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1.  Cause-specific infant mortality in a population-based Swedish study of term and post-term births: the contribution of gestational age and birth weight 
BMJ Open  2012;2(4):e001152.
To investigate infant mortality and causes of infant death in relation to gestational age (GA) and birth weight for GA in non-malformed term and post-term infants.
Observational, retrospective nationwide cohort study.
Sweden 1983–2006.
2 152 738 singleton non-malformed infants born at 37 gestational weeks or later.
Main outcome measures
Infant, neonatal and postneonatal mortality and causes of infant death.
Infant mortality rate was 0.12% (n=2687). Compared with infants born at 40 weeks, risk of infant mortality was increased among early term infants (37 weeks, adjusted OR 1.70, 95% CI 1.43 to 2.02). Compared with infants with normal birth weight for GA, very small for gestational age (SGA; <3rd percentile) infants faced a doubled risk of infant mortality (adjusted OR 2.13, 95% CI 1.80 to 2.53), and corresponding risk was also increased among moderately SGA infants (3rd to <10th percentile; adjusted OR 1.46, 95% CI 1.26 to 1.68). Sudden infant death syndrome (SIDS) was the most common cause of death, accounting for 39% of all infant mortality. Compared with birth at 40 weeks, birth at 37 weeks was associated with increased risks of death by infections, cardiovascular disorders, SIDS and malignant neoplasms. Very and moderately SGA were associated with increased risks of death by neonatal respiratory disorders, infections, cardiovascular disorders, SIDS and neuromuscular disorders. High birth weight for GA was associated with increased risks of death by asphyxia and malignant neoplasms.
Early term birth and very to moderately low birth weight for GA are independent risk factors for infant mortality among non-malformed term infants.
Article summary
Article focus
Term infants (born at 37 gestational weeks or more) contribute with 30% to all neonatal mortality. Infants born at 37 and 38 weeks have higher rates of infant mortality than infants born at 40 weeks. Little is known about the interplay between GA and birth weight for GA and its effect on infant mortality.
Key messages
This study adds detailed analyses of the relationships between GA and birth weight for GA and risks of neonatal and postneonatal mortality and causes of infant death. We conclude that induced deliveries before 39 weeks gestation should be avoided when possible and that extra caution should be taken in term pregnancies with suspected severe or moderate intrauterine growth restriction.
Strengths and limitations of this study
The main strengths of this study are related to sample size and to the large number of predefined risk factors and confounders. Limitations were that some malformations may not have been detected, causing a theoretical selection bias, and that time trends may have influenced the outcome.
PMCID: PMC3391369  PMID: 22763662
2.  Fetal Growth and Risk of Stillbirth: A Population-Based Case–Control Study 
PLoS Medicine  2014;11(4):e1001633.
Radek Bukowski and colleagues conducted a case control study in 59 US hospitals to determine the relationship between fetal growth and stillbirth, and find that both restrictive and excessive growth could play a role.
Please see later in the article for the Editors' Summary
Stillbirth is strongly related to impaired fetal growth. However, the relationship between fetal growth and stillbirth is difficult to determine because of uncertainty in the timing of death and confounding characteristics affecting normal fetal growth.
Methods and Findings
We conducted a population-based case–control study of all stillbirths and a representative sample of live births in 59 hospitals in five geographic areas in the US. Fetal growth abnormalities were categorized as small for gestational age (SGA) (<10th percentile) or large for gestational age (LGA) (>90th percentile) at death (stillbirth) or delivery (live birth) using population, ultrasound, and individualized norms. Gestational age at death was determined using an algorithm that considered the time-of-death interval, postmortem examination, and reliability of the gestational age estimate. Data were weighted to account for the sampling design and differential participation rates in various subgroups. Among 527 singleton stillbirths and 1,821 singleton live births studied, stillbirth was associated with SGA based on population, ultrasound, and individualized norms (odds ratio [OR] [95% CI]: 3.0 [2.2 to 4.0]; 4.7 [3.7 to 5.9]; 4.6 [3.6 to 5.9], respectively). LGA was also associated with increased risk of stillbirth using ultrasound and individualized norms (OR [95% CI]: 3.5 [2.4 to 5.0]; 2.3 [1.7 to 3.1], respectively), but not population norms (OR [95% CI]: 0.6 [0.4 to 1.0]). The associations were stronger with more severe SGA and LGA (<5th and >95th percentile). Analyses adjusted for stillbirth risk factors, subset analyses excluding potential confounders, and analyses in preterm and term pregnancies showed similar patterns of association. In this study 70% of cases and 63% of controls agreed to participate. Analysis weights accounted for differences between consenting and non-consenting women. Some of the characteristics used for individualized fetal growth estimates were missing and were replaced with reference values. However, a sensitivity analysis using individualized norms based on the subset of stillbirths and live births with non-missing variables showed similar findings.
Stillbirth is associated with both growth restriction and excessive fetal growth. These findings suggest that, contrary to current practices and recommendations, stillbirth prevention strategies should focus on both severe SGA and severe LGA pregnancies.
Please see later in the article for the Editors' Summary
Editors' Summary
Pregnancy is usually a happy time, when the parents-to-be anticipate the arrival of a new baby. But, sadly, about 20% of pregnancies end in miscarriage—the early loss of a fetus (developing baby) that is unable to survive independently. Other pregnancies end in stillbirth—fetal death after 20 weeks of pregnancy (in the US; after 24 weeks in the UK). Stillbirths, like miscarriages, are common. In the US, for example, one in every 160 pregnancies ends in stillbirth. How women discover that their unborn baby has died varies. Some women simply know something is wrong and go to hospital to have their fears confirmed. Others find out when a routine check-up detects no fetal heartbeat. Most women give birth naturally after their baby has died, but if the mother's health is at risk, labor may be induced. Common causes of stillbirth include birth defects and infections. Risk factors for stillbirth include being overweight and smoking during pregnancy.
Why Was This Study Done?
Stillbirths are often associated with having a “small for gestational age” (SGA) fetus. Gestation is the period during which a baby develops in its mother's womb. Gestational age is estimated from the date of the woman's last menstrual period and/or from ultrasound scans. An SGA fetus is lighter than expected for its age based on observed distributions (norms) of fetal weights for gestational age. Although stillbirth is clearly associated with impaired fetal growth, the exact relationship between fetal growth and stillbirth remains unclear for two reasons. First, studies investigating this relationship have used gestational age at delivery rather than gestational age at death as an estimate of fetal age, which overestimates the gestational age of stillbirths and leads to errors in estimates of the proportions of SGA and “large for gestational age” (LGA) stillbirths. Second, many characteristics that affect normal fetal growth are also associated with the risk of stillbirth, and this has not been allowed for in previous studies. In this population-based case–control study, the researchers investigate the fetal growth abnormalities associated with stillbirth using a new approach to estimate gestational age and accounting for the effect of characteristics that affect both fetal growth and stillbirth. A population-based case–control study compares the characteristics of patients with a condition in a population with those of unaffected people in the same population.
