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Whether environmental exposure to bacterial endotoxin protects against asthma is questionable. According to a recent review in Thorax, the evidence is equivocal. Endotoxin is common in the environment—in homes, especially those with pets, and in occupational, especially agricultural, environments. Recent studies indicate that exposure to it might reduce atopy and asthma in farmers' children.
Direct evidence for protection against atopy—that is, involving IgE sensitisation and eosinophils—rests on a single study of infants with a high risk of asthma in whom endotoxin stimulated a non-atopic immunological pathway. Atopy probably accounts for only half of asthma cases, at most.
However, endotoxin can provoke asthma too. Its recognition as a cause of occupational lung disease—including asthma—comes from inhalation experiments and field studies in farmers and other occupations, among them cotton mill, pig farm, and grain workers, and its ability to exacerbate existing asthma in adults and children comes from several indoor studies. But this is non-allergic asthma, involving inflammation and activation of neutrophils and alveolar macrophages.
The relation between endotoxin, asthma, and farming is complex and the evidence contradictory. For now it seems that endotoxin marginally protects children and adolescents but increases risk in adult farmers.
Endotoxin might prevent primary development of allergic asthma but may itself be a primary and secondary cause of non-allergic asthma. This could be explained, the authors suggest, if endotoxin differs in effect depending on exposure—during the prenatal or neonatal period versus child and adult phases—and dose. Prospective studies in progress may clarify the picture.
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