Low birth weight and neonatal mortality rate related to maternal smoking and socioeconomic status

Comstock, George W.; Shah, Farida; Meyer, Mary B.; Abbey, Helen

doi:10.1016/0002-9378(71)90926-4

Cited by 119 publications

(31 citation statements)

References 13 publications

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“…Plasma norepinephrine and epinephrine were measured by a modified single isotopic radioenzymatic assay (15). Assay reagents in a volume of 0.17 ml were mixed by 0.5-ml plasma aliquots, such that the final incubation mixture contained 0.2 M Tris, 30 mM MgCl2, 10 mM EDTA, 0.1 mM dithiothreitol, 0.4 mM S-adenosylmethionine (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15) Ci/mmol from New England Nuclear, Boston, Mass. ), 200 U/ml catechol-O-methyltransferase (Sigma Chemical Company, St. Louis, Mo.).…”

Section: Methodsmentioning

confidence: 99%

Catecholamine-mediated reduction in uterine blood flow after nicotine infusion in the pregnant ewe.

Resnik¹,

Brink²,

Wilkes³

1979

J. Clin. Invest.

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A B S T R A C T The effect of nicotine on uterine blood flow, uterine vascular resistance, and plasma catecholamine concentration was studied in chronically catheterized pregnant sheep equipped with electromagnetic flow probes. The systemic administration of nicotine (14-32 ,ug/kg body wt per min) resulted in a 44% reduction in uterine blood flow (P < 0.001) and a 203% increase in uterine vascular resistance. Both responses were inhibited by pretreatment with the alpha blocker, phentolamine. Arterial plasma concentrations of norepinephrine and epinephrine, measured by a single isotopic radioenzymatic assay, rose (from 117.9+6.7 to 201.8±+13.3 pglml, P < 0.001; and from 71.6±4.5 to 124.1±8.4 pg/ml, P < 0.001, respectively) during nicotine infusion. The findings suggest that nicotine exerts a deleterious effect on uterine blood flow mediated through the release of catecholamines.

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Section: Methodsmentioning

confidence: 99%

Catecholamine-mediated reduction in uterine blood flow after nicotine infusion in the pregnant ewe.

Resnik¹,

Brink²,

Wilkes³

1979

J. Clin. Invest.

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“…Moreover, LBW infants surviving past their first year of life face an increased risk of longterm disabilities such as cognitive deficits, obesity, hypertension, cardiovascular disease, and diabetes (Botero and Lifshitz, 1999;Ong and Dunger, 2002;Das and Sysyn, 2004;Gluckman et al, 2005). While a number of genetic and environmental risk factors for LBW have been identified, one of the best-documented environmental factors contributing to LBW is maternal smoking status (Comstock et al, 1971;Magee et al, 2004;Bailey and Byrom, 2007).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2008

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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...

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“…Vários autores têm descrito a importância do fator econômico na ocorrência do recém-nascido de baixo peso (Osofsky e Kendall 17 ; Baird 3 ; Comstock e col. 8 , Menchaca, 16 ; Drillien 11 ; Beargie e col. 4 e Ademowore e col.…”

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