November, 1997

Occupational Disease Panel (ODP)
ODP Report No. 14A
Toronto, Ontario

Occupational Disease Panel

In 1985, the Ontario legislature established the Industrial Disease Standards Panel to investigate and identify diseases related to work. The Panel is independent of both the Ministry of Labour and the Workers' Compensation Board. At the end of each fiscal year the WCB reimburses the Ministry for the Panel's expenditures. In 1995, the name was changed to the Occupational Disease Panel (ODP).

The Panel's authority flows from section 95 of the Workers' Compensation Act and its functions are set out as follows:

95(8) (a) to investigate possible occupational diseases;

(b) to make findings as to whether a probable connection exists between a disease and an industrial process, trade or occupation in Ontario;

(c) to create, develop and revise criteria for the evaluation of claims respecting occupational diseases; and

(d) to advise on eligibility rules regarding compensation for claims.

Decisions of the Panel are made by its members who represent labour, management, scientific, medical and community interests. Once the Panel makes a finding, the WCB is required to publish the Panel's report in the Ontario Gazette and solicit comments from interested parties. After considering the submissions the WCB Board of Directors decide if the Panel's recommendations are to be implemented, amended or rejected.

To assist with its work, the Panel has a small staff of researchers, analysts and support people. In addition to its own staff, the Panel relies heavily on the advice of outside experts in science, medicine and law, as well as input from parties of interest.

Additional copies of this publication are available at:
http://www.ccohs.ca/odp

Panel Membership

Panel Staff

CHAPTER I.
THE ISSUE

Pursuant to a recommendation by the Royal Commission on Asbestos (RCA) [4], the Workers' Compensation Board (WCB) made a formal request to the Industrial Disease Standards Panel (IDSP) by letter dated March 5, 1987 for a review of Schedule 3 in Regulation 951 to The Workers' Compensation Act (the Act) [1].

1. THE PANEL'S MANDATE

The Panel undertook revision of the current Schedule 3 pursuant to its mandate in s.95 of the Act. Specifically, s.95(8) states that,

(8) It shall be the function of the Panel,

(a) to investigate possible occupational diseases;

(b) to make findings as to whether a probable connection exists between a disease and an industrial process, trade or occupation in Ontario;

© to create, develop and revise criteria for the evaluation of claims respecting occupationaldiseases; and

(d) to advise on eligibility rules regarding compensation for claims respecting occupationaldiseases.

The compensation of occupational diseases happens through section 1(1) of the Act, which contains the following:

"occupational disease" includes

(a) a disease resulting from exposure to a substance relating to a particular process, a trade or occupation in an industry,

(b) a disease peculiar to or characteristic of a particular industrial process, trade or occupation,

© a medical condition that in the opinion of the Board requires a worker to be removed either temporarily or permanently from exposure to a substance because the condition may be a precursor to an occupationaldisease, or

(d) any of the diseases mentioned in Schedule 3 or 4; ("maladie professionelle").

In subparagraphs (a) to (c), a disease or medical condition¹ is compensable if it meets the requirements set out in the whole definition.² In (d) scheduled diseases are demonstrably occupational diseases because they meet the definition and can thus either be presumed or deemed to be caused by the employment.

The intent in (d) is to expedite the process of entitlement where diseases are probably work-related. A schedule of diseases gives public notice that diseases in Column 1 meet the legal criteria of the Act and are considered to be characteristic of or peculiar to the work processes specified in Column 2, unless the contrary is proved in any particular case.

Adjudication of disease claims is also aided by the evidentiary presumptions in s.134(9) and (10) of the Act, which state:

(9) If the worker at or before the date of the disablement was employed in any process mentioned in the second column of Schedule 3 and the disease contracted is the disease in the first column of the Schedule set out opposite to the description of the process, the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved.

(10) If the worker at or before the date of the disablement was employed in any process mentioned in the second column of Schedule 4 and the disease contracted is the disease in the first column of the Schedule set out opposite to the description of the process, the disease shall be conclusively deemed to have been due to the nature of the employment. 1984, c. 58, s. 34 (1).

If the prerequisites set out by these two subsections are met, then the law directs that claims for scheduled diseases are either presumed compensable until proved otherwise or deemed compensable.³ Adjudication by schedule proceeds on the basis that a probable connection between disease and work is demonstrable.

Both law and practice concerning occupational disease compensation is more or less uniform in Canada, an exception being Saskatchewan.⁴ Practice demonstrates that any disease is compensable if it can be shown to be work-related or if it is already recognized as work-related. Schedules of diseases therefore give public notice of legally recognized compensable conditions that carry an explicit presumption as to their origin.

2. HISTORY OF THE ISSUE

The IDSP, now called the Occupational Disease Panel (ODP), came into existence as the result of two separate but related events.

The Weiler Report

The first was a report by Professor Paul Weiler, known generally as the Weiler Report, on the protection of workers from disability, submitted to the Minister of Labour in 1983 [5]. The Weiler Report recommended the statutory creation of an Industrial Disease Standards Panel to oversee occupational disease compensation policy in Ontario. Membership on the IDSP was to be constituted as is the present day ODP. The purpose of the Panel was to produce scientifically sound guidelines that would also satisfy the legal requirements of the Act.

Because disease compensation could not be solely a matter for science, Weiler foresaw the "inescapable policy dimension to compensation guidelines". Hence, the Panel could investigate both the medical and legal connection between work and diseases, "either on its own initiative, or at the request of the Board, the Ministry, or an interested party". The results of the investigation would be made public after consultation with all interested parties.

The Royal Commission on Asbestos

The second impetus for creation of the IDSP came from the Royal Commission on Asbestos, which issued its Report in 1984. One of the RCA recommendations was the creation of an Advisory Council on Industrial Disease Policy, the equivalent of the IDSP. The Commission's recommendation followed the essence of Weiler's proposals for the same. Both Reports saw the need for updating and a practical revision of Schedule 3. The Schedule had fallen into disuse because of deficient wording and a lack of practical data for adjudication.

The WCB

Dr. Elgie's request was reinforced in the course of inter-agency discussions on disease compensation policy. All parties interested in the revision of Schedule 3 were agreed that to be viable the existing form and contents needed updating and that updating should be continual.

The Panel has agreed to revise Schedule 3. As part of the effort to update the Schedule, the Panel released Report No. 14 To The Workers' Compensation Board on IDSP Revisions To Schedule 3: Phase One in November, 1994.

3. THE PANEL'S INVESTIGATIONS

The Act gives the ODP the authority to investigate possible diseases and when appropriate to make findings of "probable connection" between disease and work.

The evidence that the ODP examines to find a probable connection is scientific and medical. Specifically, the ODP considers epidemiological studies, industrial hygiene information on workplace exposures, toxicological evidence on identifiable contaminants and alternative causes of disease. To evaluate this evidence, the Panel uses the concepts of Sir Austin Bradford Hill [2]. Bradford Hill argued that to determine causality, consideration should be given to the following factors:

Strength of association:

The degree of increase in the risk of disease after exposure to a substance or process (e.g., a high SMR). A statistically significant increase is usually required to confirm an excess risk of disease; however, a strong association may be relevant even if statistical significance has not been shown, particularly when the failure to show statistical significance relates to the small size of the study population.

Consistency:

There is consistency when several different studies produce similar findings. Consistency is particularly persuasive if the studies are of various designs, and are large and carefully conducted.

Specificity:

Specificity is shown when exposure to a particular substance or process is associated with one particular disease (e.g., silicosis). Specificity must be weighed with caution and is inapplicable if a certain substance is capable of causing more than one disease (e.g., lead).

Temporality:

Temporality indicates exposure took place before the disease occurred.

Dose-response (also called "biological gradient"):

There is a dose-response trend when an increase in the exposure ("dose") corresponds with an increase in the rate of disease or death ("response"). Conversely, a dose-response trend will also occur if the incidence of disease decreases with a corresponding decrease in the exposure.

Biological plausibility:

An association is biologically plausible when the connection between exposure and disease is consistent with what we already know about biological and chemical patterns.

Coherence:

There is coherence when the evidence as a whole is cogent and uncontradicted by what is known about the disease process, which also describes biological plausibility.

Experiment:

Experimental evidence is also relevant, if it is available. Often animal studies provide evidence about the effects of exposures.

Analogy:

An analogy can be drawn when the same exposure in another setting is also associated with an increased risk of the same disease.

After weighing the evidence, the Panel will decide what, if any, probable connection exists between a particular work process and a specific disease. If the results of the investigation do not indicate the existence of a probable connection, the Panel will also report those findings.

When a probable connection is identified, depending on its strength, the Panel may recommend that the WCB take certain steps to ensure compensation for occupational diseases.

The project to revise Schedule 3 began with an examination of relevant sections of the Act, the legal definition of occupational disease, the presumptive clauses pertaining to Schedule 3, current adjudicative practice and Workers' Compensation Appeal Tribunal (WCAT) decisions on occupational disease claims. The project for revision is an ongoing investigation. As investigations move forward, the revisions to Schedule 3 will move from the simple (Phase One) to the more substantive. Any new diseases that the Panel recommends for scheduling would also have a recommendation for adjudicative guides for each disease. This report on silicosis, tuberculosis, non-ionizing radiation and benzene inaugurates Phase Two.

4. PRINCIPLES FOR EVALUATING ELIGIBILITY OF DISEASE CLAIMS⁵

Schedule 3 has existed in Ontario compensation law since 1914 when it included only six diseases. Between 1914 and 1961, Schedule 3 was amended a dozen times and then again in 1994. The latest amendment added nasal cancer related to the nickel industry [3]. Over time the WCB has added to the list of eligible diseases through the use of adjudication policy guidelines without formal amendments to Regulation 951. Diseases declared by guidelines, however, were not always given the benefit of a causal presumption as were Schedule 3 diseases.⁶

The Schedule originally provided an exclusive list of work-related diseases. It gave public notice of which specific diseases were solely compensable under the Act. The list lost its exclusivity in 1947 when the definition of occupational disease was changed to include any disease peculiar to a process, trade or occupation. Claims for unlisted diseases could therefore be adjudicated case by case. In 1984, the Act was amended to make the definition of occupational disease even more inclusive. Schedule 3, however, has never lost its notice function. Diseases listed in Schedule 3 could be presumed to be caused by work, unless the contrary were proved.

Criteria need to be formulated to determine whether a disease can be added to Schedules 3 or 4, or whether guidelines alone should be used for adjudication of a certain disease. Such criteria, however, have not yet been clearly recognized by the WCB. The Panel has examined current schedule entries and attempted to identify the criteria used by the WCB in the past. The Panel has also reviewed internal WCB documents on this point.

When does the WCB list diseases in Schedule 4

Currently, only three diseases are included in Schedule 4: asbestosis, mesothelioma and nasal cancer. The guide for inclusion in Schedule 4 used by the WCB, as identified by the Panel, in practice appears to be the following:

! a consistent pattern of elevated rates of disease among workers with similar exposures that is substantially greater than the rates in the general population;

! evidence that the rate of disease increases with the extent or duration of exposure or both;

! evidence of known causative substance(s) in the Scheduled work process; and,

! a biological explanation for the development of the disease.

Diseases included in Schedule 4 are then deemed conclusively work-related; that is, these diseases have a definite connection to work. The presumption of their cause is irrebuttable.

When does the WCB list diseases in Schedule 3

The WCB has not yet articulated the process it uses to enter diseases into Schedule 3. On examining WCB practice, the Panel's understanding of the process for diseases listed in Schedule 3 is that the WCB first determines if the claimant has the disease and was exposed to the corresponding industrial process. If these conditions are satisfied,"the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved" [emphasis added].

The WCB can therefore look for evidence that might prove a non-work-related cause. At this point, the ODP believes the WCB would be better served by a set of criteria that could be used to identify facts and to weigh evidence for and against the statutory presumption.

Diseases entered in this Schedule appear to have a strong or clear but not conclusive connection to work processes. To determine if a disease should be included in Schedule 3, the WCB appears in practice to look for:

! a consistent pattern of elevated rates of disease among workers with similar exposures;

! evidence that the rate of disease increases with the extent and/or duration of exposure;

! evidence of suspected cause(s) of the disease in the work process; and,

! a reasonable biological explanation for the development of the disease.

Diseases currently listed in Schedule 3 clearly have employment related causes, but they may also have non-employment related causes. On this basis, for example, a finding of work-relatedness has allowed for scheduling diseases such as dermatitis. Hence the need to have a rebuttable causal presumption for Schedule 3.

Guidelines for diseases not listed In the Schedules

The WCB issues policy guidelines for the adjudication of both scheduled and non-scheduled diseases. Guidelines evolve from manifold investigations of recurrent claims for specific diseases. Lack of certainty about a work association may exist in some cases because there is little known about a disease or because there is an even balance of contradictory and supporting evidence about an association. Guidelines can then be used to regulate adjudication of such cases. When and if the evidence becomes stronger, the ODP has the ability to investigate and make new recommendations on guideline diseases to the Board, including a recommendation for scheduling if appropriate.

