The exposure of nonsmoking and smoking mothers to environmental tobacco smoke during different gestational phases and fetal growth

We studied the impact of maternal exposure to environmental tobacco smoke (ETS) on birth weight (BW), low birth weight (LBW), and intrauterine growth retardation (IUGR) according to self-reported maternal smoking habits in a sample of 6,866 singleton births. We obtained data about parental characteristics and maternal active smoking (AS) and passive smoking at delivery via maternal questionnaires and medical records. We used three categories of smoking habits (nonsmokers and those who smoked 1-10 or >10 cigarettes per day) and defined ETS exposure as greater than or equal to 5 cigarettes per day smoked by others in the mother's presence. We used multiple regression and logistic regression procedures with adjustment for many associated covariates. We observed a significant reduction of the mean BW in infants of AS mothers. This reduction was only marginal for mothers who stopped smoking after recognizing their pregnancy. ETS exposure in 1,797 of 5,507 nonsmoking mothers reduced the mean BW of their infants by 53 g [95% confidence interval (CI), 24-82 g]. ETS exposure also significantly reduced BW in babies of AS mothers by 92 g (CI, 21-113 g) compared with BW of ETS-nonexposed AS mothers. The adjusted odds ratio (AOR) of LBW for ETS-exposed AS mothers was two times the LBW risk of ETS-nonexposed AS mothers(2.02; CI, 1.11-3.67); the AOR of ETS-exposed nonsmoking mothers was 1.51 (CI, 1.02-2.26). The AOR of IUGR for this group did not differ from unity (1.08; CI, 0.82-1.43). However, ETS exposure increased the AOR of IUGR for AS mothers from 1.64 (CI, 1.06-2.53) to 2.13 (CI, 1.70-2.67). ETS exposure reduced the BW of infants of nonsmoking mothers and contributed to additional BW reduction in infants of AS mothers. ETS exposure increased the risk of LBW but not that of IUGR in babies of nonsmoking mothers.     

Adverse birth outcomes associated with open dumpsites in Alaska Native Villages

This retrospective cohort study evaluated adverse birth outcomes in infants whose birth records indicated maternal residence in villages containing dumpsites potentially hazardous to health and environment. Birth records from 1997 to 2001 identified 10,073 eligible infants born to mothers in 197 Alaska Native villages. Outcomes included low or very low birth weight, preterm birth, and intrauterine growth retardation. Infants from mothers in villages with intermediate (odds ratio (OR) = 1.73, 95% confidence interval (CI): 1.06, 2.84) and high (OR = 2.06, 95% CI: 1.28, 3.32) hazard dumpsites had a higher proportion of low birth weight infants than did infants from mothers in the referent category. More infants born to mothers from intermediate (OR = 4.38, 95% CI: 2.20, 8.77) and high (OR = 3.98, 95% CI: 1.93, 8.21) hazard villages suffered from intrauterine growth retardation. On average, infants weighed 36 g less (95% CI: -71.2, -0.8) and 55.4 g less (95% CI: -95.3, -15.6) when born to highly exposed mothers than did infants in the intermediate and low exposure groups, respectively, an effect even larger in births to Alaska Native mothers only. No differences in incidence were detected across exposure levels for other outcomes. This is the first study to evaluate adverse pregnancy outcomes associated with open dumpsites in Alaska Native villages.     

Low birthweight, preterm births and intrauterine growth retardation in relation to maternal smoking

The association between the intensity and duration of cigarette smoking during pregnancy and the frequency of low birthweight, preterm births and intrauterine growth retardation was investigated in a historical cohort. All 5166 livebirths occurring in the city of Pelotas, Brazil, during 1993 were identified and mothers interviewed soon after delivery. Children whose mothers smoked during pregnancy had a birthweight 142 g lower than those of non-smoking mothers. The odds ratio for low birthweight among children of smokers was 1.59 [95% CI 1.30–1.95]. There was no association between smoking and preterm delivery assessed by the Dubowitz score. In relation to intrauterine growth retardation, smoking was associated with an odds ratio of 2.07 [95% CI 1.69–2.53]. There was a direct dose–response association between the number of cigarettes smoked and the risk of growth retardation. Women whose partner smoked were also at higher risk of having a child with growth retardation. All the above results were adjusted for confounding factors. The effect of maternal smoking on low birthweight seems to be attributable to intrauterine growth retardation rather than preterm delivery.     