What Did the Researchers Do and Find?
The researchers investigated all the stillbirths and a sample of live births that occurred over 2.5 years at 59 hospitals in five US regions. They used a formula developed by the Stillbirth Collaborative Research Network to calculate the gestational age at death of the stillbirths. They categorized fetuses as SGA if they had a weight for gestational age within the bottom 10% (below the 10th percentile) of the population and as LGA if they had a weight for gestational age above the 90th percentile at death (stillbirth) or delivery (live birth) using population, ultrasound, and individualized norms of fetal weight for gestational age. Population norms incorporate weights for gestational age from normal pregnancies and from pregnancies complicated by growth abnormalities, whereas the other two norms include weights for gestational age from normal pregnancies only. Having an SGA fetus was associated with a 3- to 4-fold increased risk of stillbirth compared to having a fetus with “appropriate” weight for gestational age based on all three norms. LGA was associated with an increased risk of stillbirth based on the ultrasound and individualized norms but not the population norms. Being more severely SGA or LGA (below the 5th percentile or above the 95th percentile) was associated with an increased risk of stillbirth.
What Do These Findings Mean?
These findings indicate that, when the time of death is accounted for and norms for weight for gestational age only from uncomplicated pregnancies are used, stillbirth is associated with both restricted and excessive fetal growth. Overall, abnormal fetal growth was identified in 25% of stillbirths using population norms and in about 50% of stillbirths using ultrasound or individualized norms. Although the accuracy of these findings is likely to be affected by aspects of the study design, these findings suggest that, contrary to current practices, strategies designed to prevent stillbirth should focus on identifying both severely SGA and severely LGA fetuses and should use norms for the calculation of weight for gestational age based on normal pregnancies only. Such an approach has the potential to identify almost half of the pregnancies likely to result in stillbirth.
Additional Information
Please access these websites via the online version of this summary at
The March of Dimes, a nonprofit organization for pregnancy and baby health, provides information on stillbirth
Tommy's, a UK nonprofit organization that funds research into stillbirth, premature birth, and miscarriage and provides information for parents-to-be, also provides information on stillbirth (including personal stories)
The UK National Health Service Choices website provides information about stillbirth (including a video about dealing with grief after a stillbirth)
MedlinePlus provides links to other resources about stillbirth (in English and Spanish)
Information about the Stillbirth Collaborative Research Network is available
PMCID: PMC3995658  PMID: 24755550
3.  Do risk factors differ between explained sudden unexpected death in infancy and sudden infant death syndrome? 
Archives of Disease in Childhood  2006;92(2):133-136.
In Germany, 2910 infants died in 2004; for many infants the reason was clear, especially prematurity or congenital abnormalities. However, 394 babies die every year suddenly and unexpectedly. The cause may be immediately clear, but is often not obvious.
(1) To describe the causes of explained sudden unexpected death in infancy (SUDI) and (2) to compare risk factors for sudden infant death syndrome (SIDS) and explained SUDI.
A 3‐year population‐based case–control study in Germany, 1998–2001.
455 deaths, of which 51 (11.2%) were explained. Most of these deaths were due to respiratory or generalised infections. The risk factors for SIDS and explained SUDI were remarkably similar except for sleep position and breast feeding. Prone sleeping position is a major risk factor for SIDS (adjusted odds ratio (OR) 7.16, 95% confidence interval (CI) 3.85 to 13.31) but not for explained SUDI (adjusted OR 1.71, 95% CI 0.25 to 11.57). Not being breast fed in the first 2 weeks of life is a risk factor for SIDS (adjusted OR 2.37, 95% CI 1.46 to 3.84) but not for explained SUDI (adjusted OR 0.39, 95% CI 0.08 to 1.83).
Prone sleeping position is a unique risk factor for SIDS. Socioeconomic disadvantage and maternal smoking are risk factors for both SIDS and explained SUDI, and provide an opportunity for targeted intervention.
PMCID: PMC2083325  PMID: 16935913
4.  Causes and risk factors for infant mortality in Nunavut, Canada 1999–2011 
BMC Pediatrics  2012;12:190.
The northern territory Nunavut has Canada’s largest jurisdictional land mass with 33,322 inhabitants, of which 85% self-identify as Inuit. Nunavut has rates of infant mortality, postneonatal mortality and hospitalisation of infants for respiratory infections that greatly exceed those for the rest of Canada. The infant mortality rate in Nunavut is 3 times the national average, and twice that of the neighbouring territory, the Northwest Territories. Nunavut has the largest Inuit population in Canada, a population which has been identified as having high rates of Sudden Infant Death Syndrome (SIDS) and infant deaths due to infections.
To determine the causes and potential risk factors of infant mortality in Nunavut, we reviewed all infant deaths (<1yr) documented by the Nunavut Chief Coroner’s Office and the Nunavut Bureau of Statistics (n=117; 1999–2011). Rates were compared to published data for Canada.
Sudden death in infancy (SIDS/SUDI; 48%) and infection (21%) were the leading causes of infant death, with rates significantly higher than for Canada (2003–2007). Of SIDS/SUDI cases with information on sleep position (n=42) and bed-sharing (n=47), 29 (69%) were sleeping non-supine and 33 (70%) were bed-sharing. Of those bed-sharing, 23 (70%) had two or more additional risk factors present, usually non-supine sleep position. CPT1A P479L homozygosity, which has been previously associated with infant mortality in Alaska Native and British Columbia First Nations populations, was associated with unexpected infant death (SIDS/SUDI, infection) throughout Nunavut (OR:3.43, 95% CI:1.30-11.47).
Unexpected infant deaths comprise the majority of infant deaths in Nunavut. Although the CPT1A P479L variant was associated with unexpected infant death in Nunavut as a whole, the association was less apparent when population stratification was considered. Strategies to promote safe sleep practices and further understand other potential risk factors for infant mortality (P479L variant, respiratory illness) are underway with local partners.
PMCID: PMC3534516  PMID: 23231747
Inuit; Nunavut; Aboriginal; Infant mortality; Sudden infant death syndrome; Sudden unexpected death in infancy; Carnitine palmitoyltransferase 1 deficiency; CPT1A P479L variant
5.  A clinical comparison of SIDS and explained sudden infant deaths: how healthy and how normal? 
Archives of Disease in Childhood  2000;82(2):98-106.
OBJECTIVES—To compare the clinical characteristics associated with sudden infant death syndrome (SIDS) and explained sudden unexpected deaths in infancy (SUDI).
DESIGN—Three year population based, case control study with parental interviews for each death and four age matched controls.
SETTING—Five regions in England (population, > 17 million; live births, > 470 000).
SUBJECTS—SIDS: 325 infants; explained SUDI: 72 infants; controls: 1588infants.