5. THE PANEL'S RATIONALE FOR SUBJECTS INCLUDED IN PHASE 2

Because Phase 1 was largely an editorial revision of Schedule 3, it became apparent that WCB practice and the state of knowledge did not completely correlate with some entries. For example, tuberculosis claims in practice are not made solely by healthcare workers; silicosis is the signature disease of certain work processes and associated occupations, and diseases associated with benzene toxicity are included but not specified under poisonings.

These entries were chosen for further revision because of the enormous existing medical and scientific literature on disease causes and effects. Moreover, WCB practice both nationally and internationally reflects a consistency in the listing or adjudication of these diseases. Work-relatedness is already established.

6. REFERENCES

1. Elgie, Robert, Chairman, WCB, [letter to James Ham, Chairman, IDSP requesting a review of Schedule 3]. March 5, 1987.

2. Hill, A.B. The environment and disease: Association or causation? Proceedings of the Royal Society, Section of Occupational Medicine. Vol. 58(1965). p. 295-300.

3. Ontario Reg. 900/93, s.1; R.R.O. 1990, Reg. 1102, Sched. 3.

4. Report of the Royal Commission on Matters of Health and Safety Arising from the Use of Asbestos in Ontario. Toronto: Ontario Ministry of the Attorney General. 3 vols. 1984.

5. Weiler, Paul C. Protecting the worker from disability: Challenges for the eighties. [A report submitted to Russell H. Ramsay, Ontario Minister of Labour]. April 1983.

6. Workers' Compensation Act, R.S.O. 1990, c. W. 11.

CHAPTER 2.
SILICOSIS AND SILICO-TUBERCULOSIS

1. SILICOSIS

History and law

After oxygen, silica is the most abundant element in the earth's crust and is the main constituent of igneous rock, granite and feldspar. It also occurs in sedimentary rock, including sandstone and shale. Sandstone and flint may contain 100% silica, granite 20-70%, slate about 40%. The crystalline form of silica (silicon dioxide) that causes silicosis is called free silica because it does not exist in a compound or as a silicate. Silicates, for example, include asbestos, mica and talc. In its most common inorganic state, free silica is quartz.¹

Silicosis as a lung disease has been known by some name or other since the 16th century.[8] The alarm for prevention of this disease was sounded as early as the 18th century. By the 19th century, lung diseases were recognized causes of premature death. Silica dust was identified as one such cause.[8] Turn of the century industrial activities resulted in large outbreaks of the disease because 20th century technology made massive heavy industry, construction and mining possible [8]. Various governments then began legislating controls to prevent and to compensate silicosis.

The Ontario experience is typical of Canada. A 1926 legislative amendment added silicosis caused by mining to the original Schedule 3,² and also added a definition of silicosis to the Act, in s.1:

"silicosis" means a fibrotic condition of the lungs sufficient to to produce a lessened capacity for work, caused by the inhalation of silica dust; ("silicose").

The disease causing process was expanded in the 1950's to include quarrying, cutting, crushing, grinding or polishing stone or metal. The definition of silicosis persists in the current law.

The Act also retains the provision in s.134(12) requiring that compensation for silicosis be paid only to workers with silica exposure in Ontario, and the amount of exposure is defined as at least two years:

134 (12) Nothing in this Act entitles a worker or his or her dependants to compensation, health care or payment of burial expenses for impairment or death from silicosis unless the worker has been actually exposed to silica dust in his or her employment in Ontario for periods amounting in all to at least two years preceding his or her impairment. R.S.O. 1980, c. 539, s. 122 (11); 1982, c. 61, s. 2; 1984, c. 58, s. 4, part; 1989, c. 47, s. 26 (2).

Section 134(12) clearly makes the presumption of work-relatedness for silicosis rebuttable only by proof of less than two years exposure in Ontario. This section imposes a strict requirement for rebuttal by making silicosis a disease peculiar to the processes described in Column 2 below:

Despite the strict exposure requirement, silica exposure of sufficient dose (quantity) and sufficient duration to cause non-occupational silicosis is highly unlikely outside the work processes identified in Column 2 of the Schedule.

Schedule 3 pre-dates Schedule 4 by about 70 years. In 1984, Schedule 4 was recognized for the first time in the definition of "industrial disease" and within that part of the Act that concerned occupational disease compensation; however, no diseases were included in the Schedule.

The first diseases placed in Schedule 4 in 1992 were mesothelioma and asbestosis, followed by nasal cancer in 1994. Silicosis is a disease very much like asbestosis in its relationship to work.

Disease process

Silicosis is a non-malignant respiratory disease, one of many lung diseases classified as a pneumoconiosis [8,9,10,12]. Pneumoconiosis is the deposition of inorganic dust in the lungs through inhalation and the reaction of body tissue to that fact. The primary reaction is through the lung tissues. Other tissue may also be involved. Pneumoconioses are the result of work in dusty occupations.

Lung impairment is caused by collagenous pneumoconiosis, a fibrosis that turns healthy lung tissue into a non-elastic mass. Impairment results from breathing in excessive amounts of inorganic dusts from silica, asbestos, coal, aluminum and talc, to name only a few [5,8,9,10,12].

Silicosis is therefore a chronic fibrotic lung disease caused by prolonged or intense exposure to crystalline silica or quartz (free silica). A history of silica exposure is essential to a diagnosis of this disease. In early stages, fibrosis caused by silica may not cause lung function impairment.

Chronic silicosis typically results from prolonged low to moderate levels of exposure to respirable dusts with quartz content. In its chronic form, the disease produces nodular lesions in the upper lobes of the lungs. The disease can be progressive, producing large fibrotic lesions, even if exposure has stopped, resulting in lung function impairment [8,12].

Accelerated silicosis usually results from five to 15 years moderate to high levels of exposure to respirable dusts with more than 30% quartz content. Fibrotic nodules are smaller, and fibrosis moves to the mid-zone of the lungs. Disease progression is rapid and can lead to respiratory failure with as little as 10 years exposure [8].

Acute silicosis is said to be the rarer occurrence; nevertheless, it can result from less than a year (weeks or months) to four years heavy or very high exposure to respirable dust with high (more than 70%) silica content. Symptoms appear rapidly within a few weeks to a year from the time of first exposure, often complicated by secondary lung diseases, leading to respiratory failure with fatal outcome. Acute silicosis is most often associated with exposures to fine particles of dust in occupations such as sandblasting or coal mining and occupations with exposures to silica flour [8, 10].

Diagnosis and lung function

Chronic silicosis manifests over a long period of years but is accelerated by intense exposures. Diagnosis is based on radiologic examination and usually presents as simple nodulation without symptoms of impairment. As nodulation increases, symptoms of lung function impairment appear, namely, breathlessness on strenuous exertion. Lung pleurae may show evidence of fibrosis. Depending on exposure dose and the quartz content of the dust, breathlessness can become incapacitating.

Unlike some other pneumoconioses, silicosis in its simple stage is associated with lung function impairment in advance of the development of symptoms. The reason for this is that, while small at first, impairment will increase with disease progression. Associated lung obstruction and other disease (e.g., tuberculosis, cor pulmonale, infectious disease) may also intensify the symptoms and the degree of impairment [8,9].

Lung function impairment is usually tested by spirometry that measures the ventilatory capacity of the lungs.[1] The tests are expressed as the measure of forced vital capacity (FVC) and forced expiratory volume (FEV₁) in the first second together with the ratio FEV₁/FVC. Being a restrictive lung disease, silicosis decreases lung volumes (both FVC and FEV₁). Because both are decreased, the FEV₁/FVC ratio may appear normal. In the advanced stages of the disease, gas diffusion may be impaired.

Occupational exposure to silica dust

Occupational sources of exposure to free silica occur mostly in the following industries and occupations [8,9]:

! foundry work

! hardrock mining, including crushing and grinding

! quarrying

! stone cutting, dressing, grinding and polishing

! tunnelling and excavating

! use of abrasives

! sandblasting

! glass manufacture

! ceramics and pottery

! vitreous enamelling

2. SILICO-TUBERCULOSIS AND OTHER COMPLICATIONS

Tuberculosis may also develop as a consequence of silicosis. Silico-tuberculosis (silicosis with tuberculosis) is a notable complication for this disease [8,9,12]. (Tuberculosis is discussed in the next chapter.)

As lung fibrosis progresses in silicosis, alterations in lung structure produce emphysematous changes that obstruct the airways, and emphysema may result. Other complications include cor pulmonale (compensated in France), scleroderma, chronic bronchitis, and more rarely, collagen vascular disease.³ Besides these complications, lung cancer is also relatable to silicosis. Lung cancer secondary to silicosis was prescribed in 1992 as an occupational disease in UK [3,4]. This relationship is not yet recognized in Canada.

3. INTERJURISDICTIONAL PRACTICES

DISEASE	BC	AB	QB	NS	NB	NF	UK	FR	ON
Silico-Tuberculosis						*		*
Silicosis	*	*	*		*	*		*
•metalliferous mining	*	*						*

The asterisks in the table (see Appendix) refer to the equivalent disease and process descriptions in the respective lists of each jurisdiction. The check marks refer to listings by the International Labour Office (ILO) and proposed amendments thereto. Silico-tuberculosis is included to highlight silicosis-induced diseases, which are compensable in Ontario but not listed.

4. EVALUATION OF THE EVIDENCE

Strength of association:

All of the evidence establishes a probable connection between silicosis and occupational exposure to silica.

Consistency:

Consistency in the findings between studies of different groups of workers is established.

Specificity:

Silicosis is a disease specific to silica exposure and derives its name from this causative agent.

Temporality:

Exposure to silica must occur before the disease manifests itself.

Dose-response:

The risk of developing silicosis rises with duration of exposure or intensity of exposure (dose) or both.

Biological plausibility:

The effect of silica exposure is consistent with what is known about pneumoconiosis.

Coherence:

There is nothing that contradicts the association between this disease and its causative agent.

Experiment:

Experimental evidence has not been examined and is not needed to confirm the nature and cause of silicosis.

Analogy:

Exposure to silica in various occupational environments can result in silicosis.

5. THE PANEL'S FINDING AND RECOMMENDATION

The consistent pattern of disease among workers exposed to silica is well established historically by both research and compensation practice. The work usually associated with the disease is hardrock mining; in general, however, all work where silica dust is generated is included, such as sandblasting and stone quarrying, cutting or carving. Furthermore, this disease is not found among the general population.

The risk of disease rises with the extent and duration of exposure, with low risk at 20 years light exposure, and high risk with as little as five years of heavy exposure, and very high risk with less than four years very heavy exposure.

The only cause of this disease is exposure to crystalline silica. Silicosis, like asbestosis, is a signature disease; thus biologically, the disease can only occur as the result of chronic or acute exposure to silica dust.

As a consequence of silicosis, other diseases can also develop, which decrease lung function and increase impairment. The most notable of these is silico-tuberculosis which can be fatal for persons whose lungs are compromised by silicosis.

Silico-tuberculosis can be a consequence of silica exposure as secondary to the primary disease of silicosis. As such, this form of tuberculosis can be presumed to be an occupationally induced disease. One Panel member, John Macnamara, has noted for the record his dissent on the inclusion of silico-tuberculosis in Schedule 3 on the grounds that the current entry for tuberculosis does not exclude silico-tuberculosis and thus the disease does not need a duplicate entry.

Silicosis can be moved from Schedule 3 and placed in Schedule 4 to read as follows:

Having previously reported on the probable connection between respiratory complications and non-malignant respiratory diseases, the Panel can see no reason to exclude Silico-tuberculosis from Schedule 3 to read as follows:

6. REFERENCES - Silicosis

1. American Medical Association (AMA). Guides to the evaluation of permanent impairment. 3rd ed. rev. 1990.

2. Cotes, JE and J. Steel. Work-related lung disorders. 1987. 145-164.

3. Department of Social Security, UK. Pneumoconiosis and other prescribed respiratory diseases. NI 236. 1989.

4. Department of Social Security, UK. Lung cancer in relation to occupational exposure to silica. Cm 2043. 1992.

5. Goldsmith, DF et al., eds. Silica, silicosis and cancer: controversy in occupational medicine. Cancer Research Monographs, v.2. 1986.

6. Braunwald, E. et al., eds. Harrison's principles of internal medicine. 11th ed. 1987.

7. IARC. Silica and some silicates. IARC Monographs, v.42. 1987.

8. Morgan, WKC and A. Seaton. Occupational lung diseases. 2nd ed. 1984. A. Seaton. Silicosis. Ibid. 250-294.

9. Rom, WN. Environmental and occupational medicine. 2nd ed. 1992. MR Balaan and DE Banks. Silicosis. Ibid. 345-358.

10. Rosenstock, L and M. Cullen. Textbook of clinical occupational and environmental medicine. 1994. SL Weber and DE Banks. Silicosis. Ibid. 264-274.

11. World Health Organization. Recommended health-based limits to occupational exposure to selected mineral dusts (silica, coal). WHO Technical Report Series 734. 1986.

