Accuracy of mothers' retrospective reports of smoking during pregnancy: comparison with twin sister informant ratings.

Retrospective assessment of maternal smoking or substance use during pregnancy is sometimes unavoidable. The unusually close relationship of twin sister pairs permits comparison of self-report data versus co-twin informant data on substance use during pregnancy. Information about smoking during pregnancy has been gathered from a series of mothers from an Australian volunteer twin panel (576 women reporting on 995 pregnancies), supplemented in many cases by independent ratings of their smoking by twin sister informants (821 pregnancies). Estimates of the proportion of women who had never smoked regularly (56-58%), who had smoked but did not smoke during a particular pregnancy (16-21%), or who smoked throughout the pregnancy (16-18%), were in good agreement whether based on self-report or twin sister informant data. However, informants underreported cases who smoked during the first trimester but then quit (1-3% versus 7-9% by self-report). Women who smoked throughout pregnancy (by informant report) rarely denied a history of regular smoking (< 1%), although a small proportion of apparent false negative cases were identified where they either denied smoking during a pregnancy (9%) or denied smoking beyond the first trimester (10%). We conclude that retrospective smoking data can safely be used to identify potential associations of later child outcomes with maternal smoking during pregnancy.     

Impact of maternal lifestyle factors on newborn HPRT mutant frequencies and molecular spectrum--initial results from the Prenatal Exposures and Preeclampsia Prevention (PEPP) Study

Epidemiological studies have demonstrated associations between maternal tobacco smoke exposure and consumption of alcohol during pregnancy and increased risk of pediatric malignancies, particularly infant leukemias. Molecular evidence also suggests that somatic mutational events occurring during fetal hematopoiesis in utero can contribute to this process. As part of an ongoing multi-endpoint biomarker study of 2000 mothers and newborns, the HPRT T-lymphocyte cloning assay was used to determine mutant frequencies (M_f) in umbilical cord blood samples from an initial group of 60 neonates born to a sociodemographically diverse cohort of mothers characterized with respect to age, ethnicity, socioeconomic status, and cigarette smoke and alcohol exposure. Non-zero M_f (N=47) ranged from 0.19 to 5.62×10⁻⁶, median 0.70×10⁻⁶, mean±SD 0.98±0.95×10⁻⁶. No significant difference in M_f was observed between female and male newborns. Multivariable Poisson regression analysis revealed that increased HPRT M_f were significantly associated with maternal consumption of alcohol at the beginning [Relative Rate (RR)=1.84, 95% CI=0.99–3.40, P=0.052) and during pregnancy (RR=2.99, 95% CI=1.14–7.84, P=0.026). No independent effect of self-reported active maternal cigarette smoking, either at the beginning or throughout pregnancy, nor maternal passive exposure to cigarette smoke was observed. Although based on limited initial data, this is the first report of a positive association between maternal alcohol consumption during pregnancy and HPRT M_f in human newborns. In addition, the spectrum of mutations at the HPRT locus was determined in 33 mutant clones derived from 19 newborns of mothers with no self-reported exposure to tobacco smoke and 14 newborns of mothers exposed passively or actively to cigarette smoke. In the unexposed group, alterations leading to specific exon 2–3 deletions, presumably as a result of illegitimate V(D)J recombinase activity, were found in five of the 19 mutants (26.3%); in the passively exposed group, two exon 2–3 deletions were present among the seven mutants (28.6%); and in the actively exposed group, six of the seven mutants (85.7%) were exon 2–3 deletions. Although no overall increase in HPRT M_f was observed and the number of mutant clones examined was small, these initial results point to an increase in V(D)J recombinase-associated HPRT gene exon 2–3 deletions in cord blood T-lymphocytes in newborns of actively smoking mothers relative to unexposed mothers (P=0.011). Together, these results add to growing molecular evidence that in utero exposures to genotoxicants result in detectable transplacental mutagenic effects in human newborns.     

Smoking and the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers.

