Smoking, intra-uterine growth retardation and sudden infant death syndrome

Cooke, R W

doi:10.1093/ije/27.2.238

Cited by 37 publications

(22 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the United States, maternal smoking is responsible for 20 -30% of low-birth-weight infants and 10% of infant deaths (64,65). In addition, maternal smoking is a leading risk factor for sudden infant death syndrome in FGR infants (14,67). The growth-inhibiting effect of tobacco smoke is observed not only in cases of heavy maternal smoking (Ն10 cigarettes/day) but also in instances of light (Ͻ10 cigarettes/day) and even passive smoking (50).…”

Section: Discussionmentioning

confidence: 99%

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Yang¹,

Julan²,

Rubio³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

104

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Yang¹,

Julan²,

Rubio³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

104

View full text Add to dashboard Cite

show abstract

“…Although maternal tobacco consumption has been related to the incidence IUGR and SIDS [10], unfortunately we were unable to examine this phenomenon, as information on maternal smoking was unavailable.…”

Section: Discussionmentioning

confidence: 99%

Renal Developmental Delay Expressed by Reduced Glomerular Number and Its Association with Growth Retardation in Victims of Sudden Infant Death Syndrome and in “Normal” Infants

et al. 2000

View full text Add to dashboard Cite

In victims of sudden infant death syndrome (SIDS), renal development has been reported to be significantly impaired. In the present study, we used stereological techniques to estimate volume of kidney cortex and total number of glomeruli in a group of human infants. Infants were classified according to cause of death-SIDS or non-SIDS. Cases were further subdivided according to birth weight-normal birth weight (NBW) or low birth weight (LBW) (we were unable to identify any non-SIDS LBW infants for our study). No significant differences were found between NBW and LBW infants (irrespective of cause of death) for cortical volume, glomerular density, or total glomerular number (p > 0.140). Kidney cortical volume, glomerular density, and total glomerular number were not significantly different between SIDS and non-SIDS infants (p > 0.510). Glomerular number was only significantly less in SIDS infants of LBW (p = 0. 032) than in controls according to the Wilcoxon rank sum test; using the Kruskal-Wallis for one-way analysis, no significant difference was found (p > 0.010). These results contrast with those from previous studies, as a reduction in glomerular number was not noted in SIDS NBW infants, and the mean value for the control (non-SIDS NBW) group was significantly reduced (p < 0.01) from those of previous studies. This indicates that glomerular number reduction is seen in SIDS NBW and non-SIDS NBW cases and is therefore directly associated with growth retardation rather than with SIDS.

show abstract

“…In the United States alone, approximately one million infants are exposed prenatally to cigarette smoke each year (Centers for Disease Control and Prevention, 1998). In utero smoke exposure has been shown to result in a variety of adverse developmental outcomes, with infant LBW being the most well documented in humans (Abel, 1980;Hebel et al, 1988;Cooke, 1998;Bernstein et al, 2000;Mitchell et al, 2002). In addition to LBW, maternal smoking status has been linked to a variety of other adverse pregnancy outcomes including: placental insufficiency, placental abruption, sudden infant death syndrome (SIDS), childhood asthma/bronchitis, and cognitive and learning deficits (Klein and Koren, 1999;Lindley et al, 2000;Ernst et al, 2001;Cnattingius, 2004;Lahr et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

An animal model of cigarette smoke-induced in utero growth retardation

et al. 2008

View full text Add to dashboard Cite

Maternal/fetal genetic constitution and environmental factors are vital to delivery of a healthy baby. In the United States (US), a low birth weight (LBW) baby is born every minute and a half. LBW, defined as weighing less than 5.5 lbs at birth, affects nearly 1 in 12 infants born in the US with resultant costs for the nation of more than 15 billion dollars annually. Infant birth weight is the single most important factor affecting neonatal mortality. Various environmental and genetic risk factors for LBW have been identified. Several risks are preventable, such as cigarette smoking during pregnancy. Over one million babies are exposed prenatally to cigarette smoke accounting for over 20% of the LBW incidence in the US. Cigarette smoke exposure in utero results in a variety of adverse developmental outcomes with intrauterine growth restriction and infant LBW being the most well documented. However, the mechanisms underlying the causes of LBW remain poorly understood. The purpose of this study was: (1) to establish an animal model of cigarette smoke-induced in utero growth retardation and LBW using physiologically relevant inhalation exposure conditions which simulate "active" and "passive" tobacco smoke exposures, and (2) to determine whether particular stages of development are more susceptible than others to the adverse effects of in utero smoke exposure on embryo/fetal growth. Pregnant C57BL/6J mice were exposed to cigarette smoke during three periods of gestation: pre-/peri-implantation (gestational days [gds] 1−5), postimplantation (gds 6−18), and throughout gestation (gds 1−17). Reproductive and fetal outcomes were assessed on gd 18.5. Exposure of dams to mainstream/sidestream cigarette smoke, simulating "active" maternal smoking, resulted in decreases in fetal weight and crown-rump length when exposed throughout gestation (gds 1−17). Similar results were seen when dams were exposed only during the first 5 days of gestation (pre-/peri-implantation period gds 1−5). Exposure of dams from the post-implantation period through gestation (gds 6−18) did not result in reduced fetal weight, although a significant reduction in crown-rump length remained evident. Interestingly, maternal sidestream smoke exposure, simulating exposure to environmental tobacco smoke (ETS), during the pre-/peri-implantation period of development also produced significant decreases in fetal weight and crown-rump length. Collectively, results from the present study confirm an association between prenatal exposure to either "active" or "passive" cigarette smoke and in utero growth retardation. Publisher's Disclaimer: This article was published in an Elsevier journal. The attached copy is furnished to the author for non-commercial research and education use, including for instruction at the author's institution, sharing with colleagues and providing to institution administration. Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohi...

show abstract

Smoking, intra-uterine growth retardation and sudden infant death syndrome

Abstract: Most of the risk of SIDS associated with growth retardation may be accounted for by maternal smoking.

Cited by 37 publications

References 13 publications

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Renal Developmental Delay Expressed by Reduced Glomerular Number and Its Association with Growth Retardation in Victims of Sudden Infant Death Syndrome and in “Normal” Infants

An animal model of cigarette smoke-induced in utero growth retardation

Contact Info

Product

Resources

About