About This Special Issue
The aim of this special issue is to review the current epidemiology, diagnosis, treatment, prevention and control of the occupational and environmental lung diseases as the diseases are still emergency global health threats. Occupational and environmental lung diseases are difficult to distinguish from those of non-environmental origin. The etiology of several diseases could be multifactorial. In smoking and genetic risks, only after taking a careful exposure history that the underlying general environmental or workplace exposure is uncovered. Knowledge of occupational or environmental etiology significantly affects the patient management and prognosis. A large number of persons are at risk although the exact proportion of lung diseases due to occupational and environmental factors is unknown. Around 15-20 % of the burden of chronic obstructive pulmonary disease (COPD) and adult asthma has been hypothesized to be due to occupational factors. The relationship between particulate matter (PM) exposure and ischemic cardiovascular diseases is well developed. Nevertheless, the association between PM exposure and mortality from COPD, lung cancer, or other lung diseases is not clear. Some previous studies using data from the American Cancer Society indicated that even low-level exposure to ambient outdoor air pollution from traffic and other sources was a critical risk factor for lung diseases and deaths from COPD. The previous American Cancer Society cohorts, only NO2 had significant positive association with lung cancer mortality whereas the effects of PM and other air pollutants on infections are less definitive. The association between air pollution exposure and risk of childhood asthma has been well established while the association between ambient pollution and allergic rhinitis pathophysiology is not well understood. The patient’s history is of importance in assessing any potential occupational or environmental exposure. Current hypothesis is that air pollution acts as an inhaled adjuvant in the development of asthma. The supportive observation is that PM can activate dendritic cells, key antigen-presenting cells that instruct T-cell differentiation. Th17 cells, which secrete interleukin (IL)-17A and promote neutrophil-dominant responses, have attracted attention because these cells arise in the lung after mucosal sensitization, tend to be steroid-insensitive, and are related to severe asthma in some previous studies. Indoor air quality is increasingly associated with exacerbations of asthma and other lung diseases, but the mechanisms remain poorly know. Several previous studies suggested that controlled human exposures will continue to provide new insights into the adverse health effects of air pollution in the near-future. Considering impact of climate change on pulmonary disease burden, the collision of an aging population with warming will result in increased respiratory morbidity in the future.
Aims and Scope: