The Prevalence, Trends and Heterogeneity in Maternal Smoking Around Birth Between the 1930s and 1970s

James J.

AbstractOn March 7, 1962 the Royal College of Physicians published a report entitled Smoking and Health that made the causal link between smoking and lung cancer clear and explicit. Using a historical data set that contains information on smoking from 1958 to 1965, I find a decrease in smoking for those with more schooling after the report's publication. I do not find a difference in the effect for those with greater access to information (measured by TV ownership or newspaper readership). This suggests the education health gradient is more likely due to processing of information rather than access to information.

Singleton J.

Abstract This article examines the Attlee government’s performance as a crisis manager in relation to tobacco policy in the years prior to the publication in 1950 of research linking smoking and cancer. Health concerns played no role in tobacco policy before 1950, and the government hoped more teenagers would take up smoking and pay tobacco duty. Tobacco took on added significance as an economic issue because policy-makers had so little room for manoeuvre. Their task was to balance the desire of consumers to smoke as much as they liked at a reasonable price, the exchequer’s need to raise revenue from tobacco duties, and the imperative to conserve scarce dollars. Tobacco was an economic and financial rather than a health issue in the late 1940s and the authorities juggled competing demands creditably. This article examines previously neglected but important aspects of the histories of tobacco and of the Attlee government’s economic policies.

Becker J., Burik C.A., Goldman G., Wang N., Jayashankar H., Bennett M., Belsky D.W., Karlsson Linnér R., Ahlskog R., Kleinman A., Hinds D.A., Agee M., Alipanahi B., Auton A., Bell R.K., et. al.

Polygenic indexes (PGIs) are DNA-based predictors. Their value for research in many scientific disciplines is growing rapidly. As a resource for researchers, we used a consistent methodology to construct PGIs for 47 phenotypes in 11 datasets. To maximize the PGIs’ prediction accuracies, we constructed them using genome-wide association studies—some not previously published—from multiple data sources, including 23andMe and UK Biobank. We present a theoretical framework to help interpret analyses involving PGIs. A key insight is that a PGI can be understood as an unbiased but noisy measure of a latent variable we call the ‘additive SNP factor’. Regressions in which the true regressor is this factor but the PGI is used as its proxy therefore suffer from errors-in-variables bias. We derive an estimator that corrects for the bias, illustrate the correction, and make a Python tool for implementing it publicly available. Benjamin et al. construct polygenic indexes (DNA-based predictors) for 47 phenotypes and make them available to researchers in 11 datasets. They also present a theoretical framework and estimator to help interpret analyses using polygenic indexes.

Pereira R.D., Rietveld C.A., van Kippersluis H.

AbstractIt is well-established that both the child’s genetic endowments as well as maternal smoking during pregnancy impact offspring birth weight. In this paper we move beyond the natureversusnurture debate by investigating the interaction between genetic endowments and this critical prenatal environmental exposure – maternal smoking – in determining birth weight. We draw on longitudinal data from the Avon Longitudinal Study of Parents and Children (ALSPAC) study and replicate our results using data from the UK Biobank. Genetic endowments of the children are proxied with a polygenic score that is constructed based on the results of the most recent genome-wide association study of birth weight. We instrument the maternal decision to smoke during pregnancy with a genetic variant (rs1051730) located in the nicotine receptor gene CHRNA3. This genetic variant is associated with the number of cigarettes consumed daily, and we present evidence that this is plausibly the only channel through which the maternal genetic variant affects the child’s birth weight. Additionally, we deal with the misreporting of maternal smoking by using measures of cotinine, a biomarker of nicotine, collected from the mother’s urine during their pregnancy. We confirm earlier findings that genetic endowments as well as maternal smoking during pregnancy significantly affects the child’s birth weight. However, we do not find evidence of meaningful interactions between genetic endowments and an adverse fetal environment, suggesting that the child’s genetic predisposition cannot cushion the damaging effects of maternal smoking.

Yang Q., Millard L.A., Davey Smith G.

Abstract Background A lack of genetic data across generations makes transgenerational Mendelian randomization (MR) difficult. We used UK Biobank and a novel proxy gene-by-environment MR to investigate effects of maternal smoking heaviness in pregnancy on offspring health, using participants’ (generation one: G1) genotype (rs16969968 in CHRNA5) as a proxy for their mothers’ (G0) genotype. Methods We validated this approach by replicating an established effect of maternal smoking heaviness on offspring birthweight. Then we applied this approach to explore effects of maternal (G0) smoking heaviness on offspring (G1) later life outcomes and on birthweight of G1 women’s children (G2). Results Each additional smoking-increasing allele in offspring (G1) was associated with a 0.018 [95% confidence interval (CI): -0.026, -0.009] kg lower G1 birthweight in maternal (G0) smoking stratum, but no meaningful effect (-0.002 kg; 95% CI: -0.008, 0.003) in maternal non-smoking stratum (interaction P-value = 0.004). The differences in associations of rs16969968 with grandchild’s (G2) birthweight between grandmothers (G0) who did, versus did not, smoke were heterogeneous (interaction P-value = 0.042) among mothers (G1) who did (-0.020 kg/allele; 95% CI: -0.044, 0.003), versus did not (0.007 kg/allele; 95% CI: -0.005, 0.020), smoke in pregnancy. Conclusions Our study demonstrated how offspring genotype can be used to proxy for the mother’s genotype in gene-by-environment MR. We confirmed the causal effect of maternal (G0) smoking on offspring (G1) birthweight, but found little evidence of an effect on G1 longer-term health outcomes. For grandchild’s (G2) birthweight, the effect of grandmother’s (G0) smoking heaviness in pregnancy may be modulated by maternal (G1) smoking status in pregnancy.

