Influence on fetal growth of exposure to tobacco smoke during pregnancy
Department of Pediatrics, Clinic Hospital, Spain. Acta Paediatrica
(Impact Factor: 1.67).
03/1995; 84(2):118-21. DOI: 10.1111/j.1651-2227.1995.tb13592.x
We analysed the effect of exposure to tobacco smoke during pregnancy on fetal growth parameters in 129 term newborns. Children were classified into four depending on exposure on the basis of a questionnaire completed by the mother. The results confirmed that tobacco smoking reduced weight, length, cranial and thoracic perimeters at birth when exposure was due to either active or passive smoking. Weight deficits of infants whose mothers smoked heavily (458 g) were higher than those whose mothers were exposed to passive smoking (192 g). We conclude that passive smoking is a very important variable and should be taken into account in any study of neonatal growth parameters.
Available from: Michael Sowa
- "Cigarette smoking leads to exposure to more than 4000 known chemicals many of which are carcinogenic and is the leading cause of preventable premature death in the world. There is strong evidence that smoking during pregnancy is strongly associated with growth retardation , low birth weight, sudden infant death syndrome (SIDS), preterm delivery and higher incidence of stillbirth . Moreover, cigarette smoke absorption begins in the oral cavity and many studies have provided convincing evidence that CS exposure is a risk factor for oral pathological conditions ranging from staining of teeth, discoloration of the gingival to degradation of tooth supporting structures . "
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ABSTRACT: Cigarette smoking is the leading cause of preventable death and has been implicated in pathogenesis of pulmonary, oral and systemic diseases. Smoking during pregnancy is a risk factor for the developing fetus and may be a major cause of infant mortality. Moreover, the oral cavity, and all cells within are the first to be exposed to cigarette smoke and may be a possible source for the spread of toxins to other organs of the body. Fibroblasts in general are morphologically heterogeneous connective tissue cells with diverse functions. Apoptosis or programmed cell death is a crucial process during embryogenesis and for the maintenance of homeostasis throughout life. Deregulation of apoptosis has been implicated in abnormal lung development in the fetus and disease progression in adults. Caspases are proteases which belong to the family of cysteine aspartic acid proteases and are key components for downstream amplification of intracellular apoptotic signals. Of 14 known caspases, caspase-3 is the key executioner of apoptosis. In the present study we explored the hypothesis that cigarette smoke (CS) extract activates caspase-3 in two types of fibroblasts, both of which would be exposed directly to cigarette smoke, isolated fetal rat lung fibroblasts and adult rat periodontal ligament (PDL) fibroblasts.
Isolated fetal rat lung fibroblasts and adult PDLs were used. Cells were exposed to different concentrations of CS for 60 min. Caspase-3 activity and its inhibition by Z-VAD-fmk were measured by caspase-3 fluorometric assay. The effect of CSE on cellular viability was measured using the MTT formazan assay. Caspase-3 expression was detected by western blot analysis and cellular localization of caspase-3 was determined by immunofluorescence using fluorescence microscopy.
It was observed in fetal rat lung fibroblast cells that CSE extract significantly (p<0.05) increased caspase-3 activity and decrease cell proliferation. However, no significant changes in activity or viability were observed in PDLs.
This indicates CS activates caspase-3 the key regulatory point in apoptosis in fetal rat lung fibroblast cells suggesting that smoking during pregnancy may alter the developmental program of fetal lung, jeopardizing the establishment of critical cellular mechanisms necessary to expedite pulmonary maturation at birth.of critical cellular mechanisms necessary to expedite pulmonary maturation at birth.
Tobacco Induced Diseases 12/2013; 11(1):25. DOI:10.1186/1617-9625-11-25 · 1.50 Impact Factor
Available from: Asghar Zare
- "Heavy paternal smoking increases the risk of early pregnancy loss through maternal and/or paternal exposure (3). Mothers who smoke during pregnancy are highly likely to have a LBW infant, and LBW infants of smoking mothers weigh an average of 150 to 250 g less than nonsmoking mothers’ infants (4). It is shown that children of nonsmoking mothers generally perform better than the two smoking groups with regard to speech and language skills, intelligence, visual / spatial abilities and rating of mother's behavior tests. "
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Background: Prematurity is an issue related to increasing the neonatal morbidity and mortality and smoking pregnant women cause the risk of low birth weight and prematurity increase, compared to non-smoking ones.
Objectives: This study investigates secondhand smoke (SHS) exposure’s effects over pregnant women on gestational age and birth weight.
Patients and Methods: In this descriptive-analytic study, 205 women referred to both public and private hospitals in the third trimester were questioned about secondhand smoke (SHS) exposure during pregnancy. In addition to birth weight and gestational age, other variables including mother’s education and job and sex of the newborns were also assessed.
Results: Of all 205 women, 43 (20.97%) women exposed to SHS during pregnancy and 162 (79.02%) women did not. In SHS exposure group, 11 infant (25.6%) and in non- SHS exposure group, 17 infant (10.5%) were born prematurely (< 37 weeks) (P = 0.01). Also birth weight of newborn in non-SHS exposure group was 118 gram more than other group but the differences were not significant (P = 0.09).
Conclusions: Our findings showed that the secondhand smoke (SHS) exposure of pregnant women may be significantly associated with early preterm delivery.
Keywords: Smoke; Pregnancy; Preterm Delivery; low birth weight
02/2013; 1(4). DOI:10.5812/ijhrba.7630
Available from: Wojciech Piekoszewski
- "). Many authors underline the significant difference in the head circumference of neonates whose mothers are active smokers and nonsmokers and this difference ranges from 0.2 to 1.1 cm (Olds et al. 1994; Cliver et al. 1995; Roquer et al. 1995; Zaren et al. 1996). In this study, the neonates whose mothers were active smokers during pregnancy had statistically smaller head circumference in comparison with those whose mothers were nonsmokers. "
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ABSTRACT: The objective of the study was to assess cerebral mass, based on head circumference measurements in neonates exposed to tobacco smoke in utero, and to determine the relative proportions of the cerebral and body mass. The study included 147 neonates born in the period 2003-2004 at the Princess Anna Mazowiecka University Hospital and admitted to the Neonatal and Intensive Care Department of the Medical University in Warsaw. Subjects were divided into three groups on the basis of maternal status as active, passive, or nonsmokers determined by maternal urinary cotinine concentration and a questionnaire. Neonates whose mothers were active smokers throughout the whole period of pregnancy had a lower head circumference and in consequence a lower cerebral mass significantly more frequently when compared with those whose mothers were nonsmokers, P= 0.002. (Median difference in cerebral mass was 48.27 g.) The risk of lower cerebral mass was 3.9 (1.4-10.8, CI 95%) in the group of neonates whose mothers actively smoked cigarettes during pregnancy. A negative correlation was seen between cerebral mass and maternal urinary cotinine concentration (correlation coefficient r=-23, P= 0.006). The ratio of the cerebral to body mass was similar for neonates in all three groups. Active smoking during pregnancy had a negative effect on the cerebral mass of the neonate, however no such effect was observed in neonates whose mothers were passive smokers. The deficiency in cerebral mass increased with greater smoking intensity. Active smoking by the mother during pregnancy inhibits the growth of the brain as well as that of the body mass of the neonate.
Brain and Behavior 05/2012; 2(3):243-8. DOI:10.1002/brb3.49 · 2.24 Impact Factor
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