Influence of maternal active and passive smoking during pregnancy on birthweight in newborns

Many studies have documented a strong association of active smoking during pregnancy with fetal growth retardation. Increasing interest has also been focused on whether there is an association between exposure of pregnant women to environmental tobacco smoke (ETS) and low birthweight of their babies. In the intervention controlled study "Healthy Pregnancy--Healthy Child", mothers after delivery were interviewed by medical students who collected data about their smoking and nutrition. Students were also trained to stimulate non-smoking behaviour and to explain the risks related to smoking and exposure to ETS. Data from 1147 mothers after delivery were collected but only single births were included in the analysis of birthweight. In our study, 63.4% women never smoked and 32.2% women reported they had stopped smoking either before pregnancy or during the first trimester. Only 4.4% of mothers (n = 50) smoked during the whole pregnancy. Women with the history of smoking were exposed to ETS more often than mothers who never smoked (51.6% vs 17.4%; p < 0.001). The number of heavily exposed both at home and workplaces was more than twice higher among former smokers compared with never smokers (22.4% versus 9.4%, p < 0.01). The average birthweight of babies born to women who had stopped smoking was higher than that born to never smokers. The average birthweight of babies born to women who smoked during pregnancy was lower by 119 g and 171 g than that of the babies born to never smokers and former smokers, respectively. When pre-term neonates were excluded, differences in birthweight between babies born to never smokers and either formerly smoking or still smoking mothers were slightly lower. The greatest effect of ETS exposure on birthweight was recorded in never smoking mothers; an average reduction in birthweight was 88 g. A strong dose-effect was observed; in mothers heavily exposed to ETS both at home and at work, the babies' birthweight was lower by 189 g in comparison with the group of non-exposed, never smoking mothers and even by 70 g compared with mothers smoking during pregnancy.     

Risk factors for Aboriginal low birthweight, intrauterine growth retardation and preterm birth in the Darwin Health Region

Abstract: Risk factors for Aboriginal low birthweight (< 2500 g), preterm birth (< 37 weeks' gestation) and intrauterine growth retardation (under the tenth percentile of Australian birthweights for gestational age) were examined in 503 live–born singletons recorded as born to an Aboriginal mother and routinely delivered at the Royal Darwin Hospital between January 1987 and March 1990. Infants born to mothers with body mass index less than 18.5 kg/m² had five times the risk of having low birthweight and 2.5 times the risk of intrauterine growth retardation. Population–attributable risk percentages suggest that 28 per cent of low birthweight and 15 per cent of growth retardation could be attributed to maternal malnutrition. Risk percentages for maternal smoking of more than half a packet of cigarettes a day were 18 per cent for low birthweight and 10 per cent for growth retardation. For growth retardation, 18 per cent could be attributed to a maternal age under 20 years. Risk factors for preterm birth were predominantly obstetric: the population–attributable risk percentage for pregnancy–induced hypertension was 26 per cent and for other obstetric conditions was 16 per cent. For Aboriginal births in the Darwin Health Region, maternal malnutrition and smoking are key elements in the prevention of low birthweight and intrauterine growth retardation. Teenage pregnancy is an important risk for intrauterine growth retardation, and pregnancy–induced hypertension is a risk for preterm birth.     

Birth outcomes and prenatal exposure to ozone, carbon monoxide, and particulate matter: results from the Children's Health Study

