Relationship of Sudden Infant Death Syndrome to Maternal Smoking During and After Pregnancy

PEDIATRICS ◽  
1992 ◽  
Vol 90 (6) ◽  
pp. 905-908 ◽  
Author(s):  
Kenneth C. Schoendorf ◽  
John L. Kiely
Keyword(s):  
Odds Ratio ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Normal Birth Weight ◽  
Combined Exposure ◽  
Tobacco Exposure ◽  
Normal Birth ◽  
Passive Exposure ◽  
The Relationship

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.

Passive Tobacco Exposure and Sudden Infant Death Syndrome

PEDIATRICS ◽  
1993 ◽  
Vol 92 (3) ◽  
pp. 505-506
Author(s):  
PETER N. LEE
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Combined Exposure ◽  
Tobacco Exposure ◽  
Smoking During Pregnancy ◽  
Passive Exposure ◽  
Increased Risk

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.

scholarly journals Revisiting the Neuropathology of Sudden Infant Death Syndrome (SIDS)

2020 ◽  
Vol 11 ◽  
Author(s):  
Jessica Blackburn ◽  
Valeria F. Chapur ◽  
Julie A. Stephens ◽  
Jing Zhao ◽  
Anne Shepler ◽  
...  
Keyword(s):  
Machine Learning ◽  
Risk Factors ◽  
Birth Weight ◽  
Infant Mortality ◽  
Sudden Infant Death Syndrome ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Normal Birth Weight ◽  
Normal Birth ◽  
Extrinsic Risk

Background: Sudden infant death syndrome (SIDS) is one of the leading causes of infant mortality in the United States (US). The extent to which SIDS manifests with an underlying neuropathological mechanism is highly controversial. SIDS correlates with markers of poor prenatal and postnatal care, generally rooted in the lack of access and quality of healthcare endemic to select racial and ethnic groups, and thus can be viewed in the context of health disparities. However, some evidence suggests that at least a subset of SIDS cases may result from a neuropathological mechanism. To explain these issues, a triple-risk hypothesis has been proposed, whereby an underlying biological abnormality in an infant facing an extrinsic risk during a critical developmental period SIDS is hypothesized to occur. Each SIDS decedent is thus thought to have a unique combination of these risk factors leading to their death. This article reviews the neuropathological literature of SIDS and uses machine learning tools to identify distinct subtypes of SIDS decedents based on epidemiological data.Methods: We analyzed US Period Linked Birth/Infant Mortality Files from 1990 to 2017 (excluding 1992–1994). Using t-SNE, an unsupervised machine learning dimensionality reduction algorithm, we identified clusters of SIDS decedents. Following identification of these groups, we identified changes in the rates of SIDS at the state level and across three countries.Results: Through t-SNE and distance based statistical analysis, we identified three groups of SIDS decedents, each with a unique peak age of death. Within the US, SIDS is geographically heterogeneous. Following this, we found low birth weight and normal birth weight SIDS rates have not been equally impacted by implementation of clinical guidelines. We show that across countries with different levels of cultural heterogeneity, reduction in SIDS rates has also been distinct between decedents with low vs. normal birth weight.Conclusions: Different epidemiological and extrinsic risk factors exist based on the three unique SIDS groups we identified with t-SNE and distance based statistical measurements. Clinical guidelines have not equally impacted the groups, and normal birth weight infants comprise more of the cases of SIDS even though low birth weight infants have a higher SIDS rate.

Letters to the Editor

PEDIATRICS ◽  
1995 ◽  
Vol 96 (1) ◽  
pp. 168-168
Author(s):  
Vincent J. M. Di Maio
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Forensic Pathology ◽  
Sudden Infant Death ◽  
Laboratory Medicine ◽  
Sudden Infant ◽  
Letters To The Editor ◽  
New Information ◽  
The Relationship

In the editorial by Little and Brooks,1 the authors refer to "new information" that two of the five deaths in the study by Steinschneider2 were in fact murders. This brings into question the conclusions of the Steinschneider study, the relationship between apnea and sudden infant death syndrome (if any) and, perhaps, the use of home monitors. All of this was not "new information" to the Forensic Pathology community. That the two deaths in the study by Steinschneider were probably homicide was stated in a chapter in Clinics in Laboratory Medicine, a letter to Pediatrics, and in the textbook Forensic Pathology.3

Maternal Smoking and Pulmonary Neuroendocrine Cells in Sudden Infant Death Syndrome

PEDIATRICS ◽  
1996 ◽  
Vol 98 (4) ◽  
pp. 668-672
Author(s):  
Ernest Cutz ◽  
Donald G. Perrin ◽  
Richard Hackman ◽  
Elinor N. Czegledy-Nagy
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Airway Epithelium ◽  
Maternal Smoking ◽  
Matched Control ◽  
Sudden Infant Death ◽  
Neuroendocrine Cells ◽  
Sudden Infant ◽  
Neuroepithelial Bodies ◽  
Pulmonary Neuroendocrine Cells

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.

Smoking and the Sudden Infant Death Syndrome

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 ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Risk Of Death ◽  
Increased Risk ◽  
Wide Range ◽  
Household Members ◽  
Control Study

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.

scholarly journals What risk factors for sudden infant death syndrome are preterm and term medically complex infants exposed to at home?

2020 ◽  
Author(s):  
Ian Mitchell ◽  
Daniel Y Wang ◽  
Christine Troskie ◽  
Lisa Loczy ◽  
Abby Li ◽  
...  
Keyword(s):  
Risk Factors ◽  
Respiratory Syncytial Virus ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Term Infants ◽  
Medical Complexity ◽  
Syncytial Virus

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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