Innovation to prevent sudden infant death: the wahakura as an Indigenous vision for a safe sleep environment.

The bassinet-like wahakura is an Indigenous initiative for the prevention of Sudden Unexpected Death in Infancy (SUDI). It was developed by New Zealand Maori in 2005 when Maori were rejecting the 'stop bedsharing' SUDI prevention message and the SUDI disparity between Maori and non-Maori had become entrenched. Made of native flax, the wahakura was promoted as a culturally resonant, in-bed safe sleep device that would disrupt the SUDI risk associated with 'bedsharing where there was smoking in pregnancy' without relying on smoking cessation. A significant movement of weavers and health professionals grew around the wahakura program. A body of research, including infant care surveys, retrospective case review, qualitative enquiry and a randomised controlled trial comparing wahakura and bassinet safety demonstrated the device's public health plausibility, acceptability to Maori women and its essential safety. This facilitated the distribution, by District Health Boards, of safe sleep devices, including a related device called the Pepi-Pod, and safe sleep education to high-risk, mainly Maori, mothers. Infant mortality in New Zealand fell by 29%, primarily among Maori infants, over the period 2009-15, suggesting that Maori cultural concepts, traditional activities and community engagement can have a significant effect on ethnic inequities in infant mortality.

Smoking in pregnancy is a key factor for sudden infant death among Maori.

AIM: To examine the sudden unexpected death in infancy (SUDI) disparity between Maori and non-Maori in New Zealand. METHODS: A nationwide prospective case-control study ran from March 2012 to February 2015. Exposure to established SUDI risk factors was analysed to investigate the disparity experienced by Maori. Infant ethnicity was based on mother's ethnicity. Maori ethnicity was prioritised. Non-Maori includes Pacific, Asian, NZ European and Other. RESULTS: There were 137 cases and 649 controls. The Maori SUDI rate was 1.41/1000 live births compared to 0.53/1000 for non-Maori. Parents/caregivers of 132 cases (96%) and 258 controls (40%) were interviewed. Smoking in pregnancy was associated with an equally increased SUDI risk for Maori (adjusted OR = 8.11, 95% CI = 2.64, 24.93) and non-Maori (aOR = 5.09, 95% CI = 1.79, 14.47), as was bed-sharing (aOR = 3.66, 95% CI = 1.49, 9.00 vs aOR = 11.20, 95% CI = 3.46, 36.29). Bed-sharing prevalence was similar; however, more Maori controls smoked during pregnancy (46.7%) than non-Maori (22.8%). The main contributor relating to increased SUDI risk for Maori/non-Maori infants is the combination of smoking in pregnancy and bed sharing. CONCLUSION: The association between known SUDI risk factors, including bed sharing and/or smoking in pregnancy and SUDI risk, is the same regardless of ethnicity. Maori infants are exposed more frequently to both behaviours because of the higher Maori smoking rate.

Evaluation of a sudden unexpected death in infancy intervention programme aimed at improving parental awareness of risk factors and protective infant care practices.

AIM: Sudden unexpected death in infancy (SUDI) rates for Maori and Pacific infants remain higher than for other ethnic groups in New Zealand and bed-sharing is a major risk factor when there is smoking exposure in pregnancy. Sleep space programmes of education and Pepi-Pod baby beds require evaluation. METHODS: Two hundred and forty Maori and Pacific women and infants were randomised 1:1, to the Pepi-Pod sleep space programme, or to a control group with 'usual care'. When infants were under 2 weeks of age, baseline interviews occurred, followed up by interviews at 2 and 4 months of age to assess safe sleep knowledge, infant care practices and Pepi-Pod use and acceptability. All participants were offered a New Zealand Standard approved portable cot. RESULTS: At baseline, 25% of babies did not have a baby bed. Knowledge of smoking and bed-sharing as SUDI risks improved at follow-up in both groups. One quarter regularly bed-shared at follow-up in both groups. Intention to bed-share was a strong predictor of subsequent behaviour. Pepi-Pods were regularly used by 46% at 2 months and 16% at 4 months follow-up. CONCLUSIONS: Bed-sharing and knowledge improvement were similar irrespective of group. It is likely that the impact of the intervention was reduced because the control group received better support than 'usual care' and all participants had a baby bed. New Zealand SUDI rates have declined since sleep space programmes have been available. Sleep space programmes should be prioritised for those with modifiable SUDI risk.