RESULTS—In the univariate analysis, all the clinical features and health markers at birth, after discharge from hospital, during life, and shortly before death, significant among the infants with SIDS were in the same direction among the infants who died of explained SUDI. In the multivariate analysis, at least one apparent life threatening event had been experienced by more of the infants who died than in controls (SIDS: 12% v 3% controls; odds ratio (OR) = 2.55; 95% confidence interval (CI), 1.02 to 6.41; explained SUDI: 15% v 4% controls; OR = 16.81; 95% CI, 2.52 to 112.30). Using a retrospective illness scoring system based on "Baby Check", both index groups showed significant markers of illness in the last 24 hours (SIDS: 22% v 8% controls; OR = 4.17; 95% CI, 1.88to 9.24; explained SUDI: 49% v 8% controls; OR = 31.20; 95% CI, 6.93 to 140.5).
CONCLUSIONS—The clinical characteristics of SIDS and explained SUDI are similar. Baby Check might help identify seriously ill babies at risk of sudden death, particularly in high risk infants.

PMCID: PMC1718219  PMID: 10648361
6.  Birth weight-specific causes of infant mortality, United States, 1980. 
Public Health Reports  1987;102(2):162-171.
To describe underlying causes of infant death by birth weight, we used data from the 1980 National Infant Mortality Surveillance project and aggregated International Classification of Diseases codes into seven categories: perinatal conditions, infections, congenital anomalies, injuries, sudden infant death syndrome (SIDS), other known causes, and nonspecific or unknown causes. Compared with heavier infants, infants with birth weights of 500-2,499 grams (g) are at increased risk of both neonatal and postneonatal death for virtually all causes. Sixty-two percent of neonatal deaths (under 28 days of life) were attributed to "conditions arising in the perinatal period," as defined using codes from the International Classification of Diseases. Prematurity-low birth weight and respiratory distress syndrome (RDS) were the leading causes of such deaths among infants with birth weights of 500-2,499 g, while birth trauma-hypoxia-asphyxia and other perinatal respiratory conditions were the leading causes among heavier infants. For all birth weight groups, congenital anomalies were the second leading cause, representing 27 percent of neonatal deaths. Although perinatal conditions caused nearly one-third of postneonatal deaths (28 days to under 1 year of life) among infants with birth weights of 500-1,499 g, for the other birth weight groups these conditions were much less important; predominant causes of postneonatal death were sudden infant death syndrome (SIDS), congenital anomalies, infections, and injuries. Black infants had a roughly twofold higher risk of neonatal and postneonatal death than did white infants for all causes except congenital anomalies, which occurred with almost equal frequency in blacks and whites. However, for infants with birth weights of 500-2,499 g, blacks had lower risks of neonatal death from RDS and congenital anomalies. Between 1960 (the latest year for which national birth weight-specific mortality statistics had been available) and 1980, SIDS emerged as a major diagnostic rubric. Otherwise, except for infections and congenital anomalies among infants with birth weights of 500-1,499 g, all causes of death declined in frequency among all birth weight groups.
PMCID: PMC1477830  PMID: 3104973
7.  Cholinergic and oxidative stress mechanisms in sudden infant death syndrome 
Acta Paediatrica (Oslo, Norway : 1992)  2009;98(11):1768-1775.
To determine whether biochemical parameters of cholinergic and oxidative stress function including red cell acetylcholinesterase (AChE), serum/plasma thyroglobulin, selenium, iron, ferritin, vitamins C, E, and A affect risk in apparent life-threatening event (ALTE), sudden infant death syndrome (SIDS), and sudden unexpected death in infancy (SUDI). To assess these biochemical parameters as a function of age; and for influence of pharmacology and epidemiology, including infant health, care, and feeding practices.
A multicentre, case–control study with blood samples from 34 ALTE and 67 non-ALTE (control) infants matched for age, and 30 SIDS/SUDI and four non-SIDS/non-SUDI (post-mortem control) infants.
Levels/activity of the biochemical parameters were not significantly different in ALTE vs. control infants, with the exception of higher vitamin C levels in the ALTE group (p = 0.009). In ALTE and control groups, AChE and thyroglobulin levels increased and decreased respectively from birth to attain normal adult levels from 6 months. Levels of iron and ferritin were higher in the first 6 month period for all infant groups studied, intersecting with vitamin C levels peaking around 4 months of age.
Lower AChE levels and higher combined levels of iron and vitamin C in the first 6 months of life may augment cholinergic and oxidative stress effect, particularly at the age when SIDS is most prevalent. This may contribute to risk of ALTE and SIDS/SUDI events during infancy.
PMCID: PMC2773533  PMID: 19706020
Cholinergic; Oxidative stress; Sudden infant death syndrome
8.  The factors contributing to the risk of sudden infant death syndrome 
Hippokratia  2011;15(2):127-131.
Sudden infant death syndrome (SIDS) is defined as the sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene and review of the clinical history. SIDS is one of the leading causes of infant mortality and occurs from the first month, until the first year of life for newborns and infants.
The aim of this review was to identify and examine risk factors responsible for causing the sudden infant death and to propose certain measures in order to protect newborns and infants from sudden death. The potential factors that contribute to the occurrence of SIDS include inadequate prenatal care, low birth weight (<2499gr), premature infants, intrauterine growth delay, short interval between pregnancies and maternal substance use (tobacco, alcohol, opiates). Moreover, factors related to infant’s sleep environment such as the prone or side sleeping position and thick coverlet increase the risk of sudden death in infants. Also, the combination of risk factors such as that of prone sleeping position and soft bed mattress are linked to a 20-fold increased risk of death. Finally, polymorphisms in the serotonin transporter gene (5-HTT), viral respiratory infections, long Q-T (responsible for the presence of fatal arrhythmia) are related to the SIDS.
Literature review indicates that each individual risk factor contributes to the appearance of SIDS and the establishment of certain protective measures for parents and health professionals has reduced its prevalence. But the precise identification of the SIDS causes and how these contribute to the occurrence of sudden death in neonates and infants, remains a challenge for health professionals.
PMCID: PMC3209674  PMID: 22110293
sudden death; newborn; infant; risk factors; prevention; review
9.  Intrauterine growth pattern and birthweight discordance in twin pregnancies: a retrospective study 
Twins, compared to singletons, have an increased risk of perinatal mortality and morbidity, due mainly to a higher prevalence of preterm birth and low birthweight. Intrauterine growth restriction (IUGR) is also common and can affect one or both fetuses. In some cases, however, one twin is much smaller than the other (growth discordance). Usually, high birthweight discordance is associated with increased perinatal morbidity. The aim of this study is to describe the epidemiological features of a population of twins at birth, with particular reference to the interpretation and clinical effects of birthweight discordance.
We evaluated retrospectively the clinical features of 70 infants born from twin pregnancies and assessed birthweight discordance in 31 pregnancies where both twins were followed at our institution. Discordance was treated both as a continuous and a categorical variable, using a cutoff of 18%. Possible relationships between birthweight discordance and other variables, such as maternal age, gestational age, birthweight percentile, number of SGA newborns in the pair, Hematocrit (Ht) discordance and neonatal anemia, prevalence of malformations, neonatal morbidity and death, were analyzed.
