COPD.14 This remains an operational approach to early disease intervention rather than a statement related to disease pathophysiology.
Whether cough in COPD is a normal physiologic response to increased mucus production or is itself pathologic remains controversial. Studies in asthma have demonstrated a consistently low cough threshold to inhaled capsaicin15 possibly due to the release of inflammatory mediators.16 Data in COPD are less consistent and appear to depend upon the technique and dosimeter used. Nonetheless, we have found similar reductions in the cough threshold in both chronic asthma and COPD (Figure 20.1),17 a finding more marked in those receiving anticholinergic treatment. Subjective reports of coughing were only weakly related to these abnormalities, which also explains the poor relationship between reported cough and pathologic evidence of increased glandular hypertrophy.13