ROS production and gene expression in alveolar macrophages exposed to PM2.5 from Baghdad, Iraq: Seasonal trends and impact of chemical composition

Hamad, Samera H.; Schauer, James J.; Antkiewicz, Dagmara S.; Shafer, Martin M.; Kadhim, Ahmed Kh.

doi:10.1016/j.scitotenv.2015.11.065

Cited by 58 publications

(39 citation statements)

References 42 publications

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“…Alveolar macrophages (AM) are constantly exposed to the ambient environment. Exposure to environmental particulates such as residual oil fly ash (ROFA) [Huang et al, 2003;Magnani et al, 2013] or PM from various sources [Hamad et al, 2016;Li et al, 2015;Soukup et al, 2000], produces large quantities of ROS. The mitochondrial electron transport chain is the main source for ROS production in eukaryotic cells stimulated by PM.…”

Section: Discussionmentioning

confidence: 99%

“…Various adverse health effects, specifically respiratory diseases (such as asthma and pneumonia), cardiovascular diseases, cardiopulmonary diseases, and even mortality are associated with exposure to PM in general and to fine mineral dust particles in particular [Baccarelli et al, 2008;Badding et al, 2014;Belnap, 2003;Brook et al, 2004;Chen et al, 2006;Giannadaki et al, 2014;Lim et al, 2012;Metcalf et al, 2012;Perez Garcia-Pando et al, 2014;Soukup et al, 2000;West et al, 2016]. Exposure to PM often leads to oxidative stress in living organisms, through the formation of excess reactive oxygen species (ROS) that can induce inflammation, cell damage, and cell death [Adam-Vizi and Chinopoulos, 2006;Antognelli et al, 2014;Hamad et al, 2016;Kermanizadeh et al, 2015;Lodovici and Bigagli, 2011;Øvrevik et al, 2015;Shuster-Meiseles et al, 2016]. A recent study showed that exposure of macrophages to Asian dust particles induced tumor necrosis factor-α (TNF-α) production and nuclear factor-κB activation accompanied by ROS generation [Higashisaka et al, 2014].…”

Section: Introductionmentioning

confidence: 99%

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Mitochondria‐mediated oxidative stress induced by desert dust in rat alveolar macrophages

et al. 2017

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Exposure to ambient particulate matter (PM), including PM from resuspension of soils and dusts, increases the risk for respiratory diseases. However, the exact mechanism of PM‐mediated damage to the lungs remains unclear. Due to recent increases in the frequency of dust storms in many areas, we examined the cytotoxic effects of soil‐dust samples collected in an arid zone in Israel on rat lung macrophages. The desert soil contains soil crusts and low levels of toxic metal content. Exposure of cells to water extracts from the dust samples caused significant reduction in the concentration of live cells and overall cell viability. The dust samples induced cell death through apoptosis, mitochondrial dysfunction, and increased mitochondrial lipid peroxidation. The dust samples generated more reactive oxygen species (ROS) compared to control‐treated samples and National Institute of Standards and Technology San Joaquin Valley standard reference material. To assess whether the oxidative imbalance induced by dust extract also interferes with the antioxidant defense, we evaluated phase II detoxifying and antioxidant enzymes, which are Nrf2 classical targets. The Nrf2 transcription factor is a master regulator of cellular adaptation to stress. The dust extracts produced a significant increase in phase II detoxifying genes. This work suggests that the health‐related injury observed in rat lung cells exposed to dust extracts is associated with ROS generation, mitochondrial dysfunction, mitochondrial lipid peroxidation, and cellular antioxidant imbalance. Damage to lung mitochondria may be an important mechanism by which dust‐containing bacterial material induces lung injury upon inhalation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mitochondria‐mediated oxidative stress induced by desert dust in rat alveolar macrophages

et al. 2017

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“…Phytoplankton is one of the controlling factors of fixed nitrogen in many parts of the oceans and consequently plays a major role in the ocean's biogeochemical cycles (Baker et al, 2006;Chen and Siefert, 2004;Kraemer, 2004;Shi et al, 2012;Tagliabue et al, 2017). Also, water-soluble iron fractions are linked to the creation of reactive oxygen species (ROSs) in lung fluid and in environmental matrices through Fenton chemistry (Hamad et al, 2016). These ROSs impart oxidative stress on the respiratory system, contributing to various health effects (Landreman et al, 2008;Park et al, 2006;Verma et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Water-soluble iron emitted from vehicle exhaust is linked to primary speciated organic compounds

