Are race and length of gestation related to age at death in the sudden infant death syndrome?

Although race and preterm delivery are known to be associated with sudden infant death syndrome (SIDS), the relationships between age at death from SIDS and these factors have not been well described. To examine these relationships, we used linked infant birth and death records for the cohort of 1,204,375 White and 283,776 Black postneonates who were born from 1979 to 1981 in five states: California, Georgia, Missouri, South Carolina and Tennessee. Deaths attributable to SIDS occurred to 1404 White postneonates and to 696 Black postneonates. Although postneonatal SIDS rate among Black infants was twice that of White infants, the relative risk was smaller among infants with gestations of less than 35 weeks. For White postneonates, the median postneonatal age at death sharply declined for gestations from 28-29 weeks to 36-37 weeks and levelled off for longer gestations. For Black postneonates, the results do not support an association between length of gestation and age at death. The findings suggest that practitioners investigating approaches to avert SIDS need to maintain their interventions to an older age among White preterm infants. Researchers investigating the causes of SIDS need to consider the relationship between length of gestation and age at death from SIDS as well as possible developmental differences between White and Black preterm infants.     

Are race and length of gestation related to age at death in the sudden infant death syndrome?

Summary. Although race and preterm delivery are known to be associated with sudden infant death syndrome (SIDS), the relationships between age at death from SIDS and these factors have not been well described. To examine these relationships, we used linked infant birth and death records for the cohort of 1 204 375 White and 283 776 Black postneonates who were born from 1979 to 1981 in five states: California, Georgia, Missouri, South Carolina and Tennessee. Deaths attributable to SIDS occurred to 1404 White postneonates and to 696 Black postneonates. Although postneonatal SIDS rate among Black infants was twice that of White infants, the relative risk was smaller among infants with gestations of <35 weeks. For White postneonates, the median postneonatal age at death sharply declined for gestations from 28–29 weeks to 36–37 weeks and levelled off for longer gestations. For Black postneonates, the results do not support an association between length of gestation and age at death. The findings suggest that practitioners investigating approaches to avert SIDS need to maintain their interventions to an older age among White preterm infants. Researchers investigating the causes of SIDS need to consider the relationship between length of gestation and age at death from SIDS as well as possible developmental differences between White and Black preterm infants.     

Intrauterine growth retardation and risk of sudden infant death syndrome (SIDS)

The purpose of this study was to assess whether intrauterine growth retardation was associated with an increased risk of sudden infant death syndrome (SIDS). A total of 148 SIDS cases were identified from the Upstate New York (exclusive of New York City) live birth cohort for 1974 (n = 132,948). Dead controls represented all other sudden deaths (n = 114). Live controls were randomly selected and matched to cases on mother's age, race, parity, and residence and infant's birth date (n = 355). Data were collected from vital certificates (response, 97%), medical records (89%), and autopsy reports (100%). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated with the use of logistic regression techniques to control for confounding. With live controls, significant risks were observed for gestations less than 37 weeks (OR = 2.2, CI 1.2-4.1), birth weights less than 2,500 g (OR = 2.5, CI 1.3-5.0) and birth lengths less than or equal to 47.0 cm (OR = 3.4, CI 1.8-6.4). Birth length less than or equal to 47.0 cm was the only significant risk factor observed when dead controls were used (OR = 2.9, CI 1.3-6.8). Risk decreased with increasing gestation and birth size. Postterm infants (greater than or equal to 42 weeks) were at lowest risk (live controls OR = 0.9, CI 0.5-1.6; dead controls OR = 0.6, CI 0.3-1.1). When gestational age was controlled for, SIDS infants were found to have reductions in both weight and length; this suggests that responsible mechanisms begin early in pregnancy.     

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.     

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.     

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.     

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.     

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

Risk factors for sudden infant death syndrome (SIDS) were examined in a prospective study based on Swedish births between 1983 and 1985. All infants surviving the first week of life were included (279,938). The overall rate of SIDS was 0.7 per 1,000 first week survivors. Elevated relative risks were associated with low maternal age, multiparity, maternal smoking, and male infants. Smoking doubled the risk and a clear dose-response relation by amount smoked was observed. Maternal smoking also seemed to influence the time of death, as infants of smokers died at an earlier age. In countries like Sweden, smoking may be the single most important preventable risk factor for sudden infant death syndrome.     