OBJECTIVE--To investigate the effects of exposure to tobacco smoke and of parental consumption of alcohol and illegal drugs as risk factors for the sudden infant death syndrome after a national risk reduction campaign which included advice on prenatal and postnatal avoidance of tobacco smoke. DESIGN--Two year population based case-control study. Parental interviews were conducted for each infant who died and four controls matched for age and date of interview. SETTING--Three regions in England with a total population of 17 million people. SUBJECTS--195 babies who died and 780 matched controls. RESULTS--More index than control mothers (62.6% v 25.1%) smoked during pregnancy (multivariate odds ratio = 2.10; 95% confidence interval 1.24 to 3.54). Paternal smoking had an additional independent effect when other factors were controlled for (2.50; 1.48 to 4.22). The risk of death rose with increasing postnatal exposure to tobacco smoke, which had an additive effect among those also exposed to maternal smoking during pregnancy (2.93; 1.56 to 5.48). The population attributable risk was over 61%, which implies that the numbers of deaths from the syndrome could be reduced by almost two third if parents did not smoke. Alcohol use was higher among index than control mothers but was strongly correlated with smoking and on multivariate analysis was not found to have any additional independent effect. Illegal drug use was more common among the index parents, and paternal use of illegal drugs remained significant in the multivariate model (4.68; 1.56 to 14.05). CONCLUSIONS--This study confirms the increased risk of the sudden infant death syndrome associated with maternal smoking during pregnancy and shows evidence that household exposure to tobacco smoke has an independent additive effect. Parental drug misuse has an additional small but significant effect.     

Weight growth in infants born to mothers who smoked during pregnancy.

OBJECTIVE--To determine whether maternal smoking during pregnancy causes impairment in growth after birth. DESIGN--Longitudinal study. SETTING--Six medical university centres of six towns of north, central, and south Italy. SUBJECTS--12,987 babies (10,238 born from non-smoking mothers, 2276 from mothers smoking one to nine cigarettes a day, and 473 from mothers smoking > or = 10 cigarettes a day) entered the study. MAIN OUTCOME MEASURES--Difference in weight gain between children born to smoking mothers and those born to non-smoking mothers. Weight was measured at birth and at 3 and 6 months of age. Maternal smoking habit was derived from interview on third or fourth day after delivery. RESULTS--Compared with children born to mothers who did not smoke during pregnancy, the birth weights of children born to mothers who smoked up to nine cigarettes a day were 88 g (girls) and 107 g (boys) lower; in children born to mothers who smoked > or = 10 cigarettes a day weights were 168 g and 247 g lower. At six months of age for the first group the mean weight for girls was 9 g (95% confidence interval -47 g to 65 g) higher and for boys 64 g (-118 g to -10 g) lower than that of children born to mothers who did not smoke. The corresponding figures for the second group were 28 g (-141 g to 85 g) lower for girls and 24 g (-136 g to 88 g) lower for boys. CONCLUSIONS--The deficits of weight at birth in children born to mothers who smoked during pregnancy are overcome by 6 months of age. These deficits are probably not permanent when smoking habit during pregnancy is not associated with other unfavourable variables (such as lower socioeconomic class).     

V(D)J recombinase-mediated deletion of the hprt gene in T-lymphocytes from adult humans.

The hprt T-cell cloning assay allows the detection of mutations occurring in vivo in the hypoxanthine-guanine phosphoribosyltransferase (hprt) gene of T-lymphocytes. We have shown previously that the illegitimate activity of V(D)J recombinase accounts for about 40% of the hprt mutations in T-lymphocytes of human newborns as measured with umbilical cord blood samples (Fuscoe et al., 1991). This mechanism results in deletion of hprt exons 2 + 3. In this report, we examined a collection of 314 HPRT-deficient clones derived from adult humans for evidence that the mutations were caused by this mechanism by analyzing exons 2 + 3 deletion mutations. DNA sequence analysis of deletion breakpoint junctions showed that 8 of the mutations were the result of V(D)J recombinase activity. The frequency of the recombinase-mediated mutations was similar in the adults and newborns (2-4 x 10(-7). However, since the hprt mutant frequency is about 10-fold higher in the adult than in the newborn, the recombinase-mediated mutations account for only a few percent of the adult mutations. These mutations are likely to have occurred during early development and persist into adulthood. Unregulated expression of V(D)J recombinase activity may be an important mechanism for genomic rearrangements in the genesis of cancer.     

Maternal smoking during pregnancy predicts adult offspring cardiovascular risk factors - evidence from a community-based large birth cohort study

Background

Maternal smoking during pregnancy is associated with offspring obesity. However, little is known about whether maternal smoking in pregnancy predicts other offspring cardiovascular risk factors including waist circumference (WC), waist-hip-ratio (WHR), pulse rate (PR), systolic (SBP), and diastolic blood pressure (DBP).

