Impact of maternal cigarette smoking on fetal growth and body composition

OBJECTIVE: The aim of this study was to determine the impact of maternal cigarette smoking on the fetal accretion of fat and lean body mass. We hypothesized that maternal smoking would result in a reduction in the deposition of lean body mass. STUDY DESIGN: Longitudinal ultrasonographic examinations on 65 singleton fetuses without anomalies of smoking mothers were compared with 36 singleton fetuses without anomalies of nonsmoking mothers. A total of 214 ultrasonographic examinations were performed between 27 and 37 weeks' gestation. All subjects underwent at least 2 ultrasonographic examinations separated by 4 weeks. We compared the slopes of the growth curves for individual morphometric parameters including head circumference, femur length, abdominal circumference, thigh muscle area, thigh fat area, estimated fetal weight and percentage of thigh fat between groups. Analysis was performed with a repeated measures analysis of covariance. Potential covariates included prepregnancy body mass index (in kilograms per square meter), weight gain during pregnancy, maternal age, parity, and fetal sex recorded at birth. Demographic variables are expressed as mean +/- SD; fetal measurements are expressed as mean +/- SE. Both t tests and chi(2) analyses were used to compare groups with respect to demographic variables. P <.05 was accepted for significance. RESULTS: There were no significant differences between groups in maternal prepregnancy weight, maternal height, maternal prepregnancy body mass index, weight gain in pregnancy, parity, or fetal sex. Smokers were younger than nonsmokers (smokers, 23.7 +/- 6.0 years; nonsmokers, 31.8 +/- 6. 0 years; P <.0001), and neonatal weight was reduced among smokers (smokers, 3269 +/- 507 g; nonsmokers, 3519 +/- 411 g; P <.01). There were no differences in the growth rates of head circumference (P =. 79) and femur length (P =.67). Growth rates of abdominal circumference (smokers, 9.0 +/- 0.3 mm/wk; nonsmokers, 10.3 +/- 0.5 mm/wk; P =.01), estimated fetal weight (smokers, 171 +/- 5.4 g/wk; nonsmokers, 193 +/- 8.0 g/wk; P =.008), and muscle area (smokers, 64. 1 +/- 3.8 mm(2)/wk; nonsmokers, 76.4 +/- 5.6 mm(2)/wk; P =.03) were significantly reduced among smokers. There was a reduction in the rate of fat deposition in the thighs of fetuses of smoking mothers (smokers, 38.7 +/- 3.7 mm(2)/wk; nonsmokers, 54.6 +/- 5.4 mm(2)/wk; P =.004); however there was no absolute difference in the amount of fat measured in the thigh between 33 and 37 weeks' gestation. CONCLUSION: We detected reduced fetal growth that selectively affected abdominal circumference and peripheral muscle mass while not affecting head circumference and femur length in fetuses of smoking mothers. The effect of cigarette smoking on fetal fat deposition was less clear. Cigarette smoking appears to have a selective effect within lean body mass compartments, with affected compartments including peripheral fetal muscle. The findings of a reduction in abdominal circumference growth compared with control subjects in combination with no difference in subcutaneous fat content beyond 33 weeks' gestation are potentially explained by a reduction in fetal liver size that may result from maternal smoking.     

