Risk factors for childhood asthma and wheezing. Importance of maternal and household smoking.

Abstract

To identify modifiable risk factors for wheezing illness in childhood, the associations between current asthma or wheezing and factors such as household smoking, damp and dietary salt preference were measured in a questionnaire-based prevalence study of schoolchildren 7 to 9 yr of age in Cape Town. In a random sample of 15 schools, questionnaires were completed by parents of 1,955 children, from which 368 cases and 294 controls were selected on the basis of reported asthma diagnosis or symptoms. Urinary cotinine concentrations were measured, and the parents were interviewed. An exposure-response relationship between the urinary cotinine creatinine ratio and asthma/wheeze was observed. In multivariate analysis, predictors of asthma/wheeze were hay fever (odds ratio [OR] - 5.30; 95% confidence interval [CI] = 3.16 to 8.89), eczema (OR = 2.19; 95% CI = 1.33-3.62), parental asthma (OR = 1.77; 95% CI = 1.11 to 2.84), absence of paternal contribution to income (OR = 1.72; 95% CI = 1.17 to 2.54), maternal smoking in pregnancy (OR = 1.87; 95% CI = 1.25 to 2.81), and each additional household smoker (OR = 1.15; 95% CI = 1.01 to 1.30). Findings were similar, with higher odds ratios for most variables, except number of household smokers, when the group was restricted to children with parent-reported asthma. The findings confirm that household smoking is an important modifiable risk factor in asthma/wheeze among young schoolchildren, and they suggest that maternal smoking in pregnancy and current household exposure are independent contributors to this effect.

Étude d'association entre l'asthme et les gènes associés à ce phénotype et à la pollution de l'air, dans un échantillon d'asthme provenant d'un environnement régional caractérisé par différentes industries /

“…For example, the two associated genes (CAT and NQOl) have been associated with asthma and tobacco smoke exposures (32,33). NQOl Prol87Ser mutation was associated in our study, but was also associated with asthma and exposure to tobacco smoke in a previous study.…”

Pediatric Asthma in Southern Africa

“…Meteorologically estimated exposure (MEE), but not simple distance from the refinery, was positively associated with having to take an inhaler to school (OR per interquartile range 1.22, 95% CI 1.06-1.40), and with a number of video elicited asthma symptoms, including recent waking with wheezing (OR 1.33, 95% CI 1.06-1.66) and frequent wheezing at rest (OR 1.27, 95% CI 1.05-1.54). Symptom prevalences were higher than in other areas of the city, with frequent waking with wheezing being in great excess (OR 8.92, 95% CI 4.79-16.63) [19]. The results support the hypothesis of an increased prevalence of asthma symptoms among children in the area as a result of refinery emissions and provide a substantive basis for community concern.…”

“…In further studies, predictors of asthma/wheeze were hay fever (OR 5.30; 95% CI 3.16-8.89), eczema (OR 2.19; 95% CI 1.33-3.62), parental asthma (OR 1.77; 95% CI 1.11-2.84), absence of paternal contribution to income (OR 1.72; 95% CI 1.17-2.54), maternal smoking in pregnancy (OR 1.87; 95% CI 1.25-2.81), and each additional household smoker (OR 1.15; 95% CI 1.01-1.30). Findings were similar, with higher odds ratios for most variables, except number of household smokers, when the group was restricted to children with parent-reported asthma [19].…”

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

“…Furthermore, combined in utero plus postnatal exposures did not increase risk of asthma beyond in utero exposures alone. The finding that maternal smoking during pregnancy has a stronger relationship to asthma onset than later ETS exposures was supported by several other studies that separated maternal in utero exposures from postnatal exposures (77)(78)(79)(80)(81)(82). It is conceivable that in utero exposures to ETS shifts the immune response toward a T H 2-type pattern as a result of the adjuvant action of PAH components interacting with in utero allergen exposures, which are now believed to lead to atopic sensitization before birth (83,84).…”