A pilot study for foetal exposure to multiple persistent organic pollutants and the development of infant atopic dermatitis in modern Japanese society.
Increasing evidence supports that harmful chemicals accumulating in the human body may pose a significant threat to infant health through foetal exposure. Persistent organic pollutants (POPs) are thought to enhance the risk for later development of allergic disease like atopic dermatitis (AD). However, few studies have evaluated the effect of foetal exposure to various POPs on the development of AD in early infancy. Here, we describe the impact of foetal exposure to a number of POPs on the occurrence of AD in 7-month-old infants. The participants were 81 infants with or without AD who participated in a birth cohort study, where the concentrations of 15 polychlorinated biphenyl (PCBs) congeners, dichlorodiphenyltrichloroethane (p,p'-DDT), dichlorodiphenyldichloroethylene (p,p'-DDE), β-hexachlorocyclohexane (β-HCH), hexachlorobenzene (HCB), cis-nonachlor, trans-nonachlor, mirex, oxychlordane, and 27 polybrominated diphenyl ether (PBDEs) congeners were measured in the umbilical cord tissues collected immediately after birth. At 7 months, 27 of the 81 infants (33.8%) were diagnosed with AD. Of all POPs examined, total concentrations of 27 PBDE congeners were associated with a significantly decreased incidence of AD. Notably, the concentration of 27 PBDEs was significantly lower in AD infants than in non-AD infants (P<0.01), and the risk of AD development decreased with increasing PBDE levels. These results suggest that foetal exposure to PBDEs is a possible contributing factor to reducing AD in early infancy.
Department of Bioenvironmental Medicine, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan; Centre for Preventive Medical Science, Chiba University, Chiba 260-8670, Japan.
Shingo
S
Ochiai
Naoki
N
Shimojo
Igoshi
I
Yuka
Masahiro
M
Watanabe
Yoshiharu
Y
Matsuno
Shuichi
S
Suzuki
Yoichi
Y
Kohno
Chisato
C
Mori
D002706:Chlordan / Q000031:analogs & derivatives / Q000378:metabolism; D003634:DDT / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000139:chemically induced / Q000453:epidemiology* / Q000378:metabolism; D003633:Dichlorodiphenyl Dichloroethylene / Q000378:metabolism; D004781:Environmental Exposure / Q000032:analysis* / Q000706:statistics & numerical data; D004785:Environmental Pollutants / Q000032:analysis / Q000378:metabolism*; D005260:Female; D006581:Hexachlorobenzene / Q000378:metabolism; D001556:Hexachlorocyclohexane / Q000378:metabolism; D006801:Humans; D006843:Hydrocarbons, Chlorinated / Q000378:metabolism; D007223:Infant; D007231:Infant, Newborn; D007564:Japan; D008297:Male; D018811:Maternal Exposure / Q000706:statistics & numerical data; D008917:Mirex / Q000378:metabolism; D010865:Pilot Projects; D011078:Polychlorinated Biphenyls / Q000378:metabolism; D055815:Young Adult
D004785:Environmental Pollutants; D006843:Hydrocarbons, Chlorinated; D002706:Chlordan; C008743:oxychlordane; C001870:nonachlor; D003633:Dichlorodiphenyl Dichloroethylene; D006581:Hexachlorobenzene; D001556:Hexachlorocyclohexane; D003634:DDT; D011078:Polychlorinated Biphenyls; C023888:beta-hexachlorocyclohexane; D008917:Mirex
Atopic dermatitis; Foetal exposure; Infants; Persistent organic pollutants