Risk of childhood cancer and adult lung cancer after childhood exposure to passive smoke: A meta-analysis

We identified more than 30 studies on the association between exposure to maternal tobacco smoke during pregnancy and cancer in childhood. We combined their results in meta-analyses based on a random effects model. The results of the meta-analyses suggest a small increase in risk of all neoplasms [relative risk (RR) 1.10; 95% confidence interval (CI), 1.03-1.19; based on 12 studies], but not of specific neoplasms such as leukemia (RR 1.05; CI, 0.82-1.34; 8 studies) and central nervous system tumors (RR 1.04; CI, 0.92-1. 18; 12 studies). Results for other specific neoplasms were sparse, but the available data did not suggest a strong association for any type of tumor. No clear evidence of dose response was present in the studies that addressed this issue. The results on exposure to maternal tobacco smoke before or after pregnancy are too sparse to allow a conclusion. The results on exposure to paternal tobacco smoke suggest an association with brain tumors (RR 1.22; CI, 1.05-1. 40; based on 10 studies) and lymphomas (RR 2.08; CI, 1.08-3.98; 4 studies). The data are too sparse for the other neoplasms, although the results of a few recent large studies are compatible with a weak carcinogenic effect of paternal smoke. For exposure from either maternal or paternal smoke, bias and confounding cannot yet be ruled out. Further studies are needed to confirm the hypothesis that parental tobacco smoke, from the father in particular, is a risk factor of childhood cancer. Results on the risk of lung cancer in adulthood and childhood passive smoking exposure are available from 11 studies: they do not provide evidence of an increased risk (summary RR 0.91; CI, 0.80-1.05).     

Maternal cigarette smoking and invasive meningococcal disease: a cohort study among young children in metropolitan Atlanta, 1989-1996

OBJECTIVES: This study assessed the association between maternal cigarette smoking during pregnancy and the risk of invasive meningococcal disease during early childhood. METHODS: Using a retrospective cohort study design, cases from an active surveillance project monitoring all invasive meningococcal disease in the metropolitan Atlanta area from 1989 to 1995 were merged with linked birth and death certificate data files. Children who had not died or acquired meningococcal disease were assumed to be alive and free of the illness. The Cox proportional hazards analysis was used to assess the independent association between maternal smoking and meningococcal disease. RESULTS: The crude rate of meningococcal disease was 5 times higher for children whose mothers smoked during pregnancy than for children whose mothers did not smoke (0.05% vs 0.01%). Multivariate analysis revealed that maternal smoking (risk ratio [RR] = 2.9; 95% confidence interval [CI] = 1.5, 5.7) and a mother's having fewer than 12 years of education (RR = 2.1; 95% CI = 1.0, 4.2) were independently associated with invasive meningococcal disease. CONCLUSIONS: Maternal smoking, a likely surrogate for tobacco smoke exposure following delivery, appears to be a modifiable risk factor for sporadic meningococcal disease in young children.     

Breast cancer incidence in women prenatally exposed to maternal cigarette smoke

BACKGROUND: Clinical studies show that maternal cigarette smoking reduces pregnancy estrogen levels. Women prenatally exposed to maternal cigarette smoke may, therefore, have a lower breast cancer risk because the fetal mammary gland's exposure to maternal estrogen is decreased. Associations between prenatal maternal cigarette smoke exposure and breast cancer, however, have not been observed in previous case-control studies that relied on exposure assessment after the onset of cancer. At the start of this study, cigarette smoking history was obtained directly from the mother. METHODS: The National Cooperative DES Adenosis project was a follow-up study of health outcomes in women prenatally exposed to diethylstilbestrol (DES). At the start of the study, women's mothers provided information about cigarette smoking habits during the time they were pregnant with the study participant. In the current study, the breast cancer rates are compared among 4031 women who were or were not prenatally exposed to maternal cigarette smoke. The resultant relative rate (RR) is adjusted for potential confounding by other breast cancer risk factors using Poisson regression modeling. RESULTS: Fetal exposure to maternal cigarette smoke appeared to be inversely associated with breast cancer incidence (RR = 0.49; 95% confidence interval [CI] = 0.24-1.03). The inverse association was more apparent among women whose mothers smoked 15 cigarettes or fewer per day than among daughters of heavier smokers. There were, however, too few cases to precisely estimate a possible dose-response relationship. CONCLUSION: These results support the hypothesis that in utero exposure to maternal cigarette smoke reduces breast cancer incidence.     

