Reducing the Incidence of Sudden Infant Death Syndrome in the Delta Region of Mississippi: A Three-Pronged Approach.

ABSTRACT: Since the "Back to Sleep" campaign in 1994, which encouraged positioning infants on their backs for sleeping, the incidence of sudden infant death syndrome (SIDS) has decreased dramatically in the United states but remains high in some rural Mississippi communities. We discuss some of the hypotheses and etiologic factors of SIDS. The high incidence of SIDS in the Delta region of Mississippi could be dramatically reduced, primarily through an intensified Back to Sleep campaign. Furthermore, the importance of health education in increasing breast-feeding rates and reducing passive smoke exposure rates in this community is emphasized.

SUDDEN INFANT DEATH SYNDROME (SIDS) is defined as the sudden and unexpected death of an apparently healthy infant. A thorough history and postmortem examination are typically insufficient to explain the cause of death. It is an- affliction that has been recognized since biblical times. In the District I health region of Mississippi (where the north Delta is located), SIDS is the second highest cause of infant death after deaths from complications of prematurity and/or low birth weight or congenital anomalies (Figure) . [1] In the United States, about 3,000 infants die of SIDS annually, accounting for more than a third of all infant deaths, or 0.77 per 1,000 live births. [2] In healthy full-term infants, the peak incidence is from 2 to 4 months of age, and by 6 to 8 months, more than 95% of all cases have occurred.

While the SIDS rates in the United States have significantly decreased by almost 40% since the 1994 "Back to Sleep" campaign by the National Institute of Child Health and Development (NICHD) , [3] these rates are still lagging substantially behind those of other industrialized nations. [4-6] The most current Mississippi SIDS rate of 1.4 per 1,000 live births (almost double the national rate) [1] is among the highest in the country.

The purposes of our report are to review current literature on etiologic factors associated with SIDS and to discuss the most effective means of reducing this affliction in the Delta region of rural Mississippi, where we are pediatricians in general practice. The Delta region of Mississippi is among the poorest in the nation. Unlike most rural areas in the United States, the majority of its inhabitants are impoverished rural African Americans with an average annual income of about $10,000. [1]

CAUSES OF SUDDEN INFANT DEATH SYNDROME

The cause of SIDS remains elusive. Hypotheses abound regarding the causal mechanism of SIDS. The most compelling of these hypotheses focus on three brainstem abnormalities, which consist of abnormal sleep/wake regulation, abnormal temperature regulation, and abnormal cardiorespiratory regulation. In infants with abnormal sleep/wake regulation, arousal responsiveness is absent. These infants are incapable of responding to the normal physiologic sleep-related hypoxia. In those with abnormal temperature regulation, increased body temperature may be due to the complex interaction between dysfunctional cardiorespiratory control and a dysfunctional autonomic nervous system. Infants with abnormal cardiorespiratory control may have decreased chemoreceptor sensitivity to hypoxia and carbon dioxide.

Each of these three abnormalities can lead to prolonged apnea/bradycardia, subsequently causing SIDS. Other biologic and environmental risk factors may also interact with these brainstem abnormalities to result in SIDS. Table 1 [7-11] summarizes some of these hypotheses and possible mechanisms of SIDS. These factors may be either modifiable or nonmodifiable (Table 2). Known modifiable risk factors include the type of infant sleep position, [7-14] environmental exposure to toxins such as tobacco smoke, [15-23] type of infant feeding practices, [24-27] maternal substance abuse, [28-29] ambient temperature, [30-32] type of bedding, [33-34] cosleeping of adults and children, [35-38] prenatal care, and possibly some ill-defined infectious disease process. [39,40] Because infants with long QT syndrome are likely to have cardiac arrhythmias during certain stress situations, these infants are likely to die of SIDS. [41-45] Nonmodifiable sociodemographic risk factors include maternal age, maternal education, race, ge stational age, birth weight, and socioeconomic status. [46-53]

To reduce the incidence of SIDS in this community, a practical three-pronged approach is proposed, consisting of (1) increasing the use of correct sleep position practices, (2) decreasing the rate of passive smoke exposure in the home, and (3) increasing breast-feeding by new mothers.

INCREASING USE OF CORRECT SLEEP POSITION PRACTICES

Before 1990, mothers were always advised to place their infants in a prone position during sleep, to prevent choking if the neonate vomited. However, it is now known that normal infants do not choke on their vomitus while sleeping on their backs. In fact, infants sleeping on their stomachs are two or three times more likely to die of SIDS than those sleeping on their backs. The reason the prone sleep position is associated with increased incidence of SIDS remains to be satisfactorily explained. It has been shown that infants sleeping prone tend to have higher arousal thresholds to auditory challenges and poor or decreased cardiorespiratory responses to environmental stimuli. The cause of the increased arousal threshold is yet to be determined.

