Childhood acetaminophen exposure may wound respiratory function during adolescence

Frequent exposure to acetaminophen during early life may weaken lung function during adolescence, a recent study has shown. This is especially true among children with glutathione S-transferase (GST) genotypes associated with poorer antioxidant function.

The study included 620 infants, of whom 92.7 percent (n=575) were followed until age 2 years. Of these, 97 percent had had at least 1 day of acetaminophen exposure. Most of the exposures were for nonrespiratory reasons or for upper respiratory tract symptoms. At ages 12 and 18 years, 23.7 percent and 23.5 percent had asthma.

The researchers observed no clear link between the doubling of total acetaminophen days with asthma at either adolescence ages examined. There was, however, a significant link between acetaminophen use and lower pre-bronchodilator FEV1/FVC* at 18 years of age (β, –0.10, 95 percent confidence interval [CI], –0.19 to –0.01). A similar effect was reported at 12 years.

Interestingly, the impact of childhood acetaminophen on adolescent respiratory function was moderated by GST genotype. For example, those who had the homozygous-ileum genotype for the GSTP1 gene were significantly more likely to report asthma at age 18 years following more frequent acetaminophen exposure between birth and age 2 years (odds ratio, 1.66, 95percent CI, 1.07–2.57; p=0.02).

In addition, the researchers noted that an “increasing doubling of days of acetaminophen use was associated with increased risk of adverse respiratory health in adolescents with GSTM1/T1 null and GSTP1 Ile/Ile polymorphisms for acetaminophen used for nonrespiratory indications and total acetaminophen use, respectively.”

“These findings need to be investigated and corroborated by other studies before translation into clinical practice,” they added.

*Forced expiratory volume in 1 second/forced vital capacity