European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry · 2008
Molar-incisor-hypomineralisation and dioxins: new findings.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Laisi S, Kiviranta H, Lukinmaa P-L, Vartiainen T, Alaluusua S
Аннотация
AIM: According to our earlier study, molar-incisor-hypomineralisation (MIH) was associated with the exposure of a child via mother's milk to polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs) in a group of Finnish children born in 1987. Since the levels of PCDD/Fs and PCBs in mother's milk/placenta have remarkably decreased, it was important to find out if an association still exists.
METHODS: The study group was composed of 167 mothers and their children. Placental samples from the mothers were collected in maternity hospitals in Helsinki and Oulu in 1995--1999 and concentrations of the 17 most toxic PCDD/PCDF and 36 PCB congeners were measured. After 7-10 years the children were examined for MIH and the mothers were interviewed on the duration of breast-feeding.
RESULTS: MIH was found in 24 children (14.4%). The duration of breast-feeding ranged from 0 to 30 months (mean=7.2+/-4.7). WHOPCDD/FTEQ ranged from 2.5 to 39.1 pg/g fat (mean=13.7+/-6.8) and WHOPCBTEQ from 0.7 to 9.8 pg/g fat (mean=2.7+/-1.4). The mean sum of PCDD/Fs was 196+/-105 pg/g fat and that of PCBs was 57.2+/-28.1ng/g fat. The total exposure to PCDD/Fs, which was calculated from the placental concentration (used as a proxy for the milk concentration) and duration of breastfeeding, was not associated with the occurrence or severity of MIH. Neither was the total exposure to PCBs associated with the occurrence or severity of MIH.
CONCLUSION: At prevailing levels, exposure of a child via placenta/mother's milk to PCDD/Fs and PCBs is not associated with MIH.
METHODS: The study group was composed of 167 mothers and their children. Placental samples from the mothers were collected in maternity hospitals in Helsinki and Oulu in 1995--1999 and concentrations of the 17 most toxic PCDD/PCDF and 36 PCB congeners were measured. After 7-10 years the children were examined for MIH and the mothers were interviewed on the duration of breast-feeding.
RESULTS: MIH was found in 24 children (14.4%). The duration of breast-feeding ranged from 0 to 30 months (mean=7.2+/-4.7). WHOPCDD/FTEQ ranged from 2.5 to 39.1 pg/g fat (mean=13.7+/-6.8) and WHOPCBTEQ from 0.7 to 9.8 pg/g fat (mean=2.7+/-1.4). The mean sum of PCDD/Fs was 196+/-105 pg/g fat and that of PCBs was 57.2+/-28.1ng/g fat. The total exposure to PCDD/Fs, which was calculated from the placental concentration (used as a proxy for the milk concentration) and duration of breastfeeding, was not associated with the occurrence or severity of MIH. Neither was the total exposure to PCBs associated with the occurrence or severity of MIH.
CONCLUSION: At prevailing levels, exposure of a child via placenta/mother's milk to PCDD/Fs and PCBs is not associated with MIH.