Parental smoking: Its effects on fetus and child health

Smoking is a risk factor in pregnancy. Maternal smoking reduces the birthweight by 150–250 g (dose-response relationship), shifting the birthweight (and length) distribution to the left. Reduction of birthweight without shortening of gestation creates a group of small-for-date babies. Intrauterine hypoxia seems responsible for the growth retardation in smokers' babies as in babies of mothers living at high altitudes. Cigarette smoking of the mother affects fetal oxygenation, due to high levels of COHb in the blood of both mother and child. This observation is strongly supported by animal experiments.The total of (abortions), stillbirths, early and late neonatal mortality (especially stillbirths) is higher in babies of smoking than in those of nonsmoking mothers and highest among the poor. Approximately 5 % of all stillbirths and neonatal deaths must be attributed to the increased mortality risk for the infant of mothers who smoke during the second half of pregnancy. Pregnancies of smoking mothers show about the same increase in infant wastage as pregnancies at high altitudes. The babies of smoking mothers show little excess of congenital malformations, if any.The placenta coefficient is increased. This symptom of compensatory placental hypertrophy cannot avert some impairment of fetal nutrition. There is less preeclamptic toxemia in smokers than in nonsmokers, but a higher incidence of antepartum hemorrhage and placental separation.Concerning long-term effects, smoking during pregnancy seems to be associated with a slight impairment of mental and physical growth.When the mother is nonsmoker and the father smokes more than ten cigarettes daily, an increase in perinatal mortality seems probable.Smoke aggravates the asthma of children in about two-thirds of those whose parents smoke. Healthy children of smokers are sick more frequently (primarily respiratory illness) than those of nonsmokers. Smoking parents and teachers stimulate their children and pupils to start smoking. Once smokers children may remain smokers.From the polemics on cause (smoking) and association (smoker) regarding the effects of parental smo?ing on the health of the fetus, the conclusion must be that health workers involved in obstretrics have great responsibilities in the antismoking campaign.     

Smoking in pregnancy: the influence on percentile birth weight, mean birth weight, placental weight, menstrual age, perinatal mortality and maternal diastolic blood pressure

Smoking habits of 597 pregnant women were investigated; 48.6% of the women smoked during pregnancy. Percentile birth weight proved to be decreased compared with the Amsterdam birth weight charts. This decrease could be attributed largely to smoking in pregnancy. Mean birth weight was significantly lower in smokers than in nonsmokers (230 g; p less than 0.01). Placental weight and menstrual age were not affected by smoking during pregnancy. A statistically significant higher incidence of hypertension in pregnancy in the nonsmokers group compared with the smokers group (p less than 0.05) was established.     

Maternal cigarette smoking during pregnancy, adiposity, social class, and perinatal outcome in Cardiff, Wales, 1965-1977

There have been several reports in which maternal nutritional status has been implicated as either a mediating or moderating factor in the relationship between maternal cigarette smoking and birthweight and perinatal survival. Also, there is evidence that the effects of maternal cigarette smoking on both intrauterine growth and fetal viability are more intense among women of lower social status. The well-maintained data set of the Cardiff Births Survey from 1965-1977 afforded an opportunity to review these issues among over 50,000 births in south Wales (the survey took place in Cardiff City through 1973 and subsequently included suburban areas of South Glamorgan). The major findings were: (1) Smoking was much more common with descending maternal social status; (2) among upper status women, smokers had similar or slightly greater mean Quetelet's indices (kg/m2) than nonsmokers. Among lower status women, smokers were considerably thinner than nonsmokers; (3) the greater the adiposity of the mother, the less the association between cigarette smoking and depressed birthweight; (4) perinatal mortality was significantly higher among heavy smokers (10 or more cigarettes a day) than among nonsmokers; and (5) neither the decrease in birthweight nor the excess mortality associated with smoking was greater among those of lower rather than upper social status, except among class I women, among whom smoking was only minimally associated with depressed birthweight. With the inclusion of the South Glamorgan suburban population in the survey after 1974, the excess mortality associated with heavy smoking dropped from 53 to 16%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Maternal Weight Gain, Smoking and Other Factors in Pregnancy as Predictors of Infant Birth-weight in Sydney Women

