Frustrated phagocytes and the fibre paradigm

These were a couple of phrases from Rosemary Gibson’s presentation during the nanotechnology workshop during the recent BOHS Conference.

The fibre paradigm sets out the basis for the harmful effects caused by resistant fibres such as asbestos.  It states that fibres will damage the lung if they are

  • thin enough to enter the lungs
  • longer than the phagocytes that clear particles from the lungs
  • resilient and non-biosoluble, so that they remain in the lung

The long thin fibres that deposit and remain in the lung can’t be engulfed by the phagocytes, so that the ends of the fibre protrude from the cell.  The phagocye is said to be “frustrated”

t012365a-macrophages-on-an-asbestos-fibre1 (1)

This results in the release of chemicals that cause damage to the lung tissue leading to inflammation and, subsequently, to other damage, including the deposition of scar tissue (fibrosis).

Potentially any fibre which is thin enough to travel down to the alveoli and too long for the phagocyles to deal with it effectively could cause this to occur.  However, fibres that are biosoluble break down and can be cleared from the lung before significant damage can occur. So some materials, such as glass fibre, are deliberately formulated to dissolve in the body. Other, more resilient, fibres such as asbestos, remain in the lung long enough to allow the process to occur.

Recent research has suggested that some of the new engineered nano-materials, such as long carbon nanotubes, can cause effects similar to asbestos as their structure and dimensions means that they conform to the “fibre paradigm”

1743-8977-7-5-2
Source: Donaldson et al. Particle and Fibre Toxicology 2010 7:5

There’s a good summary of the fibre paradigm in an open access paper by Donaldson et al. published in the journal Particle and Fibre Technology last year, which is available on the web here.

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