Exposures to ambient air pollutants have been associated with adverse birth outcomes. We investigated the effects of air pollutants on birth weight mediated by reduced fetal growth among term infants who were born in California during 1975-1987 and who participated in the Children's Health Study. Birth certificates provided maternal reproductive history and residence location at birth. Sociodemographic factors and maternal smoking during pregnancy were collected by questionnaire. Monthly average air pollutant levels were interpolated from monitors to the ZIP code of maternal residence at childbirth. Results from linear mixed-effects regression models showed that a 12-ppb increase in 24-hr ozone averaged over the entire pregnancy was associated with 47.2 g lower birth weight [95% confidence interval (CI), 27.4-67.0 g], and this association was most robust for exposures during the second and third trimesters. A 1.4-ppm difference in first-trimester carbon monoxide exposure was associated with 21.7 g lower birth weight (95% CI, 1.1-42.3 g) and 20% increased risk of intrauterine growth retardation (95% CI, 1.0-1.4). First-trimester CO and third-trimester O3 exposures were associated with 20% increased risk of intrauterine growth retardation. A 20-microg/m3 difference in levels of particulate matter < or = 10 microm in aerodynamic diameter (PM10) during the third trimester was associated with a 21.7-g lower birth weight (95% CI, 1.1-42.2 g), but this association was reduced and not significant after adjusting for O3. In summary, O3 exposure during the second and third trimesters and CO exposure during the first trimester were associated with reduced birth weight.     

Fetal environment and subsequent obesity: a study of maternal smoking

BACKGROUND: The intrauterine environment may influence the development of obesity, but as yet, the long-term effect of growth in utero is unclear. We studied maternal smoking during pregnancy to gain insight on how an insult affecting fetal growth might subsequently influence obesity risk through childhood to age 33. METHODS: Data from the 1958 British birth cohort (all births in England, Wales and Scotland, 3-9 March 1958), including body mass index (BMI), maternal smoking during pregnancy and several potential confounding factors. We assessed obesity risk at ages 7, 11, 16, 23 and 33 associated with maternal smoking. Adjusted odds ratios (OR) for obesity at age 33 were estimated for 2918 men and 2921 women with complete data. RESULTS: Infants of mothers who smoked in pregnancy were lighter at birth than infants of non-smokers, but from adolescence (age 11 for females, 16 for males) they had an increased risk of being in the fattest decile of BMI. The OR for obesity associated with maternal smoking increased with age, suggesting strengthening of the relationship over time. At age 33 the OR was 1.56 (95% CI : 1.22-2.00) for men and 1.41 (95% CI : 1.12-1.79) for women. This was robust to adjustment for factors in early life, childhood and adulthood. CONCLUSIONS: An elevated risk of obesity among the offspring of smokers was not accounted for by other known influences. Findings are consistent with a long-term effect of intrauterine environment on adiposity, possibly through fetal nutrition, although other mechanisms should be investigated in future studies of obesity.     

Offspring birth weight and parental mortality: prospective observational study and meta-analysis

The authors have investigated associations between offspring size at birth and parental cardiovascular disease mortality among 12,086 mothers and 6,936 fathers of participants in the British 1958 birth cohort. Birth weight was inversely associated with all-cause mortality and cardiovascular mortality in both mothers and fathers. The adjusted hazard ratio of cardiovascular disease mortality for a 1-standard deviation increase in offspring birth weight in mothers was 0.87 (95% confidence interval (CI): 0.82, 0.93) and in fathers was 0.94 (95% CI: 0.89, 0.99). The association was not specific for cardiovascular disease. In fathers, similar weak associations with violent and accidental deaths, stomach cancer, and alcohol- and smoking-related outcomes were found. Weak associations for these outcomes were also found for mothers, but the magnitude of the association with cardiovascular disease was greater than with any other outcomes. In a meta-analysis pooling results from this study with six others, the adjusted hazard ratio of cardiovascular disease mortality among mothers was 0.75 (95% CI: 0.67, 0.84) and that among fathers was 0.93 (95% CI: 0.91, 0.95), with evidence that the difference in effect between mothers and fathers was not due to chance (p < 0.001). The weak association of offspring birth weight with cardiovascular disease in fathers may be due to residual confounding by factors such as socioeconomic position and smoking that they share with the offspring's mother and that would therefore be associated with low offspring birth weight as well as adverse outcomes in the father. The stronger association in mothers is consistent with intergenerational effects on intrauterine growth and with the fetal origins hypothesis.     

Effect of trihalomethane exposure on fetal development

Aims: To examine the effect of trimester specific and pregnancy average total trihalomethane (TTHM) exposure on infant birth weight, low birth weight, and intrauterine growth retardation in term births, as well as gestational age and preterm delivery in all births.

Methods: Cross sectional analysis of 56 513 singleton infants born to residents of Massachusetts during 1990. City specific aggregate data were used to estimate maternal exposure to TTHM concentration; individual maternal information was used to adjust for confounding.

