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From the Respiratory Epidemiology and Clinical Research Unit, Montreal Chest Institute (Becklake, Ghezzo, Ernst); and the Meakins Christie Laboratories (Becklake, Ghezzo), Montréal, Que.
Correspondence to: Dr. Margaret R. Becklake, Respiratory Epidemiology and Clinical Research Unit, Montreal Chest Institute, Rm. K1.33, 3650 St Urbain Street, Montréal QC H2X 2P4; margaret.becklake{at}mcgill.ca
| Abstract |
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Methods: To investigate these and other possible childhood predictors of teenage smoking, we gathered follow-up data on 191 Montréal schoolchildren, aged 512 years (average 9.2 yr) when first examined. At an average age of 13.0 years, they answered further questions on their health and smoking behaviour and provided a second set of spirometric measurements.
Results: At the second survey, 80% of the children had entered high school and 44% had become smokers. Reaching puberty between the surveys was the most significant determinant of becoming a smoker: 56.4% of the 124 children postpubertal at the second survey had taken up smoking, versus 17.9% of the 67 who were still prepubertal (p = 0.001). We found salivary cotinine level, a measure of uptake of environmental tobacco smoke, to be an independent predictor of becoming a teenage smoker; even after adjustment for sex, socioeconomic status of parents, a crowding index, and the numbers at home of siblings, adult smokers and cigarettes smoked, it remained significant for both groups: postpubertal (odds ratio [OR] 1.2, 95% confidence interval [CI] 1.23.0) and prepubertal (OR 2.1, 95% CI 1.0 4.5). The influence of forced vital capacity was marginally significant only in the postpubertal group (OR 5.0, 95% CI 0.8828.3).
Interpretation: The proportion of nicotine absorbed from that available in environmental tobacco smoke during childhood is associated with subsequent smoking in adolescence. The more efficient absorption of nicotine seen in some children may be related to physiological factors such as lung capacity.
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The outcome of interest was having become a smoker by the second survey, defined as an answer of "Yes" to the question, "Have you ever smoked as much as 1 cigarette a week for a month?" Social and cultural factors that may affect levels of environmental tobacco smoke in the home and physiologic data from the first survey are shown in Table 1. During the second survey, we recorded pubertal status (defined as a "yes" answer to the survey question "Have you started your menstruations?" for girls or "Has your voice changed?" for boys), the high school currently attended (a composite marker of peer pressure to smoke and the scholastic and sporting expectations attributed to each school) and changes in family smoking behaviours since the first survey, which we interpreted as indications of parental attitudes toward smoking (negative, if an increase in the number of adult smokers in the home had been allowed; and positive, if smoking cessation in the home appeared to have been encouraged). Univariate analysis was used to select potential explanatory factors, based on 2-tailed p values of 0.10 or less. Independent predictors were determined by multivariate logistic regression analyses.
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The only factor associated with becoming a teenage smoker in both pre- and postpubertal children was salivary cotinine concentration (adjusted in the analysis for sex, number of siblings, socioeconomic status of the parents, crowding index, number of smokers at home and total number of cigarettes smoked in the home). In prepubertal children, a marginally significant childhood factor was female sex; in postpubertal children, forced vital (lung) capacity and the presence of adult smokers in the home, whether single (i.e., 1 smoker) or multiple. The specific high school currently attended, which was recorded at the second survey, also showed marginal significance (p = 0.09; data not shown).
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An unexpected finding in the multivariate analysis was the lack of any significant association between becoming a teenage smoker and the number of smokers in the home in childhood (p = 0.99). Also unexpected was the association between a decrease in the number of adult smokers in the home between surveys (thought to indicate a positive parental attitude toward smoking cessation) and a decrease in the number of adolescents becoming smokers (the reduction in risk is shown in Table 2). This could have been caused not only by parental disapproval but alternatively by nonsmoking teenagers pressuring their parents to quit.8,9,10 It nonetheless shows the importance of a dynamic attitude at home against smoking.
As for the anatomic and physiologic findings, the most important observation was that salivary cotinine in childhood (a measurement of the nicotine actually entering the bloodstream) was an independent predictor of adolescent smoking, after adjustment in the analysis for amount smoked at home and other relevant factors (see final footnote, Table 1). Given also the association (admittedly not strong) between forced vital capacity and adolescent smoking, we suggest that lung size (or some associated characteristic) increases the uptake of environmental tobacco smoke, maximizes the influence of passive smoking in childhood and induces smoking in adolescence. In this context, the recently reported reduced density of dopamine D1 receptors in the ventral striatum of the brains of adult smokers of cigarettes led those investigators11 to speculate that a hypodopaminergic state may play an important role in sustaining "nicotine-seeking" behaviour and future addiction.
In conclusion, we hypothesize that enhanced susceptibility to environmental tobacco smoke in childhood increases the risk of nicotine-seeking behaviour in adolescence. If proved correct, this would be valuable information to use in the ongoing campaign against smoking in teenagers.
ß See related article page 382
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Contributors: Pierre Ernst and Margaret Becklake were responsible for data collection. Heberto Ghezzo designed this study and carried out the statistical analysis. All authors contributed equally to the writing and revision of the manuscript.
Acknowledgements: The study was funded by the Medical Research Council (Canada) in a grant to the Respiratory Health Network of Centres of Excellence (Principal Investigator, P.T. Macklem). Pierre Ernst was a Chercheur Boursier (Fonds de la recherché en Santé du Québec) and Margaret Becklake was a Career Investigator (Medical Research Council, Canada) during the original study. Dr. Maurice McGregor provided a critical review of the text.
Competing interests: None declared.
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