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CORK Bibliography: Sudden Infant Death Syndrome (SIDS)

32 citations. January 2003 to present

Prepared: March 2012

Adgent MA. Environmental tobacco smoke and sudden infant death syndrome: A review. (review). Birth Defects Research. Part B. Developmental and Reproductive Toxicology 77(1): 69-85, 2006. (90 refs.)

Environmental tobacco smoke (ETS), containing the developmental neurotoxicant, nicotine, is a prevalent component of indoor air pollution. Despite a strong association with active maternal smoking and sudden infant death syndrome (SIDS), information on the risk of SIDS due to prenatal and postnatal ETS exposure is relatively inconsistent. This literature review begins with a discussion and critique of existing epidemiologic data pertaining to ETS and SIDS. It then explores the biologic plausibility of this association, with comparison of the known association between active maternal smoking and SIDS, by examining metabolic and placental transfer issues associated with nicotine, and the biologic responses and mechanisms that may follow exposure to nicotine. Evidence indicates that prenatal and postnatal exposures to nicotine do occur from ETS exposure, but that the level of exposure is often substantially less than levels induced by active maternal smoking. Nicotine also has the capacity to concentrate in the fetus, regardless of exposure source. Experimental animal studies show that various doses of nicotine are capable of affecting a neonate's response to hypoxic conditions, a process thought to be related to SIDS outcomes. Mechanisms contributing to deficient hypoxia response include the ability of nicotine to act as a cholinergic stimulant through nicotinic acetylcholine receptor (nAChR) binding. The need for future research to investigate nicotine exposure and effects from non-maternal tobacco smoke sources in mid to late gestation is emphasized, along with a need to discourage smoking around both pregnant women and infants.

Alm B; Lagercrantz H; Wennergren G. Stop SIDS: Sleeping solitary supine, sucking soother, stopping smoking substitutes. Acta Paediatrica 95(3): 260-262, 2006. (23 refs.)

The recognition of prone sleeping and maternal smoking as modifiable risk factors for sudden infant death syndrome (SIDS), has drastically decreased SIDS incidence. However, during the last years other factors have become necessary to consider to further reduce the risk of SIDS. Side sleeping implies a greater risk than supine sleeping but is still common. Bed sharing may increase the risk of SIDS, while use of a pacifier seems to be protective. Replacement of maternal smoking with nicotine substitutes is not harmless. Conclusion: To further reduce the risk of SIDS, exclusive supine sleeping should be encouraged and side sleeping discouraged. When the breast-feeding is established, a pacifier can very well be used at bedtime. Bed sharing can increase the risk of SIDS if the infant is below 2-3 months of age, especially if the mother is a smoker. Any nicotine use should be avoided during pregnancy and breast-feeding.

Athanasakis E; Karavasiliadou S; Styliadis I. The factors contributing to the risk of sudden infant death syndrome. (review). Hippokratia 15(2): 127- 131, 2011. (40 refs.)

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.

Bailey BA; Sokol RJ. Prenatal alcohol exposure and miscarriage, stillbirth, preterm delivery, and sudden infant death syndrome. Alcohol Research & Health 34(1): 86-91, 2011. (39 refs.)

In addition to fetal alcohol syndrome and fetal alcohol spectrum disorders, prenatal alcohol exposure is associated with many other adverse pregnancy and birth outcomes. Research suggests that alcohol use during pregnancy may increase the risk of miscarriage, stillbirth, preterm delivery, and sudden infant death syndrome. This research has some inherent difficulties, such as the collection of accurate information about alcohol consumption during pregnancy and controlling for comorbid exposures and conditions. Consequently, attributing poor birth outcomes to prenatal alcohol exposure is a complicated and ongoing task, requiring continued attention to validated methodology and to identifying specific biological mechanisms.

Bajanowski T; Brinkmann B; Mitchell EA; Vennemann MM; Leukel HW; Larsch KP et al. Nicotine and cotinine in infants dying from sudden infant death syndrome. International Journal of Legal Medicine 122(1): 23-28, 2008. (31 refs.)

The aim of this component of the German Study on Sudden Infant Death was to determine (1) nicotine concentrations in hair (NCH), as a marker of long standing exposure to tobacco, (2) cotinine concentrations in pericardial fluid (CCP) and (3) cotinine concentrations in liquor cerebrospinalis (CCL), the latter measures being markers of recent exposure to tobacco in the last few hours of life. The results obtained were compared with data on parental smoking revealed from interviews. In 100 cases of sudden infant death syndrome, material was taken at autopsy to determine NCH. In 41 cases, NCH and CCP, and in 70 cases, NCH and CCL were determined. Infants of mothers who stated having smoked during pregnancy had higher NCH than infants of non-smoking mothers (p=0.008). Furthermore, there was a weak but statistically significant relationship between NCH's and the daily cigarette consumption of the mother during pregnancy (n=64, r=0.24, p=0.05). In 43% of infants, nicotine could be detected in their hair, although the mothers had said at the interview that they did not smoke during pregnancy. On the other hand, in 33% of infants whose mother stated they had smoked during pregnancy nicotine was not detectable in the infant's hair. CCP's were strongly correlated with CCL's (r=0.62, p=0.0027). For this reason, both parameters were treated as equivalent for the detection of tobacco smoke exposure in the last hours before death. The influence of breast-feeding was evaluated by comparison of the nicotine concentrations in breast fed and non-breast-fed infants from smokers and non-smokers. Fivefold higher nicotine concentrations were determined in non-breast-fed infants of parents who smoked as compared to all other groups. It can be concluded that nicotine intake by passive smoking is much more important than by breast-feeding. We conclude that both interview data and biochemical measures should be sought to understand the true exposure to tobacco smoke.

