Smoking In Offspring Research Articles

The intergenerational transmission of smoking in adulthood: A 25-year study of maternal and offspring maladaptive attributes

While smoking is a major cause of mortality and morbidity, and maternal smoking is a risk factor for smoking among their offspring, the mechanisms involved in the intergenerational transmission of smoking are not well understood. This study examines the pathways from maternal and adolescent child factors, and the parent–child relationship, to smoking among the adult offspring, approximately 25years later. Data for the present analysis were based on time waves 2 (T2; 1983) and 7 (T7; 2007–2009) of an on-going study of a community sample of mothers and their children. Offspring and mother X¯ ages were 14.1 and 40.0years, respectively, at T2, and 36.6 and 65.0years, respectively, at T7. At T2, trained interviewers administered individual structured interviews. Psychosocial questionnaires were self-administered at T7. Structural equation modeling (SEM) was used to analyze the interrelationships among maternal and offspring attributes (T2 and T7). SEM results indicated a satisfactory model fit (RMSEA=0.052; CFI=0.91; SRMR=0.057), and confirmed hypothesized pathways. One pathway linked maternal maladaptive attributes (T2) to the mother–adolescent child attachment relationship (T2), which was associated with the offspring's maladaptive attributes over time (T2 to T7), which then predicted the adult offspring's smoking (T7). Other pathways highlighted the stability of maternal smoking, the continuity of maladaptive attributes, and less offspring educational attainment as predictors of offspring smoking at T7. Findings suggest the importance of early interventions to treat maternal smoking, maternal and offspring maladaptive attributes, and the mother–child relationship in order to reduce risk factors for the intergenerational transmission of smoking behavior. Interventions which enhance educational success should also prove effective in reducing smoking.

Clinical correlates and heritability of erythrocyte eicosapentaenoic and docosahexaenoic acid content in the Framingham Heart Study

ObjectivesRed blood cell (RBC) levels of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA, the omega-3 index, expressed as a percent of total fatty acids) are inversely related to risk for cardiovascular disease (CVD). Although several mechanisms underlying this relationship have been proposed, understanding the associations between the omega-3 index and markers of CVD in the community can shed additional light on this question. The objectives of this study were to define the relations between the omega-3 index and clinical factors and to determine the heritability of the omega-3 index. MethodsRBC samples (n = 3196) drawn between 2005 and 2008 from participants in the Framingham Study [Examination 8 of the Offspring cohort plus Examination 3 of the Omni (minorities) cohort] were analyzed for fatty acid composition by gas chromatography. ResultsThe mean (SD) omega-3 index was 5.6% (1.7%). In multivariable regression models, the factors significantly and directly associated with the omega-3 index were age, female sex, higher education, fish oil supplementation, dietary intake of EPA + DHA, aspirin use, lipid pharmacotherapy, and LDL-cholesterol. Factors inversely associated were Offspring cohort, heart rate, waist girth, triglycerides and smoking. The total explained variability in the omega-3 index for the fully adjusted model was 73%, which included major components due to heritability (24%), EPA + DHA intake (25%), and fish oil supplementation (15%). ConclusionThe variability in the omega-3 index is determined primarily by dietary and genetic factors. An increased omega-3 index is associated with a generally cardioprotective risk factor milieu.

Relationship between body mass index of offspring and maternal smoking during pregnancy