12. Zenz, C et al. Occupational Medicine. 3rd ed. 1994. DP Schlueter. Silicosis and coal worker's pneumoconiosis. Ibid. 171-178.

CHAPTER 3.
TUBERCULOSIS

1. DISEASE PROCESS

Tuberculosis is normally a chronic disease caused by Mycobacterium tuberculosis, a bacterium that resides within humans.¹ The site of disease is usually the lungs, although other organs can also be affected (e.g., renal tuberculosis). Once organ tissues are infected, there is a formation of granulomas (tissue granulation in the form of nodules) with cell-mediated hypersensitivity.

Tuberculosis was once widely prevalent but has been controlled in modern times; however, there has been a rise in incidence in recent years [3,4].

The disease is transmitted from person to person through the air. Tubercle bacillus forms a nucleus for water droplets within the respiratory system that are expelled by coughing and sneezing or even talking and singing. Upon evaporation of the expelled droplets, the bacillus becomes dry and remains airborne for long periods. A susceptible individual may contract tuberculosis when the airborne bacillus is inhaled. Infection is not necessarily immediate and can require repeated exposures over time. Furthermore, susceptibility to infection is related to nutrition and the health of the immune system. The more infectious the source, however, the more likely the transmission to a susceptible individual.

Because the bacillus is adversely affected by ultra-violet light, transmission rarely occurs in the sunlight (tuberculosis sanatoria were always airy, with an abundance of natural light). Infection usually occurs with immuno-compromised or nutritionally deficient hosts, or where living conditions and social hygiene are substandard [1,3]. Transmission is thus more likely in crowded, poorly ventilated indoor or underground spaces.

Once the tubercle bacillus enters the lungs, the infection causes an inflammation that starts the disease process. The process remains undetected because there are few or no symptoms. The disease can become inactive or latent; it can be re-activated or activated (e.g., by another disease or re-infection) [3]. Tuberculosis can also manifest as a complication in the progression of other diseases (e.g., silicosis and HIV).²

2. INTERJURISDICTIONAL PRACTICES

The chart above shows Canadian jurisdictions that list occupational diseases and also compensate tuberculosis. The chart includes United Kingdom and France for greater comparison. By further comparison (see, Interjurisdictional Compensation for Silicosis, Chapter 2 above), tuberculosis is also a non-malignant respiratory condition consequent upon another occupational disease.

Compensation for occupational tuberculosis in Ontario

Tuberculosis is compensated because it is a recognized occupational disease pursuant to the current unrevised Schedule 3. In the existing entry, the process description is embodied in the disease description. The Panel has recommended inclusion of a separate process description in ODP Report No.14 on Phase One of Schedule 3 revision, which has yet to be adopted by the WCB.

Tuberculosis is an infectious disease and a continuing public health concern [3]. A specified group of workers in healthcare, provincial laboratories and correctional services are now covered by Schedule 3; however, other workers at risk because of employment are covered only on a case-by-case basis. Such workers might be found in police, firefighting, emergency, public health, social and animal services. For example, individuals have been exposed in Alberta and Quebec as recent as 1994; additionally, the Ontario Ministry of Labour has examined the threat to workers from tuberculosis exposure in a particular wildlife population.³

The current law, the Phase One revision and the proposed changes for occupational tuberculosis can be compared, in the following way:

The current law:

Phase One revision:

Proposed Phase Two revision:

The reality of occupational risk is also borne out by WCB claims statistics for tuberculosis. For example, in four years between 1990 - 1994, the total number of claims allowed for occupational tuberculosis 18. The breakdown per occupation and industry is as follows[6]:

The majority of claims come from the healthcare sector, which has the greatest potential for exposure. The sector, Hospitals, has a total of eight (8) claims, plus one from a related sector, Medical Labs, for a total of nine (9). The second largest number of claims comes unexpectedly from Metal Mines and Metal Fabrication industries (4). Next come Protection Services (2), Concrete Products (1), Telecommunications (1) and Elementary and Secondary Schools (1) for a total of 18. The public health concern is particularly noteworthy in the last sector.

3. EVALUATION OF THE EVIDENCE

Strength of association:

The total of evidence establishes a probable connection between occupational exposure to tubercle bacillus and tuberculosis.

Consistency:

Consistency in the findings between studies of different groups of workers is established.

Specificity:

The incidence of tuberculosis is specific to substandard environments that consistently demonstrate poor social hygiene, lack of sunlight, poor ventilation and nutrition; individuals living and working in such environments are usually immuno-compromised and nutritionally deficient, thereby increasing susceptibility to infection. Individuals can also be susceptible to infection through exposure in clinical and laboratory environments or by exposure to a person with the disease.

Temporality:

Exposure precedes the disease and may occur inside or outside the work environment.

Dose-response:

Repeated exposure to tubercle bacillus increases the risk of disease.

Biological plausibility:

The transmission of this disease is consistent with what is known about the transmission and development of infectious diseases.

Coherence:

There is no evidence that contradicts what is known about the transmission and development of tuberculosis.

Experiment:

Experimental studies have not been examined and are not needed to confirm the cause of disease in this case.

Analogy:

The risk of disease is also present outside the traditional environment for TB exposure (e.g., poor and crowded living conditions, lack of good nutrition and social hygiene).

4. THE PANEL'S FINDING AND RECOMMENDATION

The current limitation to certain provincial healthcare and correctional services does not reflect the reality of the risks in the present-day workplace. There is a definite pattern discernible in the claims record, with an elevated risk for some work, healthcare in particular. The pattern of risk, however, is not limited to this sector. The cause of disease is a specific bacterium and the conditions for transmission are readily identifiable. Furthermore, the risk of disease in sectors outside healthcare is biologically plausible given these conditions and the nature of the work processes. A more comprehensive Column 2 description would therefore capture workers, for example, in police, fire and emergency services, wildlife, animal, customs and immigration services, and underground mining; that is, the workers likely to be exposed to infection because of work.

A more comprehensive wording would also cover the industries and occupations revealed in the above tabulation. Any revision should foresee all relevant work exposures but still be limited by the terms, "employment" and "tuberculosis". Column 2 should be worded specifically and at the same time be inclusive enough to cover the employments where WCB practice has revealed a known risk. The revised entry for this disease should read as follows:

5. REFERENCES - Tuberculosis

1. Benenson, AS., ed. Control of communicable diseases in man. 15th ed. 1990.

2. Braunwald, E. et al., eds. Harrison's principles of internal medicine. 11th ed. 1987.

3. Markowitz, S.B. ed. Occupational Medicine: Tuberculosis in the workplace. State of the art reviews. v.9, n.4, Oct.-Dec. 1994.

4. Rom, WN. Environmental and occupational medicine. 2nd ed. 1992. MR Balaan and DE Banks. Silicosis. Ibid. 345-358.

5. Sherson, D and F. Lander. Morbidity of pulmonary tuberculosis among silicotic and nonsilicotic foundry workers in Denmark. Journal of occupational medicine. V.32; no.2; February 1990

6. Workers' Compensation Board. Corporate Data Services. June 1, 1995.

CHAPTER 4
NON-IONIZING RADIATION AND EYE INJURY

1. BACKGROUND

Retinitis is an eye "disease" listed in Schedule 3 with a presumption of work-relatedness to "electro-welding or acetylene welding". Claims for welder's flash (flash kerato-conjunctivitis) which is not scheduled, are adjudicated under Retinitis. Taking WCB practice into account, the Panel's Phase One report recommended adding flash keratoconjunctivitis to the retinitis entry. Compensation practice in other jurisdictions regarding these diseases has also been considered.

Non-ionizing radiation (NIR) lies in the region of the electromagnetic spectrum (which includes the light spectrum) where the energies are less than needed to separate an electron from an atom (i.e., to ionize the atom). This region consists of energies with frequencies below 10¹⁶ Hz and includes (in order of decreasing frequency and energy) ultra-violet (UV), visible light (VL), infra-red (IR), microwave and radiowave. The last two are not considered in this Report.

Both flash keratoconjunctivitis and retinitis are injuries associated with over-exposures to certain types of NIR. Damage occurs in different parts of the eye and is caused by different types of NIR. Retinitis, however, should be more accurately described as photo retinitis, and while flash keratoconjunctivitis is used in practice, it is more accurately described as Photo keratoconjunctivitis [4].

I) Photo keratoconjunctivitis

Keratoconjunctivitis refers to acute inflammation of the cornea (keratitis), and inflammation of the conjunctiva (conjunctivitis). Photo keratoconjunctivitis is caused by exposure to certain frequencies in the light spectrum. The symptoms range from irritation to severe pain of the eye and increased sensitivity to light. In most cases, symptoms are temporary, manifesting within 2 to 24 hours after exposure and subsiding within 1 to 5 days. "Flash" kerato-conjunctivitis, as used in the Phase One report, refers specifically to the condition caused by excess exposure of the eye to Ultra-Violet light [9].

Photo keratoconjunctivitis occurs mainly at wavelengths between 220 to 310 nm (UV-B and UV-C)¹, with a peak sensitivity around 270 nm [17]. Ultra-Violet light is heavily absorbed by the cornea and lens of the eye but is greatly attenuated by the ocular fluids. Therefore, UV damage (mainly photochemical) from excess exposure is generally limited to the anterior parts of the eye, such as the cornea and conjunctiva. Permanent corneal damage can occur with high intensity exposures or cumulative exposures over an extended period [5]. A good example is the effect of prolonged unprotected gazing at a solar eclipse.

ii) Photo retinitis

The currently used term in Schedule 3, Retinitis, refers to inflammation of the retina connecting the eye to the receptor cells that produce sight. This injury can be caused by exposing the eye to excessive Visible Light and near Infra-Red radiation. Retinal damage by Ultra-Violet light is also possible in aphakic persons (those lacking the lens of the eye) who have no UV protection over their eyes [13].

While Ultra-Violet light cannot be refracted, Visible Light and some Infra-Red radiation can be and can be transmitted and focused onto the retina. Intense visible radiation can cause severe retinal damage by causing both thermal and photochemical changes. The blue-light region of the spectrum (near UV at wavelengths between 400 and 550 nm) is particularly hazardous to the retina because its intensity is too low to cause thermal damage, thus permitting long exposure that can lead to photochemical changes to the retina.

2. OCCUPATIONAL EXPOSURES

Common sources of non-ionizing radiation in the workplace include welding arcs, lasers and the lamps used in various printing and curing processes.

Potential optical hazards from such emissions depend on the measure of individual Ultra-Violet light, Visible Light and Infra-Red output [17].¹⁴

I) Welding and cutting

Both Photo keratoconjunctivitis and photo retinitis have been commonly associated with metal welding and cutting, both common sources of intense Ultra-Violet radiation in the workplace. These processes are broadly divided into gas and electric or arc welding (and cutting).

Gas Welding/Torch Cutting

In gas welding and torch cutting, a flame is produced by combustion of a fuel gas (e.g., acetylene) with air or oxygen for the purpose of melting or joining metal pieces or to cut metal. The brightness of the flame produced by combustion is not much greater than that of a candle flame (1 to 20 cd/m2)³ and the Ultra-Violet emission is quite small [17]. These processes generally present little hazard to the eye, other than contact with spattering hot metals.

Arc Welding/Cutting

Arc welding and cutting involve striking an arc between an electrode and a metal workpiece connected to an electrical supply. The resulting arc produces high temperatures, enough to fuse or cut metal surfaces. Such arcs are also a source of intense Visible Light, Ultra-Violet and Infra-Red radiation. Depending on the metal workpiece, type of shielding gas used and the electrical current applied, the welding/cutting arc may be 1,000 times brighter than the gas welding flame, with UV at proportionately greater levels, than the gas welding flame [17].

Direct and prolonged exposure of the eye to the arc is unlikely because the arc's intense brightness triggers involuntary aversion responses (blinking, turning away). These responses, which take place within 0.25 seconds, protect the eyes from absorbing Visible Light (including blue-light radiation) or Infra-Red radiation enough to cause any serious thermal damage to the retina or other parts of the inner eye [17]. They may not, however, provide adequate protection against Ultra-Violet light because doses accumulated over a work shift can add up easily to exceed the maximum permitted exposure duration.

For this reason, arc welders wear eye safety equipment (face shields, helmets, goggles and filters) which, if properly used, effectively reduce much of the Ultra-Violet, Infra-Red and Visible Light radiations from welding arcs [11]. The likelihood of developing eye injuries from arc welding or cutting has therefore become very low. A recent WCB survey in Alberta showed that, although 21% of the claims for eye injuries came from welders, over 70% of these injuries had no direct association with welding or thermal cutting but were caused by foreign particles entering the eye [16]. In most of these cases, welders were engaged in metal handling jobs (e.g., chipping and grinding) after welding and did not have their face shields in place.

Eye injuries, however, can occur to persons who are unprotected and momentarily exposed to stray arc emissions or flashes. Such persons include welder's assistants, bystanders or welders who may not have had their eyes protected when others nearby began welding. Such brief exposure to Visible Light and Infra-Red radiation is usually not enough to cause thermal retinal damage, although photochemical retinal damage is possible [8].