The effect of maternal smoking during pregnancy on intellectual disabilities among 8-year-old children

Prenatal tobacco smoke exposure has been implicated as a risk factor for cognitive deficits in children. The purpose of this study is to examine the association between prenatal tobacco smoke exposure and diagnosis of intellectual disabilities (ID) among 8-year-old children living in Arkansas, Georgia, North Carolina and Utah. In 2002 and 2004, 965 ID case children were identified through a surveillance network and compared with the population of children born in the surveillance region during the same period ( n  = 104 607). Prenatal tobacco smoke exposure was determined from birth certificates. We estimated the effect of prenatal tobacco smoke exposure (none, <10, 10–19 and ≥20 cigarettes per day) on ID using logistic regression.
Generally, the risk of ID was mildly elevated among children whose mothers smoked ≥20 cigarettes per day during pregnancy [RR 1.34; 95% (confidence interval) CI 0.96, 1.87] after adjustment for maternal education, maternal race, maternal age, marital status, child sex, birth year and study site. However, the effect of exposure to ≥20 cigarettes per day significantly differed for males [RR 1.77, 95% CI 1.20, 2.62] compared with females [RR 0.81, 95% CI 0.44, 1.50]. Supplemental analyses reveal substantial confounding of this relationship by socio-economic indicators. A differential effect of tobacco smoke exposure on the risk of ID is suggested for males and females and deserves further investigation; however, the interpretation is tempered by the potential for residual confounding.     

Tobacco smoke exposure at one month of age and subsequent risk of SIDS--a prospective study

The aim of this investigation was to identify the sources of postnatal exposure to tobacco smoke at 1 month of age and to examine their relation to sudden infant death syndrome (SIDS). The Tasmanian Infant Health Survey was a prospective cohort study undertaken from 1988 to 1995. It involved 9,826 infants (89% of eligible infants) at higher risk of SIDS. Subsequently 53 eligible infants died of SIDS. Hospital interviews were available on 51 and home interviews on 35 SIDS infants. Urinary cotinine assays were conducted using gas-liquid chromatography (n = 100). Within a predictive model that explained 63% of urinary cotinine variance, the strongest predictor of cotinine and also of SIDS was maternal smoking, though the effects of prenatal and postnatal smoking could not be separated. However, for particular smoking-related behaviors, there was a discordance between prediction of cotinine concentration and prediction of risk of SIDS. If smoking mothers did not smoke in the room with the baby, the cotinine level in the infant's urine was reduced by a little more than a half (p = 0.009), but this was not associated with a reduction in SIDS risk (odds ratio = 1.09, 95% confidence interval 0.47-2.55). Similarly, the presence of other adult resident smokers was associated with a 63% increase in urinary cotinine (p = 0.047) but not with increased SIDS risk (odds ratio = 0.69, 95% confidence interval 0.34-1.40). However, the study lacked the power to detect modest effects, that is, those altering risk less than twofold.     

