Author: Mario Coccia
Title: Two mechanisms for accelerated diffusion of COVID-19 outbreaks in regions with high intensity of population and polluting industrialization: the air pollution-to-human and human-to-human transmission dynamics Document date: 2020_4_11
ID: lhd0jn0z_82
Snippet: or indirectly through the activation intracellular oxidant pathways (Rahman and MacNee, 2000) . Animal and human in-vitro and in-vivo exposure studies have demonstrated the powerful oxidant capacity of inhaled ozone with activation of stress signaling pathways in epithelial cells (Bayram et al., 2001) and resident alveolar inflammatory cells (Mochitate et al., 2001) . Lewtas (2007) shows in human studies that exposures to combustion emissions and.....
Document: or indirectly through the activation intracellular oxidant pathways (Rahman and MacNee, 2000) . Animal and human in-vitro and in-vivo exposure studies have demonstrated the powerful oxidant capacity of inhaled ozone with activation of stress signaling pathways in epithelial cells (Bayram et al., 2001) and resident alveolar inflammatory cells (Mochitate et al., 2001) . Lewtas (2007) shows in human studies that exposures to combustion emissions and ambient fine particulate air pollution are associated with genetic damages. Long-term epidemiologic studies report an increased risk of all causes of mortality, cardiopulmonary mortality, and lung cancer mortality associated with increasing exposures to air pollution (cf., Coccia, 2012 Coccia, , 2014 Coccia and Wang, 2015) . Although there is substantial evidence that polycyclic aromatic hydrocarbons or substituted polycyclic aromatic hydrocarbons may be causative agents in cancer and reproductive effects, an increasing number of studiesï€investigating cardiopulmonary and cardiovascular effectsï€shows potential causative agents from air pollution combustion sources.
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