Summary: Two hundred and four (204) women attending a Sydney maternity hospital and their babies were followed throughout pregnancy in a study, which aimed: 1) to describe the distribution of maternal weight gain in present day Australian women and 2) to determine the effect of weight gain and other factors on birth-weight.
Maternal weights and skinfold thicknesses were measured serially to give an indication of weight gain. Mean weight gain from conception to term was 14.2kg and mean birth-weight was 3,442g.
Maternal predictors of birth-weight such as maternal weight gain, parity, age, education, height, public or private booking status, smoking, prepregnancy weight, and sex of the infant and gestational age were explored using simple and multiple regression analysis. Weight gain was predictive of birth-weight, each kg increase in total weight gain resulting in about a 30g increase in birthweight. Other strong predictors were gestational age, maternal smoking, sex of the infant and maternal parity. Maternal height was less strongly predictive and age and prepregnant weight were not predictive.
Smoking mothers had infants who were 268g lighter than those of nonsmoking mothers. However, smokers were also younger, shorter, had less education and were more likely to book as public patients than nonsmokers. After adjusting for all other predictors, the birth-weight of infants whose mothers smoked, was still 224g less than that for nonsmoking mothers.     

How does maternal smoking affect birth weight and maternal weight gain? Evidence from the Ontario Perinatal Mortality Study

A large data set was used to examine the possibility that maternal smoking during pregnancy causes low birth weights by reducing maternal appetite, eating, and weight gain. As always, birth weight distributions shifted downward as maternal smoking level increased. Maternal weight gain distributions, on the other hand, were the same for smokers and nonsmokers. Within each level of maternal weight gain, from less than five pounds to over 40 pounds, the more the mothers smoked the greater was the percentage of neonates weighing less than 2,500 grams. This evidence supports a direct effect of maternal smoking on birth weight, possibly due to the hypoxic effects of carbon monoxide, rather than one mediated through eating. Efforts to prevent or reduce smoking should have greater benefits for mother and child than would efforts to increase food intake among pregnant women who smoke.     

Smoking during pregnancy and preterm birth

Objective To evaluate the association between smoking during pregnancy and preterm birth.
Design A follow up study.
Setting Department of Gynaecology and Obstetrics, Aarhus University Hospital, Denmark.
Participants Four thousand one hundred and eleven nulliparous women with singleton pregnancies who returned questionnaires about smoking habits at 16 weeks of gestation.
Results The overall rate of preterm delivery was 4.3 %. Smokers had a 40 % higher risk of preterm birth compared with nonsmokers. A dose response relationship was found between smoking and risk of preterm birth. Adjustment for women's height, prepregnancy weight, age of the mother, marital status, education, occupational status, and alcohol intake did not change the results. Among women with an intake of less than 400 mg of caffeine per day no difference in the risk of preterm birth between smokers and nonsmokers was found. However, among women with an intake of more than 400 mg of caffeine per day, the risk of preterm birth was increased almost threefold among smokers compared with nonsmokers. Furthermore, among women with a high intake of caffeine a dose-response relationship was found; women smoking one to five cigarettes per day had no increased risk of preterm birth compared with nonsmokers with the same intake of caffeine, women smoking six to ten cigarettes per day had almost three times higher risk of preterm birth, and women smoking more than 10 cigarettes per day had almost five times higher risk of preterm birth compared with nonsmokers with the same intake of caffeine.
Conclusions Smoking increases the risk of preterm birth. The association between smoking and preterm birth was only present among women with a high intake of caffeine. However, whether smoking alone influences the risk of preterm birth among heavy consumers of caffeine needs further investigation.     

Twenty-four-hour urinary-free cortisol in premenopausal cigarette smokers and nonsmokers

Cigarette smoking has been reported to produce acute increases in plasma ACTH and cortisol, but the effect of chronic smoking on integrated adrenal steroid production has not been studied. The effects of chronic smoking on 24-hour urinary-free cortisol, 11-deoxycortisol, DHEAS, and 17-keto-steroids were studied in 10 premenopausal smokers, and their results were compared with 15 premenopausal nonsmokers. The 24-hour excretion of urinary-free cortisol (85.0 +/- 40.8 nmol/d in smokers versus 81.7 +/- 49.7 nmol/d in nonsmokers), 11-deoxycortisol (259 +/- 170 nmol/d in smokers versus 222 +/- 147 nmol/d in nonsmokers), DHEAS (3,140 +/- 2,909 nmol/d in smokers versus 2,890 +/- 1,960 nmol/d in nonsmokers), and 17-ketosteroids (17.4 +/- 8.3 mumol/d in smokers versus 23.4 +/- 19.9 mumol/d in nonsmokers) were similar in smokers and nonsmokers (all P values not significant). We conclude that chronic smoking does not result in abnormal levels of 24-hour urinary-free cortisol.     

