You are here:
Particle exposures and infections
Citation:
Ghio, Andy. Particle exposures and infections. Infection. Urban & Vogel, , Germany, 42(3):459-67, (2014).
Impact/Purpose:
Particulate matter plays a role in respiratory infections in humans. Subsequently, it is expected that the cessation of exposure will diminish, but not totally reverse, the elevated risk for infection. Iron, a component of many particles, adds further dimensions to the particle infection interactions. This review paper discusses the role of particles in human respiratory infections.
Description:
Particle exposures increase the risk for human infections. Particles can deposit in the nose, pharynx, larynx, trachea, bronchi, and distal lung and, accordingly, the respiratory tract is the system most frequently infected after such exposure; however, meningitis also occurs. Cigarette smoking, burning of biomass, dust storms, mining, agricultural work, environmental tobacco smoke (ETS), wood stoves, traffic-related emissions, gas stoves, and ambient air pollution are all particle-related exposures associated with an increased risk for respiratory infections. In addition, cigarette smoking, burning of biomass, dust storms, mining, and ETS can result in an elevated risk for tuberculosis, atypical mycobacterial infections, and meningitis. One of the mechanisms for particle-related infections includes an accumulation of iron by surface functional groups of particulate matter (PM). Since elevations in metal availability are common to every particle exposure, all PM potentially contributes to these infections. Therefore, exposures to wood stove emissions, diesel exhaust, and air pollution particles are predicted to increase the incidence and prevalence of tuberculosis, atypical mycobacterial infections, and meningitis, albeit these elevations are likely to be small and detectable only in large population studies. Since iron accumulation correlates with the presence of surface functional groups and dependent metal coordination by the PM, the risk for infection continues as long as the particle is retained. Subsequently, it is expected that the cessation of exposure will diminish, but not totally reverse, the elevated risk for infection.