Momentary exposures to arc flashes, however, can result in enough UV light absorption and photochemical changes to cause keratoconjunctivitis [10]. This injury commonly occurs during a single working period, although a damaging dose could be accumulated over several work days [12]. Cumulative exposure can also occur to a welder who uses poorly fitting eye protection that allows some Ultra-Violet light to penetrate the eye.

ii) Lasers

Laser is an anachronym for, Light Amplification by Stimulated Emission of Radiation. The laser produces a beam of electromagnetic radiation which is both monochromatic (single wavelength) and spatially coherent (i.e., the waves are in phase with each other). There are many different types of lasers and some of them are extremely potent sources of Visible Light, Infra-Red or Ultra-Violet radiations.

The following Table lists some of the commonly used lasers and their applications.

Optical hazards include burns and inflammation to the cornea, conjunctiva and retina. Exposure to laser radiation in the Ultra-Violet region may cause only temporary damage to the cornea if the damage is limited to its outer layer. Because of its spatial coherence, however, a laser beam in the Visible Light or Infra-Red region will focus all its energy through the eye on a very small area of the retina. There the energy concentration (irradiance) can be as much as 200,000 times greater than that received at the cornea [8]. Such high energy concentration generates much heat in the tissues, resulting in rapid and irreversible retinal damage.

Classes of lasers

All lasers are classified according to their hazard potential through assessment of the maximum level of accessible radiation (accessible emission limit, or AEL). The classification scheme is as follows:

iii) Lamps

A variety of lamps can be sources of Ultra-Violet exposure in the workplace (e.g., searchlights, spotlights, lamps used in photocuring of dental resins). The eye's aversion response can usually give adequate protection from over-exposure, the exception being some of the halogen lamps (e.g., tungsten-halogen lamps) which emit a slightly greater amount of UV [11]. Gas discharge lamps (arc, mercury and metal halide lamps) can be sources of intense Ultra-Violet, Visible Light and Infra-Red radiation and are commonly used in photochemical processes.

In most workplace settings, gas discharge lamps are enclosed or fitted with safety filtres (diffusers and shields or both) to reduce hazardous emissions to workers. Therefore, barring a failure of engineering controls, workers are unlikely to develop Photo keratoconjunctivitis or photo retinitis while working near these lamps [13].

The following, however, are exceptions where acute exposure to intense UV radiation from these lamps can be more of a concern:

Non-Destructive Testin

High intensity Ultra-Violet spot lamps are used for non-destructive testing (NDT) to detect fissures in metals in the aircraft and steel industry. A fluorescent dye is drawn into the fissures by a static magnetic field and becomes brightly visible when UV is shone on it. The workers involved are necessarily situated close to the work pieces for examination and thus may be over-exposed to UV radiation. Non-destructive testing is also used in other industries, as in the textile industry to differentiate materials.

Sterilization

Germicidal lamps emit UV-C radiation and are used in hospitals and laboratories (to control bacterial contamination) and in food preparation areas of restaurants, cafeterias and food processing plants. These lamps are generally installed at ceiling level and have some shielding to protect against direct exposure. Ultra-Violet exposure, however, is possible if these lamps are placed close to the ground or when workers go to ceiling level for repairs.

Ultra-Violet Curing

Ultra-Violet lamps are installed in many workplaces to cure inks or coatings on labels (can or box manufacturers), signs (printing industry), wood flooring or circuit boards. Many of these applications involve high intensity enclosed UV lamps located on automatic production lines. Often, the enclosure is not perfectly sealed and has openings which allow UV radiation to escape [13].

iv) Solar radiation

The sun's photo emissions beyond the earth's atmosphere consist of about 5% Ultra-Violet light, 45% Visible Light and 50% Infra-Red radiation. Values for UV and IR are lower on the earth's surface and vary greatly depending on elevation, cloud cover, degree of pollution and time of day and year. The eye is normally protected from over-exposure to strong sunlight by aversion responses. Acute retinal injury, however, can occur from the blue light and Ultra-Violet light in the incident rays reflected off surfaces of water, white sand or snow. Under such conditions, outdoor workers without proper eye protection can be readily exposed to hazardous levels [11].

3. INTERJURISDICTIONAL PRACTICES

Quebec specifies retinitis related to work involving electro-or acetylene welding. There is also a separate entry for cataract caused by non-ionizing radiation (limited to Infra-Red, microwave or laser beam). New Brunswick mentions eye conditions due to welding.

British Columbia (BC) and Alberta include "radiation injuries or diseases due to Non-Ionizing Radiation" in their schedules but specify conjunctivitis and keratitis associated with an industry or process where there is significant occupational exposure to Ultra-Violet light. Cataract or other thermal damage to the eye are also specified in association with processes that have a risk of significant occupational exposure to Infra-Red, microwave or laser radiation.

In the United Kingdom (UK), various skin and eye conditions and injuries including cataract, ulceration, inflammation and cancers are prescribed in association with any occupation involving electromagnetic radiation (other than radiant heat) or ionizing particles. Heat cataract is prescribed separately in association with prolonged exposure to rays from molten or red-hot material. France refers to both welding and non-ionizing radiation.

Ontario

The existing unrevised schedule entry reads as follows:

The Phase One revision made the disease medically more precise and also added a Column 2 description; both revisions reflect current compensation practice:

The best schedule entry for this disease, however, would update the description to reflect the real nature of the injury and to reflect more accurately both workplace and compensation practice.

4. EVALUATION OF THE EVIDENCE

Strength of association:

The total of evidence establishes a probable connection between photo keratoconjunctivitis, photo retinitis and prolonged or intense exposure to Ultra-violet and Infra-red light.

Consistency:

Consistency in the findings between studies of different groups of workers is established.

Specificity:

The disease is specific to exposures to spectrum Ultra-violet and Infra-red light.

Temporality:

Exposure precedes the disease and may occur inside or outside the work environment.

Dose-response:

Repeated exposure to Ultra-violet and Infra-red light increases the risk of disease.

Biological plausibility:

The development of this diease is consistent with what is known about the cause of diseases induced by both non-ionizing and ionizing radiation.

Coherence:

There is no evidence that contradicts what is known about the devlopment of photo keratoconjunctivitis and photo retinitis.

Experiment:

Experimental studies support the association between photo keratoconjunctivitis, photo retinitis and prolonged or intense exposure to Ultra-violet and Infra-red light.

Analogy:

Exposure to Ultra-violet and Infra-red light in various occupational environments can result in these diseases.

5. THE PANEL'S FINDING AND RECOMMENDATION

Inclusion of Photo keratoconjunctivitis in Schedule 3 is reasonable and would reflect current WCB practice in Ontario and other jurisdictions. Photo keratoconjunctivitis can be caused by electro (arc)-welding, primarily as a result of over-exposure to Ultra-Violet radiation from strayed emissions. Acetylene welding generally presents very little hazardous light emission to the eyes.

Photo keratoconjunctivitis can also be caused by over-exposure to Ultra-Violet radiation emitted from gas discharge lamps used for non-destructive testing, sterilization and curing. Depending on the workplace and process design, workers involved in other processes using gas discharge lamps could also be at risk.

Photo retinitis caused by arc welding should be uncommon because welders are protected from direct exposure to the Visible Light and Infra-Red radiation generated by the arc. Exposure to stray radiation from arc welding is usually too brief to cause serious retinal damage. Retinal damage from Visible Light radiation and Infra-Red from lamp sources is uncommon because it generally requires a prolonged exposure (e.g., purposeful staring).

Exposure to the direct or reflected beam from Class 3B and 4 lasers can cause photo kerato-conjunctivitis, cataract and retinal damage. The type of damage depends on the radiation emitted (UV, VL or IR). These lasers are used in surgical procedures, material etching and for special effects in the entertainment industry and for research in laboratories.

At this time, however, the Panel is undecided on the relationship between cataract and work.

The existing disease entry of "retinitis" appears out-dated and does not fully reflect current knowledge on optical injuries where the workplace is the source of injury. The current process description appears restrictive in limiting eye injuries to welding because such injuries are commonly associated with other work processes, such as torch cutting and foundry flash, which also present a hazard of over-exposure to Ultra-Violet light, Infra-Red and Visible Light. Other processes include those involving 3B and 4 lasers and gas discharge lamps.

Most jurisdictions examined by the Panel include specific skin and eye injuries as caused by non-ionizing radiation but limit exposures to Ultra-Violet, Infra-Red, Visible Light and microwave radiation. Some jurisdictions also include cataract as a work-related disease caused by such exposures.

All the work processes listed in Ontario and other jurisdictions can be the cause of photo keratoconjunctivitis and photo retinitis or other injuries and diseases. The deletion of acetylene welding from the process description in Schedule 3 would not be a diminution of protection because most injuries that result from this process are accidental burns or lacerations caused by molten metal which would be compensated as accidents.

The revised Schedule 3 entry would read as follows:

6. REFERENCES - Non-ionizing Radiation

1. 1993-1994 Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, OH: ACGIH, 1993.

2. Anonymous. Epidemic Keratoconjunctivitis in a Factory. British Medical Journal. Vol. 2 (1975). no.5970.

3. Chatterjee, D.S. An Outbreak of Shipyard Eye in a Car Factory - A Diagnostic Dilemma. J. Society of Occupational Medicine. Vol.36, no.2(1986). p. 63-65.

4. Cullen, A.P. Non-ionizing Radiation and Work-Review, Opinion and Comments. [A Review of ODP Draft]. February 8, 1996.

5. Cullen, A.P. Personal Communication to J. Tung. February 15, 1996.

6. Cullen, A.P. and Perera, C.S. Sunlight and Human Conjunctiva Action Spectrum. SPIE Proceeding. Vol.2134B, 1994. p.24-30.

7. Curtis, R. and Nichols, M. Nonionizing Radiation. In: Rom, W.N., ed. Environmental and Occupational Medicine. Boston: Little, Brown and Company, 1983. p.6930-705.

8. Delpizzo, V. and Cornelius, W.A. Lasers. In: Repacholi, M.H., ed. Non-Ionizing Radiations: Physical Characteristics, Biological Effects and Health Hazard Assessment. Proceedings of the International Non-Ionizing Radiation Workshop, Melbourne, 5-9 April, 1988. IRPA, 1988. p.135-158.

9. Dorland's Illustrated Medical Dictionary. 26th edition. Toronto: W.B. Saunders Co., 1985.

10. Lyndon G.S. Welding and Thermal Cutting. In: Parmeggiani L., ed. Encyclopedia of Occupational Health and Safety - Vol. II. 3rd edition. Geneva: ILO, 1983. p.2290-2295.

11. McKinlay, A.F. Visible Light and Infra-red Radiations. In: Repacholi, M.H., ed. Non-Ionizing Radiations: Physical Characteristics, Biological Effects and Health Hazard Assessment. Proceedings of the International Non-Ionizing Radiation Workshop, Melbourne, 5-9 April, 1988. IRPA, 1988. p.111-133.

12. McMillan, G. Foiling Flashes. Occupational Health. Vol.38, no.1(January 1986). p.20-22.

13. Nishio, J. [Potential Acute Eye Injury due to Optical Radiation from Artificial Sources in Industry]. Personal Communication. July 24, 1995.

14. Pitts, D.G., et al. Optical Radiation and Cataracts. In: Waxler, M. and Hitchins, V.M., ed. Optical Radiation and Visual Health. Boca Raton, Florida: CRC Press Inc. 1986. p.5-41.

15. Pitts, D. A Position Paper on Ultraviolet Radiation. In: Cronly-Dillon, J.; Rosen, E.S. and Marshall J., ed. Hazards of Light, Myth and Realities. Toronto: Pergamon Press, 1986. p.197-208.

16. Reesal, M.R., et al. Welder Eye Injuries. Journal of Occupational Medicine. Vol.31, no.12(December 1989). p.1003-1006.

17. Sliney, D.H. and Wolbarsht, M.L. Safety with Lasers and other Optical Sources, A Comprehensive Handbook. New York: Plenum Press, 1980.

18. Spraque, J.B.; Hierholzer, J.C.; et al. Epidemic Keratoconjunctivitis - A Severe Industrial Outbreak due to Adenovirus Type 8. New England Journal of Medicine. Vol.289(1973). p. 134.

19. Wingrad, C.H. and Resnick, N.M. Management of Common Clinical Disorders in Geriatric Patients. Chapter 8(IX). In: Dale, D.C. and Federman, D.D., ed. Scientific American Medicine. Vol. II. New York: Scientific American Inc., 1995. p.19-21.

20. Zuclich, J.A. and Connolly, J.S. Ocular Damage Induced by Near-Ultraviolet Laser Radiation. Invest. Ophthalmol. 15,1976. p.760.

