ABSTRACT
Aerosol pollution in urban areas is highly variable due to numerous single emission sources such as automobiles, industrial and commercial activities as well as domestic heating, but also due to complex building structures redirecting air mass flows, producing leeward and windward turbulences and resuspension effects. In this publication, it is shown that one or even few aerosol monitoring sites are not able to reflect these complex patterns. In summer 2019, aerosol pollution was recorded in high spatial resolution during six night and daytime tours with a mobile sensor platform on a trailer pulled by a bicycle. Particle mass loadings showed a high variability with PM10 values ranging from 1.3 to 221 µg m-3 and PM2.5 values from 0.7 to 69.0 µg m-3. Geostatistics were used to calculate respective models of the spatial distributions of PM2.5 and PM10. The resulting maps depict the variability of aerosol concentrations within the urban space. These spatial distribution models delineate the distributions without cutting out the built-up structures. Elsewise, the overall spatial patterns do not become visible because of being sharply interrupted by those outcuts in the resulting maps. Thus, the spatial maps allow to identify most affected urban areas and are not restricted to the street space. Furthermore, this method provides an insight to potentially affected areas, and thus can be used to develop counter measures. It is evident that the spatial aerosol patterns cannot be directly derived from the main wind direction, but result far more from an interplay between main wind direction, built-up patterns and distribution of pollution sources. Not all pollution sources are directly obvious and more research has to be carried out to explain the micro-scale variations of spatial aerosol distribution patterns. In addition, since aerosol load in the atmosphere is a severe issue for health and well-being of city residents more attention has to be paid to these local inhomogeneities.
ABSTRACT
The SARS-CoV-2 virus, the causative agent of COVID-19, is undergoing constant mutation. Here, we utilized an integrative approach combining epidemiology, virus genome sequencing, clinical phenotyping, and experimental validation to locate mutations of clinical importance. We identified 35 recurrent variants, some of which are associated with clinical phenotypes related to severity. One variant, containing a deletion in the Nsp1-coding region (Δ500-532), was found in more than 20% of our sequenced samples and associates with higher RT-PCR cycle thresholds and lower serum IFN-ß levels of infected patients. Deletion variants in this locus were found in 37 countries worldwide, and viruses isolated from clinical samples or engineered by reverse genetics with related deletions in Nsp1 also induce lower IFN-ß responses in infected Calu-3 cells. Taken together, our virologic surveillance characterizes recurrent genetic diversity and identified mutations in Nsp1 of biological and clinical importance, which collectively may aid molecular diagnostics and drug design.