The combination of bed sharing and maternal smoking leads to a greatly increased risk of sudden unexpected death in infancy: the New Zealand SUDI Nationwide Case Control Study.

BACKGROUND: Despite a major reduction in overall infant mortality, sudden unexpected death in infancy (SUDI) continues to be of concern in New Zealand, as the rate is high by international standards, and is even higher in indigenous Maori. AIM: To identify modifiable risk factors for SUDI. METHODS: A three-year (1 March 2012-28 February 2015) nationwide case-control study was conducted in New Zealand. RESULTS: There were 137 SUDI cases, giving a SUDI mortality rate of 0.76/1,000 live births. The rate for Maori was 1.41/1,000, Pacific 1.01/1,000 and non-Maori non-Pacific (predominantly European) 0.50/1,000. The parent(s) of 97% of the SUDI cases were interviewed. Six hundred and forty-nine controls were selected and 258 (40%) were interviewed. The two major risk factors for SUDI were: maternal smoking in pregnancy (adjusted OR=6.01, 95% CI=2.97, 12.15) and bed sharing (aOR=4.96, 95% CI=2.55, 9.64). There was a significant interaction (p=0.002) between bed sharing and antenatal maternal smoking. Infants exposed to both risk factors had a markedly increased risk of SUDI (aOR=32.8, 95% CI=11.2, 95.8) compared with infants not exposed to either risk factor. Infants not sharing the parental bedroom were also at increased risk of SUDI (aOR=2.77, 95% CI=1.45, 5.30). Just 21 cases over the three-year study were not exposed to smoking in pregnancy, bed sharing or front or side sleeping position. CONCLUSIONS: This study has shown that many of the risk factors that were identified in the original New Zealand Cot Death Study (1987-1989) are still relevant today. The combination of maternal smoking in pregnancy and bed sharing is extremely hazardous for infants. Furthermore, our findings indicate that the SUDI prevention messages are still applicable today and should be reinforced. SUDI mortality could be reduced to just seven p.a. in New Zealand (approximately one in 10,000 live births).

Differences in Infant Care Practices and Smoking among Hispanic Mothers Living in the United States.

OBJECTIVE: To assess the association between maternal birth country and adherence to the American Academy of Pediatrics safe sleep recommendations in a national sample of Hispanic mothers, given that data assessing the heterogeneity of infant care practices among Hispanics are lacking. STUDY DESIGN: We used a stratified, 2-stage, clustered design to obtain a nationally representative sample of mothers from 32 US intrapartum hospitals. A total of 907 completed follow-up surveys (administered 2-6 months postpartum) were received from mothers who self-identified as Hispanic/Latina, forming our sample, which we divided into 4 subpopulations by birth country (US, Mexico, Central/South America, and Caribbean). Prevalence estimates and aORs were determined for infant sleep position, location, breastfeeding, and maternal smoking. RESULTS: When compared with US-born mothers, we found that mothers born in the Caribbean (aOR 4.56) and Central/South America (aOR 2.68) were significantly more likely to room share without bed sharing. Caribbean-born mothers were significantly less likely to place infants to sleep supine (aOR 0.41). Mothers born in Mexico (aOR 1.67) and Central/South America (aOR 2.57) were significantly more likely to exclusively breastfeed; Caribbean-born mothers (aOR 0.13) were significantly less likely to do so. Foreign-born mothers were significantly less likely to smoke before and during pregnancy. CONCLUSIONS: Among US Hispanics, adherence to American Academy of Pediatrics safe sleep recommendations varies widely by maternal birth country. These data illustrate the importance of examining behavioral heterogeneity among ethnic groups and have potential relevance for developing targeted interventions for safe infant sleep.

Analysis of PAC1 receptor gene variants in Caucasian and African American infants dying of sudden infant death syndrome.

AIM: Stress peptide, pituitary adenylate cyclase-activating polypeptide (PACAP), has been implicated in sudden infant death syndrome (SIDS). The aim of this exploratory study was to determine whether variants in the gene encoding the PACAP-specific receptor, PAC1, are associated with SIDS in Caucasian and African American infants. METHODS: Polymerase chain reaction and Sanger DNA sequencing was used to compare variants in the 5'-untranslated region, exons and intron-exon boundaries of the PAC1 gene in 96 SIDS cases and 96 race- and gender-matched controls. RESULTS: The intron 3 variant, A/G: rs758995 (variant 'h'), and the intron 6 variant, C/T: rs10081254 (variant 'n'), were significantly associated with SIDS in Caucasians and African Americans, respectively (p < 0.05). Also associated with SIDS were interactions between the variants rs2302475 (variant 'i') in PAC1 and rs8192597 and rs2856966 in PACAP among Caucasians (p < 0.02) and rs2267734 (variant 'q') in PAC1 and rs1893154 in PACAP among African Americans (p < 0.01). However, none of these differences survived post hoc analysis. CONCLUSION: Overall, this study does not support a strong association between variants in the PAC1 gene and SIDS; however, a number of potential associations between race-specific variants and SIDS were identified that warrant targeted investigations in future studies.