CHAPTER 5.
BENZENE AND LEUKAEMIA

1. INTRODUCTION

The information contained in the following chapter is based in large part on a detailed literature review on benzene and leukaemia conducted for the Panel by Jennifer Penney, MSc. [35]

Poisoning by benzene was added to Schedule 3 by regulation in 1925 but was referred to as benzol poisoning. The ODP's Phase One report recommended the entry be changed to benzene. In 1940, poisonings by compounds derived from or homologous to benzene were added to the Schedule. These were specified as poisoning by nitro- and amino derivatives of benzene, phenol and their homologues (trinitrotoluene, dinitrophenol, aniline and others). Included under any poisoning are its sequelae. Historically, therefore, any condition that results directly from toxic exposures to benzene at work, or to its derivatives and homologues, or that is consequent upon such exposures, is a compensable occupational disease.

About benzene

Benzene is a clear, colourless, highly volatile liquid hydrocarbon produced primarily by the petrochemical and petroleum refining industries. It is a naturally occurring constituent of crude oil and natural gas, ranging between 0.1 and 3.0 percent by volume, depending on the geographical source. Benzene is also recovered as a byproduct of the coking process in steel mills.

Benzene has been commercially produced and used since the 1860's [22]. It is widely used and ranks among the top ten chemicals produced worldwide. Canada is a major producer of benzene after the U.S., Europe and Japan [27]. Historically, benzene has been an important industrial solvent, used especially for rubber, inks, lacquers, paint removers, plastics and artificial leather [13, 14], although usage has been phased out in Canada and most of the developed world because of the chemical's toxicity. Benzene continues to be employed extensively as a laboratory solvent, however.

Benzene is an important feedstock chemical. Large quantities are used to manufacture other organic compounds, including ethyl benzene, styrene, cumene and cyclohexanol [34]. Unreacted benzene may be present in chemicals which use benzene as a feedstock.

Because of its anti-knock properties, benzene-containing substances are added to gasoline as a replacement for alkyl lead compounds [13]. Gasoline contains from less than one to five percent of benzene by volume [27].

Exposure

Benzene enters the body mostly by inhalation. Highly volatile, the chemical is easily respirable; almost 50 percent of inhaled benzene is absorbed by the body [32]. About 1% of benzene is absorbed from skin contact; however, absorption is accelerated to as much as 5% when the skin is cracked, blistered or abraded [34].

IARC identifies the following major sources of benzene emissions into the air: (1) gasoline production, storage, transport, vending and combustion; (2) production of other chemicals from benzene; (3) indirect production of benzene, as for example by coke ovens, which are also a major source of benzene contamination of water [27].

Benzene is released to the general environment from auto exhaust, partly from combustion of other aromatic compounds and is also given off as a vapour from hot engines and fuel tanks. Exposures increase with the rush of traffic and with time driving [45, 20, 1], both inside vehicles and outside on roadways and in parking garages. Self-service refueling increases environmental benzene exposure.

Benzene exposures for workers occur in a number of settings: in petrochemical plants, petroleum refineries, in tire manufacturing, coke production in steel plants; in bulk terminals, and in automotive service and gas stations.

Work involving routine exposures includes unit operators, tankcar loaders and unloaders, laboratory technicians and maintenance personnel [34]; process operators, workers who store, mix, load and unload solvents, tire builders and tubers, laboratory technicians and maintenance personnel [34, 39]; work in byproduct and benzol plants and in coke oven operations; loading benzene or gasoline, particularly in top filling operations and barge loading [29, 39, 20]; auto repair or rebuilding and gas pumping [20, 1]; and firefighting [IDSP Report No.13].

After carbon monoxide, benzene is the second most common constituent of fire smoke to which firefighters are exposed. Furthermore, benzene is a constituent of diesel emission produced by emergency fire vehicles [IDSP Report No.13].

A relatively new source of occupational exposure results from the removal of underground gasoline storage tanks [7]. Regular work with chain saws or other gasoline-powered equipment may also result in significant benzene exposures.

Mainstream and sidestream cigarette smoke may account for about 50% of non-occupational exposure.¹ Benzene emissions from smoking and from consumer products such at latex paints, marking pens, rubber products and other common materials can build up indoors in the air and produce low level exposures. Homes adjacent to service stations may have increased exposures [1]. Benzene is sometimes found in drinking water, primarily as a result of gasoline spills, or seepage from underground gasoline tanks [1].

2. THE HEALTH EFFECTS OF BENZENE EXPOSURE

Benzene has long been recognized internationally as a potent toxic substance, particularly for blood-formation from within bone marrow.

The hematological disorder caused by benzene is pancytopenia, a progressive decrease in the circulating cells of the blood: erythrocytes, thrombocytes or platelets, and each of the various types of leukocytes [16, 13]. Benzene can deplete just one or two of these cell lines, with a range of effects from the subclinical to the fatal. Benzene was first reported to cause aplastic anaemia as early as 1897 [27].

Leukaemia

Leukaemia is a progressive, malignant disease of the blood-forming organs, characterized by the proliferation of abnormal haematopoietic (blood making) cells in the blood and bone marrow. Cells show a decreased capacity for normal differentiation, expand at the expense of normal cell lines and impair normal myeloid or lymphoid cell growth. This frequently leads to death by infection or haemorrhage. Diagnosis is based on two findings: the presence of abnormal cells in peripheral blood and the presence of abnormal cells replacing normal bone marrow elements.

The neoplastic cells arise from a malignant transformation of various cell lines which proliferate initially in the bone marrow and then spill over into the peripheral blood. The particular type of disease which develops depends on the point in the cell line at which transformation occurs and further development or maturation is blocked.

Leukaemia is classified clinically on the basis of:

• the duration and character of the disease -- may be acute or chronic, relating to life expectancy and/or maturity of the leukaemic cells involved; acute leukaemias have a rapid clinical course and will result in death in a few months if not effectively treated, whereas chronic leukaemias have a more prolonged natural history; and
• the dominant type of cell involved -- myeloid (myelocytic, myelogenous or non-lymphocytic) or lymphoid (lymphatic, lymphocytic, or lymphogenous); may also be classified by more specific cell type (e.g. monocytic l. erythroleukaemia, myelomonocytic l., etc.)

There are several classification systems for leukaemia. Most of these categorize leukaemias into four major groupings:

I) Acute myelogenous leukaemia (AML): (also known as acute myelocytic leukaemia or acute non-lymphocytic or ANLL).

AML is the most common acute leukaemia among adults, where abnormal myeloid precursors infiltrate and replace bone marrow tissue.

Many patients develop AML after a preleukaemic syndrome, or myelodysplastic syndrome (MDS) usually characterized by anaemia, thrombocytopenia (decrease in platelets) and sometimes granulocytopenia (decrease in basophils, eosinophils and neutrophils), associated with a dysplastic bone marrow. Although it may not progress to AML, MDS is often fatal [13].

Several environmental exposures are suspected to cause AML, including ethylene oxide and ionizing radiation. Styrene, 1,3-butadiene, vinyl chloride, paints and nitrites have also been linked to AML [31].

ii) Acute lymphocytic (lymphoblastic) leukaemia: (ALL)

Although ALL can also be subdivided by cell type, these sub-classifications are not used in the benzene-related leukaemia literature, and so are not elaborated on here.

With ALL, abnormal lymphoid precursors infiltrate and replace bone marrow and lymphatic tissue. ALL is primarily seen in children and to a lesser extent in adolescents, although a late peak in incidence occurs after age 60. Several maternal and paternal occupations have been linked to ALL in children, especially in the nuclear industry [31].

iii) Chronic myelocytic (myeloid, myelogenous) leukaemia: (CML)

CML is one of several diseases classified as a myeloproliferative disorder and is often discovered as a result of an elevated white
cell count in the absence of symptoms. Ten to 15% of patients also have marrow fibrosis, creating difficulties in differentiating CML from myelofibrosis with myeloid metaplasia [31].

CML has been linked with benzene exposures [18, 44; 31]. Rubber workers and electrical workers are supposed to be at increased risk for CML [31].

iv) Chronic lymphocytic leukaemia: (CLL)

CLL is mainly a disease of later life and has a more favourable prognosis than the other leukaemias and often requires no therapy [31]. CLL is described as a "variant of well-differentiated non-Hodgkin's lymphoma" [31]. CLL has not been strongly associated with benzene exposures.

Nomenclature

Classification systems and diagnostic techniques have changed substantially over the last several decades which has complicated the process of linking different types of leukaemia with specific environmental agents. Kipen and Wartenberg elaborate on this issue:

The International Classification of Diseases (ICD) and clinical coding practices are not well synchronized with one another nor with trends in clinical diagnostic practice. Thus, deaths due to myelodysplastic syndrome (MDS) are sometimes classified as a type of AML and sometimes separately, and within NHLs (Non-Hodgkin's Lymphomas) there have been numerous shifts in nomenclature, whereas the ICD has retained the older terminology. Because in any population LH neoplasms are relatively rare, such inconsistency influences the relative occurrence of specific LH cancers, and thus impedes epidemiologic recognition and investigation of etiologic associations. For this reason, the total number of LH neoplasms or leukaemias based on death certificates usually is reliable, because LH tumours rarely are classified outside of the overall leukaemia and lymphoma rubric, but specific cell types cannot be reliably ascertained from death certificates.

For this reason, in many epidemiologic analyses, the leukaemias are considered as one... The paradox is that, to

the extent that the tumours are distinct entities with distinct sets of causes, imprecision in classification makes etiologic associations more difficult to observe with consistency, whereas to the extent that one cause may result in multiple distinct histologic abnormalities, splitting arbitrarily reduces epidemiologic power and the opportunity to observe statistically significant associations.

3. EVIDENCE OF CAUSATION

Benzene was first linked to leukaemia in a report published in 1928 by Delore and Borgomano [27]. Today there is no question that benzene exposures can cause this disease. The international scientific community is agreed that benzene causes acute myelogenous leukaemia (AML), also called acute non-lymphocytic leukaemia (ANLL) [27, 20, 42, 10, 9, 18, 31, 41, etc.].

I) Cohort studies

Many epidemiologists have examined benzene-exposed workers in shoemaking, rotogravure (printing), petroleum, petrochemical and rubber industries. A number of their studies followed up on case reports. The relationship between benzene and leukaemia has also been investigated in several hospital-based case-control studies. Some of the studies, however, are limited by a lack of good exposure data, losses of former workers to follow-up, incomplete or possibly faulty diagnoses on death certificates, potentially confounding exposures, as well as other problems. Several studies used general population incidence rates for comparison but neglected the healthy worker effect in the analysis of results. Nevertheless, there is an impressive mass of evidence to support the benzene-leukaemia connection.

There is clear scientific agreement that benzene causes acute myelogenous types of leukaemia (AML). Several researchers looking to investigate the effects of low-level exposures to benzene in various industries, however, appear to have focused narrowly on the incidence of AML rather than incidence of all types of leukaemia. This has reinforced the AML-benzene link, but made it more difficult to assess the linkage with other leukaemias and lymphatic disorders.

At least two key investigators -- Aksoy and Yin -- have used proportionate mortality ratios of different types of leukaemia in benzene-exposed workers and the general population to support a causal relationship with benzene [2, 46]. In some populations of benzene-exposed workers, there is a disproportionately high incidence of AML compared to other leukaemias (and disproportionately low incidence of other types). Neither of these investigators, however, argues that benzene causes only AML. Aksoy reviewed several studies of benzene-exposed workers in which AML predominates, together with two studies in which chronic types of leukaemia occur more frequently and suggests factors to explain the differences, Including:

• higher benzene content (and exposures) appear to correspond more to acute leukaemias;
• mixed solvent exposures may be more closely related to chronic leukaemias [2].

Aksoy noted the effects of benzene on lymphatic tissues and lymphocytes to support his contention that benzene is associated with Hodgkin's Disease (malignant lymphoma). Several studies have also identified an association between benzene exposure and multiple myeloma [14, 36]. OSHA drew attention to studies which linked benzene and chronic myeloid, chronic lymphatic, and acute lymphatic leukaemias among chemical workers exposed to benzene, as well as multiple myeloma, reticulum cell sarcoma, Hodgkin's disease and other lymphoid tissue neoplasms.

On the basis of information combined from epidemiology and case studies, the following hierarchy of associations between benzene and various Haematologic disorders emerges.²

Cullen (1994) and Snyder and Kalf (1994) both suggest that myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML) represent a continuum that may be induced in normal stem cells or early progenitor cells by the toxic metabolites which result from chronic exposure to benzene. MDS probably precedes leukaemia in a substantial proportion of all cases [13]. Aberrations involving chromosomes 5 and 7 have been found in many patients with radiation therapy-induced myelodysplasia prior to the development of AML.

