REPORT TO THE WORKERS' COMPENSATION BOARD ON LUNG CANCER IN THE HARDROCK MINING INDUSTRY March, 1994

Industrial Disease Standards Panel (Occupational Disease Panel)
IDSP Report No. 12
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:

(8) (a) to investigate possible industrial diseases;

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

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

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

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

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

Letter of Transmittal

Chapter 1 Introduction

(a) The IDSP Mandate and Terms of Reference
(b) How the issue arose
(c) Questions the Panel asked
(d) Investigative process

Chapter 2 The Evidence

(a) Question 1
     Is there an excess of lung cancer in the hardrock mining industry?
(i) Introduction

(b) Question 2
     If there is an excess of lung cancer in the hardrock mining industry, is there something
     in the mining environment that can be related to the excess of lung cancer?
(i) Potentially harmful agents in the hardrock mining industry

(c) Question 3
     What are the processes common to the hardrock mining industry?
(i) Processes
(ii) Conclusion

(d) Question 4
     If there is an excess of lung cancer among hardrock miners, how is smoking related to that excess?
(i) Smoking, mining and lung cancer
(ii) Conclusions

Chapter 3 Workers' Compensation Law and Policy

Chapter 4 Summary of Conclusions

Chapter 5 Findings and Recommendations

Glossary

Abbreviations

References

Appendices

Table of Appendices

Appendix

Appendix A

Appendix B

Appendix C

Appendix D

Appendix E

Appendix F

Appendix G

Appendix H

Tables and Figures

Figure 1
Lung Cancer Standardized Mortality Ratios for Ontario Hardrock Miners

Table 2
Cohort Studies of Ontario Gold Miners

Figure 2
Lung Cancer SMRs of Ontario Gold Miners

Figure 2A
Dose-Response Relationship of Lung Cancer and Ontario Gold Mining

Table 2A
Lung Cancer Mortality in Gold Miners as found in IDSP Gold Mining Industry Report

Table 3
Cohort Studies of Ontario Uranium Miners

Figure 3
Lung Cancer SMRs of Ontario Uranium Miners

Figure 3A
Dose-Response Relationship of Lung Cancer and Ontario Uranium Mining

Table 4
Cohort Studies of Ontario Nickel Miners

Figure 4
Lung Cancer SMRs of Ontario Nickel Miners

Figure 4A
Dose-Response Relationship of Lung Cancer and Ontario Nickel Mining

Table 5
Cohort Studies of Ontario Multi-Ore Miners

Figure 5
Lung Cancer SMRs of Ontario Multi-Ore Miners

Figure 5A
Dose-Response Relationship of Lung Cancer and Ontario Multi-Ore Mining

Table 6A
Ontario Radon Exposure Standards

Table 6B
Historical Radon Data

Table 6C
Comparison of Radon and Gamma Ray Levels

Table 7
Average Dust Level in Underground Mines

Figure 8
Continuum of Injuries and Illness

Working Definitions

For the purposes of this report, the Panel has adopted the following definitions:

Hardrock mining refers to all mining, excluding iron ore open pit, in igneous rock. In Ontario, this involves the Pre-Cambrian Shield which extends in a horseshoe shape around Hudson Bay and south to the Great Lakes.Metals mined from this area may include gold, zinc, nickel, copper, lead, silver, molybdenum, cadmium, selenium, iron, cobalt, uranium, yttrium, platinum metals and tellurium.*

A miner refers to any person employed underground; in shaft sinking; in surface diamond drilling; crushing; grinding; milling and tailings operations. All other surface work is excluded.

Lung cancer refers to primary neoplasm of the trachea, bronchus and lung.

* Asbestos mining is not dealt with in this report.

Chapter One Introduction

In the following pages the members of the Industrial Disease Standards Panel (IDSP) examine the issue of the probable connection between lung cancer and hardrock mining. The Panel sets out the legal framework for its work and provides a detailed explanation of the scientific knowledge which will form the foundation of its conclusions. Ultimately, the Panel explains its policy recommendations, which result from the integration of the scientific data and the legal requirements.

(a) The IDSP Mandate and Terms of Reference

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

95. ...

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

(a) to investigate possible industrial diseases;

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

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

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

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

1. (1) In this Act,

...

"industrial disease" includes,

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

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

(c) a medical condition that in the opinion of the Board requires a worker to be removed either temporarily or permanently from exposure to a substance because the condition may be a precursor to an industrial disease, or

(d) any of the diseases mentioned in Schedule 3 or 4.

An industrial disease can be identified when there is established evidence of a "probable connection" between a disease and an industrial process or a connection to a toxic agent or carcinogen.

The evidence that the IDSP weighs to find a "probable connection" is scientific and medical in nature. Specifically, the IDSP considers epidemiological studies, hygiene information about workplace exposures, toxicological evidence about the identified contaminants and alternative causes of lung cancer, in particular smoking.

When evaluating this evidence, the IDSP continues to be aided by the work of Sir Austin Bradford Hill [53]. The complete text of the discussion can be found in Appendix A. 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; and

9. analogy.

The difficult question to answer is what amount and quality of evidence will establish a "probable connection". In the chapter on "Workers' Compensation Law and Policy", the IDSP will look at various approaches to answer this question. Its deliberations will be guided by legal principles and the standards applied in this and other jurisdictions.

After weighing the evidence, the IDSP decides what, if any, association exists between hardrock mining and lung cancer. The answer to that question determines the Ultimate IDSP policy recommendations.

It is possible for the IDSP, depending on the strength of the probable connection, to recommend that the WCB:

a. enter lung cancer and hardrock mining into Schedule 4; or

b. enter lung cancer and hardrock mining into Schedule 3; and/or

c. develop guidelines for the adjudication of claims.

Of course, if a worker suffers from a non-scheduled industrial disease the WCB is required to adjudicate the worker's claim for benefits on the basis of the real merits and justice of the particular situation.

A discussion of the significance of each of these possibilities and of the significance of Schedules 3 and 4 can be found in the chapter on "Workers' Compensation Law and Policy".

An Abridged Chronology of the History of Compensation for Lung Cancer in the Ontario Mining Industry

1890		Mining Operations Act passed establishing regulations for mining in Ontario
1926		Silicosis placed in the Workman's Compensation Act as an occupational disease
1929		Silicosis Act required miners to obtain health certificates, the foundation for the Mining Master File
1930		Mines Accident Prevention Association (MAPAO) established to monitor and reduce dust levels in mines
1937		first claim for silicosis accepted by the Ontario WCB
1940s		aluminum dust employed to lessen the effects of exposure to silica dust
1974		first Muller report released on uranium mining mortality in Ontario, finding excess lung cancer deaths
1976		Report of the Royal Commission on Health and Safety of Workers in Mines was completed
1976		Board approved guidelines for the adjudication of lung cancer in uranium miners
1983		Muller report released finding excess lung cancer in gold, uranium and mixed ore miners
1985		The Industrial Disease Standards Panel (IDSP) established by statute
1986		Muller report updated, indicating an increased incidence of lung cancer among gold miners
1987		IDSP published a report on the Gold Mining Industry in Ontario establishing a probable connection between lung cancer and work in gold mining
1988		first gold/lung cancer criteria established by WCB and claims accepted
1989		IDSP report on the Ontario Uranium Mining Industry released, establishing a probable connection between lung cancer and work in uranium mining
1991		new WCB policy regarding lung cancer and gold miners adopted resulting in readjudication and compensation

(b) How the issue arose

The health of miners has been a concern of labour, management and the Ontario government for over 100 years. The original concern focused on non-malignant respiratory problems such as silicosis. In an attempt to limit the severity and incidence of these illnesses, the provincial government in 1929 began to monitor the health of miners and required them to undergo annual chest x-rays. If it became obvious on x-ray that a miner was suffering from either tuberculosis or silicosis, he was denied a license which permitted him to work underground.

The Ministry of Health was originally responsible for the chest x-ray programme. Eventually the programme was transferred to the Ministry of Labour (MOL). Regardless of which Ministry was responsible for the programme, the history of the miners' working experience was captured in the Mining Master File (MMF). This data base contains the working history of all licensed miners in the province between 1956 and 1988, approximately 90,000 entries.

While this was happening in Canada, related activity was taking place in the United States. As Dr. Yassi has observed,

During the late 1940s and into 1950s, as uranium mining expanded rapidly, excess lung cancer was observed in U.S. uranium miners. By the late 1950s the U.S. Public Health Service had documented excess lung cancer among Colorado Plateau uranium miners (cf. BEIR IV) [153A].

During the 1950s and 1960s, the union representing the majority of miners in Ontario, the United Steelworkers of America (USWA), began to actively negotiate for improved health and safety conditions and for access to more data about the health of its membership. In 1969, as a result of a strike and the collective bargaining process, the Steelworkers and INCO, the largest mining interest in the province, agreed to establish joint health and safety committees.

The MOL on its own initiative and in response to pressure from labour groups, began to match the data contained in the MMF and the Canadian Mortality Database held by Statistics Canada about the causes of death. This information, when linked and analyzed, established that some groups of miners were dying more frequently of lung cancer than would have been expected.