In our cohort birthweight percentile decreased slightly with increasing gestational age. Birthweight discordance, on the contrary, increased slightly with the increase of gestational age.
A high discordance is associated to the presence of one SGA twin, with the other AGA or LGA. In our population, all 6 pregnancies in which discordance exceeded 18% belonged to this category (one SGA twin).
Ht discordance at birth is associated to the presence of neonatal anemia in a twin, but it is not significantly related to weight discordance.
Finally, in our case history, weight discordance is not associated in any way with the prevalence of malformations, morbidity and mortality.
Birthweight discordance is an important indicator of complications that act asymmetrically on the two fetuses, affecting intrauterine growth in one of them, and usually determining the birth of a SGA infant.
Our case history shows a significant statistical association between pair discordance and IUGR in one of the twins, but we could not demonstrate any relationship between discordance and the prevalence of malformations, morbidity and mortality.
PMCID: PMC4018970  PMID: 24887062
Twins; Birthweight discordance; SGA; Weight percentile; Neonatal anemia
10.  Comparisons of mortality and pre-discharge respiratory outcomes in small-for-gestational-age and appropriate-for-gestational-age premature infants 
BMC Pediatrics  2004;4:9.
There are differences in the literature regarding outcomes of premature small-for-gestational-age (SGA) and appropriate-for gestational-age (AGA) infants, possibly due to failure to take into account gestational age at birth.
To compare mortality and respiratory morbidity of SGA and AGA premature newborn infants.
A retrospective study was done of the 2,487 infants born without congenital anomalies at ≤36 weeks of gestation and admitted to the neonatal intensive care unit (NICU) at John Dempsey Hospital, between Jan. 1992 and Dec. 1999. Recent (1994–96) U.S. birth weight percentiles for gestational age (GA), race and gender were used to classify neonates as SGA (<10th percentile for GA) or AGA (10th–90th percentile for GA). Using multivariate logistic regression and survival analyses to control for GA, SGA and AGA infants were compared for mortality and respiratory morbidity.
Controlling for GA, premature SGA infants were at a higher risk for mortality (Odds ratio 3.1, P = 0.001) and at lower risk of respiratory distress syndrome (OR = 0.71, p = 0.02) than AGA infants. However multivariate logistic regression modeling found that the odds of having respiratory distress syndrome (RDS) varied between SGA and AGA infants by GA. There was no change in RDS risk in SGA infants at GA ≤ 32 wk (OR = 1.27, 95% CI 0.32 – 1.98) but significantly decreased risk for RDS at GA > 32 wk (OR = 0.41, 95% CI 0.27 – 0.63; p < 0.01). After controlling for GA, SGA infants were observed to be at a significantly higher risk for developing chronic lung disease as compared to AGA infants (OR = 2.2, 95% CI = 1.2 – 3.9, P = 0.01). There was no significant difference between SGA and AGA infants in total days on ventilator. Among infants who survived, mean length of hospital stay was significantly higher in SGA infants born between 26–36 wks GA than AGA infants.
Premature SGA infants have significantly higher mortality, significantly higher risk of developing chronic lung disease and longer hospital stay as compared to premature AGA infants. Even the reduced risk of RDS in infants born at ≥32 wk GA, (conferred possibly by intra-uterine stress leading to accelerated lung maturation) appears to be of transient effect and is counterbalanced by adverse effects of poor intrauterine growth on long term pulmonary outcomes such as chronic lung disease.
PMCID: PMC434508  PMID: 15186501
11.  Prevalence of and risk factors for sudden infant death syndrome in Canada. 
OBJECTIVE: To analyse and describe the prevalence of sudden infant death syndrome (SIDS) in the Canadian population in relation to the distribution of known risk factors for the syndrome. To explain the observed interprovincial variation in SIDS rates. DESIGN: Retrospective population-based case-control study. SETTING: All the provinces and territories of Canada except Quebec. SUBJECTS: The birth and infant death records of singleton births for 1986-88 were linked. The linkage was successful in matching 904 (86%) of the 1053 deaths attributed to SIDS to the birth file for the infant. For each SIDS case three control babies who survived infancy were chosen at random, matched by province of birth. MAIN OUTCOME MEASURES: Infant death classified as a "sudden infant death." Independent variables included infant's sex, birth weight and gestational age, being small for gestational age, mother's age, marital status and parity, and father's age. RESULTS: The risk of SIDS was greater for boys (odds ratio [OR] 1.47, 95% confidence limits [CLs] 1.26 and 1.70) than for girls and was greater for the infants of unmarried women (OR 3.48, 95% CLs 2.94 and 4.11) than for those of married women. The risk of SIDS was inversely related to birth weight (p < 0.001), duration of pregnancy (p < 0.001) and mother's age (up to age 35) (p < 0.001) and was directly related to parity (up to four) (p < 0.001). The available information on birth and death registrations enabled about 30% of deaths from SIDS to be predicted. CONCLUSIONS: Logistic regression equations based on the risk factors available in vital statistics data have low power to predict provincial differences in rates of SIDS. Consequently, there may be additional factors that may explain provincial variation. There is a need for a well-designed case-control study that examines more variables than are available through vital registration systems.
PMCID: PMC1486006  PMID: 8364819
12.  Maternal Influenza Immunization and Reduced Likelihood of Prematurity and Small for Gestational Age Births: A Retrospective Cohort Study 
PLoS Medicine  2011;8(5):e1000441.
In an analysis of surveillance data from the state of Georgia (US), Saad Omer and colleagues show an association between receipt of influenza vaccination among pregnant women and reduced risk of premature births.
Infections during pregnancy have the potential to adversely impact birth outcomes. We evaluated the association between receipt of inactivated influenza vaccine during pregnancy and prematurity and small for gestational age (SGA) births.
Methods and Findings
We conducted a cohort analysis of surveillance data from the Georgia (United States) Pregnancy Risk Assessment Monitoring System. Among 4,326 live births between 1 June 2004 and 30 September 2006, maternal influenza vaccine information was available for 4,168 (96.3%). The primary intervention evaluated in this study was receipt of influenza vaccine during any trimester of pregnancy. The main outcome measures were prematurity (gestational age at birth <37 wk) and SGA (birth weight <10th percentile for gestational age). Infants who were born during the putative influenza season (1 October–31 May) and whose mothers were vaccinated against influenza during pregnancy were less likely to be premature compared to infants of unvaccinated mothers born in the same period (adjusted odds ratio [OR] = 0.60; 95% CI, 0.38–0.94). The magnitude of association between maternal influenza vaccine receipt and reduced likelihood of prematurity increased during the period of at least local influenza activity (adjusted OR = 0.44; 95% CI, 0.26–0.73) and was greatest during the widespread influenza activity period (adjusted OR = 0.28; 95% CI, 0.11–0.74). Compared with newborns of unvaccinated women, newborns of vaccinated mothers had 69% lower odds of being SGA (adjusted OR = 0.31; 95% CI, 0.13–0.75) during the period of widespread influenza activity. The adjusted and unadjusted ORs were not significant for the pre-influenza activity period.
