Background
The negative effect of air pollution on human health is widely reported in recent literature. It typically involves urbanized areas where the population is concentrated and where most primary air pollutants are produced. A comprehensive health risk assessment is therefore of strategic importance for health authorities.
Methods
In this study we propose a methodology to perform an indirect and retrospective health risk assessment of all-cause mortality associated with long-term exposure to particulate matter less than 2.5 microns (PM2.5), nitrogen dioxide (NO2) and ozone (O3) in a typical Monday to Friday working week. A combination of satellite-based settlement data, model-based air pollution data, land use, demographics and regional scale mobility, allowed to examine the effect of population mobility and pollutants daily variations on the health risk. A Health Risk Increase (HRI) metric was derived on the basis of three components: hazard, exposure and vulnerability, utilizing the relative risk values from the World Health Organization. An additional metric, the Health Burden (HB) was formulated, which accounts for the total number of people exposed to a certain risk level.
Results
The effect of regional mobility patterns on the HRI metric was assessed, resulting in an increased HRI associated with all three stressors when considering a dynamic population compared to a static one. The effect of diurnal variation of pollutants was only observed for NO2 and O3. For both, the HRI metric resulted in significantly higher values during night. Concerning the HB parameter, we identified the commuting flows of the population as the main driver in the resulting metric.
Conclusions
This indirect exposure assessment methodology provides tools to support policy makers and health authorities in planning intervention and mitigation measures. The study was carried out in Lombardy, Italy, one of the most polluted regions in Europe, but the incorporation of satellite data makes our approach valuable for studying global health.
Background
Influenza seasonality has been frequently studied, but its mechanisms are not clear. Urban in-situ studies have linked influenza to meteorological or pollutant stressors. Few studies have investigated rural and less polluted areas in temperate climate zones.
Objectives
We examined influences of medium-term residential exposure to fine particulate matter (PM2.5), NO2, SO2, air temperature and precipitation on influenza incidence.
Methods
To obtain complete spatial coverage of Baden-Württemberg, we modeled environmental exposure from data of the Copernicus Atmosphere Monitoring Service and of the Copernicus Climate Change Service. We computed spatiotemporal aggregates to reflect quarterly mean values at post-code level. Moreover, we prepared health insurance data to yield influenza incidence between January 2010 and December 2018. We used generalized additive models, with Gaussian Markov random field smoothers for spatial input, whilst using or not using quarter as temporal input.
Results
In the 3.85 million cohort, 513,404 influenza cases occurred over the 9-year period, with 53.6% occurring in quarter 1 (January to March), and 10.2%, 9.4% and 26.8% in quarters 2, 3 and 4, respectively. Statistical modeling yielded highly significant effects of air temperature, precipitation, PM2.5 and NO2. Computation of stressor-specific gains revealed up to 3499 infections per 100,000 AOK clients per year that are attributable to lowering ambient mean air temperature from 18.71 °C to 2.01 °C. Stressor specific gains were also substantial for fine particulate matter, yielding up to 502 attributable infections per 100,000 clients per year for an increase from 7.49 μg/m3 to 15.98 μg/m3.
Conclusions
Whilst strong statistical association of temperature with other stressors makes it difficult to distinguish between direct and mediated temperature effects, results confirm genuine effects by fine particulate matter on influenza infections for both rural and urban areas in a temperate climate. Future studies should attempt to further establish the mediating mechanisms to inform public health policies.
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