Maternal,paternal and environmental tobacco smoking and breast feeding

The effects of environmental tobacco smoke (ETS) on breast-feeding patterns are poorly understood, while those of parental smoking on breast-feeding initiation vs. duration have not been clearly delineated. We conducted a prospective, population-based birth cohort study to examine the independent effects of maternal, paternal and ETS on breast-feeding initiation and duration. A total of 6747 Hong Kong Chinese infants were recruited and followed up in 1997-8. We obtained detailed household smoking history and recorded breast-feeding patterns in three follow-up interviews over 9 months. We found that both maternal and paternal smoking were associated with not initiating breast feeding (odds ratio [OR] for ever maternal smoking = 2.51, 95% confidence interval [CI] = 1.63, 3.86; OR for ever paternal smoking = 1.22, 95% CI = 1.08, 1.39). Exposure to ETS in utero and post partum were also related to not starting breast feeding (OR(ETS in utero) = 1.10, 95% CI = 0.99,1.24; OR(ETS post partum) = 1.21, 95% CI = 1.08, 1.36). These effects, however, did not persist for breast-feeding duration of < or = 4 months. Cox proportional hazards modelling confirmed the lack of association between any form of smoking and breast-feeding duration. Our findings suggest that smoking of any kind, during or after pregnancy, is a strong risk indicator for not initiating breast feeding. Smoking as a risk indicator for underlying socio-economic, demographic and psychosocial factors is probably responsible for most of the observed adverse effects, although we cannot rule out direct contributions from pathophysiological mechanisms. Public health strategies directed at these underlying factors should be vigorously pursued to reduce the adverse effects of tobacco on breast feeding and infant health in general.     

Tobacco smoke exposure and pregnancy outcome among working women. A prospective study at prenatal care centers in Orebro County, Sweden

Among 4,687 women undergoing prenatal care in Orebro County, Sweden, from October 1980 to June 1983, 678 nonsmokers reported passive exposure to tobacco smoke. Of these women, 267 had been passively exposed at work, and the risk ratio (RR) for intrauterine death (spontaneous abortion or stillbirth) among these pregnancies was increased to 1.53 (95% confidence interval (CI) 0.98-2.38) compared with pregnancies of unexposed working women. This could not be explained by age, previous spontaneous abortion, educational level, planning of pregnancy, or alcohol use. The effect was confined to first-trimester fetal loss (adjusted RR = 2.16, 95% CI 1.23-3.81), while active smoking was associated with intrauterine death after the first trimester. Passive exposure in the workplace was weakly associated with preterm birth (less than 37 weeks) but not with low birth weight (less than 2,500 g) among full-term livebirths. Active smoking clearly increased the risk of both of these outcomes. However, passive exposure in the home only did not seem to affect pregnancy outcome. The lack of quantitative exposure data points to the need for more research before passive exposure to tobacco smoke can be regarded as an established hazard to fetal development and survival.     

Cocaine use during pregnancy: perinatal outcomes

The relation between maternal cocaine use and perinatal outcomes was investigated among 17,466 non-Asian singleton deliveries in 1988 from the University of Illinois Perinatal Network data base in the metropolitan Chicago area. Elevated adjusted relative risks (RR) of low birth weight (RR = 2.8, 95% confidence interval (CI) 2.2-3.7), prematurity (RR = 2.4, 95% CI 1.9-3.1), abruptio placentae (RR = 4.5, 95% CI 2.4-8.5), and perinatal death (RR = 2.1, 95% CI 1.1-4.0) were observed for "any" cocaine users (n = 408) compared with women who did not use cocaine or any other drugs or alcohol (n = 17,058). There was an increased (although unstable) risk of intrapartum placenta previa not previously reported (RR = 2.3, 95% CI 1.0-5.1). The relative risk of small-for-gestational-age births for cocaine users who did not smoke (RR = 3.4, 95% CI 1.8-6.5) was greater than that for cocaine users who did (RR = 2.1, 95% CI 1.1-4.1). Irrespective of smoking status, cocaine use during pregnancy increased the risk of small-for-gestational-age births.     

Parental smoking behaviour and effects of tobacco smoke on children's health in Finland and Russia