To examine the relationship between maternal smoking during pregnancy and the body composition of offspring. Grade 4 elementary school children (n=1366; boys/girls, 724/642; 9-10 years old) were enrolled in this study. All parents answered a lifestyle questionnaire, and children underwent passive smoking tests. Urinary cotinine measurement and lifestyle screening test parameters (that is, body weight, body length, body mass index (BMI), obesity index (OI), blood tests for liver function and lipid profile and questions regarding maternal smoking and lifestyle) were evaluated in terms of their relationship with maternal smoking. In addition, urinary 8-hydroxydeoxyguanosine (8-OHdG) concentration was measured in 80 randomly selected children to assess its relationship with oxidative stress. Both BMI and OI were significantly higher in children whose mothers smoked during pregnancy than in those whose mothers never smoked (BMI: 17.2±2.7 vs 16.9±2.5 kg m(-2), P=0.016; OI: 2.7±14.3% vs 0.4±14.0%, P=0.003). The degree of elevation was positively correlated with the duration of maternal smoking. The increases in BMI and OI resulted from increased body weight and reduced height. The confounding factors-'breakfast with family', 'watching television at dinner', 'eating and drinking before sleep', 'watching television for >2 h', 'sleep duration <8 h' and 'playing sports'-were statistically significant. BMI and OI were significantly high in children whose mothers smoked during pregnancy in these six confounders. On the other hand, urinary 8-OHdG concentration was negatively correlated with BMI in children who had >1.3 ng ml(-1) urinary cotinine, suggesting that it may be related to basal metabolism due to oxidative stress. Maternal smoking is a risk factor for higher BMI and OI in 9- to 10-year-old children whose mothers smoke during pregnancy and may be independent of other confounding factors.

Parent, sibling and peer influences on smoking initiation, regular smoking and nicotine dependence. Results from a genetically informative design

We sought to determine whether parenting, sibling and peer influences are associated with offspring ever smoking, regular smoking and nicotine dependence (ND) after controlling for familial factors. We used a twin-family design and data from structured diagnostic surveys of 1919 biological offspring (ages 12–32 years), 1107 twin fathers, and 1023 mothers. Offspring were classified into one of four familial risk groups based on twin fathers' and their co-twins' history of DSM-III-R nicotine dependence. Multivariate multinomial logistic regression was used to model familial risk, paternal and maternal parenting behavior and substance use, sibling substance use, and friend and school peer smoking, alcohol and drug use. Ever smoking was associated with increasing offspring age, white race, high maternal pressure to succeed in school, sibling drug use, and friend smoking, alcohol and drug use. Offspring regular smoking was associated with these same factors with additional contribution from maternal ND. Offspring ND was associated with increasing offspring age, male gender, biological parents divorce, high genetic risk from father and mother ND, maternal problem drinking, maternal rule inconsistency and sibling drug use, and friend smoking, alcohol and drug use. Friend smoking had the largest magnitude of association with offspring smoking. This effect remains after accounting for familial liability and numerous parent and sibling level effects. Smoking interventions may have greatest impact by targeting smoking prevention among peer groups in adolescent and young adult populations.

Advancing maternal age is associated with lower bone mineral density in young adult male offspring

SummaryAdvancing maternal age has been related to increased risk of fetal death and morbidity, as well as higher fracture risk during childhood, in the offspring. In the present study, we demonstrate that advancing maternal age is independently associated with reduced bone mass in the young adult male offspring.IntroductionIn Sweden the maternal age in both primi- and multipara mothers has steadily increased during the last three decades. It has been previously reported that advancing maternal age increases the risk of fetal death, but also of morbidity in the offspring, such as chromosome abnormalities, leukemia, diabetes mellitus type 1, and schizophrenia. Whether or not maternal age influences peak bone mass has not been reported. The aim of the present study was to investigate whether a high maternal age was associated with lower peak bone mass, as measured using DXA in a large cohort of male offspring [the Gothenburg Osteoporosis and Obesity Determinants study (GOOD)].MethodsThrough the Swedish multi-generation register, we identified the mothers of 1,009 GOOD study subjects. From the Swedish medical birth register detailed information about the medical circumstances at the time of child birth were obtained, including maternal and offspring anthropometrics (birth height and weight), maternal age, and smoking habits, parity and length of pregnancy.ResultsMaternal age was inversely correlated to areal BMD (aBMD) at the total body (r =−0.07, p = 0.03) and the lumbar spine (r =−0.09, p < 0.01). Using a linear regression model (with covariates including current physical activity, smoking, calcium intake, weight, present height and birth height, total body lean and fat mass in the offspring, and length of pregnancy), we found that maternal age negatively independently predicted lumbar spine aBMD (β =−0.08, p < 0.01) in the male offspring.ConclusionsIn conclusion, our results suggest that advancing maternal age could negatively affect bone mass in young adult men.

