Differential injurious effects of ambient and traffic‐derived particulate matter on airway epithelial cells

Kumar, Rakesh K.; Shadie, Alexander M.; Bucknall, Martin P.; Rutlidge, Helen; Garthwaite, Linda; Herbert, Cristan; Halliburton, Brendan; Parsons, Kristy; Wark, Peter

doi:10.1111/resp.12381

Cited by 51 publications

(48 citation statements)

References 36 publications

(50 reference statements)

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“…The localized response of soot is mainly caused by the oxidative stress and dysfunctions in the cellular machinery (Figure 4) (142, 197). One of the mechanisms by which soot or CB exert oxidative stress is the interruption of mitochondrial metabolism (142, 198).…”

Section: The Proposed Mechanisms and Future Perspectives Of Soot- Andmentioning

confidence: 99%

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

2017

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The environmental soot and carbon blacks (CBs) cause many diseases in humans, but their underlying mechanisms of toxicity are still poorly understood. Both are formed after the incomplete combustion of hydrocarbons but differ in their constituents and percent carbon contents. For the first time, “Sir Percival Pott” described soot as a carcinogen, which was subsequently confirmed by many others. The existing data suggest three main types of diseases due to soot and CB exposures: cancer, respiratory diseases, and cardiovascular dysfunctions. Experimental models revealed the involvement of oxidative stress, DNA methylation, formation of DNA adducts, and Aryl hydrocarbon receptor activation as the key mechanisms of soot- and CB-induced cancers. Metals including Si, Fe, Mn, Ti, and Co in soot also contribute in the reactive oxygen species (ROS)-mediated DNA damage. Mechanistically, ROS-induced DNA damage is further enhanced by eosinophils and neutrophils via halide (Cl− and Br−) dependent DNA adducts formation. The activation of pulmonary dendritic cells, T helper type 2 cells, and mast cells is crucial mediators in the pathology of soot- or CB-induced respiratory disease. Polyunsaturated fatty acids (PUFAs) were also found to modulate T cells functions in respiratory diseases. Particularly, telomerase reverse transcriptase was found to play the critical role in soot- and CB-induced cardiovascular dysfunctions. In this review, we propose integrated mechanisms of soot- and CB-induced toxicity emphasizing the role of inflammatory mediators and oxidative stress. We also suggest use of antioxidants and PUFAs as protective strategies against soot- and CB-induced disorders.

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Section: The Proposed Mechanisms and Future Perspectives Of Soot- Andmentioning

confidence: 99%

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

2017

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“…These cells are known to release a multitude of biochemical compounds including pro-inflammatory cytokines such as interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α in response to PM exposure [23]. Various components of PM can influence the subsequent pro-inflammatory cytokine response [24], with the inflammatory potential of PM being heterogeneous depending on the city and season [25–28]. Several studies have shown that these heterogeneous inflammatory responses may be partly attributed to the elemental composition of AD [25, 26, 29].…”

Section: Introductionmentioning

confidence: 99%

“…Various components of PM can influence the subsequent pro-inflammatory cytokine response [24], with the inflammatory potential of PM being heterogeneous depending on the city and season [25–28]. Several studies have shown that these heterogeneous inflammatory responses may be partly attributed to the elemental composition of AD [25, 26, 29]. However, the effects of fungi in airborne PM on the inflammatory response remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Association between transported Asian dust and outdoor fungal concentration during winter in a rural area of western Japan

et al. 2017

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BackgroundRecently, Asian dust (AD) has become a serious health problem and several studies have clearly proven that AD can aggravate asthma. However, it remains unclear as to which components of AD have a strong effect on the asthma exacerbation caused by AD exposure. Outdoor fungi can increase emergency department visits and hospitalization for asthma exacerbation and can aggravate asthma symptoms. Therefore, this study was aimed at investigating the relationship between AD and outdoor fungi and determining the potential of fungi to cause airborne particulate matter (PM)-related inflammatory responses.MethodsAirborne PM was collected each day from January 26, 2015 to February 27, 2015. Daily levels of outdoor fungi-associated PM were calculated using a culture-based method. Production of cytokines such as interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α was assessed in THP1 cells stimulated by the collected airborne PM each day.ResultsDaily levels of AD particles were assessed using Light Detection and Ranging and did not correlate with outdoor fungi (r = −0.17, P = 0.94). There was also no association between outdoor fungi and the daily production of IL-6 (r = 0.16, P = 0.37), IL-8 (r = 0.19, P = 0.30), or TNF-α induced by collected PM (r = 0.07, P = 0.70). However, the daily levels of AD particles were significantly associated with IL-6 (r = 0.91, P < 0.0001), IL-8 (r = 0.64, P = 0.0004), and TNF-α (r = 0.72, P < 0.0001) production.ConclusionAD did not increase the acute levels of outdoor fungi and outdoor fungi did not affect the cytokine production induced by airborne PM. These results suggest that outdoor fungi do not have any detectable effect on the asthma exacerbation caused by AD exposure.

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“…Associations have also been found between adverse respiratory health outcomes and specific constituents of PM 2.5 , such as metallic and organic species, independent of total PM 2.5 concentration (Mar et al 2000; Ostro et al 2007; Ostro et al 2009). To identify the mechanisms of ambient PM 2.5 -induced respiratory illnesses and establish the biological plausibility of epidemiological findings, toxicology studies have employed filter-based collection of ambient PM 2.5 (Choi et al 2004; Sawyer et al 2010; Kumar et al 2015). …”

Section: Introductionmentioning

confidence: 99%

Association of IL-6 with PM2.5 Components: Importance of Characterizing Filter-Based PM2.5 Following Extraction

Roper

Chubb

Cambal

et al. 2016

Water Air Soil Pollut

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Filter-based toxicology studies are conducted to establish the biological plausibility of the well-established health impacts associated with fine particulate matter (PM2.5) exposure. Ambient PM2.5 collected on filters is extracted into solution for toxicology applications, but frequently, characterization is nonexistent or only performed on filter-based PM2.5, without consideration of compositional differences that occur during the extraction processes. To date, the impact of making associations to measured components in ambient instead of extracted PM2.5 has not been investigated. Filter-based PM2.5 was collected at locations (n = 5) and detailed characterization of both ambient and extracted PM2.5 was performed. Alveolar macrophages (AMJ2-C11) were exposed (3, 24, and 48 h) to PM2.5 and the pro-inflammatory cytokine interleukin (IL)-6 was measured. IL-6 release differed significantly between PM2.5 collected from different locations; surprisingly, IL-6 release was highest following treatment with PM2.5 from the lowest ambient concentration location. IL-6 was negatively correlated with the sum of ambient metals analyzed, as well as with concentrations of specific constituents which have been previously associated with respiratory health effects. However, positive correlations of IL-6 with extracted concentrations indicated that the negative associations between IL-6 and ambient concentrations do not accurately represent the relationship between inflammation and PM2.5 exposure. Additionally, seven organic compounds had significant associations with IL-6 release when considering ambient concentrations, but they were not detected in the extracted solution. Basing inflammatory associations on ambient concentrations that are not necessarily representative of in vitro exposures creates misleading results; this study highlights the importance of characterizing extraction solutions to conduct accurate health impact research.

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Differential injurious effects of ambient and traffic‐derived particulate matter on airway epithelial cells

Cited by 51 publications

References 36 publications

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

Association between transported Asian dust and outdoor fungal concentration during winter in a rural area of western Japan

Association of IL-6 with PM2.5 Components: Importance of Characterizing Filter-Based PM2.5 Following Extraction

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