BACKGROUND: There is little information on potential differences in smoking behaviour of parents between Finland and Russia and on the effects of environmental tobacco smoke (ETS) exposure on allergic and respiratory diseases among Finnish and Russian children. The aim of the study was to compare the smoking behaviour of parents and school children and to assess the relations of tobacco smoke exposure during pregnancy and childhood with occurrence of allergic diseases and respiratory infections among school children. METHODS: We conducted a population-based cross-sectional study in the neighbour towns across the border of Imatra in Finland and Svetogorsk in Russia. The study population consisted of 512 Finnish and 581 Russian school children aged 7-16 years (response rate 79%). RESULTS: Children's tobacco smoke exposure differed markedly between Finland and Russia. The risk of asthma was particularly related to high maternal smoking exposure during pregnancy (adjusted OR 3.51, 95% CI 1.00-12.3), infancy (3.34, 1.23-9.07) and currently (3.27, 1.26-8.48), and the risk of common cold was related to high combined parental smoking during infancy (1.83, 1.06-3.17) in Finnish children. Among Russian children allergic conjunctivitis was related to maternal smoking during infancy (4.53, 1.49-13.8) and currently (2.82, 1.07-7.44). CONCLUSIONS: Smoking behaviour of parents and ETS exposure during childhood differed markedly between Finland and Russia. Asthma was particularly increased in relation to high exposure to maternal smoking in Finland. The results suggest that more efforts should be directed to reducing tobacco smoke exposure of children in both Finland and Russia. (250 words).     

Prenatal Ambient Air Exposure to Polycyclic Aromatic Hydrocarbons and the Occurrence of Respiratory Symptoms over the First Year of Life

The purpose of the study was to test the hypothesis that infants with higher levels of prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) from fossil fuel combustion may be at greater risk of developing respiratory symptoms. The study was carried out in a cohort of 333 newborns in Krakow, Poland, followed over the first year of life, for whom data from prenatal personal air monitoring of mothers in the second trimester of pregnancy were available. The relative risks of respiratory symptoms due to prenatal PAHs exposure were adjusted for potential confounders (gender of child, birth weight, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke, and moulds in households) in the Poisson regression models. Increased risk related to prenatal PAH exposure was observed for various respiratory symptoms such as barking cough (RR = 4.80; 95% CI: 2.73–8.44), wheezing without cold (RR = 3.83; 95% CI: 1.18–12.43), sore throat (RR = 1.96; 95% CI: 1.38–2.78), ear infection (RR = 1.82; 95% CI: 1.03–3.23), cough irrespective of respiratory infections (RR=1.27; 95% CI: 1.07–1.52), and cough without cold (RR = 1.72; 95% CI: 1.02–2.92). The exposure to PAHs also had impact on the duration of respiratory symptoms. The effect of PAHs exposure on the occurrence of such symptoms as runny nose or cough was partly modified by the simultaneous exposure to postnatal passive smoking. The analysis performed for the duration of respiratory symptoms confirmed significant interaction between PAHs exposure and postnatal ETS for runny or stuffy nose (RR = 1.82; 95% CI: 1.57–2.10), cough (RR = 1.18; 95% CI: 0.99–1.40), difficulty in breathing (RR = 1.39; 95% CI: 1.01–1.92) and sore throat (RR = 1.74; 1.26–2.39). Obtained results support the hypothesis that prenatal exposure to immunotoxic PAHs may impair the immune function of the fetus and subsequently may be responsible for an increased susceptibility of newborns and young infants to respiratory infections.     

Maternal smoking during pregnancy and childhood obesity

A recent cohort study suggested that maternal smoking during pregnancy might be a risk factor for childhood obesity. Data from the obligatory school entry health examination in six Bavarian (Germany) public health offices in 1999-2000 were used to assess the relation between maternal smoking during pregnancy and childhood obesity (n = 6,483 German children aged 5.00-6.99 years). A body mass index greater than the 90th percentile was defined as overweight, and a body mass index greater than the 97th percentile was defined as obesity. The main exposure was maternal smoking during pregnancy. The prevalences of overweight and obesity, expressed as percentages, increased in the following order: never smoked (overweight: 8.1, 95% confidence interval (CI): 7.2, 9.0; obesity: 2.2, 95% CI: 1.7, 2.7); less than 10 cigarettes daily (overweight: 14.1, 95% CI: 11.1, 17.7; obesity: 5.7, 95% CI: 3.7, 8.2); and 10 or more cigarettes daily (overweight: 17.0, 95% CI: 10.1, 26.2; obesity: 8.5, 95% CI: 3.7, 16.1). The adjusted odds ratios for maternal smoking during pregnancy were 1.43 (95% CI: 1.07, 1.90) for overweight and 2.06 (95% CI: 1.31, 3.23) for obesity. A dose-dependent association between overweight/obesity and maternal smoking during pregnancy was observed that could not be explained by a wide range of confounders, suggesting that intrauterine exposure to inhaled smoke products rather than lifestyle factors associated with maternal smoking accounts for this finding.     

