In utero exposure to environmental chemicals

lessons from maternal cigarette smoking and its effects on gonad development and puberty

Rebecca McKinlay, Peter J. O'Shaughnessy, Richard M Sharpe, Paul Alfred Francois Fowler

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

1 Citation (Scopus)

Abstract

Although tobacco use has declined in recent years, a signifi cant minority
of pregnant women still smoke and cessation during gestation is rare. Substantial
passive exposure to tobacco smoke is an unavoidable hazard to many more. This is
of great concern, since tobacco smoke contains a large number of toxins known to
be hazardous to foetal development. These include carbon monoxide, nicotine and
its breakdown products, polycyclic aromatic hydrocarbons, thiocyanate and many
more. Some are known or suspected endocrine-disrupting chemicals (EDCs).
In addition to providing further evidence to dissuade pregnant women and those
around them from smoking, studying the effects of tobacco smoke on human development
gives insight into effects of other EDCs and EDC mixtures which affect the
same developmental processes and end points.
In utero development of the reproductive tract is a poorly understood process that
is entirely dependent on the proper functioning of the maternal and foetal endocrine
systems. It is vulnerable to disruption in both genders. Thus far, only the physiological
effects of the disruption of oestrogen and androgen-mediated signalling and the
hypothalamic-pituitary-gonadal (HPG) axis have been investigated in detail. Our
knowledge of the process in both animals and humans is far from complete. Exposure
of animal models to EDCs affecting sex steroid-mediated processes can cause a wide range of adverse reproductive outcomes. These include impaired gametogenesis
and later subfertility, early reproductive senescence, neuroendocrine dysregulation
affecting fertility and sexual behaviour, genital deformities and increased susceptibility
to certain cancers. Effects on humans are thus far uncertain, but many epidemiological
studies have associated EDC exposure with decreasing fertility, reductions in the age
of pubertal onset and increases in susceptibility to certain cancers and deformities
of the reproductive tract. Studies of the physiological and cellular effects of individual
EDCs and EDC mixtures in vitro and in vivo have added plausibility to these
associations.
Prenatal human tobacco smoke exposure has multiple known adverse effects on
reproductive development and may affect the age of puberty in females at least.
Overall, maternal and foetal oestrogen and androgen synthesis are suppressed centrally
by suppression of the HPG axis by the activation of the hypothalamic-pituitary-
adrenal (HPA) axis and peripherally by the direct inhibition of their synthesis.
The hypothalamic-pituitary-thyroid (HPT) axis and the peripheral transformation
and utilization of thyroid hormones are also suppressed by activation of the HPA
axis. Neuroendocrine programming of the HPA, HPT and HPG is perturbed.
Decreased fertility and fecundity have been noted in both genders, and exposed
females are more likely to experience early menopause. Some epidemiological
studies have reported a connection with malformations of the male reproductive
tract (testicular dysgenesis syndrome), the plausibility of which is supported by
evidence that the production of desert hedgehog, a morphogen essential for male
sexual development, is halved by maternal smoking. These outcomes are similar to
those observed in epidemiological and animal studies of other EDCs and EDC mixtures,
but a great deal of further research is required to determine their exact physiological
effects and properly quantify the risks they pose. The effects of tobacco
smoke and other EDC mixtures and EDCs on systems other than those directly
mediated by the oestrogen receptors and androgen receptor have barely begun to be
elucidated.
Original languageEnglish
Title of host publicationEndocrine Disruptors and Puberty
Subtitle of host publicationContemporary Endocrinology
EditorsEvanthia Diamanti-Kandarakis, Andrea Gore
PublisherHumana Press
Pages11
Number of pages48
ISBN (Electronic)978-1-60761-561-3
ISBN (Print)978-1-60761-560-6
DOIs
Publication statusPublished - 2012

Fingerprint

Endocrine Disruptors
Environmental Exposure
Gonads
Puberty
Smoking
Mothers
Smoke
Tobacco
Fertility
Androgens
Pregnant Women
Thyroid Gland
Estrogens
Hedgehogs
Polycyclic Aromatic Hydrocarbons
Androgen Receptors
Tobacco Use
Carbon Monoxide
Menopause
Fetal Development

