Industrial Disease Standards Panel (Occupational Disease Panel)
IDSP Report No. 13
Toronto, Ontario

Industrial Disease Standards Panel

In 1985 the Ontario legislature established the Industrial Disease Standards Panel (IDSP) 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.

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

95(8)

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 by writing:

Industrial Disease Standards Panel
69 Yonge Street, Suite 1004
Toronto, Ontario M5E 1K3
(416) 327-4156

Panel Membership

TABLE OF CONTENTS

Chapter 1. Introduction

• Further Panel investigations
  

Appendix A: IARC Evaluation of Evidence for Carcinogenicity

Appendix B: Glossary

Appendix C: WCB Operational Policy - Heart Conditions

Appendix D: Questions asked of cardiovascular consultants

Appendix E: Questions asked of carcinogenecist consultants

References

TABLES

1. Fires, Calls, Injuries and Fatalities Among Metropolitan Toronto Firefighters from 1983 to 1989, by Municipality

2. Mortality by Detailed Cause for Total Cohort, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto

3. Standardized Mortality Ratios by Duration of Employment for Selected Causes, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto

4. Standardized Mortality Ratios by Years Since First Employment for Selected Causes, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto

5. Standardized Mortality Ratios by Age for Selected Causes, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto

6. Arteriosclerosis/ischemic heart disease combined SMRs

7. Combined arteriosclerosis/ischemic heart disease, compared to all causes of death

8. Mortality due to Aortic Aneurysms Among Northwestern US Firefighers and Police compraed to US National Rates for 1950-1989

9. Mortality due to Aortic Aneurysms Among Firefighters from Metropolitan Toronto and Northwestern US compared to Police from Northwestern US

10. Firefighter Mortality/Morbidity Studies: Cardiovascular Disease

11. Firefighter Mortality/Morbidity Studies: Lung Cancer Findings

12. Firefighter Mortality/Morbidity Studies: Brain Cancer Findings

13. Firefighter Mortality/Morbidity Studies: Lymphatic/Haematopoietic Cancer Findings

14. Firefighter Mortality/Morbidity Studies: Colon Cancer Findings

15. Firefighter Mortality/Morbidity Studies: Bladder Cancer Findings

16. Firefighter Mortality/Morbidity Studies: Kidney Cancer Findings

17. Firefighter Mortality/Morbidity Studies: Rectal Cancer Findings

FIGURES

1. Continuum of Injuries and Illness

2. Number and status of WCB claims for cardiovascular disease from firefighters since 1961

3. Cardiovascular disease findings

4. Risk factors for ischemic heart disease among Los Angeles firefighters compared to underwriters, 1975

5. Circulatory disease mortality among Seattle firefighters, 1945-1983, by duration of employment

6. Circulatory disease mortality among Buffalo firefighters, 1950-1979, by duration of employment

7. Lung cancer findings

8. Lung cancer mortality among Danish firefighters, November 9, 1975 to November 9, 1980, by age

9. Respiratory cancer mortality among New Jersey firefighters, 1974-1980, by duration of employment

10. Lung cancer mortality among Swedish firefighters, 1951-1986, by number of fires attended

11. Brain cancer findings

12. Brain cancer mortality among Swedish firefighters, 1951-1986, by duration of employment and by number of fires attended

13. Lymphatic/haematopoietic cancer findings

14. Lymphatic/haematopoietic cancers other than leukemia among Seattle firefighters with 30 or more years of service, 1945-1983, by duration of exposure

15. Cancer of blood and blood cells mortality among Swedish firefighters, 1951-1986, by number of fires attended

16. Lymphatic/haematopoietic cancer mortality among firefighters from three northwestern US cities, 1945-85, by duration of employment

17. Lymphatic leukemia mortality among Metropolitan Toronto firefighters, 1950-1989, by duration of employment, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto

18. Colon cancer findings

19. Colon cancer mortality among Buffalo firefighters, 1950-79, by duration of employment

20. Colon cancer mortality among firefighters from three northwestern US cities, 1945-89, by duration of employment

21. Bladder cancer findings

22. Bladder cancer mortality among Buffalo firefighters, 1950-1979, by duration of employment

23. Kidney cancer findings

24. Kidney and ureter cancer mortality among Alberta firefighters, 1927-1987, by duration of employment and by exposure opportunity

25. Kidney cancer mortality among Swedish firefighters, 1951-1986, by duration of employment and number of fires attended 161

26. Rectal Cancer Findings

CHAPTER 1. INTRODUCTION

a) The issues before the Panel

The Industrial Disease Standards Panel (IDSP) was asked by the representatives of firefighters to determine whether any diseases were attributable to working as a firefighter. This Report focuses specifically upon cardiovascular diseases and cancer among firefighters. Claims for heart attacks experienced by the firefighters during the course of their employment are adjudicated under the accident provisions of the Act and will not be dealt with in this Report. Occupational non-malignant respiratory disease will be the subject of a subsequent Panel Report.

b) The IDSP mandate and terms of reference

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

The evidence that the IDSP investigates to find a probable connection is scientific and medical in nature. Specifically, the IDSP considers epidemiological studies, hygiene information about firefighter exposures, toxicological evidence about the identified contaminants and alternative causes of disease.

When evaluating this evidence, the IDSP uses the concepts of Sir Austin Bradford Hill (1965). Bradford Hill argued that to determine causality, consideration should be given to the following factors.

1. strength of association
2. consistency
3. specificity
4. temporality
5. biological gradient
6. biological plausibility
7. coherence
8. experiment
9. analogy

After weighing the evidence, the Panel will decide what, if any, probable connection exists between firefighting 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 payments are made (described below).

c) How these issues arose

In April of 1986, the Ontario Professional Fire Fighters Association approached the Minister of Labour to request better emergency treatment for firefighters who suffer the effects of inhalation of toxic gases [115]. They were advised to contact the IDSP.

In March of 1988, the Provincial Federation of Ontario Fire Fighters (PFOFF) sent a detailed brief to the IDSP which asserted that firefighters' work subjected them to an increased risk of heart disease [26]. Their brief referred to other jurisdictions which have enacted legislation imposing presumptions that heart and lung disease are causally connected with firefighting.

PFOFF asked the Panel to conclude that a relationship exists between heart and lung disease and working as a firefighter, and to recommend that a legal presumption be enacted in favour of compensation for such claims from firefighters.

The Panel added the issue of cancer among firefighters to its agenda after reviewing the findings of the IDSP Mortality Study of Fire Fighters in Metropolitan Toronto (discussed below) and other studies.

d) The organization of this Report

In the following pages, the Panel explores the issues of whether there is a probable connection between cardiovascular disease or cancer and working as a firefighter.

After an outline of the investigations undertaken by the Panel and the stakeholders' views, the legal framework for this work is described. The chemicals which have been identified at fire sites are listed, together with a description of what is known about exposure levels and a summary of the known health effects of each chemical. For cardiovascular diseases and several types of cancer, this Report summarizes the scientific evidence obtained from experts consulted by the Panel and from epidemiological and other data about the rates of disease, dose-response trends and potential causative factors. Ultimately, the Panel explains its policy recommendations which result from the integration of the scientific data and the legal requirements.

e) Investigations by the Panel

After receiving the PFOFF brief, the Panel directed its staff to conduct a review of the world literature on the health effects of firefighting.

That 1988 review identified elevated risks of injury due to falls, burns and accidents, as well as potential acute effects of exposure to smoke and chemicals. The chronic health effects of firefighting were unclear because there were too few studies and the quality of evidence was too limited to answer these questions; however, there was some evidence to "suggest that it is biologically plausible that firefighting could lead to the development of respiratory, cardiovascular and neoplastic disease" [222]. The Panel then placed the issues of cardiovascular and respiratory disease among firefighters on its agenda.

A protocol for a retrospective cohort study of mortality among Toronto area firefighters from 1950 to 1989 was drafted. The protocol was revised [85] in light of comments solicited from four independent expert reviewers [9, 71, 120, 165] and data collection began in January of 1990.

Analysis of those data was carried out and after revisions in light of two additional independent reviewers' comments [66, 57], the final report of findings entitled Mortality Study of Fire Fighters in Metropolitan Toronto was released in March, 1992 [86].

Because the study identified a statistically significant increase in the rate of brain and nervous system cancers as well as other malignant neoplasms, cancer was added to the other issues on the Panel's agenda.

The firefighters' representatives and Toronto area Fire Chiefs were invited to participate in the process of selecting medical specialists to review the study's findings and the updated literature review. One expert in each medical specialty was chosen by the firefighters, the Fire Chiefs and the Panel to answer specific question [117, 118].

• about cardiovascular disease:

  Dr. James M. Melius, New York Department of Health [119];
  Dr. Chris D. Morgan, Sunnybrook Hospital [126];
  Dr. John K. Wilson, Canadian Cardiac Health Centres [208].

A list of the questions posed appears in Appendix D.

• about cancer:

  Dr. Norman Boyd, Ontario Cancer Institute [17];
  Dr. Melissa A. McDiarmid, Occupational Safety and Health Administration [111];
  Dr. Ian Quirt, University of Toronto [155].

A list of the questions posed appears in Appendix E.

All of this information was provided to the firefighters' representatives, the six Fire Chiefs and two groups of representatives of municipalities for their comments.

PFOFF, the International Association of Fire Fighters (IAFF) and the Ontario Professional Fire Fighters Association (OPFFA) provided written submissions [37, 38, 44, 114] and made oral presentations to the Panel at its meeting of October 30, 1992. Their submissions are summarized below.

The Fire Chiefs sent a representative to that meeting to observe but made no written submissions.

The Municipal WCB Users' Group and the Association of Municipalities of Ontario were invited but both declined to attend or make written submissions.

In response to the firefighters' and some of the medical reviewers' comments, the Panel sought advice from Dr. Bernard C. K. Choi, of the University of Toronto, about how to control for the "healthy worker effect" when interpreting the findings of the IDSP mortality study [24, 25].

Dr. Kristan A. L'Abbé [87, 88], Dr. Paul A. Demers [33] and George A. Tomlinson [193] provided further analyses of the cardiovascular findings. Mr. Tomlinson also conducted additional analyses of the cancer findings and provided advice on the problem of multiple tests of significance [193]. Dr. Melissa M. McDiarmid was asked to elaborate on her previous comments about cancer latency [111].

The Panel sought advice from Dr. Dwayne M. Reed, an Epidemiological Consultant formerly with the Honolulu Heart Program, who has expertise in the etiology of aortic aneurysms [157].

Dr. F. Stern of the US National Institute for Occupational Safety and Health provided additional information about mortality due to aortic aneurysm among New Jersey motor vehicle examiners [187].

Drs. Tee L. Guidotti [58], Paul Targonski [190], John Vena [203] and Kenneth Rosenman [163] were asked to provide further analyses of their data on aortic aneurysms and cancer in other firefighter cohorts.

