Article thumbnail
Location of Repository

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

By W J Catallo, C H Kennedy, W Henk, S A Barker, S C Grace and A Penn


Adverse health effects of airborne toxicants, especially small respirable particles and their associated adsorbed chemicals, are of growing concern to health professionals, governmental agencies, and the general public. Areas rich in petrochemical processing facilities (e.g., eastern Texas and southern California) chronically have poor air quality. Atmospheric releases of products of incomplete combustion (e.g., soot) from these facilities are not subject to rigorous regulatory enforcement. Although soot can include respirable particles and carcinogens, the toxicologic and epidemiologic consequences of exposure to environmentally relevant complex soots have not been well investigated. Here we continue our physico-chemical analysis of butadiene soot and report effects of exposure to this soot on putative targets, normal human bronchial epithelial (NHBE) cells. We examined organic extracts of butadiene soot by gas chromatography-mass spectrometry (GC-MS), probe distillation MS, and liquid chromatography (LC)-MS-MS. Hundreds of aromatic hydrocarbons and polycyclic aromatic hydrocarbons with molecular mass as high as 1,000 atomic mass units were detected, including known and suspected human carcinogens (e.g., benzo(a)pyrene). Butadiene soot particles also had strong, solid-state free-radical character in electron spin resonance analysis. Spin-trapping studies indicated that fresh butadiene soot in a buffered aqueous solution containing dimethylsulfoxide (DMSO) oxidized the DMSO, leading to CH(3)* radical formation. Butadiene soot DMSO extract (BSDE)-exposed NHBE cells displayed extranuclear fluorescence within 4 hr of exposure. BSDE was cytotoxic to > 20% of the cells at 72 hr. Morphologic alterations, including cell swelling and membrane blebbing, were apparent within 24 hr of exposure. These alterations are characteristic of oncosis, an ischemia-induced form of cell death. BSDE treatment also produced significant genotoxicity, as indicated by binucleated cell formation. The combination of moderate cytotoxicity and genotoxicity, as occurred here, can be pro-carcinogenic

Topics: Research Article
Year: 2001
OAI identifier:
Provided by: PubMed Central

Suggested articles


  1. (1994). A kinetic approach to the selection of a sensitive spin trapping system for the detection of hydroxyl radical.
  2. (1998). Air pollution particles induce IL-6 gene expression in human airway epithelial cells via NF-kB activation.
  3. (1993). antioxidants and the degenerative diseases of aging.
  4. (1995). Apoptosis, oncosis and necrosis.
  5. (1998). Autofluorescence of living cells.
  6. (1987). Binucleate cells in the Ehrlich ascites tumor. Action of 5-fluorouracil.
  7. (1997). Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent.
  8. (1984). Cytotoxicity of chemical carcinogens towards human bronchial epithelial cells evaluated in a clonal assay.
  9. (2000). Diesel exhaust particles activate p38 MAP kinase to produce interleukin-8 and RANTES by human bronchial epithelial cells and N-acetylcysteine attenuates p38 MAP kinase activation.
  10. (1999). Diesel exhaust particles are taken up by human airway epithelial cells in vitro and alter cytokine production.
  11. (1997). Environmental Protection Agency. National ambient air quality standards for particulate matter: final rule.
  12. (1968). Enzymatic changes in fluorescent alveolar macrophages of the lungs of cigarette smokers.
  13. (1986). G2 arrest, binucleation and single-parameter DNA flow cytometric analysis.
  14. (1996). Induction of genomic instability in normal human bronchial epithelial cells by 238Pu alpha particles.
  15. (1990). Induction of micronucleated and binucleate cells in Chinese hamster ovary (CHO) cells by cis-diaminedichloroplatinum (II): a morphological and morphometric study.
  16. (1999). Louisiana Office of Public Health.
  17. (1998). Measurement of C24H14 polycyclic aromatic hydrocarbons associated with a size-segregated urban aerosol.
  18. (2000). Mechanisms of GM-CSF increase by diesel exhaust particles in human airway epithelial cells.
  19. (1986). Metabolism of benzo(a)pyrene in monolayer cultures of human bronchial epithelial cells from a series of donors.
  20. (2001). Pollution Locator-Criteria Air Pollutants in 1998, Rank Counties by Health Risks. Environmental Defense Fund:
  21. (1998). Polycyclic aromatic hydrocarbons in combustion residues from 1,3-butadiene.
  22. (2000). Quantification of polycyclic aromatic hydrocarbons in the NIST standard reference material (SRM1649A) urban dust using thermal desorption GC/MS.
  23. (1998). Rodent models of cardiopulmonary disease: their potential applicability in studies of air pollutant susceptibility. Environ Health Perspec 106(suppl 1):111–130
  24. (1998). The effect of diesel exhaust particles on cell function and release of inflammatory mediators from human bronchial epithelial cells in vitro.
  25. (1942). The origin of binucleate and large mononucleate cells in the liver of the rat. Anat Rec
  26. Tissues and Disease: Principles of General Pathology.
  27. (2001). Unpublished data. Articles • Cyto- and genotoxicity of butadiene soot
  28. (1995). Vande Woude G. Mos overexpression in Swiss 3T3 cells induces meiotic-like alterations of the mitotic spindle.

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.