Relationship between dietary intake of cod liver oil in early pregnancy and birthweight

OBJECTIVE: To investigate the possible association between birth outcome and marine food and cod liver oil intake of healthy women in early (prior to 15 weeks of gestation) pregnancy. DESIGN: An observational study. SETTING: Free-living conditions in a community with traditional fish and cod liver oil consumption. POPULATION: Four hundred and thirty-five healthy pregnant Icelandic women without antenatal and intrapartum complications. METHODS: Dietary intake of the women was estimated with a semi-quantitative food frequency questionnaire (FFQ) covering food intake together with lifestyle factors for the previous three months. Questionnaires were filled out at between 11 and 15 weeks and between 34 and 37 weeks of gestation. The estimated intake of marine food and cod liver oil was compared with birthweight by linear and logistic regression controlling for potential confounding. MAIN OUTCOME MEASURES: Birthweight, cod liver oil intake, lifestyle factors (alcohol, smoking). RESULTS: Fourteen percent of the study population used liquid cod liver oil in early pregnancy. Regression analysis shows that these women gave birth to heavier babies (P < 0.001), even after adjusting for the length of gestation and other confounding. CONCLUSIONS: Maternal intake of liquid cod liver oil early in pregnancy was associated with a higher birthweight. Higher birthweight has been associated with a lower risk of diseases later in life and maternal cod liver oil intake might be one of the means for achieving higher birthweight.     

Smoking in pregnancy is associated with increased total maternal serum cell-free DNA levels

OBJECTIVE: Cell-free DNA is a marker of cellular apoptosis and necrosis. We wished to determine if maternal smoking affects maternal and fetal serum cell-free DNA levels. METHODS: Case-control sets of stored second-trimester serum-screening samples from 27 smoking and 90 nonsmoking pregnant women were developed. Smoking status was confirmed by measuring serum cotinine levels. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and DYS1 levels were determined using real-time polymerase chain reaction (PCR) to measure total and fetal cell-free DNA, respectively. At delivery, medical records were reviewed to confirm gender and determine other factors that could affect DNA values. RESULTS: Smoking was associated with significantly elevated GAPDH levels compared with nonsmokers (median: 97,662 genome equivalents (GE)/mL vs 38,217 GE/mL; p = 0.018). DYS1 levels were not statistically significantly elevated in smokers (p = 0.29). Other factors that affected DYS1 levels included maternal age in nonsmokers only (r(2) = 0.30, p = 0.013) and maternal Synthroid use (p = 0.0045) CONCLUSION: Pregnant smokers have threefold higher levels of total cell-free DNA compared with pregnant nonsmokers. Maternal age and Synthroid exposure may also affect circulating cell-free fetal DNA levels.     

