Elsevier

The Journal of Pediatrics

Volume 127, Issue 5, November 1995, Pages 691-699
The Journal of Pediatrics

Deficient hypoxia awakening response in infants of smoking mothers: Possible relationship to sudden infant death syndrome☆,☆☆,★,★★

Presented in part at the Western Society for Pediatric Research, February 1995, Carmel, Calif., and the Society for Pediatric Research, May 1995, San Diego, Calif.
https://doi.org/10.1016/S0022-3476(95)70155-9Get rights and content

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 ≤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. (J PEDIATR 1995;127:6919)

Section snippets

Subjects

Pregnant women were recruited through advertisements throughout the San Francisco Bay area. Histories were obtained for maternal age, parity, general health, and complications of pregnancy. Subjects who agreed to enroll their infants in the study were interviewed to determine their use of tobacco, alcohol, and other drugs. The subjects filled out a questionnaire about the number of cigarettes smoked per day, years of smoking, other tobacco smoke exposure in the household and workplace, and use

Patient population

One hundred twenty-six women (56 smokers, 70 nonsmokers) responded to advertisements about the study. Seventy-three women entered the study (29 smokers, 44 control subjects) and 47 (13 smokers, 34 nonsmokers) completed the study. Reasons for failure to complete or exclusion from the study included preterm delivery, stillbirth, congenital anomaly, and withdrawal of consent after delivery. We were unable to obtain sleep studies in four control infants and one study infant of a smoker because they

DISCUSSION

Failure to awaken in response to a hypoxia challenge occurred significantly more often in infants of smokers than in control infants. All infants in both groups responded to hypercapnia challenges with no difference in arousal threshold. In addition, the ventilatory responses to hypoxia and hypercapnia were similar in the two groups. These findings indicate that the peripheral and central chemoreceptors are functioning but that the brain-stem-mediated hypoxic arousal response is abnormal.

References (36)

  • FJ Seidler et al.

    Fetal nicotine exposure ablates the ability of postnatal nicotine challenge to release norepinephrine from rat brain regions

    Dev Brain Res

    (1992)
  • TA Slotkin et al.

    Impact of fetal nicotine exposure on development of rat brain regions: critical sensitive periods or effects of withdrawal?

    Brain Res Bull

    (1993)
  • HC Kinney et al.

    Early developmental changes in [3H]nicotine binding in the human brain stem

    Neuroscience

    (1993)
  • B Haglund et al.

    Cigarette smoking as a risk factor for sudden infant death syndrome: a population-based study

    Am J Public Health

    (1990)
  • JP Nicholl et al.

    Antenatal smoking, postnatal passive smoking and the sudden infant death syndrome

  • JH Hoffman et al.

    Risk factors for SIDS: results of the National Institute of Child Health and Human Development SIDS Cooperative Epidemiological Study

  • EA Mitchell et al.

    Smoking and the sudden infant death syndrome

    Pediatrics

    (1993)
  • FJ Murphy et al.

    The epidemiology of sudden infant death syndrome

    J Epidemiol Commun Health

    (1982)

    • Cited by (0)

    ☆

    From the Department of Pediatrics, California Pacific Medical Center, San Francisco

    ☆☆

    Supported by funds provided by the Cigarette and Tobacco Surtax Fund of the State of California through the Tobacco-related Disease Research Program of the University of California, grant No. 2RT-0048

    ★

    Reprint requests: Kathleen W. Lewis, MD, Newborn Services, California Pacific Medical Center, 3850 California St., San Francisco, CA 94118.

    ★★

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