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
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.
|Canadian Cataloguing in Publication Data
Main entry under title:
Report to the Workers' Compensation Board on lung cancer in
the hardrock mining industry
(IDSP report, ISSN 0804-7274; 12)
Includes bibliographical references.
1. Lungs-Cancer. 2. Mineral industries-Health aspects.
I. Ontario. Industrial Disease Standards Panel. II. Series.
RC280.L8R46 1994 616.99'424 C94-964021-2
Additional copies of this publication are available by writing:
Industrial Disease Standards Panel
69 Yonge Street, Suite 1004
Toronto, Ontario M5E 1K3
|Ms. Nicolette Carlan (Chair)||May 16, 1991 to May 15, 1994|
|Dr. Carol Buck||June 1, 1991 to June 16, 1994|
|Mr. James Brophy||January 23, 1992 to January 22, 1995|
|Mr. Robert DeMatteo||April 7, 1993 to April 7, 1996|
|Mr. William Elliott||November 7, 1991 to November 6, 1994|
|Ms. Nicole Godbout||December 16, 1992 to December 15, 1995|
|Mr. John Macnamara||November 7, 1991 to November 6, 1994|
|Mr. Homer Seguin||May 28, 1992 to May 27, 1995|
|Dr. Michael Wills||November 7, 1991 to November 6, 1994|
|Carolyn Archer||Senior Research Officer|
|Robert Chase||Medical Consultant|
|Martha Keil||Program Coordinator|
|Francis Macri||Policy Analyst|
|Cara Melbye||Policy Analyst|
|Susan Meurer||Policy Analyst|
|Anne Rekenye||Data Entry Clerk|
|Tracy Soyka||Administrative Co-Ordinator|
|Salima Storey||Administrative Officer|
|Jason Tung||Industrial Hygienist|
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?
(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?
(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
Chapter 3 Workers' Compensation Law and Policy
Chapter 4 Summary of Conclusions
Chapter 5 Findings and Recommendations
Lung Cancer Standardized Mortality Ratios for Ontario Hardrock Miners
Cohort Studies of Ontario Gold Miners
Lung Cancer SMRs of Ontario Gold Miners
Dose-Response Relationship of Lung Cancer and Ontario Gold Mining
Lung Cancer Mortality in Gold Miners as found in IDSP Gold Mining Industry Report
Cohort Studies of Ontario Uranium Miners
Lung Cancer SMRs of Ontario Uranium Miners
Dose-Response Relationship of Lung Cancer and Ontario Uranium Mining
Cohort Studies of Ontario Nickel Miners
Lung Cancer SMRs of Ontario Nickel Miners
Dose-Response Relationship of Lung Cancer and Ontario Nickel Mining
Cohort Studies of Ontario Multi-Ore Miners
Lung Cancer SMRs of Ontario Multi-Ore Miners
Dose-Response Relationship of Lung Cancer and Ontario Multi-Ore Mining
Ontario Radon Exposure Standards
Historical Radon Data
Comparison of Radon and Gamma Ray Levels
Average Dust Level in Underground Mines
Continuum of Injuries and Illness
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.
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.
The IDSP's authority to conduct this work is set out in Ontario's Workers' Compensation Act. Specifically, the Act reads:
(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 . 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;
5. biological gradient;
6. biological plausibility;
8. experiment; and
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".
|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|
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 .
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.
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?
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.
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.
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:
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 , 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.
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) . 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.
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.
Cohort Studies Of Ontario Gold Miners
|Author||Follow-Up||Cohort Size||SMR||(95% CI)|
|All of the studies in this table used a five year gold mining
experience as a criteria for inclusion.
Excess lung cancer in Ontario gold miners was documented by Muller . 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 . 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 . 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 . 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" . 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.
Lung Cancer Mortality in Gold Miners as found in the
IDSP Gold Mining Industry Report
|South Africa||3,971||9 years||161|
Cohort Studies of Ontario Uranium Miners
|Author||Follow-Up||Cohort Size||SMR||(95% CI)|
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) . 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) . In Muller's 1987 follow-up study, all uranium miners with previous gold mining experience were excluded from the cohort . 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 . 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 , there were too few deaths to generate statistically significant SMRs. Muller  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 . 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 . 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 .
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 . 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 . According to Muller, the median number of years worked in uranium was 1.5 years .
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.