In 1974 Dr. J. Muller, a physician employed by the MOL, published a report on uranium miners which showed a pattern of higher levels of deaths than expected from lung cancer, and raised concerns about the health of uranium miners.

Following further negotiations between INCO and the USWA in 1975, the parties agreed to begin to study the health of their employees. Management at Falconbridge, the other nickel producer in Ontario, also began to study the health of its workforce. Joint management/labour and company managed research projects were initiated and have continued to this day.

In 1975 the Royal Commission on the Health and Safety of Workers in Mines (the Ham Commission) was established by the provincial government. The Commission completed its work in 1976 and recommended that an epidemiological review of the mining workforce be carried out every five years.

In keeping with the above recommendation, Dr. Muller looked at mortality in all mining. The first of several investigations in response to the Ham Commission--the resultant 1983 "Study of Mortality of Ontario Miners"-- confirmed findings of increased incidence of some cancers among miners.

On the basis of the epidemiological evidence and continuing pressure from the USWA, the WCB asked the IDSP to investigate lung and stomach cancer mortality among gold and mixed ore miners in 1986. Subsequently, and as a separate issue, the WCB also requested that the IDSP investigate the uranium industry and possible related cancers.

In both circumstances, the IDSP agreed to undertake the investigation and report back to the WCB. The IDSP also undertook to provide eligibility criteria for entitlement to workers' compensation benefits if a probable connection could be determined.

In 1987 and 1989 respectively, the IDSP issued Reports on both gold and uranium mining. Although these Reports were met with controversy, WCB guidelines in 1988 for entitlement to benefits were established for some gold miners. That policy was revised again in 1991, compensating more gold miners. These guidelines can be found in Appendix B.

The WCB adjudicates claims for lung cancer among uranium miners under the policy for exposure to radon progency. The WCB is currently reviewing proposed changes which would create policy specifically for uranium miners. The current policy can be found in Appendix C.

There has been agreement between the WCB and all of the members of the IDSP that because of the epidemiological findings, a "probable connection" exists between lung cancer and gold and uranium mining. As a result, certain miners have been paid WCB benefits for lung cancer. The full policies can be found in Appendices B and C.

Significant numbers of miners, who also were at excess risk of lung cancer, have been excluded from the above policies. Their multi-ore mining experience made it impossible for them to accumulate sufficient specific ore exposure to qualify under those policies [85].

From 1948 to 1992, the WCB reports having compensated the following cases of lung cancer in hardrock miners:

The Board noted that these figures underestimate the number of cases actually compensated.

In 1990, in part because of the problems faced by multi-ore miners, the issue of "all" hardrock mining was again on the table for discussion at the IDSP. The Panel declined to undertake any active investigation until the results of the update of the miners' mortality study were available. The IDSP decided that the update might serve to resolve some of the problematic areas that had led to dissenting opinions in previous IDSP reports. In fact, the study update which extended the follow-up time and provided more information and which was completed in 1991, has been crucial to the IDSP's current deliberations.

With the benefit of this updated data, the IDSP has been able to investigate the incidence of lung cancer in the whole of the Ontario hardrock mining industry. This investigation explores the possibility that there is a "probable connection" between lung cancer and any or all hardrock mining.

(c) Questions the Panel asked

In order to reach a conclusion, the IDSP explores the following questions:

1. Is there an excess of lung cancer in the hardrock mining industry?

2. If there is an excess of lung cancer in the hardrock mining industry, is there something in the mining environment that can be related to the excess of lung cancer?

3. What are the processes common to the hardrock mining industry?

4. If there is an excess of lung cancer among hardrock miners, how is smoking related to that excess?

5. If there is an excess of lung cancer among hardrock miners, what criteria should the Workers' Compensation Board employ to compensate hardrock miners who have subsequently developed lung cancer?

(d) Investigative process

To investigate the scientific issues and conduct the necessary analysis the IDSP pursued many avenues. The investigation relied on the work completed independent of the IDSP, work commissioned by the IDSP, including a world literature review, and work conducted by the IDSP. The following sets out the investigative steps taken directly by the IDSP.

• An in-depth background paper which explored present and past mining techniques, potential risk factor in the mining industry and some epidemiological data wascompleted in-house.
• Dr. Annalee Yassi, Director, Department of Occupational and Environmental Medicine, Winnipeg Health Sciences Centre and of the Occupational and Environmental Health Program at the University of Manitoba, was commissioned to carry out a review of the world literature on hardrock mining and lung cancer.
• The MOL provided a statistical profile of the type of ore mined by the 90,000 registrants in the Mining Master File.
• Statistics from the MMF were assembled by the MOL staff and records of the Ontario Cancer Treatment and Research Foundation were used to compare the age specific death rates from lung cancer in miners, the Northern Ontario population and the general population of Ontario.
• IDSP staff reviewed hundreds of environmental records from Ontario mines and mills.
• IDSP staff and Panel members visited several hardrock mines to observe mining methods.
• MAPAO supplied Panel staff with micro-fiche copies of historical dust records in numerous Ontario mines and mills.
• The National Dose Registry of the Bureau of Radiation and Medical Devices, Health and Welfare Canada, provided historical records of radon and gamma radiation measurements in Ontario mines.
• IDSP staff reviewed numerous WCB claim files to gain a better understanding of the adjudicative process for lung cancer in miners.
• Dr. Yassi was asked to prepare a second paper, which considered the effect of cigarette smoking and lung cancer among miners, for the Panel's deliberations.
• On-line computer searches were carried out by IDSP staff of the following databases: Cancerlit, Medline, NIOSH, Embase, Hseline, NTIS, Biosis Prenews, RTECS, Metadex, Enviroline, Pollution abstracts, Chemsearch, CISILO, Environmental Bibliography.
• International Agency of Research into Cancer (IARC) publications were consulted to assess known and potential carcinogens.
• All Canadian and some international jurisdictions were surveyed for current policy and guidelines on lung cancer and hardrock mining.
• A study on the geological environment was prepared for the Panel by Barbara D'Silva, geologist. The paper looked at ore genesis theories; at the general characteristics of deposits; at the physical mining of ore; and, at specific agents such as arsenic and radon decay products.

In addition to these steps the IDSP consulted with several technical advisors. For a complete list refer to Appendix F.

All of the information gathered was shared throughout the process with stakeholders in both a formal and an informal way. Dr. Yassi's paper, "Hardrock Mining and Lung Cancer. A Literature Review and Discussion Paper," was sent to the United Steelworkers of America, District 6, Mine, Mill Smelter Workers' Union, the Canadian Union of Base Metal Workers, INCO Limited, Falconbridge and the Ontario Mining Association.

At the Panel's May, 1992, meeting in Sudbury, presentations were made by the United Steelworkers' National Health and Safety Representative, as well as by a representative from Mine Mill. Both INCO and Falconbridge were represented as was the Ontario Mining Association. Written submissions were received from all of the above. To date, nó submission has been received from the Base Metal Workers' Union.

Chapter Two The Evidence

(a) Question 1: is there an excess of lung cancer in the hardrock mining industry?

i) Introduction

Both the existence and the extent of the excess of lung cancer among hardrock miners are important pieces of evidence to be weighed by the IDSP.

The search for an answer to these questions is assisted to some degree by the agreement among the stakeholders. The workplace parties agree that there is an excess of lung cancer among Ontario hardrock miners when a comparison is made to the incidence of lung cancer among the general Ontario population.

In its submission to the IDSP, the Ontario Mining Association "agreed to the premise that there is an excess of lung cancer in miners." Falconbridge confirmed an excess of lung cancer but questioned the role of the workplace in the problem. INCO in its detailed comments did not deny the excess of lung cancer in the miners, but questioned the attribution to the workplace. There was also unanimity among the industry representatives that all of the excess could not necessarily be attributed to work and accordingly all of the costs should not be borne by the employers.

Both the United Steelworkers of America and ache Sudbury Mine, Mill and Smelter Workers' unions in their presentations repeated their past position that there is an excess of lung cancer in miners.

The true nature of the excess is the subject of the following pages. To answer the question of excess lung cancers, numerous statistics and reports were collected and analyzed. Particular emphasis was given to Ontario-based reports, but international studies were consulted as well.

By convention, the majority of epidemiological studies examine the experience of miners by limiting the review to single ore mining. However, most single ore cohorts include true mixed ore miners because inclusion criteria were rarely, if ever, defined as 100% experience with a single ore. Following the convention established in the published works, the IDSP organized its work by first examining single ore experience.

Figure 1 presents a summary of epidemiological evidence for some specific types of ore. Each further section contains a graph showing a dose-response relationship found for that ore type.