Exposure to tobacco smoke in utero and the risk of stillbirth and death in the first year of life

The authors examined the association between exposure to tobacco smoke in utero and the risk of stillbirth and infant death in a cohort of 25,102 singleton children of pregnant women scheduled to deliver at Aarhus University Hospital, Aarhus, Denmark, from September 1989 to August 1996. Exposure to tobacco smoke in utero was associated with an increased risk of stillbirth (odds ratio = 2.0, 95% confidence interval: 1.4, 2.9), and infant mortality was almost doubled in children born to women who had smoked during pregnancy compared with children of nonsmokers (odds ratio = 1.8, 95% confidence interval: 1.3, 2.6). Among children of women who stopped smoking during the first trimester, stillbirth and infant mortality was comparable with that in children of women who had been nonsmokers from the beginning of pregnancy. Conclusions were not changed after adjustment in a logistic regression model for the sex of the child; parity; or maternal age, height, weight, marital status, years of education, occupational status, and alcohol and caffeine intake during pregnancy. Approximately 25% of all stillbirths and 20% of all infant deaths in a population with 30% pregnant smokers could be avoided if all pregnant smokers stopped smoking by the sixteenth week of gestation.     

孕妇被动吸烟与低出生体重关系的Meta分析

目的分析孕妇孕早期和不同孕期被动吸烟对新生儿低出生体重的影响。方法通过Meta分析方法分析孕妇被动吸烟与新生儿低出生体重之间的关系。对NCBI、OVID-MEDLINE、CNKI、VIP以及CBM数据库进行检索(截止日期为2008年4月),结果报告合并OR值及95%CI。结果共获得26篇文献,其中队列研究20篇,病例对照研究6篇。总体分析,孕妇被动吸烟的合并效应值OR=1.65(95%CI:1.39～1.97);调整合并效应值OR=1.60(95%CI:1.25～2.05);最低和最高暴露量的合并效应值分别为OR=1.53(95%CI:1.14～2.04)和OR=2.53(95%CI:1.46～4.36);孕早期暴露的合并效应值OR=1.12(95%CI:0.82～1.55),没有统计学意义。结论孕妇被动吸烟增加新生儿低出生体重的危险性;孕中晚期可能是被动吸烟效应的敏感期;被动吸烟的阈值是否存在尚不明确。     

Passive smoking and behavioural problems in children: Results from the LISAplus prospective birth cohort study

Objective

To analyse the association between pre- and postnatal exposure to tobacco smoke and child behavioural problems and to further investigate the influence of trimester-specific exposure to maternal smoking and the impact of paternal smoking at home on the same outcome.

Methods

Data of 3097 German children recruited at birth for a population-based, prospective study were used. Detailed information on children's tobacco smoke exposure was collected by self-administered questionnaires at each follow-up. Behavioural outcomes were measured by the Strengths and Difficulties Questionnaire applied at 10-year follow-up.

Results

Children exposed to environmental tobacco smoke at home showed increased risks of hyperactivity/inattention problems. Only smoking during the entire pregnancy increased the risk for conduct and hyperactivity/inattention problems (proportional odds ratio (pOR)=1.58, 95% confidence interval (CI)=1.06–2.37 and pOR=1.67, CI=1.03–2.72). Pre- and postnatal exposure to paternal smoking was associated with hyperactivity/inattention problems in children of non-smoking mothers (pOR=1.97, CI=1.06–3.65). Effect estimates were adjusted for study centre, sex, parental educational level, mother's age at birth, having a single parent and time spent in front of a screen.

Conclusions

Not only maternal smoking during pregnancy but also paternal smoking at home should be considered as a risk for hyperactivity/inattention problems in children.     

