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by sharp, needle-like fibers of diameter greater than 4-5 μm. The breakage of stiff carbon fibers into smaller fragments
and rubbing against exposed skin may increase severity of the exposure and infection of the affected area.
Such irritation effects are generally not permanent. However, the inhalation exposure from fibers poses the greatest
potential for adverse health effects.
Asbestos is the most widely studied fiber for its health impact on humans. Extensive epidemiological data combined
with animal studies have been done to study the pathological impact of this silica-based fiber [10-14]. Inhalation of
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asbestos fibers in the lungs initiates an inflammatory response in that region [11]. The lung’s efforts to repair this
damage manifests as progressive scarring in the lung walls. This interstitial scarring effect caused by the deposition
of fibers is called pulmonary fibrosis, a condition in which scar tissue forms in the connective tissues that support the
alveoli in the lungs. Scarring can be a reaction to a large number of diseases and conditions. The induction of
fibrosis retards the process of fiber clearance resulting in longer fiber retention. Extended chronic exposure to
asbestos is known to result in bronchogenic carcinoma or lung cancer, and may also lead to mesothelioma - a
cancer of the pleural cells lining the lungs. The causal relationship between asbestos exposure and onset of lung
cancer has been demonstrated in numerous epidemiological studies [12-14].
The framework of information on asbestos and fiberglass has been applied for the study of health effects from new,
organic fibers such as kevlar and carbon and to delineate the contributing factors in fiber toxicity. Using the animal
models in studies with asbestos, researchers have identified the important characteristics that describe a given
material’s fiber toxicity. By definition, a particle is considered a fiber if it has a length-to-diameter ratio (L/D) of greater
than 3:1.
It appears that fiber size and geometry and its durability are the most important factors in fiber toxicity. Fiber dimension
determines whether the fiber can be inhaled deep into the lungs that lie below the larynx, tracheal conducting
airways which constitute the upper respiratory tract. Only those fibers with dimensions smaller than the bronchial
airways’ size can penetrate the deep lung (alveolar) region. Generally, fibers larger than 10 microns (μm) in diameter
can not penetrate deep enough into the alveoli to cause disease [12].
However, the respirability of fibers is not entirely governed by their physical dimensions. The respirability or the
extent fibers are deposited in the deep pulmonary region and the alveoli is primarily determined by their aerodynamic
equivalent diameter (D). The parameter D reflects the way a particle behaves when airborne. For a fiber, D
refers to the diameter of an equivalent spherical particle having the same terminal velocity as the fiber. The number
of deposited fibers increase significantly when D lies between 2-3 μm and falls off to 0 when the D is between 7and
10 μm. Long and thin, aerodynamic fibers line up straight in an airstream and are more likely to penetrate deeper
into the lungs. Studies on size analysis of fibers in human lungs exposed to asbestos fibers have shown that the
upper limits of respirable fibers are either 3.5 μm in diameter or 200 μm in length [10].
The aerodynamic character of the fibers (D) also determines the manner in which the fibers are deposited in the lung
tissue. There are five different modes of fiber deposition in the respiratory airways. In the human lung, the airways
region consists of a series of branching airways called bronchi and bronchioles that become progressively smaller.
The multiple division of the bronchi greatly increases the total cross-sectional area of the airways available for fiber
deposition. Fibers aligned vertical to the airway flow stream are primarily deposited by interception at each successive
bifurcation. The probability of interception increases when the fiber length is greater than 10 μm. The larger
airway bifurcations are the primary sites of fiber deposition and lung cancer in humans from mineral fibers [14]. In
smaller airways where the airflow velocity becomes very small, sedimentation is the primary mode of fiber deposition.
Three other mechanisms of fiber loading in lungs are interception, diffusion, and electrostatic deposition. The
durability of fibers inside the body depends on the response of the local cell tissues in the lungs. Warheit [13] has
shown that fibers can be cleared from the pulmonary region via dissolution in lung fluids or through an internal,
pulmonary self-defense mechanism. Cells known as alveolar macrophages that are present on the outer walls of
　
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