Passive Tobacco Exposure and Sudden Infant Death Syndrome

PEDIATRICS ◽  
1993 ◽  
Vol 92 (3) ◽  
pp. 505-506
Author(s):  
PETER N. LEE

To the Editor.— Drs Schoendorf and Kiely1 report increased risk of SIDS, both in mothers smoking during and after pregnancy ("combined exposure") and in mothers smoking only afterward ("passive exposure"). Most previous studies2-18 that reported that maternal smoking is associated with SIDS considered only smoking during pregnancy, but some2,4,11,15 considered smoking after pregnancy. However, I am unaware of any previous study which attempted separation of smoking during and after pregnancy. Although such an attempt is commendable, certain problems with the analysis and data of Drs Schoendorf and Kiely merit comment.

PEDIATRICS ◽  
1993 ◽  
Vol 91 (5) ◽  
pp. 893-896 ◽  
Author(s):  
E. A. Mitchell ◽  
R. P. K. Ford ◽  
A. W. Stewart ◽  
B. J. Taylor ◽  
D. M. O. Becroft ◽  
...  

Objective. Maternal smoking has been shown to be a risk factor for sudden infant death syndrome (SIDS). The effect of smoking by the father and other household members has not previously been examined. Methods. A large nationwide case-control study. Four hundred eighty-five SIDS deaths in the postneonatal age group were compared with 1800 control infants. Results. Infants of mothers who smoked during pregnancy had a 4.09 (95% confidence interval [CI] = 3.28, 5.11) greater risk of death than infants of mothers who did not smoke. Infants of mothers who smoked postnatally also had an increased risk of SIDS compared with infants of nonsmokers and, furthermore, the risk increased with increasing levels of maternal smoking. Smoking by the father and other household members increased the risk (odds ratio [OR] = 2.41, 95% CI = 1.92, 3.02 and OR = 1.54, 95% CI = 1.20, 1.99, respectively). Smoking by the father increased the risk of SIDS if the mother smoked, but had no effect if she did not smoke. In analyses controlled for a wide range of potential confounders, smoking by the mother and father was still significantly associated with an increased risk of SIDS. Conclusion. Passive tobacco smoking is causally related to SIDS.


PEDIATRICS ◽  
1992 ◽  
Vol 90 (6) ◽  
pp. 905-908 ◽  
Author(s):  
Kenneth C. Schoendorf ◽  
John L. Kiely

Sudden infant death syndrome (SIDS) is associated with maternal smoking during pregnancy. However, the relationship between tobacco exposure during infancy and SIDS is unknown. The examination of infants whose mothers smoked only after pregnancy will help determine the relationship between passive cigarette exposure during infancy and SIDS risk. This case-control analysis used data on normal birth weight (≥2500 g) infants included in the National Maternal and Infant Health Survey, a nationally representative sample of approximately 10 000 births and 6000 infant deaths. Infants were assigned to one of three exposure groups: maternal smoking during both pregnancy and infancy (combined exposure), maternal smoking only during infancy (passive exposure), and no maternal smoking. SIDS death was determined from death certificate coding. Logistic regression was used to adjust for potentially confounding variables. Infants who died of SIDS were more likely to be exposed to maternal cigarette smoke than were surviving infants. Among black infants the odds ratio was 2.4 for passive exposure and 2.9 for combined exposure. Among white infants the odds ratio was 2.2 for passive exposure and 4.1 for combined exposure. After adjustment for demographic risk factors, the odds ratio for SIDS among normal birth weight infants was approximately 2 for passive exposure and 3 for combined exposure for both races. These data suggest that both intrauterine and passive tobacco exposure are associated with an increased risk of SIDS and are further inducement to encourage smoking cessation among pregnant women and families with children.