Effect of narghile and cigarette smoking on newborn birthweight

Objective  To assess the effect of narghile smoking on the weight of newborns.
Design  Historical retrospective cohort.
Setting  Six major hospitals in Greater Beirut, Lebanon.
Population  Consecutive singleton newborns delivered from August 2000 to August 2003.
Methods  Obstetric and nursery charts were reviewed to obtain information about maternal and neonatal variables. Information concerning initiation of smoking, dose of smoking, smoking habits during pregnancy, and socio-demographic characteristics was collected through interviews with mothers.
Main outcome measures  Low birthweight and newborn birthweight.
Results  Exclusive narghile smokers constituted 4.4% (378/8592) of women. Multiparas were significantly more likely to smoke cigarettes and narghile. Mothers smoking narghile more than once per day were at 2.4 increased odds of having low birthweight infants compared with nonsmoking mothers (OR 2.4; 95% CI 1.2–5.0) after adjusting for confounding variables. No difference was noted between women smoking narghile in the first trimester and those initiating smoking in subsequent trimesters regarding low birthweight.
Conclusions  Narghile smoking more than once per day increases the odds of low birthweight by a 2.4-fold compared with nonsmokers, although to a lesser extent than cigarette smoking.     

Maternal calcium supplementation and fetal bone mineralization.

OBJECTIVE: To determine the effect of maternal calcium supplementation during pregnancy on fetal bone mineralization. METHODS: Healthy mothers with early ultrasound confirmation of dates and singleton pregnancies were enrolled in a double-masked study and randomized before 22 weeks' gestation to 2 g/day of elemental calcium or placebo until delivery. Maternal dietary intake at randomization and at 32-33 weeks' gestation was recorded with 24-hour dietary recalls. Dual-energy x-ray absorptiometry measurements of the whole body and lumbar spine of the neonates were performed before hospital discharge. RESULTS: The infants of 256 women (128 per group) had dual-energy x-ray absorptiometry measurements during the first week of life. There were no significant differences between treatment groups in gestational age, birth weight, or length of the infants, or in the total-body or lumbar spine bone mineral content. However, when bone mineral content was analyzed by treatment group within quintiles of maternal dietary calcium intake, total body bone mineral content (mean +/- standard error of the mean) was significantly greater in infants born to calcium-supplemented mothers (64.1+/-3.2 versus 55.7+/-2.7 g in the placebo group) in the lowest quintile of dietary calcium intake (less than 600 mg/day). The effect of calcium supplementation remained significant after adjustment for maternal age and maternal body mass index and after normalization for skeletal area and body length of the infant. CONCLUSION: Maternal calcium supplementation of up to 2 g/day during the second and third trimesters can increase fetal bone mineralization in women with low dietary calcium intake. However, calcium supplementation in pregnant women with adequate dietary calcium intake is unlikely to result in major improvement in fetal bone mineralization.     

Protease inhibitor therapy and fetal growth potential in HIV-positive women

Our objective was to test if protease inhibitors (PIs) increase the incidence of fetal growth restriction (FGR). Human immunodeficiency (HIV)-seropositive women were studied. At birth the neonatal weight percentile was assigned by predicted growth potential (GP), accounting for race, parity, weight, height, gestational age, birthweight, and gender (Gardosi, 1992). FGR was defined as GP < 10% percentile. Maternal age, CD4 count, viral load, weight gain, prenatal care, tobacco, alcohol, substance abuse, and PI use were related to FGR using chi-square and multiple regression analysis. Ninety-three of 191 women received PI. In these, FGR occurred in 27 (29%) compared with 15 (15.3%) in the non-PI group ( P = 0.02). Maternal CD4 count ( P < 0.0001) was the primary determinant, and smoking ( P = 0.037) was an independent cofactor for FGR (Nagelkerke r2 = 0.24). Twenty-six of 82 (31.7%) smokers had FGR, versus 16 of 109 (14.7%) of nonsmokers (odds ratio, 2.69; 95% confidence interval, 1.33 to 5.46; P = 0.005). After exclusion of the CD4 count, PI became a cofactor for FGR ( P = 0.021 and Nagelkerke r2 = 0.104). We concluded that maternal HIV status and smoking determine the risk for FGR. Although PIs increase the risk for FGR, this effect appears to depend on maternal disease severity.     

