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Diesel Exhaust

Organ Sites of Toxicity and Metabolic Considerations

Organ sites of toxicity and metabolic considerations were combined into one heading since this section will be a superficial survey of journal articles that examine both of these topics. Three articles (titles will be listed in text below; full citations will be in the reference section) will be highlighted and briefly summarized. A list of similar studies will be provided at the end of this section.

Sites of Toxicity:

From the journals surveyed and cited for this website, here is a list of the organ sites of toxicity. In general, there has been little research done directly exposing humans to diesel exhaust. Most of the research has been conducted on rats.
  • Upper and lower airway epithelial cells
  • Lung
  • Alveolar type II cells
  • Human heart
  • Reproductive system of rats
  • Ling, liver, and kidney of rats
  • Skin of mice

Journal Article #1:

“Diesel particles are taken up by alveolar type II tumor cells and alter cytokine secretion”

Diesel exhaust particles (DEP) are small enough that they can reach alveolar lung tissue. Here the DEPs interact with alveolar type II cells. This study was designed to determine whether DEPs alter the production of proinflammatory cytokines including interleukin-8 and granulocyte macrophage-colony-stimulating factor.

  • Cells from human epithelial cell line A-549 were incubated with DEPs or with inert particles.
  • Phagocytosis was monitored by an electron microscope and flow cytometry.
  • Both DEPs and inert particles were engulfed by alveolar type II cells.
  • DEPs were taken up by alveolar type II cells and altered cytokine production. Cytokines are proteins that control cell-to-cell communications and enhance the immune response.)
  • Inert particles did not.

Conclusion: Alveolar type II cells may be a target site for the adverse effects of DEPs.

Journal Article #2:

“Assessment of exposure to polycyclic aromatic hydrocarbons in police in Florence, Italy, through personal air sampling and biological monitoring of the urinary metabolite 1-hydroxypyrene.”

The purpose of this study was to assess the efficiency of urinary 1-hydroxypyrene as an indicator of exposure to polycyclic aromatic hydrocarbons(PAHs). Two groups of police officers that worked in Florence were studied. One group was highly exposed to high-density traffic emissions and the other group experienced low exposure.

  • Ambient levels of airborne PAHs were taken after each workshift using personal samplers. Eight hydrocarbons were selected as indicators of PAH pollution (such as dibenzo[a,h]anthracene, pyrene, benzo[a]anthracene, benzo[a]pyrene).
    Results: PAH concentrations were influenced both density of traffic and by season of the year. In winter, benzo{a}pyrene was twice as high in high-density traffic areas versus low-density areas. In summer, the concentrations were 6 times higher in the high-density areas.
  • Bio-monitoring was thru dosing of 1-hydroxypyrene (a pyrene metabolite) after each workshift.
    Results: The pyrene metabolite was found to be mostly influenced by traffic density, especially during the winter. It was found to be higher 199.2 ng/gm creatinine in high-density areas and 120.5ng/gm creatinine in the low-density traffic area.

Conclusion: The pyrene metabolite, 1-hydroxypyrene, can be a good bio-indicator of airborne PAH exposure in urban settings, particularily during the winter and in high-density traffic areas.

Journal #3:

“Short-term effects of particulate air pollution on cardiovascular diseases in eight European cities”

The purpose of this study was to see if there was an association between airborne particles and hospital admissions for cardiac causes. The eight cities included in this study were Barcelona, Birmingham, London, Milan, the Netherlands, Paris, Rome, and Stockholm.

  • All admissions were studied and stratified by age. Confounding by other pollutants was also examined.
  • The main results:
    *As PM (10) and black smoke levels increased by 10ug/m3 there was, respectively, a 0.5% and 1.1% increase for cardiac admissions of all ages; a 0.7% and 1.3% increase for cardiac admissions over 65 years of age; and, 0.8% and 1.1% for ischaemic heart disease over 65 years of age.