Methods

We studied a sub-sample of 2038 (50% males) young adults who were born in Brisbane, Australia to investigate the prospective association of maternal smoking during pregnancy with young adult cardiovascular risk factors. We compared offspring mean BMI, WC, WHR, SBP, DBP and PR and the risk of being overweight and obese at 21 years by three mutually exclusive categories of maternal smoking status defined as never smoked, smoked before and/or after pregnancy but not in pregnancy or smoked during pregnancy and other times.

Results

Offspring of mothers who smoked during pregnancy had greater mean BMI, WC, WHR and PR and they were at greater risk of being obese at 21 years compared to offspring of those mothers who never smoked. The mean of these risk factors among those adult offspring whose mothers stopped smoking during pregnancy, but who then smoked at other times in the child''s life, were similar to those mothers who never smoked. These results were independent of a range of potential confounding factors.

Conclusion

The findings of this study suggest a prospective association of maternal smoking during pregnancy and offspring obesity as well as PR in adulthood, and reinforce the need to persuade pregnant women not to smoke.     

Impact of maternal lifestyle factors on newborn HPRT mutant frequencies and molecular spectrum — Initial results from the Prenatal Exposures and Preeclampsia Prevention (PEPP) Study

Epidemiological studies have demonstrated associations between maternal tobacco smoke exposure and consumption of alcohol during pregnancy and increased risk of pediatric malignancies, particularly infant leukemias. Molecular evidence also suggests that somatic mutational events occurring during fetal hematopoiesis in utero can contribute to this process. As part of an ongoing multi-endpoint biomarker study of 2000 mothers and newborns, the HPRT T-lymphocyte cloning assay was used to determine mutant frequencies (M_f) in umbilical cord blood samples from an initial group of 60 neonates born to a sociodemographically diverse cohort of mothers characterized with respect to age, ethnicity, socioeconomic status, and cigarette smoke and alcohol exposure. Non-zero M_f (N=47) ranged from 0.19 to 5.62×10⁻⁶, median 0.70×10⁻⁶, mean±SD 0.98±0.95×10⁻⁶. No significant difference in M_f was observed between female and male newborns. Multivariable Poisson regression analysis revealed that increased HPRT M_f were significantly associated with maternal consumption of alcohol at the beginning [Relative Rate (RR)=1.84, 95% CI=0.99–3.40, P=0.052) and during pregnancy (RR=2.99, 95% CI=1.14–7.84, P=0.026). No independent effect of self-reported active maternal cigarette smoking, either at the beginning or throughout pregnancy, nor maternal passive exposure to cigarette smoke was observed. Although based on limited initial data, this is the first report of a positive association between maternal alcohol consumption during pregnancy and HPRT M_f in human newborns. In addition, the spectrum of mutations at the HPRT locus was determined in 33 mutant clones derived from 19 newborns of mothers with no self-reported exposure to tobacco smoke and 14 newborns of mothers exposed passively or actively to cigarette smoke. In the unexposed group, alterations leading to specific exon 2–3 deletions, presumably as a result of illegitimate V(D)J recombinase activity, were found in five of the 19 mutants (26.3%); in the passively exposed group, two exon 2–3 deletions were present among the seven mutants (28.6%); and in the actively exposed group, six of the seven mutants (85.7%) were exon 2–3 deletions. Although no overall increase in HPRT M_f was observed and the number of mutant clones examined was small, these initial results point to an increase in V(D)J recombinase-associated HPRT gene exon 2–3 deletions in cord blood T-lymphocytes in newborns of actively smoking mothers relative to unexposed mothers (P=0.011). Together, these results add to growing molecular evidence that in utero exposures to genotoxicants result in detectable transplacental mutagenic effects in human newborns.     