This study demonstrates an association between immunization with the inactivated influenza vaccine during pregnancy and reduced likelihood of prematurity during local, regional, and widespread influenza activity periods. However, no associations were found for the pre-influenza activity period. Moreover, during the period of widespread influenza activity there was an association between maternal receipt of influenza vaccine and reduced likelihood of SGA birth.
Please see later in the article for the Editors' Summary
Editors' Summary
Maternal infections during pregnancy can have harmful effects on both mother and baby. For example, influenza is associated with increased morbidity and mortality among pregnant women compared to women who are not pregnant or who acquire influenza infection after delivery. And some respiratory infections, especially those that can cause maternal pneumonia such as influenza virus, are known to be associated with the baby being small—below the 10th percentile—for gestational age and with an increased risk of preterm birth—birth before 37 weeks of gestation. Previous studies have shown that inactivated influenza vaccination during pregnancy provides protection against influenza virus for both mother and baby. As there has been an increase in the rate of preterm birth the United States from 9.5% in 1981 to 12.8% in 2006, the impact of maternal influenza immunization on birth outcomes has important public health implications and is of particular interest during influenza pandemics.
Why Was This Study Done?
Given that maternal vaccination can protect babies from influenza virus, it is plausible that influenza vaccination in pregnancy could mitigate adverse birth outcomes such as prematurity and the baby being small for gestational age. The researchers of this study set out to evaluate this hypothesis by investigating whether there was an association between women receiving inactivated influenza vaccine during pregnancy and positive birth outcomes for their babies in the population of the state of Georgia, in the United States.
What Did the Researchers Do and Find?
The researchers conducted a retrospective cohort analysis of a large surveillance dataset (the Georgia Pregnancy Risk Assessment Monitoring System) to analyze the relationship between receipt of inactivated influenza vaccine during any trimester of pregnancy by mothers of infants born between June 1, 2004, and September 30, 2006, and their baby being premature or small for gestational age. The study period encompassed the 2004–2005 and 2005–2006 influenza seasons—the two most recent seasons for which the data were available. The researchers did a stratified analysis for the overall study period, and various periods during it, and also weighted their analysis to adjust for possible oversampling. They used logistic regression to evaluate the association of maternal influenza vaccine and (a) prematurity and (b) small for gestational age, and also used linear regression to evaluate the statistical significance of differences between vaccinated and unvaccinated women for mean gestational age at first antenatal visit and mean birth weight.
During the study period, 4,168 mother–baby pairs were included in the analysis. Local influenza activity was detected during 27 weeks (22.1%), and 578 women (14.9% [weighted]) had received the influenza vaccine during pregnancy, giving a vaccination coverage of 19.2% (weighted) among mothers of infants born during the assumed influenza season. In the study sample, 1,547 babies (10.6% [weighted]) were born premature, and 1,186 babies (11.2% [weighted]) were small for gestational age. Infants who were born during the assumed influenza season (October–May) and whose mothers were vaccinated against influenza during pregnancy were less likely to be premature than infants of unvaccinated mothers born in the same period, with an adjusted odds ratio of 0.60. The effect of maternal influenza vaccine on reducing prematurity was the highest for infants born during the period of widespread influenza activity, with 72% lower odds of prematurity in infants of vaccinated mothers than infants of unvaccinated mothers. Compared with newborns of unvaccinated women, babies of vaccinated mothers also had 69% lower odds of being small for gestational age during the period of widespread influenza activity, but the adjusted and unadjusted odd ratios were not significant for the pre-influenza activity period.
What Do These Findings Mean?
These results show that there was an association between maternal immunization with the inactivated influenza vaccine during pregnancy and reduced likelihood of prematurity during local, regional, and widespread influenza activity periods. In addition, during the period of widespread influenza activity there was an negative association between maternal receipt of influenza vaccine and small for gestational age birth.
Additional Information
Please access these Web sites via the online version of this summary at
More information about influenza vaccination during pregnancy is available from the World Health Organization and the UK National Health Service
More information about the Georgia Pregnancy Risk Assessment Monitoring System is also available
PMCID: PMC3104979  PMID: 21655318
13.  Survival Analysis of Long-Term Exposure to Different Sizes of Airborne Particulate Matter and Risk of Infant Mortality Using a Birth Cohort in Seoul, Korea 
Environmental Health Perspectives  2010;119(5):725-730.
Several studies suggest that airborne particulate matter (PM) is associated with infant mortality; however, most focused on short-term exposure to larger particles.
We evaluated associations between long-term exposure to different sizes of particles [total suspended particles (TSP), PM ≤ 10 μm in aerodynamic diameter (PM10), ≤ 10–2.5 μm (PM10–2.5), and ≤ 2.5 μm (PM2.5)] and infant mortality in a cohort in Seoul, Korea, 2004–2007.
The study includes 359,459 births with 225 deaths. We applied extended Cox proportional hazards modeling with time-dependent covariates to three mortality categories: all causes, respiratory, and sudden infant death syndrome (SIDS). We calculated exposures from birth to death (or end of eligibility for outcome at 1 year of age) and pregnancy (gestation and each trimester) and treated exposures as time-dependent variables for subjects’ exposure for each pollutant. We adjusted by sex, gestational length, season of birth, maternal age and educational level, and heat index. Each cause of death and exposure time frame was analyzed separately.
We found a relationship between gestational exposures to PM and infant mortality from all causes or respiratory causes for normal-birth-weight infants. For total mortality (all causes), risks were 1.44 (95% confidence interval, 1.06–1.97), 1.65 (1.18–2.31), 1.53 (1.22–1.90), and 1.19 (0.83–1.70) per interquartile range increase in TSP, PM10, PM2.5, and PM10–2.5, respectively; for respiratory mortality, risks were 3.78 (1.18–12.13), 6.20 (1.50–25.66), 3.15 (1.26–7.85), and 2.86 (0.76–10.85). For SIDS, risks were 0.92 (0.33–2.58), 1.15 (0.38–3.48), 1.42 (0.71–2.87), and 0.57 (0.16–1.96), respectively.
Our findings provide supportive evidence of an association of long-term exposure to PM air pollution with infant mortality.
PMCID: PMC3094428  PMID: 21169127
air pollution; Cox proportional hazards model; infant mortality; long-term effect; particulate matter; PM2.5; PM10; PM10–2.5; survival analysis; time dependent; TSP
14.  The epidemiology of sudden infant death syndrome 
Background: Twins compared to singletons are at increased risk of sudden infant death syndrome (SIDS).
Aims: To compare the epidemiology of SIDS in twins and singletons and to test the hypothesis that monozygous (MZ) were at greater risk of SIDS than dizygous (DZ) twins.
Methods: Data from the Office for National Statistics on all registered live births and infant deaths with registered cause of death "sudden unexpected death in infancy" in England and Wales from 1993 to 1998 were obtained, together with the registered birth weight and, for twins, whether they were of like or unlike sex.
