|Hazardous Materials Assessment, Inc *
1933 Davis Street, Suite 303 * San Leandro, CA *
94577 (510) 638-4801
|The Respiratory System
|Every cell in the body needs a constant
supply of oxygen. The respiratory system meets this need by
bringing oxygen to the bloodstream, which delivers it to
each cell and carries away carbon dioxide. The lungs are the
focal point of the respiratory system, which also includes
the respiratory tract, the channel by which air flows into
and out of the lungs. The drawing above is an illustration
of the respiratory system. Inhaled air passes through the
nose, where moisture and tiny hairs filter dust. It then
passes down the throat where air is also humidified. Air
continues into the trachea. Just above the heart, the
trachea divides into two bronchi. Each bronchus leads into a
lung where it subdivides into bronchioles and smaller air
tubes - giving the appearance of an upside-down tree. The
tiniest tubes end in globular air sacs called alveoli.
The actual exchange of gases - respiration - takes place in the alveoli. There, blood vessels only one cell thick allow oxygen and carbon dioxide to trade places. The carbon dioxide is exhaled back up the respiratory tract. The blood picks up fresh oxygen and transports it throughout the body.
The lungs, cone-shaped, balloon-like, elasticized tissue, are located on either side of the chest. Each lung is encased by a double layer of membrane, or pleura. One layer is attached to the lung, the other to the rib cage. Space and fluid between the two layers enable the lungs to expand and contract in the chest cavity without friction. When we breathe in, the diaphragm stretches out flat and muscles between the ribs contract with it, pulling the ribs up and out. This expands the chest cavity creating a vacuum between the linings that expands the lungs and sucks in air. When breathing out, the diaphragm and rib cage muscles relax,the ribs fall in and down, and the lungs contract and push out the carbon dioxide and unused oxygen.
The respiratory system is sensitive to bacteria, viruses, and many airborne particles that can be inhaled. Reactions to these irritants can disrupt the functioning of the system, resulting in many ailments including such things as: the common cold, hay fever, sinusitis, sore throat, acute or chronic bronchitis, emphysema, and lung cancer.
Natural Filters. The body has several mechanisms by which it filters the air it breathes. The tiny hairs in the nose filter out dust and airborne particles. Like the nose, the trachea and the bronchi are lined with small fine "hairs" called cilia. Together with mucous secreted by cells lining the airways, cilia trap particles and help prevent respiratory infections. the cilia beat in an upward direction sweeping foreign particles up to the back of the mouth where they are expelled or swallowed. Viruses and bacteria are also attacked by enzymes called lysozymes in the mucous cells. Microbes that slip through are usually handled by white blood cells called phagocytes that envolope and eat these invaders in the lung.
Cigarette smoking temporarily paralyzes the cilia. If smoking continues long enough, the cilia wither and die. They are never replaced. The efficiency of the cilia is replaced by the smoker's inefficient cough which attempts to rid the respiratory tract of foreign particles and excess mucus.
Dirty, contaminated air presents the greatest challenge to the respiratory system. Some of the particles entering the airways reach the alveoli. When this occurs, white blood cells called macrophages attempt to engulf and digest the particles. In the case of asbestos, we are dealing with a mineral fiber, as a substance which macrophages can often not successfully attack. As a means of secondary defense, the macrophages deposit a coating on the fibers which are then deposited in the smaller passages. Here they clog and actually scar the tissues. The walls of the alveoli lose their elasticity and useful function in respiration. Coated asbestos fibers ("asbestos bodies") are often seen at autopsy.
|Asbestos Related Diseases
Note: all have long latency periods, from 15 to 40 years
Asbestos related diseases are DOSE-RESPONSE related
[that is, the greater the exposure, and the longer the time of exposure, the greater the risk]
Asbestos exposure can cause a number of disabling and fatal diseases. The principal rout of exposure is by inhalation through the nose and mouth. Asbestos, traditionally valued for it's indestructibility, is especially resistant to the internal defenses of the human body. Once lodged inside the lungs, most fibers will not break up or dissolve, and they cannot be neutralized or removed.