Cohort Studies of Ontario Nickel Miners
|Author||Follow-Up||Cohort Size||SMR||(95% CI)||Comments|
|Roberts [113a]||1950-76||47,890||112||(103-123)||All Sudbury non-sinter
workers, including some
smelter and refinery workers.
|Roberts [69a]||1950-76||27,611||114||(100-128)||As found in 1990 Doll nickel
|Shannon [69b]||1950-76||6,841||150||(114-191)||As found in 1990 Doll nickel
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.
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 . 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 . 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 . 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" .
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|
|Shannon [120c]||1955-81||9,524||179||(137-227||uranium/nickel-copper, no gold|
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 .
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 .
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 . 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  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 . 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].
Most of the studies confirm that
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" .
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.
|IARC's programme, initiated in 1971, relies on
international working groups of scientists expert in the
particular area under investigation. Information is analyzed
from animal studies, other relevant biological data, and case
reports and epidemiologic studies in humans. The working
group then makes an overall evaluation of the
carcinogenicity of the particular agent to humans and the
substance is designated as falling within one of four main
IARC groupings as listed below:
|Group 1||The agent is carcinogenic to humans.
There is sufficient evidence of
carcinogenicity in humans. A causal
relationship has been established between
exposure to the agent and human cancer.
|Group 2A||The agent is probably carcinogenic to humans.
This category is used when there is limited
evidence of carcinogenicity in humans and
sufficient evidence in experimental animals.
|Group 2B||The agent is possibly carcinogenic to humans.
This category is generally used when there is
limited evidence in humans in the absence of
sufficient evidence in experimental animals.
|Group 3||The agent is not classifiable as to its carcinogenicity
This category is used for agents that do not fall
into any other group.
|Group 4||The agent is probably not carcinogenic to humans.
This category is used for agents for which
there is evidence suggesting lack of
carcinogenicity in humans together with
evidence suggesting lack of carcinogenicity in
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]
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]
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)" .
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.
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 . 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.
Ontario Radon Exposure Standards Before 1975 and
Current for Underground Uranium Mining
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 . As shown in Table 6B the exposure decreased between 1960 and 1975.
Historical Radon Exposure Data in Ontario Uranium Mines
|Historical Exposure Data in WLMs|
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 .
|Comparison of Radon and Gamma Ray Levels (WLM*) in
Ontario Uranium Mines between 1987-1991.
|Gamma was originally measured in millesieverts, converted here to WLMs.
Surface includes workers other than millworkers, i.e. office, technical staff, etc.
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 .
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 .
The concentration of uranium oxide in non-uranium mines is up to 100 times less than the concentration found in uranium mines . 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 . The high levels were measured in inactive areas of the mines.
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 .
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.
According to the IARC evaluation , 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% .
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 .
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 . 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 .
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 .
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 . There continues to be controversy over which species of nickel are carcinogenic and at what levels they constitute a health hazard .
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.
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 . The Panel was not aware of similar studies for Ontario hardrock mines.
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 . 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 . It was further considered in the second idsp Report on Asbestos . 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.
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" . 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 .
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 .
Diesel-powered vehicles were first used underground in 1927 in Germany . 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 .
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 . 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 .
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 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 .
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 , 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  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 .
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 . 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 .
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 .
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 . 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 .
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.
According to IARC, silica is a probable human carcinogen, Group 2a .
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 . In light of this, total dust was measured historically as an indicator of potential silica exposure in Ontario mines (see Table 7).
Average Dust Level in Underground Mines
|(As adopted with modification from the Report of the Royal
Commission on the Health & Safety of Workers in Mines as
compiled by the Mines Accident Prevention Association of
Ontario and the Ministry of Natural Resources.)
Dust levels in particles per cubic centimetre as measured by a
*1969 Guideline of the Mines Accident Prevention Association of
Ontario for total dust.
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 .
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.
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 .
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 . 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 .
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.
Known lung carcinogens
Other agents of concern
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. 
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" . 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.
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 .
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 .
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 .
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 .
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:
|Ischaemic heart disease||80||79||98||72|
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.
Data from Case Control Study of New Mexico Uranium Miners
|Years of Underground Mining|
|1: 1+ ø(yr,n/d)||15||--121.8|
|aRelative risks from additive model, Equation VII-2
bRelative risks from multiplicative model, Equation VII-1
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.