The following explanation may assist the reader:

Results are measured in terms of a "standardized mortality ratio" (SMR"), which is an estimate computed by comparing the number of deaths observed among miners with the number of deaths which are expected based upon a comparison group of the same age and sex, during the same time period then multiply by 100:

               "observed" deaths among miners       )
SMR =     ----------------------------------------- ) X 100
          "expected" deaths among comparison group  )

For example, if among 1000 miners three died of lung cancer, whereas two of 1000 individuals in the comparison group of the same age and sex died of lung cancer:

              (observed) 3
The SMR is ----------------- X 100 = 150.
              (expected) 2

An SMR greater than 100 would suggest an excess risk of lung cancer. Epidemiologists evaluate the statistical significance of an SMR by using a 95% confidence interval, a range of numbers in which the true SMR would fall 95% of the time. If the lower end of the 95% confidence interval is above 100, the likelihood that the excess mortality is due to chance is less than 5% (or 1 out of 20). In this Report, confidence intervals, where available from the original paper, are noted. When not available, they were calculated using the following formula:

Lower limit = [Square root of Observed events - (1.96 x 0.5)]2
              ------------------------------------------------
                                   Expected

Upper limit = [Square root of Observed events + (1.96 x 0.5)]2
              ------------------------------------------------
                                   Expected

It is also important to note that the SMRs may not accurately reflect the excess mortality or true risk for the following reasons:

Healthy worker effect

Most epidemiological studies compare workers with the general population. Since the general population includes people who do not or cannot work due to illness or disability, a working population is usually healthier and is, therefore, expected to have a lower mortality rate for most causes of death. The influence of these factors on the results of studies is known as the "healthy worker effect". It results in lower SMRs than would occur if more similar groups had been compared and may conceal a real increase in deaths among workers. In other words, the phenomenon underestimates the true excess. Comparisons with another group of "healthy" workers, rather than to the general population, are therefore more likely to provide accurate statistical estimates of occupational risks.

Whether or not the healthy worker effect influences cancer mortality ratios is controversial. In a previous Report [56], the IDSP published comments on the healthy worker effect solicited from nine experts. The Panel's review of those opinions led it to conclude that the healthy worker effect must be taken into account when interpreting epidemiological studies of mortality or morbidity from any cause, including cancer.

The magnitude of the healthy worker effect on the studies discussed here remains unknown. Since no other large population is available to the Panel for a comparison study, the general population must suffice as a comparison group. The Panel will continue to explore the possibility of finding such a working group for future investigation.

Accuracy of the data

Because epidemiological cohort studies follow subjects over a long period of time many people may be difficult to trace. A portion of these subjects may die outside Ontario or Canada and their deaths would not be accurately recorded.

For example, in Kusiak's 1993 study of uranium miners, Social Insurance Numbers (SIN) were available for only 63. 1% of the men in uranium mines (largely because SINs were not issued until 1965) [79]. Without SINs the determination of vital status is much more difficult.

For the uranium miners, the SMR for those with SINs was 225, whereas for those without SINs, it was only 135 [79A]. The authors indicated 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 led to an 88% increase in SMRs when the vital status of miners with SINs was compared to the vital status of miners without SINs. In their ultimate analysis the authors chose to rely on the figures calculated for the miners with SINs. Alternatively it would be possible to determine the weighted average SMR for all uranium miners. That weighted average is 193, reduced by 15% from the SMR of 225 from the miners who could be adequately traced. The higher the proportion of miners who cannot be traced, the greater will be the reduction of the apparent SMR compared with its true value. In fact, the vital status of 25% of all miners without SINs could not be determined, compared to the ascertainment of the vital status of all but 5% of those miners with SINs.

The IDSP has concluded that the SMR for lung cancer has been underestimated in most of the studies of Ontario miners primarily because of the lack of SINs to accurately ascertain mortality.

Estimating the extent of disease when comparing working populations to the general population

When the 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: i.e., the deaths are counted for both the observed and the expected. If deaths from a disease such as nasal cancer are caused almost always by occupational factors, the SMR will thus be underestimated. Since lung cancer is caused by smoking as well as by occupational factors, this error would be present but less important.

The preceding factors constitute the framework within which reports of SMRs need to be considered. The following account of the SMRs found in mining cohort studies are affected by questions of data accuracy, the healthy worker effect and population comparisons. They should be evaluated with these factors taken into account.

ii) Establishing incidence and excess

Gold miners

Excess lung cancer in Ontario gold miners was documented by Muller [98]. For the purposes of that study, a gold miner was defined as a non-uranium miner with 85% of his mining experience in gold. The SMR for this cohort was 145 (95%CI = 126-166) [98A]. In Muller's 1986 update an SMR of 140 (95%CI = 120-163) was reported [95]. The slight difference in SMR is attributed to the exclusion of gold miners from the later cohort if they did not mine between 1955-1977.

In its 1987 Report on the Gold Mining Industry, the IDSP found a probable connection between lung cancer excess and some gold mining experience [57]. The Panel based its findings on a special report and analysis it commissioned from Dr. H. Shannon. Shannon revised the cohort definition and included additional miners categorized as mixed ore miners in Muller's 1983 study. This led to inclusion of gold miners with five years gold mining experience even if they had other ore experience. Uranium miners were excepted from this inclusion rule. Shannon assumed that this method would better reflect all gold mining experience. The SMR for lung cancer is reported to be 141 (95%CI = 122-160) [57A].

In Kusiak's 1991 investigation an overall SMR of 129 (95%CI = 115-145) was found for all gold miners [81]. Yassi noted that Kusiak's study underestimates the number of lung cancer deaths since the person-years at risk were not counted once the miner entered uranium mining. This "would tend to falsely lower the result in gold miners who began mining uranium then died from their experience in gold mining" [153B].

The dose-response relationship found in Muller's report is reproduced in Figure 2A above. The number of years worked in gold mining represents work exposure. The SMR rises over 20 years from 139 to 202.

The 1987 IDSP report included a review of the world literature. A summary of that review is included in Table 2A. Methodologies and cohort inclusion criteria differed but Shannon concluded that despite this "a fairly consistent mortality pattern was observed" [57]. All but one of the studies included in the review found a statistically significant increase in the SMRs. The authors opined that the one lower SMR was attributable to the use of an inappropriate comparison group. If an alternative comparison group had been chosen, the SMR would have been 138.

Uranium miners

Historically, radiation-exposed miners were studied to determine the effects of exposure to radiation on human health in general.

More specifically, Muller studied the incidence of lung cancer in Ontario uranium miners. In his 1974 study, Muller used a one-month minimum uranium mining criterion and at least five years mining experience for inclusion in the cohort. He found an SMR of 313 (95%CI = 225-416) [96]. In his 1983 follow-up study, a uranium worker was defined as anyone who worked two weeks or longer in that industry. The SMR computed for underground uranium miners was 181 (95%CI = 150-214) [98]. In Muller's 1987 follow-up study, all uranium miners with previous gold mining experience were excluded from the cohort [94]. The SMR was 144 (95%CI = 114-177) [94A].

In Kusiak's (1993) follow-up study, the SMR was 225 (95%CI = 191-264) for all those with at least two weeks of uranium mining experience [79]. Uranium miners with neither gold nor nickel/copper experience showed an SMR of 230 (95%CI = 164-315) [79A].

Shannon's 1989 investigation for the IDSP found an SMR of 186 (95%CI = 158-217) for all uranium miners [120B]. For this study, Shannon excluded from the cohort uranium miners who no longer worked in the industry as well as men who were identified by the Atomic Energy Control Board but not found in the MMF.

Although 1,344 uranium millworkers were included in the MMF [79], there were too few deaths to generate statistically significant SMRs. Muller [98] did find an excess of lung cancer in millworkers with an SMR of 195. The millworkers were included in the overall cohort of uranium miners in the Shannon IDSP study, but not in Muller's 1987 and 1989 updates of uranium miners.

In Figure 3A above, the SMR for lung cancer mortality rises from 168 to 282 in direct relation to increased WLM¹, or estimated exposure to radon progeny.

As early as the mid-16th century, there are reports of high rates of deaths due to respiratory disease in miners extracting radioactive ore [3]. Archer reviewed studies from Czechoslovakia, the United States and Canada, and found excess lung cancer related to radon progeny levels in several types of mines including uranium [9]. The report carried out by the Committee on the Biological Effects of Ionizing Radiation (BIER IV) was an exhaustive review of 22 international studies which all looked at miners exposed to radon progeny, many of whom were uranium miners. The Report authors concluded that without exception, the studies show excess deaths due to lung cancer [27].

A more recent study by Samet, et al., of uranium miners in New Mexico found an SMR of 400 (95%CI = 310 - 510) for 4,044 men [117]. The authors found a dose/response relationship between lung cancer and radon as measured by WLM. The relative risk for lung cancer increased by 1.8% per WLM exposure.

In considering epidemiological evidence for Ontario uranium miners, the Panel noted that this group of workers experienced a relatively short exposure, since 87% of the uranium miners worked in that ore for less than five years [77]. According to Muller, the median number of years worked in uranium was 1.5 years [98].

It is also important to note that the SMR for uranium miners is likely underestimated because the inclusion criterion of two weeks of uranium mining means that the cohort is diluted with miners who had very little exposure. In the other studies of Ontario miners, the criterion for inclusion into the cohort was six to 60 months experience.

In Figure 4, the inclusion criteria are a minimum of five years experience in the Muller, Shannon 1990 and Roberts 1990 studies. The ocher investigations by Shannon and Roberts used a six month criterion.

