Airway and systemic inflammatory responses to ultrafine carbon black particles and ozone in older healthy subjects

Holz, Olaf; Heusser, Karsten; Müller, Meike; Windt, H.; Schwarz, Katharina; Schindler, Christoph; Tank, Jens; Hohlfeld, Jens M.; Jordan, Jens

doi:10.1080/15287394.2018.1463331

Cited by 12 publications

(4 citation statements)

References 29 publications

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“…It is unclear whether ozone acts independently of other environmental factors. In some studies ozone alone enhances plasma and sputum inflammatory cells and mediators (CC16, IL-6, and matrix metalloproteinase (MMP)9) (59) with no effect seen with carbon black ultrafine particles (cbUFP). However, other studies show no effect of ozone alone (60).…”

Section: Epidemiological Impact Of Ozone In Healthy and At Risk Subjectsmentioning

confidence: 99%

Transcriptional Effects of Ozone and Impact on Airway Inflammation

2019

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Epidemiological and challenge studies in healthy subjects and in individuals with asthma highlight the health impact of environmental ozone even at levels considered safe. Acute ozone exposure in man results in sputum neutrophilia in 30% of subjects particularly young children, females, and those with ongoing cardiopulmonary disease. This may be associated with systemic inflammation although not in all cases. Chronic exposure amplifies these effects and can result in the formation of asthma-like symptoms and immunopathology. Asthmatic patients who respond to ozone (responders) induce a greater number of genes in bronchoalveolar (BAL) macrophages than healthy responders with up-regulation of inflammatory and immune pathways under the control of cytokines and chemokines and the enhanced expression of remodeling and repair programmes including those associated with protease imbalances and cell-cell adhesion. These pathways are under the control of several key transcription regulatory factors including nuclear factor (NF)-κB, anti-oxidant factors such as nuclear factor (erythroid-derived 2)-like 2 NRF2, the p38 mitogen activated protein kinase (MAPK), and priming of the immune system by up-regulating toll-like receptor (TLR) expression. Murine and cellular models of acute and chronic ozone exposure recapitulate the inflammatory effects seen in humans and enable the elucidation of key transcriptional pathways. These studies emphasize the importance of distinct transcriptional networks in driving the detrimental effects of ozone. Studies indicate the critical role of mediators including IL-1, IL-17, and IL-33 in driving ozone effects on airway inflammation, remodeling and hyperresponsiveness. Transcription analysis and proof of mechanisms studies will enable the development of drugs to ameliorate the effects of ozone exposure in susceptible individuals.

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Section: Epidemiological Impact Of Ozone In Healthy and At Risk Subjectsmentioning

confidence: 99%

Transcriptional Effects of Ozone and Impact on Airway Inflammation

2019

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“…Previous studies found correlations between air pollutants and altered immunologic/ inflammatory marker levels (Carosino et al 2015;Holz et al 2018). With respect to PM, Pope et al (2016) noted in Provo, Utah found that PM 2.5 exposure was associated with decreased circulating levels of pro-angiogenic growth factors such as epidermal growth factor (EGF), increased levels of anti-angiogenic (i.e.…”

Section: Discussionmentioning

confidence: 99%

Household coal combustion, indoor air pollutants, and circulating immunologic/inflammatory markers in rural China

Wong

Bassig

et al. 2019

Journal of Toxicology and Environmental Health, Part A

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The study aim was to investigate whether household bituminous ("smoky") coal use and personal exposure to combustion emissions were associated with immunologic/inflammatory marker levels. A cross-sectional study of healthy never-smoking women from rural Xuanwei and Fuyuan, China was conducted, which included 80 smoky coal and 14 anthracite ("smokeless") coal users. Personal exposure to fine particulate matter (PM 2.5 ) and benzo[a]pyrene (BaP) was assessed using portable devices, while 67 circulating plasma immunologic/inflammatory markers were measured using multiplex bead-based assays. Multivariable linear regression models were employed to estimate associations between smoky coal versus smokeless coal use, indoor air pollutants, and immunologic/inflammatory markers. Six markers were altered among smoky coal users compared to smokeless coal, including significantly decreased interferon-inducible T-cell alpha chemoattractant (CXCL11/I-TAC), and increased serum amyloid P component (SAP). CXCL11/I-TAC was previously found to be reduced in workers exposed to high levels of diesel engine exhaust, which exhibits similar constituents as coal combustion emissions. Further, there was evidence that elevated PM 2.5 and BaP exposure was associated with significantly diminished levels of the serum amyloid A (SAA); however, the false discovery rates (FDRs) were >0.2 after accounting for multiple comparisons. Inflammatory processes may thus mediate the carcinogenic effects attributed to smoky coal emissions.

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“…Other studies have also suggested that CB is unlikely to be directly genotoxic, or a reproductive toxicant [8]. However, recent human [9] and animal studies [10,11] suggest that age and the effects of immunosuppression may have been previously underestimated.…”

Section: Introductionmentioning

confidence: 99%

An In Vitro Model to Assess Early Immune Markers Following Co-Exposure of Epithelial Cells to Carbon Black (Nano)Particles in the Presence of S. aureus: A Role for Stressed Cells in Toxicological Testing

Brown,

Evans,

Burgum

et al. 2024

Biomedicines

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The exposure of human lung and skin to carbon black (CB) is continuous due to its widespread applications. Current toxicological testing uses ‘healthy’ cellular systems; however, questions remain whether this mimics the everyday stresses that human cells are exposed to, including infection. Staphylococcus aureus lung and skin infections remain prevalent in society, and include pneumonia and atopic dermatitis, respectively, but current in vitro toxicological testing does not consider infection stress. Therefore, investigating the effects of CB co-exposure in ‘stressed’ infected epithelial cells in vitro may better approximate true toxicity. This work aims to study the impact of CB exposure during Staphylococcus aureus infection stress in A549 (lung) and HaCaT (skin) epithelial cells. Physicochemical characterisation of CB confirmed its dramatic polydispersity and potential to aggregate. CB significantly inhibited S. aureus growth in cell culture media. CB did not induce cytokines or antimicrobial peptides from lung and skin epithelial cells, when given alone, but did reduce HaCaT and A549 cell viability to 55% and 77%, respectively. In contrast, S. aureus induced a robust interleukin (IL)-8 response in both lung and skin epithelial cells. IL-6 and human beta defensin (hβD)-2 could only be detected when cells were stimulated with S. aureus with no decreases in cell viability. However, co-exposure to CB (100 µg/mL) and S. aureus resulted in significant inhibition of IL-8 (compared to S. aureus alone) without further reduction in cell viability. Furthermore, the same co-exposure induced significantly more hβD-2 (compared to S. aureus alone). This work confirms that toxicological testing in healthy versus stressed cells gives significantly different responses. This has significant implications for toxicological testing and suggests that cell stresses (including infection) should be included in current models to better represent the diversity of cell viabilities found in lung and skin within a general population. This model will have significant application when estimating CB exposure in at-risk groups, such as factory workers, the elderly, and the immunocompromised.

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Airway and systemic inflammatory responses to ultrafine carbon black particles and ozone in older healthy subjects

Cited by 12 publications

References 29 publications

Transcriptional Effects of Ozone and Impact on Airway Inflammation

Transcriptional Effects of Ozone and Impact on Airway Inflammation

Household coal combustion, indoor air pollutants, and circulating immunologic/inflammatory markers in rural China

An In Vitro Model to Assess Early Immune Markers Following Co-Exposure of Epithelial Cells to Carbon Black (Nano)Particles in the Presence of S. aureus: A Role for Stressed Cells in Toxicological Testing

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