Cite this

McKinlay, R., O'Shaughnessy, P. J., Sharpe, R. M., & Fowler, P. A. F. (2012). In utero exposure to environmental chemicals: lessons from maternal cigarette smoking and its effects on gonad development and puberty. In E. Diamanti-Kandarakis, & A. Gore (Eds.), Endocrine Disruptors and Puberty: Contemporary Endocrinology (pp. 11). Humana Press. https://doi.org/10.1007/978-1-60761-561-3

In utero exposure to environmental chemicals : lessons from maternal cigarette smoking and its effects on gonad development and puberty. / McKinlay, Rebecca; O'Shaughnessy, Peter J.; Sharpe, Richard M; Fowler, Paul Alfred Francois.

Endocrine Disruptors and Puberty: Contemporary Endocrinology. ed. / Evanthia Diamanti-Kandarakis; Andrea Gore. Humana Press, 2012. p. 11.

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

McKinlay, R, O'Shaughnessy, PJ, Sharpe, RM & Fowler, PAF 2012, In utero exposure to environmental chemicals: lessons from maternal cigarette smoking and its effects on gonad development and puberty. in E Diamanti-Kandarakis & A Gore (eds), Endocrine Disruptors and Puberty: Contemporary Endocrinology. Humana Press, pp. 11. https://doi.org/10.1007/978-1-60761-561-3
McKinlay R, O'Shaughnessy PJ, Sharpe RM, Fowler PAF. In utero exposure to environmental chemicals: lessons from maternal cigarette smoking and its effects on gonad development and puberty. In Diamanti-Kandarakis E, Gore A, editors, Endocrine Disruptors and Puberty: Contemporary Endocrinology. Humana Press. 2012. p. 11 https://doi.org/10.1007/978-1-60761-561-3
McKinlay, Rebecca ; O'Shaughnessy, Peter J. ; Sharpe, Richard M ; Fowler, Paul Alfred Francois. / In utero exposure to environmental chemicals : lessons from maternal cigarette smoking and its effects on gonad development and puberty. Endocrine Disruptors and Puberty: Contemporary Endocrinology. editor / Evanthia Diamanti-Kandarakis ; Andrea Gore. Humana Press, 2012. pp. 11
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N2 - Although tobacco use has declined in recent years, a signifi cant minorityof pregnant women still smoke and cessation during gestation is rare. Substantialpassive exposure to tobacco smoke is an unavoidable hazard to many more. This isof great concern, since tobacco smoke contains a large number of toxins known tobe hazardous to foetal development. These include carbon monoxide, nicotine andits breakdown products, polycyclic aromatic hydrocarbons, thiocyanate and manymore. Some are known or suspected endocrine-disrupting chemicals (EDCs).In addition to providing further evidence to dissuade pregnant women and thosearound them from smoking, studying the effects of tobacco smoke on human developmentgives insight into effects of other EDCs and EDC mixtures which affect thesame developmental processes and end points.In utero development of the reproductive tract is a poorly understood process thatis entirely dependent on the proper functioning of the maternal and foetal endocrinesystems. It is vulnerable to disruption in both genders. Thus far, only the physiologicaleffects of the disruption of oestrogen and androgen-mediated signalling and thehypothalamic-pituitary-gonadal (HPG) axis have been investigated in detail. Ourknowledge of the process in both animals and humans is far from complete. Exposureof animal models to EDCs affecting sex steroid-mediated processes can cause a wide range of adverse reproductive outcomes. These include impaired gametogenesisand later subfertility, early reproductive senescence, neuroendocrine dysregulationaffecting fertility and sexual behaviour, genital deformities and increased susceptibilityto certain cancers. Effects on humans are thus far uncertain, but many epidemiologicalstudies have associated EDC exposure with decreasing fertility, reductions in the ageof pubertal onset and increases in susceptibility to certain cancers and deformitiesof the reproductive tract. Studies of the physiological and cellular effects of individualEDCs and EDC mixtures in vitro and in vivo have added plausibility to theseassociations.Prenatal human tobacco smoke exposure has multiple known adverse effects onreproductive development and may affect the age of puberty in females at least.Overall, maternal and foetal oestrogen and androgen synthesis are suppressed centrallyby suppression of the HPG axis by the activation of the hypothalamic-pituitary-adrenal (HPA) axis and peripherally by the direct inhibition of their synthesis.The hypothalamic-pituitary-thyroid (HPT) axis and the peripheral transformationand utilization of thyroid hormones are also suppressed by activation of the HPAaxis. Neuroendocrine programming of the HPA, HPT and HPG is perturbed.Decreased fertility and fecundity have been noted in both genders, and exposedfemales are more likely to experience early menopause. Some epidemiologicalstudies have reported a connection with malformations of the male reproductivetract (testicular dysgenesis syndrome), the plausibility of which is supported byevidence that the production of desert hedgehog, a morphogen essential for malesexual development, is halved by maternal smoking. These outcomes are similar tothose observed in epidemiological and animal studies of other EDCs and EDC mixtures,but a great deal of further research is required to determine their exact physiologicaleffects and properly quantify the risks they pose. The effects of tobaccosmoke and other EDC mixtures and EDCs on systems other than those directlymediated by the oestrogen receptors and androgen receptor have barely begun to beelucidated.

