BISC 312

ASBESTOS
What is asbestos?
 a group of fibrous, naturally occurring silicate
minerals that generally exist in nature as
metamorphic or igneous rocks
 classified into 2 groups according to their
physical characteristics
1) Serpentine asbestos
- develops in a layered or tiered form
2) Amphibole asbestos
- has chain like structures
 the three common types of asbestos fibres are:
Chrysotile, Amosite and Crocidolite
Asbestos Types
Name Shape/ Compsition Group Picture
Colour
Crysotile* Curly/ Magnesium silicate Serpentine
White

Amosite Straight/ Iron and Magnesium Amphibole

Grey

Crocidolite Straight/ sodium, iron, Amphibole

Blue magnesium silicate

* Crysotile is the most used form

toxicity ranking: chrysotile < crocidolite < amosite
History
 the word asbestos is derived from the
Greek word “αμίαντος” meaning
inextinguishable or indestructive
 first used in 4000 BC by the Romans in
cremation, cloths and lamp wicks
 commercially mined in 1800's
 found in rock formations in
USA, Canada, South Africa,
and the former Soviet Union
Uses
 heavily used due to its high tensile strength, thermal
stability/resistance, and electrical resistance
 fibers can be spun into material that is flame retardant
and chemically inert
 Examples:
 household appliances Uses of Asbestos in 1999
 handheld hair dryers
 insulation
(in walls and piping)
Airborne (friable) asbestos

 only dangerous if in this form

 form of asbestos released from the manufacturing
process

 exposure/dose = risk of disease

 risks associated with low-level non-occupational

exposure are not well established

 biggest concern: diameter < 3 µm

Uptake of Asbestos
Respiratory:
 friable asbestos can be deposited in both
the upper and lower respiratory tracts
 smaller fibres have greater probability of deposition
in lower respiratory tract
 fibre geometry and anatomy of the animal affect
successful entrance into the body
 fibres deposited in lungs may penetrate respiratory
membrane and be transported to other sites of body
via circulatory and lymphatic systems
Uptake of Asbestos
Gastro-Intestinal:
 Ingestion
 human water supply can be
contaminated due to mine runoff into
lakes and streams
 airborne asbestos may settle on crops
and be ingested
 then crosses the GI mucosa and
can be transported to other sites in
body
Fibre persistence
the retention of fibres in the lung over time

 depends on the relative insolubility of fibres

 long fibres generally have more biological
activity greater pathogenicity
 most carcinogenic fibres for the mesothelium have
fibre lengths > 8 µm and diameters < 0.25 µm.
 fibres that split longitudinally produce thinner and
longer respirable fibres that are more pathogenic
 non-biodegradable by aquatic organisms
Clearance of asbestos
 clearance of inhaled  ingested asbestos
asbestos occurs via cleared from the
the sputum body via feces
(mucociliary transport)

no evidence for 100% clearance

Asbestos Effects on other
Organisms
Bacteria
 addition of asbestos dust to
soil reduced the total
population of soil microflora

Plants
 dumping of asbestos-bearing
wastes onto soil results in
areas devoid of vegetation
Asbestos Effects on Humans
 biochemical alterations
 genetic impairment
 changes in the immune response and
kidney damage
 pulmonary functions are adversely
affected
 impairment of gas exchange, vital
capacity and ventilation capacity changes
 asbestos can contain the carcinogen,
Benzopyrene found to facilitate the
transfer of Benzo(a)pyrene to
phospholipid vesicles
Diseases Associated with
Asbestos
 latency period between date of first
exposure and the time when the disorder
becomes clinically apparent.
 lung disease from asbestos can be
divided into three main types:
1) asbestosis
2) mesothelioma
3) lung cancer
 Asbestosis
Disease of the lung lining
 causes inflammation, tissue damage, and scarring
around the asbestos fibers
 scarring can continue to grow and form plaques at
the surface of the lungs and in the tissue lining
 latency period of 15-30 years
 often lethal

symptoms include:
- dyspnea - basilar interstitial opacities
- inspiratory crackles - difficulty breathing
- enlarged heart - dry cough
- decreased blood flow to lungs
 Mesothelioma
Dose (mg/rat)
0.5 1 2 4 8
# of 12 11 12 12 12
Rats
Cancer of the pleural lining
 a rare cancer exclusively
# with 1 3 5 4 8
related to asbestos exposure mesothe
lioma
 affects thin membranes,
Mean 784 729 664 762 692
surrounding lungs & other survival
internal organs (days)

 latency period: 30-40 years

 by time it is diagnosed, almost
always fatal (no treatment)

symptoms include:
- dyspnea - lasting cough
- pleuritic pain - fatigue
- weight loss - chest pain Lung with Healthy Lung
- opacification Mesothelioma
Lung Cancer
 persistence of asbestos fibers in the lung tissue and the
resulting inflammation seem to initiate the process of
cancer formation.
 starts in the lining of the bronchi, bronchioles, trachea, or
alveoli
 forms malignant tumor and can spread to other parts of
the body

smoking increases the risk of lung cancer

(synergistic effect with asbestos)
 due to the weakening of the
mucocilliary defence mechanism
of the lungs caused by smoking
Other Effects
Immune system
 Impaired cell-mediated immune response
noted in asbestosis and mesothelioma
patients

