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Related Experiment Videos

Lifetime Risk Factors for Pre- and Post-Bronchodilator Lung Function Decline. A Population-based Study.

Dinh S Bui1,2, Jennifer L Perret1,3, E Haydn Walters1

  • 1Allergy and Lung Health Unit, The University of Melbourne, Melbourne, Victoria, Australia.

Annals of the American Thoracic Society
|December 5, 2019
PubMed

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Environmental epidemiology (Philadelphia, Pa.)·2026
Summary

Childhood factors like low lung function and maternal smoking amplify adult risks, accelerating lung function decline. Genetic factors, such as GSTM1 genotype, also modify susceptibility to occupational exposures and smoking.

Area of Science:

  • Pulmonology
  • Epidemiology
  • Genetics

Background:

  • Lung function decline is influenced by adult risk factors, but interactions with early life exposures are not fully understood.
  • Most prior research focused on prebronchodilator (pre-BD) forced expiratory volume in 1 second (FEV1) decline, neglecting postbronchodilator (post-BD) measures and other spirometric parameters.

Purpose of the Study:

  • To investigate the associations between adult risk factors and lung function decline, considering both pre-BD and post-BD spirometry.
  • To examine the potential effect modification of these associations by early life respiratory factors and genetic polymorphisms.

Main Methods:

  • Utilized multiple regression analysis on data from the Tasmanian Longitudinal Health Study (n=857) examining individuals aged 45-53 years.
  • Assessed associations between adult exposures (asthma, smoking, occupational exposures, traffic pollution, obesity) and decline in pre- and post-BD FEV1, forced vital capacity (FVC), and FEV1/FVC.
Keywords:
bronchodilatordeclineinteractionlung functionsusceptibility

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  • Investigated effect modification by childhood risk factors, including low childhood lung function and glutathione S-transferase (GST) gene polymorphisms.
  • Main Results:

    • Adult asthma, smoking, occupational exposure to vapors/gases/dusts/fumes, and proximity to traffic accelerated both pre- and post-BD FEV1 decline.
    • Maternal smoking intensified the impact of personal smoking on FEV1 decline. Low childhood lung function and the GSTM1 null genotype exacerbated the effects of occupational exposures and smoking on post-BD FEV1 decline.
    • Incident obesity was linked to accelerated FEV1 decline and more pronounced FVC decline.

    Conclusions:

    • Early life factors, including low childhood lung function, maternal smoking, and specific genetic profiles (GSTM1 null allele), significantly accentuate individual susceptibility to adult-onset lung function decline.
    • This highlights the critical role of early life exposures and genetic predisposition in modulating the long-term respiratory health consequences of adult risk factors.