Asbestosis is a disease which is characterized by pulmonary fibrosis, a progressive scarring of the lungs caused by the accumulation of asbestos fibers. Asbestosis is associated exclusively with chronic, occupational exposure. The build up of scar tissue interferes with oxygen uptake through the lungs and can lead to respiratory and heart failure. Often, asbestosis is a progressive disease, even in the absence of continued exposure. Symptoms include shortness of breath, cough, fatigue, and vague feelings of sickness. When the fibrosis worsens, shortness of breath occurs even at rest.
Pleural plaques and pleural calcification are markers of exposure and may develop 10 to 20 years after initial exposure. Plaques are opaque patches visible on chest x-rays that consist of dense strands of connective tissue surrounded by cells. All commercial types of asbestos induce plaques. Plaques can occur even when fibrosis is absent and do not seem to reflect the severity of pulmonary disease.
Of all the diseases related to asbestos exposure, lung cancer has been responsible for over half of the excess deaths resulting from occupational exposure. Although tissues and cells react to the presence of asbestos immediately, detectable symptoms take years, or more often decades, to manifest themselves. Asbestos-induced lung cancer may not show up on x-rays for twenty years or more after the exposure began. This delay between exposure and onset is referred to as the "latency period". Even in cases of prolonged heavy exposure, abnormalities commonly appear on x-rays only after ten or more years following exposure.
Asbestos as a Co-Factor: Other substances appear to cooperate with asbestos to multiply the risk of lung cancer. Asbestos exposure in combination with cigarette smoking can multiply the risk of developing lung cancer as much as ninety times over the risk to a non-smoker with no history of exposure to asbestos.
Mesothelioma, a malignant nodular type cancer of the membranes which line the lung cavity, is another disease related to asbestos exposure. Malignant mesotheliomas of these membranes (the pleura and the peritoneum) are extremely rare in persons with no history of asbestos exposure, but may account for 10% to 18% of excess deaths in workers exposed to asbestos. Generally, a latency period of at least 25 to 30 years is required in order to observe mesotheliomas, and some victims have had a latency period of forty years since their initial exposure to asbestos. This form of cancer is incurable and is usually fatal within a year after diagnosis. Mesothelioma has been associated with short term, incidental exposure, but here is no evidence of a relationship between cigarette smoking and mesothelioma risk.
Additional Resource for Mesothelioma information:
Mesothelioma Cancer Center
Asbestos.com has the most comprehensive information on asbestos exposure and mesothelioma. The Mesothelioma Center is an up-to-date resource on mesothelioma treatments and a mesothelioma prognosis.
Some health studies have observed increases in esophageal, stomach, colo-rectal, kidney, and possibly ovarian cancers as well as cancers in the nose and throat from exposure to asbestos. While the magnitude of increased cancer risk for these sites is not as great as for lung cancer and mesothelioma, the increased risk may be of considerable importance because of the high background rates of some of these tumors in the general population. By way of example, a 50% increase of risk in a common cancer such as colo-rectal cancer results in many more deaths than a similar 50% increase in a rare cancer.
Death Rates vs. Fiber Exposure
The Occupational Safety and health Administration has declared that they are "aware of no instances in which exposure to a toxic substance has more clearly demonstrated detrimental health effects on humans than has asbestos exposure." By one count over 21 million men and women were occupationally exposed to asbestos between 1940 and 1980 alone.
Risk of asbestos related illness is Dose-Response related. That is, the greater the amount of exposure and the longer the time of exposure, the greater the risk of asbestos related cancers.
The following chart depicts the number of deaths per 1000 workers during a working career based upon the airborne levels of asbestos fiber to which the workers were exposed.
|As a matter of comparative interest, the
original OSHA permissible exposure level from 1972 was 5.0
f/cc (which is clear off of the above chart), was then
reduced to 2.0 f/cc in the mid '70's (64 deaths per 1000).
