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Eur Respir J 2001; 17:881-886
Copyright ©ERS Journals Ltd 2001


Is the increase in childhood asthma coming to an end? Findings from three surveys of schoolchildren in Rome, Italy

R. Ronchetti, M.P. Villa, M. Barreto, R. Rota, J. Pagani, S. Martella, C. Falasca, B. Paggi, F. Guglielmi and G. Ciofetta

Paediatric Clinic of the 2nd Faculty of Medicine, University of Rome "La Sapienza", Rome, Italy

CORRESPONDENCE: R. Ronchetti, Paediatric Clinic of the 2nd Faculty of Medicine, Viale Regina Elena, 324, 00161, Rome, Italy. Fax: 39 064462767

Keywords: asthma increase, asthma prevalence, childhood asthma, family history of atopy

Received: April 27, 2000
Accepted December 6, 2000

Time trends in the prevalence of asthma, family history of asthma and atopy in Roman schoolchildren were assessed. The study population consisted of all children (aged 6–14 yrs) attending two primary schools in Rome, situated in urban areas that differed markedly in socioeconomic conditions and environmental pollution. Three questionnaire-based surveys were conducted in 1974, 1992 and 1998 in 2,259, 1,229 and 1,139 children. The prevalence of asthma in males and females increased significantly during 1974–1992 and remained stable from 1992–1998. In age groups born in the subsequent 4-yr periods it increased almost linearly, for children born from 1962–1965 to 1982–1985 (4.4%–12.5%), and remained remarkably stable in children born after 1985. Because the prevalence of asthma had a steeper trend in males than in females (approximately 0.55%·yr–1 versus 0.25%·yr–1), the male:female asthma ratio increased (1:38 in 1974; 1:84 in 1992 and 1:62 in 1998). No single environmental factor, including area of residence, seemed to influence the prevalence of asthma. Family history of asthma and atopy also increased steadily (0.72%·yr–1 and 0.30%·yr–1 respectively) more than doubling during the 24-yr study period. The strong relationship between asthma and a family history of atopy not only persisted but also strengthened over time (23.3% of asthmatic children belonged to families with atopic illnesses in 1974 but 44.2% in 1998). The environmental factors that might explain the almost three-fold rise in childhood asthma between 1974 and 1992 remain unknown but the genetic background of the disease has presumably remained unchanged since the early 1970s. The fact that the prevalence of asthma increased no further during the past 6 yrs suggests that the progressive induction of asthma symptoms in genetically predisposed subjects is a self-limiting process that has probably come to an end in the authors' study area.




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