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Pathophysiological effects of air pollutants

While experimental studies have shown a range of effects related to single pollutants, it should be emphasised that the effects of ambient air pollution cannot be assigned to a single pollutant in the mixture. As in the case of tobacco smoke, many pollutants act together in a series of partly interrelated mechanisms, which result in the observed associations between levels of air pollution and a range of health outcomes. Oxidative stress and both local and systemic inflammation are suggested to be the main harmful mechanisms set in train following the inhalation of these pollutants.  A first step may be the generation of reactive oxygen species in the lung cells (e.g. from contact with the carbon core of inhaled particles where toxic substances such as sulfates, nitrates and metals are adsorbed). PM of various sizes and highly oxidative gases (e.g. O₃ or NO_x) have been shown to induce local pulmonary reactions related to oxidative stress. Both local and systemic inflammatory reactions, mediated through cytokines and chemokines, have been found in experimental studies in cellular systems and in animals, as well as in exposure-chamber studies with human subjects.

Claims that one specific aspect or constituent of ambient air pollution is ‘more important’ than others need to be interpreted with great caution. Such comparisons are inherently difficult to make, as the effect also depends on the health outcomes under study, the timescale (e.g. acute versus long-term effects) being considered, the underlying susceptibilities of the exposed individuals, and possibly the nature and concentrations of the co-pollutants.

Table 1 – Examples of established associations between frequently used markers of ambient air pollution and various respiratory health outcomes. Markers of air pollution are often correlated with each other and the health effects are often nonspecific. While urban air pollution is considered a cause of these adverse health effects, specific effects cannot be assigned to single pollutants.

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• Respiratory research
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