278 EFFECTS OF CHEMICALS
Ingestion of azoglucoside carcinogens with Cycad plants is
probably the chief cause of liver cancer in Guam. Cancer of
the esophagus in Zambians may be related to high nitrosa-
mine content of Kachasu spirits.
There is well documented evidence of occupationally
related cancers. These include bladder cancer in the rubber
and aniline dye industries, lung cancer in uranium workers,
nasal sinus cancer in wood workers, skin cancer in shale oil
workers, and lung cancer in asbestos workers.
The question of asbestos assumed great importance in
the 1980s. Once widely used in building, it was found to be
a serious health hazard. It is now felt that no exposure to
airborne particles is safe.
The Environmental Protection Agency estimates that
30,000,000 tons were used between 1900 and 1980. Asbestos
abatement has become big business. One estimate places the
value as high as $200 billion per year. Asbestos has been used
in more than 3000 products over the years. These include
duct work, exterior shingles, floor and ceiling tiles, plaster,
pipe lagging, cement, drywalls, theater curtains, brake lin-
ings, clutch facings and baby powder.
Asbestos occurs naturally as chrysotile, crocidolite,
amosite, anthophyllite, actinolite tremolite. The thin, tiny
fibers are not dangerous until disturbed. Then particles of a
certain size can lodge in the lungs. When the substance can
be crumbled under hand pressure—friable—it is considered
extremely dangerous. Building renovation and demolition
can release particles into the air. Water damage can loosen
the binding matrix.
In the 1930s asbestos inhalation was linked to asbesto-
sis and lung cancer. It was later shown that mesothelioma,
cancer of the lining of the lung, is caused by asbestos.
Gastrointestinal and larynx cancers have also been asso-
ciated with asbestos. In the 1970s the Department of
Health, Education and Welfare estimated that 8 1/2 to
11 million workers have been exposed occupationally in
the last 40 years. Asbestos related illnesses can take 20
to 40 years to develop. World War II shipyard workers
and prewar insulation workers comprise the majority of
afflicted persons. In one study a premature death rate of
48% was found among insulation workers of the 1940s.
Custodial personnel are also thought to be at high risk.
Studies have found that wives of asbestos workers may
well be in danger. It is thought that fibers on the husbands’
clothes are the reason.
Asbestos fibers suspended in water are not thought to
pose a hazard. However, steam pipe explosions have put
fibers into the air, causing whole blocks to be evacuated and
necessitating expensive cleanup operations.
Some claims that chrysotile, the asbestos form most com-
monly used in the US, may pose less danger than other vari-
eties. This position has not yet been validated scientifically.
The variety of asbestos versus fiber size as more important in
causing disease is the current debate topic. Some European
nations and Canada make distinctions among asbestos vari-
eties but, in the US, the EPA and OSHA treat all forms the
same for rule making purpose. The UK and Scandinavia
follow closely the US approach.Considerable uncertainty exists in risk assessment for
nonoccupational and environmental settings.
Action on asbestos abatement began in the schools.
Since the period for appearance of asbestos related diseases
can be as long as 20 to 40 years, it was felt that school-age
children were at particular risk. In 1982 the EPA Asbestos-
in-Schools required all public and private schools to inspect
for friable asbestos and report to parents and employees if
any were found. The rule did not require abatement. In 1984
the Asbestos Hazard Abatement Act gave funds to assist in
abatement. The Asbestos Hazard Emergency Response Act
(AHERA) of 1986 established rules and regulations concern-
ing identification, evaluation and control of asbestos contain-
ing materials in schools. It further required schools to identify
friable and nonfriable asbestos found and submit manage-
ment plans to state governors. Provisions were included for
periodic reinspections, even though inspections were already
made as a result of the notification rule of 1982. Of great
importance was that portion of the Act dealing with removal
situations and certification of workers. In the early days of
removal, when guidelines were not yet available, there were
too many “rip and skip” operators who performed such work
without regard for proper procedures or air quality monitor-
ing. In many cases there was probably more asbestos in the
air after the operation than there was before.
It is felt that asbestos abatement in private homes will
not be covered by formal regulations. However, it is esti-
mated that about 75,000 commercial and industrial buildings
contain friable asbestos.
There are four basic abatement approaches.1) Removal
2) Encapsulation, in which friable asbestos is bound
in a matrix.
3) Isolation of the asbestos containing area
4) RepairAll of these means have a place in dealing with the
asbestos problem and it is necessary to seek advice of a qual-
ified professional before undertaking any action. It should
be noted that, in the early days of abatement efforts, some
education departments allowed only removal. Encapsulation
was forbidden. In retrospect, this inflexible position might
be criticized.
The National Institute of Building Sciences (NIBS) has
taken the position that there is no single correct answer for
all situations.
Environmental carcinogens can be classed into two
categories, potent and weak. Potent carcinogens, such as
nitrosamines and aflatoxins, can induce cancers in animals
in very low concentrations. Isolation of these substances in
food has given rise to endeavors to relate food distribution
patterns with local cancer incidence.
Weak carcinogens, such as atmospheric pollutants,
some pesticides, and food additives, have effects much more
difficult to evaluate and thus may pose as great a threat as
the potent carcinogens because they are less likely to be
recognized as a significant epidemiological factor. Often,C005_004_r03.indd 278C005_004_r03.indd 278 11/18/2005 10:21:38 AM11/18/2005 10:21:38 AM