8.22 – Particle Toxicities

The documentation of particle toxicities dates back to several centuries, with lung diseases in miners, smelters, and stonecutters being described in early scientific writings in the sixteenth and seventeenth centuries. The pathological and toxic effects of airborne particles, however, began to be aggressively studied only in the early 1900s when increased respiratory diseases were noted among people in occupations involving dusty trades (e.g., coal and granite mining and foundries). Much of the early work of assessing the hazards of airborne particles focused on crystalline silica, whereas in more recent times (specifically, the second half of the twentieth century), other nonoccupational exposures to airborne particulates (i.e., ambient air pollution, tobacco smoke, and diesel exhaust) and their relation to pulmonary disease, functional deficits, and, in some cases, mortality among healthy and susceptible populations were investigated. However, not all particles cause toxicity. Nuisance dusts (i.e., titanium dioxide (TiO2)), for example, cause very little or no toxicity or lung remodeling unless incredibly high exposures are experienced over prolonged durations. There are a number of factors that influence whether a particle is toxic or relatively inert, including its respirability (e.g., ability to enter the respiratory tract), patterns for pulmonary deposition, clearance and retention, solubility, and surface reactivity. This chapter reviews how different types of airborne particles and fibers can lead to very different biological responses, 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 toxicity, including how particle physicochemistry can influence particle deposition and clearance patterns and ultimately lead to different patterns of site-specific or broad-based structural changes in the lungs.