Observed Lung-Cancer Mortality and Calculated Lung-Cancer Mortality Rate as a Function of
Cumulative Exposure and Cigarette Consumption for the Colorado Miner Cohorta
|Cumulative||No. of Cigarettes/day|
|aCumilative exposure limited to 2,000 WLM.
bBaseline rate per 100,000 computed using expected number of cases, based on U.S. white male mortality rates for lung cancer adjusted to nonsmokers.
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 .
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.
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 years after that first exposure.
Neither individual workers nor employers generally have a sufficiently broad information base to identify patterns of disease. The long-term perspective and wide view can only be achieved by scientific research or information gathered by external bodies such as government agencies. On this point Professor Paul Weller, one of the primary architects of the IDSP, in his report entitled: Protecting the Worker from Disability: Challenges for the Eighties wrote at page 44:
This Panel should not be locked into a formal legal procedure, especially not trial-type hearings with testimony under oath and subject to cross-examination by lawyers. Issues of science policy require a more flexible, probing style of inquiry. Either on its own initiative, or at the request of the Board, the Ministry, or an interested Farm, the Panel would untertake the review of a disease to which there is, as of yet, no standard, or where the guidelines appear to be outmoded. [At the outset, the Panel would need to canvass a number of internationally recognized industrial diseases for which there is as yet no Ontario standard, although the toxic substance is to be found in Ontario industry: e.g. leukemia and benzene, angiosarcoma and vinyl chloride, lung cancer and chromium, bladder cancer and the aromatic amines in the petrochemical industry.] Probably the Panel would base its work primarily on a review of the world-wide research literature....
The IDSP was created in 1985 with the intention of bringing that broad perspective and specialized expertise to the task of identifying industrial diseases.
As set out in section 95 of the Act, the Panel is authorized to make findings of probable connection between disease and work. These findings are reported to the WCB which has the right to accept or reject the findings and declare the existence of an industrial disease in an appropriate circumstance.
At the time s. 95 was added to the Workers' Compensation Act, the Minister of Labour said:
"I believe there are very few persons who would seriously contest the need for improving our efforts in locating and identifying elements that appear to be causally associated with industrial disease and for developing standards to deal in the fairest manner possible with the compensation claims to which they give rise."
This indicates that the government of the day determined that it would be appropriate for the Panel to make findings of apparent causal connections. This suggests that it may be best to understand "probable connection" as meaning something like "apparent causal connection." This should not be confused with the concept of causation, a relationship that is the subject of medical and scientific research.
Once there is a finding of "probable connection" by the IDSP and a declaration of an industrial disease by the Board, it is then necessary to develop guidelines for the processing of claims. In accordance with its mandate under the law and often at the request of the WCB, the Panel may make recommendations to the Board on how employees with an industrial disease should be compensated.
The Workers' Compensation Act has provisions to accommodate the unique issues associated with industrial disease adjudication. Specifically, Schedules 3 and 4 have been added to legislation to make the workplace parties aware of accepted and declared industrial diseases. By entering diseases on the Schedule the work association is declared and the de facto burden of proof of work association is shifted from the worker to the WCB. Once a disease is assigned to Schedule 3 or 4, a worker need only prove that he or she suffers from the disease and was exposed to the associated industrial process. By demonstrating this, the worker has invoked the presumptions in s.134. This shifts the onus to the WCB in the case of Schedule 3 diseases to disprove the work association in the specific case. In the case of Schedule 4 diseases there is no ability to disprove an association.
When a disease is not listed on Schedule 3 or 4, in practice the affected worker has the burden of proving the work association. The standard applied by the Worker's Compensation Appeals Tribunal and endorsed by the Minister's Task Force on Occupational Disease to establish the work relationship is that work was a "significant contributing factor" to the disease. The worker may be required to present medical evidence, and perhaps epidemiological evidence about the usual causes of the disease. The worker may also have to obtain information about the chemicals he or she was exposed to at work, and investigate whether these chemicals may have "significantly contributed" to the onset of the disease.
It is possible to formulate criteria for determining whether a disease is the sort to be added to Schedule 3 or 4 or whether guidelines should be created. However, those criteria have not yet been clearly articulated by the WCB. The best guidance we currently have on this issue are the current entries in each of the Schedules. We have examined the current entries and attempted to identify the criteria used by the Board when entries were made in the past. We have also reviewed internal WCB documents on this point.
Schedule 4 is appended to Regulations1 to the Workers' Compensation Act. When a worker suffers from one of the diseases listed in Schedule 4 and can show that he or she, in the work-place, was exposed to the associated process, then the following conclusive presumption applies.
