Hazard Identification
Asbestos is the generic name used to describe naturally occurring fibrous minerals of the amphibole and serpentile groups. Chrysotile, crocidolite and amosite are the main asbestos minerals exploited commercially. The discovery of large deposit of asbestos in Canada in 1887 and the start of large-scale mining of blue asbestos in South Africa led to its large-scale exploitation. The major uses of asbestos are in asbestos-cement products (pipes and building materials), sheets, friction materials, insulation and coating materials and textile products.
There are three main hazards from asbestos exposure: asbestosis, lung cancer and mesothelioma. The first case to be described fully in the medical literature was by Cooke in 1924 and in 1927 he named the disease asbestosis. In the1930s, case reports suggested there was an association between asbestosis and carcinoma of the lung. In the 1950s, studies confirmed that lung cancer was the specific industrial hazard of asbestos workers. Doll noted that the average risk of lung cancer among the men employed for 20 years or more was of the order of ten times that of the general population. In addition to lung cancer, asbestos has been referred to be associated with primary malignant mesothelioma, a tumour principally affecting the pleura and peritoneum.
In order to quantify the risk of asbestos exposure, many studies have examined the dose-response relationship for asbestos related disease. Asbestos related diseases have a long latency period, making the determination of the attack rate among exposed persons, and its relation to the dose of asbestos inhaled, difficult to determine. Estimates of the dose have been based on: the number of years of service in an industry, the number of years since first exposure, the total years of exposure, together with an estimate of the dustiness of a worker’s job, and the cumulative dust exposure calculated from dust concentrations for given jobs. Despite the difficulties of estimating dose, studies have shown that the risk of occurrence and the severity of disease increase with the increasing dose of asbestos. This relationship has been found in all areas of asbestos exposure, mining, manufacturing and secondary stage use, including the removal of old asbestos insulation.
Exposure to tobacco smoke increases the risk and severity of asbestosis and the risk of lung cancer. In humans, the effect of smoking on the pulmonary fibrosis has been found to be additive to that of asbestos on the progression of asbestosis. The effect of smoking combined with asbestos on the rate of lung cancer appears to be more than additive effect and is possibly multiplicative.
Death from lung cancer per 100,000 among individuals with and without
exposure to cigarette smoking and asbestos (Data from Hammond Ac et al.
Ann NY Acad Sci 330:473,1979)
Asbestos exposure
| Cigarette smoking | No | Yes |
| No | 11.3 | 58.4 |
| Yes | 122.6 | 601.6 |
Although the dose of asbestos is important, other factors including individual susceptibility are dominant. When asbestos is inhaled, most of the particles are removed by mucociliary clearance or via the lymphatic after being engulfed by the macrophages and cells lining the airways, but some fibres penetrate and accumulate in the lung tissue.
A number of methods are used for measuring thefibre concentration in the lung, including phase contrast light microscopy, scanning electronic microscopy (SEM), and transmission electron microscopy (TEM) on digested lung issue. Asbestos fibre can also be counted and identified in broncheoalveolar lavage (BAL) sample. The different methods all give different estimates of the fibre concentration. Histological analysis of lungs from workers exposed to asbestos has shown a broad correlation between the degree of asbestosis and the fibre content of the lungs. However, within each grade of asbestosis, there is considerable variation and the relationship between the fibre count and grade of asbestosis is poor.
Degree of asbestosis and Fibre content per 106 gm of Dry Lung (Eplar
et al 1982)
|
|
|
|
|
| No occupational exposure | |||
| North America | <0.001 | <0.025 | < 0.05 |
| United Kingdom | ---- | 0.01 | ---- |
| Australia | ---- | 95% < 0.25 | ---- |
| Occupational Exposure Present | |||
| No fibrosis | 0.02-0.07 | 0.10-0.30 | 0.2-0.4 |
| Plaques | 0.1-0.8 | 0.3-1.0 | 0.25-2.0 |
| Mesothelioma | 0.10-10 | 0.5-50 | 0.2-100 |
| Mild Fibrosis | 0.1-20 | 1.0-50 | 1.0-60 |
| Moderate Fibrosis | 0.5-50 | 2.0-200 | 2.5-300 |
| Severe Fibrosis | 20-150 | 80-2000 | 80-2500 |
The risk due to asbestosis arises from the inhalation of fibres. A visual assessment of the workplace is the first important step. If a workplace looks dusty, no control procedures are in place and no respiratory protection is being used, workers could have excessive exposure to fibres. Correct fibre identification and fibre counting are the minimum requirements needed to assess the risk where asbestos is being used.
The following steps indicate the basic procedures used in assessing the risk due to asbestos fibre exposure.