While aplastic anaemia occurs usually as the result of fairly high exposures, leukemia has been shown to occur as a result of exposures below the current Ontario TWAEV (Infante, 1989). Several investigators have found that increased risk is associated with cumulative exposure. Others have postulated that intermittent or peak exposures are more important risk factors. With respect to latency, there appears to be a minimum lag period of 3-5 years from first exposure and a peaking of AML incidence within 8-10 years for individuals who develop therapy-related leukaemia. In the Pliofilm cohort, time from initial exposure to death due to a haematological neoplasm ranges from 3.5 to 37 years [18].

ii) Case reports

More than 150 neoplasms are described in the case reports reviewed by IARC and Goldstein. While case reports do not, by themselves, constitute sufficient evidence of causality, they play an important dual role in providing preliminary associations for further study and analysis, and as supporting evidence where population studies, experimental evidence, metabolic studies and cytogenetic investigations show a causal connection between an environmental exposure and disease. The large number of benzene-leukaemia case reports has served this dual role. The association with benzene in many of these cases is strengthened by the diagnosis of benzene-related blood disorders, especially pancytopenia or aplastic anaemia (pre-leukaemia) before the onset of leukaemia.

iii) Chromosome studies

Benzene is known to produce chromosomal abnormalities that demonstrate its mutagenic potential [41]. IARC's review of several chromosome studies, reported up to 1980, divided the studies in two general categories: (1) patients with a current or past history of benzene induced blood hemopathies; or (2) workers with current or past exposure to benzene but no obvious clinical effects.

Findings of significant increases in chromosomal aberrations in blood and bone marrow and in lymphocytes from benzene-exposed, symptomatic workers, have been confirmed by several other investigations [27, 34, 41]. Studies of asymptomatic benzene-exposed workers have also revealed chromosome abnormalities.

Several studies cited by OSHA demonstrated chromosomal damage in animals exposed to benzene at very low doses [15, 16].

iv) Metabolic studies

In a recent review of the biological basis of chemical carcinogenesis, Cox described the known and postulated pathways of benzene metabolism and leukaemogenesis [12]. Initial metabolism occurs primarily in the liver, forming benzene oxide, some of which is detoxified and excreted in the urine. The remaining benzene oxide may spontaneously rearrange to form phenol, or be converted to catechol and/or hydroquinone by liver enzymes. Phenol, catechol and hydroquinone are the three principle liver metabolites of benzene. Catechol and hydroquinone are known carcinogens: catechol causes glandular stomach cancers; hydroquinone elevates the incidence of leukemia in female rats and liver adenomas in female mice [21, 12].

Toxins are carried by the blood stream to bone marrow where they accumulate and can be found in high concentrations many hours after benzene exposure has ended [40]. In the bone marrow, these metabolites are transformed yet again. Several cell populations of the blood-forming system are susceptible to the effects of benzene metabolites [30, 41].

v) Experimental animal evidence

From animal studies, benzene appears to produce its affects on blood cell formation (hematopoiesis) in a number of ways. It can reduce the number of multipotent stem cells that differentiate into various blood-forming cells. Certain metabolites of benzene will destroy certain progenitor cells needed for human blood formation. Benzene also appears to have the same effect on certain marrow cells [30].

A number of experimental studies demonstrating chromosome damage and genotoxicity and benzene-induced cancer in animals have been reported. In these studies, benzene has been shown to induce leukaemia, lymphatic cancer and several other types of neoplasm in mice and rats. The production of cancer in more than one species and in more than one organ system reinforces the conclusion that a substance is carcinogenic.

Chromosome damage has also been seen in mice treated with benzene and benzene metabolites [19, 43, 11, 16, 8]. Sister chromatid exchanges have also been demonstrated in mice exposed to benzene by inhalation [34]; in human blood incubated with benzene metabolites [33]; and in T lymphocytes [15].

4. INTERJURISDICTIONAL PRACTICES

The following table illustrates WCB practice in other jurisdictions concerning benzene- induced disease. The asterisks in the table refer to the equivalent of Columns 1 (disease) and 2 (process) in the respective lists of each jurisdiction. The check-mark refers to listings by the International Labour Office (ILO) and proposed amendments thereto.

One Canadian jurisdiction (BC) has specified benzene-induced leukaemia and pre-leukaemia, together with benzene poisoning, and one foreign jurisdiction (France) has done exactly the same. In BC, exposure to ionizing radiation or benzene is specified as linked with leukaemia and pre-leukaemia. The ILO (check marks) has also listed benzene-induced disease.

Massachusetts set an occupational exposure limit for benzene as early as 1946 [23]. The American Conference of Governmental Industrial Hygienists (ACGIH) recommended a Threshold Limit Value (TLV) of 100 ppm in the same year [7]. In 1971, the International Labour Organization adopted a Benzene Convention that included, among other things, prohibition of the use of benzene in certain work processes; substitution with less toxic substances wherever possible; occupational hygiene measures to assure effective protection of workers; and medical surveillance of exposed workers [28].

Finland recognized benzene's leukaemogenic properties in 1973 [20]. In 1975, the ACGIH proposed classification of benzene as a suspected human carcinogen and reduced its recommended TLV to 10 ppm. In 1976, the National Institute for Occupational Safety and Health (NIOSH) concluded that benzene is leukaemogenic and recommended an occupational exposure limit of 1 ppm. [23]. Subsequently, the Occupational Safety and Health Administration (OSHA) proposed a 1 ppm permissible exposure limit, which came into effect in the U.S. in 1987. In the late 1970's and early 1980's a succession of countries including Australia, Denmark, Sweden, Norway, the Netherlands and Germany, classified benzene as a carcinogen or suspected carcinogen and prescribed restrictive occupational exposure limits and protective measures [20]. The International Agency for Research on Cancer (IARC) concluded in 1982 that there is sufficient evidence that benzene is carcinogenic to man.

Ontario passed a Designated Substance Regulation for benzene in 1984, and set the exposure limit at 5 ppm. Although the background research for the regulation discussed benzene's leukaemogenic properties at some length, the regulation did not identify benzene as a carcinogen.

In 1990, the ACGIH changed benzene's classification to confirmed human carcinogen and lowered its recommended TLV to 0.1 ppm.

5. EVALUATION OF THE EVIDENCE

The Panel uses the considerations articulated by Sir Austin Bradford Hill to evaluate the evidence of probable connection with occupation.

Strength of association:

The strength of the evidence establishes a probable connection between benzene exposure and the leukaemias.

Consistency:

Findings from cohort studies, case reports, animal experiments and chromosome studies cited above consistently support an association between benzene exposure and the leukaemias.

Specificity:

First, the Panel notes that Bradford Hill cautioned against relying on specificity. Where a particular exposure causes one particular disease, specificity is shown and is highly persuasive. Bradford Hill, however, emphasized that: "We must also keep in mind that diseases may have more than one cause."

Temporality:

Clearly, the exposure to benzene took place before the onset of the disease in the studies cited above.

Dose-response:

Research by Infante et al. (1983), Yin et al. (1989) and Wong et al. (1995) provide evidence of dose-response.

Biological plausibility:

Benzene interferes with the process of blood cell formation and induces "pre-leukaemic" pancytopenia or aplastic anaemia. The evidence that these conditions precede the onset of leukaemia supports the biological plausibility of the association between benzene and leukaemia.

Coherence:

The evidence as a whole, its consistency between studies of various types including experimental evidence, findings indicating dose-response and the biological plausibility of an association, is not contradicted by what is known about benzene exposure and leukaemia.

Experiment:

Experimental evidence establishes that tumours have been produced in more than one species of animal and in more than one organ system. This supports a causal link between benzene and the leukaemias.

Analogy:

The association between exposure to ionizing radiation and leukaemia provides an analogy to benzene exposure and leukaemia.

6. THE PANEL'S FINDING AND RECOMMENDATION

Benzene and its metabolites are toxic to almost all cells of the bone marrow. There is evidence of multiple mechanisms for benzene-related toxicity. The multiplicity of diseases associated with benzene exposure therefore makes sense.

Case reports, epidemiology, chromosome studies, metabolic studies and experimental evidence all support the conclusion that benzene exposures cause pancytopenia, aplastic anaemia, myelodysplastic syndrome and all variants of acute myelogenous leukaemia. This association is strong and constitutes a probable connection.

Considerable evidence also exists to link benzene to chronic myelogenous leukaemia, chronic lymphatic leukaemia, multiple myeloma and myelofibrosis and myeloid metaplasia. A number of studies also report an association with acute lymphoblastic leukaemia, non-Hodgkin's lymphoma, Hodgkin's disease and thrombocythemia.

A probable connection between benzene and leukaemic and pre-leukaemic cancer has been recognized in two other jurisdictions. Moreover, many jurisdictions will compensate the effects of benzene poisoning and its sequelae which includes various compounds and homologues of benzene. Compensation for work-related benzene poisoning can include compensation for neoplastic effects.

7. REFERENCES - Benzene and Leukaemia

1. Akland GG. Exposure of the general population to gasoline. Environ Health Persp Suppl 1993;101:27-32

2. Aksoy M, Erdem S, DinCol G. Leukemia in shoe-workers exposed chronically to benzene. Blood 1974;44:837-841

3. Aksoy M, Erdem, S, DinCol G. Types of leukemia in chronic benzene poisoning: a study in thirty-four patients. Acta Haemat 1976;55:65-72

4. Aksoy M. Malignancies due to occupational exposure to benzene. AJIM 1985;7:395-402

5. Aksoy M. "Leukemogenic and Carcinogenic Effects of Benzene" in M.A. Mehlman, ed. Benzene: Occupational and Environmental Hazards -- Scientific Update, Princeton Scientific Publishing Co. Inc., Princeton New Jersey, 1989

6. Amdur MO, Doull J, Klassen CD. "Aromatic Hydrocarbons" in Casarett and Doull's Toxicology: The Basic Science of Poisons, Fourth Edition, Pergamon Press, New York 1991

7. American Conference of Governmental Industrial Hygienists. "Benzene" in Documentation of the Threshold Limit Values and Biological Exposure Indices, Sixth Edition 1991

8. Anwar WA, Au WW, Legator M, Ramanujam VMS. Effect of dimethyl sulfoxide on the genotoxicity and metabolism of benzene in vivo. Carcinogenesis 1989;10:441-445

9. Austin H, Delzell E, Cole P. Benzene and leukemia. American Journal of Epidemiology 1988;127:419-439

10. Brett SM, Rodricks JV, Chinchilli VM. Review and update of leukemia risk potentially associated with occupational exposure to benzene. Environ Health Perspect 1989;82:267-281

11. Choy WN, MacGregor JT, Shelby MD, Maronpot RR. Induction of micronuclei by benzene in B6C3F1 mice. Mutat Res 1985;143:55-59

12. Cox LA. Biological basis of chemical carcinogenesis: insights from benzene. Risk Analysis 1991;11:453-464

13. Cullen MR. "Disorders of the Blood and Blood-Forming Organs" in Rosenstock L, Cullen MR. Textbook of Clinical Occupational and Environmental Medicine. W.B. Saunders Co., Philadelphia, 1994

14. Decoufle P, Blattner WA, Blair A. Mortality among chemical workers exposed to benzene and other agents. Environ Res 1983;30:16-25

15. Erexson GL, Wilmer JL, Kligerman AD. Sister chromatid exchange induction of human lymphocytes exposed to benzene and its metabolites in vivo. Cancer Res 1985;45:241-7

16. Gad-El Karim MM, Ramanujam VMS, Legator MS. Correlation between the induction of micronuclei in bone marrow by benzene exposure and the excretion of metabolites in urine of CD-1 mice. Toxic Appl Pharmacol 1986;85:464-477

17. Goldstein BD. Hematotoxicity in humans. J Toxicol Environ Health Suppl 2 1987:69-105

18. Goldstein BD. "Clinical Hematotoxicity of Benzene" in M.S. Mehlman, ed., op cit

19. Hite M, Pecharo M, Smith I, Thornton S. The Effect of benzene in the micronucleus test. Mutat Res 1980;77:149-155

20. Holmberg B, Lundberg P. Benzene: Standards, Occurrence, and Exposure. AJIM 1985;7:375-383

21. Huff JE, Haseman JK, DeMarini DM, et al. Multiple-site carcinogenicity of benzene in Fischer 344 rats and B6C3F1 mice. Environ Health Persp 1989;82:125-163

22. Illinois Environmental Protection Agency. Benzene - Chemical Information Sheet Office of Chemical Safety, Springfield, Illinois, July 1987

23. Infante PF, Rinsky RA, Wagoner JK, Young RJ. Benzene and leukemia. Lancet 1977;ii:868-869

24. Infante PF, White MC. Benzene: epidemiologic observations of leukemia by cell type and adverse health effects associated with low-level exposure. Environ Health Perspec 1983;52:75-83

25. Infante PF. Benzene toxicity: studying a subject to death. AJIM 1987;11:599-606 (letter)

26. Infante PF. Benzene and leukemia: the 0.1 ppm ACGIH proposed Threshold Limit Value. Appl Occup Environ Hyg 1992;7:253-62

27. International Agency for Research on Cancer. Benzene. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans Vol. 29, Some Industrial Chemicals and Dyestuffs. IARC, Lyon France 1982

28. International Labour Organization. International Labour Conventions and Recommendations, 1919 -1981. International Labour Office, Geneva 1982

29. Irving WS, Grumbles TG. Benzene exposures during gasoline loading at bulk marketing terminals. AIHA Journal 1979;40:468-472

30. Kalf GF. Recent advances in the metabolism and toxicity of benzene. Critical Reviews in Toxicology 1987;18:141-159

31. Kipen HM, Wartenberg D. "Lymphohematopoietic Malignancies" in Textbook of Clinical Occupational and Environmental Medicine, W.B. Saunders Company, Philadelphia, 1994

