Backgrounder on the Health Effects of Chrysotile and Other Asbestos Fibres
(Prepared by Health Canada)
Most experts and review panels on asbestos agree that the risk of lung cancer
and mesothelioma, resulting from environmental exposure to asbestos is extremely
low, and would be difficult to quantify. The risk of asbestosis is considered
to be so low as to be negligible and "virtually zero" (IPCS, 1986).
The health effects of chrysotile and other forms of asbestos are predominantly
based on occupational exposure in an industrial setting. However, it should
be noted, that there are exceptions to the industrial scenario. For instance,
there are reported incidences of mesothelioma and lung cancer in spouses of
asbestos miners, attributed to exposure from the long-term washing of contaminated
clothing (ATSDR 2001). It is also widely accepted that most of the diseases,
attributable to asbestos exposure, observed today, are a result of relatively
heavy exposure via the inhalation route, during a time when asbestos was not
controlled as rigidly as it is today. The inhalation route is considered to
be the main exposure route of concern, for manifestation of asbestos related
diseases. In general, most of the health effects of asbestos, do not manifest
themselves until 20-30 years after exposure. For the amphibole fibres, even
after exposure has terminated, the risk can remain high for many years for the
development of asbestos related diseases.
The following is a general summary of the health effects of asbestos. It is
not exhaustive, because the literature on just this aspect of chysotile and
the amphibole asbestos fibres, is very extensive. Asbestos exposure via inhalation
is associated with pleural plaques, pleural thickening, asbestosis, lung cancer
and mesothelioma. The most serious endpoints such as asbestosis and cancer will
be discussed.
Asbestosis: Asbestosis was the first disease attributed to asbestos
exposure and officially recognized for workers compensation. All forms of asbestos
can cause asbestosis. It is a diffuse interstitial fibrosis of the lungs resulting
from exposure to asbestos fibres. Breathlessness, a major symptom, is caused
by the scarring and subsequent reduction in elasticity and function of the lung.
Epidemiological data indicate that the incidence rate increases and becomes
more severe with increasing dust levels and duration of exposure. Asbestosis
can progress many years after the termination of exposure. There is some evidence
indicating that chrysotile is less potent than amphiboles in causing asbestosis.
Fibre size may be a factor in influencing this hazard. For instance, the rate
of radiologic asbestosis in Quebec textile plant workers was greater than that
observed for miners and millers in Quebec. There is a difference in fibre size
between these industries. Asbestosis related changes are common following prolonged
exposure to concentrations greater than 25 fibres/cm3
Lung Cancer: Most of the evidence for the role of asbestos in human
lung cancer originate from studies of the cause of death of occupationally exposed
workers. A substantial proportion of cases were reported for insulation workers
in the United States and Canada. This group of workers have been studied extensively.
Lung cancer rates were elevated also in household members of asbestos workers,
supposedly due to exposure following the carrying home of fibres on work clothes.
Animal and occupational studies combined suggest that all forms of asbestos
cause lung cancer. Lung cancers attributed to asbestos appear to form in the
inferior lobes of the lungs more frequently, than lung cancers derived from
other causes. There is a considerable latency period, from 10 to 40 years in
humans, from first exposure. Combined exposure to asbestos and cigarette smoke
synergistically increases the risk of lung cancer.
Studies suggest that not all asbestos fibres are equally likely to lead to
lung cancer, although there is some dispute in this area. In the scientific
literature, many scientists believe that chrysotile is less potent than the
amphiboles for inducing lung cancer. Some factors that were attributed to this
difference are differences in mineral types with respect to surface properties
such as surface charge density, iron content, and durability, but most data
indicates that fibre thickness and length may be the most important factors
in carcinogenesis. The type of industrial process may affect the incidence of
lung cancer, with studies indicating that workers in the textile industry are
at higher risk. For instance, with chrysotile, the relative risks for lung cancer
is considered to be 10-30 times greater for workers in the textile manufacturing
sector compared to workers in the milling and mining sectors. This effect was
observed for mesothelioma as well.
Mesothelioma: Mesotheliomas are tumours that arise from the thin membranes
that line the chest (thoracic) and abdominal cavities and surround the internal
organs. Mesothelioma is an effect specific to asbestos exposure with 50 % of
cases reported attributable to professional use of asbestos. This effect of
asbestos exposure was identified in 1960 in South Africa,, and was recognised
by the scientific community shortly afterwards. In a study involving insulation
workers in which 2,227 total deaths were analysed, there were 175 deaths attributable
to mesothelioma. In the general population, published results indicate that
approximately 3 males and 1 female die due to mesothelioma per million people
per year, in North America. Although there is some variation from year to year,
it is clear that mesothelioma is an extremely rare disease in the general population.
