Risk factors for sudden infant death syndrome in the US Collaborative Perinatal Project

Risk factors for sudden infant death syndrome (SIDS) were studied among infants born to the nearly 56,000 women enrolled in the US Collaborative Perinatal Project from 1959 through 1966. The 193 SIDS cases identified in the cohort were compared with 1930 controls randomly selected from infants who survived the first year of life. The previously documented excess risk associated with black race disappeared after adjusting for maternal education and family income. Maternal smoking, maternal anaemia during pregnancy, and lack of early prenatal care were all positively associated with SIDS. After adjustment for gestational age, infants with low weight and length at birth were still at increased SIDS risk, suggesting that intrauterine growth retardation may be a risk factor. Neurological abnormalities diagnosed before death were associated with SIDS, but much of the association was removed by adjusting for birthweight. The negative association of breastfeeding with SIDS was much reduced upon adjustment by maternal education and birthweight. These findings may have important implications in our understanding of the epidemiology of SIDS.     

Prenatal and intrapartum events and sudden infant death syndrome

The purpose of this study was to evaluate specific pregnancy and labour and delivery events that may increase the risk of sudden infant death syndrome (SIDS). A matched case-control study was conducted in five counties in southern California, using California death certificate records. The sample consisted of 239 Caucasian, African-American, Hispanic and Asian mothers of SIDS infants and 239 mothers of control infants matched on sex, race, birth hospital and date of birth. Mothers participated in a detailed telephone interview and provided access to obstetric and paediatric records. More case than control mothers reported a family history of anaemia (OR=2.12, P < 0.001). Placental abruptions were strongly associated with SIDS (unadjusted OR=7.94, [95% CI 1.34,47.12]). There was an increased risk of SIDS death associated with maternal anaemia during pregnancy (OR=2.51, [95% CI 1.25,5.03]), while simultaneously adjusting for maternal smoking during pregnancy, maternal years of education and age, parity, infant birthweight, gestational age, medical conditions at birth, infant sleep position and post-natal smoking. Interactions of anaemia and prenatal smoking as well as anaemia and post-natal smoking were not statistically significant. There were no other statistically significant differences between case and control mothers for pregnancy conditions, labour and delivery events (e.g. caesarean sections, anaesthesia, forceps) or newborn complications (e.g. nuchal cord, meconium aspiration). Anaemia and placental abruptions were significantly associated with an increased risk of SIDS; both are circumstances in which a fetus may become hypoxic, thereby compromising the subsequent growth, development and ultimate survival of the infant.     

Maternal smoking, birthweight and gestational age in sudden infant death syndrome (SIDS) babies and their surviving siblings

To evaluate the effect of maternal smoking on intrauterine growth of babies who died of sudden infant death syndrome (SIDS), birthweights of SIDS infants and their surviving siblings were compared with birthweights of infants in sibships were all infants survived the first year of life. We studied 184 349 mothers with at least two births registered in the population-based Swedish Medical Birth Registry during 1983–91. The mother being the unit of analysis, birthweight and gestational age of her infants were the repeated measures used in a repeated measures analysis of variance. Mothers whose first two infants survived at least 1 year, smoked less than mothers of SIDS infants, 25 and 41% ( P < 5 0.01). Overall, SIDS mothers did not smoke more while pregnant with the SIDS infant than while pregnant with the surviving sibling. SIDS siblings weighted, on average, 90 g less than infants in non-affected sibships. SIDS babies were even lighter, 193 g, and had 3.8 days shorter mean gestational age, compared with same birth-order babies in non-affected sibships. After adjustment for gestational age, the birthweight difference changed only slightly for SIDS siblings, while the difference for SIDS infants was reduced from 193 to 110 g. Further adjustment for smoking reduced the birthweight difference for SIDS siblings, from 74 to 50 g, and SIDS infants, from 110 to 82 g. Intrauterine growth retardation of sibships with a SIDS baby is explained only partly by maternal smoking. The even lower birthweight of the SIDS baby, resulting from shorter gestational age, cannot be explained by smoking, suggesting pregnancy factors specific to the SIDS baby and not to its siblings.     