Results: Increased pregnancy average and second trimester TTHM exposure were associated with small for gestational age and reductions in birth weight after adjusting for potential confounding variables. Compared to ≤60 µg/l, pregnancy average TTHM exposure over 80 µg/l was associated with a 32 g reduction in birth weight. There was a 23 g reduction in birth weight in infants born to mothers exposed to greater than 80 µg/l TTHM during the second trimester. For each 20 µg/l increase in TTHM, the estimated reduction in birth was 2.8 g for pregnancy average exposure and 2.6 g for second trimester exposure. An increased risk of small for gestational age births was found for pregnancy average (odds ratio (OR) 1.14; 95% CI 1.02 to 1.26) and second trimester (OR 1.13, 95% CI 1.03 to 1.24) TTHM levels greater than 80 µg/l. There was no evidence of an association between preterm delivery and increased TTHM levels, but there were slight increases in gestational duration associated with TTHM concentrations.

Conclusions: Maternal exposure to THMs may be associated with fetal growth retardation. Our findings are consistent with most previous work, although we generally found smaller effects of TTHMs on low birth weight and intrauterine growth retardation.

     

The Influence of Maternal Smoking and Exposure to Residential ETS on Pregnancy Outcomes: A Retrospective National Study

In a nationwide study of Serbian births, in 2008, we estimated the influence of maternal prenatal smoking and environmental tobacco smoke (ETS) exposure on birth outcomes. Using stratified two-stage random cluster sampling, 2,721 women were interviewed in-person (response rates 98.1 %), and 2,613 singleton live births were included. Date of birth, gender, birthweight, birth height and head circumference were copied from the official hospital Birth Certificate. Six exposure categories were defined according to mother’s smoking history and exposure to ETS. We calculated adjusted mean values and group differences by analysis of covariance, and adjusted odds ratios for the low birthweight (LBW < 2,500 g). Compared to the reference category (non-smoking, non-exposed to ETS) we observed birthweight reductions in infants whose mothers smoked continuously during the pregnancy and were exposed to ETS (?162.6 g) and whose mothers were not exposed to ETS (?173 g) (p = 0.000, and p = 0.003, respectively), as well as reduction in birth length (?1.01 and ?1.06 cm; p = 0.003 and p = 0.000, respectively). Reduction in birthweight and birth length related to exposure categories was not linear. Adjusted OR for LBW was almost tripled for mothers who smoked over the entire pregnancy and were non-exposed to ETS (aOR 2.85; 95 % CI 1.46–5.08), and who were exposed to ETS (aOR 2.68; 95 % CI 1.15–6.25). Our results showed strong effects of smoking throughout the pregnancy on reduced birthweight, birth length and head circumference, and increased risk for LBW. We were not able to detect an effect for ETS exposure alone.     

The influence of active and passive smoking during pregnancy on umbilical cord blood levels of vitamins A and E and neonatal anthropometric indices

Smoking during pregnancy has been shown to be detrimental for the developing fetus. The effects of active and passive maternal smoking on umbilical cord serum levels of vitamin A and vitamin E were examined. Secondary measures included anthropometric parameters in the newborn. Maternal and umbilical cord serum levels of vitamins A and E were measured at delivery. The mothers were assigned to three groups: non-smoking (n 12); passive smoking (n 13); active smoking (n 18). Based on multivariate linear regressions, active smoking during pregnancy was associated with increased umbilical cord serum levels of vitamin A and vitamin E. While enhanced circulating levels of vitamin A in cord blood were also found in non-smoking mothers exposed to tobacco smoke during pregnancy, those of vitamin E were not influenced. Further, an inverse association between smoking behaviour during pregnancy and birth length was observed, with shortest length in active smokers followed by passive smoking mothers. Active and passive maternal smoking behaviour during pregnancy increases the fetal demand for antioxidant compounds in order to counteract the oxidative burden by cigarette smoke. Against this background, the observed increase in umbilical cord serum levels of vitamins A and E may subserve antioxidative processes in response to tobacco smoke-induced oxidative stress. This would reduce the availability of vitamins A and E for fetal maturation, which is critical inasmuch as both compounds are indispensable for the developing fetus. However, due to the cross-sectional nature of our observation, this line of reasoning definitely requires validation in cause-effect experiments in the future.     

