Chronic Obstructive Pulmonary Disease (COPD): Causes

Pathogenesis (disease development)

The following factors are important in the pathogenesis of chronic obstructive pulmonary disease (COPD):

  • Insufficiency of the ciliated epithelium of the airways; continued damage – e.g., tobacco smoke – results in complete destruction of the epithelium
  • Atrophy of the bronchial mucosa
  • Abnormally increased mucus production in the bronchi
  • Infiltrations mainly of lymphocytes and plasma cells.
  • Metaplasia of the squamous epithelium

All these factors together lead to chronic bronchitis, which, if the risk factors persist, may eventually lead to emphysema (irreversible overinflation of the smallest air-filled structures (alveoli, alveoli) of the lungs) due to loss of elasticity of emphysematous lung tissue and cor pulmonale (pressure-loaded right heart due to an increase in pressure in the pulmonary circulation). Note: It is now believed that the pathogenesis of COPD begins earlier than previously thought. Destruction of terminal bronchioles (smallest bronchi) precedes the development of emphysema.

Etiology (Causes)

Biographic causes

  • Genetic burden
    • Genetic risk depending on gene polymorphisms:
      • Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
        • Genes: AQP5, FAM13A
        • SNP: rs7671167 in the gene FAM13A
          • Allele constellation: CT (1.32-fold).
          • Allele constellation: TT (1.7-fold)
        • SNP: rs3736309 in gene AQP5
          • Allele constellation: AG (0.44-fold).
          • Allele constellation: GG (0.44-fold)
    • Genetic diseases
      • Alpha-1-antitrypsin deficiency (AATD; α1-antitrypsin deficiency; synonyms: Laurell-Eriksson syndrome, protease inhibitor deficiency, AAT deficit): genetic disorder with autosomal recessive inheritance in which too little alpha-1-antitrypsin is produced due to a polymorphism, resulting in the lack of inhibition of elastase, causing the elastin of the pulmonary alveoli to degrade (SNP s. u. Laboratory parameter “alpha-1-antitrypsin deficiency“).
  • Anatomical variants – dysanapsis (compared to total lung small airways); patients have poorer lung function (FEV1) from a young age than non-smokers who do not later develop COPD (could possibly explain in part why non-smokers can also develop COPD).
  • History of bronchial hyperresponsiveness and bronchial asthma.
  • Passive smoker as a child (parents smoke).
  • Frequent respiratory infections in childhood
  • Disorders of lung growth
  • Age

Behavioral causes

  • Nutrition
    • Micronutrient deficiency (vital substances) – see Prevention with micronutrients.
  • Consumption of stimulants
    • Tobacco (smoking, passive smoking) – The most important risk factor for developing COPD is smoking. Chinese hookah smoking is also associated with a significant increase in COPD risk, although tobacco smoke is filtered by water.However, according to the CanCOLD study (5176 individuals aged 40 years and older; population-based, prospective Canadian Cohort of Obstructive Lung Disease Study (CanCOLD study)), 29% of COPD patients are nonsmokers.
  • Overweight (BMI ≥ 25; obesity).
  • Android body fat distribution, that is, abdominal/visceral, truncal, central body fat (apple type) – high waist circumference or waist-to-hip ratio (THQ; waist-to-hip ratio (WHR)) is presentWhen measuring waist circumference according to the International Diabetes Federation (IDF, 2005) guideline, the following standard values apply:
    • Men < 94 cm
    • Women < 80 cm

    The German Obesity Society published somewhat more moderate figures for waist circumference in 2006: < 102 cm for men and < 88 cm for women.

Disease-related causes

  • Bronchial asthma / “asthma-COPD overlap syndrome”
  • Chronic bronchitis (inflammation of the bronchial mucosa).
  • Cicatricial emphysema (expansion of lung tissue in the vicinity of shrinking lung districts; e.g., due to inhalation of quartz-containing dusts).
  • Subclinical inflammation (engl.”silent inflammation”) – permanent systemic inflammation (inflammation affecting the whole organism), which proceeds without clinical symptoms.
  • Hyperexpansion emphysema after partial lung resection (occurs because part of the lung has been removed and the remaining lung fills the remaining space).

Environmental pollution – intoxications (poisonings).

  • General air pollution (including NO2, oxon).
  • Occupational dusts – quartz-containing dusts, cotton dusts, grain dusts, welding fumes, mineral fibers, irritant gases such as ozone, nitrogen dioxide or chlorine gas.
  • Exposure to biogenic heating materials (coal, wood, etc. for at least ten years).
  • Wood fire
  • Indoor pollution (cooking and heating by burning natural materials).
  • Air pollutants: particulate matter, ozone, sulfur dioxide.
  • Ship emissions (heavy fuel oil; diesel)

Other causes

  • Old-age emphysema
  • Childhood hospitalizations for respiratory disease; risk factor for nonsmokers with COPD.