated with SHBG (b=-0.09, 95% CI:-0.17--0.004) in the group of 12 to 15 years old. In females, n-PFOA (b=-0.18, 95% CI:-0.29--0.07), PFHxS (b=-0.09, 95%CI:-0.16--0.01), and Sm-PFOS (b=-0.12, 95%CI:-0.22--0.02) were negatively associated with SHBG; when stratified by age, only in the group of 16 to 20 years old, PFHxS was negatively associated with SHBG (b=-0.11, 95% CI:-0.21--0.003), and PFDeA was positively associated with T (b=0.12, 95%CI:0.02-0.23).
Conclusion Exposure to certain PFASs may be associated with decreased sex hormone levels in puberty, such as lower E2 in males and lower SHBG in females, and these effects are strongest in the 16-20 years age group.
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