Ball HL; Moya E; Fairley L; Westman J; Oddie S; Wright J. Infant care practices related to sudden infant death syndrome in South Asian and White British families in the UK. Paediatric and Perinatal Epidemiology 26(1): 3-12, 2012. (28 refs.)

In the UK, infants of South Asian parents have a lower rate of sudden infant death syndrome (SIDS) than White British infants. Infant care and life style behaviours are strongly associated with SIDS risk. This paper describes and explores variability in infant care between White British and South Asian families (of Bangladeshi, Indian or Pakistani origin) in Bradford, UK (the vast majority of which were Pakistani) and identifies areas for targeted SIDS intervention. A cross-sectional telephone interview study was conducted involving 2560 families with 2- to 4-month-old singleton infants enrolled in the Born in Bradford cohort study. Outcome measures were prevalence of self-reported practices in infant sleeping environment, sharing sleep surfaces, breast feeding, use of dummy or pacifier, and life style behaviours. We found that, compared with White British infants, Pakistani infants were more likely to: sleep in an adult bed (OR = 8.48 [95% CI 2.92, 24.63]); be positioned on their side for sleep (OR = 4.42 [2.85, 6.86]); have a pillow in their sleep environment (OR = 9.85 [6.39, 15.19]); sleep under a duvet (OR = 3.24 [2.39, 4.40]); be swaddled for sleep (OR = 1.49 [1.13, 1.97]); ever bed-share (OR = 2.13 [1.59, 2.86]); regularly bed-share (OR = 3.57 [2.23, 5.72]); ever been breast-fed (OR = 2.00 [1.58, 2.53]); and breast-fed for 8+ weeks (OR = 1.65 [1.31, 2.07]). Additionally, Pakistani infants were less likely to: sleep in a room alone (OR = 0.05 [0.03, 0.09]); use feet-to-foot position (OR = 0.36 [0.26, 0.50]); sleep with a soft toy (OR = 0.52 [0.40, 0.68]); use an infant sleeping bag (OR = 0.20 [0.16, 0.26]); ever sofa-share (OR = 0.22 [0.15, 0.34]); be receiving solid foods (OR = 0.22 [0.17, 0.30]); or use a dummy at night (OR = 0.40 [0.33, 0.50]). Pakistani infants were also less likely to be exposed to maternal smoking (OR = 0.07 [0.04, 0.12]) and to alcohol consumption by either parent. No difference was found in the prevalence of prone sleeping (OR = 1.04 [0.53, 2.01]). Night-time infant care therefore differed significantly between South Asian and White British families. South Asian infant care practices were more likely to protect infants from the most important SIDS risks such as smoking, alcohol consumption, sofa-sharing and solitary sleep. These differences may explain the lower rate of SIDS in this population.

Burd L; Klug MG; Martsolf JT. Increased sibling mortality in children with fetal alcohol syndrome. Addiction Biology 9(2): 179-186, 2004. (18 refs.)

We compared the rate of all-cause mortality in siblings of children diagnosed with fetal alcohol syndrome (FAS) with the siblings of matched controls. The siblings of children with FAS had increased mortality (11.4%) compared with matched controls (2.0%), a 530% increase in mortality. The age of death in case siblings deaths occurred later (between 1 day and 7 years) compared with the controls (1 day to 4 years) [odds ratio (OR) = 2.4 (0.4-15.6)]. Siblings of children with FAS had increased risk of death due to infectious illness [OR = 13.7 (1.2-361)] and sudden infant death syndrome compared with controls [OR = 10.2 (1.2-75.1)]. A diagnosis of FAS is an important risk marker for mortality in the siblings of the proband even if they do not have FAS. Maternal alcoholism appears to be a useful risk marker for increased mortality risk in diagnosed cases and their siblings. This has important implications in the management of family members of children with FAS.

Blair PS; Sidebotham P; Evason-Coombe C; Edmonds M; Heckstall-Smith EMA; Fleming P. Hazardous co-sleeping environments and risk factors amenable to change: Case-control study of SIDS in south west England. British Medical Journal 339(b3666), 2009. (38 refs.)

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.

Blair PS; Sidebotham P; Evason-Coombe C; Edmonds M; Heckstall-Smith EMA; Fleming P. Hazardous co-sleeping environments and risk factors amenable to change: Case-control study of SIDS in south west England. British Medical Journal 339(b3666), 2009. (38 refs.)

Esani N; Hodgman JE; Ehsani N; Hoppenbrouwers T. Apparent life-threatening events and sudden infant death syndrome: Comparison of risk factors. Journal of Pediatrics 152(3): 365-370, 2008. (23 refs.)

Objective To compare the risk factors of 153 cases of apparent life-threatening event (ALTE) enrolled in the multicenter Collaborative Home Infant Monitoring Evaluation (CHIME) from 1994 to 1998 with the published risk factors for sudden infant death syndrome (SIDS). Study design Trained CHIME interviewers gathered histories of infants with ALTE who met the criteria. The following risk factors were analyed: male predominance, gestational age, low birth weight, very low birth weight, incidence of small for gestational age (SGA), age at the event, multiparity, maternal age, and smoking. Population-based SIDS studies with >100 deaths, focusing on 1 or more pertinent risk factors and earned out during the decade in which CHIME data were collected, were chosen for comparison. Results One of the 153 infants with ALTE in this study died during follow-up (0.6%). CHIME ALTE differed significantly from SIDS in 4 respects: fewer infants with low birth weight and SGA at birth, fewer teenage pregnancies, and a younger infant age at ALTE. Conclusions Although a number of risk factors for ALTE are similar to those for SIDS, the differences warrant a separate focus on ALTE beyond that on SIDS.

Chan-Yeung M; Dimich-Ward H. Respiratory health effects of exposure to environmental tobacco smoke. (review). Respirology 8(2): 131-139, 2003. (90 refs.)

