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  Vol. 158 No. 4, April 2004 TABLE OF CONTENTS
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Adult Hemoglobin Levels at Birth and Risk of Sudden Infant Death Syndrome

David B. Richardson, PhD; Steve Wing, PhD; Fred Lorey, PhD; Irva Hertz-Picciotto, PhD

Arch Pediatr Adolesc Med. 2004;158:366-371.

Background  During the final weeks of gestation, infants normally begin a transition from the production of fetal to adult hemoglobin. Delayed or faulty transition to the production of adult hemoglobin might play a role in the etiology of sudden infant death syndrome (SIDS).

Objective  To examine the association between adult hemoglobin levels measured at birth and the subsequent risk of SIDS.

Design and Setting  Cohort study of all infants born in California between March 1, 1990, and December 31, 1997, who were enrolled in the state's Newborn Screening Program and followed up during the first year of life to identify deaths attributed to SIDS.

Participants  Population-based sample of 3.2 million infants.

Main Outcome Measure  Risk of death attributed to SIDS.

Results  The study included 2425 infants whose deaths were attributed to SIDS. There was an inverse relationship between adult hemoglobin level, expressed as a percentage of total hemoglobin, and the subsequent incidence of SIDS. After adjustment for infant sex, race/ethnicity, length of gestation, maternal age, maternal education, maternal smoking, intrauterine growth restriction, and preeclampsia/eclampsia, the relative risks of SIDS for infants in the lower 4 quintiles of adult hemoglobin level were, in descending order, 1.12 (95% confidence interval [CI], 0.96-1.32), 1.38 (95% CI, 1.19-1.59), 1.55 (95% CI, 1.34-1.80), and 2.15 (95% CI, 1.87-2.47) compared with infants in the highest quintile.

Conclusions  These findings suggest that infants with low levels of adult hemoglobin in the first hours after birth are at elevated risk of SIDS. Delayed maturation in production of adult hemoglobin may play a role in the etiology of some SIDS cases.


From the Department of Epidemiology, School of Public Health, University of North Carolina at Chapel Hill (Drs Richardson, Wing, and Hertz-Picciotto); the Program Development and Evaluation Section of the Genetic Disease Branch, California Department of Health and Human Services, Berkeley (Dr Lorey); and the Department of Epidemiology and Preventive Medicine, University of California–Davis (Dr Hertz-Picciotto).



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