(10) If the worker at or before the date of the disablement was employed in any process mentioned in the second column of Schedule 4 and the disease contracted is the disease in the first column of the Schedule set out opposite to the description of the process, the disease shall be conclusively deemed to have been due to the nature of that employment.2
Currently only three diseases are included in Schedule 4, asbestosis, mesothelioma, and nasal cancer. The pattern of criteria for inclusion that we have identified by reviewing these entries is as follows:
There are no "diseases of ordinary life" included in Schedule 4.
The legislation setting out Schedule 33 reads as follows:
(9) If the worker at or before the date of the disablement was employed in any process mentioned in the second column of Schedule 3 and the disease contracted is the disease in the first column of the Schedule set out opposite to the description of the process, the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved.4
According to our understanding of the WCB process, when a worker claims to have a disease that is listed in this Schedule, the adjudicator would first determine whether the claimant has the disease, and was exposed to the corresponding industrial process. If these conditions are satisfied, the adjudicator would be required to "presume" that the disease is compensable. This does not end the matter, however, since
"the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved" (emphasis added).
This appears to direct the adjudicator to ask whether there is any other information that demonstrates that the disease was not caused by work. At this stage of the adjudication, the IDSP believes that WCB staff would be aided by a set of criteria referred to collectively as a rebuttal matrix. That matrix would assist adjudicators in the indentification of facts that would lead to the rebuttal of the statutory presumption. If evidence of this sort "proves the contrary", then the disease is no longer presumed to be due to work and compensation will be denied.
Diseases entered on this Schedule have a strong but not exclusive connection to work processes. In looking to determine if a disease should be included in Schedule 3, the WCB apparently has looked for:
For diseases currently listed in Schedule 3 there may be several possible causes for a disease. Currently in the Schedule there are diseases which are known to have both employment and non-employment etiologies. This has allowed for the scheduling of "diseases of ordinary life" such as dermatitis.
When a disease is not listed in the Schedules are there alternatives tools available to assist the adjudicators?
Employees receive compensation for a disease if it is established that the disease is caused5 by work, even when the disease is not listed in the Schedules.6 The WCB has issued many "policies" or "guidelines" that assist adjudicators on how to handle claims on an individual basis. These policies are created by the WCB as a result of the investigation of many instances of a specific disease.
In instances where the evidence is equivocal about whether a disease is caused by work, the IDSP has recommended that the Board create specific policies and guidelines concerning the disease. This approach was adopted by the IDSP in its Report of Findings on Scleroderma. The lack of certainty about the work association may exist because there is little known about the disease or because there is contradictory evidence about an association. When and if the evidence becomes stronger it may be appropriate for the IDSP to issue revised recommendations to the Board which may endorse entering the disease into a schedule.
The following outlines the current policies of the Ontario Workers' Compensation Board on lung cancer and mining as outlined in the Board's manuals. The Board's policies on other conditions that affect the lungs, such as asbestosis, mesothelioma, silicosis or tuberculosis are not discussed.
Some diseases listed on Schedule 3 of the Regulations to the Workers' Compensation Act are diseases that may be related to lung cancer in specific instances. Diseases on this schedule, which are presumed to be caused by work unless the contrary is proven, are poisonings and their sequelae by arsenic.7
Also listed on this Schedule is "Any disease due to exposure to X-rays, radium or other radioactive substances".8
The Workers' Compensation Board has also enacted policies that relate to lung cancer. One policy sets out "categories of persuasive evidence to establish work-relatedness" in regard to lung cancer in gold miners. This policy begins by stating that,
"Primary cancer of the trachea, bronchus or lung is accepted as an industrial disease under sections 1(1)n [definition of industrial disease] and 122 [section 134 of R.S.O. 1990] of the Workers' Compensation Act as characteristic of gold mining in Ontario."9
It is worth noting that according to WCB documents the Board was satisfied by the application of the Hill criteria that there was a relationship between gold mining and lung cancer. This policy was enacted with evidence of an SMR of 160 for lung cancer in gold miners, and evidence of known carcinogens in the workplace.