The Canadian National Centres for Toxicology were asked to comment on the literature about chemical exposures which firefighters may face [20]. In addition, a background paper was prepared for the Panel discussing the toxicology of common chemical constituents of fires and the effect on firefighters' incidence of brain cancer [199].

Finally, Dr. Eric Holowaty and Nelson Chong of the Ontario Cancer Treatment and Research Foundation provided a linkage between data from the Ontario Cancer Registry and the IDSP firefighter study data [140]. George Tomlinson and Dr. Rosa Hong Zhou of the University of Toronto provided analyses of those data [194, 224].

f) Submissions from stakeholders

The PFOFF, the IAFF and the OPFFA provided written submissions [37, 38, 44, 114] and made oral presentations to the Panel at its meeting of October 30, 1992. Excerpts from their unified position follow:

The IAFF also expressed concern about the risk of noise-induced hearing loss faced by firefighters [39]. They provided copies of studies that suggest that carbon monoxide and solvent exposure can also damage hearing and may potentiate the damaging effect of noise on hearing [4, 105, 45, 46, 168, 223, 134]. Hearing loss among firefighters will be considered by the Panel in a subsequent Report of Findings.

As noted above, neither the Fire Chiefs nor the invited representatives of municipalities made submissions.

CHAPTER 2. WORKERS' COMPENSATION LAW AND POLICY

a) The legal and administrative framework within which the IDSP operates

The IDSP's authority to conduct this work is set out in Ontario's Workers' Compensation Act. Specifically, the Act reads:

"95. ...

The Act also provides the following definition for an industrial disease:

"1. (1) In this Act,

Fig. 1: Example

CONTINUUM OF INJURIES AND ILLNESS

The term "industrial disease" occurs in the context of the Act and refers to an entity defined by the Act and not to a medical term. Because the term is defined by the law, the identification of an industrial disease requires the integration of law and science.

The need for and the development of industrial disease policy are distinguishable from other policy development processes at the Workers' Compensation Board. This distinction is visually captured in Figure 1 prepared by the Minister of Labour's Occupational Disease Task Force. Accidents usually are single events with an immediate onset of disability. Diseases normally develop over time and may not be apparent for many years after the initial exposure. For example, asbestos-related illnesses are usually not evident until at least 10 years after the initial exposure and may have an onset as late as 30 years after that first exposure.

Usually, individual workers and employers do not have a sufficiently broad information base to identify patterns of disease. Realistically, the long-term perspective and wide view can only be achieved by scientific research or information gathered by external bodies such as government agencies.

On this point Professor Paul Weiler, one of the primary architects of the IDSP, wrote:

The IDSP was created in 1985 with the intention of bringing that broad perspective and specialized expertise to the task of identifying industrial diseases.

As set out in section 95 of the Act, the Panel is authorized to make findings of probable connection between disease and work. These findings are reported to the WCB which has the right to accept or reject

the findings and to declare the existence of an industrial disease in an appropriate circumstance.

At the time s. 95 was added to the Workers' Compensation Act, the Minister of Labour said:

This indicates that the government of the day determined that it would be appropriate for the Panel to make findings of apparent causal connection. This suggests that it may be best to understand "probable connection" as meaning something like "apparent causal connection." This should not be confused with the concept of causation, a relationship that is the subject of medical and scientific research.

Once there is a finding of probable connection by the IDSP and a declaration of an industrial disease by the Board, it is then necessary to develop guidelines for the processing of claims. In accordance with its mandate under the law and often at the request of the WCB, the Panel may make recommendations to the Board about when employees with a disease should be compensated.

The Workers' Compensation Act has provisions to accommodate the unique issues associated with industrial disease adjudication. Specifically, Schedules 3 and 4 have been added to the legislation to make the workplace parties aware of accepted and declared industrial diseases. By entering a disease into one of these Schedules the work association is declared. Once a disease is assigned to Schedule 3 or 4, a worker need only prove that he or she suffers from the disease and was exposed to the associated industrial process. By demonstrating this, the worker has invoked the presumptions in s. 134. This shifts the onus to the WCB in the case of Schedule 3 diseases to disprove the work association in any specific case. In the case of Schedule 4 diseases there is no ability to disprove an association.

When a disease is not listed in Schedule 3 or 4, in practice the affected worker has the burden of proving the work association. The standard applied by the Worker's Compensation Appeals Tribunal, and endorsed by the Minister's Task Force on Occupational Disease, to establish a work relationship is that work was a "significant contributing factor" to the disease. The worker may be required to present medical evidence, and perhaps epidemiological evidence, about the usual causes of the disease. The worker may also have to obtain information about the chemicals to which he or she was exposed at work, and investigate whether these chemicals may have "significantly contributed" to the onset of the disease.

It is possible to formulate criteria for determining whether a disease is the sort to be added to Schedule 3 or 4 or whether guidelines should be created. However, those criteria have not yet been clearly articulated by the WCB. The best guidance available on this issue are the current entries in each of the Schedules. The Panel has examined the current entries and attempted to identify the criteria used by the Board when entries were made in the past. The Panel has also reviewed internal WCB documents on this point.

When are diseases listed in Schedule 4?

Schedule 4 is in the Regulations to the Workers' Compensation Act. When a worker suffers from one of the diseases listed in Schedule 4 and can show that he or she was exposed to the associated industrial process, then the following conclusive presumption applies:

"134. ...

Currently, only three diseases are included in Schedule 4: asbestosis, mesothelioma and nasal cancer. The pattern of criteria for inclusion that the Panel has identified by reviewing these entries is as follows:

• 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 and/or duration of exposure;

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

• a biological explanation for the development of the disease.

There are no "diseases of ordinary life" included in Schedule 4.

When are diseases listed in Schedule 3?

The legislation setting out Schedule 3 reads as follows:

"134. ...

According to our understanding of the WCB process, when a worker claims to have a disease that is listed in this Schedule, the adjudicator would first determine whether the claimant has the disease and was exposed to the corresponding industrial process. If these conditions are satisfied, the adjudicator would be required to "presume" that the disease is compensable. This does not end the matter, however, since "the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved" (emphasis added).

This appears to direct the adjudicator to ask whether there is any other information that demonstrates that the disease was not caused by work. At this stage of adjudication the IDSP believes that WCB staff would be aided by a set of criteria referred to collectively as a rebuttal matrix. That matrix would assist adjudicators in the identification of facts that would lead to the rebuttal of the statutory presumption. If evidence of this sort "proves the contrary", then the disease is no longer presumed to be due to work and compensation may be denied.

Diseases entered in this Schedule appear to have a strong but not exclusive connection to work processes. In looking to determine if a disease should be included in Schedule 3 the WCB apparently has looked 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.

For diseases currently listed in Schedule 3 there may be several possible causes for a disease. Currently in the Schedule there are diseases which are known to have both employment and non-employment etiologies. This has allowed for the scheduling of "diseases of ordinary life" such as dermatitis.

When a disease is not listed in the Schedules, are there alternative tools available to assist the adjudicators?

Employees receive compensation for a disease if it is established that the disease is caused by work, even when the disease is not listed in the Schedules.⁽³⁾ The WCB has issued many "policies" or "guidelines" that assist adjudicators on how to handle claims on an individual basis. These policies are created by the WCB as a result of the investigation of many instances of a specific disease.

In instances where the evidence is equivocal about whether a disease is caused by work, the IDSP has recommended that the Board create specific policies and guidelines concerning the disease. This approach was adopted by the IDSP in its Report on Scleroderma. The lack of certainty about the work association may exist because there is little known about the disease or because there is contradictory evidence about an association. When and if the evidence becomes stronger it may be appropriate for the IDSP to issue revised recommendations to the Board which may endorse entering the disease into a Schedule.

b) Policy and claims experience considerations regarding cardiovascular disease

(i) Ontario

No legal presumption has been applied to cardiovascular disease nor to the occupation of firefighting in Ontario. Claims are adjudicated by the Workers' Compensation Board on a case-by-case basis.

WCB policy on heart conditions states that the Board accepts entitlement if a causal relationship is shown, either as an "accident" or as a "disablement" "arising out of and in the course of employment". That policy includes, as one example of an acceptable causal circumstance, heart conditions which result from "inhalation of smoke and various noxious gases and fumes, e.g., fire fighters" [220]. The full policy is reproduced in Appendix C.

It also provides for conditions arising from unusual physical exertion and/or acute emotional stress as long as there is no significant delay in the onset of symptoms. Claims such as these may be allowed on the basis of aggravation of pre-existing non-compensable conditions, and permanent disability benefits are reduced in proportion to the contribution made by the pre-existing condition.

The Workers' Compensation Appeals Tribunal (WCAT) has allowed claims for fatal heart attacks in firefighters [213], some of which involved pre-existing coronary artery disease or atherosclerosis [216, 215], and in one case the claimant was a smoker [215]. Working as a firefighter was considered a "significant contributing factor", but not the only factor, in the development of the heart condition. In both of these cases, the firefighter was working at the time of the heart attack. Another claim [217] for a myocardial infarction was denied because it did not occur at work and was not considered caused by employment exposures.

The WCAT allowed one case involving a fatal pulmonary edema from coronary insufficiency in a firefighter who was a smoker and who had previously suffered a mild, non-compensable cardiac infarction [212]. His death did not occur while working, but while he was undergoing a stress test.

Since 1961, the WCB reports having received a total of 469 claims from firefighters [178]. The types and status are shown in Figure 1.

Fig. 2: Number and status of WCB claims for cardiovascular disease from firefighters since 1961:

DISEASE	CLAIMS FILED	ALLOWED	DENIED	PENDING
Ischemic heart disease	57	24	31	2
Aortic aneurysm	2	1	1	-
Other cardiac disease	8	4	3	1
Cerebrovascular disease	1	1	-	-

During their presentation to the Panel, the representatives of the firefighters stated that firefighters rarely file workers' compensation claims for diseases. It was their perception that the WCB takes considerable time to decide claims for disease, and such claims are likely to be rejected as unrelated to work. Moreover, many firefighters, particularly those in Metropolitan Toronto, are covered by employment insurance plans that provide benefits at least as beneficial as workers' compensation benefits, and there is no requirement that the disease be related to work. These circumstances make it likely that the number of WCB claims filed under-represents the incidence of diseases to which their work may contribute.

(ii) British Columbia

Section 6(3) of the BC Act provides:

In 1954, the BC legislature applied the rebuttable presumption in Schedule B to claims for "injury to the heart" from workers in the firefighting industry. Because the Board began receiving claims from non-firefighters who worked in the firefighting industry, the language in the Schedule was changed in 1980 to cover "[H]eart injury or disease including heart attack, cardiac arrest or arrhythmia, disease of the pericardium, heart muscle or coronary arteries" in claims "[W]here the worker is employed as a firefighter."