    *The effect of PM (10) when controlling for SO2 and ozone was little changed, but was reduced when controlled for CO and eliminated when controlled for NO2.

    *The effect of black smoke remained essentially unchanged when controlling for CO and somewhat reduced when controlling for NO2.

Conclusion: The authors conclude these effects of particulate air pollution and their association with increased cardiac admissions suggests the primary effect is probably mostly attributable to diesel exhaust.

These are just three studies demonstrating examples of organ sites of toxicity and metabolic pathways of diesel fuel. I located many more and selected a few that I will list below. As I mentioned above, it is difficult to establish exposure to diesel exhaust as it is everywhere. Therefore, it is also difficult to understand its effects on human health, as will be addressed in a later section of this website.

References for this section:

Article #1:
Juvin P, Fournier T, Boland S, et al: Diesel particles are taken up by alveolar type II tumor cells and alter cytokines secretion. Arch Environ Health 57(1):53-60, 2002.

Article #2:
Perico A, Gottardi M, Boddi V, et al: Assessment of exposure to polycyclic aromatic hydrocarbons in police in Florence, Italy, through personal air sampling and biological monitoring of the urinary metabolite 1-hydroxypyrene. Arch Environ Health 56(6):506-12, 2001.

Article #3:
Le Tertre A, Medina S, Samoli E, et al: Short-term effects of particulate air pollution on cardiovascular disease in eight European cities. J Epidemiol Community Health 56(10):773-9, 2002.

Additional Journal Articles:

Pandya RJ, Solomon G, Kinner A, Balmes JR: Diesel exhaust and asthma: hypotheses and molecular mechanisms of action. Environ Health Perspect 110 Suppl 1:
103-12, 2002.

Hatanaka N, Yamazaki H, Kizu, R et al: Induction of cytochrome P450 1B1 in lung, liver and kidney of rats exposed to diesel exhaust. Carcinogenesis 22(12):2033-2038, 2001.

Van Winkle LS, Gunderson AD, Shimizu JA, et al: Gender differences in naphthalene metabolism and naphthalene-induced acute lung injury. Am J Physiol Lung Cell Mol Physiol 282(5):L1122-34, 2002.

Seidel A, Dahmann D, Krekelerh, Jacob J: Biomonitoring of polycyclic aromatic compounds in the urine of mining workers occupationally exposed to diesel exhaust. Int J Hyg Environ Health 204(5-6):333-8, 2002.

Bonvallot V, Baeza-Squiban A, Baulig a, et al: Organic Compounds from Diesel Exhaust Particles Elicit a Proinflammatory Response in Human Airway Epithelial Cells and Induce Cytochrome p450 1A1 Expression. Am J Respir Cell Mol Biol 25(4):515-521, 2001.

Tsukue N, Tsubone H, Suzuki AK: Diesel exhaust affects the abnormal delivery in pregnant mice and the growth of their young. Inhal Toxicol 14(6):635-51, 2002.

Sato H, Sone H, Sagai M, et al: Increase in mutation frequency in lung of Big BlueR rat by exposure to diesel exhaust. Carcinogenesis 21(4):653-661, 2000.

Hatanaka N, Yamazaki H, Oda Y, et al: Metabolic activation of carcinogenic 1-nitropyrene by human cytochrome P450 1B1 in Salmonella typhimurium strain expressing an O-acetyltransferase in SOS/umu assay. Mutat Res 497(1-2):223-33, 2001.

Washburn BS, Goth-Goldstein R: Validation of the Use of 1-hydroxypyrene as a Biomarker for Exposure to Polycyclic Aromatic Hydrocarbons: The Role of Genetic Polymorphisms. As retrieved on November 20, 2002 from http://www-esd.lbl.gov/CEB/BEST/ann_rpt99/ECO_4story.html.

Knebel JW, Ritter D, Aufderheide M: Exposure of human lung cells to native diesel motor exhaust—development of an optimized in vitro test strategy. Toxicol In Vitro 16(2):185-92, 2002.

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