Related Experiment Videos
Epidemiology of asthma and recurrent wheeze in childhood
1Arizona Respiratory Center, Department of Pediatrics, University of Arizona, Tucson, AZ 85724, USA.
Insights
Childhood wheeze changes with age, evolving from early infectious/mechanical causes to later allergic asthma. Early wheeze is often benign, but persistent wheezing indicates a higher risk for asthma development.
Area of Science:
- Pediatric Pulmonology
- Allergy and Immunology
- Epidemiology
Background:
- Wheezing is a common childhood symptom with characteristics and risk factors that evolve with age.
- Early childhood wheezing is often transient and linked to mechanical or infectious factors, typically resolving without long-term consequences.
- Later childhood wheezing becomes increasingly associated with allergic mechanisms and asthma.
Purpose of the Study:
- To delineate the age-dependent characteristics, risk factors, and natural history of wheezing in children.
- To differentiate between transient early wheezing and persistent wheezing phenotypes and their associations with asthma.
- To explore the roles of genetic and environmental factors in the development of childhood wheeze and asthma.
Main Methods:
- Longitudinal studies tracking wheezing patterns from infancy through childhood.
- Assessment of risk factors including respiratory infections, passive smoke exposure, breastfeeding, and social contact.
- Evaluation of atopic markers such as total IgE levels and skin-test responses, alongside lung function and methacholine responsiveness.
Main Results:
- Transient early wheezing, common in infancy, is primarily associated with mechanical/infectious factors and is generally benign.
- Persistent wheezing by age 6 is linked to higher IgE, atopy, and a Th2-biased immune response, predicting later asthma.
- By late childhood, allergic wheezing predominates, correlating with asthma markers like methacholine responsiveness and atopy; early wheeze may be a marker, not a cause, of atopy.
Conclusions:
- Childhood wheeze is a complex phenomenon with distinct phenotypes that change with age, influenced by both genetic and environmental factors.
- Early wheezing does not necessarily predispose to atopy, but persistent wheezing is a strong predictor of asthma.
- Understanding these age-dependent patterns is crucial for elucidating causal mechanisms and developing primary prevention strategies for asthma.
Abstract:
To summarize, wheeze is common throughout childhood, although it decreases as children age. However, the characteristics of wheeze, its relations with asthma, and its risk factors all change with age. Longitudinal studies have shown that "transient early wheezing" predominates during the first years of life. The principal risks for this type of wheezing are largely mechanical, relating to small airways, and infectious, relating to the risk of becoming infected with respiratory viruses. Associated with passive exposure to cigarette smoke, exposure to other children, and not being breastfed, this form of wheezing was unrelated to increased airway liability or atopy in the child. For the majority of children, particularly those with low lung function at birth, wheezing with early LRIs is a benign condition, not associated with subsequent wheeze or risk for asthma. During the middle part of the first decade of life, wheezing appears to reflect a mix of infectious and allergic wheezing. By 6 yr of age, some children have already wheezed persistently. This group is more likely to have high total IgE levels, to be skin-test positive, and to be given a diagnosis of asthma. Further, their immunologic response to their early LRIs was consistent with a Th2 bias: persistent wheezers produced high levels of IgE, and did not demonstrate the normal pattern of decreased eosinophils. Nevertheless, the children who wheeze in middle childhood are a mixed group, with some being less allergic. Thus, although markers of allergy become increasingly important predictors of wheezing for the group as a whole, wheezing in middle childhood is not associated with later methacholine hyperresponsiveness (42). Finally, persistent allergic wheezing, usually associated with a diagnosis of asthma, predominates by the end of the first decade of life. Wheezing at this age is associated with methacholine responsiveness, peak-flow variability, and markers of atopy, such as total IgE and allergy skin-test response. Although children who wheezed early in life are more likely to wheeze later, early wheeze does not increase the risk of atopy, suggesting that early LRIs are markers of increased risk rather than causes. The gender differences in wheeze disappear, with boys becoming less likely to wheeze and to have asthma, whereas both conditions appear to increase in girls. Finally, some of the risk factors for early LRIs, such as exposure to other children in infancy, appear to be associated with protection from later allergic wheezing. Clearly, asthma and wheeze during childhood are complex entities, presenting with different characteristics at different ages, and implicating varied and changing causes. Genetic factors are important determinants of the intermediate phenotypes. However, environmental factors operating at different developmental stages also appear to influence the development of asthma. Additional research regarding these relationships is essential, both to elucidate possible causal mechanisms and to provide insight into the primary prevention of asthma.