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.     

Exposure to Tobacco Smoke in Utero and Subsequent Plasma Lipids,ApoB, and CRP among Adult Women in the MoBa Cohort

Background: Recent findings suggest that maternal smoking during pregnancy may play a role in the development of metabolic alterations in offspring during childhood. However, whether such exposure increases the risk of developing similar metabolic alterations during adulthood is uncertain.Objective: We evaluated the association of in utero exposure to maternal tobacco smoke with plasma lipids, apolipoprotein B (apoB), and C-reactive protein (CRP) in adulthood.Methods: The study was based on a subsample of the Norwegian Mother and Child Cohort Study (MoBa) and included 479 pregnant women with plasma lipids, apoB, and CRP measurements. Information on in utero exposure to tobacco smoke, personal smoking, and other factors were obtained from the women by a self-completed questionnaire at enrollment, at approximately 17 weeks of gestation.Results: Women exposed to tobacco smoke in utero had higher triglycerides [10.7% higher; 95% confidence interval (CI): 3.9, 17.9] and lower high-density lipoprotein cholesterol (HDL) (–1.9 mg/dL; 95% CI: –4.3, 0.5) compared with unexposed women, after adjusting for age, physical activity, education, personal smoking, and current body mass index (BMI). Exposed women were also more likely to have triglycerides ≥ 200 mg/dL [adjusted odds ratio (aOR) = 2.5; 95% CI: 1.3, 5.1] and HDL < 50 mg/dL (aOR = 2.3; 95% CI: 1.1, 5.0). Low-density lipoprotein cholesterol, total cholesterol, and apoB were not associated with the exposure. CRP was increased among exposed women; however, after adjustment for BMI, the association was completely attenuated.Conclusions: In this population, in utero exposure to tobacco smoke was associated with high triglycerides and low HDL in adulthood, 18–44 years after exposure.     

A case-control study of maternal smoking and congenital malformations

Summary. We conducted a population-based case-control study to assess the association between maternal smoking during pregnancy and the risk of giving birth to a child with a congenital malformation. Cases were all singleton livebirths with a congenital malformation recorded on the 1984–1986 Washington State Birth Records (n = 3284). The smoking histories of these mothers were compared to a randomly selected group of mothers with a singleton livebirth of a child without a malformation during these same years (n = 4500). When all malformations were taken as a group, there was no association with maternal smoking (relative risk (RR) = l.0, 95% CI 0.9–1.1). However, increased risks were observed for a number of specific malformations, including microcephalus (RR = 2.0, 95% CI 1.0–4.0), cleft defects (RR=1.4, 95% CI 1.0–2.0), and club foot (RR= 1.4, 95% CI 1.0–2.0). We did not find any association with Down's syndrome (RR=0.8, 95% CI 0.5–1.3) or any other malformation. We conclude that maternal smoking during pregnancy may be associated with an increased risk for some malformations.     

Does maternal smoking during pregnancy cause childhood overweight?

The objective of this study was to examine a possible association between maternal smoking in pregnancy and childhood overweight. From a population-based cohort of 5722 women from Trondheim, Bergen (Norway) and Uppsala (Sweden) enrolled in early pregnancy during 1986-92, a random sample of 482 women was selected for participation. They were followed up throughout pregnancy, and their children from birth until 5 years of age. Data on maternal smoking and diet, socio-economic determinants and breast feeding were recorded prospectively. During pregnancy and childhood, anthropometric measures were also recorded. Maternal smoking status was based on reported number of cigarettes smoked in week 17 of pregnancy. Child overweight was defined by body mass index (BMI) and sum of skinfold thickness (SFT) >or= 85th percentile at 5 years of age. Children of mothers who smoked in pregnancy had increased risk of overweight at 5 years of age (RR 2.5, 95% CI 1.5, 4.2 for BMI; and RR 1.8, 95% CI 1.1, 3.0 for SFT). Adjusting for maternal diet, breast feeding, maternal obesity and socio-economic status did not suggest confounding. However, adjustment for birthweight increased the observed risk. A linear increase in BMI and SFT was observed with increasing number of cigarettes smoked. In conclusion, smoking during pregnancy may be a risk factor for development of childhood overweight. This study may support the hypothesis of 'fetal origin of adult disease', but the risk of overweight associated with smoking during pregnancy was independent of intrauterine growth retardation, and may thus be attributed to specific effects of cigarette smoke.     