The peak incidence of SIDS coincides with the time most infants begin to sleep better, especially throughout the night. Infants are less easily aroused and less responsive to the stimulating effects of low oxygen or increased carbon dioxide. One proposed mechanism for this increase in arousal thresholds is that infants sleeping in the prone position are more likely to rebreathe their own exhaled gases, such as carbon dioxide, that may be trapped in excessively soft bedding. [54-52] The inhaled carbon dioxide further depresses the respiratory center. Furthermore, infants sleeping in the prone position tend to have longer NREM (non-rapid eye movement, or inactive) sleep and may "forget" to breathe due to relative immaturity of the cardiorespiratory control centers of the brain. [60]

Since 1992, NICHD has regularly conducted surveys on sleep position practices in the United States. Since then, use of the prone sleep position has steadily decreased. In Georgia, Saraiya et al [63] showed that the prevalence of the prone sleep position decreased from 49% in 1990 to 15% in 1995. This shift was attributed primarily to a shift in the side sleep position rather than the back. Other recent findings show that, nationally, more than 50% of infants younger than 8 months of age are placed on their backs or sides during sleep. However, the rates vary by region and by state, with the highest rates in the Midwest and Northeast and the lowest rates in the southern states. [12,14]

Rates are also lowest in low-income, inner-city communities as compared with suburban communities. [13] Currently, no published rates are available for Mississippi. However, in a recent survey of 260 low-income mothers in a rural Mississippi community (Philip Kum-Nji et al, unpublished data, 2000), only 38% of the infants younger than 12 months of age were placed on their backs or sides during sleep. When these mothers were asked to state the reason why an infant should be placed preferentially on the back or side, only 9% correctly answered that the nonprone position prevented crib death or SIDS. The results of this survey suggest a lack of information on advantages of the nonprone sleep position in this community. Although the side sleep position is also acceptable; the back sleep position should be emphasized as being the most effective in preventing SIDS. Such education should be initiated soon after birth, even if the infant is preterm, and it should be continued during all well-baby or sick visits in t he first year of life.

Because about 20% of SIDS cases in the United States occur in day-care settings, [64] daycare personnel should also be targeted for education on the advantages of the nonprone sleep position. A recent study [65] from the Washington, DC, area showed that 49% of the day-care centers placed their infants exclusively in the prone position during sleep, and only 43% of the licensed child-care workers were unaware of the association between sleep position and SIDS. Another survey [66] in this same area 4 years later showed that the proportion of licensed centers that were aware of the association of infant sleep position and SIDS had increased from 57% to 75%, while the rate of infants sleeping prone had dropped from 49% to 28%. Some contraindications to the supine sleep position include severe gastroesophageal reflux, extreme prematurity, and obstructive apnea.

DECREASING ENVIRONMENTAL TOBACCO SMOKE 

Cigarette smoke contains at least 4,000 chemical toxins. Despite the well-known hazards of environmental tobacco smoke (ETS), at least 50% of young children in the United States are exposed to these toxins in their homes. [67] Maternal smoking during pregnancy and maternal passive smoke during the postneonatal period has been shown to be one of the most significant predictors of SIDS, [15-23] including other illnesses, such as otitis media, [68-74] serious bacterial and/or respiratory tract infections, [75-86] and possibly cancer. [87-89] A dose-response relationship has also been shown in most of these studies. Recent data [90] in the Delta area of Mississippi show that 27% of mothers are regular smokers, and an additional 43% of other household members or other close relatives also smoke in homes with children. Thus, up to 75% of young children may be exposed to ETS in this community However, a survey by the Mississippi Health Department showed lower maternal smoking rates of 19% for the whole state, thoug h information on the smoking status of other household members was not obtained in this study. [91]

How ETS causes SIDS is purely speculative at this time. One view is that the toxic chemicals in tobacco (eg, nicotine and its metabolites) may actually damage the developing brain, especially the cardiorespiratory center in the midbrain. Another hypothesis is that an infectious agent interacting with the chemical products of ETS may cause SIDS. Sayers et al [39,92,93] have shown that low levels of nicotine or one of its primary metabolites, cotinine, may actually result in the potentiation of low levels of certain bacterial toxins. This could in part explain why the cause of SIDS deaths is not often apparent on postmortem examination. A third view is that nicotine from ETS may cause SIDS through impaired metabolism of catecholamines in the brain, resulting in decreased arousal and ventilatory responsiveness to hypoxia. Since relative growth failure is noted in infants exposed to ETS both prenatally and postnatally, it is reasonable to presume that brain growth, including the cardiorespiratory center, is also impaired in these infants.