Childhood obesity and parental smoking as risk factors for childhood ADHD in Liverpool children

ADHD prevalence has risen in parallel with rising prevalence of pregnancy smoking and childhood obesity. The objective was to determine the epidemiological association of pregnancy smoking and childhood obesity with ADHD. A cross-sectional community study was conducted in 2006 using a parental questionnaire. A total of 1,074 schoolchildren aged 5-11 years were enrolled from 15 primary schools in a lower socio-economic area of Merseyside. ADHD was defined by the question "does your child have Attention Deficit Hyperactivity Disorder, (ADHD), which has been diagnosed by a doctor?" The prevalence estimates for childhood obesity, maternal smoking during pregnancy and childhood ADHD were 14.9% (116/777), 28.0% (269/955), and 3.4% (32/945), respectively. ADHD prevalence increased fivefold in children with obesity (RR, 4.80, 95% CI 2.2-10.4, P < 0.001) and more than twofold in children of mothers who smoked during pregnancy (RR, 2.44, 95% CI 1.2-4.9, P = 0.02). Regression analysis adjusting for obesity, overweight, maternal smoking during pregnancy, heavy maternal smoking, household member smoking during pregnancy, doctor-diagnosed asthma, preterm birth, and low birthweight showed significant independent associations of ADHD prevalence with obesity (AOR, 4.66, 95% CI 1.57-13.89, P = 0.006) and pregnancy smoking (AOR, 3.19, 95% CI 1.08-9.49, P = 0.04). There was a positive dose-response association of ADHD with the number of maternal cigarettes smoked during pregnancy. Measures to reduce both smoking among pregnant women and childhood obesity might reduce prevalence of childhood ADHD.     

The influence of mother's active smoking during pregnancy on body mass index of newborns

Many investigations have noted bad influence of smoking during pregnancy. In the present article, the influence of mothers smoking during pregnancy on the body mass index (BMI), birth weight and birth length are examined. This retrospective research included 219 children: Group I: 109 children from rural area of east Slavonia (born in General Hospital-Vinkovci) and group II: 110 children from industrial area (born in Zagreb). The questioned subjects were divided into two groups depending on mothers smoking during pregnancy: newborns of mothers who didn't smoke during pregnancy (subgroup A) and newborns of mother who did smoke 10 or more cigarettes per day during pregnancy (subgroup B). Anthropometric parameters (BMI, birth length and birth weight) in newborns of non-smoking mothers were statistically higher (p < 0.05) than in newborns of smoking mothers. Moderate correlation between birth length and birth weight in newborns of non-smoking and smoking mothers from rural area and from non-smoking mothers in urban area was statistically significant, but correlation in the group in newborns of smoking mothers from Zagreb was not statistically significant. Results of this research show that smoking during pregnancy significantly influences the birth weight and birth length. Further investigation is needed, to investigate the lack of correlation between the birth length and birth weight in newborns of smoking mothers from industrial city.     

Smoking and health care patterns among pregnant women

A population-based hospital survey of 3628 women in the postpartum period was conducted in the Ottawa-Carleton region in 1983 to determine the prevalence of smoking before and during pregnancy, the demographic and socioeconomic characteristics of women who smoke during pregnancy and the use of health care services by these women. Of the 3628 women 91% completed a full-length questionnaire and 4% completed a shorter questionnaire. Before pregnancy 37.4% of the women smoked cigarettes. Overall, 61.1% of the smokers changed their smoking habit: 31.1% stopped, 28.1% decreased the amount smoked and 2.0% increased the amount smoked. Two thirds of the women who stopped smoking did so as soon as they realized they were pregnant. Over 50% of teenagers, single women, women living common-law and women with less than a grade 11 education smoked after the 3rd month of pregnancy. The physician is in an ideal position to identify as soon as possible pregnant women who smoke and to initiate a health education program. Only a few women who smoked during pregnancy attended early prenatal classes. Physicians and class organizers must work to improve this situation if such classes are to have an impact on smoking during pregnancy.     

Maternal Snuff Use and Smoking and the Risk of Oral Cleft Malformations - A Population-Based Cohort Study

Objective

To determine if maternal use of snuff (containing high levels of nicotine, low levels of nitrosamines and no combustion products) is associated with an increased risk of oral cleft malformations in the infant and whether cessation of snuff use or smoking before the antenatal booking influences the risk.

Method

A population-based cohort study was conducted on all live born infants, recorded in the Swedish Medical Birth Register from 1999 through 2009 (n = 1 086 213). Risks of oral clefts were evaluated by multivariate logistic regression analyses (using adjusted odds ratios, with 95% confidence intervals [CI]).