Tobacco smoke is a major component of indoor air pollution. Exposure to environmental tobacco smoke (ETS) is prevalent worldwide despite growing awareness of its adverse health effects on non-smokers. ETS contains the same toxic substances as identified in mainstream tobacco smoke. Cotinine (a metabolite of nicotine) can be measured in urine and serum of non-smokers exposed to ETS and reflects the degree of exposure. In children, exposure to ETS leads to reduced lung function, increased risk of lower respiratory tract illnesses, acute exacerbation of asthma resulting in hospitalization, increased prevalence of non-allergic bronchial hyperresponsiveness, increased risk for sudden infant death syndrome (SIDS) and possibly increased risk for asthma. Exposure to ETS is responsible for excess cost to the family's financial resources and demands on health services. In adults, exposure to ETS is associated with increased risk of lung cancer, particularly in those with high exposure and acute and chronic respiratory symptoms that improve after the cessation of exposure. Healthcare providers should advocate for non-smokers' rights in the community and support legislation to limit tobacco exposure.

Chong DSY; Yip PSF; Karlberg J. Maternal smoking: An increasing unique risk factor for sudden infant death syndrome in Sweden. Acta Paediatrica 93(4): 471-478, 2004. (28 refs.)

Aim: To assess the change of risk factors that are specific to sudden infant death syndrome (SIDS) after the initialization of a campaign to reduce the risk (RTR) of SIDS compared to non-SIDS postneonatal deaths. Methods: Data were extracted from the Swedish Medical Birth Registry, 1982-1991 and 1993-1998. 1105 infants died from SIDS during the postneonatal period, 2115 postneonatal deaths were from other causes and 11050 live birth controls were selected. Risk factors previously identified to be related to SIDS were defined as high parity, prematurity, young maternal age, low Apgar score, birth during the night, single motherhood, multiple births, maternal smoking, male gender, short length standard deviation score (SDS) and small weight-to-length SDS. Results: Non-SIDS deaths were more significantly related to a low 5-min Apgar score, smaller weight-to-length SDS, and/or short length SDS values; while SIDS deaths were more closely related to mothers with higher parity or multiple births, mothers who smoked during pregnancy and single-parent (mother) families. Maternal smoking was even more prominent among SIDS deaths in the post-campaign period. The adjusted odds ratios, compared with non-SIDS deaths, increased from 1.84 (95% CI: 1.48, 2.28) in the pre-campaign period to 4.11 (95% CI: 2.72, 6.21) in the post-campaign period. Conclusions: Maternal smoking during pregnancy remains the most important modifiable risk factor for SIDS in the post-campaign period in comparison with non-SIDS postneonatal deaths. Other than putting babies in a supine sleeping position, maternal smoking should be the next most important issue to be considered, if there is to be a second campaign.

Fleming P; Blair PS. Sudden Infant Death Syndrome and parental smoking. Early Human Development 83(11): 721-725, 2007. (21 refs.)

Prenatal exposure to tobacco smoke is a major risk factor associated with Sudden Infant Death Syndrome (SIDS) and the risk has increased despite continued advice against this practice. Evidence from the UK suggests the prevalence of maternal smoking during pregnancy has risen amongst SIDS mothers (from 50% to 80%) when the rate amongst expectant mothers in the general population has fatten (from 30% to 20%) confirming pooled estimates from recent studies of a fourfold risk. An additional risk from postnatal exposure has also been identified; increasing with the number of smokers in the household or the daily hours the infant is subjected to a smoke-fitted environment. Exposure may lead to a complex range of effects upon normal physiological and anatomical development in fetal and postnatal life that places infants at greatly increased risk of SIDS. Recent legislation prohibiting smoking in public places needs to emphasise the adverse effects of tobacco smoke exposure to infants and amongst pregnant women.

Friend KB; Goodwin MS; Lipsitt LP. Alcohol use and sudden infant death syndrome. Developmental Review 24(3): 235-251, 2004. (70 refs.)

Despite general evidence of fetal toxicities associated with sudden infant death syndrome (SIDS), there has been limited research focusing on the effects of parental alcohol use on SIDS occurrence, either directly or in interaction with other risk conditions. The purpose of this paper is to review the literature on parental, especially maternal, alcohol use and SIDS. We present a model illustrating the possible association of alcohol exposure with SIDS and then use this model to organize study findings. Results show that, despite some ambiguities, intrauterine alcohol exposure is associated with SIDS. Parental postnatal use appears to be linked as well. We conclude that alcohol ingestion is a presumptive risk factor weakening an infant's life-saving responses, and should be more rigorously studied in order to develop and implement appropriate public-health-based interventions.

Gingras JL; Mitchell EA; Grattan KJ; Stewart AW. Effects of maternal cigarette smoking and cocaine use in pregnancy on fetal response to vibroacoustic stimulation and habituation. Acta Paediatrica 93(11): 1479 -1485, 2004. (34 refs.)