Education efforts should aim at encouraging all parents and household members to refrain from smoking at home. During all encounters with the health service provider, whether for routine health checkups or an acute illness, the clinician should always seize the opportunity to educate the parents or guardians on the health hazards of ETS, including SIDS, ear infections, serious bacterial infections, and other upper and lower respiratory tract illnesses. Families should be encouraged to give up smoking or at least to start by smoking only outside using a smoking gown and smoking cap. They should be instructed that, even though they may not smoke at home in the presence of the infant, the tobacco toxins are still present on their hair or clothes and are easily transferable to their baby. They should also be directed to resources in the community that may facilitate their quitting smoking.

INCREASING THE BREAST-FEEDING RATES

Recent well-controlled studies have consistently shown that infants who were never breast-fed were two or three times more likely to die of SIDS than their breast-fed counterparts. [24-27] Because of its high content of immunoglobulins and other antibacterial agents, breast milk has also been shown to have protective effects against illnesses such as rotavirus infections, ear infections, and upper and lower respiratory tract infections. It is not clear why breast-feeding is protective against SIDS. Gordon et al [25,26] have speculated that the protective effect of breast milk could in part be attributable to the binding effects of IgA on bacterial toxins, such as staphylococcal enterotoxin C and Clostridium perfringens enterotoxin A, implicated in some cases of SIDS. Because breast-fed infants are usually healthier than their bottle-fed counterparts, they also tend to be resistant to whatever causes SIDS. Another possible explanation could be that, because of its richness in long-chain polyunsaturated fatty acids and other nutrients, breast milk enhances faster development of the central nervous system of the infants. [94-97] Also, the frequent tactile stimulation of breast-feeding during the night may actually protect against SIDS. [35]

Nationally, about 60% of new mothers initiate breast-feeding, though only about 25% continue to do so 6 months after delivery. [98] These figures vary widely depending on the region; they are highest in the Northeast and lowest in the Southeast. [99-102] These rates are consistently lower among ethnic minorities than whites. In rural Mississippi, a recent survey [102] showed that breast-feeding initiation rates were only 19% for blacks versus 44% for whites. Breast-feeding rates 6 months after delivery were not measured but were likely to have been substantially lower. Increasing the breast-feeding rates in the Delta region of Mississippi would necessitate educating and encouraging new mothers to breast-feed their infants.

Breast-feeding education programs should preferably be initiated before delivery, and efforts should be continued after delivery. Some studies have shown that most breast-feeding counseling is done by allied health care workers. [102] Physicians often report being inadequately prepared for the task during residency training. [103-107] Physicians, nurses, nutritionists, and other health care professionals should therefore all be involved in such programs. For the programs to be effective, educational programs should involve not only mothers, but also husbands, friends, family members, and significant others. Other studies also show that social support systems, such as those at the workplace and in the hospitals, are necessary for a successful breast-feeding program. [108,109]

CONCLUSION

Sudden infant death syndrome is the single most important cause of postneonatal mortality in the United States. In the Delta region of Mississippi, we recommend a three-pronged educational approach to reduce die incidence of SIDS in this region: (1) increasing the proportion of infants sleeping in the nonprone position, (2) decreasing the proportion of young infants exposed to passive smoke in homes, and (3) increasing the proportion of mothers initiating breast-feeding and continuing to breast-feed for at least 12 months after delivery. Until the cause of SIDS is found, our only hope of combating this endemic problem is through lasting changes in infant care practices in our community. Other factors, such as type of bedding, cosleeping, long QT syndrome, and ambient room temperature, may also be of some importance but, for now, too much emphasis on these may only add to parents' confusion. We believe that the three factors discussed in this paper are the most important, and health education programs focused on them will dramatically decrease the incidence of SIDS in this community.

References

(1.) Vital Statistics. Public Health Service. Jackson, Miss, Mississippi State Department of Health, 1998

(2.)Centers for Disease Control and Prevention: National Linked Birth/Infant Death Data Sets, 1983-1997. Hyattsville, Md, National Vital Statistics System, National Center for Health Statistics, 2000

(3.) Willinger M, Hoffman HJ, Wu KT, et al: Factors associated with the transition to nonprone sleep postions of infants in the United States: the National Infant Sleep Position Study. (JAMA 1998; 280:329-335

(4.) Mitchell EA, Grunt JM, Evard C: Reduction in mortality from sudden infant death syndrome in New Zealand. Arch Dis Child 1994; 70:291-294

(5.) Hiley CM, Morley CJ: Risk factors for sudden infant death syndrome: further change in 1992-1993. BMJ 1996; 312:1397-1398

