Ultrafine Particles


Characteristics of Ultrafine Particles

Transport and Fate in the Environment

Measuring Exposure

Exposure Pathways

Prevention or Control of Exposures

Human Health Effects of Ultrafine Particles


Absorption and Distribution


Risk Assessment

Works Cited

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Biomarkers of Disease

Inhalation of ultrafine particles are currently thought to effect two organ systems, the heart and the lungs. The lungs are effected by the inhalation of carbon ultrafine particles which and brought deeply into the lungs and are deposited in the alveolar sacs. Particles are deposited on to the epithelium of the lungs and are thought to be capable of also moving into the interstitial space between cells. The particles then induce an inflammatory response. This response can be measured by number of polymorphonuclear leukocytes (PMNs) in the pulmonary lavage fluid of rats. A dose response can be established not based on the amount of material retained in the lungs but on the surface area of the retained material (Oberdorster, 1996). This inflammatory response is then viewed as a cascade of events that adversely effect the health of the rat. In the Oberdorster model particle exposure leads to Alveolar Macrophage activation followed by acute inflammation and impaired clearance. This causes accelerated particle accumulation leading to chronic inflammation. This can cause fibrosis in the lung and also cause mutations followed by hyperplasia of the epithelial cells. This is followed by metaplasia and tumor formation. The final endpoint in rats may be carcinogenicity.

(Oberdorster, 1996)

This sequence of events involves the turning on of resident macrophages and the signaling to neutrophils, eosinophils, monocytes, and lymphocytes. This response can lead to the damage of DNA by reactive oxygen species due to release of signaling substances from inflammatory cells. Free radicals and oxidative stress then are able to effect gene regulation. Calcium signaling between macrophages is also stimulated. (Donaldson et al., 2003).

This sequence illustrates the idea the oxidative stress plays a major role in both mutagenesis of the DNA molecule and the factors such as nuclear factor-kappa b a transcription factor protein that is stimulated with ultrafine particle exposure.

There is also epidemiological data that supports the hypothesis that ultrafine particle can have heart effects. It is been hypothesized that the release of these chemical mediators may alter the delicate balance of the autonomic nervous system that effects cardiac rhythm (Ibald-Mulli et al., 2002).

The biomarkers of ultrafine particle inhalation are the cytokines and gene regulation factors that are increased with inflammatory response. These biomarkers are C-reactive protein, fibrinogen, and interleukin -6 (Frampton, 2001). The cascade of events has the potential to cause an increase in severity of asthma, chronic obstructive pulmonary disease, cardiovascular disease, and possibly cancer.

Organs effected by Ultrafine Particles:

  • Lung and respiratory system
  • Cardiovascular system
  • Gastrointestinal System
  • Generalized effect to the whole human body?

Effect on the respiratory system:

  • Deposition and disposition of ultrafine particles play a significant role in inducing effects in the lung.
  • The mass concentrations of urban ultrafine particles may be very low but deposition in the alveolar region is very high.
  • Deposited UF are not as readily phagocytized by alveolar macrophages.
  • The penetrate much more deeper and rapidly to the interstitial sites and may enter the blood circulations.
  • Less efficient phagocytosis by macrophages for UF.
  • Some epidemiological studies on PM show adverse effects only in compromised persons.

Diseased lung:

  • Respective animal model mimic specific human disorders.
  • One such model is inhalation of low doses of Endotoxin Lipopolysaccharide (LPS).
  • This is to induce and mimic the early stages of respiratory tract infections.

Modeling for the Diseased lung:

  • Statistical Analysis showed that ultrafine carbon particles have an inflammatory effect of their own.
  • Co exposure to LPS increases the response even more.
  • So the combined effects of ultrafine particles with LPS is significant as demonstrated by the graph.

Hypothesis to the cardiovascular injury:

  • Seaton et al have proposed that pollutant exposure induces a transient increase in blood coagulability as part of acute phase response.
  • Increase blood viscosity, increases blood coagulability could precipitate adverse cardiac events in people with coronary lesions.
  • Ultrafine particles have high propensity to penetrate the epithelium and reach interstitial sites.
  • This raises intriguing possibility that ultrafine particles could enter the systemic circulation and induce direct effect on the myocardium and coronary vasculature. Profound evidence is lacking.

Cardiovascular effects:

  • Injury to epithelial cells by reactive oxygen species and activation of regulatory factors.
  • Activation of vascular endothelium and circulating polymorph nuclear leukocytes.
  • Migration of inflammatory cells from blood to the tissue sites.
  • Up regulation of adhesion molecules on vascular endothelium.
  • Increase release of IL-6 and tissue factor by activated blood. Mononuclear cells initiate the CRP,amyloid A and fibrinogen.
  • The whole process make the person more prone to cardiovascular event.

Gastrointestinal Effects:

  • Recent data suggest that Ultrafine particulate matter is associated with Crohn’s disease.
  • Crohn’s disease is chronic relapsing inflammatory bowel disease.

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