Nickel miners

Most of the world literature on lung cancer incidence and nickel miners is based on Ontario studies. Figure 4 illustrates the incidence of lung cancer found in those studies.

Muller's 1983 study of Ontario's hardrock mining population found an SMR of 130 (95%CI = 79-193) [98D] for nickel miners who worked both surface and underground. This group would therefore include workers with possible experience in smelting and/or refining. For those miners working underground only, the SMR was 87 [98C]. Muller's criterion for inclusion in this cohort was five years mining experience, with 85% in nickel/copper. The Panel notes that the 1983 findings of nickel miners are inconsistent with later findings based on epidemiological studies conducted by McMaster University derived from company/union data.

In 1984, as a result of joint union-management agreements at Ontario's two largest nickel mining companies, mortality studies were carried out. The cohorts were assembled from company records. Shannon's study in 1984 of Falconbridge workers included all men employed between 1950 and 1976 for at least six months [121]. The SMR for miners was 141 (95%CI = 97-193) [121A]. Roberts carried out epidemiological studies at INCO. From the published results, the SMR for miners and millers with at least five years of experience and a 15 year latency period was 111 (95% CI=101-121) [113B].

One of the most important studies on nickel carcinogenesis is the Report of the International Committee on Nickel Carcinogenesis in Man [69]. The two Ontario studies were part of this investigation. The authors of the international report subdivided both cohorts so that results for mining and milling are available. For the Falconbridge mine, mill and surface workers, an SMR of 150 (95%CI = 114-191) was found [69A]. Among INCO miners and millers, an SMR of 114 (95%CI = 100-128) was found [69A].

In an effort to have comparable figures for all nickel miners, the IDSP combined the above numbers for all miners and millers from both INCO and Falconbridge. For this group there is an overall SMR of 119 (95%CI = 106-133), for a population of 34,452. All SMRs are for nickel workers with at least five years experience and a latency of 15 years.

Shannon in 1991 earned out an update of the Falconbridge cohort [122]. A significant increase of lung cancer was found: an SMR of 159 (95%CI = 118-206), for miners and millers, all win greater than five years exposure and 15 years latency [122A].

Figure 4A above plots findings from the Roberts study. The SMR rises from 115 to 134 over the exposure intervals from 5-9 to 25+ years although the intervening exposure intervals have lower SMRs. This is for all miners with at least 15 years latency.

The international report mentioned above examined other studies of nickel workers which concern mostly nickel processing, open pit mining, strip mining or small cohorts. The authors conclude, "Based on the total number of deaths, the principal lung cancer excess in the cohort was for miners and surface workers. The attribution of the increased risk to nickel is questionable, given the evidence of a similar risk among other hard-rock miners with no exposure to nickel" [69].

Table 5 Cohort Studies Of Ontario Multi-Ore Miners
Author	Follow-Up	Cohort-Size	SMR	(95% CI)	Ores Mined
Muller [98f]	1955-77	8,379	145	(118-175)	5 yrs, <85% single ore
Muller [194b]	1955-81	4,216	201	(162-245)	gold/uranium
Shannon [120c]	1955-81	9,524	179	(137-227	uranium/nickel-copper, no gold
Shannon [120d]	1955-81	5,046	195	(158-237)	gold/uranium
Kusiak [81a]	1955-86	1,586	168	(125-216)	nickel/gold
Kusiak [79a]	1955-86	13,469	225	(191-262)	uranium/gold/nickel

Multi-ore miners

The majority of Ontario miners have work experience in more than one type of ore, based on information from the MMF. According to the MMF records, 52.1% of miners worked in at least two types of ore. This is the reality of mining experience. The single ore experience consists primarily of 16.9% nickel only, 14.5% gold only and 8.9% uranium only. The remaining 7.3% is scattered among other single ores [77].

Some multi-ore experience would be undocumented. For example, according to USWA sources, during strikes at the nickel miners went to work in the uranium mines. Mobility was also common during recurring lay-offs and economic downturns in the mining industry. During World War II, gold miners in Timmins were actively recruited for work in Sudbury's nickel mines. There are some unofficial estimates that up to 15,000 miners left gold mining for the nickel mines. During the 1960s, when the number of uranium miners fell from over 10,000 to about 1,000 in Ontario, employment was sought in other types of mining both in Ontario and in other provinces. An individual miner may in fact have worked for very short periods of time, but repeatedly, in different ore mines. Considering that nickel mining was often the best paid type of mining, there would have been movement into and out of various types of mining employment whenever there were openings in the nickel industry. The large nickel companies offered work in a relatively large community--Sudbury--and good pay with benefits.

A miner might have started out in gold mining, transferred to nickel mining once it was declared a strategic metal, in the 1950s switched to the uranium mines which began to flourish, and in the 1960s, he could have returned to gold mining or commenced nickel mining. The fact that mining companies preferred to hire men with previous mining experience probably contributed to the crossover.

Just as miners found jobs in different ore types, they also moved from surface to and from underground work. Men without previous mining experience sometimes would work in processing before transferring to better paid underground or surface work. Older miners, on the other hand, would sometimes prefer to transfer from underground to surface work. According to figures from the MMF, of nearly 90,000 men, 33,210 or nearly 38% have both underground and surface experience. This number excludes nickel surface workers unless they were employed in crushing or grinding operations [77].

Muller consistently found n excess of lung cancer in multi-ore miners. Muller's definition for "mixed ore" miner was anyone who did not fit the 85% criterion for one ore, or the two-week criterion for uranium [98]. In fact, most uranium miners defined in cohort studies worked in mines other than uranium. In the 1983 paper, Muller found an SMR of 145 (95% CI = 118-175) for multi-ore miners [98F], and in his 1987 follow-up, an SMR of 201 (95% CI = 162-245) for gold/uranium miners [94B].

In the 1989 IDSP Report on the uranium mining industry, Shannon found an SMR of 179 (95% CI = 137-227) for uranium/nickel (no gold) miners [120C], and an SMR of 195 (95% CI = 158-237) for miners with gold and uranium experience [120D]. It is also important to note that the SMR for uranium miners is likely underestimated because the inclusion criterion of two weeks of uranium mining means that the cohort is diluted with miners who had very little exposure.

In 1991, Kusiak found an SMR of 168 (95% CI = 125-216) for gold/nickel miners, [81A] and in 1993, an SMR of 225 (95% CI = 191-262) for gold/uranium/nickel miners [79A].

None of the papers mentioned above examined a dose-response relationship between mixed ore mining experience and lung cancer incidence. However, based on records in the MMF, MOL staff was able to generate a graph showing dose as measured by years worked as a multi-ore miner. Any miner with experience in more than one ore was included.

When Kusiak [78] analyzed the data from the MMF for all men who worked more than one ore, excluding uranium, he found an overall SMR of 132 (95% CI= 120-147). A dose-response relationship, as is seen in Figure A, shows an increase in SMRs from 112 for miners with less than five years worked to 167 for miners with 20-24 years experience.

In a paper for the IDSP, Yassi undertook a review of the world literature on lung cancer and hardrock mining. Yassi singled out Archer's 1988 summary of 21 studies which addressed issues of methodology, follow-up, lung cancer cell type and smoking [10]. Yassi also considered a broad population-based study. "It is noteworthy that the highest risk occupation for lung cancer was miners (OR=4.01). Mining as an industry also carried the highest risk of lung cancer (OR=2.98)" [153C].

Yassi concluded, "Epidemiological studies have documented increases in lung cancer in Ontario uranium miners, gold miners and nickel-copper miners. As more studies are conducted, and increasingly complex models are applied to the data, different permutations and combinations of relevant factors (including age, duration of exposure, years of exposure, confounding exposures, dose rate, etc.) have revealed different levels of risk in different subgroups" [153D].

(iii) Conclusions

Most of the studies confirm that

(b) Question 2: If there is an excess of lung cancer in the hardrock mining industry, is there something in the mining environment that can be related to the excess of lung cancer?

i) Potentially harmful agents in the hardrock mining industry

The Panel considered a large body of scientific literature on the mining environment and lung cancer and, as a result identified a number of potential carcinogens in that environment. Among these agents, the Panel was unable to identify any single agent to which excess cancer could be attributed.

As part of that process, the Panel looked at the natural or intrinsic elements found in the ore as well as at the potential carcinogens that would be introduced by its processing. The Panel relied particularly on the critical reviews and evaluations conducted and published by the International Agency for Research on Cancer (IARC).

For a detailed description of IARC criteria, please see Appendix G.

Frequently, where evidence for carcinogenicity in animals is judged to be sufficient, there is insufficient or nonexistent data on humans. IARC's policy has been that, "In the absence of adequate data on humans, it is reasonable, for practical purposes, to regard chemicals for which there is sufficient evidence of carcinogenicity in animals as if they presented a carcinogenic risk to humans" [66].

IARC has used its unique international position to develop a system for classification that has been praised for its elegant set of scientific criteria for selecting and evaluating published evidence on cancer. The Agency is widely recognized as an authoritative source of information on the carcinogenicity of chemicals and complex exposures.

The following agents have been consistently addressed by most of the sources which the Panel consulted in the preparation of the paper. For organizational purposes and based on their perceived presence in the mining environment,we have grouped the agents in the following categories. The IARC designation is noted where available.