Contribution of Parental Psychopathology to Offspring Smoking and Nicotine Dependence in a Genetically Informative Design

It is not known if parental psychiatric disorders have an independent effect on offspring smoking after controlling for genetic and environmental vulnerability to nicotine dependence. We tested if parental alcohol, drug, or conduct disorders; antisocial personality disorder; depression; and anxiety disorders remained significant predictors of offspring smoking initiation, regular smoking, and nicotine dependence before and after adjusting for genetic and environmental risk for nicotine dependence. Data were obtained via semi-structured interviews with 1,107 twin fathers, 1,919 offspring between the ages of 12 and 32, and 1,023 mothers. Genetic and environmental liability for smoking outcomes was defined by paternal and maternal nicotine dependence. Multinomial logistic regression models were computed to estimate the risk for offspring trying cigarettes, regular smoking, and the Fagerström Test for Nicotine Dependence (FTND) as a function of parental psychopathology and sociodemographics before and after adjusting for genetic and environmental vulnerability to nicotine dependence. Before adjusting for genetic and environmental risk for nicotine dependence, ever trying cigarettes was associated with maternal depression, regular smoking was associated with maternal alcohol dependence and maternal conduct disorder, and FTND was associated with paternal and maternal conduct disorder and antisocial personality disorder. No parental psychopathology remained significantly associated with regular smoking and FTND after adjusting for genetic and environmental vulnerability to nicotine dependence in a multivariate model. The association between parental psychopathology and offspring smoking outcomes is partly explained by genetic and environmental risk for nicotine dependence. Point estimates suggest a trend for an association between parental antisocial personality disorder and offspring regular smoking and nicotine dependence after adjusting for genetic and environmental vulnerability. Studies in larger samples are warranted.

Parental Smoking and Adolescent Smoking Initiation: An Intergenerational Perspective on Tobacco Control

Adolescence is an important period of risk for the development of lifelong smoking behaviors. Compelling, although inconsistent, evidence suggests a relationship between parental smoking and the risk of smoking initiation during adolescence. This study investigates unresolved issues concerning the strength and nature of the association between parent smoking and offspring smoking initiation. We enrolled 564 adolescents aged 12 to 17, along with 1 of their parents, into the New England Family Study between 2001 and 2004. Lifetime smoking histories were obtained from parents and their adolescent offspring. Discrete-time survival analysis was used to investigate the influence of parental smoking histories on the risk of adolescent smoking initiation. Parental smoking was associated with a significantly higher risk of smoking initiation in adolescent offspring. In addition, the likelihood of offspring smoking initiation increased with the number of smoking parents and the duration of exposure to parental smoking, suggesting a dose-response relationship between parental smoking and offspring smoking. Offspring of parents who had quit smoking were no more likely to smoke than offspring of parents who had never smoked. The effects of parental smoking on offspring initiation differed by sex (with a stronger effect of fathers' smoking on boys than girls), developmental period (with a stronger effect of parental smoking before the adolescent was age 13 than afterward), and residence of parents (with effects of fathers' smoking being dependent on living in the same household as the adolescent). Parental smoking was also associated with stronger negative reactions to adolescents' first cigarette, a potential marker of the risk of progression to higher levels of use. Parental smoking is an important source of vulnerability to smoking initiation among adolescents, and parental smoking cessation might attenuate this vulnerability.