Active and passive smoking and risk of breast cancer by age 50 years among German women

Recent studies suggest that both active and passive smokers have an increased risk of breast cancer compared with women who have never been either actively or passively exposed. Data on lifetime active and passive smoking were collected in 1999-2000 from 468 predominantly premenopausal breast cancer patients diagnosed by age 50 years and 1,093 controls who had previously participated in a German case-control study conducted in 1992-1995. Compared with never active/passive smokers, former smokers and current smokers had odds ratios of 1.2 (95% confidence interval (CI): 0.8, 1.7) and 1.5 (95% CI: 1.0, 2.2), respectively, and ever active smokers had an odds ratio of 1.3 (95% CI: 0.9, 1.9). The risk increased with duration of smoking and decreased after cessation of smoking. Among never active smokers, ever passive smoking was associated with an odds ratio of 1.6 (95% CI: 1.1, 2.4). Exposure to environmental tobacco smoke during childhood or before the first pregnancy did not appear to increase breast cancer risk. At greatest risk were women who had a high level of exposure to both passive and active smoking (odds ratio = 1.8, 95% CI: 1.2, 2.7). This study strengthens the hypothesis of a causal relation between active and passive smoke exposures and breast cancer risk.     

Cigarette smoking during pregnancy in rural Nepal. Risk factors and effects of beta-carotene and vitamin A supplementation

OBJECTIVE: We examined risk factors of smoking and the association between smoking and pregnancy-related and 6-month infant mortality in rural Nepal, where 30% women reported smoking during pregnancy. DESIGN: Cross-sectional analysis of risk factors associated with smoking status and health consequences of smoking, using prospective data collected as part of a randomized community trial to examine the effect of maternal vitamin A or beta-carotene supplementation on maternal mortality. SETTING: Rural, southeastern plains of Nepal. SUBJECTS AND METHODS: A total of 17 767 women contributed at least one pregnancy during 3.5 y of the study. Data on cigarette or bidi (rolled tobacco) smoking were collected using a 7-day recall, twice during pregnancy. Associations between smoking status and maternal diet, morbidity profile, household socioeconomic status and serum concentration of retinol, carotenoids and tocopherols were examined. Further, relative risk (RR) and 95% confidence intervals (CI) were calculated to estimate supplement effects on pregnancy-related mortality, stratified by smoking status during pregnancy. RESULTS: Smokers were more likely to be older, illiterate and poor compared to nonsmokers. Fruit and vegetable consumption among smokers and nonsmokers did not vary. However, smokers were more likely to consume meat/fish/eggs and less likely to consume milk than nonsmokers. They were also more likely to report symptoms of vaginal bleeding, edema, severe headache and convulsions during pregnancy relative to nonsmokers. Mortality per 100,000 pregnancies appeared to be higher among smokers than nonsmokers in the placebo group (915 vs 584, RR=1.57, 95% CI: 0.80-3.08). beta-Carotene supplementation reduced pregnancy-related mortality both among smokers (RR=0.31 95% CI: 0.11-0.89) and nonsmokers (RR=0.41, 95% CI: 0.19-0.89). Similar results obtained with vitamin A supplementation were not statistically significant. Infant mortality up to 6 months was approximately 30% higher among smokers compared to nonsmokers in the placebo group both before and after adjusting for confounding factors. Neither supplement given to women reduced infant mortality. CONCLUSIONS: Cigarette smoking during pregnancy is associated with an increased risk of maternal and infant mortality in rural Nepal. beta-Carotene and to some extent vitamin A may reduce the risk of pregnancy-related mortality, but not infant mortality, among both smokers and nonsmokers.