A review of reported cases showed that, in practice, the presumption is virtually never rebutted [89].

(iii) Saskatchewan

In response to the Firefighters' Association's position that heart and lung disease in firefighters should be presumed to be work-related, the Saskatchewan WCB commissioned a review of the world literature on heart and lung disease in firefighters, which was completed in 1986 [73]. The author concluded that there was insufficient evidence to show that firefighters' overall risk of heart disease is increased by their occupation and accordingly, no presumption has been enacted. In fact, presumptions are not used in the adjudication of any disease or injury claims in Saskatchewan [167].

(iv) United States

The laws in several US states contain presumptions that heart disease is related to firefighting. Those presumptions are all described as rebuttable; however, because there are widely divergent tests applied to rebut the presumptions, the practical effect varies from irrebuttable to virtually meaningless [91].

c) Policy and claims experience considerations regarding cancer

There is presumptive legislation in some Canadian provinces covering claims for cancer. While some of these presumptions may apply to claims made by firefighters because of their individual circumstances, none of them pertains specifically to firefighters.

(i) Ontario

Schedule 3 of the Workers' Compensation Act includes, at entry 4:

"Description of Disease	Process
Epitheliomatous cancer or ulceration of the skin due to tar, pitch, bitumen, mineral oil or paraffin or any compound, product or residue of any of these substances.	Handling or use of tar, pitch, bitumen, mineral oil or parrafin or any compound, product or residue of any of these substances."

There is little doubt that fighting fires involves exposure to compounds, products or residues of tar, pitch, etc. since these are substances which are widely used in construction materials, etc. The WCB has advised the Panel that it interprets "epitheliomatous cancer" of the skin as meaning all skin cancer types including malignant melanoma [42]. This entry provides a rebuttable presumption to firefighters' claims for skin cancer.

The Ontario WCB has no policies about cancer claims specific to firefighters. There are several policies that have identified cancer as an industrial disease, such as lung cancer in gold miners and gastro-intestinal cancer in asbestos workers.

(ii) British Columbia

Section 6(3) of the BC Act provides:

"If the worker at or immediately before the date of the disablement was employed in a process or industry mentioned in the second column of Schedule B, and the disease contracted is the disease in the first column of the schedule set 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."

This presumption applies to claims for "[P]rimary cancer of the skin" "[W]here there is prolonged contact with coal tar products, arsenic or cutting oils or prolonged exposure to solar ultra-violet light."

On January 29, 1993, the BC Workers' Compensation Board's Appeal Division granted the claim of a firefighter for malignant melanoma, a cancer of the skin. Although the worker was not able to describe in detail the nature of his exposure over his 22 year career, the Panel considered the available general evidence which indicates that a firefighter is likely to come into repeated intermittent contact with "coal tar products, arsenic or cutting oils". Since, in this case, the contrary was not proved, his disease was presumed to have been work-related [218].

On December 12, 1993, however, that decision was set aside by the Supreme Court of British Columbia on the ground that the Appeal Panel erred by applying too high a standard of proof for rebutting the Schedule B presumption. The case has been returned to the Appeal Division for reconsideration [201].

In another case, the BC WCB Appeal Division granted a firefighter's claim for multiple myeloma (cancer of plasma cells in bone marrow[183]). It was accepted because the evidence supported a link between the disease and occupational exposure to benzene and because there was no evidence to support any alternate hypothesis [219].

(iii) Manitoba

In 1977, the Manitoba Board passed Regulation #24/77 which stated:

That provision was struck down by the Manitoba Court of Appeal in 1988. The Court found that, under the specific terms of the Manitoba Workers' Compensation Act, the Board's power to make regulations is limited to administrative and procedural matters and that the Board does not have the power to make regulations which will expand coverage by the Act. Consequently, that regulation no longer applies. There have been no attempts by the WCB to introduce guidelines that would apply to claims from firefighters.

(iv) United States

According to our research, twenty-four US states apply presumptions, all rebuttable, to firefighters' claims for cancer but, again, the tests used to rebut those presumptions vary widely.

Alabama, California, Illinois, Minnesota, Nevada, Oklahoma and Rhode Island apply a presumption to claims for "cancer". In Maryland, a presumption is applied to claims for "throat, prostate, rectal or pancreatic cancer, or leukemia". The states of Louisiana, New Hampshire, North Dakota, Oregon, Pennsylvania, Washington, Missouri, Wisconsin, Virginia, South Carolina, Michigan, Maine, Hawaii, Iowa and Tennessee apply a presumption to claims for lung or respiratory disease [116], which is usually held to include lung cancer by the courts [91].

In 1990, the state of Massachusetts applied a rebuttable presumption in favour of work-relatedness to firefighters' claims for "any condition of cancer affecting the skin or the central nervous, lymphatic, digestive, haematological, urinary, skeletal, oral or prostate systems" [108]. That presumption was applied after researchers at the University of Lowell in co-operation with the Massachusetts Department of Public Health reported findings from their study of the incidence of cancer among firefighters from 1982 to 1986. Those findings were acknowledged to be conservative estimates because about 50% of Cancer Registry records did not indicate any occupation.

The terms of the Massachusetts legislation require active firefighting duty and reflect internationally recognized knowledge about toxicology and latency in the development of cancer. Specifically, it provides that:

1) the firefighter must have undergone a pre-service examination which did not reveal cancer;

2) the firefighter must have served for at least five years before diagnosis, and must have regularly responded to fire calls;

3) the type of cancer must be one which may result from exposure to heat, radiation or a known or suspected carcinogen as determined by the International Agency for Research on Cancer (IARC); and,

4) the presumption ceases to apply five years after the firefighter leaves active fire service.

Despite its efforts, the Panel was unable to identify the reasoning behind the application of legal presumptions in other US and Canadian jurisdictions.

Table 1: FIRES, CALLS, INJURIES AND FATALITIES AMONG METROPOLITAN TORONTO FIREFIGHTERS FROM 1983 TO 1989, BY MUNICIPALITY

	City of Toronto	Scarborough	East York	North York	City of York	Etobicoke	TOTAL
1983: fires other calls FF injured FF killed	2541 24778 138 -	718 84 108 -	250 2636 9 -	1173 12177 117 1	224 24 14 -	624 8 4 -	5530 39707 390 1
1984: fires other calls FF injured FF killed	2428 33850 153 -	740 52 48 -	258 3242 12 -	1144 16272 128 -	255 54 19 -	544 12 4 -	5369 53482 364 -
1985: fires other calls FF injured FF killed	2398 30138 172 1	924 10495 27 -	272 2894 3 -	1120 14425 135 -	198 33 10 -	545 7 4 -	5457 57992 351 1
1986: fires other calls FF injured FF killed	2247 31197 216 -	803 11323 68 -	243 2997 4 -	1103 15190 131 -	256 32 18 -	561 23 4 -	5213 60762 441 -
1987: fires other calls FF injured FF killed	2877 32828 245 -	914 11977 90 -	244 3056 12 -	1108 16903 196 -	197 34 7 -	625 15 8 -	5965 64813 558 -
1988: fires other calls FF injured FF killed	2751 35040 258 -	895 13523 104 -	254 3268 10 -	1145 19000 132 -	191 46 3 -	523 19 6 -	5759 70896 513 -
1989: fires other calls FF injured FF killed	2634 37706 316 -	831 14940 74 -	217 3693 21 -	1139 21115 118 -	251 57 8 -	526 18 24 -	5598 77529 561 -

CHAPTER 3. THE EVIDENCE

a) About firefighting

Fire protection in Ontario is a municipal responsibility. As of 1986 (when the most recent figures were available to the Panel), 706 of the approximately 800 municipalities in Ontario operated 656 fire departments. Those Departments employed 9,127 full-time and 16,994 part-time (volunteer) firefighters, for a total of 26,121.

Table 1 shows the number of fires, other calls, firefighter injuries and line-of-duty deaths from 1983 to 1989 in each municipality included in the IDSP study. It is important to note that firefighters' illnesses and deaths which were caused by diseases are not included in Table 1. It is clear, however, that some municipalities responded to many more actual fires than others [135, 136].

There are two main phases of firefighting. The process of extinguishing the main fire is called the "knockdown" phase. The "overhaul" phase involves searching for and extinguishing hidden fires.

Self-contained breathing apparatus (SCBA) was introduced in the last 20 years or so [60]. SCBA includes a pressurized bottle of air carried on the firefighter's back. A hose leading from the air tank feeds clean air into a mask covering the face. Because of its "positive pressure", any leaks flow out from the mask, rather than allowing contaminated outside air to enter the mask. When used properly, SCBA provides very effective, but not complete, protection from carbon monoxide and other chemical exposures [101, 94].

The oxygen provided by most SCBA is designed to last thirty minutes [61]. Since firefighters must allow about ten minutes to get out of a burning building in order to change air tanks, and since the air supply is consumed more quickly during heavy exertion, each tank effectively provides only 15 minutes' breathing protection. The firefighters' representatives explained that there is often an inadequate number of air tanks available to them at fire sites. They said that, in recent years, Toronto fire departments have been equipped with compressors which produce air for refilling used tanks, but that these are rarely if ever available to firefighters who work outside Metropolitan Toronto.

SCBA was generally under-utilized or used inconsistently in many fire departments until the 1980's [59]. The firefighters' representatives advised the Panel that in recent years most of them use SCBA during the knockdown phase. Once the main fire has been extinguished, it appears that the danger has been reduced and firefighters often remove their SCBA because it is heavy, hot and cumbersome [19]. Its use actually interferes with breathing, particularly during strenuous work [102] and even moreso when the tank's air supply has been reduced to 30% of capacity [110]. Regular use of SCBA is particularly difficult under extreme weather conditions [59].

Firefighters who remove their SCBA during overhaul work could suffer the most dangerous exposures [60]. Researchers who have measured carbon monoxide levels in blood (carboxyhemoglobin) report that intermittent use of SCBA offers as little protection as no use at all [94, 95, 60].

It is estimated that 80% of firefighters' injuries are due to smoke inhalation or oxygen deficiency and that over 50% of line-of-duty deaths are due to smoke exposures [60].

Smoke is a suspension of carbon particles in air and in other gases [166]. All smoke is hazardous and is potentially lethal at high enough concentrations. The degree of hazard depends on the chemistry and quantity of gases, concentrations reached, size of particulate, solubility of gases and duration of exposure [60].

Particulates become adsorbed (coated) with chemicals in smoke and carry those chemicals deeper into the lungs during active firefighting than they would during normal, less strenuous activities. The heavy exertion demanded by fighting a fire causes more rapid and deeper breathing which increases delivery of toxins to deep within the lungs [60].

Carbon monoxide is a by-product of all fire and is one of the most hazardous chemical exposures encountered by firefighters. Since carbon monoxide is odourless, colourless and tasteless, the amount present at a fire site cannot be

judged by the firefighter. There is no correlation between the apparent intensity of smoke and the amount of carbon monoxide in the air [60, 94, 95].

