Chronic airway inflammation and oxidative stress are
important features of chronic obstructive pulmonary
disease (COPD), a condition that is characterised by a
progressive and irreversible airflow limitation [1–3].
More than90%ofCOPD-affectedpatients are smokers;
cigarette smoking and inhalation of airborne pollutants
including oxidant gases such as ozone, nitrogen dioxide
or particulate air pollution lead to lung damage and
activation of pulmonary inflammatory processes [3].
Cadmium (Cd) is an important component of tobacco
smoke [4] and has been shown to accumulate during
exposure to tobacco in man [5,6]. In animal models of
COPD or emphysema, intra-tracheal administration or
inhalation of Cd has been shown to induce a pulmonary
inflammatory response as well as the subsequent
development of emphysema [7–12], which mirrors the
conditions observed in COPD-affected patients.