Educational attainment and smoking among women: Risk factors and consequences for offspring

We examine the association between education and smoking by women in the population, including smoking during pregnancy, and identify risk factors for smoking and the consequences of smoking in pregnancy for children's smoking and behavioral problems. Secondary analyses of four national data sets were implemented: The National Survey of Drug Use and Health (2006), the National Longitudinal Survey of Youth (1979–2004); the National Longitudinal Survey of Adolescent Health (Wave III); National Health and Nutrition Examination Survey (2005–2006). The lower the level of education, the greater the risk of being a current smoker, smoking daily, smoking heavily, being nicotine dependent, starting to smoke at an early age, having higher levels of circulating cotinine per cigarettes smoked, and continuing to smoke in pregnancy. The educational gradient is especially strong in pregnancy. Educational level and smoking in pregnancy independently increase the risk of offspring smoking and antisocial and anxious/depressed behavior problems. These effects persist with control for other covariates, except maternal age at child's birth, which accounts for the impact of education on offspring smoking and anxious/depressed behavior problems. Women with low education should be the target of public health efforts toward reducing tobacco use. These efforts need to focus as much on social conditions that affect women's lives as on individual level interventions. These interventions would have beneficial effects not only for the women themselves but also for their offspring.

Parental Smoking and Vascular Damage in Young Adult Offspring: Is Early Life Exposure Critical?

Our purpose was to study the association between familial and particularly fetal tobacco smoke exposure and vascular damage in young adulthood. From a cohort of 732 young adults, birth data were collected and in young adulthood ultrasound measurement of common carotid artery intima-media thickness (CIMT) was performed. Data on parental smoking were obtained by standardized questionnaires. Twenty-nine percent of the mothers smoked during pregnancy. Offspring of mothers who smoked had 13.4 microm thicker CIMT (95% CI: 5.5, 21.3; P=0.001) than offspring of mothers who did not smoke in pregnancy. Adjustment for known CIMT risk factors (participant's age, gender, BMI, pulse pressure, and LDL-cholesterol) yielded no change (9.4 microm, 95% CI: 1.9, 16.3, P=0.01) nor did adjustment for current smoking of parents (10.6 microm, 95% CI: 0.4 to 20.8, P=0.04), for participants' current smoking and pack-years (11.5 microm, 95% CI: 3.5 to 19.4, P=0.004) or for parental socioeconomic status (SES; 13.0 microm, 95% CI: 5.0, 21.1, P=0.002). Thicker CIMT was associated with exclusive paternal smoking in pregnancy, somewhat stronger with exclusive maternal smoking and strongest with both parents smoking (P (linear trend)=0.001). Offspring of particularly mothers who smoked an above median number of cigarettes in pregnancy had thicker CIMT than those smoking less than median or no cigarettes (P (linear trend) <0.0001). Permanent vascular damage is partly attributable to familial tobacco smoke exposure, an association that might be initiated in gestation.

Maternal smoking during pregnancy and multiple sclerosis amongst offspring

An association between parental smoking and multiple sclerosis (MS) in offspring has been reported. This study examined whether maternal smoking during pregnancy is associated with MS in offspring. Swedish general population registers provided prospectively recorded information on maternal smoking during pregnancy. The study identified 143 cases with MS diagnosed by 2006 and 1730 matched controls. Subjects were born since 1982 and individually matched by year of birth, age, sex and region of residence. Conditional logistic regression assessed the association of maternal smoking with MS in offspring with adjustment for socioeconomic index. Maternal smoking during pregnancy was not associated with MS in offspring, with an odds ratio (and 95% confidence interval) of 0.96 (0.65-1.44). When stratified by paediatric or later MS onset there was no association with maternal smoking in either stratum. It is unlikely that smoking during pregnancy represents a risk for early-onset MS amongst offspring.