Other dangerous products of combustion also continue to be chemically reactive after the main fire has been extinguished and they continue to form additional chemical substances [60, 30]. For example, one of the fuel components of the original material in upholstery, wire, pipe coating and wall, floor and furniture coverings is polyvinyl chloride. Hydrogen chloride and phosgene are produced as decomposition products when these materials are burned [60].

Synthetic materials, such as polyethylene and polyvinyl chloride, have been widely used since the 1950's in furniture and building construction [60]. These substances are often more dangerous when they are smouldering than in high heat. In addition to carbon monoxide [41], synthetic materials cause large numbers of other hazardous chemicals, such as hydrogen cyanide and hydrochloric acid, to be present at fire sites [60, 40, 83, 210]. Moreover, concrete retains heat and gasses, acting like a sponge, then releases toxic fumes as cooling takes place and for long after the fire has been extinguished [60, 40].

Chemical hazards of firefighting

Fire smoke has so far not been well characterized [119]. The chemicals present at fire sites are extremely variable depending upon the type of fire and local physical conditions [60]. As their representatives told the Panel, firefighters can be exposed to a myriad of substances in unknown quantities, which are heated and mixed together [114]. The synergistic effects of these substances are unknown.

In this Report, the Panel has focused on those chemicals which have been identified at fire sites and for which there is evidence of a potential link with cardiovascular disease or cancers. The chemicals discussed below

• were measured in studies of actual fires as reviewed by McDiarmid and colleagues [112];
• were reported to be present in a subsequent survey of the fire environment by Jankovic et al. [82]; or
• were included in two toxicological reviews prepared for the Panel [20, 199].

The following discussion summarizes the reported levels of these chemicals at fire sites and includes, for comparison purposes, a brief description of their current Ontario exposure limits. (In some cases the exposure limits are too detailed to be included in the text of this report and the reader should consult the Regulation.) The Ontario Ministry of Labour's bipartite Occupational Exposure Limits Task Force conducted a review of the current exposure limits and has recommended lowering all of the current limits listed below [137].

Most of the limits given below are Short-Term Exposure Values (STEV) or Ceiling Exposure Values (CEV). The STEV is a 15-minute time-weighted average concentration which may not be exceeded at any time during a workday, while a CEV is the maximum airborne concentration of a chemical to which a worker may be exposed at any time during a workday.

It should be noted that an STEV is set on the basis of preventing the acute adverse effects which have been observed in humans or animals after high short-term exposures. Thus, comparisons between firefighters' exposures and STEVs or CEVs may have little significance in estimating the risk of long-term health effects such as cancers and chronic cardiovascular diseases.

Where an STEV or CEV is not available, a Time-Weighted Average Exposure Value (TWAEV) may be mentioned instead. A TWAEV is the average airborne concentration of a chemical agent to which a worker may be exposed in a workday or work week.

In most cases, a comparison between airborne contaminant measurements at a fire site and a TWAEV is inappropriate because of firefighters' relatively short period of exposure to airborne contaminants at most fires.

Several of the chemicals mentioned below (i.e. acrylonitrile, benzene, asbestos and vinyl chloride) are also regulated as designated substances in Ontario. This means that permissible exposure levels, methods of use and control in the workplace are specifically prescribed by Regulation.

The Panel's work has been aided by the critical reviews and evaluations conducted by the International Agency for Research on Cancer. IARC has used its unique international position to develop a system for classification that has been praised for the elegant scientific criteria used for selecting and evaluating published evidence on cancer. IARC is widely recognized as an authoritative source of information on the carcinogenicity of chemicals and complex exposures. For a detailed description of the IARC criteria, please see Appendix A.

The Panel wishes to emphasize that the following alphabetical list is far from exhaustive.

Acrolein

Acrolein is present in most fires as a combustion product of wood, cotton, carpeting and upholstery [60]. Its vapour may also be found at fire sites where acrolein is stored and used for the manufacturing of products such as metals, plastics, perfumes and methyl chloride refrigerants [20].

In a study of various building fires, 56% of the measurements reported for airborne acrolein were above 3 ppm (ranging from below detection to 98 ppm) [198]. These measurements exceed the STEV of 0.7 ppm (0.3 mg/m3) for airborne acrolein by at least four times [143].

A later study of various types of fires reported lower levels during different phases of firefighting, ranging from not detectable to 3.2 ppm in the knockdown phase and 0.2 ppm in the overhaul phase [82]. The study also showed that significant exposure to acrolein could occur amongst firefighters even with the use of self-contained breathing apparatus since levels as high as 0.9 ppm were measured in air samples collected from inside the masks of these devices worn by firefighters at fire sites.

Acrolein is a severe eye and respiratory tract irritant. It has also been shown to interfere with lung function in animals [20]. The carcinogenicity of acrolein has not been well investigated and the evidence in both humans and animals is inadequate (Group 3) according to IARC. One of its metabolites, glycidaldehyde, is considered to be carcinogenic [79].

Acrylonitrile

Acrylonitrile is a flammable liquid used in the manufacture of acrylic fibres and various rubber products. At fire sites, firefighters can be exposed to vapours from heated acrylonitrile or from the combustion of products in which acrylonitrile is an ingredient [12].

Acrylonitrile is irritating to the skin, eyes and respiratory tract. It is metabolized to form cyanide which inhibits respiratory enzymes and can cause death [154].

Systemic effects are non-specific but may include the central nervous system (headache and nausea) and hepatic (liver dysfunction), renal, cardiovascular and gastrointestinal (diarrhoea and vomiting) systems [154].

Acrylonitrile has been described as carcinogenic by some researchers [191], particularly in lung and prostate cancers [176]. IARC classifies acrylonitrile as Group 2A, probably carcinogenic in various cancers such as lung, prostate, stomach, colon, brain, lymphatic and haematopoietic system [79].

Acrylonitrile is a "designated substance" in Ontario. The conditions under which most workers may be exposed to it are set out in Ontario Regulation 733/84 under the Occupational Health and Safety Act [145].

Asbestos

Because of its insulating qualities, asbestos has been widely used in building materials for residential, commercial and industrial settings [160]. Therefore, asbestos fibres are likely to be present in a wide variety of fires.

In a 1990 study of 226 metropolitan New York firefighters, almost all of whom had worked as firefighters for at least twenty years, forty-nine percent had abnormalities on chest x-ray that are characteristically caused by prior exposure to asbestos. It was concluded that firefighters are at risk for scarring

of the lungs and pleura due to occupational asbestos exposure. It was thought that much of that exposure occurred during the overhaul phase of firefighting [107].

The fact that asbestos causes mesothelioma and lung cancer in humans is clearly established [160, 76]. IARC has classified asbestos as a Group 1 carcinogen for which the evidence is sufficient [79]. The Panel has previously reported that it can also cause laryngeal and gastrointestinal cancers [77, 160]. It is also carcinogenic to animals [79].

Asbestos is a designated substance in Ontario. Regulations limiting most workers' exposure to asbestos in workplaces, construction projects and in buildings and repair operations are prescribed by Regulation [142, 143].

Benzene

Benzene may be present at fire sites where it is being used as an ingredient for the manufacture of various products (e.g. medicinal chemicals, dyes, artificial leather, linoleum, oil cloth, varnishes and lacquers) and as a solvent for waxes, resins and oils [20]. It is also a common decomposition product of many organic materials.

After carbon monoxide, benzene is generally the second most commonly found organic constituent of fire smoke, typically present in high concentrations in the fire environment [19]. Mean airborne concentrations ranging from 28-63 ppm of benzene were measured from grab samples collected at various content/building or car fires. These concentrations were two to four times Ontario's current maximum allowable concentration of 15 ppm at any time [144]. The measurements from individual air samples were as high as 16 times this maximum allowable concentration (ranging from not detectable to 250 ppm). These findings are similar to previous reports of benzene measurements at fire sites which reached levels greater than 150 ppm [198].

A more recent study showed that firefighters could be highly exposed to benzene even with the use of self-contained breathing apparatus since levels as high as 21 ppm were measured from air samples collected from inside SCBA masks worn at fire sites [82].

In addition to its irritative and narcotic effects, benzene damages the bone marrow resulting in reduced red and white blood cells and platelets. This can lead to anemia, susceptibility to infection and clotting disorders [20]. It is also known to produce both non-malignant tumours and leukemia in rats and cause mutation and DNA damage in rodent cell cultures [79].

IARC has classified benzene as Group 1, for which there is sufficient evidence of carcinogenicity to humans (causing several types of leukemia) and to animals (causing cancer of multiple sites). It has also produced both non-malignant tumours and leukemia in rats and caused mutation and DNA damage in rodent cell cultures. Lymphoid cancer has been induced in mice by inhalation of benzene [79].

Benzene is a designated substance in Ontario [144].

Carbon monoxide/dioxide

Carbon monoxide and carbon dioxide are common occupational exposures of firefighters because they are natural products of combustion and are necessarily present at every fire. The health effects of exposure to each of them are very different.

Mean carbon monoxide concentrations measured from grab samples ranged from 22.7 ppm (auto fire), 235 ppm (content fires) to 272 ppm (building fires) [19], all of which were well below the current Ontario STEV of 400 ppm; however, a much higher mean of 500 ppm was reported in another study [5]. The difference may be due to the nature and intensity of the fires studied, as well as the sampling duration and location selected.

Studies using rats exposed to varying concentration ratios of carbon monoxide and carbon dioxide showed that carbon monoxide in the presence of 5% carbon dioxide is twice as toxic as carbon monoxide alone. Apparently, carbon dioxide acts to increase uptake of carbon monoxide and to prolong its effects [30].

Unlike carbon monoxide, carbon dioxide is a simple asphyxiant. It is also considered a potent stimulus to respiration, as well as being both a depressant and an excitant of the central nervous system [154].

No mean concentration was reported for carbon dioxide in any of the available studies. Grab sample measurements reported in several studies ranged from below 1,000 ppm to 60,000 ppm (a difference of at least 60 times), the latter being twice the STEV of 30,000 ppm for carbon dioxide. However, such levels may be uncommonly high for carbon dioxide at most fires. A recent study of various fires reported carbon dioxide levels to be 300-5410 ppm during the knockdown phase and 130-1420 ppm in the overhaul phase [82].

When inhaled, carbon monoxide is quickly absorbed into the blood stream and bind with red blood cells to form carboxyhemoglobin. This complex displaces oxygen on red blood cells by a factor of 200 times and interferes with the transfer of essential oxygen to body tissues [60, 205, 222]. Carbon monoxide is directly toxic to the heart [20] and may be involved in the development of atherosclerosis [222]. Atherosclerosis may predispose an individual to aortic aneurysm [158].

