Childhood environment and adult atopy: Results from the European Community Respiratory Health Survey,☆☆,

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Abstract

Background: Previous literature has indicated that environmental exposures in childhood influence development of atopic sensitization. Objective: We sought to study the association between childhood environment and adult atopy. Methods: Thirteen thousand nine hundred thirty-two subjects aged 20 to 44 years from 36 areas in Europe, New Zealand, the United States, and Australia took part in the European Community Respiratory Health Survey, answering interviewer-led questionnaires and providing blood tests for measurement of specific IgE to grass, house dust mite, cat, and Cladosporium allergens. Results: Atopy was negatively associated with family size (OR = 0.93; 95% CI = 0.90-0.96 per 1 sib), partly attributable to an independent protective effect of a greater number of brothers (OR = 0.92; 95% CI = 0.89-0.95 per 1 brother). Accounting for total number of siblings, no further influence was detected for number of older or younger siblings. Bedroom sharing was associated with a lower prevalence of atopy, particularly to cat allergen. A protective effect of family size and bedroom sharing could only be detected in subjects reporting no parental allergy (family size, test for interaction P = .012). The presence of a dog in the home in childhood was negatively associated with adult atopy (OR = 0.85, 95% CI = 0.78-0.92), an effect that remained after adjustment for parental allergy, sibling allergy, and adult pet ownership. Conclusion: Subjects from large families with brothers, shared bedrooms, and dogs in childhood were less often atopic as adults. Our findings are consistent with the hypothesis that infectious agents could inhibit development of atopy during childhood. However, in subjects with a strong genetic predisposition, environmental factors in childhood are possibly of less importance. (J Allergy Clin Immunol 1999;103:415-20.)

Section snippets

Data collection

The methodology for the ECRHS has been fully described elsewhere.16, 17 Briefly, participating centers selected an area defined by preexisting administrative boundaries with a population of at least 150,000. When possible, an up-to-date sampling frame was used to select randomly at least 1500 men and 1500 women aged 20 to 44 years. In stage I, subjects were sent the ECRHS screening questionnaire, a self-completed 9-item questionnaire asking about symptoms suggestive of asthma, the use of

Family size, brothers and sisters, older and younger siblings

Specific IgE to one or more allergens decreased with increasing number of siblings (Table I).

. Unadjusted prevalence and adjusted odds ratios for atopy (specific IgE to 1 or more allergen) and serum-specific IgE to 4 common allergens according to family size

No of siblingsPrevalence of sensitization (%)OR (95% CI)*P value
01234+
Atopy (4522/13,932†)34.034.532.932.028.60.93 (0.90-0.96)<.001
IgE grass (2660/13,929†)19.821.420.017.915.20.93 (0.89-0.96)<.001
IgE house dust mite (2754/13,931†)19.119.920.1

DISCUSSION

Subjects from large families with brothers, shared bedrooms, and dogs in childhood had a lower risk of atopic sensitization in adulthood. This was found in a large study of men and women from 36 centers from different parts of the Western world, strongly supporting the concept that environmental factors in childhood influence development of the immune system in an allergic or nonallergic direction. Some environmental influences, however, seem to be of less importance in subjects with a family

Acknowledgements

We thank Seif Shaheen for valuable discussions and Jonathan Sterne for preparing the program used for metaanalyses in Stata. The coordination of this work was supported by the European Commission and we are grateful to the late Colette Baya and Dr Manuel Hallen for their help during the study and to Professor K. Vuylsteek and the members of the COMAC for their support.

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    Supported by the European Commission. The following grants helped to fund the local studies: Australia, Allen and Hanbury’s, Australia; Belgium, Belgian Science Policy Office, National Fund for Scientific Research; France, Ministère de la Santé, Glaxo France, Institut Pneumologique d’Aquitaine, Contrat de Plan Etat-Région Languedoc-Rousillon, CNMATS, CNMRT (90MR/10, 91AF/6), Ministre delegué de la santé, RNSP; Germany: GSF, and the Bundesminister für Forschung und Technologie, Bonn; Greece, The Greek Secretary General of Research and Technology, Fisons, Astra and Boehringer-Ingelheim; India, Bombay Hospital Trust; Italy, Ministero dell’Università e della Ricerca Scientifica e Tecnologica, CNR, Regione Veneto grant RSF n. 381/05.93; New Zealand, Asthma Foundation of New Zealand, Lotteries Grant Board, Health Research Council of New Zealand; Norway, Norwegian Research Council project no. 101422/310; Portugal, Glaxo Farmacêutica Lda, Sandoz Portugesa; Spain, Ministero Sanidad y Consumo FIS grants #91/0016060/00E-05E and #93/0393, and grants from Hospital General de Albacete, Hospital General Juan Ramón Jiménenz, Consejeria de Sanidad Principado de Asturias; Sweden, The Swedish Medical Research Council, the Swedish Heart Lung Foundation, the Swedish Association against Asthma and Allergy; Switzerland, Swiss National Science Foundation grant 4026-28099; United Kingdom, National Asthma Campaign, British Lung Foundation, Department of Health, South Thames Regional Health Authority; USA, United States Department of Health, Education and Welfare Public Health Service Grant #2 S07 RR05521-28.

    ☆☆

    Reprint requests: Cecilie Svanes, PhD, Department of Thoracic Medicine, N-5021 Haukeland Hospital, Norway.

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