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. 2021 Jul 13;106(8):2495-2504.
doi: 10.1210/clinem/dgab267.

Life-course Exposure to Perfluoroalkyl Substances in Relation to Markers of Glucose Homeostasis in Early Adulthood

Damaskini Valvi  1   2 , Kurt Højlund  3 , Brent A Coull  4 , Flemming Nielsen  5 , Pal Weihe  6   7 , Philippe Grandjean  1   5
Affiliations

Life-course Exposure to Perfluoroalkyl Substances in Relation to Markers of Glucose Homeostasis in Early Adulthood

Damaskini Valvi et al. J Clin Endocrinol Metab. .

Abstract

Objective: To investigate the prospective associations of life-course perfluoroalkyl substances (PFASs) exposure with glucose homeostasis at adulthood.

Methods: We calculated insulin sensitivity and beta-cell function indices based on 2-h oral glucose tolerance tests at age 28 in 699 Faroese born in 1986-1987. Five major PFASs were measured in cord whole blood and in serum from ages 7, 14, 22, and 28 years. We evaluated the associations with glucose homeostasis measures by PFAS exposures at different ages using multiple informant models fitting generalized estimating equations and by life-course PFAS exposures using structural equation models.

Results: Associations were stronger for perfluorooctane sulfonate (PFOS) and suggested decreased insulin sensitivity and increased beta-cell function-for example, β (95% CI) for log-insulinogenic index per PFOS doubling = 0.12 (0.02, 0.22) for prenatal exposures, 0.04 (-0.10, 0.19) at age 7, 0.07 (-0.07, 0.21) at age 14, 0.05 (-0.04, 0.15) at age 22, and 0.04 (-0.03, 0.11) at age 28. Associations were consistent across ages (P for age interaction > 0.10 for all PFASs) and sex (P for sex interaction > 0.10 for all PFASs, except perfluorodecanoic acid). The overall life-course PFOS exposure was also associated with altered glucose homeostasis (P = 0.04). Associations for other life-course PFAS exposures were nonsignificant.

Conclusions: Life-course PFAS exposure is associated with decreased insulin sensitivity and increased pancreatic beta-cell function in young adults.

Keywords: beta-cell function; developmental exposures; endocrine disruptors; insulin resistance; perfluoroalkyl substances; type 2 diabetes.

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Figures

Figure 1.
Figure 1.
Adjusted mean change (beta, 95% CI) in markers of glucose homeostasis per doubling of exposure to PFOS, PFOA, or PFHxS, in the population overall and in specific strata according to sex. Effect estimates from longitudinal Multiple informant GEE models adjusted for an interaction term between each PFAS and age at exposure assessment, exact age at examinations, sex, order of birth, maternal prepregnancy BMI, and maternal smoking and fish intake during pregnancy.
Figure 2.
Figure 2.
Adjusted mean change (beta, 95% CI) in markers of glucose homeostasis per doubling of postnatal exposure to PFDA or PFNA in the population overall, and in specific strata according to sex. Effect estimates from longitudinal multiple informant GEE models including an interaction term between each PFAS and age at exposure assessment and additionally adjusted for exact age at postnatal examinations, sex, order of birth, maternal prepregnancy BMI, maternal smoking and fish intake during pregnancy, and breastfeeding duration.
Figure 3.
Figure 3.
Path diagram and standard error of the mean effect estimates for the association between life-course latent PFAS exposure functions and the latent glucose homeostasis function estimated based on observed markers of insulin sensitivity and beta-cell function. aChange in the standard deviation of the glucose homeostasis function per 1 SD increase in life-course PFAS exposures, adjusted for sex, order of birth, maternal prepregnancy BMI, maternal smoking and fish intake during pregnancy, and breastfeeding duration.
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References

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