Then in 1986 OHSA reduced the PEL from 2.0 to 0.2 f/cc and
then recently to 0.1 f/cc. Even at the present PEL of 0.1
f/cc there are an estimated 3.2 to 3.7 asbestos related
deaths per 1000 workers expected. Present EPA "clearance"
levels following abatement work are 0.01 f/cc, 1/10th of the
OSHA permissible exposure level.
It may be noted in the above chart that while the death rate decreases with reduced exposure, there is no level at which the death rate reaches zero (0.0).
Similarly, asbestos is present in the air in our atmosphere. There is no "zero" exposure. This is partly due to the fact that asbestos is a naturally occurring mineral, and partly due to man's usage (and disturbance) of the material.
Although the initial focus of inquiry was on the exposures associated with the manufacture of asbestos products (estimated over 3000 such building material products), after World War II the focus shifted to include exposure associated with product use. Research on short term occupational exposure and on workers with low cumulative exposures has confirmed that excess mortality can be expected at low occupational exposure levels.
In 1980, a National Institute of Occupational Safety and Health (NIOSH)/OSHA work group concluded that there was no level of exposure to asbestos below which clinical effects did not occur. They recommended a Permissible Exposure Limit (PEL) based on the lowest measurable airborne fiber level, 0.01 f/cc. EPA has accepted this conclusion and recommends that 0.01 fibers per cubic centimeter be used to define the successful completion of asbestos abatement work. The risks associated with low levels of cumulative exposure are not well-established, and considerable debate surrounds the issue.
There are many factors which complicate studies of non-occupational exposure, including a lack of data on incidental exposures which may occur, lack of data on non-occupational levels (f/cc) of exposure, and the lack of a control group (zero, or at least known "near zero" exposure). Confounding variables such as migration into and from communities and multiple exposures to other toxic chemicals and carcinogens consistently frustrate attempts to generalize about the risk of low level exposure.
At low levels of exposure, for example, asbestos may serve only as a "cancer promoter", acting as a co-factor along with other substances and carcinogens to elevate the risk of developing cancer above normal. This is clearly the case with asbestos and cigarette smoke, but other chemicals and agents may react in a similar way to the presence of asbestos fibers.
Because asbestos fibers do accumulate in the lungs, and because the risk of developing disease does increase as the cumulative dose increases, exposure to asbestos should be controlled or eliminated whenever possible. Even a relatively minor source of airborne asbestos fibers should be abated, avoided, or minimized in order to maintain the cumulative dose at a minimum.
In order to prevent outbreaks of asbestos disease in the future, asbestos exposure must be controlled today. When asbestos materials are managed calmly and deliberately and handled properly when removed (or abated) the potential for non-occupational exposure can be significantly reduced.
Detectable levels of asbestos fibers in the ambient air are a fact of life. Studies have reported typical levels of 0.005 f/cc in urban or metropolitan areas. HMA's own testing and air level measurements have supported these studies. For the major urban areas here in the San Francisco Bay Area, such as San Francisco and Oakland, levels of 0.004 f/cc to 0.005 f/cc are common. Suburban areas are typically lower, usually in the 0.003 f/cc to 0.004 f/cc range. A few years ago, HMA had occasion to conduct air testing 13 miles out in the Pacific Ocean off the California coast, and found levels of 0.002 f/cc (TEM), lower than urban areas but not zero.
Principal sources of ambient asbestos are typically listed in the text books as "quarrying,mining and milling, and manufacturing". Here in the USA, most (but not all) manufacturing of asbestos-containing products has ceased. For example, many automobile and truck brake shoes and clutch linings were manufactured with asbestos, and many such vehicles are on the roadways today. Friction applied during braking (and clutch use) releases fibers.
Many buildings were constructed with Asbestos Containing Materials. The present OSHA standards reflect that buildings constructed prior to January 1, 1981 are presumed to be constructed with asbestos-containing building materials (PACM). Again, proper maintenance and management of the asbestos containing materials can significantly reduce potentials for exposures.