Maisonet Mildred, Calafat Antonia M, Marcus Michele, Jaakkola Jouni J K, Lashen Hany
Department of Biostatistics and Epidemiology, College of Public Health, East Tennessee State University, Johnson City, Tennessee, USA.
Environ Health Perspect. 2015 Dec;123(12):1325-30. doi: 10.1289/ehp.1408847. Epub 2015 Jun 2.
Exposure to perfluorooctane sulfonic acid (PFOS) or to perfluorooctanoic acid (PFOA) increases mouse and human peroxisome proliferator-activated receptor alpha (PPARα) subtype activity, which influences lipid metabolism. Because cholesterol is the substrate from which testosterone is synthesized, exposure to these substances has the potential to alter testosterone concentrations.
We explored associations of total testosterone and sex hormone-binding globulin (SHBG) concentrations at age 15 years with prenatal exposures to PFOS, PFOA, perfluorohexane sulfonic acid (PFHxS), and perfluoronanoic acid (PFNA) in females.
Prenatal concentrations of the perfluoroalkyl acids (PFAAs) were measured in serum collected from pregnant mothers at enrollment (1991-1992) in the Avon Longitudinal Study of Parents and Children (ALSPAC). The median gestational age when the maternal blood sample was obtained was 16 weeks (interquartile range, 11-28 weeks). Total testosterone and SHBG concentrations were measured in serum obtained from their daughters at 15 years of age. Associations between prenatal PFAAs concentrations and reproductive outcomes were estimated using linear regression models (n = 72).
Adjusted total testosterone concentrations were on average 0.18-nmol/L (95% CI: 0.01, 0.35) higher in daughters with prenatal PFOS in the upper concentration tertile compared with daughters with prenatal PFOS in the lower tertile. Adjusted total testosterone concentrations were also higher in daughters with prenatal concentrations of PFOA (β = 0.24; 95% CI: 0.05, 0.43) and PFHxS (β = 0.18; 95% CI: 0.00, 0.35) in the upper tertile compared with daughters with concentrations in the lower tertile. We did not find evidence of associations between PFNA and total testosterone or between any of the PFAAs and SHBG.
Our findings were based on a small study sample and should be interpreted with caution. However, they suggest that prenatal exposure to some PFAAs may alter testosterone concentrations in females.
接触全氟辛烷磺酸(PFOS)或全氟辛酸(PFOA)会增加小鼠和人类过氧化物酶体增殖物激活受体α(PPARα)亚型的活性,这会影响脂质代谢。由于胆固醇是合成睾酮的底物,接触这些物质有可能改变睾酮浓度。
我们探讨了15岁女性的总睾酮和性激素结合球蛋白(SHBG)浓度与产前接触PFOS、PFOA、全氟己烷磺酸(PFHxS)和全氟壬酸(PFNA)之间的关联。
在雅芳亲子纵向研究(ALSPAC)中,对1991 - 1992年入组时从怀孕母亲采集的血清中全氟烷基酸(PFAA)的产前浓度进行测量。采集母亲血样时的中位孕周为16周(四分位间距,11 - 28周)。在其女儿15岁时采集的血清中测量总睾酮和SHBG浓度。使用线性回归模型估计产前PFAA浓度与生殖结局之间的关联(n = 72)。
与产前PFOS处于低浓度三分位数的女儿相比,产前PFOS处于高浓度三分位数的女儿经调整后的总睾酮浓度平均高0.18 nmol/L(95%置信区间:0.01,0.35)。与浓度处于低三分位数的女儿相比,产前PFOA(β = 0.24;95%置信区间:0.05,0.43)和PFHxS(β = 0.18;95%置信区间:0.00,0.35)处于高三分位数的女儿经调整后的总睾酮浓度也更高。我们未发现PFNA与总睾酮之间或任何PFAA与SHBG之间存在关联的证据。
我们的研究结果基于一个小样本研究,应谨慎解读。然而,它们表明产前接触某些PFAA可能会改变女性的睾酮浓度。