Skip to main content
Log in

Effects of carbon black to inflammation and oxidative DNA damages in mouse macrophages

  • Original Paper
  • Published:
Molecular & Cellular Toxicology Aims and scope Submit manuscript

Abstract

Carbon black is classified as carcinogen group 2B by International Agency for Research on Cancer (IARC). But it uncertained the effects of ultrafine carbon black particles on oxidative damage or inflammation. So we were focused to evaluate the oxidative damage or inflammation with ultrafine carbon black particles at gene expression level by using mouse macrophage cell line, and the co-effects with solvent coating to it. It was evaluated the changes of gene expression with real time RT-PCR, and oxidative DNA damage with Fragment Length Analysis with Restriction Enzyme (FLARE) assay in mouse macrophage (RAW264.7) cell line. Two kinds of carbon black induced the gene expression of cytokines related to acute inflammation, and with 0.1% methylcyclohexane coating were regulated conversely each other. The oxidative DNA damage with smaller size carbon black was increased than bigger one (the range with 500–30 nm). The 0.1% methylcyclohexane increased the damage by binding with each carbon black (the dose range with 100 ng/mL-100 μg/mL). In this study, we got the conclusion that the genotoxicity of carbon blacks are elevated with its size get smaller and their surface area wider, and with methylcyclohexane coating. It could cause DNA damage by promoting oxidative stress and inflammatory responses.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Lyon (France): World Health Organization; International Agency For Research On Cancer 93:43–190 (2010).

    Google Scholar 

  2. Surveys on Work Environment in Korea, Incheon (Korea): Korea Occupational Safety and Health Agency, Ministry of Labor (KR) (2009).

  3. Dannenberg, E. M., Paquin, L. & Gwinnell, H. Carbonblack. In: Kroschwitz JI, Howe-Grant M, eds, Kirk-Othmer Encyclopedia of Chemical Technology, 4th Ed, Vol. 4, New York, John Wiley & Sons; 631–666 (1992).

    Google Scholar 

  4. Kuhlbusch, T. A., Neumann, S. & Fissan, H. Number size distribution, mass concentration, and particle composition of PM1, PM2.5, and PM10 in bag filling areas of carbon black production. J Occup Environ Hyg 1: 660–671 (2004).

    Article  PubMed  CAS  Google Scholar 

  5. Criteria for a Recommended Standard [Internet]. Occupational Exposure to Respirable Coal Mine Dust. Publication No. 95106. Cincinnati, Ohio (U.S.A): National Institute for Occupational Safety and Health (URL: http://www.cdc.gov/niosh/95-106.html) (1995).

    Google Scholar 

  6. Documentation of the TLVs® and BEIs® with Other Worldwide Occupational Exposure Values, 2005. Cincinnati, Ohio (U.S.A): American Conference of Governmental Industrial Hygienists® Worldwide (2005).

  7. Test for hazardous substance 527 (carbon black) from OSHA Inception through January 1977. Washington DC. (U.S.A): Occupational Safety and Health Administration (1977).

  8. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Lyon (France): World Health Organization; International Agency For Research On Cancer 65:1–578 (1996).

    Google Scholar 

  9. Hodgson, J. T. & Jones, R. D. A mortality study of carbon black workers employed at five United Kingdom factories between 1947 and 1980. Arch Environ Health 40:261–268 (1985).

    PubMed  CAS  Google Scholar 

  10. Sorahan, T. et al. A cohort mortality study of U.K. carbon black workers, 1951–1996. Am J Ind Med 39:158–170 (2001).

    Article  PubMed  CAS  Google Scholar 

  11. Ingalls, T. Incidence of Cancer in the Carbon Black Industry. Arch Ind Hyg & Occup Med 1:662–676 (1950).

    CAS  Google Scholar 

  12. Robertson, J. & Inman, K. Mortality in carbon black workers in the U.S.; Brief Communication. J Occup Environ Med 38:569–570 (1996).

    Article  PubMed  CAS  Google Scholar 

  13. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Lyon (France): World Health Organization; International Agency For Research On Cancer 46:1–458 (1989).

    Google Scholar 

  14. Muhle, H. et al. Pulmonary response to toner upon chronic inhalation exposure in rats. Fundam Appl Toxicol 17:280–299 (1991).

    Article  PubMed  CAS  Google Scholar 

  15. Morrow, P. E. Possible mechanisms to explain dust overloading of the lungs. Fundam Appl Toxicol 10:369–384 (1988).

    Article  PubMed  CAS  Google Scholar 

  16. Morrow, P. E. Dust overloading of the lungs: update and appraisal. Toxicol Appl Pharmacol 113:1–12 (1992).

    Article  PubMed  CAS  Google Scholar 

  17. Tran, C. L., Jones, A. D., Cullen, R. T. & Donaldson, K. Exploration of the mechanisms of retention and clearance of low-toxicity particles in the rat lung using a mathematical model. Inhal Toxicol 11:1077–1108 (1999).

    Article  PubMed  CAS  Google Scholar 

  18. Renwick, L. C., Donaldson, K. & Clouter, A. Impairment of alveolar macrophage phagocytosis by ultrafine particles. Toxicol Appl Pharmacol 172:119–127 (2001).

    Article  PubMed  CAS  Google Scholar 

  19. Ferin, J., Oberdörster, G. & Penney, D. P. Pulmonary retention of ultrafine and fine particles in rats. Am J Respir Cell Mol Biol 6:535–542 (1992).

    PubMed  CAS  Google Scholar 

  20. Muhle, H. et al. Dust overloading of lungs after exposure of rats top articles of low solubility: comparative studies. J Aerosol Sci 21:374–377 (1990).

