METALS ASSOCIATED WITH BOTH THE WATER-SOLUBLE AND INSOLUBLE FRACTIONS OF AN AMBIENT AIR POLLUTION PARTICLE CATALYZE AN OXIDATIVE STRESS

1999 ◽  
Vol 11 (1) ◽  
pp. 37-49 ◽  
Author(s):  
Andrew J. Ghio
PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0233425 ◽  
Author(s):  
Zaira Leni ◽  
Laure Estelle Cassagnes ◽  
Kaspar R. Daellenbach ◽  
Imad El Haddad ◽  
Athanasia Vlachou ◽  
...  

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.


1999 ◽  
Vol 107 (3) ◽  
pp. 233 ◽  
Author(s):  
Herman Autrup ◽  
Bahram Daneshvar ◽  
Lars Ove Dragsted ◽  
Mikael Gamborg ◽  
Ase Marie Hansen ◽  
...  

2021 ◽  
Vol 2 (10) ◽  
pp. 964-976
Author(s):  
Mojtaba Ehsanifar ◽  
Banihashemian SS ◽  
Masoud Ehsanifar

Urban air pollutants exposure is known as a source of neuroinflammation and oxidative stress that causes the Central Nervous System (CNS) and neuropathology disease. Transition metals, Particulate Matter (PM), including PM 2.5 (PM <2.5 μm) and PM 0.1 (PM <0.1μm), nitrogen oxides and ozone are of potent or oxidant capable of producing Reactive Oxygen Species (ROS). Redox-sensitive pathways can be caused by oxidative stress, leading to various biological processes, including inflammation and cell death. The incidence of Alzheimer's Disease (AD) and Parkinson's Disease (PD) and stroke are associated with exposure to air pollution. Some recent findings suggest that urban air pollutants reach the brain in addition to pulmonary and cardiovascular diseases and affect the CNS health too. While the underlying CNS pathology mechanisms induced air pollutants exposure are not well understood, recent studies show that changes in Blood Brain Barrier (BBB) and microglial activation are key components. In this work, we reviewed the new evidence of the mechanisms by which ambient air pollution reach the brain and activate innate immune response as a source of oxidative stress and neuroinflammatory factors.


2020 ◽  
Vol 21 (12) ◽  
pp. 4306 ◽  
Author(s):  
Omar Hahad ◽  
Jos Lelieveld ◽  
Frank Birklein ◽  
Klaus Lieb ◽  
Andreas Daiber ◽  
...  

Exposure to ambient air pollution is a well-established determinant of health and disease. The Lancet Commission on pollution and health concludes that air pollution is the leading environmental cause of global disease and premature death. Indeed, there is a growing body of evidence that links air pollution not only to adverse cardiorespiratory effects but also to increased risk of cerebrovascular and neuropsychiatric disorders. Despite being a relatively new area of investigation, overall, there is mounting recent evidence showing that exposure to multiple air pollutants, in particular to fine particles, may affect the central nervous system (CNS) and brain health, thereby contributing to increased risk of stroke, dementia, Parkinson’s disease, cognitive dysfunction, neurodevelopmental disorders, depression and other related conditions. The underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests inflammation and oxidative stress to be crucial factors in the pathogenesis of air pollution-induced disorders, driven by the enhanced production of proinflammatory mediators and reactive oxygen species in response to exposure to various air pollutants. From a public health perspective, mitigation measures are urgent to reduce the burden of disease and premature mortality from ambient air pollution.


2018 ◽  
Vol 24 (1) ◽  
Author(s):  
V. S. CHAUHAN ◽  
BHANUMATI SINGH ◽  
SHREE GANESH ◽  
JAMSHED ZAIDI

Studies on air pollution in large cities of India showed that ambient air pollution concentrations are at such levels where serious health effects are possible. This paper presents overview on the status of air quality index (AQI) of Jhansi city by using multivariate statistical techniques. This base line data can help governmental and non-governmental organizations for the management of air pollution.


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