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Published on: August 7, 2017
Parental smoking and airway reactivity in healthy infants
Robert S Tepper1, Tamica Williams-Nkomo, Tanya Martinez
1Department of Pediatrics, Indiana University Medical Center, James Whitcomb Riley Hospital for Children, 702 Barnhill Drive, ROC 4270, Indianapolis, IN 46202-5225, USA. rtepper@iupui.edu
Insights
Parental smoking lowers infant airway function but does not increase airway hyperreactivity. However, a family history of asthma is linked to heightened airway reactivity in infants.
Area of Science:
- Pediatric Pulmonology
- Environmental Health
- Respiratory Medicine
Background:
- Parental tobacco smoking is linked to reduced infant lung function and increased respiratory illnesses.
- Airway hyperreactivity may mediate the association between smoking exposure and impaired airway function.
Purpose of the Study:
- To investigate the association between parental tobacco smoking and airway hyperreactivity in healthy infants.
- To determine if airway hyperreactivity contributes to lower airway function in infants exposed to secondhand smoke.
Main Methods:
- Evaluated 76 healthy infants using the raised-volume rapid thoracic compression technique for airway function.
- Assessed airway reactivity via methacholine challenge, measuring the decline in forced expiratory flow (FEF(75)).
Main Results:
- Parental smoking was associated with lower baseline airway function (FEF(50), FEF(25-75)).
- Infants exposed to smoking showed reduced likelihood of developing significant FEF(75) decline during methacholine challenge (HR=0.4, p=0.001).
- Family history of asthma increased the likelihood of FEF(75) decline (HR=1.7, p=0.04).
Conclusions:
- Infant exposure to parental smoking is associated with diminished airway function.
- Parental smoking exposure was not associated with increased airway hyperreactivity.
- A family history of asthma independently predicts heightened airway reactivity in infants.
Abstract:
Parental tobacco smoking is associated with lower airway function and an increased incidence of wheezy respiratory illnesses in infants. We evaluated in 76 healthy infants whether exposure to parental tobacco smoking was associated with airway hyperreactivity, which could contribute to lower airway function and the increased wheezy illnesses. Airway function was measured using the raised-volume rapid thoracic compression technique, and airway reactivity was assessed by methacholine challenge (0.015-10 mg/ml), which was stopped for a more than 30% decrease in forced expiratory flow (FEF)(75) or the final dose with a less than 30% decrease. Parental tobacco smoking was associated with lower baseline airway function (FEF(50), 600 vs. 676 ml/second, p < 0.04; FEF(25-75), 531 vs. 597 ml/second, p < 0.05). Infants exposed to tobacco smoking were approximately half as likely to develop a more than 30% decline in FEF(75) at any given methacholine dose (hazard ratio = 0.4, p = 0.001). In addition, a history of asthma in an extended family member increased the likelihood that an infant would develop a more than 30% decline in FEF(75) (hazard ratio = 1.7, p = 0.04). We conclude that exposure to parental smoking is associated with lower airway function but not increased airway reactivity; however, family history of asthma is associated with heightened airway reactivity.
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