Maternal pre-eclampsia/eclampsia and the risk of sudden infant death syndrome in offspring

To determine whether maternal exposure to pre-eclampsia/eclampsia during pregnancy increases the risk of sudden infant death syndrome (SIDS) in offspring, we conducted a population-based case-control study using the California linked birth and death certificate data. All infants who died of SIDS (ICD-9 code 798.0) during 1989-91 were identified as cases. More than 96% of the identified SIDS cases were diagnosed through autopsy. Ten controls who did not die from SIDS were randomly selected for each case from the birth certificate matched to the case on the year of birth. Among 2,029 cases and 21,037 controls included in the final analysis, mothers of 49 cases (2.4%) and 406 controls (1.9%) had a diagnosis of either pre-eclampsia or eclampsia noted on the birth certificate. After adjustment for maternal age, prenatal smoking, race/ethnicity, parity, maternal education, gestational age at the initial visit for prenatal care, infant year of birth and infant sex, maternal pre-eclampsia/ eclampsia during pregnancy was associated with a 50% increased risk of SIDS in the offspring (odds ratio = 1.5, 95% confidence interval 1.1, 2.0). Potential under-reporting of pre-eclampsia/eclampsia on the birth certificates was likely to be non-differential and is unlikely to explain the finding. Fetal hypoxia resulting from pre-eclampsia/ eclampsia or immunological aetiology affecting the risk of both pre-eclampsia/eclampsia and SIDS may explain the finding.     

Sudden infant death syndrome and reported maternal smoking during pregnancy

We investigated the effect of maternal smoking during pregnancy on the relative risk of sudden infant death syndrome (SIDS) by linking data from Georgia birth and death certificates from 1997 to 2000. We estimated the effect of misclassifying smokers as non-smokers and the effect of being misclassified on SIDS rates, and we calculated the fraction of cases caused by exposure. Of all SIDS cases, 21% were attributable to maternal smoking; among smokers, 61% of SIDS cases were attributable to maternal smoking. Maternal smoking during pregnancy is associated with a significantly increased risk of SIDS.     

Secular trends of sudden infant death syndrome in Norway 1967–1988: application of a method of case identification to Norwegian registry data

Summary. In Norway, towards the end of the 1980s, sudden infant death syndrome (SIDS) was the most frequent cause of infant death. Both SIDS and the total post-perinatal mortality rates had increased. This paper presents a procedure for identifying SIDS from death certificates. Supplemented with additional information, a database was established to evaluate secular trends of SIDS and for further analytical research. The Medical Birth Registry of Norway comprises 1.3 million births from 1967 to 1988. Of these, 5447 infants died in the post-perinatal period. The cause of death was reviewed by an expert panel and 1984 cases of SIDS were retrieved.
Low maternal age, higher birth order, male gender, and lower birthweight were confirmed as risk factors for SIDS. In 1988, the rate for SIDS and for total post-perinatal deaths reached 2.69 and 5.02 per 1000 infants at risk. The incidence of SIDS increased 2.2 times from the period 1967–1971 to the period 1987–1988. Adjusted for maternal age, birth order, and birthweight, the odds ratio was 3.1. The increase is due to factors not yet accounted for. Adjusted mortality rates for the other post-perinatal deaths were not different from the crude rates.     

