Biology Reference
In-Depth Information
Table 21.1
Comparison of E2,
BPA, PCB, and GEN levels in newborns, infants
,
and adults
GEN
ng/mL
BPA
ng/mL
PCBs
ng/mL
E2 ng/mL
References
Plasma, adult Western
woman (across the cycle)
0.25-5.4
1-2
0.3-5
0.1-14.3
[
59
-
65
]
Amniotic fl uid, Western
0.4-1.7
[
66
,
67
]
Cord blood, Western
1-3
0.1-7.2
[
62
,
64
]
Plasma, adult Japanese
woman
7.2-83
1.4-2
[
58
,
68
-
70
]
Cord blood, Japan
19.4-45
2.2
[
58
,
68
,
70
,
71
]
Breast milk
8-13.5
1.3
5.4-63.1
[
64
,
72
,
73
]
Plasma, breast-fed infant
<0.04-0.08
2-4.7
[
56
,
74
]
Plasma, infant-fed bovine
formula
<0.04-0.08
9.4
[
56
]
Plasma, infant-fed soy
formula
<0.04-0.08
684-757
[
56
,
75
]
GEN levels are typically higher than BPA or PCB levels for all age groups and in all fl uids listed
Compiled values represent the range of those previously reported and do not take into account
methodological differences (including controlling for lipid levels for the PCB values listed), sam-
ple sizes, or differences between steady state and peak levels. Thus, values presented should be
considered representative. Circulating E2 levels were obtained from references [
76
-
78
] and the
UK General Practice Notebook (
http://www.gpnotebook.co.uk/simplepage.cfm?ID=570818627&
linkID=24801&cook=yes
) (Table adapted from [
19
])
to GEN and other phytoestrogens is typically much higher than for most synthetic
EDCs, even among individuals that do not consume a legume-rich diet (Table
21.1
).
Thus, it is important to consider the potential long-term impacts of exposure, particu-
larly during development. Concern regarding the use of soy-based infant formula is
emerging because epidemiology studies have associated its use with elevated risk of
menstrual irregularities and uterine fi broids [
33
,
34
]. Infants maintained on these for-
mulas consume as much as 6-9 mg/kg of isofl avone phytoestrogens per day, which is
6-11-fold higher than a typical adult exposure [
56
]. GEN exposure can also occur in
utero through placental transfer or after birth via lactation [
57
,
58
].
Mechanisms of Kisspeptin System Endocrine Disruption
The detailed neuroanatomy, sexual differentiation, and steroid hormone regulation of
the kisspeptin system are provided in other chapters, and thus will not be repeated here.
Key aspects that make this system vulnerable to endocrine disruption, including how
kisspeptin is infl uenced by perinatal estrogens, are worth highlighting (Fig.
21.2
). In
rodents, two primary hypothalamic populations of kisspeptin neurons have been charac-
terized: one in a region comprising the anteroventral periventricular (AVPV) nucleus
and the medial aspects of the rostral periventricular nucleus (AVPV/PeN, an area some-
times referred to as the rostral periventricular area of the third ventricle (RP3V)), and a
second in the arcuate (ARC) nucleus. Additionally, a third, smaller population was sub-
sequently identifi ed in the medial amygdala (MeA) [
79
,
80
]. There is now evidence that
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