Mean carboxyhemoglobin levels of about 4% were measured in non-smoking firefighters exposed to carbon monoxide concentrations as low as 200-1000 ppm [55]. These levels approach those in smokers (5-7%) who consume an average of 1.5 packs of cigarettes per day [180].

The maximum concentration of carbon monoxide in samples measured typically exceeded 1,000 ppm [19, 53, 82] and sometimes reached potentially lethal levels of 3,000 ppm [5] to 5,000 ppm [198]. Levels measured during the knockdown phase (up to 1900 ppm) were substantially higher than during the overhaul phase (up to 82 ppm) [82].

Carbon monoxide may also worsen the damage to hearing caused by noise [46, 223]. Occupational hearing loss among firefighters will be discussed in detail in a subsequent Panel Report.

Chloroform (trichloromethane)

Chloroform may be found as a constituent of solvents and as a decomposition product of organic materials in fires.

Chloroform has been quantified in the fire environment, but at relatively low concentrations [112].

It is known as a skin and eye irritant [20], a central nervous system depressant and a cause of liver and kidney damage [149]. Cardiovascular and carcinogenic effects in humans are generally not known. However, IARC did report sufficient evidence that chloroform is carcinogenic to animals (Group 2B), causing cancers of the liver and kidney [79]. This substance can also cause genetic damage and is a reproductive toxin in rodents [20].

Diesel exhaust

Diesel exhaust is a complex mixture which includes polycyclic aromatic hydrocarbons (PAHs), benzene, formaldehyde, etc. There is to date no single exposure standard or guideline available for diesel exhaust exposure. The combined particulate fraction of diesel exhaust is usually determined as total particulates and as methylene chloride extract of the total particulate fraction. The latter is used as an indicator of the content of PAHs.

A survey of 23 Ontario fire stations concluded that firefighters may be significantly exposed intermittently to diesel exhaust in the fire station from the operation of diesel-powered vehicles. Carbon monoxide levels were used as a marker for diesel exhaust concentration. For purposes of comparison, carbon monoxide concentration was measured directly from the vehicle exhaust and averaged about 200 ppm (ranging from 60 to 750 ppm). Carbon monoxide levels were found to be less than 5 ppm (background level) in the fire stations but were higher than 50 ppm (up to 120 ppm) on the apparatus floor when vehicles were started or returned to the station. Levels as high as 33 ppm were measured in the living quarters of the fire station during these two periods [97].

In most cases, carbon monoxide measured on the apparatus floor decreased to levels below 10 ppm within ten minutes after reaching peak concentration. This was largely attributed to the different types of control measures used in fire stations, such as mechanical tailpipe exhaust, structural barriers, natural and mechanical ventilation, and pole hole location [97].

A union representative of firefighters advised the Panel that in some fire stations, it is common practice to regularly start the vehicle engines while they are inside the station to ensure that they are in working order. Diesel exhaust exposure could also be significant when, for example, only one vehicle in a multi-vehicle station responds to a call. In such a circumstance, the vehicle is started indoors and those firefighters who remain in the station are exposed. The Panel was advised that the walls and floors in most fire stations are washed every year, but in some cases the walls become "black" with diesel exhaust particulate within about six months. Most but not all urban stations have adequate separation between living quarters and the apparatus floor [28].

IARC has classified diesel engine exhaust as probably carcinogenic to humans, particularly in the cases of lung and bladder cancers (Group 2A). It reports sufficient evidence that diesel exhaust is carcinogenic to animals in lung cancer [80].

Formaldehyde

Formaldehyde is used in the manufacture of resins, textiles, embalming fluids, fungicides, air fresheners [20], plastics, adhesives, wood products, insulation, paints, leather and rubber [164]. It may therefore be present as a decomposition product in fires involving such materials.

Brandt-Rauf (1988) studied different types of fires and reported mean (grab sample) formaldehyde concentrations of 0.8 ppm and 0.5 ppm in the air at content fires and building fires, respectively. Airborne formaldehyde was not detected in the automobile fires observed. These means are two to four times below Ontario's STEV of 2 ppm for formaldehyde in workplace air, although levels as high as 3.3 ppm and 8.3 ppm were measured in content fires and building fires, respectively [19]. Thus, formaldehyde levels

which could cause acute health effects in humans may be present in certain areas or during certain phases of a fire.

In another study, formaldehyde levels as high as 8 ppm were measured during the knockdown phase of the fires, as well as a maximum level during the overhaul phase of 0.4 ppm [82].

Formaldehyde is a primary irritant to the mucous membranes of the eyes, nose and respiratory system and can cause headaches, cough, difficulty sleeping, diarrhoea, nausea, phlegm, weakness, vomiting, dizziness, wheezing, chest pain and tightness, breathlessness, rash, bronchitis and pneumonia [196]. Acute respiratory tract irritation can lead to pulmonary edema and pneumonitis [131].

According to IARC, formaldehyde is probably carcinogenic (Group 2A) [79]. Cancers which occurred in excess in more than one study were: Hodgkin's disease, leukemia, and cancers of the buccal cavity and pharynx (particularly nasopharynx), lung, nose, prostate, bladder, brain, colon, skin and kidney [79].

An excess of deaths from lymphopoietic cancer was found among formaldehyde-exposed workers by Levine et al. (1984).

Thomas and Waxweiler report an association between occupational exposure to formaldehyde and brain cancer [191]. The incidence of brain cancer was consistently elevated among professional groups (embalmers, pathologist, anatomists) but not among industrial workers exposed to formaldehyde. There was correlation between these professionals' years of exposure and brain cancer [14]. For the pathologists studied, chronic exposure to other substances such as organic solvents, tuberculosis infection and drugs have also been implicated [64].

Halons

Halons are fire extinguishing agents. Halon fire extinguishers are present in offices, factories, public buildings, etc. [20].

As a rule, Halon gases are not lung irritants except at high concentrations. The most important toxicological effects of Halons are on the central nervous system (CNS) and on the cardiovascular (CV) system. Clinically important CNS effects almost always appear at lower levels of exposure than do CV effects. CNS effects resulting from Halon overexposure are: alterations in perception, increase in reaction time, and reduced ability to concentrate on complex intellectual tasks [197].

The cardiovascular effects of Halons are the most significant hazard of their use. They can cause decreased blood pressure and cardiac arrhythmias. Halons appear to interact with endogenous catecholamines (chemical messengers in the body) such as adrenalin. It is thought that Halons sensitize the heart to the arrhythmogenic action of adrenalin. This assumption is based on the supposed release of adrenalin from the adrenal medulla during excitement, fear or other stressful stimuli such as that experienced by firefighters. Exposure to other toxicants such as chloroform in fires which can also cause similar effects would potentiate the cardiac effects of Halons [20].

Hydrogen chloride

Hydrogen chloride is used in the manufacture of pharmaceuticals, chlorine, vinyl chloride and alkyl chlorides, and in the chlorination of rubber [20]. Hydrogen chloride gas is one of at least 75 identifiable potentially toxic compounds produced by the combustion of polyvinyl chloride [40]. Since polyvinyl chloride is widely used in home construction, furnishings, electric wire, telephone cables, office equipment [40] and wallcoverings [30], hydrogen chloride is likely to be present in most fires [2, 112].

In a study of different fires, mean hydrogen chloride concentrations of 0.1 ppm and 3.3 ppm (grab samples) were measured in the air of building and content fires, respectively [19]. These concentrations are below Ontario's CEV of 5 ppm [143]. Levels exceeded twice that CEV (ranging from not detectable to 13.3 ppm), however, were measured in some samples collected from content fires. Other studies reported similar and even higher findings, with levels as high as 40 ppm [103], 150 ppm [43] and 200 ppm [198] of hydrogen chloride at sites of "non-specified mixed" fires.

Acute effects of hydrogen chloride exposure include eye, skin and throat irritation [106], as well as impairment to respiratory functions [30]. It has also been found to have cardiotoxic effects in rats [138].

Hydrogen cyanide

Hydrogen cyanide is commonly used in the production of chemicals such as resin monomers, cyanide salts, nitriles (e.g. acrylonitrile) [22] as well as rodenticides and insecticides [20]. It is produced by the incomplete combustion of both natural fibres (such as wool and silk) and synthetic polymers (such as polyurethane, polyacrylonitrile, nylon and

melamine) widely used in building materials and furnishings [175].

While one study reported hydrogen cyanide in only 10-15% of the fires surveyed [103], others have detected it in as many as 47% of the fires studied [112]. Since polyvinyl chloride is a pyrolysis product of polyvinyl chloride, which is a very widely used polymer, hydrogen cyanide is likely to be involved in most fires [2].

Mean or average concentrations of hydrogen cyanide reported in different studies ranged from 0.04 [53] to 3.7 ppm [103] and from 2.9 to 15 ppm [19]. The highest level was reported for content fires and exceeded the CEV of 10 ppm [143]. The measurements from such fires ranged from below detection to 75 ppm [19], a level five times the CEV.

Hydrogen cyanide is much more potent and faster acting than carbon monoxide [2] and can be rapidly fatal [30]. Both hydrogen cyanide and carbon monoxide are chemical asphyxiants that render the body incapable of utilizing an adequate supply of oxygen. While carbon monoxide interferes with the transport of oxygen to the tissues by its affinity to haemoglobin, cyanide alters the cellular use of oxygen in energy production [30]. Carbon monoxide and cyanide are additive in producing changes in blood flow within the brain but may act synergistically on cerebral metabolism, so that their combined effects are greater than that expected by either substance alone [153].

Nitrogen dioxide

Nitrogen dioxide is a common decomposition product of fires. It may also be present in fires which occur where it is being used as an ingredient in the manufacture of chemicals [20], nitric and sulphuric acids, and explosives.

A mean concentration of 0.47 ppm was reported for nitrogen dioxide in 8-minute air samples collected at non-specified mixed fires [53]. This concentration is well below the STEV of 5 ppm set for nitrogen dioxide in Ontario workplaces [143]. In another study, nitrogen dioxide levels as high as 10 ppm [198] were observed in some of the samples, although no mean values were reported.

Nitrogen dioxide is a strong lung irritant and can cause pulmonary edema [20]. NIOSH considers it a suspected carcinogen based upon animal studies and limited epidemiologic evidence [149].

Organic solvents

Organic solvents are widely used in various workplaces to dissolve other organic materials and are classified into several broad categories⁽⁵⁾.

Firefighters may be exposed to a complex mixture of organic solvents present in fire stations, at fire sites, and from decomposition products of materials involved in the fires.

After carbon monoxide, benzene is generally the second most commonly found organic constituent of fire smoke [19]. In a review of various studies, grab sampling measurements of other solvents such as chloroform, dichlorofluoromethane, methylene chloride, perchloroethylene, toluene and trichloroethylene were well below the respective exposure limits used for comparison by the authors[]. These limits are comparable to the STEVs or TWAEVs prescribed for the individual chemical agents mentioned.

