Serum hormones in boys prenatally exposed to polychlorinated biphenyls and dibenzofurans
- PMID: 16076757
- DOI: 10.1080/15287390590967360
Serum hormones in boys prenatally exposed to polychlorinated biphenyls and dibenzofurans
Abstract
Polychlorinated biphenyls (PCBs) and dibenzofurans (PCDFs) are persistent environmental pollutants shown to adversely interact with several functions of the endocrine system. In 1978-1979, over 2000 Taiwanese people ingested rice oil accidentally contaminated with PCBs and PCDFs. This is one of the major toxic exposure episodes that occurred globally and was later called Yucheng (oil disease in Chinese). The children born to exposed Yucheng women were therefore exposed in utero to high doses of PCBs/PCDFs. In 1995, 60 Yucheng and 61 control boys participated in physical examination, and serum hormones were measured by radioimmunoassay (RIA). Age, body weight, body height, Tanner status, testicular size, serum luteinizing hormone (LH), prolactin (PRL), thyroxine (T4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) levels were not statistically different between Yucheng and control boys in the subgroups of before and at the age of puberty. However, the serum estradiol (E2) levels were significant higher in Yucheng boys at the age of puberty. Yucheng and control boys were further divided into two subgroups, those before (age <13 yr) and those at the age of puberty (age > or = 13 yr). There was a decrease of serum testosterone (TT) levels and increase of serum follicle-stimulating hormone (FSH) levels in Yucheng boys at the age of puberty as compared with controls. There was a significant decrease of the square root of TT/E2 and TT/FSH; however, the square root of E2/FSH was increased in Yucheng boys at the age of puberty as compared with controls. Data indicated that prenatal exposure to PCBs and PCDFs may have implications for boys' sex hormone homeostasis at puberty. Further studies are needed to identify the congeners of PCBs/PCDFs responsible for disruption of the endocrine system, as well as the mechanisms of such disruption.
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