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increased the obesity rates followed by intake of high energy meals and deficiency of
physical activities. On the other hand, at population level genomic causes are insufficient to clarify the reasons for arising obesity. Epidemiological studies in the last
40 years suggested that chemical changes in environment have played a major role
in arising obesity through interfering with major pathways (Fig. 17.11) such as lipid
metabolism, energy homeostasis, and adipogenesis [89]. In utero exposure to EDCs
has provided the correlations between obesity and environmental obesogens [90].
Grun et al. [91] have also investigated that continuous exposure of MDCs to in
vivo animal models during embryonic developments cause the adipogenesis.
Newborns also showed that exposure of diethylstilbestrol may increase the risk of
miscarriage in pregnant women followed by initial loss of body weight in infant. It
leads to sudden gain of body weight at puberty, finally causing increased body
weight [92]. This study provides the evidences that pesticides as MDCs act on specific targeted pathway to boost up obesity [93].
Influence on Reproductive and Developmental Processes
Pesticides as EDCs damage many physiological reaction of reproductive system
which can be manifested in vivo or in vitro with ovarian and testicular abnormalities [92]. These pesticides increase the rate of breast/prostate cancer, increase testicular occurrence, reduce quality and number of sperms [94]. Effect of these
environmental pollutants as sexual defects can also be visualized in wildlife species
[95]. These environmental recalcitrants (Fig. 17.12) are also responsible for testicular dysgenesis syndrome (TDS) which includes low sperm count, testicular carcinoma, poor quality of sperms in males whereas diethylstilbestrol (DES) in female
reproductive systems [96]. Organochlorine pesticides like chlorpyrifos and
methoxychlor alter the biosynthetic pathway of gonadotropin hormones in GT1–7
cells of hypothalamus cells [97]. A study on effect of polychlorinated biphenyl
(PCBs) in baby girls reported that PCBs damage the reproductive system in the
developmental stages [98]. Reproductive malfunctioning is also observed in the
persons working with bisphenol A. Bisphenol A has a property to leach out from
plastic utensils, so infants are also at higher danger of ED problems [48]. In females,
exposure of BPA is one cause of miscarriage [99]. Miscarriage in experimental
animals due to aneuploidy with BPA exposure is also reported [100]. In short,
whole hormone release system of humans is a prone target of these recalcitrants.
Effects on Sexual Dimorphism
Many pesticides such as dieldrin being EDCs have ability to interfere with sex limited effects. Data regarding sex is very limited because most of the experiments
were performed on males. It is admitted fact that deposition of subcutaneous fats as
S. Kamal et al.
increased the obesity rates followed by intake of high energy meals and deficiency of
physical activities. On the other hand, at population level genomic causes are insufficient to clarify the reasons for arising obesity. Epidemiological studies in the last
40 years suggested that chemical changes in environment have played a major role
in arising obesity through interfering with major pathways (Fig. 17.11) such as lipid
metabolism, energy homeostasis, and adipogenesis [89]. In utero exposure to EDCs
has provided the correlations between obesity and environmental obesogens [90].
Grun et al. [91] have also investigated that continuous exposure of MDCs to in
vivo animal models during embryonic developments cause the adipogenesis.
Newborns also showed that exposure of diethylstilbestrol may increase the risk of
miscarriage in pregnant women followed by initial loss of body weight in infant. It
leads to sudden gain of body weight at puberty, finally causing increased body
weight [92]. This study provides the evidences that pesticides as MDCs act on specific targeted pathway to boost up obesity [93].
Influence on Reproductive and Developmental Processes
Pesticides as EDCs damage many physiological reaction of reproductive system
which can be manifested in vivo or in vitro with ovarian and testicular abnormalities [92]. These pesticides increase the rate of breast/prostate cancer, increase testicular occurrence, reduce quality and number of sperms [94]. Effect of these
environmental pollutants as sexual defects can also be visualized in wildlife species
[95]. These environmental recalcitrants (Fig. 17.12) are also responsible for testicular dysgenesis syndrome (TDS) which includes low sperm count, testicular carcinoma, poor quality of sperms in males whereas diethylstilbestrol (DES) in female
reproductive systems [96]. Organochlorine pesticides like chlorpyrifos and
methoxychlor alter the biosynthetic pathway of gonadotropin hormones in GT1–7
cells of hypothalamus cells [97]. A study on effect of polychlorinated biphenyl
(PCBs) in baby girls reported that PCBs damage the reproductive system in the
developmental stages [98]. Reproductive malfunctioning is also observed in the
persons working with bisphenol A. Bisphenol A has a property to leach out from
plastic utensils, so infants are also at higher danger of ED problems [48]. In females,
exposure of BPA is one cause of miscarriage [99]. Miscarriage in experimental
animals due to aneuploidy with BPA exposure is also reported [100]. In short,
whole hormone release system of humans is a prone target of these recalcitrants.
Effects on Sexual Dimorphism
Many pesticides such as dieldrin being EDCs have ability to interfere with sex limited effects. Data regarding sex is very limited because most of the experiments
were performed on males. It is admitted fact that deposition of subcutaneous fats as
S. Kamal et al.