All organic solvents affect the central nervous system to some extent, acting as depressants and anaesthetics. They also cause dermatitis and other health effects depending on the solvent and the route and extent of exposure. These effects range from narcosis to death from respiratory arrest. While some (e.g. n-hexane and methyl n-butyl ketone) cause peripheral neuropathy when chronically exposed, others (e.g. carbon tetrachloride) are recognized more for their acute injuries to the liver, kidneys and gastrointestinal tract [81]. Exposure to trichloroethylene, a commonly used solvent, has been found to cause liver cancer in mice [154]. Benzene causes considerable adverse effects on the blood-forming tissues and bone marrow (see "Benzene", above). Carbon disulphide has been linked to cardiovascular disease [84]. There is evidence to suggest that solvent exposure can also exacerbate the damage to hearing caused by excessive noise [168].

Polycyclic aromatic hydrocarbons (PAHs)

PAHs are multi-ring aromatic compounds found widely dispersed in nature. They are formed during the combustion of many organic materials (for example, diesel fuel) and high-temperature processing of crude oil, coal and

coke. They also occur in tobacco smoke and grilled, smoked and fried foods [81].

Only one study reported concentration of airborne PAHs in fire smoke. The measurements ranged from below detection to 0.5 mg/m³ during knockdown and below detection to 0.02 mg/m³ during overhaul. Personal samples from firefighters showed no measurable exposure to PAHs when the SCBA was worn [82].

No short-term exposure limit has been prescribed in Ontario for PAHs per se, although a TWAEV of 0.2 mg/m³ has been set for coal tar pitch volatiles (total benzene-solubles). As already mentioned, a comparison of the aforementioned measurements with a TWAEV may not be meaningful because of the short-term or intermittent exposure profile of firefighters to contaminants in fire smoke.

In the human body, PAHs are metabolized to more water soluble compounds which are excreted through urine or bile. While many PAHs, such as naphthacene and anthracene, are not known to be carcinogenic, others (eg. benzo(a)pyrene, benzo(a)anthracene and pyrene) and their metabolites have shown to be slight to potent carcinogens. These PAHs, particularly benzo(a)pyrene, may be linked to increased risk of cancer of the lungs, colon, pancreas, stomach, pharynx and bladder reported in petroleum refinery workers and in workers exposed to coke, coal tar pitch and asphalt. Tar and pitch exposure is associated with benign and malignant skin tumours [81, 79].

A detailed review of the epidemiological literature by Thomas and Waxweiler identified an association between PAHs and brain cancer (1986). Other authors have suggested a link between exposure to PAHs and leukemia [62] and cancers of the bladder, kidney and ureter [59].

Soots

Since all fires create soots, it is likely that firefighters are also significantly exposed during firefighting. Soots contain polycyclic aromatic hydrocarbons (PAHs), many of which are known carcinogens in humans. These particulates have been measured in detectable amounts in the smoke of building fires [82].

IARC reports that there is sufficient evidence to establish soots as carcinogenic to humans (Group 1) in the cases of skin, scrotal and lung cancer. Statistically significant excesses in mortality from esophageal and liver cancer and leukemia were also found among chimney-sweeps exposed to soots [79].

Vinyl chloride

Vinyl chloride is used primarily to manufacture plastic articles (from polyvinyl chloride) such as building and construction materials (pipes, ducts, floor tiles, electrical wire and cable), packaging (films, sheets, bags and bottles), clothing, insulation, automobile upholstery and mats, records, toys and a variety of consumer goods [21]. When sufficiently heated, these articles can release vinyl chloride and other products of decomposition which are health hazards. In all, at least 75 potentially toxic products have been identified in the thermal degradation of polyvinyl chloride [40].

The Panel is aware of only one study which reported measurements of vinyl chloride in fire smoke, by Markowitz et al.(1989). Only a small amount of vinyl chloride was detected in the smoke from the decomposition of plastics. Measurements from a fire involving polyvinyl chloride showed that the products of pyrolysis consisted mostly of nitrogen, hydrogen, carbon monoxide and hydrogen chloride [106]. Also identified in lesser amounts were carbon dioxide, hydrogen cyanide, benzene and methane. The concentration of vinyl chloride itself was, however, below the limit of detection (less than 0.2 ppm) in that study.

Short-term exposures to high concentrations of vinyl chloride have resulted in euphoria, dizziness, respiratory irritation, headache, nausea, irritability, poor memory and tingling sensations [20]. A high incidence of Raynaud's syndrome, hypertension and coronary deficiencies had also been reported in workers exposed for at least 5 years [90].

According to IARC, there is sufficient evidence (Group 1) that vinyl chloride is carcinogenic, causing cancers of the liver, brain, lung and haematolymphopoietic system in humans. IARC also noted findings of excessive melanoma, gastric and gastrointestinal cancers in exposed individuals [79]. Several authors also reported an association between vinyl chloride and brain tumours, particularly gliomas [191, 93]. It has also shown to be carcinogenic, mutagenic and genotoxic in studies on rodents and cell cultures [79].

Vinyl chloride is a designated substance in Ontario [141].

Other

Methylene chloride and sulphur dioxide have also been identified at fire sites. They cause eye and skin irritation but are not known to lead to the major health outcomes upon which the Panel has decided to focus in this Report.

SUMMARY

There is evidence that many of the chemical substances to which firefighters may be exposed are carcinogenic to humans and animals. Some of these substances cause cardiovascular, respiratory and central nervous system effects. In addition, carbon monoxide and solvent exposure may worsen the damage to hearing caused by excessive noise exposure.

Other hazards of firefighting

The physical activities demanded by their work may also affect firefighters' cardiovascular health.

In 1992, a York University research team published a detailed study of the activities involved in firefighting [51]. Based upon that information, they developed a fitness screening protocol for firefighter applicants [52] which has recently been adopted by several Fire Departments.

This research identified the following physical tasks which are commonly required during active firefighting:

• carrying equipment up stairs in high-rise buildings while wearing breathing apparatus and turnout gear, which together weigh 48.4 pounds dry and are heavier when wet;

• advancing charged hoses, sometimes from a distant hydrant, outdoors around obstacles or in icy conditions and indoors through hallways or stairs;

• carrying heavy equipment long distances from the truck to a fire site, particularly when garbage and furniture interfere with access to the fire site;

• breaking down doors, walls, ceilings and roofs; forcible entry through walls or steel security doors using hand tools;

• raising ladders, sometimes with an insufficient number of firefighters; using an axe while on a ladder;

• working overhead with a pike pole or other equipment; for example, breaking through a roof while on a ladder;

• rescuing victims from a roof or window using a ladder, or from confined areas using hand and power tools; moving victims from damaged cars or collapsed buildings;

• raising and lowering equipment or victims from high-rise windows using ropes;

• fighting fires for extended periods of time; conducting lengthy extrication and rescue operations, for example, in multi-vehicle accidents, industrial fires, train derailments, etc.; and working overhead or in awkward positions for extended periods of time [51].

A firefighter's endurance is reduced by self-contained breathing apparatus and other protective clothing which is hot, cumbersome and heavy [179]. The extra weight and effort causes more rapid breathing which is made even more difficult by using the respirator [51]. As mentioned above, the heavy exertion demanded by fighting a fire causes more rapid and deeper breathing which increases delivery of toxins to deep within the lungs [60].

In older buildings composed of heavier construction materials, fires reach higher temperatures and spread more rapidly. Firefighters must work more quickly, encumbered by these physical constraints and in even higher heat [51].

Fighting high-rise building fires requires climbing several flights of stairs carrying the weight of protective gear, tools and hoses, and removing heavy windows or opening concrete walls. Newer buildings often involve concrete construction and toxic materials [51]. Concrete absorbs heat and toxins, then releases them gradually as it cools [51, 60].

Obviously, firefighters are exposed to very high temperatures. Heat stress is compounded by the insulating properties of the protective clothing and by physical exertion, which result in endogenous heat production [60]. Research indicates that heat stress contributes to ischemia [6] and to the risk of a myocardial infarction in a predisposed individual [126].

In addition to burns, radiant heat may cause skin injuries such as erythema and telangiectasia [60].

Firefighting in winter conditions can pose special problems as water freezes and firefighters undergo large fluctuations in body temperature when they repeatedly enter and exit the fire site [51].

Darkness and smoke decrease visibility, impede search and firefighting procedures and may lead to accidents and traumatic injuries [51].

High noise levels make firefighting more difficult and dangerous. Noise interferes with speech and hazard communications and drowns out warning signals, which can eliminate firefighters' ability to prevent traumatic injuries. Loud noise can also cause stress reactions which are measurable in increased heart rate and elevated blood pressure [110] and some studies have documented noise-induced hearing loss among firefighters [159].

Firefighters routinely face unknown personal danger and, unlike most other workers in Ontario, they have no legal right to refuse work which is unsafe⁽⁶⁾. They are often responsible for the safety of other people. These

responsibilities, quite understandably, cause high levels of psychological stress [60, 16].

Finally, there is some evidence that shiftwork has a negative effect on subjective, and to a lesser extent, objective measures of health. Normal 24-hour (circadian) rhythms are disturbed by shiftwork, which can interfere with sleep patterns. Family and social activities may also suffer [50].

b) Considerations for interpreting epidemiological evidence

(i) Selected terms⁽⁶⁾

Dose-response:

A dose-response trend is shown when an increase in the "dose" (exposure level, intensity or duration) corresponds to an increase in the "response" (death or disease). In the studies of firefighters, dose is usually measured by duration of employment.

Latency period:

The period of time between first exposure to a substance(s) and the appearance of the disease which it has caused. In the studies discussed below, latency is usually measured by time since first employment.

Standardized Mortality Ratio (SMR):

An SMR is computed by comparing the number of deaths observed (i.e. that occurred) among firefighters with the number of deaths which are expected based upon a comparison group of the same age and sex, during the same time period:

            "observed" deaths among firefighters }   				
SMR =  ----------------------------------------  } (x100)
                   "expected" deaths             } 

Most authors multiply the ratio by 100, but some do not. An SMR greater than 100 (or 1) suggests an excess risk of death. Epidemiologists evaluate the statistical significance of an elevated SMR by using the 95% confidence interval, which is the range in which the true SMR would fall 95% of the time.

If the lower end of the 95% confidence interval is above 100 (or 1), the likelihood that the excess mortality is due to chance is less than 5% (or 1 out of 20). If the SMR is under 100 (or 1) and the upper 95% end of the confidence interval is under 100 (or 1), a statistically significant decrease in deaths is indicated, compared to the number of deaths that would normally be expected.

(ii) Potential sources of bias

When evaluating epidemiological evidence, it is important to consider the following factors.