Mesotheliomas are difficult to diagnose, therefore death certificate information
may lead to an underestimate or overestimate of the true incidence of this disease.
The risk of mesothelioma appears to be more elevated with crocidolite and tremolite
than with amosite. The risk of mesothelioma is lower with chrysotile, than with
amphibole fibres. These observations have been repeated in several studies.
The degree or importance of the risk differential between fibre types is an
area of considerable debate and there are several theories that have evolved.
One theory is that amphibole fibres stay in the lungs longer than chrysotile
fibres. There is major debate over the degree of risk attributable to chrysotile,
but for a comparison of chrysotile and crocidolite, studies have indicated that
crocidolite is significantly more potent in elevating the risk of mesothelioma.
For mesothelioma, there does not appear to be an interaction between asbestos
and tobacco smoking, nor an independent risk of mesothelioma attributable to
tobacco smoking.
The latency period of mesothelioma is significantly longer than for lung cance,
usually between 25 and 50 years. A median latency period of 32 years has been
estimated in a review of 1,105 cases of malignant mesotheliomas.
Animal studies, using rats, indicate the inhalation exposure to all forms of
asbestos produces mesotheliomas.
An Australia Mesothelioma Surveillance (AMS) Program was established in 1980
to monitor the incidence of the disease and to explore occupational and other
associations with mesothelioma. This program has indicated that mesothelioma
is elevated in the following industries; repair and maintenance of asbestos
materials (13 %), shipbuilding (3%), asbestos cement production (4%), railways
(3%), power stations (3%), boilermaking (3%), mining (Wittenoom) (5%), wharf
labour (2%), para-occupational, hobby, environmental (4%), carpentry (4%), building
(6%), navy (3%), plumbing (2%), brake linings (manufacture/repair) (2%), and
combinations of the above (12%). As to asbestos exposure, this program indicated
that the pattern of exposure shifted away from the older traditional industries,
towards product, domestic, and environmental exposure.
Other effects: Cancers of the larynx, oropharynx, esophagus, stomach,
colon, kidney, and upper and lower digestive tract have been reported in some
studies. The cancers of the larynx and esophagus are strongly associated with
work related exposure to asbestos. For chrysotile exposed cohorts of workers,
there appears to be no consistent evidence of excess mortality from stomach
or colorectal cancer. A significant excess of stomach cancer was observed in
a study of Quebec chrysotile miners and millers, but it is suspected that possible
confounding factors such as diet, infections, or other risk factors were not
addressed. Cancers other than lung cancer or mesothelioma, are less extensively
studied in government surveys due to their much lower frequency. Cardiovascular
disease related to heavy asbestos exposure has been documented (Leman et
al.1980), but has not been considered in any risk assessment on asbestos
health effects.
Effects of asbestos exposure in animals: Studies using animals such
as mice, rats, hamsters, and rabbits provide similar results to observations
made in epidemiological studies. For instance, all types of commercial asbestos
fibres that have been tested are carcinogenic in these animals, producing mesotheliomas
and lung cancer after inhalation exposure and after administration intrapleurally,
intratracheally, or intraperitoneally. Animal studies have indicated that chrysotile
may affect the immune system (Rosenthal et al.1998).
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Factors to Consider for Asbestos Toxicity
With the exception of fibrosis of the lung, in vivo studies indicate
that fibres longer than 5 µm are the more toxic. The ability to cause fibrosis
is strongly associated with a fibre length of greater than 2 µm and a diameter
of less than 0.15 µm. Asbestos fibres with a length greater than 10 µm and a
diameter greater than 0.15 µm increase the risk of broncio-pulmonary cancer.
Mesothelioma appears to be associated with fibres that are 5-10 µm long and
have a diameter less than 0.1 µm.
When asbestos fibres are inhaled, many are deposited on the epithelial surface
of the lung. The amount and location of the fibres deposited will depend on
the aerodynamic properties of the fibre. For the upper airway of the lung, ,
mostly thick fibres (> 3 µm), are deposited while thinner fibres will be
carried to deeper and alveolar regions of the lung. Animal studies indicate
that 30-40 % of typical fibres of chrysotile, amosite, and crocidolite , are
retained, with most of these being deposited in the upper airways such as the
nose, throat and trachea. The median length for these fibres was 1-2 µm, while
the median diameter was 0.2-0.4 µm.
