Effect Of Maternal Cigarette Smoking Research Articles

Maternal Smoking and Fetal Growth Retardation

To determine whether the fetal growth-retarding effect of maternal cigarette smoking could be due to lower dietary intake in smokers than in nonsmokers, the pediatric group of the Children's Hospital of Winnipeg assessed the energy and nutrient intake of 302 smoking and 234 nonsmoking women toward the end of the last trimester of pregnancy. The smokers had significantly smaller infants, but pregnancy weight gain was not different. Daily dietary intake of the smokers was not less than that of the nonsmokers; in fact, for some nutrients it was significantly greater. Therefore, the authors concluded that fetal growth retardation due to smoking is not caused by the mother's diminished intake of food.

Smoking and Pregnancy

Sir .—The article entitled Effect of Maternal Cigarette Smoking on Apgar Scores by Garn et al (Journal1981;135:503-506) is a valuable contribution to the medical literature because data are presented to show a statistical relationship between maternal cigarette smoking and lower infant Apgar scores. The correlation of an increased incidence of low Apgar scores with maternal smoking is quite convincing. However, this correlation is the only fact demonstrated by the data presented and it is scientifically unsound to assume that a cause-and-effect relationship is demonstrated as well. It seems that such a relationship is implied by the comments of the authors and by themarginal commentby T. A. Merritt in the same issue (1981;135:595-596). If this is so, where are the data to support it? If one adopts the very reasonable hypothesis that a cause-and-effect relationship does exist between maternal smoking and lower Apgar scores, then one is bound

476 CHILDHOOD RENAL AND RESPIRATORY DISEASE AS A MATERNAL RISK FACTOR IN LOW BIRTH WEIGHT

In a recent study which assessed the effect of “healed” renal disease on pregnancy outcome the incidence of low birth weight infants born to women with previous illness requiring hospitalization as children was unexpectedly higher than that among siblings of the renal disease cohort (p < 0.05). Further analysis of data from birth certificates of 88 live births to the 109 women with previous respiratory disease and 57 infants to the 64 siblings of the renal disease group indicate that these differences persist. 12 (13.6%) low birth weight infants were born to the renal disease mothers and 11 (18.3%) low birth weight infants were delivered to the women in the respiratory disease group. 2 (3.5%) of the infants born to the sibling cohort were low birth weight. Gestational age was calculated against LMP. The curves generated by plotting gestational age vs birth weight of the three cohorts were compared to the birth weight curves of Lubchencko and Babson. When race, socioeconomic status and the effect of maternal cigarette smoking were controlled, the differences also persisted. These data challenge the current concept that low socioeconomic status per se is a risk factor for low birth weight. Women with disease severe enough to be hospitalized as children may represent a risk factor for preterm and small for gestational age infants.

Fetal growth retardation in cigarette-smoking mothers is not due to decreased maternal food intake

To determine whether the fetal growth-retarding effect of maternal cigarette smoking could be due to a lower dietary intake in smokers than in nonsmokers, the energy and nutrient intake of 302 smoking and 234 nonsmoking women were assessed toward the end of the last trimester of pregnancy. The women were from two socioeconomic groups which differed greatly in age, height, education, family income, racial origin, and pregnancy weight gain. Within each group, smokers had significantly smaller infants, but pregnancy weight gain was not different. Daily dietary intake of the smokers was not less than that of the nonsmokers; in fact, for some nutrients it was significantly greater. Therefore, fetal growth retardation due to smoking is not caused by the mother's diminished intake of food.

Effect of maternal cigarette smoking on 3,4-benzpyrene and N-methylaniline metabolism in human fetal liver and placenta

The effect of maternal cigarette smoking on the metabolism of 3,4-benzpyrene (BP) and N-methylaniline (MA) was studied in human fetal liver and placenta. Maternal cigarette smoking apparently had no effect on fetal hepatic drug metabolism. Placentas from smokers, unlike those from nonsmokers, were able to metabolize BP both in the first half of pregnancy and at term. The critical duration of gestation for the appearance of the effect of cigarette smoking seemed to be about 10–11 wk. Metabolism of MA by placental homogenates was very low during the pregnancy, and maternal cigarette smoking had no effect on it. No correlation was established between the level of BP hydroxylase activity in the fetal liver and the level of BP hydroxylase activity in the placenta of the same mother. The fetal hepatic and placental BP hydroxylase systems were shown to differ in their response to maternal cigarette smoking, their subcellular location and their kinetic characteristics.