Sudden infant death syndrome in an urban Aboriginal community.

AIM: The study aims to understand sudden infant death syndrome (SIDS) risk and preventive practices in an urban Aboriginal community, through exploration of mothers' knowledge and practices and examination of coroner case records. METHODS: Data were collected from the mothers of Aboriginal infants participating in the Gudaga Study, a longitudinal birth cohort study. At 2-3 weeks post-natal, mothers were asked about SIDS risk-reduction practices, infant sleeping position and smoking practices within the home. Questions were repeated when study infants were 6 months of age. During the first 18 months of the study, three infants within the cohort died. All deaths were identified as SIDS related. The Coroner reports for these infants were reviewed. RESULTS: At the 2-3 weeks data collection point, approximately 66.2% (n = 98) of mothers correctly identified two or more SIDS risk-reduction strategies. At this same data point, approximately 82% (n = 122) of mothers were putting their infants to sleep on their backs (supine). Higher maternal education was significantly associated (P < 0.01), with identification of two or more correct SIDS risk-reduction strategies and supine sleeping position at 2-3 weeks. The Coroner considered two infants who had been sleeping in an unsafe sleeping environment. CONCLUSION: Rates of SIDS deaths within the study community were much higher than the national average. Most mothers were putting their infant to sleep correctly even though they may be unaware that their practice was in accordance with recommended guidelines. Best practice safe sleeping environments are difficult to achieve for some families living in low socio-economic settings.

Sudden infant death syndrome: review for the obstetric care provider.

Sudden infant death syndrome (SIDS) is the leading cause of death among infants aged 1 to 12 months. In this article, we review risk factors that may predispose infants to increased vulnerability. Maternal characteristics, including nonmodifiable and modifiable factors, antenatal medical conditions, labor and delivery events, and infant characteristics, are reviewed, with the purpose of helping obstetric care providers target risk reduction efforts. We have reviewed over 85 case-control, retrospective, and prospective cohort studies published between 1975 and 2011. Major modifiable risk factors include maternal and paternal smoking, drug use, alcohol use, and insufficient prenatal care. Infants at increased risk include males, premature infants, infants of low birth weight or growth-restricted infants, and infants in multiple gestations. By targeting modifiable and nonmodifiable risk factors, it may be possible to decrease the incidence of SIDS. Efforts should be put on decreasing high-risk behaviors and encouraging sufficient antenatal follow-up. In view of recent increases in ethnic and social disparity with SIDS, it is essential that risk reduction guidelines, which have recently been expanded by the American Association of Pediatrics, be explained in a culturally sensitive manner.

Infant care practices related to sudden infant death syndrome in South Asian and White British families in the UK.

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.

Bed sharing among black infants and sudden infant death syndrome: interactions with other known risk factors.

OBJECTIVE: Bed sharing has been associated with sudden infant death syndrome (SIDS) and may contribute to the racial disparity seen in infant mortality. It is unclear how bed sharing interacts with other factors to impact SIDS risk. We aimed to measure the effects of bed sharing on risk of SIDS in blacks and to determine whether the risk is modified by other characteristics of the sleep environment. METHODS: Characteristics of 195 black infants who died of SIDS were compared with matched controls. The moderating influence of known SIDS risk factors on the effect of bed sharing on risk of SIDS was examined using logistic regression. RESULTS: Almost half (47.4%) of the study population bed shared during the last/reference sleep (58% cases and 37% controls). Bed sharing was associated with 2 times greater risk of SIDS compared with not bed sharing. The deleterious effect of bed sharing was more pronounced with a soft sleep surface, pillow use, maternal smoking, and younger infant age. However, bed sharing was still associated with an increased risk of SIDS, even when the infant was not using a pillow or sleeping on a firm surface. The strongest predictors of SIDS among bed-sharing infants were soft sleep surface, nonuse of a pacifier, and maternal smoking during pregnancy. CONCLUSIONS: Bed sharing is a common practice among black infants. It is associated with a clear and strong increased risk of SIDS, which is even greater when combined with other known risk factors for SIDS. This practice likely contributes to the excess incidence of SIDS among blacks, and culturally competent education methods must be developed to target this high-risk group.