Results: The crude relative risk of SIDS in twins is twice that in singletons. There has been a significant temporal decline in SIDS mortality. There is also a significant increase in risk with decreasing birth weight for both twins and singletons. The birth weight specific risk of SIDS in all except for those ≥3000 g is greater in singletons than in twins. There is no significant difference in risk of SIDS in like compared with unlike sex twins.
Conclusions: In spite of a lower risk of SIDS in twins compared with singletons for each birth weight group <3000 g, one component of the higher crude relative risk of SIDS in twins is attributable to the higher proportion of twins that are of low birth weight. A second component is the higher risk in twins compared with singletons for those of birth weight ≥3000 g. Like sex are at no greater risk than unlike sex twins, which suggests that zygosity is not a significant factor in SIDS.
PMCID: PMC1719293  PMID: 12495955
15.  The UK accelerated immunisation programme and sudden unexpected death in infancy: case-control study 
BMJ : British Medical Journal  2001;322(7290):822.
To investigate whether the accelerated immunisation programme in the United Kingdom is associated, after adjustment for potential confounding, with the sudden infant death syndrome.
Population based case-control study, February 1993 to March 1996. Parental interviews were conducted for each death and for four controls matched for age, locality, and time of sleep. Immunisation status was taken from records held by the parents.
Five regions in England with a combined population of over 17 million.
Immunisation details were available for 93% (303/325) of infants whose deaths were attributed to the sudden infant death syndrome (SIDS); 90% (65/72) of infants with explained sudden deaths; and 95% (1515/1588) of controls.
After all potential confounding factors were controlled for, immunisation uptake was strongly associated with a lower risk of SIDS (odds ratio 0.45 (95% confidence interval 0.24 to 0.85)). This difference became non-significant (0.67 (0.31 to 1.43)) after further adjustment for other factors specific to the infant's sleeping environment. Similar proportions of SIDS deaths and reference sleeps (corresponding to the time of day during which the index baby had died) among the controls occurred within 48 hours of the last vaccination (5% (7/149) v 5% (41/822)) and within two weeks (21% (31/149) v 27% (224/822)). No longer term temporal association with immunisation was found (P=0.78). Of the SIDS infants who died within two weeks of vaccination, 16% (5/31) had signs and symptoms of illness that suggested that medical contact was required, compared with 26% (16/61) of the non-immunised SIDS infants of similar age. The findings for the infants who died suddenly and unexpectedly but of explained causes mirrored those for SIDS infants.
Immunisation does not lead to sudden unexpected death in infancy, and the direction of the relation is towards protection rather than risk.
What is already known on this topicSome studies have suggested a link between the sudden infant death syndrome and primary immunisation, but most have failed to show a linkPotential bias in the studies includes lack of a comparative control group with similar low immunisation uptake and misclassification of cause of deathWhat this study addsThis study investigated explained sudden infant deaths as well as the sudden infant death syndrome and took into account potential biasAfter confounding was controlled for, immunisation uptake was lowest among the infants who died, with no temporal relation or correlation with signs and symptoms of illness
PMCID: PMC30557  PMID: 11290634
16.  Temporal trends in sudden infant death syndrome in Canada from 1991 to 2005: contribution of changes in cause of death assignment practices and in maternal and infant characteristics 
Gilbert NL, Fell DB, Joseph KS, Liu S, León JA, Sauve R, for the Fetal and Infant Health Study Group of the Canadian Perinatal Surveillance System. Temporal trends in sudden infant death syndrome in Canada from 1991 to 2005: contribution of changes in cause of death assignment practices and in maternal and infant characteristics. Paediatric and Perinatal Epidemiology 2012; 26: 124–130.
The rate of sudden infant death syndrome (SIDS) declined significantly in Canada and the US between the late 1980s and the early 2000s. In the US, this decline was shown to be due in part to a shift in diagnosis, as deaths from accidental suffocation and strangulation in bed and from other ill-defined and unspecified cause increased concurrently. This study was undertaken to determine whether there was such a shift in diagnosis from SIDS to other causes of death in Canada, and to quantify the true temporal decrease in SIDS. Cause-specific infant death rates were compared across three periods: 1991–95, 1996–2000 and 2001–05 using the Canadian linked livebirth-infant death file. The temporal decline in SIDS was estimated after adjustment for maternal and infant characteristics such as maternal age and small-for-gestational age using logistic regression. Deaths from SIDS decreased from 78.4 [95% confidence interval (CI) 73.4, 83.4] per 100 000 livebirths in 1991–95, to 48.5 [95% CI 44.3, 52.7] in 1996–2000 and to 34.6 [95% CI 31.0, 38.3] in 2001–05. Mortality rates from other ill-defined and unspecified causes and accidental suffocation and strangulation in bed remained stable. The temporal decline in SIDS between 1991–95 and 2001–05 did not change substantially after adjustment for maternal and infant factors. It is unlikely that the temporal decline of SIDS in Canada was due to changes in cause-of-death assignment practices or in maternal and infant characteristics.
PMCID: PMC3321219  PMID: 22324498
SIDS; time trend; Canada
17.  SIDS 
BMJ Clinical Evidence  2009;2009:0315.
By definition, the cause of sudden infant death syndrome (SIDS) is not known. Observational studies have found an association between SIDS and several risk factors, including prone sleeping position, prenatal or postnatal exposure to tobacco smoke, soft sleeping surfaces, hyperthermia/overwrapping, bed sharing (particularly with mothers who smoke), lack of breastfeeding, and lack of soother use. The risk of SIDS is increased in families in which there has been a prior sudden infant death.
Methods and outcomes
We conducted a systematic review and aimed to answer the following clinical question: What are the effects of interventions to reduce the risk of SIDS? We searched: Medline, Embase, The Cochrane Library, and other important databases up to April 2007 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
We found 28 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
In this systematic review, we present information relating to the effectiveness and safety of the following interventions: advice to avoid prone sleeping; advice to avoid tobacco-smoke exposure; advice to avoid soft sleeping surfaces; advice to avoid overheating or overwrapping; advice to avoid bed sharing; advice to breastfeed; advice to promote soother/pacifier use; and advice to promote room sharing (without bed sharing).
Key Points
Sudden infant death syndrome (SIDS) is the sudden death of an infant under 1 year of age that remains unexplained after review of the clinical history, examination of the scene of death, and postmortem. The incidence varies among countries, with 0.32 cases being reported per 1000 live births in England and Wales in 2004, and 0.55 cases per 1000 in the US for the same period.We found no systematic review or RCTs studying the effects of interventions to reduce the risk of SIDS due to the obvious difficulties in performing these trials. Therefore, we report only observational evidence in this review.
Campaigns that have advised avoiding prone sleeping have significantly reduced the incidence of SIDS. Observational studies have additionally shown that the incidence of prone positioning is dramatically reduced after national advice campaigns.