Parental smoking and vascular damage in young adult offspring: is early life exposure critical? The Atherosclerosis Risk in Young Adults study

Parental smoking and vascular damage in young adult offspring: is early life exposure critical? The Atherosclerosis Risk in Young Adults study

Adolescent Environmental Tobacco Smoke Exposure Predicts Academic Achievement Test Failure

Purpose Research has linked prenatal tobacco exposure to neurocognitive and behavioral problems that can disrupt learning and school performance in childhood. Less is known about its effects on academic achievement in adolescence when controlling for known confounding factors (e.g., environmental tobacco smoke [ETS]). We hypothesized that prenatal tobacco exposure would decrease the likelihood of passing academic achievement tests taken at 16 and 18 years of age. Methods This study was a longitudinal analysis of birth cohort data including 6,380 pregnant women and offspring from the 1958 National Child Development Study (NCDS). Academic pass/fail performance was measured on British standardized achievement tests (“Ordinary Level” [O-Level] and Advanced Level: [A-Level]). Prenatal tobacco exposure plus controlling variables (ETS, teen offspring smoking and gender, maternal age at pregnancy, maternal smoking before pregnancy, and socioeconomic status) were included in regression models predicting O- and A-Level test failure. Results Significant predictors of test failure in the O-Level model included exposure to maternal (OR = 0.71, p < .0001) and paternal (OR = 0.70, p < .0001) ETS, as well as teen smoking, female gender, and lower SES. Prenatal tobacco exposure did not influence failure. Similar factors emerged in the A-Level model except that male gender contributed to likelihood of failure. Prenatal exposure remained nonsignificant. Conclusions Our model suggests that adolescent exposure to ETS, not prenatal tobacco exposure, predicted failure on both O- and A-Level achievement tests when controlling for other factors known to influence achievement. Although this study has limitations, results bolster growing evidence of academic-related ETS consequences in adolescence.

Gender-Specific Effects of Prenatal and Adolescent Exposure to Tobacco Smoke on Auditory and Visual Attention

Prenatal exposure to active maternal tobacco smoking elevates risk of cognitive and auditory processing deficits, and of smoking in offspring. Recent preclinical work has demonstrated a sex-specific pattern of reduction in cortical cholinergic markers following prenatal, adolescent, or combined prenatal and adolescent exposure to nicotine, the primary psychoactive component of tobacco smoke. Given the importance of cortical cholinergic neurotransmission to attentional function, we examined auditory and visual selective and divided attention in 181 male and female adolescent smokers and nonsmokers with and without prenatal exposure to maternal smoking. Groups did not differ in age, educational attainment, symptoms of inattention, or years of parent education. A subset of 63 subjects also underwent functional magnetic resonance imaging while performing an auditory and visual selective and divided attention task. Among females, exposure to tobacco smoke during prenatal or adolescent development was associated with reductions in auditory and visual attention performance accuracy that were greatest in female smokers with prenatal exposure (combined exposure). Among males, combined exposure was associated with marked deficits in auditory attention, suggesting greater vulnerability of neurocircuitry supporting auditory attention to insult stemming from developmental exposure to tobacco smoke in males. Activation of brain regions that support auditory attention was greater in adolescents with prenatal or adolescent exposure to tobacco smoke relative to adolescents with neither prenatal nor adolescent exposure to tobacco smoke. These findings extend earlier preclinical work and suggest that, in humans, prenatal and adolescent exposure to nicotine exerts gender-specific deleterious effects on auditory and visual attention, with concomitant alterations in the efficiency of neurocircuitry supporting auditory attention.

Chronic neonatal nicotine increases anxiety but does not impair cognition in adult rats.