Pre-pregnancy body mass, gestational weight gain and birth weight

OBJECTIVE: This study was undertaken to determine the effect of pregravid body weight and weight gain during pregnancy on birth weight of term newborns. MATERIALS AND METHODS: The study population consisted of 1443 healthy women, who delivered of singleton, live infants at or beyond 38 weeks of gestation. Maternal pregravid weight was obtained by recall and categorized into quartiles: < or = 53, < or = 58, < or = 65, > 65 (kg). Women were further divided according to their gestational weight gain into quartiles: < or = 10.5; < or = 12.5; < or = 15.5; > 15.5 (kg). Birth weight was measured and recorded at delivery. Newborns were classified as hypotrophic (SGA; < 10th percentile for the study population) and hypertrophic (LGA; > 90th percentile). RESULTS: The mean birth weight in the study population was 3499 +/- 447 g, 8.5% infants met the criteria for SGA, and 9.4%--for LGA. Studies showed that a progressive increase in maternal pregravid weight as well as gestational weight gain effect independently on increase birthweight, although the effect of weight gain during pregnancy was lessened as weight before gestation increased. For example, increasing gestational weight gain from < or = 10.5 kg to > 15.5 kg increased mean birthweight by 385 g (12.1%) for pregravid weight of 53 kg or less, compared with 142 g (4.0%) for weight of more than 65 kg. They were also associated with decreased frequency of hypotrophic infants and increased frequency of hypertrophic neonates. CONCLUSIONS: Both maternal prepregnancy weight and weight gain during gestation are important factors affecting fetal growth and birth weight. Increasing maternal weight before pregnancy diminishes the influence of weight gain on birthweight. As pregravid weight and prenatal weight gain increase, the incidence of LGA also increase, whereas the frequency of SGA decreases.     

Smoking During Pregnancy: Prevalence,Effects, and Intervention Strategies

ABSTRACT: Smoking prevalence rates have been declining in the United States, but an estimated 25 percent of pregnant women continue to smoke. Smoking during pregnancy is considered one of the leading, preventable causes of low birthweight. Research attributes 21 to 39 percent of low birthweight to smoking during pregnancy, although the exact mechanism of the effect is not completely understood. Several well-designed studies have shown that pregnant smokers are more likely to stop smoking if they are provided with systematic interventions. This overview describes adverse consequences, prevalence, possible mechanisms of action, and prenatal smoking-cessation programs that have proved effective. A five-step approach is outlined for clinicians who want to counsel their prenatal clients.     

Profile of maternal smokers and their pregnancy outcomes in south western Sydney

OBJECTIVE: The prevalence of maternal smoking remains high in New South Wales. In order to better understand the profile of maternal smokers, a study has been conducted to examine the social and demographic characteristics and pregnancy outcomes of women who smoked during their pregnancy in south western Sydney. METHODS: Women and babies of a retrospective cohort of 7,191 singleton births between March 1996 and December 1998, at Liverpool Hospital were analyzed. RESULTS: The prevalence of maternal smoking for the study population was 18.8%. The study found that the sociodemographic factors, such as marital status, ethnic origin, English speaking background, working status during pregnancy, and private health insurance status were independent risk factors for maternal smoking, but maternal age was not. Women who smoked during their pregnancy had higher rates of abruptio placenta, threatened premature labour, and premature labour. The adverse neonatal outcomes due to maternal smoking were low birth weight and increased neonatal morbidity. Smoking appears to have a protective effect on pregnancy induced hypertension. CONCLUSION: The findings of this study suggests that future smoking cessation programs should pay more attention to addressing sociodemographic and cultural factors that influence the behaviour of maternal smokers.     

Smoking and its effect on maternal plasma volume during and after normal pregnancy

Smoking during pregnancy decreases birthweight significantly. The mechanisms causing this decrease have not yet been clarified. Plasma volume (expansion) is positively related to birthweight. There are indications that plasma volume expansion in pregnancy is lower among smokers. A group of healthy women (n = 70) producing healthy mature babies after an uncomplicated pregnancy was studied. No difference in plasma volume was observed between non-smokers and smokers during and after pregnancy. It is unlikely that the growth-depressing effect of smoking during pregnancy is mediated by an influence on plasma volume expansion.     