Known Lung Carcinogens

Radiation [Group 1]

Arsenic and its compounds [Group 1]

Nickel and nickel compounds [Group 1]

Sulphuric Acid Mist [Group 1]

Asbestos [Group 1]

Suspected Carcinogens

Diesel Emissions [Group 2A]
(polycyclic aromatic hydrocarbons or PAHs)

Oil Mist- untreated and mildly treated [Group 1] highly refined [Group 3]

Blasting Agents [Not specifically classified by IARC-nitrosamines are by-products of the blasting process and are classified as Group 2A]

Silica, crystalline [Group 2A]

Other Agents of Concern

Chromium and compounds [Groups 1 and 3]

Cadmium [Group 2A]

Known lung carcinogens

Radiation

Studies of miners have confirmed the association between exposure to radon progeny and lung cancer [27, 62]. IARC concluded, "Radon and its decay products are carcinogenic to humans (Group 1)" [62].

The Panel investigated the types of radiation found in hardrock mining and the relationship between them. In its deliberations the Panel was guided by the explanation found in the Ham Report:

The ionizing radiation in mines arises from the spontaneous radioactive disintegrations associated with the decay chains of the naturally occurring isotopes of the elements uranium and thorium. There is a stage in each of these chains at which a gas is produced. The hazard of radiation in air breathed into the lungs arises mainly from the emanation into mine air from rock faces, broken rock, and mine water of the radioactive gas radon; thoron and actinon are radioactive gases of relatively lower hazard.

Throughout the rock in the Canadian Shield, uranium is present in about 3 parts per million and thorium in about 9 parts per million. These elements are more concentrated in many mineral deposits, especially in uraniferous ores. Wherever they are present in significant quantities there is a potential hazard from ionizing radiation in mine air if ventilation is not adequate. There is evidence from several countries, including Canada, of hazard from ionizing radiation in mines other than uranium mines... [52a].

The radiation associated with radon and thoron disintegration and further decays of their progeny are largely alpha and beta particles and gamma radiation.

The International Commission on Radiological Protection (ICRP) recommends that, when determining a worker's exposure to radiation, "the sum of both external and internal dose contributions" be considered [67a]. This would include external gamma radiation and internal exposure to alpha and beta particles which are emitted from radon and thoron progeny attached to the ore dust.

Radiation in uranium mines

Significant concentration of radon and radon progeny is expected from both underground and surface mining processes of uranium ore. Measurements from Ontario uranium mines indicated that the potential cumulative exposure to radioactivity from radon progeny between 1955 and 1961 was greater than 100 WLMs and could have reached over 300 WLMs [52]. Over the years, significant improvements in ventilation were made to meet regulations and the actual levels of radon progeny decreased. The annual exposure considered acceptable in Ontario also has decreased, see Table 6A.

The lowering of the exposure limit had a real effect on the exposure to radon progeny experienced by underground miners. As a result, by 1974, less than 9% of Denison mine workers and 0.3 % of Rio Algom workers had annual exposures above 4 WLMs. The average annual exposure in the two mining populations ranged from 1.2 to 1.7 WLM [52]. As shown in Table 6B the exposure decreased between 1960 and 1975.

According to a 1980 study comparing several Canadian and U.S. uranium mines, the exposures for milling ranged from below detection limit to 1.4 wlm, average 0.1 wlm. The exposures in the mill varied depending upon location, efficiency of local exhaust ventilation and atmospheric conditions. Maximum readings were from tailings, grinding and leeching processes, and from areas where radon had been concentrated during failures of local or general ventilation or during periods of climatic inversion [90].

Table 6c shows a comparison of radon and gamma ray levels in Ontario mines and surface operations between 1987 and 1991. Measurable levels of gamma radiation contributed to a worker's total radiation exposure but were not included in the calculation of his WLMs. According to Bush:

Gamma radiation was negligible relative to radon daughters in the early mines, but would have remained essentially unchanged in magnitude as the radon daughter concentration was reduced by improved ventilation. Consequently, for every Wlm of exposure to radon daughters, there is a greater exposure to gamma radiation in today's mines than in the earlier mines [18a].

In the uranium mills, where workers were exposed to concentrated ore and yellow cake, they were exposed to levels of gamma which were disproportionate to other levels of radiation, for the reasons cited above. Although the exposure was not consistently measured, a survey of the mills as cited in Table 6c supports the concept of high levels of gamma in the mills. The specific gamma exposure continued to be a source of whole body irradiation.

A 1980 Ministry of Labour report did measure gamma radiation levels in the Denison Mills. The report found, "Radiation levels in the mill from gamma radiation are not insignificant." Further, "Results obtained in the uranium precipitation shows that gamma and beta radiation increase with time. Close measurements (at 3 cm) of old uranium caked on the drum filter gave a beta reading of 14mR/h." In fact, the gamma radiation levels in a room adjacent to a maintenance area gave a reading of 3.0 mR/h which would suggest a yearly dose of just gamma radiation of 6 rems. The recommended occupational exposure limit is 5 rem per year [70].

In its recommendations for the monitoring of workers in the mining industry, the ICRP suggests a combination of personal and area sampling to provide a proper indication of exposure [67].

Radiation in gold and nickel mines

The concentration of uranium oxide in non-uranium mines is up to 100 times less than the concentration found in uranium mines [88]. Therefore, levels of radon progeny in non-uranium mines are likely to be much lower than those levels commonly found in uranium mines--except in areas where there is no or poor ventilation.

Radiation measurements in Ontario gold and nickel mines were not nearly as extensive as they were in uranium mines. Annual exposure based on levels measured in a 1982 Ontario gold mines survey ranged from 0.24 to above 3.6 Wlm [79]. The high levels were measured in inactive areas of the mines.

Considerations for the Evaluation of Radiation Exposure

It is important to exercise caution in assessing exposure to radon progeny in mines. While air monitoring measurements can reasonably reflect the levels of radon progeny within a short period of time, they may not necessarily be indicative of the general atmospheric conditions in the mine or of instances when the working environment or process is atypical. Variations in the level of radon and radon progeny are common in the same area or between different areas of a mine as a result of temperature and atmospheric changes.

Furthermore, data available on radon in mines is frequently based on instantaneous readings, which may miss peak radon concentrations, or on area sampling, which may not be representative of a worker's exposure under different work conditions over the course of a work day or week. Therefore, measurements of radon progeny are only estimates and should be used only as guidelines.

According to A. Dory, Manager, Uranium Mine Division for the Atomic Energy Board of Canada, as cited in the idsp's 1989 Uranium Report, pre-1960 measurements were very inexact and known to be incorrect up to one order of magnitude. This would mean that a wlm exposure of 15 could in fact be as high as 150. From 1960-70, wlm uncertainty can be plus or minus 200%, from 1970 plus or minus 100%. As late as 1978, the uncertainty is within plus or minus 50%. Exposure measurements of radon decay products did not begin in Ontario mines until 1958 [54].

Further, estimated personal exposures in the form of WLMs do not consider the synergistic effect of various risk factors in the mining environment. This effect may be multiplicative, or additive. Even at present times, WLMs do not include estimates of individual exposure to thoron progeny, gamma and beta radiation. Gamma radiation is now measured separately in uranium mines.

Arsenic

According to the IARC evaluation [64], arsenic is deemed to be a Group 1 carcinogen. IARC does not exclude any forms of arsenic in this evaluation, and includes occupational exposure among miners as a potential source of arsenic.

Arsenic is found in Ontario ore in the form of arsenopyrite and is particularly notable in gold mines. It is found combined with nickel ore in Sudbury. The concentration is low "but differed by as much as two orders of magnitude between mines" [141a]. Arsenic levels in Sudbury ore range from 0.096% to as low as 0.0004% [141].

In 1983 when the Ministry of Labour proposed regulating arsenic as a designated substance, numerous stakeholders, including various mining companies, made submissions. The mining companies were uniformly opposed to the proposal to include all forms of arsenic under the regulation and argued that the predominant form in ore, arsenopyrite, was probably not bioavailable and there was insufficient knowledge of health effects. Control in the mining industry was described as adequate in any case. The companies maintained that its designation would cause undue economic hardship and divert funds from more generally accepted health hazards. Designated Substance Regulation for Arsenic 176/86 subsequently excluded underground mining operations and construction from its authority.

In the Panel's evaluation of this issue the mining companies raised two issues:

In their written submissions, the management stakeholders questioned the extent to which arsenic is present in mining operations. It was argued that, if there had been sufficient levels of arsenic to be problematic, there would have been evidence of arsenic poisoning.

In response to that concern the Panel reviewed documentation that was available at the Ministry of Labour's office in Sudbury. The Ontario time-weighted average exposure limit for arsenic was 0.05 mg/m³ and was then lowered to 0.01 mg/m³ after 1986. Personal and area monitoring records established measurable levels of arsenic in gold mines. There was also evidence that the arsenic level in the gold mills occasionally exceeded the former exposure limit by a factor of 10. It should be noted that the highest levels were taken in areas in or near the roasting operation, a process which has been discontinued. Workers in gold mines who had been classified as millers would also have had exposure to roasting because of the application of union seniority lists in promotions, demotions and transfers or because of organizational practices in non-unionized mines.

