Lung injury after cigarette smoking is particle related

Abstract

The specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking are yet to be delineated. We propose that 1) injury and disease following cigarette smoking are associated with exposure to and retention of particles produced during smoking and 2) the biological effects of particles associated with cigarette smoking share a single mechanism of injury with all particles. Smoking one cigarette exposes the human respiratory tract to between 15,000 and 40,000 μg particulate matter; this is a carbonaceous product of an incomplete combustion. There are numerous human exposures to other particles, and these vary widely in composition, absolute magnitude, and size of the particle. Individuals exposed to all these particles share a common clinical presentation with a loss of pulmonary function, increased bronchial hyperresponsiveness, pathologic changes of emphysema and fibrosis, and comorbidities, including cardiovascular disease, cerebrovascular disease, peripheral vascular disease, and cancers. Mechanistically, all particle exposures produce an oxidative stress, which is associated with a series of reactions, including an activation of kinase cascades and transcription factors, release of inflammatory mediators, and apoptosis. If disease associated with cigarette smoking is recognized to be particle related, then certain aspects of the clinical presentation can be predicted; this would include worsening of pulmonary function and progression of pathological changes and comorbidity (eg, emphysema and carcinogenesis) after smoking cessation since the particle is retained in the lung and the exposure continues.

Pleural plaques in smoking-associated fibrosis and pulmonary asbestosis

“…Clinical and radiographic characteristics of lung injury following particle exposure (including fibers in which one diameter of the particle is 3× that of the other by definition) are often comparable. 2 The results of this investigation 1 support further evaluation of a role for cigarette smoking in interstitial fibrosis. Furthermore, asbestos exposure can cause several non-malignant diseases of the pleura and lungs (ie, pleural effusions, pleural plaques, diffuse pleural fibrosis, rounded atelectasis, and asbestosis).…”

COPD: balancing oxidants and antioxidants

“…Almost all of these exposures are particle related. 63 , 64 Such exposures can include environmental tobacco smoke, burning of biomass, and air pollution particles. All these particle exposures, environmental and occupational, can result in oxidative stress.…”

Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

“…Ambient air pollution, containing PM smaller than aerodynamic diameter of 2.5 μm (PM 2.5 ), has gained particular attention in recent years as a causative factor in the increased incidence of respiratory diseases, including lung cancer [1,2,3,4]. Tobacco smoke also plays a very important role in increasing the risk for epithelial inflammation and lung cancer due to its high carcinogenic potential and the synergistic effects with other respirable particulate to generate reactive oxygen species (ROS) and catalyze redox reactions in human lung epithelial cells, leading to oxidative stress and increased production of mediators of pulmonary inflammation [5,6,7,8,9]. …”