Results

Among 975 866 infants that had information on maternal tobacco use, 1761 cases of oral clefts were diagnosed. More than 50% of the mothers who used snuff or smoked three months prior pregnancy stopped using before the antenatal booking. Almost 8% of the mothers were smoking at the antenatal booking and 1,1% of the mothers used snuff. Compared with infants of non-tobacco users, the adjusted odds ratios (95% CI) of any oral cleft for infants of mothers who continued to use snuff or to smoke were 1.48 [1.00–2.21] and 1.19 [1.01–1.41], respectively. In contrast, in infants of mothers who stopped using snuff or stopped smoking before the antenatal booking, the corresponding risks were not increased (adjusted odds ratios [95% CI] were 0.71 [0.44–1.14] and 0.88 [0.73–1.05], respectively).

Conclusion

Maternal snuff use or smoking in early pregnancy is associated with an increased risk of oral clefts. Infants of mothers who stopped using snuff or stopped smoking before the antenatal booking had no increased risk of oral cleft malformations. Oral snuff or other sources of nicotine should not be recommended as an alternative for smoke-cessation during pregnancy.     

Planning elective operations on patients who smoke: survey of North American plastic surgeons.

Patient smoking status affects many aspects of plastic surgery, including patient selection, counseling, management, and outcomes. No specific recommendations for performing elective procedures on patients who smoke are available. The goal of this study was to determine the current practice standards and attitudes toward this often controversial topic. In September of 2000, 1600 members of the American Society for Aesthetic Plastic Surgery were sent questionnaires, 955 of which were returned. Questions elicited categorical answers, either dichotomous or multiple choice. Data were evaluated using logistic regression and the chi-square and binomial tests. Our results show that 60 percent (p < 0.01) of plastic surgeons routinely perform a less than optimal procedure on their patients who smoke. The survey measured willingness to perform various operative procedures on patients who smoke and types of smoking cessation aids offered. Of those physicians who require patients to quit smoking before surgery, only 16.7 percent (p < 0.01) would perform a nicotine test if they suspected noncompliance. Interestingly, 28.6 percent (p < 0.01) of the physicians responding admit to a smoking history, whereas only 1.5 percent (p < 0.01) continue to smoke, compared with the national smoking rate of almost 25 percent. Physicians who are previous smokers are less likely to offer smoking cessation aids than those who have never smoked, and the proportion not offering aids increases as the amount of previous smoking increases (p = 0.02). This study shows that a wide range of opinions exists on which elective surgical procedures should be performed on patients who smoke. Furthermore, the physician's prior smoking history influences this decision. No clear consensus exists on how best to treat patients who smoke who request elective surgeries. Although surgeons would prefer to operate on nonsmokers, they are faced with a significant population of patients who use tobacco. No clear consensus exists on how best to treat these individuals. Advancements in wound healing research and smoking cessation aids will provide more insight into this treatment dilemma.     

Dental asymmetry,maternal obesity,and smoking

This study examines the levels of fluctuating dental asymmetry in four samples of school children: those whose mothers were obese and had smoked during the pregnancy concerned (n = 111); those whose mothers were obese non-smokers (n = 114); those whose mothers were non-obese smokers (n = 104); and those whose mothers were lean non-smokers (n = 111). The degree of fluctuating asymmetry was assessed by means of a rescaled asymmetry measure. Obesity was defined as Quetelet's index in excess of 30, and smoking status as at least 20 cigarettes per day during the pregnancy concerned. When the magnitudes of fluctuating asymmetry in children of lean smokers were compared to the control group of lean non-smokers, no significant univariate differences were found. Children of obese mothers, whether these smoked or not, were found to have significantly raised levels of asymmetry. An analysis of variance confirmed that the combination of obesity and maternal smoking was a significant predictor of fluctuating dental asymmetry. The teeth involved tended to be the maxillary first incisor and molars. It is concluded that maternal obesity has a destabilizing effect on the developing fetus and that this effect appears to be enhanced in obese mothers who smoked. This effect was absent in lean mothers, irrespective of their smoking status. Am J Phys Anthropol 102:133–139. © 1997 Wiley-Liss, Inc.     

Orofacial clefts, parental cigarette smoking, and transforming growth factor-alpha gene variants.

