Fetal growth and the timing of exposure to maternal smoking

Ohmi, Hiroki; Hirooka, Kenzou; Mochizuki, Yoshikatsu

doi:10.1046/j.1442-200x.2002.01495.x

Cited by 35 publications

(20 citation statements)

References 10 publications

(19 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because infant mean birthweight decreased to 2922 and 2911 g when women quit smoking during the second and third trimester, respectively, these women were grouped with women who smoked throughout pregnancy. This agrees with previous findings that quitting smoking early in pregnancy does not greatly affect infant birth size (25).…”

Section: Study Participantssupporting

confidence: 93%

“…Additionally, the individual effect of smoking on birth size was analyzed because of its known impacts on fetal growth (25,28). The main linear regression model included mean infant birth size as the dependent variable, caffeine intake as a categorical variable, the CYP1A2 genotype (CC/CA vs. AA), and the CYP1A2 and caffeine gene-environment interaction variable (the product term of maternal caffeine intake and CYP1A2 genotype) adjusted by the confounders listed above.…”

Section: Statistical Analysesmentioning

confidence: 99%

See 1 more Smart Citation

Interaction between maternal caffeine intake during pregnancy and CYP1A2 C164A polymorphism affects infant birth size in the Hokkaido study

et al. 2017

View full text Add to dashboard Cite

show abstract

Section: Study Participantssupporting

confidence: 93%

Section: Statistical Analysesmentioning

confidence: 99%

Interaction between maternal caffeine intake during pregnancy and CYP1A2 C164A polymorphism affects infant birth size in the Hokkaido study

et al. 2017

View full text Add to dashboard Cite

show abstract

“…While there is some evidence that specific trimester effects occur in association with birth weight (Ohmi et al, 2002), it is important to note that one well-designed study (Toschke et al, 2003) found no significant increase in the odds ratios for childhood BMI in association with first trimester smoking versus smoking throughout pregnancy. At any rate, it appeared that women in the present study may not have been able to make distinctions by trimester accurately, requiring analyses of data for the entire pregnancy.…”

Section: Discussionmentioning

confidence: 98%

Offspring from families at high risk for alcohol dependence: Increased body mass index in association with prenatal exposure to cigarettes but not alcohol

Hill¹,

Shen²,

Wellman³

et al. 2005

Psychiatry Research

View full text Add to dashboard Cite

The prevalence of overweight and obese children is increasing, a tendency that can be expected to increase the risk of adverse outcomes in adulthood. The aim of this study was to determine if prenatal exposure to alcohol, cigarettes, and street drugs would be associated with differences in body mass index (BMI) in childhood and adolescence in offspring from families at high and low genetic risk for developing alcohol dependence. Annual follow-up of offspring (N =288) provided 1200 height and weight assessments for analysis. Maternal substance use data were available for 235 offspring from families stratified for familial/genetic risk for alcohol dependence (high or low risk), providing the opportunity to assess prenatal exposure and familial/genetic risk in relation to BMI in the offspring. When data were grouped by the presence or absence of any prenatal cigarette exposure, a significant difference in offspring BMI was seen for 8-to 11-year-olds. Significant group differences were also seen at ages 12-15 and 16-18 years. A dose-response relationship between cigarette use by the mother and offspring BMI was also seen. With the strong tendency for individuals who are overweight in childhood and adolescence to become overweight adults, prenatal exposure to nicotine may be a harbinger of increased risk for numerous adultonset, weight-related health problems.

show abstract

“…In some cases, the etiology of these disorders is already well known whereas in some other cases it is still under study. Poor or inadequate nutrition, smoking, alcohol abuse, lower genital tract infections, anemia, hypertension, gestational or non-gestational diabetes, obesity, metabolic and antiphospholipid syndromes, among others, are some of the maternal conditions that may have an effect on fetal growth [1][2][3][4][5][6][7][8]. These maternal disorders affect the environment where the fetus is developing and may produce metabolic, immune, vascular, hemodynamic and renal alterations [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Biochemical Profiling Study in Umbilical Cord Blood as Predictors of Neonatal Damage

Gruccio¹

2014

Int J Clin Pediatr

View full text Add to dashboard Cite

Background: During pregnancy inflammatory, metabolic and immunologic disorders that affect differently the fetus, are known. These could be early disorders: abortion, intrauterine growth retardation, low birth weight and neonatal death; or late disorders: cardiovascular and metabolic disease in adults. The objective was to analyze different biochemical parameters in maternal venous blood and newborn's umbilical cord blood (UCB) from healthy and pathological mothers for early detection of future perinatal complications. Methods:Maternal venous blood (283) and UCB (283) were analyzed. The patients were consecutively, prospectively and transversally studied. Delivery: cesarean section. Mothers and newborns were classified: control group (C) (n = 99) and pathological group (P) (n = 184). Glucose, urea, creatinine, uric acid (UA), bilirubin (Bi), proteins (PT), albumin (Alb), transaminases (ALT/AST), alkaline phosphatase, gamma-glutamyl transpeptidase (GGT), creatinkinasa (CK), lactate dehydrogenase (LDH), iron, calcium, phosphorus, magnesium, sodium, potassium (K), chlorine, cholesterol (Chol), triglycerides (TG) and hsCRP were determined by recommended methods. Student's t and Mann-Whitney tests were applied, P < 0.05.Results: P newborns from P mothers showed significant decrease: in gestation weeks (GW) and newborn weight (NW) with respect to C newborns from C mothers (P < 0.001); significant increases in Chol, TG, UA, K, Bi, AST and GGT (P: 0.01, < 0.001, 0.03, < 0.001, 0.04, < 0.001, < 0.001, respectively) and significant decreases in CK, PT and Alb (P < 0.001). P mothers showed significant increase in UA, ALT, AST, GGT (P: 0.04, 0.02, 0.04, < 0.001, respectively) with respect to C mothers. Conclusions:The decrease in GW and NW in P newborns with respect to C would be related to intrauterine growth restriction (IUGR) accompanying these disorders; increases in Chol, TG, UA, K, Bi, AST and GGT would be related to cellular destruction associated to maternal disorders and deficit in pulmonary development by IUGR respectively, whereas decreases in CK, PT and Alb to IUGR. Increase in UA, ALT, AST and GGT from P mothers with respect to C would be associated to inflammatory process with liver alterations. A future study including greater number of samples and analysis of each maternal disorder is proposed to obtain early markers of neonatal damage and to prevent future perinatal complications.

show abstract

Fetal growth and the timing of exposure to maternal smoking

Abstract: Maternal smoking during any trimesters increased the risk of preterm birth. Maternal smoking during the third trimester reduced the body length of both full-term and preterm neonates, and the birthweight of the full-term neonate in a somewhat dose-dependent manner.

Cited by 35 publications

References 10 publications

Interaction between maternal caffeine intake during pregnancy and CYP1A2 C164A polymorphism affects infant birth size in the Hokkaido study

Interaction between maternal caffeine intake during pregnancy and CYP1A2 C164A polymorphism affects infant birth size in the Hokkaido study

Offspring from families at high risk for alcohol dependence: Increased body mass index in association with prenatal exposure to cigarettes but not alcohol

Biochemical Profiling Study in Umbilical Cord Blood as Predictors of Neonatal Damage

Contact Info

Product

Resources

About