32. Landrigan PJ, Nicholson WJ. "Benzene" in WN Rom, ed. Environmental and Occupational Medicine, Little, Brown and Company, Boston, 1992

33. Morimoto K, Wolff S. Increase of sister chromatid exchanges and perturbations of cell division kinetics in human lymphocytes by benzene metabolites. Cancer Res 1980;40:1189-1193

34. Occupational Safety and Health Administration (OSHA). Final Rule on Occupational Exposure to Benzene. Fed Regist 1987;52:34460-34578

35. Penney, J. Report to the Occupational Disease Panel on occupational exposure to benzene and leukemia. 1995.

36. Rinsky RA, Young RJ, Smith AB. Leukemia in benzene workers. AJIM 1981;2:217-245

37. Rinsky RA, Smith AB, Hornung R, et al. Benzene and leukemia: an epidemiological risk assessment. N Engl J Med 1987;316:1044-1050

38. Rinsky RA. Benzene and leukemia: and epidemiological risk assessment. Environ Health Perspect 1989;82:189-191

39. Runion HE, Scott LM. Benzene exposure in the United States 1978-1983: an overview. AJIM 1985;7:385-393

40. Sawahata T, Rickert DE, Greenlee WF. "Metabolism of Benzene and its Metabolites in Bone Marrow." In: Irons RD, Toxicology of the Blood and Bone Marrow. Raven Press, New York, 1985

41. Snyder R, Kalf GF. A Perspective on Benzene Leukomogenesis. Critical Reviews in Toxicology 1994;24:177-209

42. Swaen GMH, Meijers JMM. Risk assessment of leukemia and occupational exposure to benzene. BJIM 1989;46:826-830

43. Tunek A, Hogstedt G, Olofsson T. Mechanism of benzene toxicity: Effects of benzene metabolites on bone marrow cellularity, number of granulopoietic stem cells and frequency of micronuclei in mice. Chem Biol Interact 1982;39:129-138

44. Vigliani EC, Saita G. Benzene and leukemia. New Engl J Med 1964;271:872-876

45. Wallace, Lance A. "The Exposure of the General Population to Benzene" in M.A. Mehlman, ed., op cit

46. Wong O. An industry wide mortality study of chemical workers occupationally exposed to benzene. I. General Results. Br J Ind Med 1987;44:365-381

47. Wong O. An industry wide mortality study of chemical workers occupationally exposed to benzene. II. Dose response analyses Br. J Ind Med 1987;44:382-395

48. Wong O, Raabe GH. Cell-type-specific leukemia analyses in a combined cohort of more than 208,000 petroleum workers in the United States and the United Kingdom, 1937-1989. Regulat Toxicol Pharmacol 1995;21:307-321

49. Yin SN, Li GL, Tian F, et al. Leukemia in benzene workers: a retrospective cohort study. Br J Ind Med 1987;44;124-128

50. Yin SN, Li Q, Tian F, et al. Occupational exposure to benzene in China. Br J Ind Med 1987;44:192-195

51. Yin SN, Li GL, Tain FD, Fu C, et al. A retrospective study of leukemia and other cancers in benzene workers. Environ Health Persp 1989;82:207-213

CHAPTER 6.
SUMMARY OF THE PANEL'S FINDINGS

Silicosis and silico-tuberculosis

The nature of silicosis and the sources of exposure make the disease peculiar to work processes using crystalline silica or generating silica dust. This peculiarity presents a very strong or definite association between silicosis and specific occupations or industries. The Panel finds that because the disease is almost always caused by a specific agent in particular employments, there is a conclusive connection between silicosis and work-related exposure to silica.

Silico-tuberculosis is a disease linked only to silicosis and therefore associated with workplace exposure to silica dust. The Panel feels this disease should be a listed disease in Schedule 3. Panel member, John Macnamara did not agree with the need for a separate listing.

Tuberculosis

The current schedule recognition of tuberculosis as characteristic of some employments is public notice of a probable connection between work and the disease. Adjudication experience shows that the disease is also characteristic of other additional specific employments. The Panel finds that the probable connection between tuberculosis and work is well established and that there is sufficient evidence to recognize a probable connection in other employments. These findings call for a revision of the Schedule 3 entry for tuberculosis.

Non-ionizing radiation and eye Injury

There are good reasons to expand the process description to include other work processes associated with photo and thermal eye injuries. Non-ionizing radiation sources in industrial settings are largely controlled by safety measures; however, toxic exposures can and do occur. The Panel finds there is sufficient evidence to revise the entry for non-ionizing radiation but chooses not to include cataract or gas discharge/arc lamps at this time.

The workplace eye injuries associated with excess ocular exposure to Ultra-Violet, Infra-Red and Visible Light are photo retinitis, photo keratitis and photo conjunctivitis. There is a probable connection between certain work processes, specifically arc and laser welding, and these diseases. Other injuries (e.g., cataract) and those injuries caused by related work processes using NIR (e.g., gas discharge/arc lamps, microwaves and radio waves) should be considered on a case-by-case basis. The effects of such processes are still very controversial and should be left for future investigations.

Benzene and leukaemia

The weight of evidence establishes a probable connection between occupational exposure to benzene and leukaemia and pre-leukaemia. Benzene and its metabolites are toxic to almost all cells of the bone marrow. A multiplicity of diseases is associated with benzene exposure. Case reports, epidemiology, chromosome studies, metabolic studies and experimental evidence all support the conclusion that benzene exposures cause pancytopenia, aplastic anaemia, myelodysplastic syndrome and all variants of acute myelogenous leukaemia. This association is strong and constitutes a probable connection.

Considerable evidence also exists to link benzene to chronic myelogenous leukaemia, chronic lymphatic leukaemia, multiple myeloma and myelofibrosis and myeloid metaplasia. A number of studies also report an association with acute lymphoblastic leukaemia, non-Hodgkin's lymphoma, Hodgkin's disease and thrombocythemia.

A probable connection between benzene and leukaemic and pre-leukaemic cancer has been recognized in two other jurisdictions. Moreover, many jurisdictions will compensate the effects of benzene poisoning, which would include the effects of various compounds and homologues of benzene, and its sequelae.

CHAPTER 7.
THE PANEL'S RECOMMENDATIONS

1. The Panel recommends that the entry for Silicosis be moved from Schedule 3 and placed in Schedule 4, to read as follows:

2. The Panel, having also previously reported on the probable connection between respiratory complications and non-malignant respiratory diseases, now recommends that Silico-tuberculosis be entered into Schedule 3 as follows:

4. The Panel recommends that the Schedule 3 entry for diseases caused by Non-ionizing radiation be changed to read as follows:

5. The Panel recommends that the connection between benzene exposures and leukaemic and pre-leukaemic diseases be entered into Schedule 3 as follows:

APPENDIX:
INTERJURISDICTIONAL COMPARISON TABLE (1995)

The interjurisdictional Table is an updated version of the 1992 comparison. The updated table represents the various provincial jurisdictions in Canada and includes the United Kingdom and France.

Prince Edward Island is no longer included because it has removed its Industrial Disease list from the provincial Workers' Compensation Act and has adopted a generalized procedure for adjudication on individual merit. The new legislation, proclaimed in January 1995, states that a worker who is found to suffer from a disease related to employment is entitled to compensation. There is no automatic presumption of occupational origin for diseases originally recognized on the old disease list. The WCB decision to discontinue the Industrial Disease list is the result of the low number of occupational disease claims filed in P.E.I. each year. Prince Edward Island has always been and still remains an agricultural province with limited industrialization.

The comparison table is set up so that all the diseases recognized in the various industrial disease lists are identified by individual entry.¹ Chemical agents have been grouped into their respective family groups for clarification and to avoid duplication. All other diseases have been divided into specific categories: "infections," "pneumoconioses," "cancers" and "others." In many cases, the diseases listed in these categories are divided into subgroups of diseases or disease causes.

By looking at the table one should be able to identify prescribed diseases and prescribed processes for each jurisdiction. To make this distinction, the numeric symbol 1' has been used to denote column 1 which lists occupational diseases, and the numeric symbol 2' has been used to denote column 2 which lists the occupational processes for each disease.² In the case of the French occupational disease list, the coding is handled a little differently.

The French Tableaux des Maladies Professionnelles lists a specific column 1 agent with an enumeration of the various diseases caused by this particular agent.³ The typographic symbol * is used to show that diseases and conditions specified in the French list are not all included in the comparison (many are not included because they are really symptoms, side effects or related conditions). The ^* symbol is therefore used as in the following example:

The above diagram illustrates that the chemical agent lead is recognized under column 1 as an occupational disease or as the cause of an occupational disease, and that there are various conditions caused by this agent specified in the original French table not listed in the comparison (e.g., saturnism).

Identifying Criteria are used in the comparison table to describe how other jurisdictions have scheduled particular diseases wherever a disease is recognized in Ontario by guideline alone. This is done to highlight the difference between Ontario and other jurisdictions in order to suggest which diseases Ontario might consider investigating for scheduling. The identifying criteria are characterized as follows:

C  general
C  limited
C  restricted

A General approach means a jurisdiction does not identify criteria per se; there is either no process attached to the disease or poisoning, or there is no mention of the type or length of exposure. This approach is open to interpretation. A Limited approach means a jurisdiction may describe the type of exposure (airborne dust, rawhide, cement) or the type of work that causes the disease (mining, farming, welding). A Restricted approach, however, means a jurisdiction has established definite criteria such as type, length and amount of exposure, as well as the type of work.

Comparison Table Symbols:

1	denotes prescribed disease (Column 1)
2	denotes occupations, substances or processes (Column 2)
*	denotes specific diseases or conditions not listed here
)	denotes current ILO listing
	denotes Ontario WCB guideline
8	denotes proposed ILO listing
G	denotes general approach to a prescribed disease (see definition p. 10)
L	denotes limited approach to a prescribed disease (see definition p. 10)
R	denotes restricted approach to a prescribed disease (see definition p. 10)