Advice to avoid tobacco-smoke exposure seems to reduce the incidence of SIDS. National campaigns that advise mothers to avoid tobacco-smoke exposure also seem to lead to a reduction in maternal smoking rates.
Some campaigns included advice to avoid overheating, overwrapping, and bed sharing, and advice to breastfeed, although it is not clear whether this contributed to the observed reduction in SIDS.
We found no studies looking at the effects of advice to avoid soft sleeping surfaces, to promote soother/pacifier use, or to promote room sharing (without bed sharing).
PMCID: PMC2907828  PMID: 21726486
18.  Hazardous cosleeping environments and risk factors amenable to change: case-control study of SIDS in south west England 
Objectives To investigate the factors associated with sudden infant death syndrome (SIDS) from birth to age 2 years, whether recent advice has been followed, whether any new risk factors have emerged, and the specific circumstances in which SIDS occurs while cosleeping (infant sharing the same bed or sofa with an adult or child).
Design Four year population based case-control study. Parents were interviewed shortly after the death or after the reference sleep (within 24 hours) of the two control groups.
Setting South west region of England (population 4.9 million, 184 800 births).
Participants 80 SIDS infants and two control groups weighted for age and time of reference sleep: 87 randomly selected controls and 82 controls at high risk of SIDS (young, socially deprived, multiparous mothers who smoked).
Results The median age at death (66 days) was more than three weeks less than in a study in the same region a decade earlier. Of the SIDS infants, 54% died while cosleeping compared with 20% among both control groups. Much of this excess may be explained by a significant multivariable interaction between cosleeping and recent parental use of alcohol or drugs (31% v 3% random controls) and the increased proportion of SIDS infants who had coslept on a sofa (17% v 1%). One fifth of SIDS infants used a pillow for the last sleep (21% v 3%) and one quarter were swaddled (24% v 6%). More mothers of SIDS infants than random control infants smoked during pregnancy (60% v 14%), whereas one quarter of the SIDS infants were preterm (26% v 5%) or were in fair or poor health for the last sleep (28% v 6%). All of these differences were significant in the multivariable analysis regardless of which control group was used for comparison. The significance of covering the infant’s head, postnatal exposure to tobacco smoke, dummy use, and sleeping in the side position has diminished although a significant proportion of SIDS infants were still found prone (29% v 10%).
Conclusions Many of the SIDS infants had coslept in a hazardous environment. The major influences on risk, regardless of markers for socioeconomic deprivation, are amenable to change and specific advice needs to be given, particularly on use of alcohol or drugs before cosleeping and cosleeping on a sofa.
PMCID: PMC2762037  PMID: 19826174
19.  Outcomes of Small for Gestational Age Infants < 27 Weeks’ Gestation 
The Journal of pediatrics  2013;163(1):55-60.e1-3.
To determine whether small for gestational age (SGA) infants <27 weeks gestation is associated with mortality, morbidity, growth and neurodevelopmental impairment at 18–22 months’ corrected age (CA).
Study design
This was a retrospective cohort study from National Institute of Child Health and Human Development Neonatal Research Network’s Generic Database and Follow-up Studies. Infants born at <27 weeks’ gestation from January 2006 to July 2008 were included. SGA was defined as birth weight <10th percentile for gestational age by the Olsen growth curves. Infants with birth weight ≥10th percentile for gestational age were classified as non-SGA. Maternal and infant characteristics, neonatal outcomes and neurodevelopmental data were compared between the groups. Neurodevelopmental impairment was defined as any of the following: cognitive score <70 on BSID III, moderate or severe cerebral palsy, bilateral hearing loss (+/− amplification) or blindness (vision <20/200). Logistic regression analysis evaluated the association between SGA status and death or neurodevelopmental impairment.
There were 385 SGA and 2586 non-SGA infants. Compared with the non-SGA group, mothers of SGA infants were more likely to have higher level of education, prenatal care, cesarean delivery, pregnancy-induced hypertension and antenatal corticosteroid exposure. SGA infants were more likely to have postnatal growth failure, a higher mortality and to have received prolonged mechanical ventilation and postnatal steroids. SGA status was associated with higher odds of death or neurodevelopmental impairment [OR 3.91 (95% CI: 2.91–5.25), P<0.001].
SGA status among infants <27 weeks’ gestation was associated with an increased risk for postnatal steroid use, mortality, growth failure and neurodevelopmental impairment at 18–22 months’ CA.
PMCID: PMC3947828  PMID: 23415614
extremely preterm infants; neurodevelopmental follow-up
20.  Sudden Unexpected Death in Infancy: place and time of death 
The Ulster Medical Journal  2006;75(1):65-71.
In recent years, many babies who die of Sudden Unexpected Death in Infancy (SUDI) in Northern Ireland are found dead in bed – i.e. co-sleeping – with an adult. In order to assess its frequency autopsy reports between April 1996 and August 2001 were reviewed and linked to temporal factors. The day and month of death, and the place where the baby was found were compared to a reference population of infant deaths between one week of age and the second birthday.
Although the rate of SUDI was lower than the UK average, 43 cases of SUDI were identified, and two additional deaths with virtually identical autopsy findings that were attributed to asphyxia caused by suffocation due to overlaying. Thirty-two of the 45 (71%) were less than four months of age. In 30 of the 45 cases (67%) the history stated that the baby was bed sharing with others; 19 died sleeping in an adult bed, and 11 on a sofa or armchair. In 16 of the 30 (53%) there were at least two other people sharing the sleeping surface, and in one case, three. SUDI was twice as frequent at weekends (found dead Saturday – Monday mornings) compared to weekdays (p<0.02), and significantly more common compared to reference deaths (p<0.002). Co-sleeping deaths were also more frequent at weekends. Almost half of all SUDI (49%) occurred in the summer months – more than twice the frequency of reference deaths.
While sharing a place of sleep per se may not increase the risk of death, our findings may be linked to factors such as habitual smoking, consumption of alcohol or illicit drugs as reported in case-control studies. In advising parents on safer childcare practices, health professionals must be knowledgeable of current research and when, for example, giving advice on co-sleeping this needs to be person-specific cognisant of the risks within a household. New and better means of targeting such information needs to be researched if those with higher risk life-styles are to be positively influenced.
PMCID: PMC1891806  PMID: 16457407
21.  Air Pollution and Postneonatal Infant Mortality in the United States, 1999–2002 
Environmental Health Perspectives  2007;116(1):110-115.
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.
We linked county-specific monitoring data for particles with aerodiameter of ≤ 2.5 μm (PM2.5) and ≤ 10 μm (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.
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-μg/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).
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.
PMCID: PMC2199284  PMID: 18197308
carbon monoxide; ozone; particulate matter air pollution; postneonatal infant mortality; respiratory-related deaths; sudden infant death syndrome; sulfur dioxide
22.  Safe sleep practices in a New Zealand community and development of a Sudden Unexpected Death in Infancy (SUDI) risk assessment instrument 
BMC Pediatrics  2014;14(1):263.