Association of low birth weight with passive smoke exposure in pregnancy

In a prospective study of 3,891 antenatal patients at Yale-New Haven Hospital between 1980 and 1982, one fourth (23.6%) had not smoked cigarettes during pregnancy but had been exposed to sidestream smoke for at least two hours per day. Among the nonsmokers, passive smoke exposure was significantly related to delivering a low birth weight (less than 2,500 g) newborn. This relation only occurred in term (greater than or equal to 37 weeks) deliveries. Compared with unexposed women, the relative risk of low birth weight after adjustment for confounding factors was 2.17 (95% confidence interval (CI) = 1.05-4.50). Those exposed to passive smoke delivered infants 24 g lighter on average. There was no additive effect of passive smoking on smokers themselves. Repeating the analysis on all women with term deliveries, therefore, resulted in a slightly diminished risk of low birth weight due to passive smoking of 1.52 (95% CI = 0.90-2.56). The risk of low birth weight at term due to direct cigarette smoking was 3.54 (95% CI = 1.62-7.71). Gestational age was unrelated to passive smoking, which appears to exert its effect primarily through growth retardation in term newborns.     

Folic acid supplements modify the adverse effects of maternal smoking on fetal growth and neonatal complications

Maternal smoking during pregnancy leads to increased risks of neonatal complications. The use of folic acid supplements might reduce the adverse effects of smoking. We examined whether folic acid supplement use modifies the associations of maternal smoking with first trimester plasma homocysteine concentrations, fetal growth characteristics, and risks of neonatal complications. The associations were studied in 6294 mothers participating in a prospective population-based cohort study in The Netherlands. Main outcomes measurements were first trimester plasma homocysteine concentrations, fetal growth characteristics, and neonatal complications, including preterm birth, low birth weight, and small-size-for-gestational-age. Continued maternal smoking was associated with higher first trimester plasma homocysteine concentrations [difference 0.52 μmol/L (95% range = 0.20, 2.14)], lower third trimester fetal weight (difference -44 g (95% CI = -57, -31)], and birth weight [difference -148 g (95% CI = -179, -118)]. There were significant interactions between maternal smoking and folic acid supplements on all outcome measures (all P-interaction < 0.040). Among mothers who continued smoking during pregnancy, those who did not use folic acid supplements had the highest risk of delivering a child with low birth weight [OR = 3.45 (95% CI = 1.25, 9.54)] compared to those who did use periconceptional folic acid supplements. No significant effects were observed for the risks of preterm birth and small-size-for-gestational-age at birth. Our results suggest that some adverse effects of maternal smoking on fetal growth and neonatal outcomes might be reduced by the use of folic acid supplements. The observed interaction seems to be mainly driven by smoking in the first trimester only.     

Interpregnancy interval and low birth weight: findings from a case-control study

In a case-control study in Natal, northeast Brazil, conducted between September 1984 and February 1986, 303 cases of intrauterine growth retardation and 282 cases of preterm delivery were compared with 1,710 normal controls to ascertain the effects of the preceding birth-to-conception interval on pregnancy outcome. The risk of intrauterine growth retardation associated with interpregnancy intervals of six months or less was 1.38 (95% confidence interval (CI): 1.02-1.86) after adjustment for maternal age, education, smoking, and prior fetal loss or low birth weight. When maternal postpartum body weight was introduced into the logistic model, the risk of intrauterine growth retardation decreased slightly to 1.25 and was no longer significant (95% CI: 0.91-1.72). Short interpregnancy intervals (six months or less) were more frequently observed in women with postpartum body weight of less than 45 kg (31.1%) than in women weighing 50 kg or more (18.9%), which might suggest that the effect of short intervals on the risk of intrauterine growth retardation is mediated through maternal nutritional status. No association was found between birth-to-conception intervals and preterm delivery.     

