We would like to draw attention to a recent finding by Neupane and colleagues in an article entitled "Long-term Exposure to Ambient Air Pollution and Risk of Hospitalization with Community-acquired Pneumonia in Older Adults". The study investigated a long-term effect of environmental air pollution, assessed over the previous 12 months, on hospitalization for community-acquired pneumonia (CAP) in a case-control study of elderly patients (>/=65 yr of age). The results show that environmental exposure to nitrogen dioxide (NO2) and particulate matter (PM2.5) was significantly associated with hospitalization for CAP. Another important finding from the public health point of view, not discussed in the article or mentioned in the abstract, was a highly positive association between CAP hospitalization and a history of regular exposure to gases, fumes, or chemicals at work (odds ratio [OR] 5.8; 95% confidence interval [CI] 4.2-7.9; P < 0.001). Furthermore, there is an association between CAP and smoking (>/=100 cigarettes over a lifetime), albeit a lower odds ratio (OR = 2.9; 95% CI 2.2-3.9). Although occupational exposure to gases, fumes (especially metal fumes), and chemicals is known to be associated with increased risk of pneumonia-related morbidity and mortality, this study is unique in that occupational risk for CAP was assessed in elderly subjects who retired from work and who were simultaneously investigated for environmental air-pollution exposure. The population-based study was conducted in the Canadian city of Hamilton, which had an extensive heavy industrial base, including metal foundries. Thus, occupational exposure was potentially highly prevalent and their contribution to respiratory disease such as CAP was likely to have public health significance given the strength of the observed association. The study is also interesting because of the potential pathogenic mechanism of environmentally related CAP. Metals in fumes and fly ashes have been shown to have the capacity to induce oxidative damage to the lung's immune defense. The damage is thought to be mediated by metal-induced generation of reactive hydroxyl radicals that can impair the function of lymphocytes and normal immune responses. Furthermore, fine metal particles are also cytotoxic to macrophages, and the presence of metals may also enhance bacterial pathogenicity in the lung. However, the above proposed mechanisms are thought to be only temporary and cease when the excess of free iron in the lung is removed. In humans, the increased susceptibility to infectious pneumonia from exposure to metal fumes is thought to be reversible following cessation of exposure. The pathological mechanism for long-term environmental and occupational exposure that may lead to increased susceptibility to CAP is not that well established. It is hypothesized that NO2 and sulfuric acid (H2SO4) exposure may lead to epithelial cell damage and impaired mucociliary clearance. The long-term damage associated with occupational exposure may lead to permanent airways remodeling that increases an individual's long-term susceptibility to CAP. It is also possible that the permanent damage to the lung associated with occupational exposure can potentiate the effect of environmental exposure to NO2 and PM. It would be of interest to investigate whether there was an interaction between occupational exposure and environmental pollution and what type of occupational exposure (e.g., industry and job) was associated with the increased risk of hospitalization for CAP. The study supports the hypothesis that regular occupational exposure to gases, fumes, or chemicals at work is associated with increased susceptibility to infectious pneumonia such as CAP and that the effect on increased susceptibility is long-lasting following cessation of exposure. These results are important in clinical practice for prevention. Clinical observations support the epidemiological and experimental studies, in that workers with occupational lung disease often present with pneumonia and because of this it has been routine practice for years to provide pneumococcal and influenza vaccine to workers with occupational lung diseases.
Respiratory-system-disorders; Occupational-exposure; Lung-disease; Pulmonary-congestion; Pulmonary-disorders; Gases; Fumes; Chemical-hypersensitivity; Risk-factors; Public-health; Environmental-exposure; Industrial-emissions; Air-contamination; Particulates; Metal-fumes; Fly-ash; Hydroxyl-groups; Vaccines; Age-groups; Clinical-pathology; Smoking; Health-care; Medical-treatment; Surveillance