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Advisory Committee on Health Effects of Endocrine Disruptors
The Supplement II to the Intermediary Report
1.4.2.2_10 |
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(iii) Studies on children from lightly exposed general
populations
A population of children in North Carolina was followed up from
the birth to adolescence by Rogan et al. (1985, 1986, 1991) and
Gladen et al. (1988, 1991, 2000). Higher exposure tended to be
associated with lower PDI (motor development) scores in Bayley
scale, but the results were not consistent because of
non-uniformity of the timing and method of evaluation.
Exposure of a population of children, half of whom breast-fed,
was evaluated by analysis of cord blood, maternal blood and
breast milk. Patandin et al. (1999) followed body growth of the
children from the birth to the 42th month, and reported a
inverse correlation of prenatal exposure to an ordinary
environmental level of PCBs with body weight of the newborns and
growth up to the third month. Neurological evaluation of
neonates (Huisman et al., 1995), evaluation of nerve development
at the 3rd, 7th and 18th months (Huisman, 1995; Koopman-Esseboom
et al., 1996), and neurobehavioral evaluation at the 42th month
(Lanting et al., 1998; Patandin et al., 1999) showed inverse
correlation between the exposure and motor development at the
3rd, 7th and 18th months.
Vreugdenhil et al. (2002) followed up 372 mother-child pairs.
The cognitive and motor performance of the children was
evaluated at 6-7 years of age to know if effects of PCB or
dioxin exposure last until the schooling age. The exposure level
was defined as the sum of PCB-118, 138, 153 and 180
concentrations in cord and maternal blood. Additionally, 17
dioxins, 6 dioxin-like PCBs and 20 non-dioxin-like PCBs in
breast milk were determined. Analysis showed that prenatal PCB
exposure influences inversely the cognitive and motor
development of the children in less-than-optimum parental and
home environments. It was thus suggested that the effects of
prenatal exposure to PCBs and dioxins last until schooling ages
but can be mitigated by favorable home environment and adequate
intellectual stimulation by the parents.
Vreugdenhil et al. (2002) further evaluated the playing behavior
of 158 children, 7.5 years of age, according to PSAI (Pre-School
Activity Inventory) to discern effects of prenatal exposure to
PCBs or dioxins. Effects of prenatal PCB exposure, as measured
in maternal and cord blood, on the masculine and androgynous
scores were significantly different between boys and girls (p <
0.5). Evaluation on the feminine scale showed that high prenatal
dioxin exposure was associated with predominance of feminine
play behavior in both sexes. These results suggest that prenatal
exposure to PCBs, dioxins and other organochlorines at
environmental level may induce imbalance in prenatal steroid
hormones. Vreugdenhil et al. (2004) further conducted
neuropsychological tests on 83 children (all 9 years of age;
including breast-fed and artificially fed groups as well as high
and low exposure groups) to evaluate perinatal exposure. High
PCB levels before the birth were correlated with slower
response, greater scattering of response time, and lower scores
in the Tower of London test. The same subjects were also tested
for central nerve functions by the P300, one of ERPs
(event-related potentials). Higher prenatal PCB exposure was
associated with longer P300 latent times. PCB exposure via
breast feeding showed no influence on the latent times. Children
breast-fed for 16 weeks or longer showed shorter P300 latent
times than those breast-fed for 6-16 weeks or artificially fed.
P300 amplitudes were not related to perinatal PCB exposure or
breast feeding. It was suggested that breast feeding promotes
adequate recognition and handling of stimulation by the central
nerve system, as reflected in ERPs, while prenatal exposure to
PCBs or related compounds at the environmental level in Holland
retards maturation of central nerve mechanisms.
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