153
Epigenetic Mechanism
DNA methylation is one of the mechanisms through which EDCs induce obesity.
DNA methylation is the addition of methyl groups to the DNA, resulting in the
alteration of functions of DNA and gene repression [33]. Most organic pollutants
and BPA are capable of initiating DNA methylation. Numerous studies had also
revealed that perfluorooctane sulfonic acid (PFOS) and BPA promote adipogenesis
through DNA methylation and nuclear factor erythroid 2-related factor 2 (Nrf2)
pathways [33, 34].
Estrogen Receptor
EDCs also show obesogenic action through estrogen receptors. BPA is one of the
first recognized estrogenic EDCs [35]. Exposure to estrogenic EDCs may modify
the development of adipocytes. Although there is a scarcity of data reporting EDCs
effects on human beings, animal studies report marked increase in weight on prenatal exposure to BPA [36].
Endocrine Disrupting Chemicals and Childhood Obesity:
Epidemiological Evidence
There is a strong linkage between EDCs and childhood obesity. BPA has been
broadly reported to be associated with childhood obesity. BPA is readily absorbed
from gastrointestinal tract after oral consumption mainly through contaminated
food and forms soluble conjugates after metabolism. As the newborns lack matured
glucuronidase enzyme, BPA concentration is three times higher in them as compared to adults. The higher levels of BPA are mainly reported in babies using polycarbonate bottles for feeding [37]. Similarly, the measurement of BPA levels in
pregnant females and their children reported a positive relationship between BPA
concentration and fat mass in children [38]. Further investigations suggest that the
urinary BPA concentrations in late pregnancy are correlated with leptin and adiponectin levels in newborn babies [39]. However, it was reported that among 8–11 years
children, the urinary BPA concentration was directly proportional to the BMI of the
children [40].
Besides BPA, phthalates are also declared to be an emerging cause of childhood
obesity. Several investigations proclaimed a higher body mass index, waist circumference, and obesity with increasing urinary concentration of phthalates in
children [41–43]. DDT has also been equally reported to be a source of childhood
obesity. An increased prenatal DDT concentration in pregnant females and their
newborn is linked with obesity in children during their early life [44]. Additionally,
10 Endocrine Disrupting Chemicals Induced Childhood Obesity
Epigenetic Mechanism
DNA methylation is one of the mechanisms through which EDCs induce obesity.
DNA methylation is the addition of methyl groups to the DNA, resulting in the
alteration of functions of DNA and gene repression [33]. Most organic pollutants
and BPA are capable of initiating DNA methylation. Numerous studies had also
revealed that perfluorooctane sulfonic acid (PFOS) and BPA promote adipogenesis
through DNA methylation and nuclear factor erythroid 2-related factor 2 (Nrf2)
pathways [33, 34].
Estrogen Receptor
EDCs also show obesogenic action through estrogen receptors. BPA is one of the
first recognized estrogenic EDCs [35]. Exposure to estrogenic EDCs may modify
the development of adipocytes. Although there is a scarcity of data reporting EDCs
effects on human beings, animal studies report marked increase in weight on prenatal exposure to BPA [36].
Endocrine Disrupting Chemicals and Childhood Obesity:
Epidemiological Evidence
There is a strong linkage between EDCs and childhood obesity. BPA has been
broadly reported to be associated with childhood obesity. BPA is readily absorbed
from gastrointestinal tract after oral consumption mainly through contaminated
food and forms soluble conjugates after metabolism. As the newborns lack matured
glucuronidase enzyme, BPA concentration is three times higher in them as compared to adults. The higher levels of BPA are mainly reported in babies using polycarbonate bottles for feeding [37]. Similarly, the measurement of BPA levels in
pregnant females and their children reported a positive relationship between BPA
concentration and fat mass in children [38]. Further investigations suggest that the
urinary BPA concentrations in late pregnancy are correlated with leptin and adiponectin levels in newborn babies [39]. However, it was reported that among 8–11 years
children, the urinary BPA concentration was directly proportional to the BMI of the
children [40].
Besides BPA, phthalates are also declared to be an emerging cause of childhood
obesity. Several investigations proclaimed a higher body mass index, waist circumference, and obesity with increasing urinary concentration of phthalates in
children [41–43]. DDT has also been equally reported to be a source of childhood
obesity. An increased prenatal DDT concentration in pregnant females and their
newborn is linked with obesity in children during their early life [44]. Additionally,
10 Endocrine Disrupting Chemicals Induced Childhood Obesity