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The article by Perzanowski et al in this issue of Thorax (see page 118) adds one more piece of evidence supporting a possible role for acetaminophen in the development of asthma in children.1 Five previous studies, including three prenatal prospective cohorts,2–5 have suggested that in utero ingestion of acetaminophen may increase the risk of asthma and respiratory symptoms in children.2–7 Increased risk of asthma from postnatal use of acetaminophen is also suggested by reports of children8–12 and adults.8 13–17 The possibility that acetaminophen may contribute to the development of asthma is supported by parallel time trends in dramatic increases in use of the medication in response to reports of associations of aspirin use with Reye syndrome18–20 and increases in asthma prevalence between the mid 1970s and mid 1990s.21
There is also biological plausibility. Acetaminophen,22–24 as well as one of its metabolites, the highly reactive N-acetyl-p-benzoquinoneimine,23 has been associated with decreased glutathione. There is substantial literature documenting the antioxidant capacity of glutathione25 as well as the role of reactive oxygen species in asthma morbidity.26 In addition, decreased glutathione may affect the development of asthma by altering antigen recognition towards favouring T helper 2 (Th2) over Th1 cytokines.23 27 Other, less likely, possibilities relate to decreased suppression of cyclo-oxygenase or direct antigenicity of acetaminophen.23
The study by Perzanowski et al notes that associations of prenatal acetaminophen use …
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