The mechanisms by which asbestos fibres cause fibrogenic and carcinogenic
effects are not well understood. Some possible mechanisms are 1) a chronic inflammation
process mediated by production of growth factors (TNF-alpha), and 2) reactive
oxygen species. For fibre-induced carcinogenicity, there are several hypothesis
: 1) DNA damage by reactive oxygen species induced by fibres; 2) direct DNA
damage by physical interactions between fibres and target cells; 3) enhancement
of cell proliferation by fibres; 4) fibre-provoked chronic inflammatory cytokines
and growth factors; and 5) action by fibres as co-carcinogens or carriers of
chemical carcinogens to the target tissues.
Lung burden or loading: Pulmonary loading with amphiboles is proportional
to the duration and intensity of asbestos exposure, and is practically independent
of time since the last exposure. Pulmonary loading with chrysotile is proportional
to duration and the intensity of asbestos exposure, but it is inversely proportional
to the elapsed time since the last exposure, due to the lower biopersistance
of chrysotile.
Fibre Durability: Fibre biopersistance is believed to be a major mechanism
of fibre-induced pathogenicity (Hesterberg et al.1998a, 1998b). It is
not known for what duration a fibre must be resident in the lung , to induce
preneoplastic (precancerous) effects. The biopersistance of chrysotile verses
the amphiboles is actively debated because it is often used to justify why the
potency, with respect to carcinogenicity, is less for chrysotile. Recently,
several studies have highlighted that chrysotile is considerably less biopersistent
(Bernstein et al., in press; Berstein et al., in press). They
have provided evidence that chrysotile asbestos is less persistent that the
amphibole asbestos, particularly tremolite. Calidria chrysotile fibres, a standard
chrysotile used for testing, clear from the lung more rapidly, with a half life
of 7 hours, for fibres longer than 20 µm (asbestos fibres with a length of less
than 20 µm, are considered to be less persistent). . This was much faster than
clearance observed for tremolite or man made vitreous fibres. When experimental
animals were challenged with calidria chrysotile there were no signs of inflamation
in the lungs. In contrast, after 5 days of exposure, tremolite was not removed
from the lung, and inflamation was observed. In another study by this group
of researchers, further evidence of the much shorter half-life of chrysotile
in animal lungs, after a 5-day exposure (6-hour per day) regimen, was provided.
The amphiboles were described as solid rod-like fibres in comparison to chrysotile
which was described as ropelike with many fine fibrils.
Fibre Type: Many reviews have been conducted in order to determine if
chrysotile is less potent than the amphiboles for inducing lung cancer and mesothelioma.
Some epidemiological studies have been assessed with this in mind but epidemiological
studies that have involved amphibole-free chrysotile are rare. There is a diversity
of opinion regarding relative potencies of various asbestos fibre types with
respect to fibrogenicity and carcinogenicity. However, there is general agreement
that the potency of amphibole fibres to produce mesothelioma is greater than
chrysotile (ATSDR, 2001).
In a recent study conducted in China, the use of amphibole free chrysotile
was reported. An epidemiological study, (Yano et. al., 2001), (25-year, 1972-1996)
conducted in Chongqin, China is considered unique due to the very low (<
0.001%) contamination of chrysotile, by tremolite. The issue with this study
was to determine if amphibole-free chrysotile would increase lung cancer and
mesothelioma. The results of the study suggest that heavy exposure(~ 6 fibres/cm3)
to pure chrysotile asbestos can cause lung cancer and malignant mesothelioma
in exposed workers. Five hundred and fifteen males asbestos workers were exposed
to chrysotile, while the control cohort included 650 non-dust-exposed workers.
The relative risk for lung cancer (adjusted for smoking) was determined to be
6.6 (6.6 fold increase compared to the nonsmoking population) . There were 2
cases of mesothelioma (out of 132 deaths) which is considered to be high in
comparison to what would be expected in the general population. Some of the
study conditions reported were: 1) work-places smoking was permitted, and 2)
improper personnel protection were commonplace. The authors of this report suggest
that there is a strong potential for chrysotile alone to cause lung cancer and
mesothelioma.
While there is some evidence that chrysotile may increase the incidence of
mesothelioma, there is considerable debate on the "degree" or the
potency of chrysotile to cause this health effect
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Occupational and Environmental Exposure Levels of Asbestos (predominantly
chrysotile).
Occupational:
The risks are greatest for workers in industries which produce and use asbestos,
such as mining and milling. In the past, workers in these environments were
exposed to 100 - 1,000 times more asbestos than today’s workers. Today’s strict
standards limit workers’ exposure and the ban of most uses of amphibole asbestos
have reduced the risks. Construction workers, tradespeople and other building
maintenance/repair workers can be exposed during renovations and repairs to
very high concentrations of amphibole asbestos fibres in older buildings. The
environment and work methods of these occupations are more difficult to control
than fixed workplaces, but most tradespeople are trained in the proper handling
of asbestos-containing materials.