INTERJURISDICTIONAL COMPARISON 19954
Legend:                             (1 = disease in Column 1)                             (2 = disease, substance or process in Column 2)                             ( = Ontario WCB guideline)                             ( = ILO listing); ( = proposed amendments to ILO)
CHEMICAL AGENTS
Metals
DISEASE (Poisoning)	BC	AB	QB	NS	NB	NF	UK	FR	ON
Aluminum	2	2
Arsenic                                 5	1	1	1	1	1	1	1	1*6	1
Beryllium	2	2				1	1	1*	1
Boron			1
Brass					1				1
Cadmium	1	1				1	1	1*	1
Chromium	2		2			1		2	1
Iron			1					1
Lead	1	1		1	1	1	1	1*	1
Manganese	1	1				1	1	1
Mercury	1	1	2	1	1	1	1	1*	1
Nickel	2		2		1			1*	1
Selenium			1
Tungsten carbide	2	2
Zinc	2				1			2	1
All metals			1
Acetone	1	1
Benzene	1	1				1	1	1*	1
Carbon Tetrachloride	1	1					2	1*	1
Chlorinated naphthalene							1	1	1
Hexane	1	1					2	1*
Paints					1			2
Tetra- chloroethane		1					1	1*	1
Toluene	1	1						1	7
Trichloroethane	1	1						1*
Trichloroethylene	1	1						1*	1
Xylene	1	1						1
Others	1	1
Gases
Arsenic Hydride								1*
Carbon Dioxide									1
Carbon Monoxide	1	1		1	1	1			1
Carbon Oxide								1*
Carbon Disulfide				1			1		1
Carbon Sulphide								1*
Manganese Dioxide								1*
Phosgene	1	1
Nitrogen Compounds
Ammonia					1
Anilin									1
Benzene homologues & nitro & amino        derivatives						1	1	1*	1
Dinitrophenol							1	1*	1
Hydrogen Cyanide	1	1				1
Nitrile	1	1						1*
Nitrogen Oxides	2	2					1
Nitrogen compounds			1
Nitrous Fumes	1	1							1
Pesticides	2	2
Phenol									1
Halogens
Alicyclic Hydrocarbons			1					1*
Aliphatic Hydrocarbons			1			1		1*
Aromatic Hydrocarbons			1			1		1*
Carbon tetrachloride	1	1					1	1*	1
Chlorinated Hydrocarbons									1
Chloroform							1	1*
Fluorine	2					1		2
Methyl Bromide							1	1*
Methyl Chloride							2	1*
Halogens			1			1		1*
Antibiotics
Antibiotics			2				2
Penicillin								1*
Streptomycin								1*
Others
Acrylamide Monomer							1
Alcohols						1
Allergens			1
Anthracene								1*
Bitumen								1*
Carbonic Acid Gas					1
Cement			2					1*
Charcoal								1*
Chlorinated compounds	2
Chlorpromazine								1*
Chromic acid								1*
Coal	2	2						1*
Diethylene Dioxide							1
Epoxy Resins			2					1*
Exotic/wood dusts	2	2					1	1*
Formaldehyde								1*
Glycols						1
Hydrogen compounds								1*
Hydrogen Sulphide	1	1				1
Isocyanates	2	2					2	1*	8
Ketones						1
Metals			1
Nickel Carbonyl							1
Nitric Acid Esters						1
Nitroglycerine						1
Oxygen compounds			1
Phenylhydrazine								1*
Phosphate	1							1*
Phosphine	1
Phosphorus	1	1	1	1	1	1	1	1*	1
Polyvinyl Chloride								1*
Proteolytic Enzymes							2	1*
Silicium			1
Sulphur			1		1			1*
Tar								1*
Tellurium			1
Vinyl chloride							2	1*
Other Toxins (dust, gases, vapours, mists)	1	1
INFECTIONS
DISEASE	BC	AB	QB	NS	NB	NF	UK	FR	ON
Amebiasis								1
Ankylostomiasis				1			1	1*
Anthrax			1	1	1		1		1
• animal products							2
• bristles			2	2	1				2
• hair			2	2	1				2
• hides			2	2	1				2
• skins			2	2	1				2
• wool			2	2	1				2
Bacterial cutaneous/Fungal infection			1
Brucellosis	1	1	1		1		1	1*
Campylobacteriosis	1
Chicken pox	1
Epicondylitis	1
Giardia lambia	1
Glanders (equine)					1		1
Hepatitis B	1	1
Herpes simplex	1
Infectious/ parasitic diseases in risky   occupations			1			1
•pediculus human			2
•sarcoptes scabies			2
Leptospira							1	1
Meningitis	1							1
Multiple warts, hands			1
Mumps	1
Polio								1
Psittacosis	1
Rabies								1
Red measles	1
Rickettsial diseases								1
Ringworm	1
Rubella	1
Salmonella	1	1
Scabies	1
Shigellosis	1
Staph aureus	1	1
Staphylococci infections	1
Streptococci infections	1
Streptococcus suis							1
Sugar infections					1
Tetanus								1
Toxoplasmosis	1
Tuberculosis	1	1	1				1	1*	1
Typhoid	1
Viral hepatitis			1				1	1*
Whooping cough	1
Yersiniosis	1
PNEUMOCONIOSES
Anthraco-silicosis						1
Asbestosis	1	1	1			1		1*	19
Bilat. Diffuse pleural thickening   (asbestos)	1						1	1
• sclerogenic mineral dust)	1
Coal workers		2		1
Fibrosis	1						1	1
Legionellosis	1
Pneumoconioses	1	1			1	1	1		1
Siderosis			1					1*
•iron oxide/dust			2
Silico-TB						1		1
Silicosis	1	1	1		1	1		1*	1
•metalliferous mining	2	2						2
Talcosis			1
CANCERS
Angiosarcoma/liver	1						1	1
• vinyl chloride monomer	2						2
Bilateral diffuse pleural thickening							1
Bladder, ureter, renal, pelvis	1						1
• alpha-naphthyl amine							2
• beta-naphthyl amine	2						2
• benzidine	2						2
• methylene-bis ortho chloroaniline							2
• 4-nitrodiphenyl	2
GI (asbestos)	1R10
Larynx/pharynx (asbestos/nickel)	1L11
Leukemia/pre-leukemia	1							1
Lung	1R		1G12			1G	1	1
• arsenic	2
• asbestos	1		1			1		1
• bilat. diffuse pleural thickening	1						1	1
• bis chlormethyl-ether	2
• chromium	2
• nickel	2
• polycly. aromatic hydrocarbons	2
• uranium/radon	2
Mesothelioma	1L		1L				1	1	113
• asbestos	2		1			1	2	1
Nasal/sinus	1						1		114
• hardwood dust	2
• nickel	2						2		2
Sarcoma								1
Skin/Epitheliomatous	1			1		1	1	1	1
• anthracene						1
• arsenic	2
• coal tar	2
• cutting oils	2
• mineral oil				1		1	1		1
• paraffin				1			1		1
• soot							1
• tar, bitumen, pitch				1		1	1	1	1
• UV light	2
OTHERS
Asthma	1	1	1			1	1	1
• isocyanates	2	2
• red cedar dust	2	2					2
Bronchitis	1							1
Bronchopulmonary Disease			1			1		1
• asbestos								1
• flax						1
• hard metal			1			1
• hemp						1
• sisal dust						1
• cotton dust (Byssinosis)			1			1	1
Bursitis         •elbow         •knee	1		1	1	1		1 1	1	1
Conjunctivitis/retinitis from welding			1		1			1	1
Corneal dystrophy							1	1	1
• arsenic							2
• tar							2		2
Cubital tunnel syndrome	1
Cutaneous telangiectasia			1					1
Dermatitis	1	1			1		1	1*	1
• allergic	2	2	1
• irritative			1					1
• radiodermatitis/ionizing			1				1	1
• venenata				1					1
Dermatoses								1*
•chemical folliculitis           •keratoderma/callosities           •phytodermatosis (plants)			1 1 1
• lubricants								1*
Disease from high/low temperature			1					1*
Dysbarism (compressed air)	1		1		1	1	1	1*	1
Emphysema	1G
Episodic blanching of phalanges							1
Erosion of incisor teeth (acid fumes)	1	1
Extrinsic allergic alveolitis	1	1	1			1	1
• organic dusts	2	2
Fluorosis	1
Food poisoning	1
Frostbite				1
Hand cramps Grinder's disease								1
Head lice	1
Heart disease (Firefighter)	1
Heat cataract							1
Infected blisters									1
Inflam./ulcer. upper resp. pass, mouth   dust, liquid, vapour							1
Lyme disease	1
Metal fume fever	1
• zinc	2
• other metals	2
Miner's nystagmus							1	1
Neurosensory hearing loss	1G	1L	1G		1L	1G	1	1
New growth of skin							1
Plantar fasciitis	1
Radiation Injury				1			2	1*	1
(ionizing)	1	1	1			1
(non-ionizing)                                               • conjunctivitis, t cataract (heat)         • keratitis (UV)	1 1 1	1 1 1	1				1	1 1 1
Repetitive strain of hand/forearm							1
Resp disease, non-offset sprays									1
Respiratory Irritation	1
Skin diseases (chemical, biological,   physical)						1G
Subcutaneous Cellulitis         •hand (beat hand)         •patella (beat knee)				1 1			1 1
Tendinitis	1L		1G				1	1*
Tenosynovitis	1		1	1			1		1
Thoracic outlet syndrome	1
Vibration Induced disease	1L	1R	1G			1G		1*
4 This Table also contains diseases listed in Ontario's Schedule 4                 5 Proposed revisions to the ILO list of occupational diseases also include chemical and physical agents as well as specific diseases that are not listed in the comparison table, per "Revisions of the ILO List of Occupational Diseases Appended to Convention No. 121: Working Document". Dr. M. Lesage. International Labour Office, 1991.                 6 The * indicates that related conditions unlisted in this table are specified in the original reference; "Tableaux des Maladies Professionnelles". Paris, 1976.                  7 Toluene is recognized by guideline not as a poison but as fume toxicity caused by toluene   diisocyanate (TDI), a misnomer because TDI is not a metal.                  8 Limited to TDI                  9 Asbestosis is a Schedule 4 disease, which means that the disease in column 1 is conclusively presumed to be caused by processes in column 2; however, claims filed before May 28, 1995 are determined in accordance with the real merits and justice of the case (policy document).                  10 R - indicates that a restricted approach is attached to the definition of the specified disease. A Restricted approach establishes definite criteria such as type, length and amount of exposure as well as the type of work; e.g., a period of 20 years of continual exposure to asbestos dust between the first exposure and the diagnosis of disease, where exposure represents the major component of the occupational activity.                  11 L- indicates that a limited approach is attached to the definition of the specified disease. A Limited approach usually describes the type of exposure; e.g., airborne dust, raw hide, cement, or the type of work that causes the disease.                  12 G- indicates that a general approach is attached to the definition of the specified scheduled disease. A General approach does not identify criteria per se; either there is no process attached to the disease or poisoning, or there is no mention of the type or length of exposure. This approach is broad, intuitive and open to interpretation.                  13R.R.O. 1990. Reg. 1102, Sched. 4.                  14Schedule 4 disease.

Endnotes

¹ In this Report, the term "disease" means disease or condition or both.

² As revealed in the qualifying language of each subparagraph.

³ Until such time as the law is changed to say otherwise. Another example of statutory direction is s.134(12), which stipulates that notwithstanding other provisions in the Act, compensation for silicosis is only payable if work exposure to silica in Ontario amounts to at least two years before impairment. Section 134(16) does the same for asbestosis. The presumption in s.134(9) is rebutted if the evidence shows less than the minimum stipulated exposure.

⁴ Saskatchewan has no schedule or definition of disease and compensates diseases case-by-case as injuries. Manitoba defines occupational disease and includes disease in the definition of accident but has no schedule and uses guidelines. In 1995, PEI abolished the disease list and adjudicates case by case. Nova Scotia now allows exclusion of a particular injury or disease from eligibility, while retaining a schedule of diseases.

⁵ See ODP Reports Nos. 12 and 13 on lung cancer and hardrock mining; cardiovascular disease and cancer among firefighters, both 1994. See also ODP occasional paper "Decision Making: Theory and Practice", 1994.

⁶ Made explicit in s.134(9) of the Act and its predecessors.

¹ Silica in organic form is freely ingested in water and foods and is found in the bones and cartilage, as well as in connective tissue including the lungs, skin and arteries. It is important for the growth and strength of hair and nails.

² An Act To Amend The Workmen's Compensation Act, s.3, c.42. S.O. 1926. A section defining who was deemed to have silicosis was also added. The Silicosis Act, c.363, R.S.O. 1950, did not deal with or affect compensation issues but provided for regulation of industrial processes where there was silica exposure.

³ See IDSP Report No. 11 on respiratory complications among workers receiving compensation for non-malignant respiratory diseases, March 1993, for further data on the effects of silico-tuberculosis on a silicotic.

¹ Types that affect birds and cattle can also affect humans.

² All authorities recognize tuberculosis as a complicating factor in the progression of other diseases; from a public health perspective, tuberculosis as a complication of HIV positive status is drawing more clinical concern [Markowitz, 1994].

³ The Globe and Mail newspaper; A7. Aug.17, 1994; and MOL, Occupational exposure to Mycobacterium Bovis infection in deer and elk in Ontario, 1992. The Globe and Mail has also reported that TB is making a comeback among the homeless and the poor, with an infection rate of about 30% among the homeless; A1/10. March 7, 1996. The occupational risks for those serving the poor and homeless rise concomitantly.

¹ UV-A ranges from 315-400 nm: UV-B, 280-320; and UV-C, 100-280 nm. Adverse effects from UV- A typically require exposure levels thousands of times greater and thus far less hazardous than the other two. UV-B and UV-C are referred to as "actinic UV radiation".

² Threshold Limit Values (TLVs) are used world-wide for controlling occupational exposure to continuous optical sources [ACGIH]; however, TLVs do not apply to lasers.

³ A measurement of luminance which is often associated with the "brightness" of a light source.

¹ Smoking has been weakly associated with an increased incidence of leukaemia in several studies (Hoffman, 1989).

² Kipen and Wartenberg adapted this table from Goldstein (1989), to which we have added MDS.

¹ Industrial Disease lists, or schedules, are either attached to individual provincial Acts (WCA) or contained in their regulations.

² In Ontario and other Canadian jurisdictions, schedules are divided into 2 columns that separate diseases and related work processes.

³ Considering that the disease tables try to be exhaustive, only those diseases also recognized in Canadian jurisdictions and in the UK are noted; however, sometimes causative agents are also noted.

November 5, 1997

Mr. Glen Wright
Chairman
Workers' Compensation Board
200 Front Street West, 18th floor
Toronto, Ontario
M5V 3J1

Dear Mr. Wright:

The Occupational Disease Panel is pleased to provide you with its second Report on recommended revisions to Schedule 3. This Report addresses a number of issues including silicosis, silico-tuberculosis, non-ionizing radiation and eye injury and the relationship between benzene and leukaemia. All of the items addressed were chosen because of existing international recognition that these diseases are occupationally related. Additionally, IARC has lately recognized silica as a Group 1 carcinogen (v.68, 1997).

It came to our attention that in addition to the well established link between benzene exposure and leukaemia, there is a growing body of evidence which supports a relationship between benzene exposure and lymphatic cancers. The most recent data comes from a very large Chinese study conducted by Hayes et al. and published in the Journal of the National Cancer Institute, July 16, 1997 (copy enclosed). This study, together with other research, strongly suggests that there may be an association between benzene exposure and all haematological neoplasms. Since this current Report was limited to reporting on established and recognized occupational diseases we did not address the broader effects of benzene. We would, however, strongly recommend that the WCB in its new research role review the literature and rule on the association between benzene and haematological neoplasms other than leukaemia.

As is always the case I would be pleased to address this Report with you and your colleagues at your convenience.

Yours sincerely.

Nicolette Carlan
Chair