title: Neonatal thyroid function in Seveso 25 years after maternal exposure to dioxin.
abstract: BACKGROUND
  Neonatal 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.
  
  
  RESULTS
  Between 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 microU/ml (95% confidence interval [CI] 0.90-1.08) in the reference area (n = 533), 1.35 microU/ml (95% CI 1.22-1.49) in zone B (n = 425), and 1.66 microU/ml (95% CI 1.19-2.31) in zone A (n = 56) (p < 0.001). The proportion of children with b-TSH > 5 microU/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, beta = 0.47, p < 0.001) and plasma toxic equivalents of coplanar dioxin-like compounds (n = 51, beta = 0.45, p = 0.005).
  
  
  CONCLUSIONS
  Our data indicate that environmental contaminants such as dioxins have a long-lasting capability to modify neonatal thyroid function after the initial exposure.
authors.affiliation: Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, United States of America. abaccare@hsph.harvard.edu
authors.forename: Andrea
authors.initials: A
authors.lastname: Baccarelli
authors.forename: Sara M
authors.initials: SM
authors.lastname: Giacomini
authors.forename: Carlo
authors.initials: C
authors.lastname: Corbetta
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: Landi
authors.forename: Matteo
authors.initials: M
authors.lastname: Bonzini
authors.forename: Dario
authors.initials: D
authors.lastname: Consonni
authors.forename: Paolo
authors.initials: P
authors.lastname: Grillo
authors.forename: Donald G
authors.initials: DG
authors.lastname: Patterson
authors.forename: Angela C
authors.initials: AC
authors.lastname: Pesatori
authors.forename: Pier Alberto
authors.initials: PA
authors.lastname: Bertazzi
mesh_terms: D000328:Adult; D004785:Environmental Pollutants / Q000633:toxicity*; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000139:chemically induced; D007231:Infant, Newborn; D007558:Italy; D008297:Male; D018811:Maternal Exposure; D000072317:Polychlorinated Dibenzodioxins / Q000097:blood / Q000633:toxicity*; D011247:Pregnancy; D013960:Thyroid Function Tests; D013961:Thyroid Gland / Q000378:metabolism*
chemical_list: D004785:Environmental Pollutants; D000072317:Polychlorinated Dibenzodioxins