The effectiveness of cigarette regulations in reducing cases of Sudden Infant Death Syndrome

Sudden Infant Death Syndrome (SIDS) is a leading cause of mortality among infants and is responsible for thousands of infant deaths every year. Prenatal smoking and postnatal environmental smoke have been identified as strong risk factors for SIDS. Given the link between smoking and SIDS, this paper examines the direct effects of cigarette prices, taxes and clean indoor air laws in explaining changes in the incidence of SIDS over time in the United States. State-level counts of SIDS cases are generated from death certificates for 1973-2003. After controlling for some observed and unobserved confounding factors, the results show that higher cigarette prices and taxes are associated with reductions in SIDS cases. Stronger restrictions on smoking in workplaces, restaurants and child care centers are also effective in reducing SIDS deaths.     

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.     

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.     

Month of birth as an independent variable in the sudden infant death syndrome

Well-known epidemiological features of sudden infant death syndrome (SIDS) are age at death and the increased numbers in winter. There are more SIDS deaths in late autumn/early winter and there is a seasonal rhythm of births with a peak in late summer and early autumn. The data set was 14 033 SIDS deaths from Scotland, England and Wales over the 11 years 1982–92. Using log-linear models, which accounted for age at death and month of death, birth month was found to be a statistically significant risk factor for SIDS independent of age at death and winter environment ( P <0.001). Although winter season had the largest effect (relative risk 2.7 in January compared with August), the independent effect of birth month was of clinical as well as statistical significance with a relative risk for August births of 1.37 compared with those born in April. The analysis of each birth month cohort revealed a change in age distribution with infants born in early winter (December) dying at a younger age (mean 108 days) than those born in midsummer (June) (mean 146 days). Although winter season and age are the most influential factors, the substantial effect of month of birth requires explanation and points to as yet unidentified environmental influences during pregnancy.     

The Tasmanian SIDS Case-Control Study: univariable and multivariable risk factor analysis

Summary. A population-based retrospective case-control study has been conducted in Tasmania since October 1988. Study measurements pertained to the scene of death of last sleep, as well as a verbal questionnaire on relevant exposures. From 1 October 1988 to 1 October 1991, 62 cases of sudden infant death syndrome (SIDS) occurred. Case response rate for retrospective interviews was 94% (58/62). The initial control response rate was 84% (101/121). After stratification for maternal age and birthweight, there was no increase in risk associated with the usual side position (odds ratio [OR] 1.05 [0.27, 5.02]), compared with the supine position (OR 1.00, reference). The prone position was associated with increased risk [OR 5.70 (1.67,25.58)], relative to the supine position. In the final multivariable model, predictors of SIDS in this study were usual prone position (P < 0.001), maternal smoking (P = 0.008), a family history of asthma (P = 0.045) and bedroom heating during last sleep (P = 0.039). Protective factors were maternal age over 25 years (P = 0.013) and more than one child health clinic attendance (P = 0.003). The results provide further support for current health education activities which aim to inform parents of modifiable risk factors for SIDS, including the prone sleeping position, thermal stress and infant exposure to tobacco smoke.     

Risk factors for early infant mortality in Sarlahi district, Nepal

OBJECTIVES: Early infant mortality has not declined as rapidly as child mortality in many countries. Identification of risk factors for early infant mortality may help inform the design of intervention strategies. METHODS: Over the period 1994-97, 15,469 live-born, singleton infants in rural Nepal were followed to 24 weeks of age to identify risk factors for mortality within 0-7 days, 8-28 days, and 4-24 weeks after the birth. FINDINGS: In multivariate models, maternal and paternal education reduced mortality between 4 and 24 weeks only: odds ratios (OR) 0.28 (95% confidence interval (CI) = 0.12-0.66) and 0.63 (95% CI = 0.44-0.88), respectively. Miscarriage in the previous pregnancy predicted mortality in the first week of life (OR = 1.98, 95% CI = 1.37-2.87), whereas prior child deaths increased the risk of post-neonatal death (OR = 1.85, 95% CI 1.24-2.75). A larger maternal mid-upper arm circumference reduced the risk of infant death during the first week of life (OR = 0.88, 95% CI = 0.81-0.95). Infants of women who did not receive any tetanus vaccinations during pregnancy or who had severe illness during the third trimester were more likely to die in the neonatal period. Maternal mortality was strongly associated with infant mortality (OR = 6.43, 95% CI = 2.35-17.56 at 0-7 days; OR = 11.73, 95% CI = 3.82-36.00 at 8-28 days; and OR = 51.68, 95% CI = 20.26-131.80 at 4-24 weeks). CONCLUSION: Risk factors for early infant mortality varied with the age of the infant. Factors amenable to intervention included efforts aimed at maternal morbidity and mortality and increased arm circumference during pregnancy.     

