Acute effects of motor vehicle traffic-related air pollution exposures on measures of oxidative stress in human airways

Abstract

Epidemiological studies have linked exposure to traffic-related air pollutants to increased respiratory and cardiovascular morbidity and mortality. Evidence from human, animal, and in vitro studies supports an important role for oxidative stress in the pathophysiological pathways underlying the adverse health effects of air pollutants. In controlled-exposure studies of animals and humans, emissions from diesel engines, a major source of traffic-related air pollutants, cause pulmonary and systemic inflammation that is mediated by redox-sensitive signaling pathways. Assessment of human responses to traffic-related air pollution under realistic conditions is challenging due to the complex, dynamic nature of near-roadway exposure. Noninvasive measurement of biomarkers in breath and breath condensate may be particularly useful for evaluating the role of oxidative stress in acute responses to exposures that occur in vehicles or during near-roadway activities. Promising biomarkers include nitric oxide in exhaled breath, and nitrite/nitrate, malondialdehyde, and F2-isoprostanes in exhaled breath condensate.

Figure 1

Hypothesized pathways by which traffic-related air pollutants cause oxidative stress and cell damage. NO, nitric oxide; O₂-, superoxide anion; ONOO-, peroxynitrite; H₂O₂, peroxide; OH·, hydroxyl radical; NADPH, nicotinamide adenine diphosphate; PAH, polycyclic aromatic hydrocarbon; NF-κB, nuclear factor kappa beta; AP-1, activator protein-1; Fe, iron; V, vanadium; Cr, chromium; Cu, copper.