Abstract
Ambient air pollution is one of the leading five health risks worldwide. One of the most harmful air pollutants is particulate matter (PM), which has different physical characteristics (particle size and number, surface area and morphology) and a highly complex and variable chemical composition. Our goal was first to comparatively assess the effects of exposure to PM regarding cytotoxicity, release of pro-inflammatory mediators and gene expression in human bronchial epithelia (HBE) reflecting normal and compromised health status. Second, we aimed at evaluating the impact of various PM components from anthropogenic and biogenic sources on the cellular responses. Air-liquid interface (ALI) cultures of fully differentiated HBE derived from normal and cystic fibrosis (CF) donor lungs were exposed at the apical cell surface to water-soluble PM filter extracts for 4 h. The particle dose deposited on cells was 0.9–2.5 and 8.8–25.4 μg per cm2 of cell culture area for low and high PM doses, respectively. Both normal and CF HBE show a clear dose-response relationship with increasing cytotoxicity at higher PM concentrations. The concurrently enhanced release of pro-inflammatory mediators at higher PM exposure levels links cytotoxicity to inflammatory processes. Further, the PM exposure deregulates genes involved in oxidative stress and inflammatory pathways leading to an imbalance of the antioxidant system. Moreover, we identify compromised defense against PM in CF epithelia promoting exacerbation and aggravation of disease. We also demonstrate that the adverse health outcome induced by PM exposure in normal and particularly in susceptible bronchial epithelia is magnified by anthropogenic PM components. Thus, including health-relevant PM components in regulatory guidelines will result in substantial human health benefits and improve protection of the vulnerable population.
Highlights
Ambient air pollution has negative impacts on human health resulting in more than 4.5 million premature deaths each year [1,2,3]
The result of such an approximation shows the high and low doses applied in this study to correspond to a deposited dose in the human tracheobronchial tract of days up to weeks in highly polluted areas reaching 1000 μg/m3, PM2.5, e.g. China [38], and of several months to years in urban areas in Europe, with typical concentrations of 20 μg/m3 [39]
The evidence of health effects associated with source-specific particulate matter (PM) does not indicate a clear ‘hierarchy’ of harmfulness for PM from different emission sources [2, 41]
Summary
Ambient air pollution has negative impacts on human health resulting in more than 4.5 million premature deaths each year [1,2,3]. PM mass concentration has been considered as the only appropriate metric to describe its impact on health [4]. This metric has been used to assess the global burden of premature deaths due to PM [1]. There are increasing indications that anthropogenic components of PM, transition metals and SOA, are of particular concern due to their ability to induce oxidative stress through the generation of reactive oxygen species (ROS) [8,9,10,11]. It is important to identify PM components that lead to an OP responsible for impairing human health
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