Background: Cigarette smoking and cocaine use in pregnancy are common in the US and both are risk factors for sudden infant death syndrome (SIDS). Although the cause of SIDS is not known, one postulated mechanism involves abnormalities of arousal and arousal regulation. Cigarette smoking and cocaine use may cause deficits of arousal. Many believe arousal deficits occur prenatally. Aims: The aim of this study was to assess the effects of cigarette smoke and cocaine exposure during pregnancy on measures of fetal arousal and arousal competency: 1) the fetal response to vibroacoustic stimulation (VAS) and 2) habituation to VAS. Hypothesis: Maternal cigarette smoking and cocaine use in pregnancy are associated with altered arousal and arousal regulation in the fetus. Methods: Three groups of mother-fetal dyads were enrolled: 1) cigarette smokers (n = 54), 2) cocaine users (n = 30), and 3) controls (n = 60). One hundred eight fetuses were tested at 29-31 wk gestation, 119 at 32-35 wk, and 118 at 36+ wk. The fetal response to VAS was assessed using real-time ultrasound and a paradigm of arousal responsiveness. Responders were tested with repeated VAS to assess habituation. Also, the quality of fetal reactivity to repeated stimuli was assessed as a measure of arousal and arousal regulation competence (Behavioral Reactivity Scale). Results: The control group had a larger proportion of fetuses who were too active to initiate testing ("too active to test") (p = 0.013); the proportion of fetuses too active to test decreased with increasing gestational age. The majority of the fetuses who could be tested responded to the initial VAS, and there were no group differences. The proportion of fetuses that habituated and the rate of habituation did not differ between the groups. Behavioral reactivity did not differ between groups. Conclusions: The original hypotheses were not confirmed. However, the chosen assessment paradigms may have lacked sensitivity. The proportion of fetuses that were "too active to test" decreased with gestational age. The control group had a larger proportion of fetuses that were "too active to test" compared with the exposure groups. We speculate that these findings indicate that prenatal exposure to these neuroteratogens may have produced an acceleration of the behavioral response to vibroacoustic stimulation.

Hafstrom A; Milerad J; Sandberg KL; Sundell HW. Cardiorespiratory effects of nicotine exposure during development. Respiratory Physiology and Neurobiology 149(1-3): 325-341, 2005. (91 refs.)

Exposure to tobacco smoke is a major risk factor for the sudden infant death syndrome. Nicotine is thought to be the ingredient in tobacco smoke that is responsible for a multitude of cardiorespiratory effects during development, and pre- rather than postnatal exposure is considered to be most detrimental. Nicotine interacts with endogenous acetylcholine receptors in the brain and lung, and developmental exposure produces structural changes as well as alterations in neuroregulation. Abnormalities have been described in sympathicovagal balance, arousal threshold and latency, breathing pattern at rest and apnea frequency, ventilatory response to hyperoxia or hypoxia, heart rate regulation and ability to autoresuscitate during severe hypoxia. This review discusses studies performed on infants of smoking mothers and nicotine-exposed animals yielding varying and sometimes inconsistent results that may be due to differences in experimental design, species and the dose of exposure. Taken together however, developmental nicotine exposure appears to induce vulnerability during hypoxia and a potential inability to survive severe asphyxia.

Horne RSC; Franco P; Adamson TM; Groswasser J; Kahn A. Influences of maternal cigarette smoking on infant arousability. Early Human Development 79(1): 49-58, 2004. (54 refs.)

Since the reduction in the incidence of the prone sleeping position, maternal cigarette smoking has become the strongest modifiable risk factor for Sudden Infant Death Syndrome (SIDS). This risk is dose dependent. Various mechanisms have been postulated to explain the increased risk of SIDS associated with maternal smoking, among these, impairment of arousal from sleep. This paper reviews the effects of maternal smoking on infant arousability from sleep, cardiorespiratory controls and sleep architecture. Infants exposed to maternal smoking have been shown to have both decreased spontaneous and evoked arousability from sleep. Such impairment of arousal has been demonstrated to be associated with changes in control of autonomic cardiac function. Sleep architecture appears not to be altered by smoking. During arousal, heart rate, blood pressure and breathing movements increase, while gross body movements occur to avoid the stimulus. Any impairment in arousability from sleep could occur when infants are exposed to maternal cigarette smoking, and could possibly contribute to the final pathway to SIDS.

Howard LM; Hannam S. Sudden infant death syndrome and psychiatric disorders. British Journal of Psychiatry 182(5): 379-380, 2003. (21 refs.)

Discusses sudden infant death syndrome (SIDS) in the context of psychiatric disorders in mothers. SIDS is defined as the sudden death of a baby that is unexpected from the baby's history and unexplained by a thorough post-mortem examination. The article cites the studies which describe the association between SIDS and mothers suffering from postnatal depression and those suffering from schizophrenia. Postnatal depression is consistently found in 12-13% of mothers and is associated with deficits in maternal-infant interactions. It is possible that mothers with depression are less attuned to their infant's health status and well being and are less able to respond appropriately to any changes in the infant. Similarly, women with schizophrenia have a higher incidence of stillbirths and neonatal deaths. The article also discusses disguised homicides of infants and substance misuse among mothers as other risk factors associated with SIDS. It is therefore important that childbearing women with psychiatric disorders are helped to decrease potential risk factors for SIDS. Close liaison between all health care professionals involved in the care of mothers and babies is essential to ensure that these patients receive optimal antenatal and postnatal care.

Hunt CE; Hauck FR. Sudden infant death syndrome. (review). Canadian Medical Association Journal 174(13): 1861-1869, 2006. (96 refs.)

Sudden infant death syndrome ( SIDS) continues to be the most common cause of postneonatal infant death. SIDS is a complex, multifactorial disorder, the cause of which is still not fully understood. However, much is known now about environmental risk factors, some of which are modifiable. These include maternal and antenatal risk factors such as smoking during pregnancy, as well as infant-related risk factors such as non-supine sleeping position and soft bedding. Emerging evidence also substantiates an expanding number of genetic risk factors. Interactions between environmental and genetic risk factors may be of critical importance in determining an infant's actual risk of SIDS. Although no practical way exists to identify which infants will die of SIDS, nor is there a safe and proven prevention strategy even if identification were feasible, reducing exposure to modifiable risk factors has helped to lower the incidence of SIDS. Current challenges include wider dissemination of guidelines to all people who care for infants, dissemination of guidelines in culturally appropriate ways, and surveillance of SIDS trends and other outcomes associated with implementation of these guidelines.

Hutton HE; McCaul ME; Santora PB; Erbelding EJ. The relationship between recent alcohol use and sexual behaviors: Gender differences among sexually transmitted disease clinic patients. Alcoholism: Clinical and Experimental Research 32(11): 2008-2015, 2008. (44 refs.)

