Effects of Inhaled Ambient Particulate Matter on Pulmonary Antimicrobial Immune Defense

Abstract

Respiratory-tract infection, specifically pneumonia, contributes substantially to the increased morbidity and mortality among elderly individuals exposed to airborne particulate matter of <10 microm diameter (PM(10)). These epidemiological findings suggest that PM(10) may act as an immunosuppressive factor that can undermine normal pulmonary antimicrobial defense mechanisms. To investigate whether, and how, compromised pulmonary immunocompetence might contribute to increased mortality, two sets of laboratory studies were performed. The first examined the effects of a single inhalation exposure to concentrated ambient PM(2.5) (CAPS) from New York City air on pulmonary/systemic immunity and on the susceptibility of exposed aged rats to subsequent infection with Streptococcus pneumoniae. The second set of studies determined whether CAPS exposure, at a concentration approximating or somewhat greater than the promulgated 24-h NAAQS of 65 microg/m(3), could exacerbate an ongoing infection. Taken together, results demonstrated that a single exposure of healthy animals to CAPS had little effect on pulmonary immune function or bacterial clearance during subsequent challenge with S. pneumoniae. Alternatively, CAPS exposure of previously infected rats significantly increased bacterial burdens and decreased percentages of lavageable neutrophils and proinflammatory cytokine levels compared to those in infected filtered-air-exposed controls. These studies demonstrate that a single exposure to ambient PM(2.5) compromises a host's ability to handle ongoing pneumococcal infections and support the epidemiological findings of increased pneumonia-related deaths in ambient PM-exposed elderly individuals.

A role for associated transition metals in the immunotoxicity of inhaled ambient particulate matter.

“…PM emissions from oil-burning power plants and other industries that contribute to air pollution contain large amounts of metals such as V, Fe, Ni, Zn, and Cu (15,16). Moreover, studies from this laboratory have demonstrated the presence of Mn in concentrated NYC PM (29). Although inflammation was not observed in this study, human exposure to airborne metals have been shown to induce pulmonary inflammatory responses such as tracheobronchitis, asthma, chemical pneumonitis, and alveolitis.…”

Health Effects of Fine Particulate Air Pollution: Lines that Connect

“…Recent animal studies suggest that PM or its constituents play a role in affecting host defenses and increase susceptibility to pulmonary infections. [411][412][413] Hypoxemia Another mechanistic pathway involves PM-induced lung damage (potentially including oxidative lung damage and inflammation), declines in lung function, respiratory distress, and hypoxemia. In the case report discussed above, 332 exposure to high levels of aerosolized oil fly ash particles eventually led to the experiencing of hypoxic respiratory failure.…”

Particulate Air Pollutants and Respiratory Diseases

“…The inflammatory effects of PM 10 were demonstrated in experimental animal studies following direct instillation into the lung, prior to human studies that showed the pulmonary effects after experimental exposure to PM (Ghio & Devlin, 2001). Clinically, PM 10 particles likely provoke airway inflammation via the release of mediators that exacerbate lung disease in susceptible individuals (Seaton et al, 1995); even a single exposure compromises a host's ability to handle ongoing pulmonary infections (Zelikoff et al, 2003). Fine and ultra-fine particles directly stimulate macrophages and epithelial cells to produce inflammatory cytokines such as TNF-, TGF-1, GM-CSF, PDGF, IL-6, and IL-8 (Fugii et al, 2001), and reactive oxygen species are responsible for acute and chronic lung inflammation .…”