A. Ascertaining the presence of asbestos in the work place.
Microscopic identification is most commonly used to distinguish asbestos from other fibres. A representative sample is needed for laboratory analysis. There may be more than one kind of fibre in the sample. Enough material should be collected in order to sample all types of fibres present. Usually 100-250 gm is sufficient. It should be packed carefully in a sealed container for the transport.
B. Identification of the asbestos fibre type.
Crocidolite and amosite are considerably more hazardous than chrysotile, so it is important to know the actual type of fibre dealing with. Ideal techniques available for the identification of asbestos are polarising light microscopy (PLM) and dispersion staining microscopy.
C. Quantity of asbestos in the source.
PLM and dispersion staining method can give some estimates of the asbestos present in the sample. When a mixture of chrysotile and other asbestos fibres is detected, the mixture is usually regarded on the basis of the more hazardous type of fibre.
D. Procedures for handling the material in the workplace.
Using processes that minimise airborne fibre will reduce he risk. Special low speed, high torque tools are available for working asbestos products. Use of wet dust suppressing methods is important, especially for removal processes.
E. Presence of respiratory protection in place.
Control processes are crucial to the safe handling of the asbestos. Methods that prevent dust from escaping are the primary means of control. Respiratory protection is only added when dust control procedures cannot control the fibre release.
Threshold limit value (TLV) for the exposure to different types of asbestos is as follows:
Chrysotile 1.0 fibres/ml
Amosite
0.1 fibres/ml
Crocidolite 0.1 fibres/ml
Exposure to asbestos fibres in different types of work settings:
Machining of asbestos fibres 1 fibre/ml
Grinding, drilling, sanding
2-5 fibres/ml
(Using power tools)
Grinding, drilling, sanding
1 fibre/ml
Blowing down
1 fibre/ml
Asbestos stripping operations 5000 fibres/ml
Risk is the function of probability and consequence. In the asbestos exposure, probability is equivalent to exposure to asbestos and the consequence is the adverse health effect due to asbestos as asbestosis, mesothelioma and lung cancer.
Health effect rating
Inhaled asbestos is now known to produce the following adverse health
effects:
· Asbestosis- fibrosis of the lung
· Lung cancer
· Mesothelioma – cancer of pleura
· Pleural plaques and pleural effusion
· Laryngeal cancer
· Some workers also suffer from cancer of the gastrointestinal
tract.
Studies show that even an exposure of only 2 years lung cancer may occur after 16 years and a massive exposure to crocidolite may lead to mesothelioma after 72 hours.
Tobacco smokers are more likely to suffer from asbestos related diseases than non- smokers. Life expectancy is also shorter among smokers than non-smokers. Asbestos workers who stop smoking, can within 5-10 years reduce their risk of dying with lung cancer by about one half to one third that of their colleagues who continue to smoke.
As the adverse health effect of asbestos is irreversible and only the smoking habit can alter the consequence to a certain extent, it has been decided to rate the health effect into the following two groups:
Severe: non-smokers exposed to asbestos
Fatal: smokers exposed to asbestos
Exposure rating to the asbestos will be done on the basis of following
table:
| RATING | EXPOSURE LEVEL |
| 1 | No exposure (PPE) |
| 2 | C < 10% of TLV |
| 3 | C = 10 – 50% of TLV |
| 4 | C = 50-100 % of TLV |
| 5 | C> TLV |
A table for the risk matrix for the workers exposed to asbestos has
been drawn on the basis of the above mentioned health effect rating and
exposure rating.
| CONSEQUENCES | ||
| PROBABILITY | Severe | Fatal |
| Likely (5) | High risk | High risk |
| Probable (4) | High risk | High risk |
| Possible (3) | High risk | High risk |
| Improbable (2) | Moderate risk | High risk |
| Remote (1) | Moderate risk | Moderate risk |
Exposure to asbestos with the use of PPE and within the level of less than 10%of TLV is a moderate risk job for the non-smokers. Where as the smokers exposed to asbestos without any personal protective equipment are always exposed to high risk.
Occupational exposure limits for asbestos in air have been set at levels that will preclude any occurrence of asbestosis and lung cancer. These values may vary from country to country. Sometime it might be difficult to comply with the international accepted exposure limits due to economic reason. Some standards for occupational exposure are as follows:
Asbestos type
USA
Norway
Australia
Chrysotile
2 fibres/cc 1 fibre/ml
1 fibre/ml
Crocidolite
0.5 fibres/cc 0.1 fibre/ml
0.1 fibre/ml
Amosite
0.2 fibre/cc 0.1 fibre/ml
0.1 fibre/ml
Other fibres
0.2 fibre/cc 0.1 fibre/ml
0.2 fibre/ml
Dr. Sunil Kumar Joshi, Norway 2001