Developmental nicotine exposure has been implicated in the association between maternal smoking and adverse outcomes in offspring. The 3rd trimester of human pregnancy is equivalent to the 1st postnatal week in rodents; both are periods of active brain growth during which nicotinic acetylcholine receptors are transiently upregulated. Chronic neonatal nicotine (CNN; 6 mg/kg/day) from postnatal Days 1 to 7 was given orally to rat pups to evaluate long-term behavioral effects. Males and females were tested as adolescents or as young adults. CNN significantly decreased center time, ambulatory behavior, and rearing in the open-field test and decreased the number of entrances and time spent in the open arm of the elevated plus-maze in both sexes and ages. CNN did not change performance in the T maze or in the water maze in adult males or females. Motor coordination was not altered. In summary, CNN had long-term effects on anxiety-like behavior but did not affect spatial learning and memory functions. This finding is particularly important when evaluating the benefits of nicotine-replacement therapies during human pregnancies, which may improve smoking cessation rates but could result in long-term behavioral consequences.

Increased nicotine self-administration following prenatal exposure in female rats

There is a significant association between maternal cigarette smoking during pregnancy and greater subsequent risk of smoking in female offspring. In animal models, prenatal nicotine exposure causes persistent alterations in cholinergic and monoaminergic systems, both of which are important for nicotine actions underlying tobacco addiction. Accordingly, the current study was conducted to determine if there is a cause-and-effect relationship between prenatal nicotine exposure and nicotine self-administration starting in adolescence. Pregnant rats were administered nicotine (6 mg/kg/day) by osmotic minipump infusion throughout gestation and then, beginning in adolescence and continuing into adulthood, female offspring were given access to nicotine via a standard operant IV self-administration procedure (0.03 mg/kg/infusion). Gestational nicotine exposure did not alter the initial rate of nicotine self-administration. However, when animals underwent one week of forced abstinence and then had a second opportunity to self-administer nicotine, the prenatally-exposed animals showed a significantly greater rate of self-administration than did the controls. Prenatal nicotine exposure causes increased nicotine self-administration, which is revealed only when the animals are allowed to experience a period of nicotine abstinence. This supports a cause-and-effect relationship between the higher rates of smoking in the daughters of women who smoke cigarettes during pregnancy and implicates a role for nicotine in this effect. Our results further characterize the long-term liabilities of maternal smoking but also point to the potential liabilities of nicotine-based treatments for smoking cessation during pregnancy.

Cohort trends in prevalence and spousal concordance for smoking

Evaluation of the pattern of smoking prevalence over time could provide insight for disease prevention and tobacco control policy. Examination of assortative mating is important in assessing the relative contribution of genetic and environmental influences in behavior genetics. A significant spousal concordance for smoking could imply assortative mating behavior and have potential influence on the risk for offspring smoking. Using intergenerational data from large scale adult twin panels in Australia, the present study examined the patterns of prevalence and spousal concordance of lifetime smoking across a wide range of birth cohorts. Data were collected for more than 16,000 twins, their spouses, parents, and parents-reported grandparents. The measurement models were used to calculate prevalence and spousal concordance for smoking. Prevalence of lifetime smoking for females increased significantly over successive cohorts, and was higher for twins (0.28–0.49) than for their parents or grandparents (0.06–0.42). Smoking prevalence was still higher in males than in females for the twins (0.49–0.69), and parental or grandparental (0.62–0.77) generations, but the gender differences largely decreased in younger cohorts. Moderate but significant spousal correlations were found across cohorts and generations, which were higher for twins (0.39–0.55) than for their parents and grandparents (0.19–0.49). Despite using a simplified smoking assessment, findings in this study demonstrated changes of lifetime smoking patterns across birth cohorts and the presence of assortative mating for smoking behavior.

