The detrimental affect on the health of people exposed to asbestos fibers has been well documented. Many studies have been conducted on laboratory animals and cell cultures to investigate the specific mechanism by which asbestos initiates or promotes disease.
Like any hazardous material, asbestos must first travel to the site where it can cause disease. The primary route of exposure is through the air. There have been reports of asbestos warts due to asbestos fibres becoming imbedded in the skin; however, this appears to be a rare occurrence. There is also some concern that excessive exposure through ingestion, such as in drinking water, may lead to an increased rate of disease. The greatest concern is exposure through inhalation.
Since the primary route of exposure is through inhalation, it is important to
review the respiratory system and gain a brief understanding of its defense
mechanisms. As air is inhailed through the nose or mouth it must pass across
membranes that are covered with a sticky mucous. Large particles of dust and
fibers, which are often visible to the naked eye, are trapped at this point and
and prevented from going further into the respiratory system. Smaller particles
will be carried along into the air passages, including the trachea, bronchi,
and bronchioles.
The air passageways have numerous turns ans branches
making it a turbulent trip for dust particles and fibres. These passageways are
also lined with special cells that have hairlike projections into the cavities of
the air passageways. These "cilia" are hair-like projections and beat upward in
a wave-like fashion. They are also covered with a sticky mucous which forms a layer
across the surface of the passageways. When particles of dust impact this sticky
coating, they dhere and are propelled upeard by the cilia. Eventually the mucus
layer with dust imbedded in it is carried out of the lung and into the back of the
mouth where it is expelled or swallowed.
The smallest dust particles may travel through the air passageways and be deposited
into terminal air sacs called "alveoli". the exchange of oxygen and carbon
dioxide takes place within the alveoli. With the incoming air also comes dust,
pollen, and other particles such as asbestos fibres.
When dust and asbestos fibres are deposited inside the alveoli, they thrgger a
response. Large cells, called "macrophages" move across the surface of the air sac
and engulf the invading particle. When the particle is a mineral, such as silica
(quartz) or asbestos, it cannot digest it. Eventually, layer upon layer is built
up to form scar tissue. This buildup of scar tissue in the lungs leads to a disease
called "asbestosis".
Abestosis, or scarring of the lungs was first ddescribed in England in 1907.
It was the first disease recognized as linked to asbestos fiber exposure. The
alveolar wall thickening reduces the ability of the lung to expand and contract
normally. This results in a retracted or restricted lung with an inability to
exchange oxygen and, to a lesser degree, carbon dioxide in a normal manner.
The buildup of scar tissue in the lung occurs gradually over many years. A
worker exposed to high concentrations of asbestos may not experience any overt
symptoms for 10 to 30 years after the start of the exposure.