(6.) Wennergren G, Alm B, Oyen N, et al: The decline in the incidence of SIDS in Scandinavia and its relation to risk-intervention campaigns. Nordic Epidemiological SIDS Study. Acta Paediatr 1997; 86:963-968

(7.) Kemp JS, Unger B, Wilkins D, et al: Unsafe sleep practices and an analysis of bedsharing among infants dying suddenly and unexpectedly: results of a four-year, population-based, death-scene investigation study of sudden infant death syndrome and related deaths. Pediatrics 2000; 106:E41

(8.) Nelson EA, Schiefenhovel W, Haimerl F: Child care practices in nonindustrialized societies. Pediatrics 2000; 105:E75

(9.) Gibson E, Dembofsky CA, Rubin S, et al: Infant sleep position practices 2 years into the "back to sleep" campaign. Clin Pediatr 2000; 39:285-289

(10.) Willinger M, Ko CW, Hoffman HJ, et al: Factors associated with caregivers' choice of infant sleep position, 1994-1998: the National Infant Sleep Position Study. JAMA 2000; 283:2135-2142

(11.) Havens T, Skadberg B, Hordvik E, et al: Sleep position and sudden infant death syndrome (SIDS): effect of an intervention program to avoid prone sleeping. Acta Paediatr 1995; 84:375-378

(12.) Centers for Disease Control and Prevention: Progress in reducing risky infant sleeping positions-13 states, 1996-1997. MMWR Morb Mortal Wkly Rep 1999; 48:878-882

(13.) Johnson CM, Borkowski MM, Hunter KE, et al: Infant sleep position: a telephone survey of inner-city parents of color. Pediatrics 1999; 104:1208-1211

(14.) Centers for Disease Control and Prevention: Assessment of infant sleeping position-selected states, 1996. MMWR Morb Mortal Wkly Rep 1998; 47:873-877

(15.) Poole KA, Hallinan H, Beardmore CS, et al: Effect of maternal smoking on ventilatory responses to changes in inspired oxygen levels in infants. Am J Respir Crit Med 2000; 162:801-807

(16.) Wisborg K, Kesmodel U, Henriksen TB, et al: A prospective study of smoking during pregnancy and SDS. Arch Dis Child 2000; 83:203-206

(17.) Haglund B, Cnattingius 5, Otterblad-Olausson P: Sudden infant death syndrome in Sweden, 1983-1990: season at death, age at death, and maternal smoking. Am J Epidemiol 1995; 142:619-624

(18.) Klonoff-Cohen HS, Edelstein SL, Lefkowitz ES, et al: The effect of passive smoking and tobacco exposure through breast milk on sudden infant death syndrome. JAMA 1995; 273:795-798

(19.) Milerad J, Rajs J, Gidlund E: Nicotine levels in pericardial fluid in victims of SIDS. Acta Paediatr 1994; 83:59-62

(20.) Mitchell EA, Ford RP, Stewart AW, et al: Smoking and the sudden infant death syndrome. Pediatrics 1993; 91:893-896

(21.) Schoendorf KG, Kiely JL: Relationship of sudden infant death syndrome to maternal smoking during and after pregnancy. Pediatrics 1992; 90:905-908

(22.) Malloy MH, Kleinman JC, Land GH, et al: The association of maternal smoking with age and cause of infant death. Am J Epidemiol 1988; 128:46-55

(23.) Bergman AB, Wiesner LA: Relationship of passive cigarette-smoking to sudden infant death syndrome. Pediatrics 1976; 58:665-668

(24.) Milligan RA, Pugh LC, Bronner YL, et al: Breastfeeding duration among low income women. J Midwifery Womes Health 2000; 45:246-252

(25.)Gordon AE Saadi AT, MacKenzie DA, et al: The protective effect of breast feeding in relation to sudden infant death syndrome (SIDS): III. Detection of IgA antibodies in human milk that bind to bacteria toxins implicated in SIDS. FEMS Immunol Med Microbiol 1999; 25:175-182

(26.)Gordon AE, Saadi AT, MacKenzie DA, et al: The protective effect of breast feeding in relation to sudden infant death syndrome: II. The effect of human milk and infant formula preparations on binding of Clostridium perfriagens to epithelial cells. FEMS Immunol Med Micrombiol 1999; 25:167-173

(27.) Ford RP, Taylor BJ, Mitchell EA, et al: Breastfeeding and the risk of sudden infant death syndrome. Int J Epidemiol 1993; 22:885-890

(28.) Fox CH: Cocaine use in pregnancy. Am Board Fam Pract 1994; 7:225-228

(29.) Kandall SR, Gaines J, Habel L, et al: Relationship of maternal substance abuse to subsequent sudden infant death syndrome in off spring. J Pediatr 1993; 123:120-126