Parental smoking and allergic sensitisation in offspring defined by skin prick testing

Pediatric Allergy and ImmunologyVolume 17, Issue 4 p. 314-314 Parental smoking and allergic sensitisation in offspring defined by skin prick testing Scott M Montgomery, Scott M Montgomery The Clinical Research Centre, Örebro University Hospital, Örebro Clinical Epidemiology Unit, Departement of Medicine, Karolinska Hospital, Karolinska Institutet, StockholmSearch for more papers by this authorMatz L Larsson, Matz L Larsson Department of Lung Medicine, Örebro University Hospital, Örebro, Sweden E-mail: matz.larsson@orebroll.seSearch for more papers by this author Scott M Montgomery, Scott M Montgomery The Clinical Research Centre, Örebro University Hospital, Örebro Clinical Epidemiology Unit, Departement of Medicine, Karolinska Hospital, Karolinska Institutet, StockholmSearch for more papers by this authorMatz L Larsson, Matz L Larsson Department of Lung Medicine, Örebro University Hospital, Örebro, Sweden E-mail: matz.larsson@orebroll.seSearch for more papers by this author First published: 06 June 2006 https://doi.org/10.1111/j.1399-3038.2006.00384.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume17, Issue4June 2006Pages 314-314 RelatedInformation

Maternal smoking during late pregnancy and offspring smoking behaviour

We explored the influence of maternal smoking during late pregnancy on the likelihood of smoking among offspring in adolescence and adulthood, using birth cohort data collected in the United Kingdom as part of the 1958 National Child Development Study. Longitudinal analysis indicated that maternal smoking during late pregnancy was associated with an increased likelihood of being a non-smoker at 16-year, 23-year and 33-year follow-up. This association differed between male and female offspring, with women showing no significant association and men showing an increased likelihood of being a non-smoker. There did not appear to be any association between maternal smoking during late pregnancy and cigarette consumption among offspring who reported smoking for either sex. These results are inconsistent with some previous reports that maternal smoking during pregnancy increases the likelihood of smoking among female offspring, although the observation of a moderating effect of sex on smoking behaviour is consistent with several previous reports. We discuss possible mechanisms for this association, and suggest factors that may account for the observed sex differences in this association, and the discrepancy between our results and some previous reports.

Parental and peer influences on smoking among young adults: ten-year follow-up of the Oslo youth study participants.

This study was designed to investigate the impact of family and peer role models during the early adolescent years on smoking onset and on subsequent daily smoking among young adults. Baseline data were collected from a sample of 827 students and their parents in 1979. Participating students were recruited among 5th, 6th and 7th graders (11-14 years old) attending six schools in Oslo, Norway. The same students were invited to participate in a 2-year follow-up survey in 1981 and in a 10-year follow-up survey in 1989 when their average age was 23.4 years. Both at baseline and in 1981, smoking (experimental or regular) was strongly associated with smoking behaviour of friends and siblings. Parental smoking and parents' educational level were not significant predictors of their offspring's smoking in 1979. While friends' smoking in 1979 or 1981 remained a significant bivariate predictor of daily smoking in 1989, mother's baseline smoking emerged, in multivariate analysis, as the most important long-term predictor of daily smoking among young adults. These results point to the importance of including parents in smoking prevention efforts targeting adolescents.

Longitudinal analysis of the effect of prenatal nicotine exposure on subsequent smoking behavior of offspring

We explored the influence of maternal smoking during pregnancy on the likelihood of smoking among offspring in adolescence and adulthood using data from two similar British birth cohort surveys, the 1958 National Child Development Study and the 1970 British Birth Survey. Similar information was available in each cohort on maternal age at delivery, offspring sex, maternal smoking during pregnancy, parental and offspring socioeconomic status, and parental smoking at the time offspring smoking was assessed at age 16 years. Offspring smoking at 16 years and at 30/33 years were the primary outcomes of interest. Our data support an association between maternal smoking during pregnancy and an increased risk of offspring smoking later in life among female offspring but not among male offspring. Female offspring of mothers who smoked during pregnancy were more likely to smoke at 16 years than were their male counterparts. Moreover, in this same subgroup, female offspring smoking at 16 years was associated with an increased likelihood of smoking at 30/33 years. Further investigation in larger studies with greater detail of factors shaping smoking in childhood and adulthood and biochemically verified outcome measures would be desirable to clarify the relationship.