Preterm delivery and age of SIDS death

PURPOSE: The aim of the study is to (i) reexamine risk factors for sudden infant death syndrome (SIDS) and (ii) describe the relationship between length of gestation and age at death from SIDS. METHODS: To evaluate risk factors for SIDS, we used multivariable logistic regression and included maternal demographic characteristics, maternal health and behavioral factors, and infant characteristics, including fetal growth, using US national linked birth and death files from 1996 to 1998. We used multivariable linear regression with mean postnatal age of death as the outcome of interest, controlling for the factors listed (referent length of gestation, 40 to 41 weeks). RESULTS: The crude SIDS rate was 0.7 deaths/1000 live births (8199 deaths). Length of gestation was a strong risk factor for SIDS, with the adjusted odds ratio (OR) greatest at shorter gestations: 28 to 32 weeks (OR, 2.9; 95% confidence interval, 2.6-3.2). Infants with gestations of 22 to 27 and 28 to 32 weeks died at mean ages of 20.9 (SD = 0.8) and 15.3 (SD = 0.5) weeks, respectively (p < or = 0.002). Term infants (40 to 41 weeks) died of SIDS at an adjusted mean age of 14.5 (SD = 0.4) weeks. CONCLUSIONS: Preterm birth continues to be a strong risk factor for SIDS after controlling for fetal growth. With increasing gestational age, mean age of SIDS death decreases considerably, with the postnatal age of death of very preterm infants 6 weeks later than that of term infants.     

Tobacco smoke exposure at one month of age and subsequent risk of SIDS--a prospective study

The aim of this investigation was to identify the sources of postnatal exposure to tobacco smoke at 1 month of age and to examine their relation to sudden infant death syndrome (SIDS). The Tasmanian Infant Health Survey was a prospective cohort study undertaken from 1988 to 1995. It involved 9,826 infants (89% of eligible infants) at higher risk of SIDS. Subsequently 53 eligible infants died of SIDS. Hospital interviews were available on 51 and home interviews on 35 SIDS infants. Urinary cotinine assays were conducted using gas-liquid chromatography (n = 100). Within a predictive model that explained 63% of urinary cotinine variance, the strongest predictor of cotinine and also of SIDS was maternal smoking, though the effects of prenatal and postnatal smoking could not be separated. However, for particular smoking-related behaviors, there was a discordance between prediction of cotinine concentration and prediction of risk of SIDS. If smoking mothers did not smoke in the room with the baby, the cotinine level in the infant's urine was reduced by a little more than a half (p = 0.009), but this was not associated with a reduction in SIDS risk (odds ratio = 1.09, 95% confidence interval 0.47-2.55). Similarly, the presence of other adult resident smokers was associated with a 63% increase in urinary cotinine (p = 0.047) but not with increased SIDS risk (odds ratio = 0.69, 95% confidence interval 0.34-1.40). However, the study lacked the power to detect modest effects, that is, those altering risk less than twofold.     

Sudden infant death syndrome and social deprivation: assessing epidemiological factors after post-matching for deprivation

As part of the confidential enquiry into stillbirths and deaths in infancy (CESDI), a 3-year population-based case-control study was specifically designed to look at risk factors associated with sudden infant death syndrome (SIDS) after the dramatic fall in incidence. The study was conducted between 1993 and 1996 in five English Health Regions (population 17 million) with parental interviews for each death and four age-matched controls. The aim of this analysis was to investigate the extent to which epidemiological characteristics associated with SIDS were particular to the syndrome or more general markers for socio-economic deprivation. One control was reassigned to each case post-matched for infant age, time of sleep and socio-economic status using components of the Townsend Deprivation Score. The post-matched analysis involved 323 SIDS infants and 323 controls with a similar socio-economic profile. Notable factors significant in the original univariable analysis that became non-significant after post-matching included young maternal age (median: 23 years 4 months SIDS vs. 23 years 11 months post-matched controls), being an unsupported mother (13.6% SIDS vs. 11.1% post-matched controls) and being bottle-fed (56.7% SIDS vs. 55.4% post-matched controls). Other factors, although clearly related to deprivation, such as parental smoking, remained significant in both the univariable and multivariable post-matched analyses.     

