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Link to original content: https://pubmed.ncbi.nlm.nih.gov/28713383
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Review
. 2017 Jun 30:8:763.
doi: 10.3389/fimmu.2017.00763. eCollection 2017.

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

Rituraj Niranjan  1 , Ashwani Kumar Thakur  1
Affiliations
Review

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

Rituraj Niranjan et al. Front Immunol. .

Abstract

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.

Keywords: air pollution; carbon black; inflammation; oxidative stress; polyunsaturated fatty acids; soot (black carbon).

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Figures

Figure 1
Figure 1
The major health problems due to soot and carbon black (CB). Figure shows soot- and CB-induced major health problems. The first hazard is cancer that is caused by DNA adducts formation, DNA strands breaks, or mutation in genes. Second is the respiratory toxicity caused by dysfunctional immune response involving activation of eosinophils and mast cells. The third is cardiovascular toxicology that also includes the coronary heart disease. Apart from these, soot also causes damage to the different organs of the body by some unknown mechanisms.
Figure 2
Figure 2
Historical perspective of soot-induced health hazards. Diagrammatic representation of major breakthrough studies due to soot and carbon black exposure (62). The left panel shows the pathological manifestation and right panel shows the corresponding year of study.
Figure 3
Figure 3
Number of publication found in PubMed related to soot. Histograms represent decade wise publications in the area of soot toxicity, collected from PubMed search using the word soot.
Figure 4
Figure 4
The proposed mechanism of soot- and carbon black (CB)-induced toxicity. The toxicological mechanisms of soot or CB can be theoretically classified into two types. The one is direct toxicity or localized damage, and the other is systemic toxicity. In direct toxicity, soot/CB comes into contact with lung epithelial cells, produces oxidative stress by affecting mitochondria, and upregulates calcium influx in the cells. The soot-induced oxidative stress initiates the cell survival or death mechanisms such as autophagy and apoptosis. Soot may lead to cancer development by interruption of autophagic and apoptotic cell death. Soot or CB also induces DNA methylation, DNA adducts formation, Aryl hydrocarbon receptor (AhR) activation, DNA double-strand breaks, and failure to DNA repair mechanisms, resulting in cancer. In systemic toxicity, soot triggers an inflammatory response in lungs and causes various symptoms. Due to soot or CB exposure, lung epithelial cells secrete inflammatory mediators (chemokine and cytokines), which further amplify the immune response. Immune cells produce interleukin-13 (IL-13) and transforming growth factor beta (TGF-beta) which activate fibroblast cells to acquire fibrotic phenotype (production and accumulations of fibrous proteins in extracellular space). Monocytes and macrophage produce a large number of matrix metalloproteases (MMPs) and other toxic mediators that alter many physiologic functions including brain and cardiovascular systems. Serum amyloid A (SAA) produced in response to soot causes problems to the liver and kidney.
Figure 5
Figure 5
The mechanism of mast cells mediated allergic response due to soot and carbon black. Soot triggers activation of mast cells that in turn release the mediators of inflammation. These mediators subsequently activate fibroblast cells. The fibroblast dysfunctions by these mediators is caused by two receptors (heparin 1 and protease-activated receptor 2) leading to excess production of collagen and other fibrous proteins of the extracellular space.
Figure 6
Figure 6
New aspects that need to be explored in the area of soot or carbon black (CB) toxicity. This figure shows new research areas, which need to be explored in soot or CB toxicity. The role of resistin-like molecule-α (RELM-alpha), role of eosinophils and mast cells, activation of invariant natural killer (iNKT) and Th17 cells, and involvement of serum amyloid protein leading to amyloidosis are some of the important areas that still need to be explored in detail.
Figure 7
Figure 7
The possible therapeutic strategies to combat soot or carbon black (CB) toxicity. The therapeutic strategies are shown in the figure targeting oxidative stress (in the center) and immune cells (in the periphery) involved in soot or CB toxicity. Red signs show the inhibitors capable of arresting the appropriate response. Anti-eosinophils based antibodies to prevent eosinophils mediated toxic effects are shown. The microRNAs and some noble inhibitors can also be used to downregulate the mast-associated toxicities. N3 fatty acids (polyunsaturated fatty acids) based therapies may be useful to minimize the T cell-associated effects. Importantly, the PPR-γ-based therapeutic interventions become more interesting to target various cell-specific functions.
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