(30.) Williams SM, Mitchell EA, Stewart AW, et al: Temperature and the sudden infant death syndrome. Paediatr Perinat Epidemiol 1996; 10:136-149

(31.) Helweg-Larsen K, Lundemose JB, Bille H: Overheating and sudden infant death. temperature regulation in relation to the prone position, the possible pathogenesis of sudden infant death. (Danish) Ugeskr Loeger 1994; 156:7193-7196

(32.)Sawczenko A, Fleming PJ: Thermal stress, sleeping position, and the sudden infant death syndrome. Sleep 1996; 19:S267-S270

(33.)Carleton JN, Donoghue AM, Porter WK: Mechanical model testing of rebreathing potential in infant bedding materials. Arch Dis Child 1998; 78:323-328

(34.) Kemp JS, Livne M, White DK, et al: Softness and potential to cause rebreathing: differences in bedding used by infants at high and low risk for sudden infant death syndrome. J Pediatr 1998; 132:234-239

(35.) McKenna JJ, Mosko SS, Richard CA: Bedsharing promotes breastfeeding. Pediatrics 1997; 100:214-219

(36.) Mosko S, Richard C, McKenna J, et al: Maternal proximity and infant [CO.sub.2] environment during bedsharing and possible implications for SIDS research. Am] Phys Anthropol 1997; 103:315-328

(37.) Rath FH Jr, Okum ME: Parents and children sleeping together: cosleeping prevalence and concerns. Am J Orthopsychiatry 1995; 65:411-418

(38.) Mosko S, McKenna J, Dickel M, et al: Parent-infant cosleeping: the appropriate context for the study of infant sleep and implications for sudden infant death syndrome (SIDS) research. J Behav Med 1993; 16:589-610

(39.) Sayers NM, Drucker DB: Animal models used to test the interactions between infectious agents and products of cigarette smoke implicated in sudden infant death syndrome. FEMS Immunol Med Microbiol 1999; 25:115-123

(40.) Morris JA: The common bacterial toxins hypothesis of sudden infant death syndrome. FEMS Immunol Med Microbial 1999; 25:11-17

(41.) Davies DP: Short QTc interval as an important factor in sudden infant death syndrome. Arch Dis Child 1999; 80:105-106

(42.) Schwartz PJ, Stramba-Badiale M, Segantini A, et al: Prolongation of the QT interval and sudden infant death syndrome. N Engl J Med 1998; 338:1709-1714

(43.) Perticone F, Ceravolo R, Mattioli PL: Prolongation of QT interval: a marker of sudden infant death syndrome? Clin Cordial 1991; 14:417-421

(44.) Krahe J, Neudorf U, Hentrich F: The QT syndrome in newborn infants. (German) Monatsschr Kinderheilkd 1989; 137:463-465

(45.) Kaada B: Sudden infant death--the QT interval in EGG and bradyarrhythmias. (Norwegian) Tidsskr Nor Laegeforen 1989; 109:186-192

(46.) Leach CE, Blair PS, Flemming PJ, et al: Epidemiology of SIDS and explained sudden infant deaths. CESDI SUDI Research Group. Pediatrics 1999; 104:E43

(47.) Lesko SM, Corwin MJ, Vezina RM, et al: Changes in sleep position during infancy: a prospective longitudinal assessment. JAMA 1998; 280:336-340

(48.) Kohlendorfer U, Kiechl S, Sperl W: Sudden infant death syndrome: risk factor profile distinct subgroups. Am J Epidemiol 1998; 147:960-968

(49.) Daltveit AK, Irgens LM, Oyen N, et al: Sociodemiographic risk factors for sudden infant death syndrome: associations with other risk factors. The Nordic Epidemiological SIDS Study. Acta Paediatr 1998; 87:284-290

(50.) Oyen N, Markestad T, Skaervin T, et al: Combined effects of sleeping position and prenatal risk factors in sudden infant death syndrome: The Nordic Epidemiological SIDS Study. Pediatrics 1997; 100:613-621

(51.) Daltveit AK, Oyen N, Skjaerven R, et al: The epidemic of SIDS in Norway 1967-1993: changing effects of risk factors, Arch Dis Child 1997; 77:23-27

(52.) Sanghavi DM: Epidemiology of sudden infant death syndrome (SIDS) for Kentucky infants born in 1990: maternal, prenatal, and perinatal risk factors. J Ky Med Assoc 1995; 93:286-290

(53.) Arntzen A, Moum T, Magnus P, et al: Is the higher postneonatal mortality in lower social status groups due to SIDS? Acta Paediatr 1995; 84:188-192

(54.) Guntheroth WG, Spiers PS: Are bedding and rebreathing sufforation a cause of SIDS? Pediatr Pulmonol 1996; 22:335-415

