In the 1980’s large cohort studies showed that ETS exposure, assessed by parental questionnaire, was associated with increased risk for BHR in children
[
8]. Subsequently, investigators moved to gathering biomarkers of exposure from the children themselves. Children’s urinary cotinine was demonstrated as a biomarker of risk for asthma and wheeze
[
9]. Subsequently, the use of biomarkers for ETS has expanded considerably and several reports have directly compared the various measures as exposure metrics
[
6,
7,
10], revealing complex dynamics dependent on several variables. In our initial analysis of risk factors for asthma at age seven
[
2], we were surprised to find that questionnaire data suggested that maternal smoking was not a significant risk factor and could be a significant “protective” factor. The questionnaire-based data in the current study again suggests “protection” from maternal smoking, though with a less focused confidence interval due to a smaller sample size (in our previous paper
[
2] biomarkers were not required for inclusion in analysis). As we speculate that maternal smoking is unlikely to be truly protective, these findings motivated our exploration of more objective measurement of exposure, and our findings reinforce that motivation.
Limitations to our data include lack of questionnaire data regarding maternal smoking from the period prior to the 3
rd trimester and sample size affecting the confidence limits for the effect of various metrics. This is important because Neuman and colleagues
[
11] have documented a time-dependency to ETS exposures during early life, though their analysis focused on pregnancy versus post-pregnancy ETS rather than on trimester-specific ETS. Duijts and colleagues
[
12] did look at trimester-specific effects but for wheeze only (not asthma). Note however that given our specific motivation to compare questionnaire-based data versus that biological sampling, the 3
rd trimester would correspond most closely with cord-blood at birth. Another potential limitation is that concern for familial asthma risk led to behavioral changes (decreased smoking) of some family members to reduce the risk of asthma in their children, thus limiting generalizability of our findings in this cohort of children at high risk for asthma, relative to other cohorts with average asthma risk and more typical smoking prevalence. Finally, we did note that amongst those 31 children in the cohort that had both frequent “colds”, defined as at least 3 per year, the risk for wheeze at 2 years (45%) was higher than in those with fewer colds (6% of these children had wheeze at 2 years). Though we were underpowered for a specific analysis of interactions between ETS and upper respiratory tract infections, potential such interactions remain an important concern, as highlighted by Ciprandi and others
[
13].
In spite of these limitations, our study is unique in evaluating various measures of ETS, in association with multiple respiratory endpoints; we believe that this is further unique in the context of a birth cohort at high risk for asthma but with modest maternal smoking rates. In spite of self-reported maternal smoking occurring in reportedly less than 10% of the families, this metric appears to be the robust for predicting early life recurrent wheeze, and similar risk estimates for this endpoint were noted when ETS was represented by either a broader sampling of family members or by cord blood cotinine. This latter similarity in risk is remarkable since cotinine, while more comprehensively measuring inhaled ETS (including that due to paternal and incidental exposures), has a relatively short half-life of approximately 20 hours
[
14] and thus may not represent averaged exposure over the specific time period.
1 Helen Dimich-Ward,1 Anne DyBuncio,1 Allan B Becker,2 and Moira Chan-Yeung1
publication history
