ABSTRACT
The pathological effects of airborne particles have been documented in historical writings dating back for millennia. In the first century, for example, the Greeks described a lung disease that appeared to cause a wasting away of the body (1,2). By the 16th and 17th centuries, lung diseases among miners, smelters, and stone cutters were described by a number of physicians, and occasionally, autopsies were performed on workers, revealing the presence of dust in the lungs (1). Early occupational studies generally did not distinguish among lung diseases caused by different types of dust (e.g., coal, silica, metal, asbestos), chemicals, or bacterial agents. Originally, nearly all respiratory diseases were termed “phthisis” or “consumption.” It was not until the early to mid 1900s with the development of new medical diagnostic methods, such as Mycobacterium tuberculosis detection in sputum samples (a causative agent of tuberculosis and frequent confounder for diagnosing pulmonary disease caused by mineral dusts) and chest X rays, that pulmonary disease began to be defined according to specific agents (e.g., silicosis, asbestosis, coal miners’ pneumoconiosis). Chronic obstructive pulmonary disease, emphysema, and other forms of structural remodeling of the lungs (granulomas of berylliosis, interstitial fibrosis of hard metal disease, macules of siderosis) are additional pulmonary diseases that were historically identified through occupational exposure to airborne particles. In more recent times (specifically, the second half of the 20th century), other nonoccupational sources of airborne particulates (i.e., ambient air pollution, tobacco smoke, diesel exhaust) have been reportedly associated with lung remodeling, ultimately leading to lung structural changes and functional deficits, and, in some cases, mortality among healthy and susceptible populations. This chapter reviews how different types of airborne particles and fibers can lead to very different lung remodeling, depending on their physicochemical characteristics, biopersistence, and internal dose. This chapter will also touch upon the theoretical or known mechanisms by which some airborne particles cause site-specific or broad-based structural changes in the lungs.
