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Abstract

In discussing our recent article concerning the protective effects of breast-feeding against asthma and wheeze,1Chulada PC Arbes Jr, SJ Dunson D Zeldin DC Breast-feeding and the prevalence of asthma and wheeze in children: analyses from the Third National Health and Nutrition Examination Survey.J Allergy Clin Immunol. 2003; 111: 328-336Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar Per Nafstad and Jouni Jaakola discuss two earlier studies in which breast-feeding lowered the risk of acute respiratory illnesses in infants exposed to maternal smoking.2Woodward A Douglas RM Graham NMH Miles H Acute respiratory illness in Adelaide children: breast feeding modifies the effect of passive smoking.J Epidemiol Community Health. 1990; 44: 224-230Crossref PubMed Scopus (84) Google Scholar, 3Nafstad P Jaakkola JJK Hagen JA Botten G Kongerrud J Breastfeeding, maternal smoking, and lower respiratory tract infections.Eur Respir J. 1996; 9: 2623-2629Crossref PubMed Scopus (137) Google Scholar We thank Drs Nafstad and Jaakola for mentioning these studies because the results support our findings as well. In contrast to these studies, however, we examined recurrent wheeze (3 or more episodes in the past 12 months) and physician-diagnosed asthma to gain new insight into the effects of breast-feeding on chronic childhood respiratory illnesses.1Chulada PC Arbes Jr, SJ Dunson D Zeldin DC Breast-feeding and the prevalence of asthma and wheeze in children: analyses from the Third National Health and Nutrition Examination Survey.J Allergy Clin Immunol. 2003; 111: 328-336Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar Recurrent wheeze was used to discriminate children with transient, early infectious wheeze from children with chronic, possibly atopic disease. We found that breast-feeding lowered the risks of both chronic outcomes in children <2 years of age. Except for the interaction between age and outcome, both findings had previously been published. In addition, we also found a strong protective relation between breast-feeding and environmental tobacco smoke–related (ETS-related), physician-diagnosed asthma in children up to 6 years of age, which had never been reported. Our results expand the growing body of evidence that breast-feeding protects against ETS-related childhood illnesses to include chronic and atopic respiratory disease. Is this a general protective effect or a specific ETS-related effect? The protective mechanisms of breast-feeding are likely to be multiple, highly complex, and depend on the pathogenesis of the illness. Before we can understand how breast-feeding is protective, we must first understand how ETS is toxic. For example, why does ETS increase a child's susceptibility to infectious agents and how does ETS exacerbate atopic disease? We do know that breast milk contains a myriad of compounds that are anti-infectious and anti-inflammatory. The latter can reduce respiratory tract inflammation associated with asthma or associated with ETS acting as an irritant (or both in combination). These more general breast-feeding benefits probably target nonspecific consequences of ETS exposure (susceptibility to infectious agents and inflammation). On the basis of our study and others, these general benefits appear to be most effective during the first year or two of life. Breast-feeding likely also exerts multiple protective mechanisms specifically against ETS-induced respiratory pathology. The large difference in the period of breast-feeding protection (2 years for general asthma and recurrent wheeze versus 6 years for ETS-related asthma and recurrent wheeze) clearly supports such a hypothesis. In spite of this longer period of breast-feeding protection against the ETS-related outcomes, we observed an interaction with age. the anti-ETS protection was stronger in children <2 years of age than in children <6 years of age (adjusted HR, 0.48 vs 0.61 for children up to 6 years old; both P < .05). This suggests that specific breast-feeding protections might act in “addition to” the general mechanisms described earlier. Little is known about the toxic mechanisms used by ETS. ETS exposure can enhance asthma by increasing airway mucosal permeability to allergens or by affecting immune function. For example, ETS might interfere with postnatal switching from a TH2 lymphocyte subset to a TH1 phenotype, thus increasing or accelerating allergic sensitization. On the other hand, breast milk might contain one or more compounds that promote TH2/TH1 switching that counteracts such an interference. Just recently, high levels of IL-18 were measured in colostrum and early human breast milk.4Takahata Y Takada H Nomura A Ohshima K Nakayama H Tsuda T et al.Interleukin-18 in human milk.Pediatr Res. 2001; 50: 268-272Crossref PubMed Scopus (43) Google Scholar In vitro evidence indicates that IL-18 and other cytokines are involved in lymphocyte differentiation. In summary, we have presented only one possibility of how ETS might exacerbate asthma and a possible specific breast-feeding countermeasure. There probably are many more, and their identification through future research will lead to better strategies for the prevention and/or treatment of childhood respiratory illness.