Author(s):  
Qiaoxia Zhou ◽  
Daoyin Gong ◽  
Yu Zhang ◽  
Feijun Huang

Abstract Introduction The etiology of sudden infant death syndrome (SIDS) remains an unsolved problem. The aim of this meta-analysis is to investigate the potential association between monoamine oxidase A (MAOA) promoter variable number tandem repeat (VNTR) polymorphism and SIDS risk. Methods A systematic review and meta-analysis were conducted on studies from accessible electronic databases. Each VNTR variant was examined in each gender independently by comparing with the pooled results of other alleles. Results A total of six independent case–control studies including 1022 SIDS cases and 1839 controls were enrolled in this meta-analysis. In both of the whole populations and Caucasian populations, male infants with the low-MAOA-expression alleles (2R+3R) were found to exhibit a statistically significant increased risk of SIDS, whereas those with a 4R allele exhibited a reduced risk of SIDS. Besides, an increased risk of SIDS was detected in male Caucasian infants with 2R or 3R alleles. However, none of the allele or genotype variants was associated with SIDS in female victims. Conclusion In male Caucasian infants, the low expression of MAOA promoter VNTR alleles (2R and 3R) is associated with an increased risk of SIDS, and the existence of the 4R allele could be regarded as a protective factor.


PEDIATRICS ◽  
1996 ◽  
Vol 98 (4) ◽  
pp. 668-672
Author(s):  
Ernest Cutz ◽  
Donald G. Perrin ◽  
Richard Hackman ◽  
Elinor N. Czegledy-Nagy

Background. Maternal smoking is a well-recognized risk factor for sudden infant death syndrome (SIDS), but the precise mechanism is unknown. We tested a hypothesis that maternal smoking affects pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs), which are innervated PNEC clusters and presumed airway chemoreceptors. Methods. Lung sections from infants who died of SIDS and whose mothers smoked during pregnancy (n = 22), infants who died of SIDS and whose mothers were nonsmokers (n = 17), and age-matched control infants (n = 15) who died of other causes were immunostained for bombesin (a PNEC and NEB marker) and assessed morphometrically. Results. The frequency of PNEC (the percentage of airway epithelium immunoreactive for bombesin) was increased up to twofold in the lungs of infants who died of SIDS (7.7 ± 0.4%) compared with controls (4.9 ± 0.4%), as was the frequency (40 ± 3.5 vs 23 ± 3.7/cm2) and size (748 ± 46.5 vs 491 ± 25.8,µm2) of NEBs. In infants who died of SIDS and who were born to smoking mothers, PNEC frequency was increased significantly compared with that in those born to nonsmoking mothers, but the frequency and size of NEBs were not significantly different between the two groups. Conclusion. Our findings suggest that maternal smoking potentiates hyperplasia of the PNEC system in the lungs of infants who die of SIDS and that a dysfunction of these cells may contribute to the pathophysiology of SIDS.


Author(s):  
Ian Mitchell ◽  
Daniel Y Wang ◽  
Christine Troskie ◽  
Lisa Loczy ◽  
Abby Li ◽  
...  

Abstract Objectives Risk factors for sudden infant death syndrome include premature birth, maternal smoking, prone or side sleeping position, sleeping with blankets, sharing a sleeping surface with an adult, and sleeping without an adult in the room. In this study, we compare parents’ responses on sleep patterns in premature and term infants with medical complexity. Methods Parents of children enrolled in the Canadian Respiratory Syncytial Virus Evaluation Study of Palivizumab were phoned monthly regarding their child’s health status until the end of each respiratory syncytial virus season. Baseline data were obtained on patient demographics, medical history, and neonatal course. Responses on adherence to safe sleep recommendations were recorded as part of the assessment. Results A total of 2,526 preterms and 670 term infants with medical complexity were enrolled. Statistically significant differences were found in maternal smoking rates between the two groups: 13.3% (preterm); 9.3% (term) infants (χ 2=8.1, df=1, P=0.004) and with respect to toys in the crib: 12.3% (term) versus 5.8% preterms (χ 2=24.5, df=1, P<0.0005). Preterm infants were also significantly more likely to be placed prone to sleep (8.8%), compared with term infants (3.3%), (χ 2=18.1, df=1, P<0.0005). Conclusion All the infants in this study had frequent medical contacts. There is a greater prevalence of some risk factors for sudden infant death syndrome in preterm infants compared to term infants with medical complexity. Specific educational interventions for vulnerable infants may be necessary.


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