Background: In animal studies, in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a known endocrine disruptor, has been associated with altered thyroid homeostasis and thyroid hormone concentrations.Limited epidemiologic evidence suggests in utero dioxin exposure alters neonatal thyroid function. Aim: On July 10,1976, as a result of a chemical explosion, residents of Seveso, Italy experienced the highest levels of TCDD in a human population. In 1996, we initiated the Seveso Women's Health Study (SWHS), a retrospective cohort study of the health of the women. In 2008, we followed up the SWHS cohort to determine if maternal TCDD exposure is associated with neonatal thyroid function. Methods:Between the start of the Regione Lombardia neonatal thyroid registry (January 1,1994) and December 31, 2009, 209 SWHS women reported 303 singleton live births. We abstracted neonatal TSH levels for 235 (～77%) births. We examined the relation of maternal serum TCDD levels (1976,1996, at pregnancy) with neonatal TSH levels using generalized estimating equations and considered interaction by menarche status and age at explosion. Results: The geometric mean (±GSD) TSH level for neonates was 1.3 (±3.0) μU/ml, and ranged from 0.1 to 67.0 μU/ml; 13 neonates (5.5%) had TSH levels ＞5 μU/ml. There was a significant interaction with age at explosion (p＜0.05). Among women who were ＜5 years in 1976, there was a significant positive association of neonatal TSH with 1996 TCDD (adj-β = 0.19; 95%CI 0.01, 0.37) and TCDD at pregnancy (adj-β=0.21; 95%CI 0.04, 0.39), but not with 1976 TCDD (adj-β=0.00; 95%CI -0.12, 0.13). Among women ≥5 years in 1976, neonatal TSH was not related to any measure of TCDD exposure. Conclusions: Our results confirm earlier epidemiologic findings that in utero dioxin exposure alters neonatal thyroid function and provides support for the hypothesis that TCDD exposure during developmentally vulnerable windows may increase susceptibility.
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