Air pollution and postneonatal infant mortality in the United States, 1999-2002

OBJECTIVE: Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States. METHODS: We linked county-specific monitoring data for particles with aerodiameter of < or = 2.5 microm (PM2.5) and < or = 10 microm (PM10), ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS), and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity), percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths. RESULTS: After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI), 1.06-1.27] for a 10-mug/m3 increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09-1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category). CONCLUSIONS: This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.     

Overview of the National Infant Mortality Surveillance (NIMS) project--design, methods, results

The recent slowdown in the decline of infant mortality in the United States and the continued high risk of death among black infants (twice that of white infants) prompted a consortium of Public Health Service agencies to collaborate with all States in the development of a national data base from linked birth and infant death certificates. This National Infant Mortality Surveillance (NIMS) project for the 1980 U.S. birth cohort provides neonatal, postneonatal, and infant mortality risks for blacks, whites, and all races in 12 categories of birth weights. (Note: Neonatal mortality risk = number of deaths to infants less than 28 days of life per 1,000 live births; postneonatal mortality risk = number of deaths to infants 28 days to less than 1 year of life per 1,000 neonatal survivors; and infant mortality risk = number of deaths to infants less than 1 year of life per 1,000 live births.) Separate tabulations were requested for infants born in single and multiple deliveries. For single-delivery births, tabulations included birth weight, age at death, race of infant, and each of these characteristics: infant's live-birth order, sex, gestation, type of delivery, and cause of death; and mother's age, education, prenatal care history, and number of prior fetal losses at 20 weeks' or more gestation. An estimated 95 percent of eligible deaths were included in the NIMS tabulations. The analyses focus on three components of infant mortality: birth weight distribution of live births, neonatal mortality, and postneonatal mortality. The most important predictor for infant survival was birth weight, with an exponential improvement in survival by increasing birth weight to its optimum level. The nearly twofold higher risk of infant mortality among blacks was related to a higher prevalence of low birth weights and to higher mortality risks in the neonatal period for infants weighing 3,000 grams or more, and in the postneonatal period for all infants, regardless of birth weight. Regardless of other infant or maternal risk factors, the black-white gap persisted for infants weighing 2,500 grams or more.     

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.     

A Secondary Analysis of Race/Ethnicity and other Maternal Factors Affecting Adverse Birth Outcomes in San Bernardino County

Objectives Though it is the largest county in the lower United States, minimal attention has been given to the elevated rates of poor perinatal outcomes and infant mortality in San Bernardino County. This study sought to analyze adverse birth outcomes such as low birth weight, and infant mortality as an outcome of specific proxy maternal sociodemographic factors. Methods Data from the California Department of Health Services Office of Vital Statistics birth cohort of mothers delivering between 1999 and 2001 (N = 1,590,876 participants) were analyzed. Of those, 5.5% (n = 86,736) were births in San Bernardino County. Low birth weight, very low birth weight, death in infants less than one year of age, and other maternal sociodemographic factors were explored. All events of low birth weight and deaths among infants less than one year of age were used as significant variables in statistical models. Results Black mothers experienced more than twice the rate of very low birth weight (3.89) than their White counterparts (1.39). The most significant contributors to adverse birth outcomes among Black women were length of gestation and maternal education, whereas the most significant predictor of infant mortality was birth weight. Conclusions This study demonstrates that traditional risk factors such as length of gestation and maternal age only partially explain adverse birth outcomes. These findings highlight the need to advocate for the systematic collection of data on maternal education and length gestation and for the promotion of public health initiatives that address these inequities in our most vulnerable of populations.     

Ascorbic Acid and the Premature Infant

Little information exists about the plasma target nutritional needs of the >15 million premature infants <37 weeks gestation. Investigating ascorbic acid’s (AscA) role in infant health, our study details the relationship of infant characteristics and maternal health on infant plasma AscA level (pAscA) during postnatal development. Furthermore, we determined pAscA influence during the first week of life (EpAscA) with later infant morbidities. We hypothesize that pAscA is influenced by gestational organ immaturity, as well as maternal factors, with EpAscA associated with greater morbidity risk. We conducted a prospective longitudinal observational study of pAscA, demographics and hospital course detailed in infants ≤34 weeks. Sixty-three subjects were included, with >200 urine and plasma data points analyzed. Maternal smoking, exposure to magnesium sulfate (MgSO4) and advancing gestational and postnatal age were associated with lower pAscA. Non-white infants and those ≤30 weeks that developed bronchopulmonary dysplasia or retinopathy of prematurity had lower pAscA. Prenatal smoking, MgSO4, birth gestational age and race negatively influence pAscA. These results show prenatal and postnatal developmental factors influencing initial pAscA and metabolism, potentially setting the stage for organ health and risk for disease. Assessment of dietary targets may need adjustment in this population.