Another policy addresses lung cancer in workers at the Deloro Smelting and Refining Company who were exposed to arsenic, and states that for these workers their lung cancer,
"is accepted as an industrial disease under sections 1(1)n [definition of industrial disease] and 122 [now s. 134 of R.S.O. 1990] of the Act as peculiar to, and characteristic of, processes and trades involving exposure to arsenic."10
A policy of the Board deals with workers suffering from lung cancer who were exposed to radon gas and radon progeny, and states that for these workers their lung cancer,
"is accepted as an industrial disease under Schedule 3, item 9 for the purposes of section 122 [now s. 134 of R.S.O. 1990] of the Act."11
Another policy concerns lung cancer in coke oven workers in the steel industry, and states that for these workers their lung cancer,
"is an industrial disease under sections 1(1)n [definition of industrial disease] and 122 [now s. 134 of R.S.O. 1990] of the Act as peculiar to and characteristic of exposure to coke oven emissions in the steel industry."12
And finally a further Board policy deals with lung and sinus cancer in workers,
"exposed to operations in the calipers, cupola furnaces, and sinter plant at Port Colborne, and in the sinter plant at Copper Cliff at INCO Metals Limited,"
and states that for these workers their lung or sinus cancers,
"are industrial diseases under sections 1(1)n [definition of industrial disease] and 122 [now s. 134 of R.S.O. 1990] of the Act as peculiar to, and characteristic of processes and trades involving such employment."13
On December 7, 1993, the WCB approved the inclusion of nasal cancer for any process at the Copper Cliff sinter plant of INCO Ltd., and any process in the Port Colborne leaching, calcining and sintering department of INCO Ltd. that was practiced before January 1, 1966, in Schedule 4. This addition to the Schedule will probably require a modification to the policy.
Other jurisdictions in Canada and the jurisdiction of Massachusetts in the U.S.A. have laws and policies that affect the manner in which compensation is paid to miners suffering from lung cancer. These policies are summarized in Appendix H.
Most of the studies confirm that
Known lung carcinogens
Other agents of concern
On the evidence available to it the Panel has come to the following conclusions:
Accordingly the IDSP finds that:
|A probable connection exists between all hardrock
mining and lung cancer.
Because of the strong evidence of a probable connection between lung cancer and hardrock mining the Panel concludes that the disease and the process should be included in a Schedule appended to the Workers' Compensation Act. The high rates of lung cancer in the general population and the known non-work related causes for lung cancer have persuaded the Panel that the entries should be included in Schedule 3 not 4. This recommendation would require the wcb to "prove" in the appropriate circumstances that a miner's lung cancer was not related to his mining exposure.
The evidence to prove the contrary is complex. There are significant and numerous differences in the experience of the majority of miners. The majority of miners worked in different kinds of ore, at different times and for different lengths of time. They also worked underground and on surface. These variations have resulted in varying degrees of risk. The risk is greatest for those miners with mixed ore experience, especially gold/uranium, and least for those miners who worked only in nickel. The extent to which a miner smoked, if at all, is also a factor that must be considered when assessing the overall risk due to exposures in the mining environment. To allow the wcb adjudicators to fairly and equitably assess the evidence that would be used to rebut the presumption, it is critical to develop a "rebuttal matrix". The Panel unanimously concludes that the scheduling of the lung cancer should not take place until this "rebuttal matrix" is created.
The Panel recommends:
|"Primary lung cancer" and the associated process,
trade or occupation of "hardrock mining" should be
placed on Schedule 3, but only after the Panel has
approved a rebuttal matrix that has been created with
the assistance of the Board. The industrial processes
included in the term hardrock mining are underground
mining, shaft sinking, surface diamond drilling,
crushing, grinding, milling, and tailings work.
A model in which the combined effects of several factors is the sum of the effects that would be produced by each of the factors in the absence of the others.
A compound mineral form in which arsenic in its natural state is found with a sulphide of iron. It is found with gold ore and is considered to be an inert mineral.
A connection between two phenomena which can be causal, biased, random or seeming. A statistical association does not automatically mean causation.
Waste rock, sand or gravel used in mining to fill up underground a void, preventing rock movement.
A metal of less monetary value as compared to gold and silver. The term is generally applied to copper, lead, nickel, zinc, etc.
Substance(s) or preparation(s) which, by inhalation, ingestion or cutaneous (through the skin) penetration can induce cancer in humans or increase its frequency.
A designated group of people with one or more features in common, such as type of exposure or common employment, followed over a period of time.
A situation in which a measure of the effect of an exposure or risk is distorted because of the association of exposure with other factor(s) influencing the outcome being studied. Common confounders are smoking, alcohol intake, socio-economic status, diet.