Kuehnle D.

Studies examining the introduction of pictorial warnings on cigarette packages provide inconclusive evidence due to small samples and methodological issues. We use individual-level panel data from Australia to examine the association between pictorial warnings and smoking behaviour - prevalence, quitting, initiating and relapsing. The pictorial warnings were accompanied by a reference to a smoking cessation helpline and supportive television commercials. Applying an event study framework, we show that the reform reduced smoking rates by around 4% within the first year of the policy. The effect decreases with age, is similar for men and women, and is slightly larger for low-educated compared to high-educated individuals. The reform permanently lowered smoking rates primarily due to increased quitting in the year of the reform. Thus, pictorial warnings combined with a reference to a smoking cessation helpline and supportive media campaigns are an important tobacco control measure to reduce the social costs of smoking.

Liu M., Jiang Y., Wedow R., Li Y., Brazel D.M., Chen F., Datta G., Davila-Velderrain J., McGuire D., Tian C., Zhan X., Choquet H., Docherty A.R., Faul J.D., Foerster J.R., et. al.

Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders1. They are heritable2,3 and etiologically related4,5 behaviors that have been resistant to gene discovery efforts6–11. In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association. Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco and alcohol use, including genes involved in nicotinic, dopaminergic, and glutamatergic neurotransmission. The results provide a solid starting point to evaluate the effects of these loci in model organisms and more precise substance use measures. Association studies of up to 1.2 million individuals identify 566 genetic variants in 406 loci associated with tobacco use and addiction (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci showing pleiotropic association.

Almond D., Currie J., Duque V.

That prenatal events can have life-long consequences is now well established. Nevertheless, research on the fetal origins hypothesis is flourishing and has expanded to include the early childhood (postnatal) environment. Why does this literature have a “second act?” We summarize the major themes and contributions driving the empirical literature since our 2011 reviews, and try to interpret the literature in light of an overarching conceptual framework about how human capital is produced early in life. One major finding is that relatively mild shocks in early life can have substantial negative impacts, but that the effects are often heterogeneous reflecting differences in child endowments, budget constraints, and production technologies. Moreover, shocks, investments, and interventions can interact in complex ways that are only beginning to be understood. Many advances in our knowledge are due to increasing accessibility of comprehensive administrative data that allow events in early life to be linked to long-term outcomes. Yet, we still know relatively little about the interval between, and thus about whether it would be feasible to identify and intervene with affected individuals at some point between early life and adulthood. We do know enough, however, to be able to identify some interventions that hold promise for improving child outcomes in early life and throughout the life course. (JEL I12, J13, J16, Q51, Q53)

Kong A., Thorleifsson G., Frigge M.L., Vilhjalmsson B.J., Young A.I., Thorgeirsson T.E., Benonisdottir S., Oddsson A., Halldorsson B.V., Masson G., Gudbjartsson D.F., Helgason A., Bjornsdottir G., Thorsteinsdottir U., Stefansson K.

Genetic variants provide a nurturing environment Genetic variants in parents may affect the fitness of their offspring, even if the child does not carry the allele. This indirect effect is referred to as “genetic nurture.” Kong et al. used data from genome-wide association studies of educational attainment to construct polygenic scores for parents that only considered the nontransmitted alleles (see the Perspective by Koellinger and Harden). The findings suggest that genetic nurture is ultimately due to genetic variation in the population and is mediated by the environment that parents create for their children. Science , this issue p. 424 ; see also p. 386

Fry A., Littlejohns T.J., Sudlow C., Doherty N., Adamska L., Sprosen T., Collins R., Allen N.E.

The UK Biobank cohort is a population-based cohort of 500,000 participants recruited in the United Kingdom (UK) between 2006 and 2010. Approximately 9.2 million individuals aged 40-69 years who lived within 25 miles (40 km) of one of 22 assessment centers in England, Wales, and Scotland were invited to enter the cohort, and 5.5% participated in the baseline assessment. The representativeness of the UK Biobank cohort was investigated by comparing demographic characteristics between nonresponders and responders. Sociodemographic, physical, lifestyle, and health-related characteristics of the cohort were compared with nationally representative data sources. UK Biobank participants were more likely to be older, to be female, and to live in less socioeconomically deprived areas than nonparticipants. Compared with the general population, participants were less likely to be obese, to smoke, and to drink alcohol on a daily basis and had fewer self-reported health conditions. At age 70-74 years, rates of all-cause mortality and total cancer incidence were 46.2% and 11.8% lower, respectively, in men and 55.5% and 18.1% lower, respectively, in women than in the general population of the same age. UK Biobank is not representative of the sampling population; there is evidence of a "healthy volunteer" selection bias. Nonetheless, valid assessment of exposure-disease relationships may be widely generalizable and does not require participants to be representative of the population at large.

