Secondary effects of urban heat island mitigation measures on air quality

This study presents numerical simulations analysing the effect of urban heat island (UHI) mitigation measures on the chemical composition of the urban atmosphere. The mesoscale chemical transport model WRF-Chem is used to investigate the impact of urban greening and highly reflective surfaces on the concentrations of primary (CO, NO) as well as secondary pollutants (O$_{3}$) inside the urban canopy. In order to account for the sub-grid scale heterogeneity of urban areas, a multi-layer urban canopy model is coupled to WRF-Chem. Using this canopy model at its full extend requires the introduction of several urban land use classes in WRF-Chem. The urban area of Stuttgart serves as a test bed for the modelling of a case scenario of the 2003 European Heat Wave. The selected mitigation measures are able to reduce the urban temperature by about 1 K and the mean ozone concentration by 5–8%. Model results however document also negative secondary effects on urban air quality, which are closely related to a decrease of vertical mixing in the urban boundary layer. An increase of primary pollutants NO and CO by 5–25% can be observed. In addition, highly reflective surfaces can increase peak ozone concentration by up to 12% due to a high intensity of reflected shortwave radiation accelerating photochemical reactions

In vitro activation of complement and contact system by lactic acidosis.

The activation of complement and contact systems occurs in reperfusion injuries with initial tissue hypoxia, and lactic acidosis such as mycardial infarction and birth asphyxia. The aim of our experiment was the formal proof of activation by sole lactic acidosis. Lactic acid was added to blood and plasma samples from 10 healthy volunteers. C5a and factor XIIa were measured by EIA after incubation at 37 degrees C for 1 h. Both concentrations increased (P < 0.0001 by Friedman analysis) in blood and plasma samples with increasing amount of added lactic acid. Lactic acidosis can activate C5 from the complement system and factor XII from the contact system directly, even in the absence of cellular components