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Breast-feeding, aeroallergen sensitization, and environmental exposures during infancy are determinants of childhood allergic rhinitis.
J Allergy Clin Immunol 2010; 125(5):1054-1060.e1JA

Abstract

BACKGROUND

Infant predictors of early childhood allergic rhinitis (AR) are poorly understood.

OBJECTIVE

We sought to identify environmental exposures and host factors during infancy that predict AR at age 3 years.

METHODS

High-risk children from greater Cincinnati were followed annually from ages 1 to 3 years. AR was defined as sneezing, runny, or blocked nose in the prior 12 months and a positive skin prick test (SPT) response to 1 or more aeroallergens. Environmental and standardized medical questionnaires determined exposures and clinical outcomes. Primary activity area dust samples were analyzed for house dust endotoxin (HDE) and (1-3)-beta-D-glucan. Fine particulate matter sampled at 27 monitoring stations was used to estimate personal elemental carbon attributable to traffic exposure by using a land-use regression model.

RESULTS

Of 361 children in this analysis, 116 had AR, and 245 were nonatopic and nonsymptomatic. Prolonged breast-feeding in African American children (adjusted odds ratio [aOR], 0.8; 95% CI, 0.6-0.9) and multiple children in the home during infancy was protective against AR (aOR, 0.4; 95% CI, 0.2-0.8). Food SPT response positivity and tree SPT response positivity in infancy increased the risk of AR at age 3 years (aOR of 4.4 [95% CI, 2.1-9.2] and aOR of 6.8 [95% CI, 2.5-18.7], respectively). HDE exposure was associated with AR; the effect was dependent on exposure level. Elemental carbon attributable to traffic and environmental tobacco smoke exposure showed no effect on AR.

CONCLUSION

Prolonged breast-feeding in African American subjects and multiple children in the home during infancy reduced the risk of AR at age 3 years. SPT response positivity to food and tree allergens enhanced risk. The HDE effect on AR was related to exposure.

Authors+Show Affiliations

Department of Internal Medicine, Division of Immunology, Allergy and Rheumatology, University of Cincinnati, Cincinnati, Ohio 4267-0563, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

20392478

Citation

Codispoti, Christopher D., et al. "Breast-feeding, Aeroallergen Sensitization, and Environmental Exposures During Infancy Are Determinants of Childhood Allergic Rhinitis." The Journal of Allergy and Clinical Immunology, vol. 125, no. 5, 2010, pp. 1054-1060.e1.
Codispoti CD, Levin L, LeMasters GK, et al. Breast-feeding, aeroallergen sensitization, and environmental exposures during infancy are determinants of childhood allergic rhinitis. J Allergy Clin Immunol. 2010;125(5):1054-1060.e1.
Codispoti, C. D., Levin, L., LeMasters, G. K., Ryan, P., Reponen, T., Villareal, M., ... Bernstein, D. I. (2010). Breast-feeding, aeroallergen sensitization, and environmental exposures during infancy are determinants of childhood allergic rhinitis. The Journal of Allergy and Clinical Immunology, 125(5), pp. 1054-1060.e1. doi:10.1016/j.jaci.2010.02.004.
Codispoti CD, et al. Breast-feeding, Aeroallergen Sensitization, and Environmental Exposures During Infancy Are Determinants of Childhood Allergic Rhinitis. J Allergy Clin Immunol. 2010;125(5):1054-1060.e1. PubMed PMID: 20392478.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Breast-feeding, aeroallergen sensitization, and environmental exposures during infancy are determinants of childhood allergic rhinitis. AU - Codispoti,Christopher D, AU - Levin,Linda, AU - LeMasters,Grace K, AU - Ryan,Patrick, AU - Reponen,Tiina, AU - Villareal,Manuel, AU - Burkle,Jeff, AU - Stanforth,Sherry, AU - Lockey,James E, AU - Khurana Hershey,Gurjit K, AU - Bernstein,David I, Y1 - 2010/04/14/ PY - 2009/08/30/received PY - 2010/01/27/revised PY - 2010/02/02/accepted PY - 2010/4/16/entrez PY - 2010/4/16/pubmed PY - 2010/6/22/medline SP - 1054 EP - 1060.e1 JF - The Journal of allergy and clinical immunology JO - J. Allergy Clin. Immunol. VL - 125 IS - 5 N2 - BACKGROUND: Infant predictors of early childhood allergic rhinitis (AR) are poorly understood. OBJECTIVE: We sought to identify environmental exposures and host factors during infancy that predict AR at age 3 years. METHODS: High-risk children from greater Cincinnati were followed annually from ages 1 to 3 years. AR was defined as sneezing, runny, or blocked nose in the prior 12 months and a positive skin prick test (SPT) response to 1 or more aeroallergens. Environmental and standardized medical questionnaires determined exposures and clinical outcomes. Primary activity area dust samples were analyzed for house dust endotoxin (HDE) and (1-3)-beta-D-glucan. Fine particulate matter sampled at 27 monitoring stations was used to estimate personal elemental carbon attributable to traffic exposure by using a land-use regression model. RESULTS: Of 361 children in this analysis, 116 had AR, and 245 were nonatopic and nonsymptomatic. Prolonged breast-feeding in African American children (adjusted odds ratio [aOR], 0.8; 95% CI, 0.6-0.9) and multiple children in the home during infancy was protective against AR (aOR, 0.4; 95% CI, 0.2-0.8). Food SPT response positivity and tree SPT response positivity in infancy increased the risk of AR at age 3 years (aOR of 4.4 [95% CI, 2.1-9.2] and aOR of 6.8 [95% CI, 2.5-18.7], respectively). HDE exposure was associated with AR; the effect was dependent on exposure level. Elemental carbon attributable to traffic and environmental tobacco smoke exposure showed no effect on AR. CONCLUSION: Prolonged breast-feeding in African American subjects and multiple children in the home during infancy reduced the risk of AR at age 3 years. SPT response positivity to food and tree allergens enhanced risk. The HDE effect on AR was related to exposure. SN - 1097-6825 UR - https://www.unboundmedicine.com/medline/citation/20392478/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-6749(10)00283-6 DB - PRIME DP - Unbound Medicine ER -