There is also anecdotal evidence indicative of significant arsenic exposure in gold mining. According to a 1978 study, there were numerous reports of symptoms commonly related to arsenic exposure including dryness, itching, burning and cracking of the skin. Five of six miners studied also displayed abnormalities such as pitting of the nails, thickening of the soles and palms, linear markings, hyperpigmentation of the hands, feet and legs, and hyperkeratosis. It was also reported that arsenic, produced as a by-product of gold, was stored underground [20].

The accumulation of this evidence has led the Panel to conclude that there is arsenic in the Ontario ore body. Clearly, the highest levels are most commonly associated with gold ore but that does not exclude the existence of arsenic in other ores.

There remained a question from management regarding the bioavailability of arsenopyrite.

Arsenopyrite in its undisturbed state is relatively inert. However, once disturbed by the mining process, natural leaching, microbial action, blasting and contact with water, the potential exists for the formation of more soluble compounds which may be bioavailable. Furthermore, inhaled dust particles in the presence of oxygen, enzymes and body fluids may undergo transformation which increases the availability of soluble arsenic compounds [21]. In addition, a 1987 Ministry of Labour report, which while limited in scope, demonstrated that arsenic underground was bioavailable since its increase in the urine of miners over the course of a workweek was demonstrated [107].

On the basis of this study and in conjunction with other findings, the stakeholders and the Ministry agreed during the consultative process for the Regulation 176/86 that arsenic in Ontario underground hardrock mining is bioavailable to a certain degree [147].

Nickel

A strong body of evidence exists to link nickel with increased lung cancer risk in exposed workers. Both IARC and the American Conference of Government Industrial Hygienists (acgih) have classified nickel, including nickel sulfide, as carcinogenic in humans [1, 61]. There is epidemiological evidence and experimental data which indicate that certain nickel compounds are more potent carcinogens than others. In the absence of detailed dose-response relationships, the acgih did not propose different exposure limits for soluble and insoluble compounds. Instead, the acgih recommended that the Al designation as a confirmed human carcinogen be applied to all chemical forms of nickel [1]. There continues to be controversy over which species of nickel are carcinogenic and at what levels they constitute a health hazard [48].

The Sudbury area is one of the world's largest producers of nickel. This metal makes up about 0.008% of the earth's crust. Nickel in igneous rocks is approximately 0.01%. In Ontario, these ores occur predominantly as iron-nickel sulfides, most commonly pentlandite and pyrrhotite [134, 141].

Although little exposure data is available, the exposure of underground nickel miners to nickel is probably low. Since the 1970s, when systematic gravimetric dust sampling examined the nickel content of airborne dust, there is no record of findings exceeding the Ontario exposure guideline of 0.1 mg/m³ for soluble nickel. The exposure guideline for airborne insoluble nickel is 1 mg/m³ , and is rarely exceeded.

Sulphuric Acid Mist

Surface processes introduce chemicals which could contribute to an excess risk of lung cancer. With the exception of sulphuric acid mist, most of the chemicals used as additives in the milling process have not been investigated.

Occupational exposure to sulphuric acid mist has recently been evaluated as a Group 1 carcinogen by IARC. "There is sufficient evidence that occupational exposure to strong-inorganic-acid mists containing sulphuric acid is carcinogenic" [63a]. Sulphuric acid mist is present in gold milling (cyanidation), uranium milling (the leaching process), zinc milling, iron ore milling (electrolysis) and in modifiers for base metal flotation [71, 110].

Sulphuric acid mist is also found underground as a component of diesel exhaust. According to the Ontario Regulation respecting Control of Exposure to Biological or Chemical Agents--made under the Occupational Health and Safety Act 654/86, the twae value for sulphuric acid mist is 1 mg/m³ . A study of 24 us mines, as cited by IARC, reported a mean concentration of 12.8 mg/m³ (< 0.2-46) for sulphuric acid mist in diesel emissions and 0.3 mg/m³ (< 0.004-2) for personal and area samples [65]. The Panel was not aware of similar studies for Ontario hardrock mines.

Asbestos

IARC has designated asbestos as belonging to Group 1, sufficient evidence of carcinogenicity.

Asbestos may be present in the mining environment both intrinsically and extrinsically. Veins of tremolite, a form of asbestos in the group amphiboles, have been identified in underground mines [134]. Its presence in the natural state may not present much of a danger to non-asbestos miners. However, once disturbed and made airborne, its presence in dust can be an inhalation hazard.

Asbestos is also brought into the mining environment in its processed form. It is found in the brakes of motorized mining equipment and in insulating material around pipes.

The association of asbestos mining, working in asbestos-contaminated mines and lung cancer,was initially addressed in the Report of the Royal Commission on Asbestos [32]. It was further considered in the second idsp Report on Asbestos [59]. Both the rca and the idsp confirmed an association between lung cancer and occupational exposure to asbestos, although the association for miners and millers was considered not as great as for insulation workers.

In its Report, the Panel recommended that lung cancer and work with asbestos be included in Schedule 3 of the Workers' Compensation Act. This recommendation has not been implemented; however, the wcb has placed the issue on its policy agenda for 1994 as a priority item. Asbestos miners and millers will be included in a broader ongoing discussion. Therefore, the Panel does not deal with that issue in this report.

Suspected Carcinogens

Diesel Emissions

The exhaust from diesel engines has been found to contain various known and suspected human carcinogens: benzo(a)pyrene which is a polycyclic aromatic hydrocarbon (pah), benzene, soot, nitrites and formaldehyde. In its 1989 monograph, IARC found "Diesel engine exhaust is probably carcinogenic to humans" [65]. This complex mixture is present in the form of particulates, gases and vapours.

How these various components may interact with each other, with other carcinogens and with human tissue is in itself complex. PAHs, for example, are known to have a special affinity for lung tissue. Sulphur dioxide enables and promotes PAHs to become more carcinogenic in its presence [45].

Smith and Stayner point out that PAHs adsorbed to diesel particles may be only one link to lung cancer. In fact, the gas phase of diesel exhaust may be carcinogenic or cocarcinogenic as well. The authors conclude that diesel exhaust is a potential human carcinogen and exposures should be reduced to the lowest feasible concentrations [127].

Diesel-powered vehicles were first used underground in 1927 in Germany [65]. Diesel engines were introduced in underground mining in Ontario in the early 1960s. By the 1970s, these engines were widely used in all underground metal mines for generating power to operate various processing machinery. Diesel engines may produce more emissions when idling, during acceleration, when carrying heavy loads or when they are poorly maintained [45].

Evidence linking diesel exhaust and lung cancer specifically in the mining environment is difficult to find. The lack of evidence is in part due to the difficulty of assessing the exposure retrospectively and uncertainty about the specific substance(s) to measure [128]. If diesel exhaust is linked to lung cancer in the mines, the latency factor may mean that the effects of diesel could be expected to increase over the next years.

In an Ontario study, Westaway postulated that even ventilation may not help reduce exposure as was assumed since PAHs remain in the mine air longer than particulate and are not removed completely with the ventilation [142].

There are presently no Ontario standards for occupational exposure to diesel exhaust. This issue is currently before the Ontario Mining Legislative Review Committee which is recommending an exposure level of 1.5 mg/m³.

Oil Mist

Oil mist refers to airborne particulates generated from oil used to lubricate drills and other equipment.

IARC has designated oil mists into two groups. Untreated and mildly treated oils are Group 1; highly refined oils are Group 3.

Over time, the composition of lubricating oils has changed. There are few, if any, records of the types of oils used. In pre-World War ii mining, the type of oil used was likely straight oil, a mineral oil-based cutting fluid. Water soluble oils became available in the 1940s, and these contained many different types of additives: emulsifiers, biocides, corrosion inhibitors, etc. In the 1970s, synthetic oils were introduced containing at least traces of polycyclic aromatic hydrocarbons (PAHs), a known human carcinogen [143].

The issue of possible cancer mortality and exposure to lubricating oils is being investigated as a separate issue by the idsp. a paper on the topic was commissioned by the idsp and written by Dr. Paige Tolbert, Assistant Professor of Environmental and Occupational Health, Emory University. According to her paper [138], other suspected carcinogenic components of the oils include long-chain aliphatics, nitrosamines, formaldehyde, and chlorinated paraffins which may form dioxins. It is also thought that some of these combine with metal particles and as a result become more carcinogenic.

One recent study [8] found that the concentration of PAHs in lubricating oil increased over three to nine months. Benzo(a)pyrene, for example, was measured at 2.7 µg/g oil at the outset, increasing to 48.3 µg/g after nine months. The authors found that in assay testing, the oils also increased in mutagenicity.

The introduction of diesel equipment into the mining environment in the 1960s complicates the measuring of oil mists. They are hard to distinguish from oil in diesel emissions. Any dust sample could contain both diesel soot and oil mist [45].

