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Risk factors for obstructive lung disease

R Madison, C Mittman, A A Afifi

    The American Review of Respiratory Disease
    |August 1, 1981
    PubMed
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    Male subjects with the PiMZ phenotype and a family history of lung disease experienced accelerated loss of lung function, indicating significant chronic obstructive lung disease (COLD) risk. This combination of factors impacts disease progression and research outcomes.

    Area of Science:

    • Pulmonology
    • Genetics
    • Epidemiology

    Background:

    • Chronic obstructive lung disease (COLD) pathogenesis is multifactorial.
    • Antitrypsin deficiency phenotypes (PiZ, MZ) are known risk factors.
    • Previous studies on COLD risk factors have yielded conflicting results.

    Purpose of the Study:

    • To evaluate the combined impact of specific risk factors on COLD development.
    • To investigate the role of PiMZ phenotype and family history in lung function decline.
    • To understand how population characteristics influence COLD research outcomes.

    Main Methods:

    • Longitudinal study of 163 subjects over approximately 6 years.
    • Inclusion of community volunteers and relatives of patients with antitrypsin deficiency.

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  • Covariance analysis to assess expiratory airflow rates and risk factor interactions.

    • Main Results:

    • Male subjects with both PiMZ phenotype and family history of lung disease showed excessive decline in expiratory airflow.
    • Lung function loss in this subgroup approximated that of individuals with established COLD.
    • Subjects with only one or two risk factors exhibited less pronounced changes in lung function.

    Conclusions:

    • The combination of PiMZ phenotype and family history significantly accelerates lung function decline, mimicking established COLD.
    • Investigator-assessed population characteristics can influence study outcomes, potentially explaining conflicting previous research.
    • Identifying individuals with multiple risk factors is crucial for understanding COLD pathogenesis and progression.