Ascertainment bias

The results of epidemiological studies can sometimes be skewed by an ascertainment bias. This may occur when the total cohort is not (or usually, cannot be) traced in order to identify illness or death; in other words, they are "lost to follow-up". In order to err on the side of caution, epidemiological studies assume that subjects lost to follow up are alive. This means that they contribute "person-years" throughout the study period even if they have died. This has the effect of overestimating the time subjects worked and remained healthy as well as underestimating the "observed" number of deaths. If the outcomes for those lost to follow-up were known, their deaths would raise the mortality rates in one or more categories of disease, because death is a common reason for the inability to trace members of a cohort.

For example, in a study by Kusiak et al. (1993) of lung cancer among uranium miners, Social Insurance Numbers (SINs) were available for only 63% of the men in uranium mines (largely because SINs were not issued until 1965). The SMR for those with SINs was 225, whereas for those without SINs, it was only 135. The authors indicated that the "additional identifying information obtained from the SIN Registry permitted the identification of a much higher proportion of the deaths of Ontario miners." According to the calculations of the IDSP, improved ascertainment contributed significantly to a 67% increase in SMRs when the vital status of miners with SINs was compared to the vital status of miners without SINs. (This may also be partly due to differences in exposure and follow-up between the two groups.)

Whenever fewer than 100% of the cohort is traced, an ascertainment bias will cause an underestimation of risk, unless the author specifically adjusts for this bias. The larger the number of subjects who are not traced, the larger the underestimation of risk.

The Panel reviewed the percentage of subjects whose health outcomes were traced in each firefighter cohort study discussed in this Report and found that all but one study traced 90% of the members of each cohort, usually more than 90%.

Proportion of subjects traced in firefighter mortality studies:

Beaumont et al., 1991	97%
Demers et al., 1992	98%
Eliopulos et al., 1984	97.3%
Guidotti, 1993	96%
Hansen, 1990	over 99%
Heyer et al., 1990	95.4%
L'Abbé & Tomlinson, 1992 (IDSP)	97.8%
Lewis et al., 1982	95%
Mastromatteo, 1959	78.4%
Musk et al., 1978	92.1%
Tornling et al., 1994	100%
Vena & Fiedler, 1987	97.5%

As shown above, in one very early study [109] 21.6% of firefighters were lost to follow-up which could introduce ascertainment bias. Nevertheless, that study identified statistically significant increases in cardiovascular-renal deaths among Toronto firefighters. Its findings were probably one of the reasons for the subsequent emphasis and concern about the risk of cardiovascular disease among firefighters.

The healthy worker effect

Many epidemiological studies compare workers to the general population. Since the general population includes people who do not or cannot work due to illness or disability, including work-related disability, a working population is usually healthier overall and usually has a lower rate of mortality for most causes of death. The influence of these factors on the results of epidemiological studies is known as the healthy worker effect. This effect results in lower SMRs than would occur if comparisons had been made with a working population.

Almost all authors of firefighter studies commented that the healthy worker effect had influenced the cardiovascular findings. The influence of the healthy worker effect on findings for cancer, however, is somewhat controversial.

There is no screening test for the susceptibility to cancer, but some experts believe that workers who are selected for being at low risk for cardiovascular and respiratory disease are healthier overall and are therefore less likely to develop cancer [111, 184]. Others think that if those who are susceptible to heart and lung disease are excluded from the fire service, the ones who are admitted will have a statistically higher chance of developing cancer [155]. Monson's review of studies of ten groups of workers concluded that the healthy worker effect had little or no effect on cancer mortality [125]. Alternatively, Sterling and Weinkam concluded that a healthy worker effect amounting to 20% to 40% reduced mortality was shown to persist over the entire age range for various causes including cancers [184].

The IDSP, in its Report Number 3 (July, 1988), concluded that the healthy worker effect must be taken into account when interpreting epidemiological studies of mortality or morbidity from any cause, including cancer. No uniform correction factor should be used because each study requires individual interpretation.

Comparing working populations to the general population

When an SMR is computed, the general population, on which the expected number of deaths is based, includes the observed number of deaths from the study population. This is because these deaths contribute to both populations, that is, the deaths are counted for both the observed and the expected. For example, deaths due to nasal cancer are almost always caused by occupational factors. An SMR for nasal cancer will thus be underestimated.

Multiple tests of significance

This refers to the possibility that when numerous disease outcomes are examined, statistically significant associations will be found for some of them by chance alone.

The survivor effect

Because adequate health is required for continuing employment, workers with cardiovascular disease may leave firefighting service, or transfer to positions where they do not encounter these exposures. It is likely that only the healthiest workers continue to be employed for a long term. The influence of this phenomenon is known as the survivor effect.

Since duration of employment was the only way that exposure could be estimated for most firefighter studies, a survivor effect would obscure a dose-response relationship. That is, a correlation between the length of exposure and illness would be reduced by the fact that those with the longest exposure would mainly be the healthiest workers [86].

c) The IDSP Mortality Study of Firefighters in Metropolitan Toronto

The purpose of the IDSP study was to examine mortality by cause of death for firefighters in Metropolitan Toronto, with particular emphasis on cardiovascular diseases.

This original research was undertaken because a literature review conducted for the Panel found too few studies to provide answers about the chronic health effects of firefighting. There was, however, some evidence to "suggest that it is biologically plausible that firefighting could lead to the development of respiratory, cardiovascular and neoplastic disease" [222]. While the Panel has considered all the available evidence, it has chosen to highlight this study because its subjects are Ontario workers, the jurisdiction for which the IDSP is responsible for making policy recommendations. The IDSP study is one of the largest studies of mortality among firefighters ever conducted.

In this study, a Standardized Mortality Ratio (SMR) of more than 100, with the lower end of the 95% Confidence Interval exceeding 100, was interpreted by authors Kristan A. L'Abbé and George A. Tomlinson as a statistically significant increase in firefighter deaths. Ontario males in the same age groups, and whose deaths occurred during the same time periods, were used to make these comparisons.

Name, sex, date of birth, date of hire and termination, reason for termination (where available), job titles and assignments, social insurance and employee numbers were obtained from employment records kept by all six Metropolitan Toronto fire departments (the Cities of Toronto, North York, Scarborough, Etobicoke, York, and the Borough of East York).

The size of the cohort was 5995 before exclusions. Since there were only 146 females, they were excluded. Also excluded were those who were aged 85 or more or who had died before the study period began on January 1, 1950 and those for whom vital information was unavailable. There were 5414 males with six months or more employment as firefighters in the cohort for the principal analysis, which included 777 deaths. The analyses which used duration of employment included fewer, 5373 firefighters including 753 deaths, because some who were not currently employed had no known termination date [86].

Identifying information was linked by Statistics Canada with records from the Canadian Mortality Data Base to identify each cause of death. Any information which might identify individual firefighters was removed from the data returned to the IDSP by Statistics Canada.

The principal tables from the Scientific Report are reproduced below. Table 2 shows the overall SMRs, Table 3 by duration of employment, Table 4 by years since first employment as a firefighter and Table 5 by age.

As shown, the study identified statistically significant increases in mortality rates for brain and nervous system cancers and for other malignant neoplasms (including largely secondary or unspecified types) among Toronto firefighters. Aortic aneurysm mortality was also increased to a statistically significant degree, but other cardiovascular causes of death were not comparably elevated. The rate of death from gallbladder diseases was elevated but did not reach statistical significance overall.

The Panel cautions against complete reliance upon these findings because the statistically significant increase in "other malignant neoplasms" probably reflects increases in cancers whose primary type was not identified. This would tend to underestimate the reported rate of cancer in some of the other categories.

In their original work, L'Abbé and Tomlinson included the deaths which occurred during the five years immediately following first exposure to firefighting. Since it is generally recognized that it takes a minimum of five years after first exposure to a carcinogen for cancer to develop [111], the Panel was concerned that including deaths which occurred during the five years after first exposure could be misleading [75]. To examine this possibility, the Panel asked Mr. Tomlinson to re-analyze the cancer data after eliminating deaths and person-years during the five years since first employment. That analysis showed that, since there were so few cancer deaths within five years of first employment, the SMRs for these analyses are very similar to those for the complete analysis [193].

It might have been informative to analyze causes of death by municipality to see whether any trend in disease patterns exists; however, that was not possible for several reasons. First, data about the number of fires in each municipality, as distinguished from the number of other calls, has been compiled by Ontario's Office of the Fire Marshall only since 1983 [135]. Firefighters routinely transfer within different platoons and fire halls. The number of fires attended by individual firefighters during the period covered by the study (1950-1989) was not available from any of the Fire Departments studied [113, 123, 148, 156, 182]. For all these reasons, it was impossible to conduct more detailed analyses and, in any event, the breakdowns required to do so would involve numbers too small to provide reliable data. More general information from published literature about other jurisdictions is, therefore, the best exposure evidence currently available to the Panel.

Most of the other studies of firefighters' mortality have had insufficient exposure information to conduct such an analysis. Some researchers have attempted to design other ways to approximate firefighters' exposure to fire and chemical hazards [59, 8, 129, 195]. Since there is usually insufficient information about job assignments and activity levels, most studies have had to use duration of employment as a crude measure of exposure [86].

TABLE 2

Mortality by Detailed Cause for Total Cohort, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto (L'Abbé and Tomlinson, 1992)

Cause of death (ICD 9)					OBS.	EXP.	SMR		95% C.I.