In Ontario, the current time-weighted standard for oil mist is under review and may be lowered to 1 mg/m³ from the present 5 mg/m³ [143]. A study of Finnish sulphide ore miners reported that the average airborne concentration of oil mist during drilling was as high as 3 mg/m³ in the 1970s, ranging from 0.1 to 17 mg/m³ . The authors estimated that in the 1950s and 1960s, when airleg drillers were used underground, exposure to oil mist might have been double the exposure of the 1970s [4].

Blasting Agents

IARC has not investigated blasting agents per se. However, the potential exists for the formation of nitrosamines from by-products of the blasting process and several of these compounds are Group 2a--probably carcinogenic to humans. PAHs are also designated Group 2A.

Until 1955, nitroglycerin-based dynamite was the most widely used explosive in mines. It was gradually replaced by a mixture of ammonium nitrate (94%) and fuel oil (6%) called anfo. anfo accounts for more than 95% of the explosives used underground today. In some mines, water gel explosives are also used [134].

Historically, blasting in underground mining was carried out in two phases: primary and secondary. Large rock surfaces would initially be blasted to be followed by a second blast to reduce large chunks of rock to smaller pieces. There was usually a waiting period of 30 minutes between blasts, but miners would still be exposed to smoke and airborne dust from the primary blast if ventilation was inadequate. Since the 1980s, most primary blasting occurs between shifts. Most miners, therefore, are exposed only to secondary blasting and the quantity of explosives used is small.

The gases produced by underground blasting, called afterdamp, may include carbon monoxide, carbon dioxide, oxides of nitrogen, ammonia and methane [31]. None of the above are currently identified as a known human carcinogen, but there is some concern that exposure to oxides of nitrogen may be related indirectly to cancer. This may occur since nitrite, produced from nitrogen dioxide in blood, may be converted in the body to nitrosamines, some of which are known human carcinogens. As well, inhaled nitrogen dioxide may act to modulate the cancer process in the lungs [134].

As DeSouza and Katsabanis point out, even with sufficient ventilation, blasting fumes may present a hazard to miners underground:

The toxic fumes liberated from blasting operations underground will mix quickly with the ventilation air stream and, if not diluted to acceptable levels, represent potential hazards to the mine environment. In addition, as much as 60% of the fumes or gases produced during blasting underground can remain entrapped in the adjacent rock mass or in the muck pile. These gases are slowly liberated into the mine air, primarily during mucking, hauling and dumping operations [31A].

Nitrosamines and PAHs may also be found in the ANFO itself. The oil constituent in ANFO is frequently Fuel Oil No. 2; this resembles diesel oil and is a complex mixture of straight chain and aromatic hydrocarbons. Additional PAHs may also be released even if the explosive was not completely detonated. The nitrosamines and PAHs from blasting would add to those from diesel emissions and oil mist found in the mining environment.

Silica

According to IARC, silica is a probable human carcinogen, Group 2a [64].

Crystalline silica was regulated as a designated substance in Ontario in 1983 [O. Reg. 769/83]. The TWAE to airborne silica is to be reduced to the lowest practical level with a view to achieving at least 0.1 mg/m³ but shall not exceed 0.2 mg/m³.

Silica is present in the hardrock mining environment. The content of free crystalline silica in uranium, gold and nickel ore is 60-70%, 15-35% and 10%, respectively. Similar concentrations have also been reported for crystalline silica in total dust samples collected from Ontario mines [39]. In light of this, total dust was measured historically as an indicator of potential silica exposure in Ontario mines (see Table 7).

Since 1960, dust levels in all three types of mine have gradually decreased so that the 1975 level was about half of that measured in 1960. In the 1970s, air sampling measurements were made on the respirable crystalline silica itself. One record of uranium, gold and nickel mines in Ontario showed average measurements in 1975 of 0.11, 0.06-0.13 and 0.03 mg/m³, respectively which were at or below the current TWAE of 0.1 mg/m³. More recently, a study of an Ontario gold mine reported that the silica concentration in almost all of the air samples collected was well below the TWAE [50].

In examining the possible carcinogens associated with hardrock mining, the Panel agreed there may be an association between silica exposure and lung cancer, but that the evidence is inconclusive.

Other Agents of Concern

Chromium

Chromium is found in varying amounts in hardrock ore bodies and is commonly associated with gold ores. IARC found it unlikely that chromium in its metallic form would be a carcinogen. However, in a combined state, certain chromium compounds are strongly linked to various forms of cancer [61].

Chrome underground is in the form of fuchsite, a chromian mica, and chromite, a chrome oxide. Exposure levels to chromium in Ontario mines are estimated based on rock samples and tailings piles.

Chromium has been linked to increased incidence of stomach cancer in Ontario gold miners [80]. Cancers have also been reported in the respiratory tract of some chromium-exposed workers. There are also numerous experimental and epidemiological studies linking chromium compounds and lung cancer, but none of these involves hardrock miners [131].

Cadmium

IARC has classified cadmium as a probable human carcinogen (Group 2a).

Cadmium is a relatively rare metal found in the crust of the earth. It generally occurs in zinc ores as the mineral sphalerite (0.1-0.5%), but can also be found in zinc-bearing lead ores or complex copper/lead/zinc ores. Ontario hardrock miners may be exposed to cadmium during the mining and milling of ore through inhalation of dust.

While certain cadmium compounds, for example chloride, oxide, sulphide or sulphate, have been shown to be carcinogenic in animals, the evidence in humans is less conclusive. Despite findings showing small but significant increases in the incidence of cancers (lung and prostate) in cadmium-exposed workers [73, 137], exposures are confounded by concurrent occupational exposure to nickel and arsenic in the same mining environment.

The Panel found that, although chromium, asbestos and cadmium are present in most ore mined in Ontario, there were few studies which looked at these agents strictly in the mining environment.

(ii) Conclusions

Known lung carcinogens

Suspected carcinogens

Other agents of concern

(c) Question 3: What are the processes common to the hardrock mining industry?

i) Processes

Drilling, blasting, mucking, slushing, hoisting, crushing, grinding and conveying are carried out much the same way in all types of mines. Bulk, open-stope mining using heavy equipment is the preferred method today. Past mining methods were varied and significantly different. [134]

The mining process begins with prospecting and shaft sinking. Once access has been established, ore extraction can begin. Work areas are secured throughout the process by screening, roof bolting, timbering or backfilling, or a combination of methods. Blasting holes are drilled into the rock face to receive the explosives. In the past, dynamite was a common explosive. It contained nitroglycerine and some sodium or ammonium nitrate. As noted in the previous section, the more common blasting agent found in mining today is ANFO. The ANFO is detonated by the use of blasting caps made of an aluminium shell containing pentaerythritol tetranitrate. If there is wetness in the blasting hole, a plastic liner may be used as well. Moving the resulting broken ore, or muck, is carried out in a number of ways. Diesel equipment and diverse conveying and chute systems are common today. The most common conveyance for carrying ore to the surface is a hoist called a skip.

Once brought to the surface, the ore undergoes dry crushing and wet and dry grinding to prepare the ore for milling. Crushing and grinding reduce the size of the ore from the mine, about 12 inches in diameter, to a very fine size for the milling process.

In the milling process, there are some differences between ore types and differences between current and past practices. In general, the processes are wet and various agents are added to make the ore more reactive. Flotation reagents and brothers are used to improve the collection of the valuable ore parts which can then be skimmed off the surface. Throughout the milling process, brothers create surface bubbles. As the bubbles burst, a mist is formed and ore dust particles, total and respirable, are released. Spillage is a common occurrence in flotation and as these spills dry, further dust may be released into the air from the floor. The process of thickening and filtering dries the final concentrate which then contains 5 to 10% moisture.

For some ores, milling activities are separated physically from other processes. In other cases, milling is associated with crushing, grinding, packaging, etc. in close proximity, (i.e. within the same building or in an adjacent building.) In still other cases, refining is in close proximity mill, and shared ventilation cannot be avoided.

Mill, crushing and grinding workers rotate jobs so it would be unlikely that any person would work solely in one operation. Union seniority lists for mill, crushing and grinding workers covered all types of work throughout the process. This means that these workers would have performed any of the jobs on any given day.

Tailings, which are materials rejected from the mill following processing, may be used as back fill underground or they are stored outside the mine. "Tailing workers" monitor the transport of this residue and the areas of confinement. These workers might be exposed to natural elements previously discussed. Occasionally during tailing storms the workers would experience extremely dusty conditions.

Although mining and milling are distinct processes, it would be artificial to view them separately. Some of the same agents which have been identified as risk hazards underground are present in the milling process, in a more concentrated form. The intrinsic factors which may represent potential health hazards and are related to geological factors remain the same both in the underground environment and on the surface.

According to Thompkins, both blasting, crushing and grinding dramatically change the levels of radon and decay products in the environment. For example, blasting releases radon contained in rock. Grinding and crushing change more than just the size of the ore. "It is believed that the ore crystal grains are fractured with fine grinding and microfracturing is increased with crushing, both of which would account for the increasing rates of radon gas release" [135]. This would clearly have an effect on both underground and surface operations. As particles decrease in size through crushing, milling and grinding, more radon is released into the mine environment. As more surface area is formed through these processes, more radon is "available."