Sudden infant death syndrome (SIDS) in African Americans: polymorphisms in the gene encoding the stress peptide pituitary adenylate cyclase-activating polypeptide (PACAP).

AIMS: Mice lacking pituitary adenylate cyclase-activating polypeptide (PACAP) are prone to sudden death in the second post-natal week, having respiratory and metabolic disturbances reminiscent of the human Sudden Infant Death Syndrome (SIDS). Here we test the hypothesis that the human PACAP gene is a site of genetic variance associated with SIDS in a cohort of 92 victims and 92 matched controls. METHODS: Using polymerase chain reaction and sequencing, we examined the PACAP gene in 92 SIDS cases (46 Caucasians and 46 African Americans) and 92 race- and gender-matched controls. RESULTS: We found no significant associations between PACAP and SIDS in Caucasians. However, in the African Americans, a non-synonymous single nucleotide polymorphism (i.e. an aspartic acid/glycine coding variant, rs2856966) within exon 2 of PACAP was significantly associated with SIDS (p = 0.004), as were haplotypes containing this polymorphism (p < 0.0001). Glycine was three times more likely at this location in the African-American SIDS victims (17 cases) than African-American controls (5 cases). CONCLUSION: These data are the first to suggest an association between a variant within the coding region of the PACAP gene and SIDS. Based on these findings, further investigations are warranted into the functional importance of PACAP signaling in neonatal survival and the role of PACAP-signaling abnormalities in SIDS.

Cardiac ion channel gene mutations in sudden infant death syndrome.

Sudden infant death syndrome (SIDS) is multifactorial and may result from the interaction of a number of environmental, genetic, and developmental factors. We studied three major genes causing long QT syndrome in 42 Japanese SIDS victims and found five mutations, KCNQ1-K598R, KCNH2-T895M, SCN5A-F532C, SCN5A-G1084S, and SCN5A-F1705S, in four cases; one case had both KCNH2-T895M and SCN5A-G1084S. All mutations were novel except for SCN5A-F532C, which was previously detected in an arrhythmic patient. Heterologous expression study revealed significant changes in channel properties of KCNH2-T895M, SCN5A-G1084S, and SCN5A-F1705S, but did not in KCNQ1-K598R and SCN5A-F532C. Our data suggests that nearly 10% of SIDS victims in Japan have mutations of the cardiac ion channel genes similar to in other countries.

The effect of maternal smoking and drinking during pregnancy upon (3)H-nicotine receptor brainstem binding in infants dying of the sudden infant death syndrome: initial observations in a high risk population.

The high rate of the sudden infant death syndrome (SIDS) in American Indians in the Northern Plains (3.5/1000) may reflect the high incidence of cigarette smoking and alcohol consumption during pregnancy. Nicotine, a neurotoxic component of cigarettes, and alcohol adversely affect nicotinic receptor binding and subsequent cholinergic development in animals. We measured (3)H-nicotine receptor binding in 16 brainstem nuclei in American Indian SIDS (n = 27) and controls (n = 6). In five nuclei related to cardiorespiratory control, (3)H-nicotinic binding decreased with increasing number of drinks (P < 0.03). There were no differences in binding in SIDS compared with controls, except upon stratification of prenatal exposures. In three mesopontine nuclei critical for arousal there were reductions (P < 0.04) in binding in controls exposed to cigarette smoke compared with controls without exposure; there was no difference between SIDS cases with or without exposure. This study suggests that maternal smoking and alcohol affects (3)H-nicotinic binding in the infant brainstem irrespective of the cause of death. It also suggests that SIDS cases are unable to respond to maternal smoking with the "normal" reduction seen in controls. Future studies are needed to establish the role of adverse prenatal exposures in altered brainstem neurochemistry in SIDS.

IL6 G-174C associated with sudden infant death syndrome in a Caucasian Australian cohort.