Background: Binge drinking is associated with risky sexual behaviors and sexually transmitted diseases (STDs). Few studies have investigated this by gender or in an STD clinic. This cross-sectional study examined the association between binge drinking and risky sexual behaviors/STDs among patients attending an urban STD clinic. Method: A total of 671 STD clinic patients were tested for STDs, and queried about recent alcohol/drug use and risky sexual behaviors using audio computer-assisted-self-interview. The association between binge drinking and sexual behaviors/STDs was analyzed using logistic regression adjusting for age, employment, and drug use. Results: Binge drinking was reported by 30% of women and 42% of men. Gender differences were found in rates of receptive anal sex which increased linearly with increased alcohol use among women but did not differ among men. Within gender analyses showed that women binge drinkers engaged in anal sex at more than twice the rate of women who drank alcohol without binges (33.3% vs. 15.9%; p < 0.05) and 3 times the rate of women who abstained from alcohol (11.1%; p < 0.05). Having multiple sex partners was more than twice as common among women binge drinkers than women abstainers (40.5% vs. 16.8%; p < 0.05). Gonorrhea was nearly 5 times higher among women binge drinkers compared to women abstainers (10.6% vs. 2.2%; p < 0.05). The association between binge drinking and sexual behaviors/gonorrhea remained after controlling for drug use. Among men, rates of risky sexual behaviors/STDs were high, but did not differ by alcohol use. Conclusion: Rates of binge drinking among STD clinic patients were high. Among women, binge drinking was uniquely associated with risky sexual behaviors and an STD diagnosis. Our findings support the need to routinely screen for binge drinking as part of clinical care in STD clinics. Women binge drinkers, in particular, may benefit from interventions that jointly address binge drinking and risky sexual behaviors. Developing gender-specific interventions could improve overall health outcomes in this population.

James C; Klenka H; Manning D. Sudden infant death syndrome: bed sharing with mothers who smoke. Archives of Disease in Childhood 88(2): 112-113, 2003. (10 refs.)

Aim: To examine the sleeping arrangements of sudden infant death syndrome (SIDS) cases on the Wirral. In particular to determine the prevalence of bed sharing with mothers who smoke, a known risk factor for SIDS. Methods: Retrospective study of postmortem determined cases of SIDS from 1995 to 2000 on the Wirral peninsula (population 350 000, 3500 annual births). Ambulance crew reports, case notes, health visitor reports, postmortem reports, and case discussion records were studied for each case. Results: There were 25 cases of SIDS in the postneonatal age group over the six year period. In nine cases the baby was bed sharing with the mother, of whom seven were smokers. Five of these mothers reported using alcohol or illicit drugs on the night of their infant's death. In two further cases the baby slept on a sofa with a parent. Conclusions: Bed sharing and smoking remain important risk factors for SIDS. Mothers should be advised ante-and postnatally of this combination of risk factors. Such advice should also include a recommendation not to sleep with their baby if under the influence of alcohol or illicit drugs, and never to sleep on a sofa with their baby. All "Child Health Record" books given to parents on the Wirral now include this advice. "Reduce the Risk" advice leaflets given to parents pre- and postnatally also now carry the recommendation, and health visitors and midwives have been educated with respect to these additions.

Liaropoulos D; Belis V; Hostiuc S. Risk factors for sudden infant death syndrome in Romanian population. Romanian Journal of Legal Medicine 18(1): 27-30, 2010. (20 refs.)

Sudden Infant Death Syndrome represents one of the most frequent causes of death in children of one year or less. We analyzed SIDS cases from Bucharest and surrounding areas on a ten year period (1999-2008), totaling a number of 298 cases, in order to determine the most important risk factors and possible interventional strategies. Our study revealed five major risk factors for SIDS on which we can intervene: bedding, supine sleeping position, maternal smoking, prematurity, and low birth weight. Awareness increasing campaigns, similar to "Back to sleep", associated with a better legal framework for child supportan decrease the total number of SIDS cases.

Liebrechts-Akkerman G; Lao O; Liu F; van Sleuwen BE; Engelberts AC; L'Hoir MP et al. Postnatal parental smoking: An important risk factor for SIDS. European Journal of Pediatrics 170(10): 1281-1291, 2011. (21 refs.)

Sudden infant death syndrome (SIDS) is the unexpected death of an infant that remains unexplained after a thorough investigation of the circumstances, family history, paediatric investigation and complete autopsy. In Western society, it is the leading cause of post-neonatal death below 1 year of age. In the Netherlands, the SIDS incidence is very low, which offers opportunities to assess the importance of old and new environmental risk factors. For this purpose, cases were collected through pathology departments and the working group on SIDS of the Dutch Paediatrician Foundation. A total of 142 cases were included; these occurred after the parental education on sleeping position (1987), restricted to the international age criteria and had no histological explanation. Age-matched healthy controls (N = 2,841) came from a survey of the Netherlands Paediatric Surveillance Unit, completed between November 2002 and April 2003. A multivariate analysis was performed to determine the risk factors for SIDS, including sleeping position, antenatal maternal smoking, postnatal parental smoking, premature birth, gender, lack of breastfeeding and socio-economic status. Postnatal smoking was identified as an important environmental risk factor for SIDS (OR one parent = 2.5 [1.2, 5.0]; both parents = 5.77 [2.2, 15.5]; maternal = 2.7 [1.0, 6.4]; paternal = 2.4 [1.3, 4.5] ) as was prone sleeping (OR put prone to sleep = 21.5 [10.6, 43.5]; turned prone during sleep = 100 [46, 219]). Premature birth was also significantly associated with SIDS (OR = 2.4 [1.2, 4.8]). Postnatal parental smoking is currently a major environmental risk factor for SIDS in the Netherlands together with the long-established risk of prone sleeping.