A dose-response trend is shown when an increase in the "dose" (exposure level, intensity, duration, etc.) corresponds to an increase in the "response" (usually an smr for a particular cause of death). A dose-response relationship is shown when more disease occurs after higher exposure to a substance.
A process in mining whereby blasting holes are mechanically made in the rock face. It is one of the dustiest operations in mining.
Is the study of disease patterns in groups of people. In the context of the idsp, the groups reflect occupational exposures to potentially hazardous substances.
A wet process in milling which separates the valuable ore from rock waste. Various chemicals are added as reagents.
Observation over a fixed period of time in a group to record changes to health status during that time. If the follow-up period is too short, findings may not reflect the true number of cases.
Modern method of sampling and measuring the amount of dust in a mine.
All exploitation of ore in igneous rock which is common in the Canadian Shield. Granite is the most common igneous rock and consists chiefly of quartz.
An early measuring instrument used to estimate dust levels in mines. Konimeters did not measure personal exposure.
The period of time between exposure to a substance(s) and the appearance of disease which it has caused.
The process of concentrating mined ore through physical and chemical manipulation. The processes differ by type of metal and by company. Waste rock is separated from the valuable minerals. Some of the stages are: crushing, grinding, flotation, separation, leaching, ion exchange, calcination, concentration, cyanidation and drying.
Ore or rock that has been broken by blasting.
A model in which the joint effect of two or more causes is greater than the sum of their individual effects. The resulting effect could not occur without the presence of each.
Refers to the odds ratio. This represents the likelihood that observed cases had a certain exposure, compared to the likelihood that controls had that exposure. An equal likelihood is expressed as 1.
Any rock containing minerals whose extraction and processing can be marketed.
Polycyclic aromatic hydrocarbons (PAH)
Also called polynuclear aromatic hydrocarbons. PAHs are nonpolar, fat soluble compounds that can be absorbed into the body through the skin, the lungs or the digestive system. PAHs are inhaled in particulate form from tobacco smoke and from air contaminated with combustion products such as vehicle exhaust. The carcinogenicity of PAHs has been demonstrated in animal experiments and more recently in epidemiological studies.
Radon decay products, progeny, daughters
Radioactive elements derived from the decomposition of radium into radon gas as a naturally occurring process. Radon undergoes a series of 11 decay events which emit irradiation energy (alpha, beta and gamma types), and produces non-gaseous radioactive progeny that tend to adsorb on dust particles and thus are deposited in the respiratory tract and elsewhere of those exposed.
The ratio of the risk of disease or death among exposed people as compared to the risk among unexposed people.
Treatment of ore, especially gold, to remove sulphur and arsenic.
Pulmonary fibrosis or scarring of lung tissue caused by the inhalation of dust containing free crystalline silica (SiO2).
A statistical method which looks at the degree to which an observed association between independent and dependent variables is probable, or is attributable to chance. The degree of certainty could be as high as 99 percent. In most epidemiological studies, a 95 percent level is the agreed-upon standard.
Includes the processing of ore through crushing, grinding and milling, and further, to smelting and refining.
The final reject product as a result of processing. It resembles a watery clay and contains little or no ore of value. It is sometimes used for backfill.
Hernberg,S. Introduction to Occupational Epidemiology. Lewis. Chelsea, 1992.
Last,J.M. ed. A Dictionary of Epidemiology. Oxford. New York, 1988.
Olsen,J., Merletti,F., et al. Searching for Causes of Work-Related Diseases: An Introduction to Epidemiology at the Work Site. Oxford. Oxford, 1991.
|ACGIH||American Conference of Government Industrial
|IDSP||Industrial Disease Standards Panel|
|IARC||International Agency of Research into Cancer|
|ICRP||International Commission on Radiological
|MAPAO||Mines Accident Prevention Association|
|MMF||Mining Master File|
|MOL||Ministry of Labour|
|PAH(s)||Polycyclic Aromatic Hydrocarbons|
|SIN||Social Insurance Numbers|
|SMR||Standardized Mortality Ratios|
|TWAE||Time-weighted Average Exposure|
|USWA||United Steelworkers of America|
|WLM||Working Level Month|
1. American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices, Nickel and Inorganic Compounds. In: Draft New or Amended Permissible Concentrations for Selected Substances. Secretariat for Regulation Review, Board of Governors, Workers' Compensation Board of B.C. 1993.