The aims of this study were to analyze IL6 G-174C in relation to high interleukin (IL)-6 concentrations found in some sudden infant death syndrome (SIDS) infants, and to assess the effects of IL6 G-174C, smoking status, and gender on IL-6 responses. SIDS infants, parents of SIDS infants, and populations with high (Aboriginal Australian), medium (Caucasian) or low (Bangladeshi) SIDS incidences were genotyped. Leukocytes were stimulated in vitro with endotoxin and IL-6 responses were assessed in relation to IL6 G-174C genotype, smoking status, and gender. The study findings showed that GG genotype, associated with high IL-6 responses, was predominant among Australian SIDS infants (58%) compared with control subjects (38%, p = 0.02), as well as Bangladeshis (94%) and Aboriginal Australians (88%) compared with Caucasians (42%, p < 0.01). GC smokers had higher median IL-6 responses (8.4 ng/ml(-1)) than GG (3.5 ng/ml(-1), p = 0.01) or CC smokers (2.4 ng/ml(-1), p < 0.01). GG nonsmokers had higher median IL-6 responses (4.9 ng/ml(-1)) than GG smokers (p < 0.05). Gender did not affect IL-6 responses. In conclusion, an association between IL6 G-174C and Australian SIDS infants was observed. IL6 G-174C alone cannot explain observed differences in the incidence of SIDS in the Bangladeshi and Aboriginal Australian populations. Further investigations are needed on interactions between smoking and gene polymorphisms in relation to proinflammatory responses implicated in SIDS.

Nicotine metabolizing genes GSTT1 and CYP1A1 in sudden infant death syndrome.

Exposure to tobacco, both to the developing fetus as well as in the postnatal period, has been identified as a key risk factor in the etiology of sudden infant death syndrome (SIDS). Polymorphisms in both the GSTT1 and CYP1A1 genes have been reported to impact the metabolic detoxification process for cigarette smoke and have been associated with low birth weight. Thus, expression of polymorphisms in these genes may account for the varying susceptibility to the adverse health consequences of tobacco exposure, including SIDS. We hypothesized that functional polymorphisms in GSTT1 (gene deletion) and CYP1A1 (m1, m2, and m3) might be associated with SIDS risk. DNA was prepared from 106 SIDS cases and 106 ethnicity- and gender-matched controls using standard methods. Regions of interest were amplified using PCR, subjected to enzyme digestion, and analyzed on agarose gel. No association was observed between the GSTT1 gene deletion or the CYP1A1 m1, m2, and m3 polymorphisms with SIDS risk when considered independently or in combination. These results indicate that the GSTT1 gene deletion and polymorphisms of CYP1A1 are not responsible for increased SIDS risk in our dataset. However, because SIDS cases with confirmed history of nicotine exposure were limited (7/106 cases), a relationship that might be apparent in a cohort with a large subset of SIDS cases with known history of nicotine exposure cannot be ruled out. A prospective study of SIDS cases with nicotine exposure history is necessary to resolve the relationship between nicotine metabolizing genes and SIDS.

Widening social inequalities in risk for sudden infant death syndrome.

OBJECTIVES: In 1994, the US Public Health Service launched the "Back to Sleep" campaign, promoting the supine sleep position to prevent sudden infant death syndrome (SIDS). Studies of SIDS in the United States have generally found socioeconomic and race disparities. Our objective was to see whether the "Back to Sleep" campaign, which involves an effective, easy, and free intervention, has reduced social class inequalities in SIDS. METHODS: We conducted a population-based case-cohort study during 2 periods, 1989 to 1991 and 1996 to 1998, using the US Linked Birth/Infant Death Data Sets. Case group was infants who died of SIDS in infancy (N = 21 126); control group was a 10% random sample of infants who lived through the first year and all infants who died of other causes (N=2241218). Social class was measured by mother's education level. RESULTS: There was no evidence that inequalities in SIDS were reduced after the Back to Sleep campaign. In fact, odds ratios for SIDS associated with lower social class increased between 1989-1991 and 1996-1998. The race disparity in SIDS increased after the Back to Sleep campaign. CONCLUSIONS: The introduction of an inexpensive, easy, public health intervention has not reduced social inequalities in SIDS; in fact, the gap has widened. Although the risk of SIDS has been reduced for all social class groups, women who are more educated have experienced the greatest decline.

Risk factors for sudden infant death syndrome among northern plains Indians.

