The relationship between urban airborne pollution and short-term mortality: quantitative and qualitative aspects.

The influence of airborne pollution on mortality rates has been examined since the well known severe pollution episodes of Pennsylvania (1948) and London (1952). Three main epidemiological approaches are available: transversal studies, time series studies, prospective studies. The most frequently used method is the time series analysis, which retrospectively determines daily mortality rates as compared to daily pollution levels in a defined period. The vast majority of studies applying this approach confirm the existence of a positive correlation between mortality and airborne pollution. The relative risk of death during the most severely polluted days as compared to the least polluted days ranges between 1.02 and 1.13. Airborne pollution affects mortality as related to cardiovascular and chronic obstructive pulmonary diseases mainly in subjects previously affected by these pathologies. The dose-response mortality-pollution curve shows linear increments of mortality at low pollution levels, weak increments at high pollution levels. This phenomenon is attributed to the existence of subjects highly susceptible to pollution induced adverse health effects. These subjects, dying at low pollution levels, are not available to increase mortality rates at high pollution levels. Mortality is mainly related to the concentration of single pollutants, such as suspended particle matter, sulfur oxides, nitric oxides and ozone. Elderly are highly susceptible to pollution-induced mortality increases. Therefore, the study of mortality-pollution correlation is of particular interest in cities characterized by a relative prevalence of the elderly in the population. The latency period between pollution increases and related mortality increases falls in the 1-3 days interval range. The pollution-mortality relationship is influenced by many factors, such as the occurrence of exceedingly high or low environmental temperatures, influenza epidemics, etc. Many hypotheses has been raised to support the causality of the mortality-pollution association, including a direct effect of pollutants on cardiovascular and respiratory apparatus, and the release of inflammatory mediators affecting blood viscosity and pneumocytes homeostasis. On the whole, available data suggest that pollution is able to increase mortality only if associated to other risk factors determining an increased susceptibility in the exposed population.