Risk factors of sudden infant death syndrome and risk factors for sleep disturbances

Relationship between major risk factors of sudden infant death syndrome (SIDS) and sleep disorders in the infants is the subject of review and discussion. Improper micro‐environmental characteristics (especially poor environmental organisation and lack of developmental stimulation), pre‐term delivery and/or infant low birth weight, prone sleep position, maternal smoking during pregnancy, and infant–parent(s) bed‐sharing are among well‐established risk factors of SIDS. These factors may also be associated with sleep disorders in infants, principally with bedtime problems, abnormal night awakenings, and arrhythmic sleep. As an attempt to fix sleep problems, some inexperienced parents may try infant‐rearing practices that may only aggravate sleep troubles and lead to further increased risk of SIDS, thus giving start to a vicious circle. Health care providers need to be aware of such situations as an opportunity to provide parents with guidance with respect for individual infant and family characteristics.     

Smoking and the sudden infant death syndrome

The aims of this review are (a) to critically examine the epidemiologic evidence for a possible association between smoking and the sudden infant death syndrome (SIDS), (b) to review the pathology and postulated physiological mechanism(s) by which smoking might be causally related to SIDS, and (c) to provide recommendations for SIDS prevention in relation to tobacco smoking. Over 60 studies have examined the relation between maternal smoking during pregnancy and risk of SIDS. With regard to prone-sleep-position intervention programs, the pooled relative risk associated with maternal smoking was RR = 2.86 (95% CI = 2.77, 2.95) before and RR = 3.93 (95% CI = 3.78, 4.08) after. Epidemiologically, to distinguish the effect of active maternal smoking during pregnancy from involuntary tobacco smoking by the infants of smoking mothers is difficult. Clear evidence for environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking when the mother is a non-smoker. Seven such studies have been carried out. The pooled unadjusted RR was 1.49 (95% CI = 1.25, 1.77). Consideration of the pathological and physiological effects of tobacco suggests that the predominant effect from maternal smoking comes from the in utero exposure of the fetus to tobacco smoke. Assuming a causal association between smoking and SIDS, about one-third of SIDS deaths might have been prevented if all fetuses had not been exposed to maternal smoking in utero.     

Sudden infant death syndrome: seasonality and a biphasic model of pathogenesis.

STUDY OBJECTIVE--This paper examines the relationship between season, age, and the sudden infant death syndrome (SIDS). It provides a theoretical model for the pathogenesis of SIDS and uses it as a framework to consider risk factor mechanism. DESIGN--A case series analysis was used to examine season and age in relation to SIDS and seasonal pattern and age at death distribution of perinatal risk factors. SETTING--The source population for the SIDS cases in this study was all live births in the state of Tasmania, Australia, 1975 to 1987 inclusive. SUBJECTS--Cases were all infants born 1975 to 1987 who died of SIDS on whom birth notification information was available (n = 348). The live birth cohort 1980-87 (n = 55,944) was used as the control population for risk factor identification. MEASUREMENTS AND MAIN RESULTS--The median ages of death for spring, summer, autumn, and winter born infants were 115, 103.5, 91 and 78 days. Spring and summer born infants died at a significantly older median age than winter born infants. The month of birth distribution of SIDS cases did not alter significantly from a uniform, nonseasonal distribution (p greater than 0.25) but month of death was seasonally distributed (p less than 0.01). Premature and low birthweight infants died at an older median age (p less than 0.05) than term and non-low-birthweight infants. An excess of male infant deaths and infant deaths to older mothers occurred during winter (p less than 0.05). CONCLUSIONS--The pathogenesis of SIDS can be represented as a biphasic model with three pathways of risk factor operation. In this study, season influenced the age at death of SIDS infants. We propose that risk factors with a strong seasonal distribution are likely to be operating in the postnatal period.     

Epidemiologic comparisons of the sudden infant death syndrome with other major components of infant mortality

All 1998 resident infant deaths in the 1969--1977 King County, Washington birth cohort of 139,132 resident live births comprise the data base for epidemiologic comparisons of the sudden infant death syndrome (SIDS) with eight other major infant mortality components: hyaline membrane disease; respiratory distress syndrome; asphyxia of the newborn; immaturity; birth injury; congenital malformation; infection; and "all other." These components were compared with respect to age at death; sex; race; prior fetal loss; prior live-born, now dead; birth plurality; birth weight; maternal age; birth order; marital status; prenatal care; and season of death in an attempt to determine the uniqueness of these purported SIDS risk factors. Only the age at death distribution unequivocally distinguished SIDS from the other components. The combination of low maternal age and multiparity was demonstrated to be putatively synergistic for risk of SIDS, hyaline membrane disease, and respiratory disease syndrome. Only deaths from infection exhibited seasonal variation similar to SIDS. These observations probably reflect secondary associations with as yet unidentified primary risk factors relatable to maternal experience.     

