Gender, environmental tobacco smoke, and pulmonary function in rural children and adolescents: the Humboldt study.

We examined the gender-related association between household exposure to environmental tobacco smoke (ETS) and pulmonary function among 862 children and adolescents aged 6 to 17 years living in the town of Humboldt, Saskatchewan, in 1993. Pulmonary function tests included forced vital capacity (FVC), forced expiratory volume in one second (FEV1), maximum mid-expiratory flow rate (FEF25-75), and flow rates at 75%, 50%, and 25% of vital capacity (Vmax75, Vmax50, and Vmax25). Each pulmonary function test variable was regressed on age, height, weight, and their quadratic and cubic polynomials, with the terms significant at the alpha level of 0.10 being retained. Residuals for the pulmonary function test variables, which are the differences between the observed and predicted values, were calculated. Estimations of ETS exposure were parental smoking status, number of household smokers, total daily cigarette consumption, and number of cigarettes smoked daily at home by household members. Maternal smoking status was significantly related to residual FEF25-75, Vmax75, Vmax50, and Vmax25. Number of household smokers and daily cigarette consumption by household members were significantly associated with FEV1, FEF25-75, Vmax75, Vmax50, and Vmax25, and the association between ETS exposure and pulmonary function was stronger in girls than in boys. Interaction of gender and number of cigarettes smoked daily at home was significantly related to FEF25-75, Vmax75, Vmax50, and Vmax25 among the non-smoking subjects. We concluded that ETS exposure had a larger effect on pulmonary function in girls than in boys.

Segregation analyses of asthma and respiratory allergy: the Humboldt family study.

We performed segregation analyses of asthma and respiratory allergy based on data from 309 nuclear families comprising 1,053 individuals living in the town of Humboldt, Saskatchewan, in 1993, using the REGD program of the S.A.G.E. program package. For adults, information on asthma and history of respiratory allergy was provided by the subjects themselves, and for children by their parents. When asthma was considered as the trait in segregation analysis, models of no major effect, with or without familial effects, were rejected, but they were not rejected after adjusting for history of respiratory allergy. The major gene hypothesis was not rejected before adjusting for history of respiratory allergy. When respiratory allergy was analyzed as the trait, both major gene and multifactorial models fitted the data well, regardless of whether there was adjustment for asthma or not. Other covariates adjusted for in the segregation analyses were age, sex, number of household smokers, current smoking, number of household members, generation, and house type. The data suggest that a major gene related to respiratory allergy may explain the familial aggregation of asthma.

Major genetic effects on airway-parenchymal dysanapsis of the lung: the Humboldt family study.

We examined familial resemblance and performed segregation analysis for the maximal expiratory flow rate at 50% of vital capacity (Vmax50) and the ratio of Vmax50 to forced vital capacity (FVC), based on data from 309 nuclear families with 1,045 individuals in the town of Humboldt, Saskatchewan, in 1993. Vmax50 is considered as an index of airway function and Vmax50/FVC is considered as an index of airway-parenchymal dysanapsis. Both Vmax50 and Vmax50/FVC were preadjusted for host characteristics (age, height, and weight), environmental factors, and history of respiratory symptoms and diseases in four separate groups (mothers, fathers, daughters, and sons). Both Vmax50 and Vmax50/FVC showed low father-mother correlations and significant parent-offspring and sibling-sibling correlations. Segregation analysis indicated that for residual Vmax50, the model of no-parent-offspring transmission with possible heterogeneity between two generations fitted the data as well as did the general model with arbitrary transmission probabilities. The Mendelian hypothesis for Vmax50 was rejected, which was consistent with our previous findings for other indexes of airway function. For residual Vmax50/FVC, however, a single locus explained all the familial resemblance and both no-parent-offspring-transmission hypotheses [tau(AA) = tau(AB) = tau(BB) = qA and tau(AA) = tau(AB) = tau(BB)] were rejected. The study provides evidence for a single locus influencing airway-parenchymal dysanapsis.

Association between obesity and high blood pressure: reporting bias related to gender and age.

OBJECTIVE: To examine the validity of self-reported information on obesity and high blood pressure (HBP) in relation to gender and age, and to explore the impacts of their misclassification on the association between obesity and HBP. DESIGN: Community based cross-sectional study. SUBJECTS: 1791 adult subjects living in Humboldt, Saskatchewan, Canada. MEASUREMENTS: Objectively measured HBP was positive if systolic blood pressure (BP) was > or = 140 mm Hg, diastolic BP was > or = 90 mm Hg or the subject was currently using antihypertensive medication. Self-reported HBP was positive if the subjects gave an affirmative response to the question: 'Has a doctor ever said you had high blood pressure?' Body mass index (BMI) was calculated as weight (kg)/height (m)2. Obesity was defined as a BMI > 27 kg/m2. Measured obesity and reported obesity were based on measured and self-reported information on height and weight, respectively. RESULTS: The sensitivity of self-reported HBP was low, and was lower for men than for women, and for younger subjects than for older subjects. The specificity was similar for both genders. Obese individuals had higher sensitivity and lower specificity than non-obese individuals. The differential misclassification of self-reported HBP caused a bias away from the null when the relative risk for HBP in relation to obesity was estimated. CONCLUSIONS: As a result of the gender- and age-related misclassification of self-reported HBP, the modification role of gender and age on the association between obesity and HBP could be altered. The bias caused by self-reported obesity was relatively small and was either toward or away from the null.