ALL CAUSES (000-999)					777	823.50	 94		( 88-101)

INFECTIVE, PARASITIC DISEASES (1-39)			  1	  7.21	 14		(  0- 77)


ALL MALIGNANT NEOPLASMS (140-208)			199	190.39	105		( 90-120)
	Pharynx (146-149)				  4	  2.87	139		( 38-357)
	Oesophagus (150)			 	  2	  5.04	 40		(  5-143)
	Stomach (151)					  7	 13.79	 51		( 20-105)
	Colon (153)					 11	 18.25	 60		( 30-108)
	Rectum and rectosigmoid junction (154)  	 13	  7.60	171		( 91-293)
	Liver and bile ducts (155)			  2	  2.37	 84		( 10-305)
	Pancreas (157)					 14	  9.98	140		( 77-235)
	Larynx (161)					  1	  2.70	 37		(  1-206)
	Trachea, bronchus & lung (162)			 54	 57.08	 95		( 71-123)
	Malignant melanoma (172)			  2	  2.76	 72		(  9-262)
	Prostate (185)					 16	 12.09	132		( 76-215)
	Testis (186)					  3	  1.22	246		( 51-719)
	Bladder (188)					  7	  5.49	128		( 51-263)
	Kidney and ureter (189)				  2	  4.63	 43		(  5-156)
	Brain and other nervous system (191-192)	 14	  7.00	200		(109-336)
	Lymphatic & haematopoietic tissue (200-208)	 18	 18.39	 98		( 58-155)
		Lymphosarcoma (200)			  3	  1.48	203		( 42-592)
		Hodgkin's disease (201)			  1	  2.19	 46		(  1-254)
		Multiple myeloma (203)			  1	  2.59	 39		(  1-215)
		Lymphatic leukaemia (204)		  4	  2.11	190		( 52-485)
		Myeloid leukaemia (205)			  4	  3.35	119		( 33-306)
		Other 					  5	  6.67	 75		( 24-175)
	Other malignant (195-199)			 20	  7.08	282		(172-436)

ENDOCRINE, NUTRITIONAL DISEASES (240-279)		  5	 14.61	 34		( 11- 80)

CIRCULATORY SYSTEM (390-459)				384	387.79	 99		( 89-109)
	Ischemic heart disease (410-414,429.2)		289	278.38	104		( 92-117)
		Acute myocardial infarction (410)	205	191.65	107		( 93-122)
	Cerebrovascular disease (430-438)		 41	 54.02	 76		( 55-103)
	Arteriosclerosis (440-448)			 24	 16.98	141		( 91-210)
		Aortic aneurysm (441)			 19	  8.40	226		(136-353)
	Diseases of veins, etc. (415, 451-459)		  8	  4.78	167		( 72-330)

RESPIRATORY SYSTEM (460-519)				 45	 46.12	 98		( 71-131)
	Chronic bronchitis, emphysema, asthma		 28	 21.47	130		( 87-189)
		(490-493, 496)


DIGESTIVE SYSTEM (520-579)				 45	 36.85	122		( 89-163)
	Gallbladder diseases				  5	  1.69	296		( 96-690)

GENITOURINARY SYSTEM (580-629)				 11	 10.41	106		( 53-189)

SYMPTOMS/ILL-DEFINED (780-799)				  1	  6.06	 17		(  0- 92)

EXTERNAL CAUSES (E800-999)				 70	100.72	 69		( 54- 88)
	Motor vehicle traffic accidents (810-825)	 22	 31.10	 71		( 44-107)
	Accidental falls (880-888)		  	  9	  7.82	115		( 53-219)
	Accidents caused by fire & flames (890-899)	  4	  3.23	124		( 34-317)
	Suicide (950-959)			 	 18	 26.68	 67		( 40-107)

OTHER KNOWN CAUSES					 16	 22.81	 70	 

TABLE 3: Standardized Mortality Ratios by Duration of Employment for Selected Causes, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto (L'Abbé and Tomlinson, 1992)

						Duration of Employment
		                                                                                           
			< 15 Years			15-29 Years			 >=30 Years       
		                       		                        		                        
Cause           Obs.    SMR     95% CI       	Obs.    SMR     95% CI         Obs.    SMR     95% CI   
                                                                                                             
All Causes	130	 88	 74-104		240	 97	 85-110		383	 91	 82 101
All Cancers	 36	137	 96-190	 	 53	 87	 65-114		100	100	 81-122
-pharynx	  1	227	  6-1265	  0	  0	*******	  	  3	236	 49-699
-rectum	  	  0	  0	*******	  	  5	220	 71-513	  	  8	180	 78-355
-pancreas	  2	172	 21-621	  	  3	 92	 19-269	  	  9	165	 75-313
-lung		  8	129	 56-254	 	 16	 83	 47-135	 	 27	 87	 57-127
-melanoma	  1	109	  3-607	  	  1	 89	  2-496	  	  0	  0	*******
-prostate	  1	152	  4-847	  	  5	213	 69-497	  	  9	101	 46-192
-testis	  	  3	353	73-1032	  	  0	  0	*******	  	  0	  0	*******
-brain & other 
 nervous system   5	258	 84-602	  	  3	105	 22-307	  	  5	233	 76-544
-lymphatic 
 leukaemia	  0	  0	*******	  	  0	  0	*******	  	  4	364	 99-932
-other malignant  4	426	116-1091	  3	134	 28-392	 	 13	340	181-581

Circulatory 
System	 	 40	 97	 69-132		126	113	 94-135		207	 91	 79-104
-acute myocardial 
 infarction	 23	108	 68-162	 	 73	120	 94-151		105	 98	 80-119
-arterio-
 sclerosis	  2	145	 18-254	  	  5	128	 42-299	 	17	148	 86-237
-aortic aneurysm  1	143	  4-797	  	  5	242	 79-565	 	13	239	127-409
Respiratory 
System	  	  4	 80	 22-205	  	  7	 62	 25-128	 	32	109	 75-154
-chronic 
 bronchitis, 
 asthma & 
 emphysema	  3	175	 36-511	  	  4	 76	 21-195	 	19	133	 80-208

Digestive System  4	 59	 16-151	 	 19	135	 82-256	 	21	134	 83-205
-cirrhosis of 
 the liver  	  4	100	 27-256	 	 17	189	110-303	  	5	 78	 25-182
-gallbladder 
 diseases	  0	  0	*******	  	  0	  0	*******	  	5	472	153-1101

TABLE 4: Standardized Mortality Ratios by Years Since First Employment for Selected Causes, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto (L'Abbé and Tomlinson, 1992)

                                                                                                                                                       
						Years Since First Employment
		                                                                                             	 
		< 20 	Years			    20-29 Years		              >=30 Years       
		                       		                        		                           
Cause 	        Obs.    SMR     95% CI         Obs.    SMR     95% CI    	Obs.    SMR       95% CI   
                                                                                                              
                                    
All Causes	120	 79	 65- 94		143	 95	 80-112		514	 99	 91-108
All Cancers	 28	120	 77-170	 	 36	 94	 66-131		135	106	 89-125
-pharynx	  0	  0	*******	  	  1	122	  3-679	  	  3	188	 39-549
-rectum	  	  1	125	  3-696	  	  2	146	 18-527	 	 10	179	 86-329
-pancreas	  1	100	  3-557	  	  2	 95	 12-344 	 11	157	 78-281
-lung		  1	 23	  1-128	 	 13	103	 55-176	 	 40	100	 71-136
-melanoma	  1	 91	  2-507	  	  1	130	  3-724	  	  0	  0	*******
-prostate	  0	  0	*******	  	  2	244	 30-881	 	 14	126	 69-211
-testis	  	  3	333	 69-973	  	  0	  0	******* 	  0	  0	*******
-brain & 
 other nervous 
 system	  	  6	286	105-623	  	  2	 99	 12-356	  	  6	222	 81-483
-lymphatic 
 leukaemia	  0	  0	*******	  	  0	  0	*******	  	  4	267	 73-684
-other malignant 
 neoplasms	  1	143	  4-797	  	  4	288	 78-737	 	 15	306	171-505
Circulatory System 37	 93	 65-128	 	 77	118	 93-147		267	 96	 85-108
-acute 
 myocardial 
 infarction	  22	102	 64-154	 	 48	126	 93-167		135	102	 86-121
-arteriosclerosis  1	100	  3-557	  	  3	165	 34-482	 	 20	141	 86-218
-aortic aneurysm   0	  0	*******	  	  3	303	 62-886	 	 16	232	133-377
-diseases of 
 veins, 
 lymphatics, etc.  1	143	  4-797	  	  2	211	 25-760  	  5	161	 52-376
Chronic 
bronchitis, 
asthma & emphysema 0	  0	*******	  	  2	 80	 10-290	 	 26	146	 95-214
Cirrhosis of 
the liver	   4	 87	 24-223	 	 10	152	 73-280 	 12	141	 73-246
Gallbladder 
diseases	   0	  0	*******	  	  0	  0	*******	  	  5	385	125-898

TABLE 5: Standardized Mortality Ratios by Age for Selected Causes, IDSP Mortality Study of Fire Fighters in Metropolitan Toronto (L'Abbé and Tomlinson, 1992)

								Age
				                                                                             
					< 60 Years					 >=60 Years   
				                            			                           
Cause				Obs. 	SMR	95% CI				Obs. 	SMR	95%CI
                                                                                                           
All Causes			337	 91	 81-101				440	 97	 88-107
All Cancers			 87	107	 86-132				112	104	 86 125
 pharynx			  1	 61	  2-340			  	  3	240	 49-701
-rectum			  	  4	138	 38-353			  	  9	191	 87-363
-pancreas			  4	 97	 26-248			 	 10	170	 81-313
-lung				 22	 91	 57-138			 	 32	 97	 66-137
-melanoma			  2	 93	 11-336			  	  0	  0	*******
-prostate			  2	153	 19-553			 	 14	130	 71-218
-testis			  	  3	268	 55-783			  	  0	  0	*******
-brain & other nervous
 system			 	 10	198	 95-364			  	  4	204	 56-522
-lymphatic leukaemia		  0	  0	*******			  	  4	336	 92-860
-other malignant		  9	304	139-577			 	 11	266	133-476

Circulatory System		150	110	 93-129				231	 93	 81-106
-acute myocardial
 infarction			 93	117	 94-146				112	100	 82-120
-arteriosclerosis		  4	113	 31-289			 	 20	149	 91-230
 aortic aneurysm		  3	163	 33-473			 	 16	245	140-398
-veins, lymphatics & other	  3	148	 31-433			  	  5	181	 59-422

Respiratory System 		  7	 57	 23-117			 	 38	112	 79-154
-chronic bronchitis, asthma
 & emphysema			  2	 43	  5-155			 	 26	155	101-227

Digestive System		 20	 96	 58-148			 	 24	156	100-232
-cirrhosis of the liver	 	 18	130	 77-205			  	  8	138	 60-272
-gallbladder diseases		  0	  0	*******			  	  5	420	136-980

d) Cardiovascular disease among firefighters

Parameters of this Report

An acute cardiac event such as a heart attack is adjudicated as a "chance event" or an "accident" by the WCB. Firefighters who have had heart attacks during the course of their employment have been compensated, albeit not always, for the period of disability resulting from the heart attack. The Ontario WCB, like most other Boards, does not usually compensate workers for periods of chronic disability resulting from cardiovascular disease.

The questions put to the Panel by the representatives of the firefighters concerned the relationship between cardiovascular disease and firefighting. While the Panel acknowledges that heart attacks or acute events are most often preceded by cardiovascular disease, the purpose of this Report is limited to a review of the data necessary to examine the relationship, if any, between cardiovascular disease and firefighting. The Panel will not be addressing specific compensation issues concerning acute events.

Medical terms

It may be useful to define briefly the medical conditions which will be discussed below.

Atherosclerosis, which is a specific type of arteriosclerosis, results from the accumulation of cholesterol and other substances within the arteries. It has major effects on the coronary arteries, the cerebral arteries and the aorta, the main artery of the body. It causes a decrease in the coronary arteries' ability to allow blood flow to the heart muscle (coronary artery disease). Known risk factors for atherosclerosis are high blood pressure, high levels of cholesterol in the blood and cigarette smoking [158]. It may also produce narrowing of large arteries such as the aorta and its immediate branches, or weakening of the aortic wall leading to aortic aneurysm.