The national cot death prevention program in New Zealand

Abstract: A case-control study examining the risk factors for sudden infant death syndrome (SIDS) in New Zealand identified three risk factors that are potentially amenable to modification: prone sleeping position of the infant, maternal smoking and lack of breastfeeding. In total these three risk factors may account for 79 per cent of deaths from SIDS in New Zealand. We describe the planning and implementation of the cot death prevention program, which has involved a wide range of groups and different strategies. The outcome of the prevention program is being evaluated.     

Ethnic differences in the incidence of the sudden infant death syndrome (SIDS) in Victoria, Australia 1985–1989

Summary. In order to describe ethnic differences in the incidence of the sudden infant death syndrome (SIDS) records of all livebirths in the State of Victoria, Australia, 1985–1989, excluding those who died in the first month of life, were linked to death certificates. Cases were defined as infants dying with a diagnosis of SIDS between 1 month and 1 year of age ( n = 601) from the cohort of 308052 neonatal survivors. Ethnicity was defined by the mother's country of birth. The SIDS incidence was 2.04/1000 in infants of Australian-born mothers. The relative risk of SIDS was 0.28 (95% confidence interval (CI) 0.15,0.55) in infants whose mothers had been born in Southern Europe and 0.48 (95% CI 0.29, 0.78) in infants whose mothers had been born in Asia. SIDS in infants of Australian-born mothers was associated with low maternal age, high parity, marital status other than married, male sex, multiple birth, low birthweight and preterm birth. After adjustment for those factors in a case-control analysis using a logistic regression model the adjusted odds ratio for SIDS was 0.34 (95% CI 0.17, 0.69) comparing infants whose mothers were born in Southern Europe with infants of Australian-born mothers, and 0.60 (95% CI 0.35, 1.04) for infants whose mothers were born in Asia, compared with infants of the Australian-born. Thus there are substantial ethnic differences in SIDS which are not explained by the classic social and perinatal risk factors.     

Sudden infant death syndrome in Australian Aboriginal and non-Aboriginal infants: an analytical comparison

Summary. Our previous research has shown that the sudden infant death syndrome (SIDS) rate for Aboriginal infants in Western Australia (WA) is markedly higher than that for non-Aboriginal infants. The aim of this study was to identify factors that may be important in explaining this disparity. A case-control study was conducted based on routinely collected data for the population of WA singleton births from 1980 to 1990 inclusive. Cases were infants bom and classified as dying from SIDS in WA (Aboriginal n = 88; non-Aboriginal n = 409). Controls were infants born in WA and not classified as dying from SIDS; 2% samples of both Aboriginal and non-Aboriginal infants were included. The risk of dying from SIDS in Aboriginal infants was 3.86 times [95% confidence interval (CI) = 2.98 to 5.02] that in non-Aboriginal infants. Statistically significant univariable risk factors for SIDS in Aboriginal infants were preterm birth, low birthweight and small-for-gestarional-age; for non-Aboriginal infants they included these factors as well as single marital status, young maternal age, parity of one or greater and male sex. Comparing Aboriginal with non-Aboriginal controls, most of the risk factors were more common in the Aboriginal population. Multiple logistic regression analysis indicated that Aboriginal infants were 1.43 times [95% CI = 1.04 to 1.95] more likely to die from SIDS than non-Aboriginal infants. Differences in the risk factor profile for Aboriginal and non-Aboriginal infants were sought using interaction terms. The only important differences were that the risk of SIDS in Aboriginal infants, unlike that in non-Aboriginal infants, appeared not to be strongly related to male sex or to single marital status. Thus, the results show that the disparity between the incidence of SIDS in the Aboriginal and non-Aboriginal populations can be explained largely, although not totally, by the high prevalence of routinely recorded risk factors in the Aboriginal population. A limitation of this study is that data on the postnatal nsk factors of prone sleeping, maternal smoking and non-breastfeeding were unavailable. The residual excess risk for Aboriginal infants may be a result of these recognised postnatal risk factors and /or other infant care practices that are not routinely recorded in our data base, or to underlying social and economic conditions. Further study of all these potential risk factors is warranted.     