Interventions to prevent sudden unexpected death in infancy (SUDI) have generally been population wide interventions instituted after case–control studies identified specific childcare practices associated with sudden death. While successful overall, in New Zealand (NZ), the rates are still relatively high by international comparison. This study aims to describe childcare practices related to SUDI prevention messages in a New Zealand community, and to develop and explore the utility of a risk assessment instrument based on international guidelines and evidence.
Prospective longitudinal study of 209 infants recruited antenatally. Participant characteristics and infant care data were collected by questionnaire at: baseline (third trimester), and monthly from infant age 3 weeks through 23 weeks. Published meta-analyses data were used to estimate individual risk ratios for 6 important SUDI risk factors which, when combined, yielded a “SUDI risk score”.
Most infants were at low risk for SUDI with 72% at the lowest or slightly elevated risk (combined risk ratio ≤1.5). There was a high prevalence of the safe practices: supine sleeping (86-89% over 3–19 weeks), mother not smoking (90-92% over 3–19 weeks), and not bed sharing at a young age (87% at 3 weeks). Five independent predictors of a high SUDI risk score were: higher parity (P =0.028), younger age (P =0.030), not working or caring for other children antenatally (P =0.031), higher depression scores antenatally (P =0.036), and lower education (P =0.042).
Groups within the community identified as priorities for education about safe sleep practices beyond standard care are mothers who are young, have high parity, low educational levels, and have symptoms of depression antenatally. These findings emphasize the importance of addressing maternal depression as a modifiable risk factor in pregnancy.
PMCID: PMC4286917  PMID: 25308713
Bed sharing; Breastfeeding; Environmental risk factors; Maternal depression; Prone sleeping; SIDS; Parental smoking
23.  Fine Particulate Matter (PM2.5) Air Pollution and Selected Causes of Postneonatal Infant Mortality in California 
Environmental Health Perspectives  2006;114(5):786-790.
Studies suggest that airborne particulate matter (PM) may be associated with postneonatal infant mortality, particularly with respiratory causes and sudden infant death syndrome (SIDS). To further explore this issue, we examined the relationship between long-term exposure to fine PM air pollution and postneonatal infant mortality in California. We linked monitoring data for PM ≤2.5 μm in aerodynamic diameter (PM2.5) to infants born in California in 1999 and 2000 using maternal addresses for mothers who lived within 5 miles of a PM2.5 monitor. We matched each postneonatal infant death to four infants surviving to 1 year of age, by birth weight category and date of birth (within 2 weeks). For each matched set, we calculated exposure as the average PM2.5 concentration over the period of life for the infant who died. We used conditional logistic regression to estimate the odds of postneonatal all-cause, respiratory-related, SIDS, and external-cause (a control category) mortality by exposure to PM2.5, controlling for the matched sets and maternal demographic factors. We matched 788 postneonatal infant deaths to 3,089 infant survivors, with 51 and 120 postneonatal deaths due to respiratory causes and SIDS, respectively. We found an adjusted odds ratio for a 10−μg/m3 increase in PM2.5 of 1.07 [95% confidence interval (CI), 0.93–1.24] for overall postneonatal mortality, 2.13 (95% CI, 1.12–4.05) for respiratory-related postneonatal mortality, 0.82 (95% CI, 0.55–1.23) for SIDS, and 0.83 (95% CI, 0.50–1.39) for external causes. The California findings add further evidence of a PM air pollution effect on respiratory-related postneonatal infant mortality.
PMCID: PMC1459937  PMID: 16675438
air pollution; infant mortality; particulate matter air pollution; PM2.5; postneonatal
24.  Trends in socioeconomic inequalities in risk of sudden infant death syndrome, other causes of infant mortality, and stillbirth in Scotland: population based study 
Objectives To compare changes in inequalities in sudden infant death syndrome with other causes of infant mortality and stillbirth in Scotland, 1985-2008.
Design Retrospective cohort study.
Setting Scotland 1985-2008, analysed by four epochs of six years.
Participants Singleton births of infants with birth weight >500 g born at 28-43 weeks’ gestation.
Main outcome measures Sudden infant death syndrome, other causes of postneonatal infant death, neonatal death, and stillbirth. Odds ratios expressed as the association across the range of seven categories of Carstairs deprivation score.
Results The association between deprivation and the risk of all cause stillbirth and infant death varied between the four epochs (P=0.04). This was wholly explained by variation in the risk of sudden infant death syndrome (P<0.001 for interaction). Among women living in areas of low deprivation, there was a sharp decline in the rate of sudden infant death syndrome from 1990 to 1993. Among women living in areas of high deprivation, there was a slower decline in sudden infant death syndrome rates between 1992 and 2004. Consequently, the odds ratio for the association between socioeconomic deprivation and sudden infant death syndrome increased from 2.04 (95% confidence interval 1.53 to 2.72) in 1985-90, to 7.52 (4.62 to 12.25) in 1991-6, and 9.50 (5.46 to 16.53) in 1997-2002 but fell to 1.78 (0.87 to 3.65) in 2002-8. The interaction remained significant after adjustment for maternal characteristics.
Conclusion The rate of sudden infant death syndrome declined throughout Scotland in the early 1990s. The decline had a later onset and was slower among women living in areas of high deprivation, probably because of slower uptake of recommended changes in infant sleeping position. The effect was to create a strong independent association between deprivation and sudden infant death syndrome where one did not exist before.
PMCID: PMC3307809  PMID: 22427307
25.  Sudden infant death syndrome: a re-examination of temporal trends 
While the reduction in infants’ prone sleeping has led to a temporal decline in Sudden Infant Death Syndrome (SIDS), some aspects of this trend remain unexplained. We assessed whether changes in the gestational age distribution of births also contributed to the temporal reduction in SIDS.
SIDS patterns among singleton and twin births in the United States were analysed in 1995–96 and 2004–05. The temporal reduction in SIDS was partitioned using the Kitagawa decomposition method into reductions due to changes in the gestational age distribution and reductions due to changes in gestational age-specific SIDS rates. Both the traditional and the fetuses-at-risk models were used.
SIDS rates declined with increasing gestation under the traditional perinatal model. Rates were higher at early gestation among singletons compared with twins, while the reverse was true at later gestation. Under the fetuses-at-risk model, SIDS rates increased with increasing gestation and twins had higher rates of SIDS than singletons at all gestational ages. Between 1995–96 and 2004–05, SIDS declined from 8.3 to 5.6 per 10,000 live births among singletons and from 14.2 to 10.6 per 10,000 live births among twins. Decomposition using the traditional model showed that the SIDS reduction among singletons and twins was entirely due to changes in the gestational age-specific SIDS rate. The fetuses-at-risk model attributed 45% of the SIDS reduction to changes in the gestational age distribution and 55% of the reduction to changes in gestational age-specific SIDS rates among singletons; among twins these proportions were 64% and 36%, respectively.
Changes in the gestational age distribution may have contributed to the recent temporal reduction in SIDS.
PMCID: PMC3437219  PMID: 22747916
SIDS; Temporal trend; Gestational age

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