Effect of environmental tobacco smoke on cough in children with a history of tonsillectomy or adenoidectomy.

We examined the possible impact of tonsillectomy or adenoidectomy (T/A) on the relationship between environmental tobacco smoke (ETS) exposure and respiratory outcomes. This study was conducted in Humboldt, Saskatchewan, in 1993. The target population included all residents aged 6-17 yrs. Of the 1,019 eligible subjects, 892 participated (88%). Estimates of ETS exposure were based on the reported smoking habits of the children's household members. We defined current cough as a positive response to the question: "Does this child usually have a cough?". Information also included morning cough, night cough and a history of T/A. For children with no history of T/A, the prevalence of current cough was 8.9%, 12.2% and 14.5% for those living in families with 0, 1, and 2+ smokers respectively. The corresponding prevalence was 7.0%, 30.2% and 36.8% for children with history of T/A. Similar effects of ETS exposure were observed on morning cough and night cough. The results did not change significantly when we used various ETS measures and controlled for confounding factors. Compared to children living in nonsmoking families and without history of T/A, the adjusted odds ratio for children with a history of T/A was 7.19 (p<0.001) if they were living in families smoking >20 cigarettes x day(-1) at home. The corresponding odds ratio was only 1.64 (p=0.11) for children without a history of T/A. We concluded that children living in smoking family were more likely to cough than those living in nonsmoking families and tonsillectomy or adenoidectomy increased the apparent influence of environmental tobacco exposure on cough.

Evidence for major genetic control of wheeze in relation to history of respiratory allergy: Humboldt family study.

We report the results of segregation analyses for wheeze before and after a history of respiratory allergy was taken into consideration. The analyses were based on data from 309 nuclear families with 1,053 individuals living in the town of Humboldt, Saskatchewan in 1993, and were performed by using the REGD program of the SAGE package. For adults, information on wheeze and history of respiratory allergy was provided by themselves, and for children, by their parents. Segregation analyses were first conducted before adjustment for history of respiratory allergy. Other covariates were adjusted including sex, current smoking, household exposure to tobacco smoke, and type of house. A single locus model with residual familial effects fit the data well, but none of the Mendelian models (recessive, dominant, and codominant) could be distinguished. The no-parent-offspring-transmission hypothesis was rejected. However, when the variable of respiratory allergy was included in the models as a covariate, both Mendelian and environmental hypotheses were rejected. The Mendelian model had a relatively lower value of Akaike's Information Criterion than did the environmental model (1095.56 versus 1111.24). The data suggest that a single locus gene explains a portion of wheeze that is related to respiratory allergy, and that common environmental factors and/or polygenes also account for a certain familial aggregation of wheeze.

Major genetic effect on forced vital capacity: the Humboldt Family Study.

Familial correlation and segregation analyses of forced vital capacity (FVC) were performed on data from 309 nuclear families with 1,045 individuals in the town of Humboldt, Saskatchewan, in 1993. FVC was preadjusted for age, height, and weight in four separate groups (mothers, fathers, daughters, and sons). Residual FVC was standardized within the four groups. Class D regressive model was first used to examine the familial resemblance of FVC without a major gene. While mother-father correlation was not significantly different from zero and mother-sibling and father-sibling correlations were not significantly different from each other, sibling-sibling correlation was greater than parent-sibling correlation. Segregation analysis for all 309 families indicated that both the Mendelian and no-parent-offspring-transmission models fitted the data as did the general model with arbitrary transmission probabilities. Likelihoods under the Mendelian model (LMendelian) and the environmental model (Lenvironmental) were calculated. Based on the value of In(LMendelian/Lenvironmental), 309 families were divided into two groups: 196 families with the value of In(LMendelian/Lenvironmental) greater than zero (group I) and 113 families with the value In(LMendelian/Lenvironmental) less than zero (group II). The Mendelian transmission model without familial correlations was the most parsimonious model for the families in group I. For group II, there were two best models of choice: 1) no-parent-offspring-transmission model with possible heterogeneity plus familial correlations [Akaike's information criterion (AIC) = 1,213.76] and 2) Mendelian transmission plus sibling-sibling correlation model (AIC = 1,202.36). The results suggest there are major genetic mechanisms in FVC with possible heterogeneity.