Smoking in pregnancy revisited: findings from a large population-based study

OBJECTIVE: The purpose of this study was to characterize the effect of smoking on the incidence of various pregnancy complications. STUDY DESIGN: A population-based retrospective analysis with a perinatal database of 170,254 singleton pregnancies was performed. The rate of pregnancy complications was calculated in 4 strata of smokers: Nonsmokers, 1 to 5 cigarettes per day, 6 to 10 cigarettes per day, and >10 cigarettes per day. Logistic regression was used to calculate odds ratios as measures of an association of smoking with various pregnancy complications after correction for confounding factors. RESULTS: The mean age of the study population was 29 +/- 4.8 years. The odds ratio for preeclampsia was 0.64 (95 % CI, 0.59-0.70), for intrauterine growth restriction was 2.4 (95% CI, 2.34-2.53), and for preterm delivery was 1.2 (95% CI, 1.13-1.28). CONCLUSION: Smoking decreased the incidence of preeclampsia in a dose-effect manner and was shown to increase the rate of intrauterine growth restriction and preterm delivery.     

Influence of maternal nutrition on infant birthweight

OBJECTIVES: The aim of the study was to examine relation between maternal prepregnancy BMI, pregnancy weight gain and infant birthweight. MATERIALS AND METHODS: In 1998 the questionnaire was sent to 227 women who were pregnant in 1993. RESULTS: 56.4% of the women under study responded the questionnaire. We excluded 33 answers because of miscarriage, stillbirths, twin pregnancies and also missing data. In the remaining 95 women 37.9% had low prepregnancy BMI (< 19.8 kg/m2). 83 women gave birth to a child at term. There was a statistically significant difference in mean birthweight of infants born by women of various prepregnancy BMI (BMI < 19.8 kg/m2, 19.8-26 kg/m2, > 26 kg/m2) and also of various pregnancy weight gain (according to IOM recommendations). Underweight women gave birth to infants of lower mean birthweight than women of normal or excessive weight (p<0.05). 10.7% of underweight women gave birth to infants of low birthweight (< 2500 g). None of the women who were not underweight before pregnancy gave birth to a child of low birthweight. Women of low pregnancy weight gain gave birth to infants of lower mean birthweight than women of normal or excessive weight pregnancy weight gain. It seems that lower birth weight of infants could result from lower maternal energy, protein, calcium and iron consumption. CONCLUSIONS: 1) Large proportion (37.8%) of women under study were underweight before pregnancy. 2) Birthweight was related to maternal prepregnancy BMI and pregnancy weight gain. Women who were underweight before pregnancy and those whose weight gain was too low gave birth to smaller infants than women who were not underweight before pregnancy and those who gained more weight during pregnancy.     

Maternal smoking and infant respiratory distress syndrome

The relationship between maternal smoking and infant respiratory distress syndrome (RDS) was investigated among 550 premature (36 weeks or less) births delivered at the University of Washington Hospital from 1977 to 1980. Forty-five percent of the mothers were smokers. To avoid bias due to the reduced birth weight of infants of smokers, infants of smokers and nonsmokers were compared within small gestational age categories (two-week intervals) and not by birth weight categories. Infants of mothers who smoked had a reduced incidence of RDS for their gestation compared with infants of nonsmokers. The probability of RDS (adjusted for gestational age and method of delivery) was 25% for the infants of smokers versus 38% for the infants of nonsmokers (odds ratio = 0.55, P = .005), equivalent to approximately a 1.5-week acceleration in lung maturity for infants of smokers. The smoking effect was not explained by demographic differences between smokers and nonsmokers, nor by differences in the incidence of pregnancy complications between the two groups. This study adds support to the theory that adverse pregnancy conditions may lead to an acceleration in pulmonary maturity to allow earlier extrauterine adaptation.