Smoking and damages of reproduction: evidence of ELSPAC

The international longitudinal prospective ELSPAC study also includes women from the Czech Republic: the results sum up data from 4530 women from City of Brno and District of Znojmo who had different exposure to active and passive smoking. Anamnestic data were collected by fulfilling the internationally unified questionnaires during pregnancy and at the 2nd month after delivery. Gynaecologists, obstetricians and pediatricians, using the unified procedures, were collecting objective data in the course of the pregnancy, delivery, monitoring health status of women and newborns. Significant differences were found between smoking and non-smoking women in the prevalence of alcohol and marihuana consumers both before and during pregnancy and after delivery. In personal health history, smoking women more often reported their self-perceived poor health, panic and loss of self-control during the delivery. In the current pregnancies, smoking women suffer more often with placenta praevia, placental abnormalities, fetal growth retardation and fetal malformations. On the other hand, the prevalence of preeclampsia was decreased among smokers. The children of mothers who were moderate/heavy smokers during pregnancy, had on average by 245 g lower birth weight, 1.22 cm shorter body length and by 0.66 cm smaller head circumference than those of non-smokers. These measures were on average also decreased in the groups of newborns whose mothers were light smokers or non-smokers heavy exposed to environmental tobacco smoke. On the contrary, the average gestational age was similar both in case of active smoking, passive smoking, and non-smoking women. In spite of the fact that most of smokers would give up smoking after getting pregnant, it is necessary to place the antismoking interventions and nutrition advisory service within the routine duty of physicians.     

Relation of Maternal Low Birth Weight to Infant Growth Retardation and Prematurity

Objectives: This study sought to determine the relationship between maternal birth weight, infant intrauterine growth retardation, and prematurity. Methods: Stratified and logistic regression analyses were performed on a dataset of computerized Illinois vital records of African American (N = 61,849) and White (N = 203,698) infants born between 1989 and 1991 and their mothers born between 1956 and 1975. Results: Race-specific rates of small-for-gestational age (weight-for-gestational age <10th percentile) and preterm (<37 weeks) infants rose as maternal birth weight declined. The adjusted (controlling for maternal age, education, marital status, parity, prenatal care utilization, and cigarette smoking) odds ratio (95% confidence interval) of small-for-gestational age for maternal low birth weight (<2500 g) among African Americans and Whites were 1.7 (1.1.4–1.9) and 1.8 (1.7–2.0), respectively. The adjusted odds ratio (95% confidence interval) of prematurity for maternal low birth weight (<2500 g) among African Americans and Whites were 1.6 (1.3–1.9) and 1.3 (1.0–1.6), respectively. The racial disparity in the rates of small-for-gestational age and prematurity persisted independent of maternal birth weight: adjusted odds ratio equaled 2.2 (2.1–2.4) and 1.5 (1.4–1.7), respectively. Conclusions: Maternal low birth weight is a risk factor for infant intrauterine growth retardation and prematurity among African Americans independent of maternal risk status during pregnancy; it is a risk factor for infant intrauterine growth retardation among Whites. Maternal low birth weight fails to explain the racial disparity in the rates of small-for-gestational age and premature infants.     

Paternal smoking and birthweight in Shanghai.

OBJECTIVES. Although maternal active smoking has been established to be associated with fetal growth retardation, evidence of an effect of environmental tobacco smoke exposure on birthweight is still limited and inconclusive. This study addressed the relationship between prenatal environmental tobacco smoke exposure and birthweight and fetal growth retardation in Shanghai, China. METHODS. Data on 1785 full-term live-born normal infants of nonsmoking mothers were used from the Shanghai Birth Defects and Perinatal Death Monitoring conducted between October 1986 and September 1987. Environmental tobacco smoke exposure was defined as exposure to paternal smoking. RESULTS. Infants with environmental tobacco smoking exposure were, on average, 30 g lower in birthweight than nonexposed infants, after adjustment for gestational age, parity, maternal age, and occupation. CONCLUSION. Consistent with previous research, this study suggests that environmental tobacco smoking exposure may have a modestly adverse effect on birthweight.     