Results of studies to determine whether women who smoke during early pregnancy are at increased risk of delivering infants with orofacial clefts have been mixed, and recently a gene-environment interaction between maternal smoking, transforming growth factor-alpha (TGFa), and clefting has been reported. Using a large population-based case-control study, we investigated whether parental periconceptional cigarette smoking was associated with an increased risk for having offspring with orofacial clefts. We also investigated the influence of genetic variation of the TGFa locus on the relation between smoking and clefting. Parental smoking information was obtained from telephone interviews with mothers of 731 (84.7% of eligible) orofacial cleft case infants and with mothers of 734 (78.2%) nonmalformed control infants. DNA was obtained from newborn screening blood spots and genotyped for the allelic variants of TGFa. We found that risks associated with maternal smoking were most elevated for isolated cleft lip with or without cleft palate, (odds ratio 2.1 [95% confidence interval 1.3-3.6]) and for isolated cleft palate (odds ratio 2.2 [1.1-4.5]) when mothers smoked > or =20 cigarettes/d. Analyses controlling for the potential influence of other variables did not reveal substantially different results. Clefting risks were even greater for infants with the TGFa allele previously associated with clefting whose mothers smoked > or =20 cigarettes/d. These risks for white infants ranged from 3-fold to 11-fold across phenotypic groups. Paternal smoking was not associated with clefting among the offspring of nonsmoking mothers, and passive smoke exposures were associated with at most slightly increased risks. This study offers evidence that the risk for orofacial clefting in infants may be influenced by maternal smoke exposures alone as well as in combination (gene-environment interaction) with the presence of the uncommon TGFa allele.     

Revisiting the Effect of Maternal Smoking during Pregnancy on Offspring Birthweight: A Quasi-Experimental Sibling Analysis in Sweden

Maternal smoking during pregnancy (SDP) seems associated with reduced birthweight in the offspring. This observation, however, is based on conventional epidemiological analyses, and it might be confounded by unobserved maternal characteristics related to both smoking habits and offspring birth weight. Therefore, we apply a quasi-experimental sibling analysis to revisit previous findings. Using the Swedish Medical Birth Register, we identified 677,922 singletons born between 2002 and 2010 from native Swedish mothers. From this population, we isolated 62,941 siblings from 28,768 mothers with discrepant habits of SDP. We applied conventional and mother-specific multilevel linear regression models to investigate the association between maternal SDP and offspring birthweight. Depending on the mother was light or heavy smoker and the timing of exposition during pregnancy (i.e., first or third trimester), the effect of smoking on birthweight reduction was between 6 and 78 g less marked in the sibling analysis than in the conventional analysis. Sibling analysis showed that continuous smoking reduces birthweight by 162 grams for mothers who were light smokers (1 to 9 cigarettes per day) and 226 g on average for those who were heavy smokers throughout the pregnancy in comparison to non-smoker mothers. Quitting smoking during pregnancy partly counteracted the smoking-related birthweight reduction by 1 to 29 g, and a subsequent smoking relapse during pregnancy reduced birthweight by 77 to 83 g. The sibling analysis provides strong evidence that maternal SDP reduces offspring birthweight, though this reduction was not as great as that observed in the conventional analysis. Our findings support public health interventions aimed to prevent SDP and to persuade those who already smoke to quit and not relapse throughout the pregnancy. Besides, further analyses are needed in order to explain the mechanisms through which smoking reduces birthweight and to identify other maternal characteristics that are common causes of both birthweight reduction and maternal smoking.     

Craniosynostosis and maternal smoking

BACKGROUND: Several previous studies suggested increased risk of craniosynostosis among infants born to women who smoked. METHODS: This study used data from the National Birth Defects Prevention Study, a multi‐state, population‐based case‐control study of infants delivered from 1997–2003. Nonmalformed, liveborn controls were selected randomly from birth certificates or birth hospitals. Data from maternal telephone interviews were available for 531 cases and 5008 controls. RESULTS: Smoking during the first month of pregnancy was not associated with craniosynostosis. Smoking later in pregnancy was associated with increased risk, but only among mothers who smoked at least one pack/day. For example, during the second trimester, the odds ratio for smoking <5 cigarettes/day was 1.0 (95% confidence interval [CI] 0.6, 1.8), but the odds ratio (OR) for smoking 15 or more cigarettes/day was 1.6 (95% CI 0.9, 2.8), after adjustment for maternal age, education, race‐ethnicity, sub‐fertility, parity, folic acid supplement intake, body mass index, and study center. Among women who did not smoke, adjusted odds ratios suggested that secondhand smoke exposure at home, but not at work/school, was associated with modestly increased risk; the OR for home exposure was 1.3 (95% CI 0.9, 1.9). Results followed a similar pattern for some, but not all, specific suture types, but numbers for some groupings were small. CONCLUSIONS: The results suggest moderately increased risk of craniosynostosis among mothers who were the heaviest smokers and who continued to smoke after the first trimester. Results are somewhat equivocal, given that most confidence intervals included one. Birth Defects Research (Part A), 2008. © 2007 Wiley‐Liss, Inc.     