Chromosome abnormalities
eg) Chinese hamster cells exposed in vitro to
0.01 mg/ml chrysotile, crocidolite, amosite or
anthophyllite
Who is at Risk?
Industries commonly associated with
asbestos exposure
 mining and milling
 manufacturing
 construction industry
 ship building industry
 insulation workers
 brake repair and maintenance
 building demolition workers
 asbestos abatement workers
Factors in determining
risk of asbestos exposure:
 fibre characteristics
(type, physical properties, length to width ratio)
 dose and duration of exposure
 confounding variable (i.e. smoking)
 biopersistence of the fibre
 surface reactivity of the material
(wet, dry, in concrete, in insulation, etc.)
Two hypotheses of asbestos
exposure
1) The “One Hit” hypothesis:
 assumes cancer is an expression of a
permanent replicable change in
cellular genetics resulting from the
interaction of one molecule of
carcinogen with a critical receptor in
one cell.
 thus the curve passes through zero
and any dose above zero will exert an
effect
2) The “Threshold” hypothesis:
 assumes a no effect dose of
carcinogen below which cancer cannot
occur (occurs with near zero
probability).
 an exposure to small amounts is
considered hazard-free
Exposure Dose
What is a safe amount of asbestos?
 experimenters expose animals to high doses and
extrapolate data to humans who typically receive
low doses

Exposure risk is difficult to quantify:

 humans are exposed repeatedly and to varying
mixtures of fibres
 the mortality and disease presently being studied
is the result of exposure 20 to 50 years ago when
fibre levels were unregulated and exposure levels
were much higher
 individuals respond differently to a given dose
Protection
 Two main ways:
1) respiratory masks
 half-face mask
 full-face mask
 helmet
 hooded respirator

Levels of protection:
half mask < full mask < helmets < hooded respirators

2) protective clothing
 disposable coveralls
 hard hats
 safety shoes/boots
 eye protection
Regulations
 Environmental Protection Agency (EPA) require
that all asbestos be thoroughly wet with a
water and surfactant mixture (low pressure
water stream spraying) prior to removal
 1970’s: began regulation of asbestos use
 Occupational Safety and Health Administration
(OSHA) has set Permissible Exposure Limit
(PEL) at 0.1 fibers per cubic centimeter (f/cc)
for an 8 hour time weighted average
Regulations
 Under EPA and OSHA, asbestos
containing waste must be properly
containerized with warning labels
SUMMARY
1. asbestos is extremely persistent
2. problems mostly in humans
3. hard to study because its effects can
take decades to show
4. can be effectively protected against with
the right equipment and handling
5. still being used today in a more
controlled manner
References:
 Associate Committee on Scientific Criteria for Environmental Quality, Effects
of Asbestos in The Canadian Environment, NRCC NO. 16452
13,(19,106)1979
 Kamp DW, Weitzman SA. Asbestosis: clinical spectrums and pathogenic
mechanisms. Proc Soc Exp Biol Med 214: 12-26 (1997)
 Jaurand M. Mechanisms of fiber-induced genotoxicity. Environ Health
Perspect 105(suppl 5):1073-1084 (1997)
 Vu VT, Lai DY. Approaches to characterizing human health risks of exposure
to fibers. Environ Health Perspect 105(suppl 5):1329-1336 (1997)
 http://www.bigclassaction.com/asbestos/descriptive.html
 http://www.findarticles.com/p/articles/mi_m0984/is_2_124/ai_107395165
 http://www.asbestosnetwork.com/asbestos/de_history_usage.htm
 http://www.asbestosnetwork.com/asbestos/de_type.htm
 http://www.co.fairfax.va.us/service/hd/atphotos.htm http://www.active-
 asbestos.co.uk/frame_centre_about_history.html
 http://www.asbestosresource.com/asbestos/
 http://www.nsc.org/library/chemical/asbestos.htm
 http://www.dnr.state.wi.us/org/aw/air/reg/asbestos/asbes3.htm
 THANK YOU
GROUP #9
 Douglas Campbell  Andy Chan
 Wesley Chan  Don Dang
 Rebecca Eastman  Nassim Ghani
 Ann Ho  Mirian Lee
 Beth O’Donoghue  Devika Sharma
 Linda Tang