Active and passive smoking during pregnancy and risk of central nervous system tumours in children

The effects of maternal active and passive smoking during pregnancy on childhood central nervous system (CNS) tumours were assessed in a population-based case-control study. The mothers of 244 children aged 0-15 years with CNS tumours and 502 control mothers were interviewed about their smoking habits. All families were resident in the region of Lombardy, Italy. Risk estimates were calculated by unconditional logistic regression, adjusted for age, sex and area of residence. Active smoking by the parents before pregnancy was not associated with increased risk of CNS tumours in the children. Active smoking by the mother during early pregnancy (approximately the first 5 weeks) was associated with a slightly increased risk of the child developing a CNS tumour (odds ratio [OR] 1.5 [95% CI 1.0, 2.3]). An increased risk of CNS tumours was found in the children of non-smoking mothers exposed regularly to tobacco smoke both in early pregnancy (OR 1.8 [95% CI 1.2, 2.6]) and in late pregnancy (OR 1.7 [95% CI 1.2, 2.5]). Although this study was retrospective, the results confirm our previous findings and suggest an association between the risk of developing CNS tumours in children and regular passive smoking by the mother during pregnancy.     

Passive smoking, metabolic gene polymorphisms, and infant birth weight in a prospective cohort study of Chinese women

The authors investigated whether polymorphisms in two maternal metabolic genes, cytochrome P-450 1A1 (CYP1A1) MspI and epoxide hydrolase 1 (EPHX1) Tyr113His, affect the association of maternal passive smoking with infant birth weight. The study was conducted in a cohort of 1,388 newly married mothers of liveborn singletons who worked in textile mills in Anqing, China, from 1996 to 2000. Multiple linear regression models were used to estimate the associations of passive smoking and genetic susceptibility with birth weight, with adjustment for important potential confounders. In the passive smoking group, there was a remarkable decrease in birth weight with the C/C6235 genotype (156.3 g, 95% confidence interval (CI): -283.6, -29.0) for CYP1A1 MspI and with Tyr/His113 (93.8 g, 95% CI: -188.6, -1.1) as compared with His/His113 (244.6 g, 95% CI: -491.0, -1.9) for EPHX1. When results were stratified by maternal genotype, passive smoking conferred a significantly negative effect in the EPHX1 Tyr/His113 group (103.5 g, 95% CI: -205.8, -9.2) and in the His/His113 group (687.3 g, 95% CI: -748.3, -178.3). The data further showed that there was a significant interaction between maternal passive smoking and maternal EPHX1 genotype for birth weight. The authors conclude that the CYP1A1 MspI and EPHX1 genotypes modified the association between maternal passive smoking and infant birth weight in this study, which is suggestive of possible gene-environment interaction.     

Increased burden of respiratory disease in the first six months of life due to prenatal environmental tobacco smoke: Krakow birth cohort study

The main purpose of our study was to assess the effects of prenatal tobacco smoke on respiratory symptoms and on doctor consultations in a birth cohort of 445 infants who had no smoking mothers and who had no postnatal exposure to environmental tobacco smoke (ETS). Before and after delivery, questionnaires and interviews with mothers were administered to solicit information on prenatal and postnatal ETS exposure. Newborns were followed-up over six months of life, and respiratory outcomes such as runny or stuffed nose, cough with or without cold, difficult (puffed) breathing, wheezing or whistling in the chest irrespective of respiratory infection were considered. In addition, medical visits related to the occurrence of respiratory symptoms were recorded for each child over a six-month study period. In the multivariate Poisson regression analysis, a set of potential confounders has been taken into account such as gender of child, season of birth, gestational age, maternal education, maternal atopy, presence of moulds in households and prenatal level of personal exposure to fine particles. The adjusted rate ratio (RR) estimated for the occurrence of episodes of running nose was significantly higher in infants exposed to prenatal ETS (1.40; 95% confidence interval [CI]: 1.11-1.68) and the corresponding RR estimates for cough, difficult breathing and wheezing were 1.49 (95% CI: 1.15-1.93), 1.96 (95% CI: 1.22-3.16) and 5.12 (95% CI: 2.86-9.16). The rate ratios of doctor consultations attributable to prenatal ETS because of cough was 1.94 (95% CI: 1.49-2.54). The risk estimate for consultations due to difficult breathing was 2.77 (95% CI: 1.76-4.36), and that for wheezing was 5.86 (95% CI: 3.56-9.64). The data strongly support the view about the impact of the in-utero effect of passive smoking on children's respiratory health. Higher utilization rates of doctor consultations in infants attributable to prenatal ETS exposure demand the revision of public health policy, which should be focused also on cessation of smoking practices by all household members during and after the pregnancy period.