(55.) Tolcos M, McGregor H, Walker D, et al: Chronic prenatal exposure to carbon monoxide results in a reduction in tyrosine hydroxylase-immunorcactivity and an increase in choline acetyltransferase-immunoreactivity in the fetal medulla: implications for sudden infant death syndrome. J Neuropathol Exp Neurol 2000; 59:218-228

(56.) Hale TM, Valea FA Stelling JR, et al: A new method and apparatus that prevents the rebreathing of expired carbon dioxide of sleeping neonates and infants. Am J Perinatol 1995; 12:164-167

(57.) Carolan PL, Wheeler WB, Ross JD, et al: Potential to prevent carbon dioxide rebreathing of commercial products marketed to reduce sudden infant death syndrome risk. Pediatrics 2000; 105:774-779

(58.) Katz-Salamon M, Milerad J: The divergent ventilatory and heart rate response to moderate hypercapnia in infants with apnoea of infancy. Arch Dis Child 1998;79:231-236

(59.) Funayama M, Mimasaka S, Iwashiro K, et al: Inhaled air trapping effect of Japanese bedding as a risk of sudden unexpected death in infancy. Tohoku J Exp Med 1998; 185:55-65

(60.) Martin RJ, Difiore JM, Korenke CB, et al: Vulnerability of respiratory control in healthy preterm infants placed supine. J Pediatr 1995; 127:609-614

(61.) Skadberg BT, Oterhals A, Finborad K, et al: [CO.sub.2] rebreathing: a possible contributory factor to some cases of sudden infant death? Acta Paediatr 1995; 84:998-1005

(62.) Home RS, Sly DJ, Cranage SM, et al: Effects of prematurity on arousal from sleep in the newborn infant. Pediatr Res 2000; 47:468-474

(63.) Saraiya M, Serbanescu F, Rochat R, et al: Trends and predictors of infant sleep positions in Georgia, 1990 to 1995. Pediatrics 1998; 102:E33

(64.) Moon RY, Patel KM, Shaefer SJ: Sudden infant death syndrome in child care settings. Pediatrics 2000; 106:295-300

(65.) Gershon NB, Moon RY: Infant sleep position in licensed child care centers. Pediatrics 1997; 100:75-78

(66.) Moon RY, Biliter WM: Infant sleep position policies in licensed child care centers after back to sleep campaign. Pediatrics 2000; 106:576-580

(67.) Hopper JA, Craig KA: Environmental tobacco smoke exposure among urban children. Pediatrics 2000; 106:E47

(68.) Ey JL, Holberg CJ, Aldous MB, et al: Passive smoking exposure and otitis media in the first year of life. Pediatrics 1995; 95:670-677

(69.) Strachan DP, Cook DG: Health effects of passive smoking. 4. Parental smoking, middle ear disease and adenotonsillectomy in children. Thorax 1998; 53:50-56

(70.) Paradise JL, Rockette HE, Colborn K, et al: Otitis media in 2,253 Pittsburgh-area infants: prevalence and risk factors during the first 2 years of life. Pediatrics 1997; 99:318-333

(71.) Duncan B, Ey J, Holberg CJ, et al: Exclusive breast-feeding for at least 4 month protects against odds media. Pediatrics 1993; 91:867-872

(72.) Saarinen UM: Prolonged breast feeding as prophylaxis for recurrent otitis media. Acta Paediatr Scand 1982; 71:567-571

(73.) Kero P, Piekkala P: Factors affecting the occurrence of acute otitis media during the first year of life. Acta Paediatr Scand 1987; 76:618-623

(74.) Narayanan I, Singh S, Mathur R, et al: Ear infection and infant feeding practices. Indian J Pediatr 1989; 56:399-402

(75.) Nuorti JP, Butler JC, Farley MM, et al: Cigarette smoking and invasive pneumococcal disease. N Engl J Med 2000; 342:681-689

(76.) el-Nawawy A, Soliman AT, el-Azzouni O, et al: Effect of passive smoking on frequency of respiratory illnesses and serum immunoglobulin-E (IgE) and interleukin-4 (IL-4) concentrations in exposed children. J Trop Pediatr 1996; 42:166-469

(77.) Haby MM, Peat JK, Woolcock AJ, et al: Effect of passive smoking, asthma, and respiratory infection on lung function in Australian children. Pediatr Pulmonol 1994; 18:323-329

(78.) Narce-Valente S, Kligman EWJ: Increasing physician screening and counseling or passive smoking. Fam Pract 1992; 34:722-728

(79.) Guyatt GH, Newbouse MT: Are active and passive smoking harmful? determining causation. Chest 1985; 88:445-451

