K W Lewis1, E M Bosque. 1. Department of Pediatrics, California Pacific Medical Center, San Francisco 94118, USA.
Abstract
OBJECTIVE: To determine whether fetal exposure to cigarette smoke impairs postnatal chemoreceptor control of ventilation and hypercapnic and hypoxic awakening responses. STUDY DESIGN: Smoking (n = 13) and nonsmoking (n = 34) women were recruited during pregnancy. Serum cotinine levels were measured to assess level of nicotine exposure. The infants were studied at 2 to 3 months of age for ventilatory and awakening responses to hypoxia (17%, 15% and 13% inspired O2) and hypercapnia 4%, 6%, and 8% inspired CO2). Continuous measures were analyzed with unpaired t tests and analysis of variance for repeated measures. Proportions of awakening and periodic breathing were analyzed by means of a comparison of proportions. RESULTS: The infants of smokers had lower birth weights (3022 +/- 566 vs 3518 +/- 491 gm; p < or = 0.005) and were older at the time of study (10.4 +/- 2.8 vs 8.7 +/- 1.3 weeks; p < 0.01) than the control infants. Maternal cotinine levels were higher in smokers (97.8 +/- 107 ng/ml vs no cotinine; p < 0.0001). More infants of smokers failed to awaken with hypoxia than did control infants (54% vs 15%; p = 0.006). The ventilatory responses to hypoxia and hypercapnia were similar in the two groups. All infants awakened with hypercapnia, and there was no difference in the awakening threshold for carbon dioxide (50.3 +/- 4.5 vs 48.3 +/- 5.4 mm Hg; p = 0.28). CONCLUSION: Infants of mothers who smoked during pregnancy have deficient hypoxic awakening responses, which may contribute to the increased risk of sudden infant death syndrome in infants of smoking mothers.
OBJECTIVE: To determine whether fetal exposure to cigarette smoke impairs postnatal chemoreceptor control of ventilation and hypercapnic and hypoxic awakening responses. STUDY DESIGN: Smoking (n = 13) and nonsmoking (n = 34) women were recruited during pregnancy. Serum cotinine levels were measured to assess level of nicotine exposure. The infants were studied at 2 to 3 months of age for ventilatory and awakening responses to hypoxia (17%, 15% and 13% inspired O2) and hypercapnia 4%, 6%, and 8% inspired CO2). Continuous measures were analyzed with unpaired t tests and analysis of variance for repeated measures. Proportions of awakening and periodic breathing were analyzed by means of a comparison of proportions. RESULTS: The infants of smokers had lower birth weights (3022 +/- 566 vs 3518 +/- 491 gm; p < or = 0.005) and were older at the time of study (10.4 +/- 2.8 vs 8.7 +/- 1.3 weeks; p < 0.01) than the control infants. Maternal cotinine levels were higher in smokers (97.8 +/- 107 ng/ml vs no cotinine; p < 0.0001). More infants of smokers failed to awaken with hypoxia than did control infants (54% vs 15%; p = 0.006). The ventilatory responses to hypoxia and hypercapnia were similar in the two groups. All infants awakened with hypercapnia, and there was no difference in the awakening threshold for carbon dioxide (50.3 +/- 4.5 vs 48.3 +/- 5.4 mm Hg; p = 0.28). CONCLUSION:Infants of mothers who smoked during pregnancy have deficient hypoxic awakening responses, which may contribute to the increased risk of sudden infant death syndrome in infants of smoking mothers.
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