Seasonality in the sudden infant death syndrome

Distinctive epidemiological features of the sudden infant death syndrome (SIDS) are its age at death distribution and pronounced winter excess. Whether or not these effects are independent of the month of birth of the infant is uncertain. We used a loglinear model to separate the effects of age at death, month of death and month of birth amongst 6229 infants who died from SIDS in England and Wales during the period 1979-1983. The results suggest that month of birth and month of death independently influence the risk of the infant dying from SIDS, the risk related to month of death being much greater.     

Sudden infant death syndrome in New Zealand: are risk scores useful? New Zealand National Cot Death Study Group.

STUDY OBJECTIVE--To evaluate the Christchurch, Invercargill, Dunedin (CID) and Oxford record linkage study (ORLS) risk scores in five regions of New Zealand and examine the effect of risk factors for sudden infant death syndrome (SIDS), such as prone sleeping position, maternal smoking, breast feeding, measures of illness, the use of antenatal classes, community health care, and medical services on a high and low risk group delineated by the CID score. DESIGN--This was a case-control study of infants dying of SIDS. SETTING--Both the cases and controls were born in one of five health districts in New Zealand and their parents were interviewed between 1 November 1987 and 31 October 1990. PARTICIPANTS--The cases were 485 infants who died of SIDS. The controls were a random sample drawn from the same five regions in which the cases were born, chosen so that their age on the day on which they were interviewed was similar to the age at death of the cases. Risk scores were calculated for 387 case and 1579 controls. MEASUREMENTS AND MAIN RESULTS--Using the recommended cut off points the sensitivity and specificity of the CID and ORLS were found to be similar to those described for other samples. The differences among the regions were significant. There was, however, no evidence that the association between SIDS and the risk factors considered was different in the high and low risk groups delineated by the CID score. The relative attributable risk for smoking was 32.3% in the high risk group. The excess risk that could be attributed to a different prevalence of any of the other risk factors in the high risk group was small when compared with the low risk group. CONCLUSIONS--Health care resources should be spent on promoting and evaluating good child care practices for all, rather than identifying and promoting special interventions for those in the high risk category.     

The association of maternal smoking with age and cause of infant death

Linked birth certificate and infant death certificate data from Missouri for 1979-1983 were used to explore the association of maternal smoking with age and cause of infant death. The data included 305,730 singleton white livebirths, of which 2,720 resulted in infant deaths. Using multiple logistic regression to control for the confounding effects of maternal age, parity, marital status, and education, the authors found that smoking was associated with both neonatal and post-neonatal mortality and with each cause of death except congenital anomalies. The adjusted odds ratio for smoking was higher for postneonatal deaths than neonatal deaths and was particularly high for two causes: respiratory disease (odds ratio = 3.4) and sudden infant death syndrome (odds ratio = 1.9). A moderate odds ratio (about 1.4) was found for causes attributed to the International Classification of Diseases, 9th Revision Perinatal Conditions Chapter. Although the associations for neonatal deaths and perinatal conditions were partially attributable to the effect of maternal smoking in lowering birth weight, virtually none of the excess respiratory mortality and sudden infant death syndrome mortality among the offspring of smokers was attributable to birth weight differences between the infants of smokers and nonsmokers. This suggests that respiratory deaths and sudden infant death syndrome deaths may be related to the effect of passive exposure of the infant to smoke after birth.