Machaalani R; Say M; Waters KA. Effects of cigarette smoke exposure on nicotinic acetylcholine receptor subunits alpha 7 and beta 2 in the sudden infant death syndrome (SIDS)// brainstem. Toxicology and Applied Pharmacology 257(3): 396-404, 2011. (57 refs.)

It is postulated that nicotine, as the main neurotoxic constituent of cigarette smoke, influences SIDS risk through effects on nicotinic acetylcholine receptors (nAChRs) in brainstem nuclei that control respiration and arousal. This study compared alpha 7 and beta 2 nAChR subunit expression in eight nuclei of the caudal and rostral medulla and seven nuclei of the pons between SIDS (n = 46) and non-SIDS infants (n = 14). Evaluation for associations with known SIDS risk factors included comparison according to whether infants had a history of exposure to cigarette smoke in the home, and stratification for sleep position and gender. Compared to non-SIDS infants, SIDS infants had significantly decreased alpha 7 in the caudal nucleus of the solitary tract (cNTS), gracile and cuneate nuclei, with decreased beta 2 in the cNTS and increased beta 2 in the facial. When considering only the SIDS cohort: 1-cigarette smoke exposure was associated with increased alpha 7 in the vestibular nucleus and increased beta 2 in the rostral dorsal motor nucleus of the vagus, rNTS and Cuneate, 2-there was a gender interaction for alpha 7 in the gracile and cuneate, and beta 2 in the cNTS and rostral arcuate nucleus, and 3-there was no effect of sleep position on alpha 7, but prone sleep was associated with decreased beta 2 in three nuclei of the pons. In conclusion, SIDS infants demonstrate differences in expression of alpha 7 and beta 2 nAChRs within brainstem nuclei that control respiration and arousal, which is independent on prior history of cigarette smoke exposure, especially for the NTS, with additional differences for smoke exposure (beta 2), gender (alpha 7 and beta 2) and sleep position (beta 2) evident.

Moon RY; Darnall RA; Goodstein MH; Hauck FR; Willinger M; Shapiro-Mendoza CK et al. SIDS and other sleep-related infant deaths: Expansion of recommendations for a safe infant sleeping environment. Pediatrics 128(5): 1030-1039, 2011. (92 refs.)

Despite a major decrease in the incidence of sudden infant death syndrome (SIDS) since the American Academy of Pediatrics (AAP) released its recommendation in 1992 that infants be placed for sleep in a non-prone position, this decline has plateaued in recent years. Concurrently, other causes of sudden unexpected infant death that occur during sleep (sleep-related deaths), including suffocation, asphyxia, and entrapment, and ill-defined or unspecified causes of death have increased in incidence, particularly since the AAP published its last statement on SIDS in 2005. It has become increasingly important to address these other causes of sleep-related infant death. Many of the modifiable and nonmodifiable risk factors for SIDS and suffocation are strikingly similar. The AAP, therefore, is expanding its recommendations from focusing only on SIDS to focusing on a safe sleep environment that can reduce the risk of all sleep-related infant deaths, including SIDS. The recommendations described in this policy statement include supine positioning, use of a firm sleep surface, breastfeeding, room-sharing without bed-sharing, routine immunizations, consideration of using a pacifier, and avoidance of soft bedding, overheating, and exposure to tobacco smoke, alcohol, and illicit drugs. The rationale for these recommendations is discussed in detail in the accompanying "Technical Report-SIDS and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment," which is included in this issue of Pediatrics

Moon RY; Darnall RA; Goodstein MH; Hauck FR; AAP Task Force of SIDS. Technical Report. SIDS and Other Sleep-Related Infant Deaths: Expansion of recommendations for a safe infant sleeping environment. Pediatrics 128(5): e1341-e1367, 2011. (357 refs.)

Despite a major decrease in the incidence of sudden infant death syndrome (SIDS) since the American Academy of Pediatrics (AAP) released its recommendation in 1992 that infants be placed for sleep in a non-prone position, this decline has plateaued in recent years. Concurrently, other causes of sudden unexpected infant death occurring during sleep (sleep-related deaths), including suffocation, asphyxia, and entrapment, and ill-defined or unspecified causes of death have increased in incidence, particularly since the AAP published its last statement on SIDS in 2005. It has become increasingly important to address these other causes of sleep-related infant death. Many of the modifiable and nonmodifiable risk factors for SIDS and suffocation are strikingly similar. The AAP, therefore, is expanding its recommendations from being only SIDS-focused to focusing on a safe sleep environment that can reduce the risk of all sleep-related infant deaths including SIDS. The recommendations described in this report include supine positioning, use of a firm sleep surface, breastfeeding, room-sharing without bed-sharing, routine immunization, consideration of a pacifier, and avoidance of soft bedding, overheating, and exposure to tobacco smoke, alcohol, and illicit drugs. The rationale for these recommendations is discussed in detail in this technical report. The recommendations are published in the accompanying "Policy Statement-Sudden Infant Death Syndrome and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment," which is included in this issue

Ottaviani G. Sudden infant and perinatal unexplained death: are we moving forward yet? (review). Cardiovascular Pathology 20(5): 302-306, 2011. (41 refs.)

Autonomic nervous system and cardiac conducting system dysfunctions have been proposed to be implied in the pathogenesis of sudden infant death syndrome (SIDS). However, most clinicians and even pathologists lack experience with detailed examination of the brainstem and cardiac conducting system and may not recognize lesions within those systems that potentially could be crucial factors in the sudden unexpected perinatal and infant death. Recent anatomical, pathological, and bacteriological studies in SIDS confirm that the multidisciplinary approach provides the best approach to the challenging problems of SIDS and sudden unexplained perinatal death.

