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Published on: August 7, 2017
Fetal Origins of Asthma: A Longitudinal Study from Birth to Age 36 Years
Stefano Guerra1,2,3, Enrico Lombardi1,4, Debra A Stern1
1Asthma and Airway Disease Research Center.
Insights
Infant lung function deficits, including expiratory flow timing (tptef/te) and maximal expiratory flow (V̇maxFRC), predict childhood asthma risk. These early markers are linked to adult asthma and airway structural changes, highlighting fetal origins of the disease.
Area of Science:
- Respiratory Medicine
- Pediatric Pulmonology
- Developmental Origins of Health and Disease
Background:
- Infant lung function deficits, specifically the ratio of the time to reach peak tidal expiratory flow to the total expiratory time (tptef/te) and maximal expiratory flow at FRC (V̇maxFRC), are associated with increased childhood asthma risk.
- Understanding these early markers is crucial for predicting long-term respiratory health outcomes.
Purpose of the Study:
- To investigate the individual and combined effects of infant tptef/te and V̇maxFRC on the risk of developing asthma into mid-adulthood.
- To examine the association between these infant lung function measures and airway structural abnormalities in later life.
Main Methods:
- Utilized data from the Tucson Children's Respiratory Study birth cohort, including 180 participants.
- Measured infant lung function using the chest-compression technique (mean age 2.0 months).
- Assessed active asthma via questionnaires up to age 36 and evaluated airway structure using HRCT imaging at age 26.
Main Results:
- A 1-SD decrease in infant tptef/te and V̇maxFRC independently increased asthma risk by 70% (P=0.001) and 55% (P=0.005), respectively.
- Infants with the lowest tertile for both measures had a two-thirds likelihood of developing active asthma by mid-adulthood.
- Infant V̇maxFRC predicted reduced airflow, and infant tptef/te predicted reduced airway caliber on HRCT at age 26.
Conclusions:
- Early-life deficits in tptef/te and V̇maxFRC have lasting impacts on respiratory health, supporting the concept of fetal origins of asthma.
- These infant lung function parameters contribute independently to asthma development and are linked to structural airway changes in adulthood.
Abstract:
Rationale: Deficits in infant lung function-including the ratio of the time to reach peak tidal expiratory flow to the total expiratory time (tptef/te) and maximal expiratory flow at FRC (V̇maxFRC)-have been linked to increased risk for childhood asthma.Objectives: To examine the individual and combined effects of tptef/te and V̇maxFRC in infancy on risk for asthma and abnormalities of airway structure into mid-adult life.Methods: One hundred eighty participants in the Tucson Children's Respiratory Study birth cohort had lung function measured by the chest-compression technique in infancy (mean age ± SD: 2.0 ± 1.2 mo). Active asthma was assessed in up to 12 questionnaires between ages 6 and 36 years. Spirometry and chest high-resolution computed tomographic (HRCT) imaging were completed in a subset of participants at age 26. The relations of infant tptef/te and V̇maxFRC to active asthma and airway structural abnormalities into adult life were tested in multivariable mixed models.Measurements and Main Results: After adjustment for covariates, a 1-SD decrease in infant tptef/te and V̇maxFRC was associated with a 70% (P = 0.001) and 55% (P = 0.005) increased risk of active asthma, respectively. These effects were partly independent, and two out of three infants who were in the lowest tertile for both tptef/te and V̇maxFRC developed active asthma by mid-adult life. Infant V̇maxFRC predicted reduced airflow and infant tptef/te reduced HRCT airway caliber at age 26.Conclusions: These findings underscore the long-lasting effects of the fetal origins of asthma, support independent contributions by infant tptef/te and V̇maxFRC to development of asthma, and link deficits at birth in tptef/te with HRCT-assessed structural airway abnormalities in adult life.
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Asthma-III: Symptoms and Complications
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Longitudinal Research
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