(80.) Joad JP: Smoking and pediatric respiratory health. Clin Chest Med 2000; 21:37-46 vii-viii

(81.) Cook DG, Strachan DP: Health effects of passive smoking. 10. Summary of effects of parental smoking on the respiratory health of children and implications for research. Thorax 1999; 54:357-366

(82.) Lister SM, Jorm LR: Parental smoking and respiratory illnesses in Australian children aged 0-4 years: ABS 1989-90 National Health Survey results. Aust N Z J Public Health 1998; 22:781-786

(83.) Komoroski EM, Kirby RS, Rickert VI, et al: Risk factors for febrile, presumed viral illness in the first ten weeks of life. J Perinatol 1997; 17:288-291

(84.) Jedrychowski W, Flak E: Maternal smoking during pregnancy and postnatal exposure to environmental tobacco smoke as predisposition factors to acute respiratory infections. Environ Health Perspect 1997; 105:302-306

(85.) Barber K, Mussin E, Taylor DK: Fetal exposure to involuntary maternal smoking and childhood respiratory disease. Ann Allergy Asthma Immunol 1996; 76:427-430

(86.) Mannino DM, Siegel M, Husten C, et al: Environmental tobacco smoke exposure and health effects in children: results from the 1991 National Health Interview Survey. Tob Control 1996; 5:13-18

(87.) Sasco AJ, Vainio H: From in utero and childhood exposure to parental smoking to childhood cancer: a possible link and the need for action. Human Exp Toxicol 1999; 18:192-201

(88.) Pershagen G: Childhood cancer and malignancies other than lung cancer related to passive smoking. Mutat Res 1989; 222:129-135

(89.) Tredaniel J, Boffetta P, Little J, et al: Exposure to passive smoking during pregnancy and childhood, and cancer risk: an epidemiological evidence. Paediatr Perinat Epidemiol 1994; 8:233-255

(90.) Kum-Nji P, Mangrem CL, Wells PJ, et al: The effect of smoking exposure on infant illnesses: the experience of a private pediatric practice in rural Mississippi. (Abstract) J Invest Med 1998; 46:26A

(91.) Mississippi State Department of Health Tobacco Program Statistics. Mississippi SIDS Risk Reduction Task Force, Jackson, Miss, AAP News 1997; 13:22

(92.) Sayers NM, Drucker DB, Morris JA, et al: Significance of endotoxin in lethal synergy between bacteria associated with sudden infant death syndrome: follow-up study. J Clin Pathol 1996; 49:245-249

(93.) Sayers NM, Drucker DB, Telford DR, et al: Effects of nicotine on bacterial toxins associated with cot death. Arch Dis Child 1995; 73:549-555

(94.) Xiang M, Alfven G, Blennow M, et al: Long-chain ployunsaturated fatty acids in human milk and brain growth during early infancy. Acta Paediatr 2000; 89:142-147

(95.) Pan XL, Izumi T: Variation of the ganglioside compositions of human milk, cow's milk and infant formulas. Early Hum Dev 2000; 57:25-31

(96.) Uauy R, Hoffman DR: Essential fat requirements of preterm infants. Am J Clin Nutr 2000; 71 (suppl 1):245S-250S

(97.) Koletzko B, Rodriguez-Palmero M: Polyunsaturated fatty acids in human milk and their role in early infant development. J Mammary Gland Biol Neoplasia 1999; 4:269-284

(98.) US Department of Health and Human Services: Child Health USA '95. Washington, DC, US Government Printing Office, Publication No. HRSA-M-DSEA-96-5, 1996

(99.) Zimmerman DR: You can make a difference: increasing breastfeeding rates in an inner-city clinic. J Hum Lact 1999; 15:217-220

(100.) Grummer-Strawn LM, Rice SP, Dugas K, et al: An evaluation of breastfeeding promotion through peer counseling in Mississippi WIC clinics, Matern Child Health J 1997; 1:35-42

(101.) Ahluwalia IB, Tessaro I, Grummer-Strawn LM, et al: Georgia's breastfeeding promotion program for low-income women. Pediatrics 2000; 105:E85

(102.) Kum-Nji P, Mangrem CL, Wells PJ, et al: Breast-feeding initiation: predictors, attitudes, and practices among blacks and whites in rural Mississippi. South Med J 1999; 92:1183-1188

(103.) Izatt SD: Breastfeeding counseling by health care providers. J Hum Lact 1997; 13:109-113

(104.) Freed GL, Clark SJ, Curtis P, et al: Breast-feeding education and practice in family medicine. J Fam Pract 1995; 40:263-269

(105.) Freed GL, Clark SJ, Lohr JA, et al: Pediatrician involvement in breast-feeding promotion: a national study of residents and practitioners. Pediatrics 1995; 96:490-494