Ostfeld BM; Esposito L; Perl H; Hegyi T. Concurrent risks in sudden infant death syndrome. Pediatrics 125(3): 447-453, 2010. (54 refs.)

BACKGROUND: Despite improved education on safe sleep, infants are still exposed to multiple risks for sudden infant death syndrome (SIDS). Variability among health care providers continues to exist regarding knowledge of risk factors and the provision of education to caregivers. OBJECTIVE: To enhance the content and delivery of SIDS risk-reduction initiatives by physicians and other health care providers and to provide them with a context for evaluating their discussions of risks and compensatory strategies, we sought to raise awareness of the frequency of risk factors in SIDS cases, patterns of co-occurrence, associations between modifiable and nonmodifiable risks, and the rarity of cases without risk. DESIGN and METHODS: In a population-based retrospective review of 244 (97%) New Jersey SIDS cases (1996-2000), we assessed the frequencies and co-occurrences of modifiable (maternal and paternal smoking, nonsupine sleep or prone status at discovery, bed-sharing, or scene risks) and nonmodifiable (upper respiratory infection or <37 weeks' gestational age) risks. RESULTS: Nonsupine sleep occurred in 70.4% of cases with data on position (159 of 226). Thirteen cases were of infants who were discovered prone, with an increased positional risk to 76.1%, in which 87% contained additional risks. Maternal smoking occurred in 42.6% (92 of 216) of the cases with data on this risk, and 98% among those cases had additional risks. At least 1 risk was found in 96% of the cases, and 78% had 2 to 7 risks. Of the 9 of 244 risk-free cases (3.7%), 7 lacked data on 2 to 5 risks per case. On the basis of the complete data, only 2 (0.8%) of all 244 cases were risk free. When nonmodifiable risks were excluded, 5.3% of the cases met this definition. CONCLUSIONS: Risk-free and single-risk SIDS cases are rare, and most contain multiple risks. Parent education should be comprehensive and address compensatory strategies for nonmodifiable risks.

Rushton L; Courage C; Green E. Estimation of the impact on children's health of environmental tobacco smoke in England and Wales. Journal of the Royal Society for the Promotion of Health 123(3): 175-180, 2003. (44 refs.)

In this paper, the population attributable risk (PAR), a measure of the excess risk of disease associated with a risk factor, is calculated for some of the common adverse health effects that have been associated with exposure of children to environmental tobacco smoke (ETS): childhood lower respiratory illness, chronic middle ear disease, asthma and sudden infant death syndrome (SIDS). Published data on both risk estimates and the percentage of children exposed to ETS in the home (prevalence of ETS) have been utilised. The percentage of childhood tower respiratory illness and middle ear disease typically attributable to ETS from either parent smoking ranged from 97. for asthma prevalence and for referral for glue ear, to 25% for hospital admission for tower respiratory illness. Where data were available to calculate PARS separately for mother only smoking and father only smoking, the PARS were generally larger for mothers only smoking, due mainly to higher odds ratios for mothers only smoking. The PAR for SIDS attributable to ETS from mother only smoking was 11%. Although based on a small number of studies, the PAR for SIDS attributable to smoking of fathers only was similar to that attributable to the smoking of mothers only, largely due to the higher prevalence of households where only the father smokes. This study has shown that the impact of ETS on childhood illness can be considerable, emphasising the importance of the need to develop effective strategies for reducing the risk of ETS exposure in the home and elsewhere.

Sawnani H; Jackson T; Murphy T; Beckerman R; Simakajornborn N. The effect of maternal smoking on respiratory and arousal patterns in preterm infants during sleep. American Journal of Respiratory and Critical Care Medicine 169(6): 733-738, 2004. (55 refs.)

Prenatal exposure to cigarette smoke is associated with an increased risk of sudden infant death syndrome. The effect of maternal smoking on apnea and arousal patterns in preterm infants is currently unknown. Multichannel polysomnographic studies were performed in preterm infants. Thirty infants were enrolled into the study: 16 exposed prenatally to cigarette smoke (S) and 14 control infants (C). There was no difference in the gestational and postconceptional ages at the time of study. Maternal smoking was associated wit a significant increase in the apneic index in these infants (28.6 +/- 6.4/hour [S] vs. 13.2 +/- 3.9 [C]; p < 0.05), and the difference was noted for obstructive events and only during active sleep. The arousal index was significantly decreased in the maternal smoking group (34.5 +/- 2.3/hour [S] vs. 46.3 +/- 5.6/hour [C]; p < 0.05), with a specific decrease in percentage of arousal after respiratory events (10.7 +/- 2.1% [S] vs. 29.4 +/- 5.4% [C]; p < 0.05). In conclusion, preterm infants exposed prenatally to cigarette smoke have increased respiratory events during active sleep, predominantly due to obstructive apnea, and possibly a higher arousal threshold during apneic events. These alterations in respiratory and arousal patterns in preterm infants born to smoking mothers may lead to significant vulnerability in this population.

Shea AK; Steiner M. Cigarette smoking during pregnancy. (review). Nicotine & Tobacco Research 10(2): 267-278, 2008. (118 refs.)

Maternal smoking during pregnancy is associated with several adverse developmental outcomes in the offspring. These include preterm delivery, spontaneous abortion, growth restriction, increased risk of sudden infant death syndrome (SIDS), as well as long-term behavioral and psychiatric disorders. However, the underlying physiological mechanisms for these ill-effects are not fully understood. The aim of this paper is to review the animal and human data to date, linking in utero smoke exposure to negative neurodevelopmental outcomes. It is known that nicotine from cigarette smoke exerts its effects by affecting placental vasculature, and also by nicotinic acetylcholine receptor binding in fetal membranes. Thus, subsequent consequences involve a cascade of events causing not only dysregulation of the nicotinic and muscarinic, but also catecholaminergic and serotonergic neurotransmitter systems. These observations provide some insight into how smoking can impair neurodevelopment, but the long-term neurotransmitter involvement in dysregulation of emotion and attention awaits further elucidation. It is important that pregnant women are warned of the detrimental effects of smoking, and encouraged to abstain for healthy fetal development.