et al. 2020

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Abstract. Iron is the most abundant transition element in airborne particulate matter (PM), primarily existing as Fe(II) or Fe(III). Generally, the fraction of water-soluble iron is greater in urban areas compared to areas dominated by crustal emissions. To better understand the origin of water-soluble iron in urban areas, tailpipe emission samples were collected from 32 vehicles with emission certifications of Tier 0 low emission vehicles (LEV I), Tier 2 low emission vehicles (LEV II), ultralow emission vehicles (ULEVs), super-ultralow emission vehicles (SULEVs), and partial-zero emission vehicles (PZEVs). The components quantified included gases, inorganic ions, elemental carbon (EC), organic carbon (OC), total metals, and water-soluble metals. Naphthalene and intermediate-volatility organic compounds (IVOCs) were quantified for a subset of vehicles. The IVOCs quantified contained 12 to 18 carbons and were divided into three subgroups: aliphatic, single-ring aromatic (SRA), and polar (material not classified as either aliphatic or SRA). Iron solubility in the tested vehicles ranged from 0 % to 82 % (average 30 %). X-ray absorption near-edge structure (XANES) spectroscopy showed that Fe(III) was the primary oxidation state in 14 of the 16 tested vehicles, confirming that the presence of Fe(II) was not the main driver of water-soluble Fe. The correlation of water-soluble iron with sulfate was insignificant, as was correlation with every chemical component except naphthalene and some C12–C18 IVOCs with R2 values as high as 0.56. A controlled benchtop study confirmed that naphthalene alone increases iron solubility from soils by a factor of 5.5 and that oxidized naphthalene species are created in the extract solution. These results suggest that the large driver in water-soluble iron from primary vehicle tailpipe emissions is related to the organic composition of the PM. We hypothesize that, during the extraction process, specific components of the organic fraction of the PM are oxidized and chelate the iron into water.

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“…Transition metals present in ambient PM reportedly promote the formation of reactive oxygen species (ROS) and result in exacerbation of lung inflammation and symptoms of asthma (Gavett & Koren, 2001;Gehring et al, 2015;Godri Pollitt et al, 2016;Hamad, Schauer, Antkiewicz, Shafer, & Kadhim, 2016;Hou et al, 2016;Zhang, Cui, & Qi, 2001). However, the role of oxidative stress in urban PM2.5 and desert dust, and trace metals present in these PM, in particular iron, in the exacerbation of asthma, is not fully understood.…”

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confidence: 99%

Role of iron and oxidative stress in the exacerbation of allergic inflammation in murine lungs caused by urban particulate matter <2.5 μm and desert dust

Ichinose

Yoshida

et al. 2019

J of Applied Toxicology

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Simultaneous exposure of lipopolysaccharide (LPS) and urban particulate matter <2.5 μm (PM2.5) or desert dust exacerbated murine asthma. In the present study, the role of iron (Fe) contained in particles and oxidative stress was investigated using Fe chelator deferoxamine (DFO) and oxidative stress scavenger N‐acetylcysteine (NAC) in a murine asthma model exacerbated by LPS + PM2.5 or LPS + Asian sand dust (ASD). When BALB/c mice were intratracheally challenged with ovalbumin (OVA) + LPS and either urban PM2.5 or ASD, LPS + PM2.5 and LPS + ASD caused exacerbation of OVA‐induced lung eosinophilia along with T‐helper 2 cytokine and eosinophil‐relevant chemokine production in bronchoalveolar lavage fluid as well as the production of OVA‐specific IgE in serum. LPS + PM2.5 with NAC tended to reduce the lung eosinophilia compared to the LPS + PM2.5 host, whereas LPS + PM2.5 with DFO did not reduce them. LPS + ASD with NAC moderately reduced the lung eosinophilia compared to the LPS + ASD host. LPS + ASD with DFO drastically reduced the lung eosinophilia compared to the LPS + ASD host. The concentration of Fe in urban PM2.5 and ASD were almost the same. However, the concentrations of trace metals Pb, Cu, As, Ni, Cr, Mo, Sb, Co, Se and Cd were greater in PM2.5 than in ASD. These results suggested that Fe and oxidative stress are at least partly involved in lung eosinophilia exacerbation caused by LPS + ASD. However, trace metals (except Fe) might also be involved in lung eosinophilia exacerbated by LPS + PM2.5.

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ROS production and gene expression in alveolar macrophages exposed to PM2.5 from Baghdad, Iraq: Seasonal trends and impact of chemical composition

Cited by 58 publications

References 42 publications

Mitochondria‐mediated oxidative stress induced by desert dust in rat alveolar macrophages

Mitochondria‐mediated oxidative stress induced by desert dust in rat alveolar macrophages

Water-soluble iron emitted from vehicle exhaust is linked to primary speciated organic compounds

Role of iron and oxidative stress in the exacerbation of allergic inflammation in murine lungs caused by urban particulate matter <2.5 μm and desert dust

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