Date Published: July 29, 2008
Publisher: Public Library of Science
Author(s): Andrea Baccarelli, Sara M Giacomini, Carlo Corbetta, Maria Teresa Landi, Matteo Bonzini, Dario Consonni, Paolo Grillo, Donald G Patterson, Angela C Pesatori, Pier Alberto Bertazzi, Bruce Lanphear
Abstract: BackgroundNeonatal hypothyroidism has been associated in animal models with maternal exposure to several environmental contaminants; however, evidence for such an association in humans is inconsistent. We evaluated whether maternal exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a persistent and widespread toxic environmental contaminant, is associated with modified neonatal thyroid function in a large, highly exposed population in Seveso, Italy.Methods and FindingsBetween 1994 and 2005, in individuals exposed to TCDD after the 1976 Seveso accident we conducted: (i) a residence-based population study on 1,014 children born to the 1,772 women of reproductive age in the most contaminated zones (A, very high contamination; B, high contamination), and 1,772 age-matched women from the surrounding noncontaminated area (reference); (ii) a biomarker study on 51 mother–child pairs for whom recent maternal plasma dioxin measurements were available. Neonatal blood thyroid-stimulating hormone (b-TSH) was measured on all children. We performed crude and multivariate analyses adjusting for gender, birth weight, birth order, maternal age, hospital, and type of delivery. Mean neonatal b-TSH was 0.98 μU/ml (95% confidence interval [CI] 0.90–1.08) in the reference area (n = 533), 1.35 μU/ml (95% CI 1.22–1.49) in zone B (n = 425), and 1.66 μU/ml (95% CI 1.19–2.31) in zone A (n = 56) (p < 0.001). The proportion of children with b-TSH > 5 μU/ml was 2.8% in the reference area, 4.9% in zone B, and 16.1% in zone A (p < 0.001). Neonatal b-TSH was correlated with current maternal plasma TCDD (n = 51, β = 0.47, p < 0.001) and plasma toxic equivalents of coplanar dioxin-like compounds (n = 51, β = 0.45, p = 0.005).ConclusionsOur data indicate that environmental contaminants such as dioxins have a long-lasting capability to modify neonatal thyroid function after the initial exposure.
Partial Text: Variations in neonatal thyroid function evaluated at birth through blood thyroid-stimulating hormone (b-TSH) are associated with changes in iodine availability and maternal intake . According to the World Health Organization (WHO), the percentage of newborns with b-TSH > 5 μU/ml should be less than 3% in iodine-replete populations . Aside from iodine deficiency, no environmental exposure has been conclusively associated with reduced neonatal thyroid function in humans [2–4].
Neonatal b-TSH, which is used in most countries to screen for congenital hypothyroidism, is considered a sensitive marker of subclinical primary hypothyroidism and a suitable index of the presence of factors causing thyroid enlargement and potential alterations in function [1,29,30]. Our results from the Seveso population showed that newborns of mothers with high body burdens of TCDD, resulting from accidental dioxin exposure occurring approximately 20–30 y earlier, had higher neonatal b-TSH concentrations compared to newborns of nonexposed women.