Many aspects of milling can be as dusty as underground work. Environmental records found at the Ministry of Labour confirm this. For every type of ore and mill, there was some incidence of surface operations producing readings equivalent to underground measurements. This was true for radon decay products, dust and silica. The majority of records consulted showed mining companies in compliance with historical guidelines for dust.

(ii) Conclusion

(d) Question 4: If there is an excess of lung cancer among hardrock miners, how is smoking related to that excess?

i) Smoking, mining and lung cancer

There is complete agreement that the primary cause of lung cancer is smoking. It is also an undisputed Act that miners smoke. Therefore, there is no doubt that smoking contributes to the incidence of lung cancer among miners.

This fact does not, however, preclude the possibility that the mining environment could also have an impact on the rate of lung cancer among miners. The IDSP is required to determine, if possible, the significance of the impact. If the impact from mining were to be insignificant, it would be open to the Panel to conclude that there is not a probable connection between mining and cancer. Alternatively, if it were to be determined that the mining environment was independently responsible for a number of lung cancer cases, the probable connection between work and disease would be undisputed. A third possibility is that smoking and mining work together or synergistically to increase the rate of lung cancer among miners.

The Panel has taken a great deal of time to address this issue. As a result of the request from the mining companies, the Panel asked Dr. Yassi to address this issue in a collateral document to her original paper. That paper was shared with the stakeholders and will be referred to in detail below.

The analysis conducted by the Panel to address the inter-relationship takes the following course. In the first instance, the Panel determines if there was a histological difference between the kinds of lung cancer attributable to smoking and the kinds of lung cancer attributable to work in the mining environment. It also looks at the pathological process to determine if the mining environment contaminants had different effects on the lung than did cigarette smoke. Finally it looks at statistical evidence to determine if there was any evidence to differentiate between smoking and non-smoking miners.

Turning to the first item--the histology--it is not possible to distinguish by cell type whether lung cancer was induced by smoking or induced by exposure to contaminants. The four main types of lung cancer (small cell, epidermoid, adenocarcinoma, and large cell) occur in both smokers and miners.

The next question deals with pathological process. This requires an examination of the differences in the disease processes, if any, between the lung cancer associated with smoking and lung cancer associated with mining which would allow individuals to distinguish the causal agent.

The following excerpt from Dr. Yassi's report explains the process by which smoking affects the anatomy of the lung. She wrote:

In the large airways, cigarette smoking produces mucous gland thickening and alteration (hyperplasia). Cigarette smoking also stimulates mucous production from the goblet cells in the small airways. These changes lead to the well recognized clinical condition of chronic bronchitis, defined as regular sputum production over the course of several months for at least two consecutive years. The lining of the airways (bronchial epithelium) becomes abnormal structurally, predisposing it to malignant changes. The physiological changes which accompany these structural abnormalities are also significant. The increased permeability caused by cigarette smoking facilitates the passage of inhaled carcinogenic agents across the epithelium. The defence mechanism whereby gases and particulates are cleared from the large airways (the mucociliary clearance) is slowed in cigarette smokers. Thus carcinogens reside in the lungs for a longer period of time. It has indeed been shown that there is greater deposition of particles in the airways of smokers compared to non-smokers. This is clinically consistent with the impaired lung function well documented in smokers, as well as the chronic airflow obstruction that develops due to cigarette smoking.

Smoking-related changes in the lung structure and function alter the dose of carcinogens to target cells at any particular level of exposure. Specifically, the impaired mucociliary transport, the increased airway permeability, and the greater central deposition all combine to increase the dose of carcinogens received by smokers compared to non-smokers at the same level of exposure. The lung impairment that is often found in smokers also leads to an increased respiratory rate for any particular level of activity, thus again increasing the risk of carcinogenesis [154].

The relationship between the inhalation of contaminants from the mining environment and the effects on the lung have also been described in a paper prepared by Dr. Chase, a physician in the employ of the IDSP. He wrote as follows:

It is important to note that the defences the lung mounts to counter the effects of smoking, and the chronic changes that result from cumulative cigarette fumes and gases (producing chronic bronchitis, emphysema, and other chronic obstructive lung diseases) are nonspecific in nature. Similar changes: mucous gland thickening; inflammation of the epithelial lining with increased membrane permeability, etc. occur in association with other forms of respiratory exposure to dusts, chemicals, and gases, many of which occur in the mining environment. In normal subjects, there is an increase in mucociliary clearance in response to exercise, hyperventilation, smoking and after inhaling dust (Cotes and Steel p74), but this is known to fail in the presence of chronic lung changes [21].

As described in the preceding passages, the natural defense process employed by the lungs is the same regardless of the nature of the offending agent. This common defense mechanism makes it difficult, if not impossible, to distinguish the course of a lung cancer induced by cigarette smoke and a lung cancer induced by another agent.

What does vary, as pointed out by Dr. Yassi, Dr. Warner and Dr. Cecutti, is the time it takes for the body to react. That reaction time or latency varies significantly from agent to agent and is further influenced by individual susceptibility. A very short latency may be important when attempting to exclude certain causes of cancer. However an analysis of latency will be much less useful when attempting to differentiate between two competing and concurrent exposures.

Finally, the Panel looks to the epidemiological evidence concerning the contribution of mining to lung cancer after allowance for smoking.

There is very limited evidence about the contribution of smoking to lung cancer in miners because many of the studies have omitted any record of the smoking habits. There are some studies, primarily of uranium miners, however, which attempt to disentangle the smoking risk from the mining risk because smoking habits were recorded.

Dr. Yassi reported:

Several U.S. studies have also provided detailed information concerning the roles of cigarette smoking and radiation in the production of lung cancer. The first report by Archer et al. 1973, found lung cancer rates of 1.1 and 4.4 per 10,000 person-years for non-smokers and smokers respectively in the population, whereas the rates among uranium miners were 7.1 and 42.2 per 10,000 respectively. Thus an almost 4-fold population base for excess smoking and a 5.9-fold excess for uranium mining was found and a multiplicative interaction of these agents was suggested [154].

The evidence for miners exposed to lower levels of radon is less complete. In Kusiak's 1991 study of Ontario gold miners, the authors determined that the smoking habits of gold miners were similar to the smoking habits of nickel miners. That same study showed that the lung cancer rate of the gold miners was higher than the rates of the other miners. The authors concluded that the excess of lung cancer among gold miners could not be attributed to smoking alone, but to something in the mining environment [81].

In addition to the evidence specifically related to lung cancer rates, there is evidence about deaths attributable to cardiovascular disease which is acknowledged to be associated with smoking. If smoking were responsible for the elevated lung cancer rates, it would be expected that rates of death for cardiovascular disease would also be elevated. The rates for heart disease are consistently not raised. For example two studies of Ontario miners produced the following SMRs:

Dr. Yassi in her review also considered the studies which looked at the combined effect of smoking and exposure to radon progeny. Her conclusions, which were not disputed by the stakeholders, are as follows:

BEIR IV felt that the data sets from the case-control studies of New Mexico uranium miners, Japanese atomic bomb survivors, and the cohort study of Colorado Plateau miners were the best data sets from which to perform a detailed analysis of radiation exposure and cigarette consumption as related to the risk of lung cancer. Table 2, also taken directly from the BEIR IV report, shows the distribution of cases and controls for the cross-classification of years of underground mining and smoking. It can be seen that risks are increased with years of underground mining within each cigarette use category. Detailed analysis suggested that the multiplicative model provided the best fit.

Table 3 shows the results of lung cancer mortality rate as a function of cumulative radon exposure and cigarette consumption for the Colorado Plateau miner cohort. BEIR IV's analysis of the interaction between smoking and cumulative exposure supported the conclusions of Whittmore and McMillan (1983) that a multiplicative combination of relative risks provided an acceptable fit. However, the committee noted that a range of sub-multiplicative to super-multiplicative models was equally compatible with the data.

Thus it can be concluded that radon progeny exposure and cigarette smoking interact synergistically, (ie. the combined effect is greater than the sum of the individual effects), although the interaction may be sub-multiplicative to super-multiplicative. It should be noted that international authorities all seem to agree with this conclusion, including the Atomic Energy Control Board of Canada, the regulatory authority for uranium mines in this country [154].

(ii) Conclusions

In summary, the Panel has found that the epidemiological evidence is the most useful in assessing the relationship between the mining environment and lung cancer. Neither the histological or pathological evidence is of much assistance.

The available evidence indicates that the rates of lung cancer among non-smoking uranium miners are similar to the rates of smokers in the general population. The rates increase significantly when smoking and mining are added to the mix. Furthermore the lower than expected SMRs for heart disease leads to the conclusion the smoking among miners is not the only reason for increased lung cancer rates.

Chapter Three Workers' Compensation Law and Policy

Criteria for making recommendations about industrial disease

There are many factors that must be considered when formulating recommendations about industrial disease. Some of these factors will be briefly described here. A more detailed discussion of these issues can be found in a forthcoming occasional paper to be published by the Industrial Disease Standards Panel in 1994.

The term "industrial disease" occurs in the context of the Workers' Compensation Act and in that context these words refer to an entity defined by the Act and not 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 8 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 year