Ethnicity, infection and sudden infant death syndrome

• Published in: FEMS Immunology and Medical Microbiology Vol. 42; no. 1; pp. 53 - 65
• Main Authors: Blackwell, C.Caroline, Moscovis, Sophia M., Gordon, Ann E., Al Madani, Osama M., Hall, Sharron T., Gleeson, Maree, Scott, Rodney J., Roberts-Thomson, June, Weir, Donald M., Busuttil, Anthony
• Format: Book Review Journal Article
• Language: English
• Published: Oxford, UK Elsevier B.V 01.09.2004; Blackwell Publishing Ltd; Oxford University Press
• Subjects: Aboriginal australian; Bacteria; Bangladeshi; Cigarette smoke; Cigarettes; Colonization; Continental Population Groups; Density; Economic factors; Environmental risk; Epidemiology; Ethnic factors; Gene polymorphism; Health problems; Humans; Incidence; Indigenous peoples; Indigenous populations; Infant; Infants; Infection - complications; Infection - immunology; Infections; Inflammation; Inflammatory cytokine genes; Interleukin 10; Minority & ethnic groups; Native Americans; Native peoples; Nucleotides; Polymorphism; Population genetics; Population studies; Populations; Respiratory tract; Respiratory tract diseases; Risk analysis; Risk Factors; Risk groups; SIDS; Single-nucleotide polymorphism; Smoke; Smoking; Social factors; Socioeconomics; Sudden Infant Death - epidemiology; Sudden Infant Death - etiology; Sudden Infant Death - genetics; Sudden infant death syndrome; Toxins; United Kingdom > UK; Aboriginal australian; Bangladeshi; Interleukin-10; Sudden infant death syndrome; Indigenous populations; Inflammatory cytokine genes; Cigarette smoke; Risk factors
• ISSN: 0928-8244; 1574-695X; 2049-632X; 1365-2567
• DOI: 10.1016/j.femsim.2004.06.007

Epidemiological studies found the incidence of SIDS among Indigenous groups such as Aboriginal Australians, New Zealand Maoris and Native Americans were significantly higher than those for non-Indigenous groups within the same countries. Among other groups such as Asian families in Britain, the incidence of SIDS has been lower than among groups of European origin. Cultural and childrearing practices as well as socio-economic factors have been proposed to explain the greater risk of SIDS among Indigenous peoples; however, there are no definitive data to account for the differences observed. We addressed the differences among ethnic groups in relation to susceptibility to infection because there is evidence from studies of populations of European origin that infectious agents, particularly toxigenic bacteria might trigger the events leading to SIDS. The risk factors for SIDS parallel those for susceptibility to infections in infants, particularly respiratory tract infections which are also major health problems among Indigenous groups. Many of the risk factors identified in epidemiological studies of SIDS could affect three stages in the infectious process: (1) frequency or density of colonisation by the toxigenic species implicated in SIDS; (2) induction of temperature-sensitive toxins; (3) modulation of the inflammatory responses to infection or toxins. In this review we compare genetic, developmental and environmental risk factors for SIDS in ethnic groups with different incidences of SIDS: low (Asians in Britain); moderate (European/Caucasian); high (Aboriginal Australian). Our findings indicate: (1) the major difference was high levels of exposure to cigarette smoke among infants in the high risk groups; (2) cigarette smoke significantly reduced the anti-inflammatory cytokine interleukin-10 responses which control pro-inflammatory responses implicated in SIDS; (3) the most significant effect of cigarette smoke on reduction of IL-10 responses was observed for donors with a single nucleotide polymorphism for the IL-10 gene that is predominant among both Asian and Aboriginal populations. If genetic makeup were a major factor for susceptibility to SIDS, the incidence of these deaths should be similar for both populations. They are, however, significantly different and most likely reflect differences in maternal smoking which could affect frequency and density of colonisation of infants by potentially pathogenic bacteria and induction and control of inflammatory responses.