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Correlation of Serum Hormone Concentrations in Maternal and Umbilical Cord Samples¹

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892 [R. T., R. N. H.], Dartmouth Medical School, Hanover, New Hampshire 03755 [R. T., B. C.]; Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland 20892 [N. P.]; Magee Women’s Hospital, University of Pittsburgh, Pittsburgh, Pennsylvania 15238 [J. M. R., G. H., N. M., D. L.]; and University of California San Francisco School of Medicine, San Francisco, California 94122 [P. S.]

Evidence suggests that adult cancer risk of hormonally related tumors may be influenced by the in utero environment, and most speculation on the biological mechanism has focused on the hormonal component. Epidemiological studies investigating the biological nature of pregnancy and maternal factors associated with offspring’s cancer risk have relied on maternal hormone measurements. The degree to which maternal hormone levels represent the fetal environment, however, is not widely known. Pregnancy estrogen, androstenedione, testosterone, dehydroepiandrosterone (DHEA), and DHEA-sulfate concentrations were measured in maternal and mixed umbilical cord sera from 86 singleton pregnancies. Spearman correlations between maternal and cord hormone levels generally ranged between 0.2 and 0.3. The correlation was 0.26 for estriol, the estrogen of highest concentration in pregnancy, and 0.27 for estradiol, the most biologically active estrogen. The correlations between mother and offspring for the estrogens and DHEA appeared similar for males and females, whereas there was a suggestion that the maternal-umbilical cord correlations for other androgens varied in magnitude by fetal sex, and all correlations appeared higher in pregnancies lasting <38 weeks compared with longer gestational lengths, although these stratified findings may have been attributable to chance. These data show a moderate degree of correlation in hormone concentrations between the maternal and fetal circulation. Studies using maternal hormone concentrations as a proxy for the fetal environment should consider the misclassification resulting with the use of this marker.

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