    Article  Google Scholar 

  21. Vallyathan, V. et al. Changes in bronchoalveolar lavage indices associated with radiographic classification in coal miners. Am J Respir Crit Care Med 162:958–965 (2000).

    PubMed  CAS  Google Scholar 

  22. Bellmann, B. et al. Lung clearance and retention of toner, utilizing at racer technique, during chronic inhalation exposure in rats. Fundam Appl Toxicol 17:300–313 (1991).

    Article  PubMed  CAS  Google Scholar 

  23. Snipes, M. B. Long-term retention and clearance of particles inhaled by mammalian species. Crit Rev Toxicol 20:175–211 (1989).

    Article  PubMed  CAS  Google Scholar 

  24. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Lyon (France): World Health Organization; International Agency For Research On Cancer 33:1–222 (1984).

    Google Scholar 

  25. Eom, H. J. & Choi, J. H. Oxidative stress of CeO2 nanoparticles via p38-Nrf-2 signaling pathway in human bronchial epithelial cell, Beas-2B. Toxicology Letters 187:77–83 (2009).

    Article  PubMed  CAS  Google Scholar 

  26. Geiser, M. et al. Ultrafine particles cross cellular membranes by nonphagocytic mechanisms in lungs and in cultured cells. Environ Health Perspect 113:1555–1560 (2005).

    Article  PubMed  Google Scholar 

  27. Chen, M. & Von, M. A. Formation of nucleoplasmic protein aggregates impairs nuclear function in response to SiO2 nanoparticles. Exp Cell Res 305:51–62 (2005).

    Article  PubMed  CAS  Google Scholar 

  28. Neenu, S. et al. NanoGenotoxicology: The DNA damaging potential of engineered nanomaterials. Biomaterials 30:3891–3914 (2009).

    Article  Google Scholar 

  29. Toyokuni, S. Oxidative stress and cancer: the role of redox regulation. Biotherapy 11:147–154 (1998).

    Article  PubMed  CAS  Google Scholar 

  30. Karlsson, H. L., Cronholm, P., Gustafsson, J. & Moller, L. Copper oxide nanoparticles are highly toxic: a comparison between metal oxide nanoparticles and carbon nanotubes. Chem Res Toxicol 21:1726–1732 (2008).

    Article  PubMed  CAS  Google Scholar 

  31. Abe, S., Takizawa, H., Sugawara, I. & Kudoh, S. Diesel exhaust (DE)-induced cytokine expression in human bronchial epithelial cells: a study with a new cell exposure system to freshly generated DE in vitro. Am J Respir Cell Mol Biol 22:296–303 (2000).

    PubMed  CAS  Google Scholar 

  32. Donaldson, K. & Tran, C. L. An introduction to the short-term toxicology of respirable industrial fibres. Mutat Res 553:5–9 (2004).

    Article  PubMed  CAS  Google Scholar 

  33. Ohshima, H., Tazawa, H., Sylla, B. S. & Sawa, T. Prevention of human cancer by modulation of chronic inflammatory processes. Mutat Res 591:110–122 (2005).

    Article  PubMed  CAS  Google Scholar 

  34. Oberdorster, G. et al. Ambient ultrafine particles: inducers of acute lung injury? In: Mohr, U. et al. editors. Relationships between respiratory disease and exposure to air pollution. Washington: ILSI Press. p. 216–229 (1998).

    Google Scholar 

  35. Don Porto Carero, A. et al. Genotoxic effects of carbon black particles, diesel exhaust particles, and urban air particulates and their extracts on a human alveolar epithelial cell line (A549) and a human monocytic cell line (THP-1). Environ Mol Mutag 37:155–163 (2001).

    Article  Google Scholar 

  36. Borm, P. J. A. et al. Formation of PAH-DNA adducts after in vivo and vitro exposure of rats and lung cells to different commercial carbon blacks. Toxicol Appl Pharmacol 205:157–167 (2005).

    Article  PubMed  CAS  Google Scholar 

  37. Jiang, J., Oberdorster, G. & Biswas, P. Characterisation of size, surface charge and agglomeration state of nanoparticle dispersions for toxicological studies. J Nanopart Res 11:77–89 (2009).

    Article  CAS  Google Scholar 

  38. Nan, A. et al. Cellular uptake and cytotoxicity of silica nanotubes. Nano Lett 8:2150–2154 (2008).

    Article  PubMed  CAS  Google Scholar 

  39. Oberdorster, G., Oberdorster, E. & Oberdorster, J. Nanotoxicology: an emerging discipline evolving from studies of ultrafine particles. Environ Health Perspect 113:823–839 (2005).

    Article  PubMed  CAS  Google Scholar 

  40. Mroz, R. M. et al. Nanoparticle carbon black driven DNA damage induces growth arrest and AP-1 and NFκB DNA binding in lung epithelial A549 cell line. J Phys and Pharmacol 58:461–470 (2007).

    Google Scholar 

  41. Tice, R. R. et al. Single cell gel/comet assay: guidelines for in vitro and in vivo genetic toxicology testing. Environ Mol Mutagen 35:206–221 (2000).

    Article  PubMed  CAS  Google Scholar 

  42. Olive, P. L. & Banath, J. P. Detection of DNA doublestrand breaks through the cell cycle after exposure to X-rays, bleomycin, etoposide and 125IdUrd. Int J Radiat Biol 64:349–358 (1993).

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Kyung-Taek Rim.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Rim, KT., Kim, SJ., Han, JH. et al. Effects of carbon black to inflammation and oxidative DNA damages in mouse macrophages. Mol. Cell. Toxicol. 7, 415–423 (2011). https://doi.org/10.1007/s13273-011-0052-7

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s13273-011-0052-7

Keywords

Navigation