(106.) Goldstein AO, Freed GL: Breast-feeding counseling practices of family practice residents. Fam Med 1993; 25:524-529

(107.) Howard CR, Schaffer SJ, Lawrence RA: Attitudes, practices, and recommendations by obstetricians about infant feeding. Birth 1997; 24:240-246

(108.) Reif MI, Essock-Vitale SM: Hospital influences on early infant feeding practices. Pediatrics 1985; 76:872-879

(109.) Labbok MH, Simon SR: A community study of a decade of in-hospital breastfeeding: implications for breast-feeding promotion. Am J Prev Med 1988; 4:62-67

TABLE 1.
Hypotheses on the Causes of Sudden Infant Death Syndrome
(SIDS)
Thermal stress                       Excessively bundled infants can
                                     lead to sharp increases in body
                                     temperature, resulting in sudden
                                     brian injury and death.
Prone sleep position                 Increased [CO.sub.2] rebreathing,
                                     which occurs in the prone sleep
                                     position, is dangerous to the
                                     infant brian and can depress the
                                     cardiorespiratory center.
Prematurity                          Preterm infants sleep deeply during
                                     NREM sleep and may "forget" to
                                     breathe due to immaturity of the
                                     cardiorespiratory control centers.
Infectious disease                   Sudden overwhelming production of
                                     bacterial toxins can kill the
                                     infant instantly; eg,
                                     staphylococcal toxins have been
                                     found at autopsy and are not
                                     necessarily due to contaminants
                                     after death. History of URI often
                                     reported before SIDS.
Type of infant feeding               Breast-fed infants are healthier
neonates' CNS.                       than bottle-fed infants and resist
                                     viral and bacterial infections,
                                     which may play a role in SIDS,
                                     Human milk (high in PUFA) may also
                                     enhance the development of
                                     neonates' CNS.
Environmental tobacco exposure       Toxins (eg, nicotine) in tobacco
                                     may injure the developing brain,
                                     resulting in impaired cardiores-
                                     piratory drive, or may interact
                                     with bacterial toxins to cause
                                     SIDS.
Type of bedding                      Compared with conventional bedding,
                                     very soft bedding, very soft
                                     beeding disperses [CO.sub.2]
                                     poorly, leading to increased
                                     [CO.sub.2] rebreathing.
Cosleeping (bed-sharing)             This may result in increased
stimulation (as a result of increas  [CO.sub.2] (derived from adults)
                                     rebreathing. Can also lead to
                                     overlying or stradding. However,
                                     cosleeping also results in
                                     increased breast-feeding and
                                     increased tactile stimulation (as
                                     a result of increased bodily
                                     contact), both of which are
                                     protective against SIDS.
Long QT syndrome                     Causes arrhythmia, which can result
                                     in sudden death.
Maternal substance abuse             Substance abuse during gestation
                                     may impair developing
                                     cardiorespiratory centers.
NREM = Non-rapid eye movement;
URI = upper respiratory infection;
PUFA= polyunstaturated fatty acids;
CNS = central nervous system.

KEY POINTS

* There is as yet no known direct cause of SIDS, though various hypotheses abound as to possible mechanisms of causation. These hypotheses and other epidemiologic risk factors are briefly reviewed.

* in the Delta region of Mississippi, SIDS is second only to complications of prematurity and congenital heart diseases as a cause of infant mortality.

* Improvement of three epidemiologic risk factors is crucial in reducing the incidence of SIDS in this region: increasing the prevalence of the supine sleep position for infants, decreasing passive smoke exposure rates in homes, and increasing breast-feeding rates.

TABLE 2. Epidemiologic Risk Factors for Sudden Infant Death Syndrome

Modifiable risk factors

Infant sleep position (prone vs non-prone)

Environmental tobacco smoke (homes with smokers vs smoke-free homes)

Type of infant feeding (bottle-feeding vs breast-feeding)

Maternal substance abuse (history of drug/alcohol use vs none)

Ambient room temperature (too warm vs normal temperature)

Type of bedding (sheepskins or natural fiber mattresses vs conventional bedding)

Cosleeping (bed-sharing with adults vs cots)

Prenatal care (little or no prenatal care vs early care)

History of mild infection (vs none)

Nonmodifiable risk factors 

Parental age (teen mothers vs older mothers)

Parental education (at least high school education vs none)

Race (eg, blacks or American Indians vs whites)

Maturity status (premature vs full-term infant)

Infant birth weight ([less than]2,500 g vs [greater than or equal to]2500 g)

Socioeconomic status (low income vs higher income)

Seasonal variations (eg, winter vs summer)

[Graph omitted]