The effect of tobacco tax cuts on cigarette smoking in Canada

OBJECTIVE: To assess the effect of the tobacco tax cuts made in 1994 on the smoking habits of Canadians. DESIGN: Population-based retrospective cohort study. DATA: Data from the Survey on Smoking in Canada conducted by Statistics Canada on 11,119 respondents 15 years of age and older, who were interviewed about their smoking habits on 4 occasions, approximately every 3 months from January 1994 to February 1995. OUTCOME MEASURES: Changes in smoking prevalence, incidence, quit rates and mean number of cigarettes smoked per day in the provinces where tobacco taxes were cut and in those where taxes were not cut. RESULTS: During the survey, smoking prevalence decreased in all provinces, whether or not cigarette taxes had been cut. However, the prevalence of smoking was greater in the provinces where tobacco taxes had been cut than in those where they had not, and this difference increased from 2.0% at the beginning of the survey to 3.4% by the end (p < 0.001). In addition, rates of starting cigarette smoking were higher and smoking quit rates were lower in the provinces where taxes had been cut than in those where taxes had not been cut. CONCLUSION: Although smoking rates are declining in Canada, tobacco tax cuts appear to have slowed the rate of decline by inducing more nonsmokers to take up smoking and leading fewer smokers to quit.     

Maternal smoking in pregnancy and sex differences in perinatal death between boys and girls

The sex difference in perinatal mortality in developed countries is largely unexplained. The current study evaluated the differences in the impact of maternal smoking during pregnancy on the risk of perinatal death between males and females. The analysis involved 11,469 and 9,404 newborns derived from two population-based birth cohorts in Northern Finland, for 1966 and 1985-86, respectively. The perinatal mortality rate was 23 per thousand in the 1966 cohort and 9 per thousand in the 1985-86 cohort. The rate ratio (RR) for mortality for males over females is 1.15 and 1.60 in the two cohorts, respectively. Among children whose mothers smoked during pregnancy, the RR was 2.2 (95% CI 1.0, 4.7) for the former cohort and 4.8 (95% CI 1.5, 15.2) for the later cohort; and among the children whose mothers did not smoke the corresponding RR was 1.2 (95% CI 0.9, 1.6) and 1.1 (95% CI 0.6, 1.9). Maternal smoking during pregnancy could be an important determinant accounting for the excess perinatal death for males over females. Our results encourage evaluation of the findings among other populations.     

Role of maternal exposures and newborn genotypes on newborn chromosome aberration frequencies

Maternal exposures may induce chromosome damage and birth defects in the fetus. Polymorphic variation in genes coding for enzymes involved in metabolic activation and detoxification of environmental procarcinogens may account for some of the differences in chromosome aberration frequencies in newborns. In this study, 40 mothers completed questionnaires regarding exposures they received during their pregnancy. Umbilical cord blood samples were analyzed for chromosome aberrations. An average of 1020 metaphase cell equivalents (equal to 1020 G-banded cells) were examined from each newborn. In 26 of the newborns, genotyping analysis was performed for genes functioning in metabolic activation and detoxification (cytochrome P450 genes: CYP2D6 and CYP1A1, and phase II genes: NAT1, NAT2, GSTT1, GSTM1, GSTP1, and epoxide hydrolase). A significant association between the CYP1A1 MspI polymorphism and chromosome aberration frequencies was observed in the newborns (p=0.02), with heterozygotes showing higher aberration frequencies than the wild type homozygotes. Some large differences in chromosome aberration frequencies for other genotypes were also noted, but these were not statistically significant. Exposure to tobacco smoke in utero also appeared to increase translocation frequencies. The mean frequency of translocations per 100 cell equivalents from newborns of mothers who smoked during pregnancy was significantly higher than that of newborns whose mothers did not smoke (0.21 vs. 0.11, respectively, p=0.045).