Maternal smoking during pregnancy affects adult onset of asthma in offspring: a follow up from birth to age 46†years.

RATIONALE: Environmental tobacco smoke (ETS) exposure increases asthma risk in children. There is limited knowledge of prenatal ETS for adult-onset asthma. OBJECTIVES: To determine the association between prenatal ETS and adult onset asthma. MEASUREMENTS AND MAIN RESULTS: The questionnaire and clinical data of 5200 people, free of physician-diagnosed asthma by 31 years of age, who were included in the Northern Finland Birth Cohort 1966 Study was used. The association of maternal smoking during the last 3 months of pregnancy with onset of physician-diagnosed asthma and with lung function in adult offspring was studied using adjusted multivariate regression analyses. The cumulative incidence of physician-diagnosed asthma between the ages of 31 and 46 years was 5.1% among men and 8.8% among women. Gestational smoke exposure was associated with adult-onset asthma among offspring (adjusted OR 1.54, 95% CI 1.04-2.29), namely among offspring who reported either past non-diagnosed asthma (OR 9.63, 95% CI 2.28-40.67) or past cough with wheeze (3.21, 95% CI 1.71-6.05). A significant association was detected between gestational smoke exposure and the offspring's forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ratio at 31 years of age. In offspring with the haplotype rs11702779-AA of RUNX1, gestational smoke exposure was associated with adult-onset asthma (5.53, 95% CI 2.11-14.52, adjusted p-value for interaction 0.10). CONCLUSION: Maternal smoking during pregnancy is associated with the cumulative incidence of asthma in offspring between the ages of 31 and 46 years. The association was accentuated in offspring who at age 31, reported having past respiratory problems and/or who had haplotype rs11702779-AA. A reduction in FEV1/FVC ratio was also observed at age 31 years in offspring with gestational smoke exposure. These results could reflect the early vulnerability of offspring's airways to ETS and its putative long-term effects.

Early life factors and blood pressure at age 31 years in the 1966 northern Finland birth cohort.

Data on the birth weight-blood pressure relationship are inconsistent. Although an inverse association has been suggested in several large studies, interpretation is complicated by publication and other biases. Few data are available on the relationship between other early growth measures and blood pressure. We examined the shape and size of association between determinants of fetal growth, size at birth, growth in infancy, and adult systolic and diastolic blood pressure at 31 years in the prospective northern Finnish 1966 birth cohort of 5960 participants. Birth weight, birth length, gestational age, ponderal index, and birth weight relative to gestational age showed a significant inverse association with blood pressure at age 31. Rapid growth in infancy ("change-up") was positively associated with blood pressure. Adjusted regression coefficients for birth weight indicated systolic/diastolic blood pressure lower by -1.7 (95% confidence interval [CI], -2.5, -1.0)/-0.7 (95% CI, -1.4, -0.02) mm Hg for 1 kg higher birth weight. The significant inverse association between birth weight and systolic blood pressure persisted without adjustment for adult body mass index for males. Among females, gestational age showed a stronger association with blood pressure than birth weight: gestational age higher by 7 weeks (equivalent to an average of 1 kg higher birth weight) among singletons associated with -2.9 (95% CI, -4.7, -1.1) mm Hg lower systolic blood pressure. Our results support the concept that birth weight, other birth measures, and infant growth are important determinants of blood pressure and hence cardiovascular disease risk in later life.

Maternal sex hormones in early pregnancy and asthma among offspring: a case-control study.

BACKGROUND: Sex hormones may be associated with the risk of onset of asthma. OBJECTIVE: To study the association between maternal sex hormone concentrations during early pregnancy and the risk of asthma among offspring. METHODS: A case-control study of 129 asthmatic children and 125 control children 5 to 6 years of age. Maternal sera in early pregnancy were obtained from the Finnish Maternal Cohort serum bank. RESULTS: The means of serum progesterone and estradiol and free estradiol in mothers of asthmatic and control children were 81.0 and 82.8 nmol/L (P =.60), 7.87 nmol/L and 7.65 nmol/L (P =.99), and 149.5 pmol/L and 148.0 pmol/L (P =.95), respectively. There were also no differences in the mean concentrations of maternal sex hormones according to the presence of allergic rhinitis or atopic eczema among the children. CONCLUSIONS: The current results do not support an association between maternal sex hormone concentrations during early pregnancy and onset of allergic disease in early childhood.

Body build from birth to adulthood and risk of asthma.

BACKGROUND: Few reports aimed at the study of adulthood obesity and asthma have taken into account the effects of size at birth and obesity in adolescence. This paper examines the combined effect of size at birth and obesity in both adolescence and adulthood on the risk of asthma at age 31 years. METHODS: The study was derived from a prospectively population-based Finnish birth cohort born in 1966, for which data were collected in pregnancy and at various ages. Adulthood doctor-diagnosed asthma with current symptoms and results of skin prick tests were obtained in 1997. The analysis was limited to 4719 subjects with complete information on asthma and atopy and anthropometric measures at various ages. RESULTS: Ponderal index at birth had a U-shaped association with adult atopy, OR 1.30 (95% CI: 1.11-1.52) for the lowest tertile and OR 1.33 (95% CI: 1.13-1.55) for the highest tertile, as compared to the middle tertile. The association was independent of obesity later in life. Those obese (BMI > or = 95th percentile) in adolescence (OR 2.09, 95% CI: 1.23-3.57) and in adulthood (OR 1.99, 95% CI: 1.14-3.47) had a higher occurrence of adult asthma than those with BMI < 85th percentile. Both estimates were reduced after mutual adjustment. CONCLUSIONS: Size at birth has a long-lasting effect on atopy in adulthood, which is independent of weight in adolescence and adulthood. Those who were obese in adolescence and adulthood tended to have a higher risk of asthma in adulthood. These findings underline the importance of considering the life course of obesity in the analyses of asthma and atopy.

Association between skin test diagnosed atopy and professionally diagnosed depression: a Northern Finland 1966 Birth Cohort study.

BACKGROUND: Several studies have suggested an association between IgE-mediated atopic allergies and depression, although thus far no epidemiologic evidence involving a large, unselected, general-population sample and valid methods in diagnosing atopy support this putative association. METHODS: We used the Northern Finland 1966 Birth Cohort, which was followed prospectively to age 31. Of the total cohort, 5428 individuals underwent skin tests for three of the most common allergens (i.e., cat, birch, and timothy grass) and for dust mites (Dermatophagoides pteronyssinus). Data on doctor-diagnosed lifetime depression were obtained from questionnaires. RESULTS: After adjusting for social class, mothers' parity, place of residence, and psychiatric morbidity, the logistic regression analysis showed that the risk of developing depression when compared with nonatopic subjects increased up to 1.8-fold in atopic women (adjusted odds ratio 1.8, 95% confidence interval [CI] 1.2-2.6) and, when compared with skin-test-negative female subjects without allergic symptoms, reached 2.7-fold increases (95% CI 1.6-4.6) in those suffering from clinically manifest atopic disorders. Corresponding associations were not found among male subjects. CONCLUSIONS: Our results indicate that women suffering from atopic diseases may possess an elevated risk for developing depression during early adulthood. Possible background theories (i.e., genetic abnormalities in serotonin metabolism, hypothalamic-pituitary-adrenal axis dysfunction, and histamine theory) are discussed.