Receptor modelling studies of airborne particulate matter in the United Kingdom and India

Research described in this thesis was conducted in the United Kingdom and India, and although the overall subject was source apportionment of traffic emissions, specific objectives as well as research design were different in each case. In the UK, composite PM$_{2.5}$ traffic profiles were derived from ambient data including tunnel and twin-site measurements, and sensitivity of a CMB model to various traffic profiles was tested. The two composite profiles were found to be similar, although lower uncertainties were observed for the tunnel profile. The UK-based traffic profile was found to quantify the traffic contribution consistently, and independent estimates of traffic contribution were found to correlate well with the CMB output. PM10 road dust was chemically characterized in Birmingham and New Delhi, and detailed chemical source profiles were prepared for both cities. Source contributions from dust and non-exhaust emissions were estimated for both cities. In New Delhi, ambient PM$_{2.5}$ and size-segregated PM data were collected at a high-traffic location. Ambient PM$_{2.5}$ concentrations were found to be very high, especially in the winter. Source inferences were derived based on mass closure and traffic emissions were found to contribute between 15 and 25% across seasons

Zika virus E protein modulates functions of human brain microvascular endothelial cells and astrocytes: implications on blood-brain barrier properties

Neurotropic viruses can cross the otherwise dynamically regulated blood-brain barrier (BBB) and affect the brain cells. Zika virus (ZIKV) is an enveloped neurotropic Flavivirus known to cause severe neurological complications, such as encephalitis and fetal microcephaly. In the present study, we employed human brain microvascular endothelial cells (hBMECs) and astrocytes derived from human progenitors to establish a physiologically relevant BBB model. We used this model to investigate the effects of ZIKV envelope (E) protein on properties of cells comprising the BBB. E protein is the principal viral protein involved in interaction with host cell surface receptors, facilitating the viral entry. Our findings show that the presence of ZIKV E protein leads to activation of both hBMECs and astrocytes. In hBMECs, we observed a decrease in the expression of crucial endothelial junction proteins such as ZO-1, Occludin and VE-Cadherin, which are vital in establishment and maintenance of the BBB. Consequently, the ZIKV E protein induced changes in BBB integrity and permeability. We also found upregulation of genes involved in leukocyte recruitment along with increased proinflammatory chemokines and cytokines upon exposure to E protein. Additionally, the E protein also led to astrogliosis, evident from the elevated expression of GFAP and Vimentin. Both cell types comprising the BBB exhibited inflammatory response upon exposure to E protein which may influence viral access into the central nervous system (CNS) and subsequent infection of other CNS cells. Overall, our study provides valuable insights into the transient changes that occur at the site of BBB upon ZIKV infection

Systematizing the approach to air quality measurement and analysis in low and middle income countries

Peer reviewe