Throughout the 1990s, many epidemiological studies consistently reported adverse health effects at unexpectedly low levels of ambient air pollution . Identification of susceptible sub-populations and mechanisms of effect involved are two clear research priorities [2,3]. Several chronic clinical conditions are good candidates to define the "frail" population susceptible to the acute effects of PM pollution: chronic obstructive pulmonary disease (COPD) including asthma, ischemic heart diseases (IHD), congestive heart failure, heart rhythm disorders, and diabetes .
The mechanisms of lung injury caused by particles among people with COPD have been reviewed . The ability of particulate matter to induce oxidative stress in the airways has been proposed as an important biological mechanism . The oxidative stress mediated by particles may arise from direct generation of reactive oxygen species from the surface of particles or from soluble compounds such as transition metals or organic compounds (poly-aromatic hydrocarbons) . Oxidative stress might up-regulate redox sensitive transcription factors (via nuclear factor kappa B, NF-kB) in airway epithelial cells, thus increasing the synthesis of proinflammatory cytokines and resulting in cell and tissue injury .
In healthy and asthmatic volunteers, airborne particles increase bronchial responsiveness, airway resistance, and bronchial tissue mast cell, neutrophil, and lymphocyte counts . A specific role for ultrafine particles and metallic content of PM (especially iron) has been advocated [10,11].
The relationship between daily levels of air pollutants and respiratory function in patients with chronic respiratory diseases has been analyzed in various panel studies, with inconsistent results [12,13]. Most studies concern asthmatic children, while far fewer observations relate to changes in peak expiratory flow rate [14-22] or in spirometric flow and volume [23-26] among adult or elderly asthmatics or COPD patients.
We conducted a time-series panel study of subjects with COPD, asthma, and IHD with the aim of answering the following question: have daily fluctuations of selected air pollutants a measurable impact on the lung function of subjects with pre-existing lung or heart disease?