Sundell HW. SIDS prevention: Good progress, but now we need to focus on avoiding nicotine. (editorial). Acta Paediatrica 93(4): 450-452, 2004. (12 refs.)

Chong et al. examined risk factors for sudden infant death syndrome (SIDS) before and after the start of the Swedish campaign to reduce the risk of SIDS. They found that maternal smoking was the strongest risk factor for SIDS in the post-campaign compared to the pre-campaign period. Conclusion: After successful results of the SIDS campaigns to prevent prone sleeping, strong efforts need to be undertaken to eliminate maternal smoking during pregnancy altogether without replacing cigarette smoking with other nicotine delivery devices such as snuff, gum or patches.

Vennemann MM; Hense HW; Bajanowski T; Blair PS; Complojer C; Moon RY et al. Bed sharing and the risk of sudden infant death syndrome: Can we resolve the debate? Journal of Pediatrics 160(1): 44-U88, 2012. (40 refs.)

Objective: To conduct a meta-analysis on the relationship between bed sharing and sudden infant death syndrome (SIDS) risk. Study design: Data from PubMed and Medline were searched for studies published after Jan 1, 1970. The search strategy included articles with the terms "sudden infant death syndrome," "sudden unexpected death," and "cot death" with "bed sharing" or "co-sleeping." To further specify the potential risk of bed sharing and SIDS, subgroup analyses were performed. Results: Eleven studies met inclusion criteria and were included in the final meta-analysis. The combined OR for SIDS in all bed sharing versus non-bed sharing infants was 2.89 (95% CI, 1.99-4.18). The risk was highest for infants of smoking mothers (OR, 6.27; 95% CI, 3.94-9.99), and infants <12 weeks old (OR, 10.37; 95% CI, 4.44-24.21). Conclusions: Bed sharing is a risk factor for SIDS and is especially enhanced in smoking parents and in very young infants.

Viskari-Lahdeoja S; Hytinantti T; Andersson S; Kirjavainen T. Heart rate and blood pressure control in infants exposed to maternal cigarette smoking. Acta Paediatrica 2008(97): 11, 2008. (30 refs.)

Aim: Exposure to maternal cigarette smoking is a major risk factor for sudden infant death syndrome (SIDS). Foetal and postnatal smoke-exposure may alter cardiovascular control in infants. We studied heart rate (HR) and blood pressure (BP) responses in smoke-exposed infants. Methods: Eleven infants exposed to maternal cigarette smoking were studied at the age of 12 +/- 2.1 (range 10-16) weeks. Twenty healthy, age-matched infants from non-smoking families served as controls. During confirmed slow-wave sleep (NREM3), 3-5 sec side motion and 45 sec 45 degrees head-up tilt tests were performed. Results: Control infants showed consistent biphasic HR and BP responses to side motion, with an initial 2-5% increase followed by a 2% decrease (p < 0.0001). In smoke-exposed infants, the initial HR (p = 0.009) and BP responses (p < 0.0001) were markedly reduced, and the subsequent decrease in BP was more prominent (systolic blood pressure, SBP, p = 0.005; diastolic blood pressure, DBP, p = 0.03). No differences were observed between the groups in tilt test results, HR variability or HR responses to spontaneous arousals. Conclusion: Maternal cigarette smoking may alter vestibulo-mediated cardiovascular control in early infancy. This may contribute to increased SIDS risk.

Webb RT; Wicks S; Dalman C; Pickles AR; Appleby L; Mortensen PB et al. Influence of environmental factors in higher risk of sudden infant death syndrome linked with parental mental illness. Archives of General Psychiatry 67(1): 69-77, 2010. (42 refs.)

Context: Since national risk reduction campaigns have been conducted, sudden infant death syndrome (SIDS) has become increasingly concentrated among disadvantaged families, including those affected by mental illness. However, causal mechanisms specific to this group are poorly understood. Objectives: To estimate relative risk and compare risk factor prevalence in infants with and without parental psychiatric inpatient history, and to explore effect modification after the 1992 Swedish risk reduction campaign. Design: National birth cohort. Parental psychiatric admissions, maternal prenatal smoking, obstetric and social risk factors, and cause-specific infant death were ascertained via linkage between national registers. Setting: The Swedish population, 1978 through 2004. Participants: All singleton live births (N = 2.5 million). Main Outcome Measure: Incidence of SIDS. Results: Risk of SIDS was higher with a history of parental inpatient care, especially if both parents were admitted with any mental illness (odds ratio, 6.8; 95% confidence interval, 4.7-10.0), or if the mother (6.5; 4.9-8.7) or both parents (9.5; 5.5-16.4) had an alcohol/drug disorder. A 2-fold higher risk was also seen if the mother or father was admitted with any psychiatric illness other than alcohol or other drug disorders. Elevated risk persisted even if the last maternal inpatient episode had occurred 5 or more years before the infant's birth. After the national campaign, risk factor prevalence (especially maternal antenatal smoking) remained high in this population, and relative risks therefore increased. During 1992 through 2004, smoking and individual social adversity measures jointly accounted for approximately half the excess risk linked with maternal psychiatric inpatient history, whereas the confounding effects of obstetric factors were minimal. Conclusions: Tailored approaches are needed to ensure that standard safety advice is effectively communicated to these vulnerable families. In particular, mentally ill pregnant women should be encouraged and better supported to stop smoking. Families with 2 affected parents require particularly strong support. A clearer understanding is needed as to why high risk factor prevalence persists among these parents.