School of Public Health

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Note: Prior to July 1, 2007, the School of Public Health was named the College of Health & Human Performance.

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Author: search.filters.author.Milton, Donald KSubject: search.filters.subject.Allergic Disease

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    Temporal changes in the prevalence of childhood asthma and allergies in urban and rural areas of Cyprus: results from two cross sectional studies
    (Springer Nature, 2011-11-11) Kolokotroni, Ourania; Middleton, Nicos; Nicolaou, Nicolas; Pipis, Spyros; Priftis, Kostas N; Milton, Donald K; Yiallouros, Panayiotis K
    The prevalence of childhood asthma and allergies in Cyprus was significantly higher in urban compared to rural areas back in the year 2000, against a background of an overall low prevalence (e.g. current wheeze 6.9%) by comparison to northern European countries. In this study we aimed to assess temporal changes in the prevalence of asthma and allergies in Cyprus after an 8-year interval and to examine whether any differential changes have occurred in urban and rural parts of the island. During the academic years 1999-2000 and 2007-2008, the parents of 7-8 year old children residing in the same set of urban and rural areas completed the ISAAC core questionnaire. In addition to providing prevalence estimates of allergic diseases in 2000 and 2008, changes between the two periods were expressed as odds ratios estimated in multiple logistic regression models adjusting for survey participants' characteristics. The prevalence of current wheeze was higher in 2008 (8.7%, 95% confidence interval 7.5%-9.9%, n = 2216) than the previously recorded figure in 2000 (6.9%, 95% CI 6.2%-7.6%, OR = 1.25, 95% CI: 1.02-1.53, n = 4944). Significant increases were also seen in the prevalence of lifetime asthma (11.3% vs. 17.4%, OR = 1.59, CI: 1.36-1.86), eczema (6.8% vs. 13.5%, OR = 1.91, CI: 1.59-2.29) and allergic rhinoconjuctivitis (2.6% vs. 5.2%, OR = 1.82, CI: 1.39-2.41). The prevalence of current wheeze nearly doubled between 2000 and 2008 in rural areas (5.4% vs. 9.7%, OR 1.81, CI: 1.24-2.64) while no significant change was observed in urban areas (7.5% vs. 8.4%, OR 1.08, CI: 0.84-1.37); p value for effect modification = 0.04. Rises in asthma and rhinitis prevalence, but not eczema were also more pronounced in rural compared to urban areas. The prevalence of allergic diseases in Cyprus is still on the rise; recent increases appear more pronounced among children living in rural areas possibly indicating recent environmental and lifestyle changes in these communities.
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    Effects of endotoxin exposure on childhood asthma risk are modified by a genetic polymorphism in ACAA1
    (Springer Nature, 2011-12-08) Sordillo, Joanne E; Sharma, Sunita; Poon, Audrey; Lasky-Su, Jessica; Belanger, Kathleen; Milton, Donald K; Bracken, Michael B; Triche, Elizabeth W; Leaderer, Brian P; Gold, Diane R; Litonjua, Augusto A
    Polymorphisms in the endotoxin-mediated TLR4 pathway genes have been associated with asthma and atopy. We aimed to examine how genetic polymorphisms in innate immunity pathways interact with endotoxin to influence asthma risk in children. In a previous analysis of 372 children from the Boston Home Allergens and the Connecticut Childhood Asthma studies, 7 SNPs in 6 genes (CARD15, TGFB1, LY96, ACAA1, DEFB1 and IFNG) involved in innate immune pathways were associated with asthma, and 5 SNPs in 3 genes (CD80, STAT4, IRAK2) were associated with eczema. We tested these SNPs for interaction with early life endotoxin exposure (n = 291), in models for asthma and eczema by age 6. We found a significant interaction between endotoxin and a SNP (rs156265) in ACAA1 (p = 0.0013 for interaction). Increased endotoxin exposure (by quartile) showed protective effects for asthma in individuals with at least one copy of the minor allele (OR = 0.39 per quartile increase in endotoxin, 95% CI 0.15 to 1.01). Endotoxin exposure did not reduce the risk of asthma in children homozygous for the major allele. Our findings suggest that protective effects of endotoxin exposure on asthma may vary depending upon the presence or absence of a polymorphism in ACAA1.