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Does environment mediate earlier onset of the persistent childhood asthma phenotype?
Ramesh J Kurukulaaratchy1, Sharon Matthews, S Hasan Arshad
1The David Hide Asthma and Allergy Research Centre, St Mary's Hospital, Newport, Isle of Wight, United Kingdom.
Insights
Genetic factors are key in persistent childhood wheeze. Early environmental exposures, like infections and parental smoking, combined with heredity, can lead to early-onset wheezing in children.
Area of Science:
- Pediatric Allergy and Immunology
- Environmental Health
- Genetics
Background:
- Persistent childhood wheeze is a common respiratory condition with complex etiology.
- Understanding the interplay of genetic and environmental factors is crucial for effective prevention and management.
Purpose of the Study:
- To investigate the distinct roles of environmental and hereditary factors in the development of early-onset versus late-onset persistent childhood wheezing phenotypes.
Main Methods:
- A prospective birth cohort study of 1456 children, with assessments at birth and ages 1, 2, 4, and 10 years.
- Wheeze prevalence was prospectively collected to classify phenotypes.
- Genetic and environmental risk factors, including skin-prick testing for allergens, were assessed.
Main Results:
- Late-onset persistent wheeze (onset after 4 years) was significantly associated with inherited factors (parental asthma, rhinitis, eczema, atopic status).
- Early-onset persistent wheeze (onset within 4 years) showed independent significance for both environmental factors (low social class, recurrent infections, parental smoking) and inherited factors (eczema, food allergy, parental/sibling asthma, urticaria, atopic status).
Conclusions:
- Inherited predisposition appears to be the primary driver of persistent childhood wheeze.
- Early-life environmental exposures can interact with genetic tendencies to precipitate early-onset wheezing.
- While environmental factors may delay onset in atopic children, they do not prevent wheezing if the hereditary predisposition is present.
Objective:
We investigated the role of environmental and hereditary factors in determining whether persistent childhood wheezing phenotypes had an early or late onset.
Methods:
In a whole population birth cohort (n = 1456), children were seen at birth and at 1, 2, 4, and 10 years. At each visit, information was collected prospectively regarding wheeze prevalence and used to classify subjects into wheezing phenotypes. Information on genetic and environmental risk factors in early life was also obtained prospectively, and skin-prick testing to common allergens was performed at 4 years.
Results:
Early-onset persistent wheezers (n = 125) had wheeze onset in the first 4 years, still present at age 10, whereas late-onset persistent wheezers (n = 81) had wheeze onset after age 4 years that was still present at 10 years. Multivariate logistic regression analysis identified independent significance only for inherited factors (parental asthma, family history of rhinitis, eczema at 4 years, and atopic status at 4 years) in the development of late-onset persistent wheeze. However, low social class at birth, recurrent chest infections at 2 years, and parental smoking at 2 years plus inherited factors (eczema at 2 years; food allergy at 4 years; maternal asthma, sibling asthma, maternal urticaria, and atopic status at 4 years) demonstrated independent significance for early-onset persistent wheeze.
Conclusion:
Inheritance seems to be of prime significance in the cause of persistent childhood wheeze. Environmental exposure in early life may combine with this tendency to produce an early onset of persistent wheeze. Absence of these environmental factors might delay but not prevent the onset of wheeze in children with atopic heredity.
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