Monitoring of asbestos levels in air, in the workplace started in the 1930s,
with air levels reaching 20-30 fibres/cm3 or higher. In countries,
such as Canada, where controls were implemented these high levels were brought
down to less than 1 fibre/cm3 Occupational health standards today
are usually 1 fibre /cm3 for 8-hour exposure period. Some countries
are moving towards 0.1-0.2 fibres/cm3 (4-8 hr exposures), but for
the most part 1 fibres/cm3 appears to be widely used standard for
many jurisdictions.
Environmental:
Negligible levels of asbestos fibres occur in the soil, water and air, both
naturally and from man-made sources. Asbestos concentrations in the air in rural
areas are about 10 times lower than those in larger cities, which are about
1,000 times lower than levels accepted in today’s asbestos-related jobs. With
such low exposure, environmental risks are negligible.
Due to natural erosion, high concentrations of chrysotile asbestos fibres may
be found in some raw water supplies. Conventional water treatment methods can
substantially reduce asbestos levels and there is no evidence that ingested
chrysotile fibres are a health hazard
Typical concentrations measure in outdoor air in Canada, Austria, Germany,
South Africa and the USA ranged from < 0.0001 to about 0.01 f/cm3.
Most recorded values tend to be less than 0.001 fibres/cm3. In most
samples, fibre concentrations (> 5 µm in length) measured in various buildings
in Canada and Germany ranged form values below the limit of detection to 0.01
fibres/cm3. The highest concentrations were found in buildings with
spray-on friable fibres. For the Quebec mining industry, levels of chrysotile
in the air have dropped to approximately < 1 fibre/cm3. The ambient
air levels of chrysotile in Quebec chrysotile mining towns was reported to be
less than 0.01 fibres/cm3 since 1981.
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How the Government Protects Against Asbestos
Health Canada has encouraged provincial occupational health authorities to
adopt stringent workplace exposure limits for asbestos. Consumer products that
release asbestos fibres as well as the sale of pure asbestos have been banned
under the Hazardous Products Act. In addition, the emissions of asbestos into
the environment from mining and milling operations are limited under the Canadian
Environmental Protection Act.
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Conclusion
All forms of asbestos are regulated extensively in Canada. Human exposure to
chrysotile, the major form of asbestos produced in Canada, is considerably lower
today in comparison to that predicted for the early half of the twentieth century.
Exposure to chrysotile fibre levels in the industrial setting is now mandated
to be less than 1 fibre/cm3, which is a level determined to be of
very low risk for affecting human heath aversely. The adverse health effects
observed over the last half century, are attributed predominantly to exposures
to an earlier time when fibre counts in industry often exceeded 20 fibres /cm3.
Although it is established that chrysotile has significant serious health effects
associated with it, the consistent and inexorable pursuit of reducing exposure
to this substance, where possible, will be effective in reducing adverse health
effects.
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Key References
Agency for Toxic Substances and Disease Registry (ATSDR). 2001. Toxicological
profile for asbestos. Atlanta, GA: U.S. Department of Health and Human Services,
Public Health Service.
Hughes JM & Weill H (1986) Asbestos exposure- quantitative assessment of
risk. American Review of Respiratory Diseases, 133:5-13.
IPCS (1998) Environmental Health Criteria 203: Chrysotile Asbestos. Geneva,
World Health Organization, International Programme on Chemical Safety, 197 pp
IPCS (1998) Environmental Health Criteria 53: Asbestos and other natural mineral
fibres. . Geneva, World Health Organization, International Programme on Chemical
Safety.
Leigh J (19944 The Australian Mesothelioma Program 1979-1994. In: G.A. Peters
and B. J. Peters ed. Sourcebook on Asbestos Diseases. Garland Law Publishers,
9: 1-73.
Meldrum M (1996) Review of fibre toxicology. Health and Safety Executive, UK.
Rogers AJ, Leigh J, Berry G et al. (1994). Dose-response relationships
between airborne and lung asbestos fibre type, length and concentration, and
the relative risk of mesothelioma. Ann Occ Hyg, 38, Supplement 1: 631-638.
Stayner LT, Dankovic DA, & Lemen RA (1996). Occupational exposure to chrysotile
asbestos and cancer risk: a review of the amphibole hypothesis. American Journal
of Public Health, 86 (2): 179-186.
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