Hansen B., Sabia J.J., Rees D.I.

AbstractUsing data from the state and national Youth Risk Behavior Surveys for the period 1991–2005, Carpenter and Cook (2008) find a strong, negative relationship between cigarette taxes and youth smoking. We revisit this relationship using four extra waves of YRBS data (from 2007, 2009, 2011, and 2013). Our results suggest that youths have become much less responsive to cigarette taxes since 2005. In fact, we find little evidence of a negative relationship between cigarette taxes and youth smoking when we restrict our attention to the period 2007–13. We conclude that policy makers interested in reducing youth smoking may have to adopt alternative strategies.

Noar S.M., Francis D.B., Bridges C., Sontag J.M., Ribisl K.M., Brewer N.T.

Cigarette pack warnings are a tobacco control strategy used globally. To understand their impact, we systematically reviewed longitudinal observational studies examining national implementation of strengthened warnings.We used comprehensive search procedures to identify observational studies examining the impact of strengthening cigarette pack warnings. We report longitudinal changes in knowledge, beliefs, attitudes, intentions, and behavior.We identified 32 studies conducted in 20 countries with 812,363 participants. Studies commonly examined changes from text to pictorial warnings (64%); the remainder examined strengthened text or strengthened pictorial warnings. Knowledge increased in all 12 studies that assessed it. Studies of beliefs/attitudes and intentions showed mixed results. Quitline calls increased in four of six studies, while foregoing of cigarettes did not increase. Cigarette consumption decreased in three of eight studies; quit attempts increased in four of seven studies; and short-term cessation increased in two of three studies. Smoking prevalence decreased in six of nine studies.Strengthening warnings was associated with longitudinal increases in knowledge, quitline calls and reductions in smoking behavior. Strengthening warning policies should be a priority for tobacco control globally.

Dolan C.V., Geels L., Vink J.M., van Beijsterveldt C.E., Neale M.C., Bartels M., Boomsma D.I.

Maternal smoking during pregnancy (SDP) is associated with increased risk of externalizing and internalizing behaviors in offspring. Two explanations (not mutually exclusive) for this association are direct causal effects of maternal SDP and the effects of genetic and environmental factors common to parents and offspring which increase smoking as well as problem behaviors. Here, we examined the associations between parental SDP and mother rated offspring externalizing and internalizing behaviors (rated by the Child Behavior Checklist/2–3) at age three in a population-based sample of Dutch twins (N = 15,228 pairs). First, as a greater effect of maternal than of paternal SDP is consistent with a causal effect of maternal SDP, we compared the effects of maternal and paternal SDP. Second, as a beneficial effect of quitting smoking before pregnancy is consistent with the causal effect, we compared the effects of SDP in mothers who quit smoking before pregnancy, and mothers who continued to smoke during pregnancy. All mothers were established smokers before their pregnancy. The results indicated a greater effect of maternal SDP, compared to paternal SDP, for externalizing, aggression, overactive and withdrawn behavior. Quitting smoking was associated with less externalizing, overactive behavior, aggression, and oppositional behavior, but had no effect on internalizing, anxious depression, or withdrawn behavior. We conclude that these results are consistent with a causal, but small, effect of smoking on externalizing problems at age 3. The results do not support a causal effect of maternal SDP on internalizing behaviors.

MacLean J.C., Kessler A.S., Kenkel D.S.

In this study, we use the Health and Retirement Study to test whether older adult smokers, defined as those 50 years and older, respond to cigarette tax increases. Our preferred specifications show that older adult smokers respond modestly to tax increases: a $1.00 (131.6%) tax increase leads to a 3.8-5.2% reduction in cigarettes smoked per day (implied tax elasticity = -0.03 to -0.04). We identify heterogeneity in tax elasticity across demographic groups as defined by sex, race/ethnicity, education, and marital status and by smoking intensity and level of addictive stock. These findings have implications for public health policy implementation in an aging population.

Monárrez-Espino J., Liu B., Greiner F., Bremberg S., Galanti R.

We used a structured approach to assess whether active smokers presented with pictorial warnings on cigarette packages (PWCP) had a higher probability of quitting, reducing, and attempting to quit smoking than did unexposed smokers. We identified 21 articles from among nearly 2500 published between 1993 and 2013, prioritizing coverage over relevance or quality because we expected to find only a few studies with behavioral outcomes. We found very large heterogeneity across studies, poor or very poor methodological quality, and generally null or conflicting findings for any explored outcome. The evidence for or against the use of PWCP is insufficient, suggesting that any effect of PWCP on behavior would be modest. Determining the single impact of PWCP on behavior requires studies with strong methodological designs and longer follow-up periods.