title: Effects of prenatal exposure to dioxin-like compounds on allergies and infections during infancy.
abstract: Dioxin-like compounds are endocrine disruptors. The effects of prenatal exposure to environmental levels of dioxins on immune function during infancy have not been clarified, although dioxins induce immunosuppression in offspring of animals. Moreover, human studies have not assessed the effects of gender- or congener-specific differences. The purpose of this study was to investigate the association between dioxin levels in maternal blood and the risk of infection and allergies in infancy. We examined 364 mothers and their infants enrolled in a Hokkaido Study on Environment and Children's Health between 2002 and 2005 in Sapporo, Japan. Relevant information was collected from a baseline questionnaire during pregnancy, medical records at delivery, and a follow-up questionnaire when the child was 18 months of age that assessed development of allergies and infections in infancy. Dioxin-like compound levels in maternal blood were measured with high-resolution gas chromatography/high-resolution mass spectrometry. Relatively higher levels of polychlorinated dibenzofuran were associated with a significantly increased risk of otitis media, especially among male infants (odds ratio=2.5, 95% confidence interval=1.1-5.9). Relatively higher levels of 2,3,4,7,8-pentachlorodibenzofuran were also associated with a significantly increased risk of otitis media (odds ratio=5.3, 95% confidence interval=1.5-19). However, we observed a weak association between dioxin-like compound levels and allergic symptoms in infancy. At environmental levels, prenatal exposure to dioxin-like compounds may alter immune function and increase the risk of infections in infancy, especially among males. The compound 2,3,4,7,8-pentachlorodibenzofuran may be responsible for this.
authors.affiliation: Department of Public Health, Hokkaido University Graduate School of Medicine, North 15 West 7 Kita-ku, Sapporo, Hokkaido, Japan.
authors.forename: Chihiro
authors.initials: C
authors.lastname: Miyashita
authors.forename: Seiko
authors.initials: S
authors.lastname: Sasaki
authors.forename: Yasuaki
authors.initials: Y
authors.lastname: Saijo
authors.forename: Noriaki
authors.initials: N
authors.lastname: Washino
authors.forename: Emiko
authors.initials: E
authors.lastname: Okada
authors.forename: Sumitaka
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Kanae
authors.initials: K
authors.lastname: Konishi
authors.forename: Jumboku
authors.initials: J
authors.lastname: Kajiwara
authors.forename: Takashi
authors.initials: T
authors.lastname: Todaka
authors.forename: Reiko
authors.initials: R
authors.lastname: Kishi
mesh_terms: D000328:Adult; D004147:Dioxins / Q000097:blood / Q000633:toxicity*; D052244:Endocrine Disruptors / Q000097:blood / Q000633:toxicity*; D004785:Environmental Pollutants / Q000097:blood / Q000633:toxicity*; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000453:epidemiology*; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D018811:Maternal Exposure / Q000706:statistics & numerical data; D010033:Otitis Media / Q000453:epidemiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology*; D012737:Sex Factors
chemical_list: D004147:Dioxins; D052244:Endocrine Disruptors; D004785:Environmental Pollutants