B Br re ea as st tf fe ee ed di in ng g, , m ma at te er rn na al l s sm mo ok ki in ng g a an nd d P. Nafstad*, J.J.K. Jaakkola* + , J.A. Hagen*, G. Botten*, J. Kongerud** Breastfeeding, maternal smoking and lower respiratory tract infections. P. Nafstad, J.J.K. Jaakkola, J.A. Hagen, G. Botten, J. Kongerud. ERS Journals Ltd 1996. ABSTRACT: The objective of the study was to assess the relationship between breastfeeding and lower respiratory tract infections (LRTIs) during the first year of life, with special reference to maternal smoking.A cohort of 3,754 children born in 1992-1993 in the City of Oslo, Norway was recruited and data were collected at birth, 6 and 12 months of age. Complete information was obtained from 3,238 children (follow-up rate 86%). The main outcome was an episode of a LRTI, such as pneumonia, bronchitis or bronchiolitis, based on a self-administered questionnaire addressed to parents when the child was 6 and 12 months old. The outcome was specified as physician-diagnosed.In logistic regression analysis adjusting for confounding, maternal smoking increased the risk of LRTIs in children breastfed for 0-6 months (odds ratio (AOR) 1.7; 95% confidence interval (95% CI) 1.2-2.4), but not essentially when the child was breastfed for more than 6 months (AOR 1.1; 95% CI 0.7-1.6). Short-term breastfeeding (0-6 months) and no maternal smoking was related to an adjusted AOR of LRTIs of 1.3 (95% CI 1.0-1.7), and short-term breastfeeding combined with maternal smoking was related to an adjusted AOR of 2.2 (95% CI 1.6-3.1), as compared with long-term breastfeeding and no maternal smoking.The present study indicates a protective effect of long-term breastfeeding on the risk of lower respiratory tract infection during the first year of life. The results suggest that the protective effect is strongest in children exposed to environmental tobacco smoke.

The healthy worker effect and incomplete exposure information have been problems in former studies regarding the association between exposure to Portland cement dust and respiratory effects. We included former workers and made an individual estimation of particle exposure to reduce the selection bias in this controlled cross-sectional study on the effects of cement dust exposure on respiratory symptoms and ventilatory function in long-term exposed Norwegian cement plant workers. A total of 119 workers from the largest cement plant in Norway and 50 workers from a nearby control plant, born 1918 to 1938, performed spirometry and gave information on respiratory symptoms in 1998 and 1999. The prevalence of symptoms and mean pulmonary function indices were similar for exposed workers and controls. There was no dose-response-related increase in symptoms or decrease in lung function indices. The estimated power to detect a true difference between forced expiratory volume in one second (FEV1) in the two groups of 0.3l was 0.90, assuming 95% significance level. The prevalence of chronic obstructive pulmonary disease was 14.3% in the exposed group and 14.0% among the controls. These findings do not support the hypothesis that cement dust exposure has a negative impact on lung function or gives an increase in respiratory symptoms.