AB - Although tobacco use has declined in recent years, a signifi cant minorityof pregnant women still smoke and cessation during gestation is rare. Substantialpassive exposure to tobacco smoke is an unavoidable hazard to many more. This isof great concern, since tobacco smoke contains a large number of toxins known tobe hazardous to foetal development. These include carbon monoxide, nicotine andits breakdown products, polycyclic aromatic hydrocarbons, thiocyanate and manymore. Some are known or suspected endocrine-disrupting chemicals (EDCs).In addition to providing further evidence to dissuade pregnant women and thosearound them from smoking, studying the effects of tobacco smoke on human developmentgives insight into effects of other EDCs and EDC mixtures which affect thesame developmental processes and end points.In utero development of the reproductive tract is a poorly understood process thatis entirely dependent on the proper functioning of the maternal and foetal endocrinesystems. It is vulnerable to disruption in both genders. Thus far, only the physiologicaleffects of the disruption of oestrogen and androgen-mediated signalling and thehypothalamic-pituitary-gonadal (HPG) axis have been investigated in detail. Ourknowledge of the process in both animals and humans is far from complete. Exposureof animal models to EDCs affecting sex steroid-mediated processes can cause a wide range of adverse reproductive outcomes. These include impaired gametogenesisand later subfertility, early reproductive senescence, neuroendocrine dysregulationaffecting fertility and sexual behaviour, genital deformities and increased susceptibilityto certain cancers. Effects on humans are thus far uncertain, but many epidemiologicalstudies have associated EDC exposure with decreasing fertility, reductions in the ageof pubertal onset and increases in susceptibility to certain cancers and deformitiesof the reproductive tract. Studies of the physiological and cellular effects of individualEDCs and EDC mixtures in vitro and in vivo have added plausibility to theseassociations.Prenatal human tobacco smoke exposure has multiple known adverse effects onreproductive development and may affect the age of puberty in females at least.Overall, maternal and foetal oestrogen and androgen synthesis are suppressed centrallyby suppression of the HPG axis by the activation of the hypothalamic-pituitary-adrenal (HPA) axis and peripherally by the direct inhibition of their synthesis.The hypothalamic-pituitary-thyroid (HPT) axis and the peripheral transformationand utilization of thyroid hormones are also suppressed by activation of the HPAaxis. Neuroendocrine programming of the HPA, HPT and HPG is perturbed.Decreased fertility and fecundity have been noted in both genders, and exposedfemales are more likely to experience early menopause. Some epidemiologicalstudies have reported a connection with malformations of the male reproductivetract (testicular dysgenesis syndrome), the plausibility of which is supported byevidence that the production of desert hedgehog, a morphogen essential for malesexual development, is halved by maternal smoking. These outcomes are similar tothose observed in epidemiological and animal studies of other EDCs and EDC mixtures,but a great deal of further research is required to determine their exact physiologicaleffects and properly quantify the risks they pose. The effects of tobaccosmoke and other EDC mixtures and EDCs on systems other than those directlymediated by the oestrogen receptors and androgen receptor have barely begun to beelucidated.

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BT - Endocrine Disruptors and Puberty

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