CONTEXT: Sudden infant death syndrome (SIDS) is a leading cause of postneonatal mortality among American Indians, a group whose infant death rate is consistently above the US national average. OBJECTIVE: To determine prenatal and postnatal risk factors for SIDS among American Indians. DESIGN, SETTING, AND PARTICIPANTS: Population-based case-control study of 33 SIDS infants and 66 matched living controls among American Indians in South Dakota, North Dakota, Nebraska, and Iowa enrolled from December 1992 to November 1996 and investigated using standardized parental interview, medical record abstraction, autopsy protocol, and infant death review. MAIN OUTCOME MEASURES: Association of SIDS with maternal socioeconomic and behavioral factors, health care utilization, and infant care practices. RESULTS: The proportions of case and control infants who were usually placed prone to sleep (15.2% and 13.6%, respectively), who shared a bed with parents (59.4% and 55.4%), or whose mothers smoked during pregnancy (69.7% and 54.6%) were similar. However, mothers of 72.7% of case infants and 45.5% of control infants engaged in binge drinking during pregnancy. Conditional logistic regression revealed significant associations between SIDS and 2 or more layers of clothing on the infant (adjusted odds ratio [aOR], 6.2; 95% confidence interval [CI], 1.4-26.5), any visits by a public health nurse (aOR, 0.2; 95% CI, 0.1-0.8), periconceptional maternal alcohol use (aOR, 6.2; 95% CI, 1.6-23.3), and maternal first-trimester binge drinking (aOR, 8.2; 95% CI, 1.9-35.3). CONCLUSIONS: Public health nurse visits, maternal alcohol use during the periconceptional period and first trimester, and layers of clothing are important risk factors for SIDS among Northern Plains Indians. Strengthening public health nurse visiting programs and programs to reduce alcohol consumption among women of childbearing age could potentially reduce the high rate of SIDS.

Are risk factors for sudden infant death syndrome different at night?

AIMS: To determine whether the risk factors for SIDS occurring at night were different from those occurring during the day. METHODS: Large, nationwide case-control study, with data for 369 cases and 1558 controls in New Zealand. RESULTS: Two thirds of SIDS deaths occurred at night (between 10 pm and 7 30 am). The odds ratio (95% CI) for prone sleep position was 3.86 (2.67 to 5.59) for deaths occurring at night and 7.25 (4.52 to 11.63) for deaths occurring during the day; the difference was significant. The odds ratio for maternal smoking for deaths occurring at night was 2.28 (1.52 to 3.42) and that for the day 1.27 (0.79 to 2.03); that for the mother being single was 2.69 (1.29 to 3.99) for a night time death and 1.25 (0.76 to 2.04) for a daytime death. Both interactions were significant. The interactions between time of death and bed sharing, not sleeping in a cot or bassinet, Maori ethnicity, late timing of antenatal care, binge drinking, cannabis use, and illness in the baby were also significant, or almost so. All were more strongly associated with SIDS occurring at night. CONCLUSIONS: Prone sleep position was more strongly associated with SIDS occurring during the day, whereas night time deaths were more strongly associated with maternal smoking and measures of social deprivation.

Sudden infant death syndrome risk factors in north Queensland: a survey of infant-care practices in Indigenous and non-Indigenous women.

OBJECTIVE: To assess the prevalence of sudden infant death syndrome (SIDS) risk factors in the Indigenous and non-Indigenous community of Townsville, a large remote urban centre in north Queensland, Australia. METHODS: Thirty Indigenous and 30 non-Indigenous women with young children were surveyed using sections of the West Australian Infancy and Pregnancy Survey 1997-1998. The prevalence of SIDS risk factors was compared between the two groups and medians and univariate associations were generated where appropriate. RESULTS: The Indigenous women were significantly younger and more likely to be single. The median age of the infants was 8 months (range 0.3-26 months) with no difference between the two groups. Thirty-seven per cent of Indigenous infants slept prone (cf. 17% of non-Indigenous infants; P = 0.03), and 77% shared a bed (cf. 13% of non-Indigenous infants; P < 0.001). The Indigenous households had significantly more members, with 57% including extended family members (cf. 20% non-Indigenous group; P = 0.003). Fifty-three per cent of the Indigenous women smoked during pregnancy (cf. 23% of non-Indigenous women; P = 0.017), 60% were smokers at the time of the interview, and smoking occurred inside 40% of Indigenous houses (cf. 20% and 20% for non-Indigenous women, respectively; P < 0.001, 0.09). CONCLUSION: This small survey suggests that the prevalence of SIDS risk factors is higher in the Indigenous population, and a new approach to education is needed urgently to promote SIDS awareness among Indigenous women.