Secondhand Smoke Exposure and Serum Trypsinogen in Cystic Fibrosis Carriers

Abstract

Supplemental digital content is available in the text. Objective The objective of this study was to determine if infants carrying 1 cystic fibrosis transmembrane receptor (CFTR) mutation demonstrate pancreatic inflammation in response to tobacco exposure. Methods Cystic fibrosis carrier infants aged 4 to 16 weeks were prospectively enrolled. Tobacco exposure was assessed by survey and maternal hair nicotine analysis. Serum immunoreactive trypsinogen (IRT) levels at birth and at the time of recruitment were analyzed relative to the presence or absence of tobacco exposure. The effect of the severity of the CFTR mutation carried by the infant on the tobacco-IRT relationship was also analyzed. Results Forty-eight infants completed the study. Newborn screen and follow-up IRT levels were not different between exposed infants (19 by hair analysis) and nonexposed infants (29 by hair analysis). Follow-up IRT levels were lower in infants with more severe CFTR mutations (P = 0.005). There was no difference in follow-up IRT based on CFTR mutation severity in exposed infants. Nonexposed infants with milder CFTR mutations had higher median IRT values on follow-up testing than those with more severe CFTR mutations (P < 0.05). Conclusions The pancreas of cystic fibrosis carrier infants is affected by tobacco exposure, and those carrying less severe CFTR mutations may be more susceptible to tobacco effects.