2. American Conference of Governmental Industrial Hygienists. 1992-1993 Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati: acgih, 1992.
3. Agricola, G. De Re Metallica. New York:Dover Publications, 1950.
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by Sir Austin Bradford Hill (be dsc frcp(hon) frs (Professor Emeritus of Medical Statistics, University of London)
Amongst the objects of this newly-founded Section of Occupational Medicine are firstly "to provide a means, not readily afforded elsewhere, whereby physicians and surgeons with a special knowledge of the relationship between sickness and injury and conditions of work may discuss their problems, not only with each other, but also with colleagues in other fields, by holding joint meetings with other Sections of the Society; and, secondly, "to make available information about the physical, chemical and psychological hazards of occupation, and in particular about those that are rare or not easily recognized.
At this first meeting of the Section and before, with however laudable intentions, we set about instructing our colleagues in other fields, it will be proper to consider a problem fundamental to our own. How in the first place do we detect these relationships between sickness, injury and conditions or work? How do we determine what are physical, chemical and psychological hazards of occupation, and in particular those that are rare and not easily recognized?
There are, of course, instances in which we can reasonably answer these questions from the general body of medical knowledge. A particular, and perhaps extreme, physical environment cannot fail to be harmful; a particular chemical is known to be toxic to man and therefore suspect on the factory floor. Sometimes, alternatively, we may be able to consider what might a particular environment do to man, and then see whether such consequences are indeed to be found. But more often than not we have no such guidance, no such means of proceeding; more often than not we are dependent upon our observation and enumeration of defined events for which we then seek antecedents. In other words we see that the event B is associated with the environmental feature A, that, to take a specific example, some form of respiratory illness is associated with a dust in the environment. In what circumstances can we pass from this observed association to a verdict of causation? Upon what basis should we proceed to do so?
I have no wish, nor the skill, to embark upon a philosophical discussion of the meaning of "causation". The "cause" of illness may be immediate and direct, it may be remote and indirect underlying the observed association. But with the aims of occupational and almost synonymously preventive, medicine in mind the decisive question is whether the frequency of the undesirable event B will be influenced by a change in the environmental feature A. How such a change exerts that influence may call for a great deal of research. However, before deducing "causation" and taking action we shall not invariably have to sit around awaiting the results of that research. The whole chain may have to be unravelled or a few links may suffice. It will depend upon circumstances.
Disregarding then any such problem in semantics we have this situation. Our observations reveal an association between two variables, perfectly clear-cut and beyond what we would care to attribute to the play of chance. What aspects of that association should we especially consider before deciding that the most likely interpretation of it is causation?
(1) Strength. First upon my list I would put the strength of the association. To take a very old example, by comparing the occupations of patients with scrotal cancer with the occupations of patients presenting with other diseases. Percival Pott could reach a correct conclusion because of the enormous increase of scrotal cancer in the chimney sweeps. "Even as late as the second decade of the twentieth century", writes Richard Doll (1964), "the morality of chimney sweeps from scrotal cancer was some 200 times that of workers who were not specially exposed to tar or mineral oils and in the eighteenth century the relative difference is likely to have been much greater."
To take a more modern and more general example upon which I have now reflected for over fifteen years, prospective inquires into smoking have shown that the death rate from cancer of the lung in cigarette smokers is nine to ten times the rate in non-smokers and the rate in heavy cigarette smokers is twenty to thirty times as great. On the other hand the death rate from coronary thrombosis in smokers is no more than twice, possibly less, the death rate in nonsmokers. Though there is good evidence to support causation it is surely much easier in this case to think of some features of life that may go hand-in-hand with smoking--features that might conceivably be the real underlying cause or, at the least, an important contributor, whether it be lack of exercise, nature of diet or other factors. But to explain the pronounced excess in cancer of the lung in any other environmental terms requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic "you can't prove it, there may be such a feature."
Certainly in this situation I would reject the argument sometimes advanced that what matters is the absolute difference between the death rates of our various groups and not the ratio of one to other. That depends upon what we want to know. If we want to know how many extra deaths from cancer of the lung will take place through smoking (i.e. presuming causation), then obviously we must use the absolute differences between the death rates--0.07 per 1,000 per year in nonsmoking doctors, 0.57 in those smoking 1-14 cigarettes daily, 1.39 for 15-24 cigarettes daily and 2.27 for 25 or more daily. But it does not follow here, or in more specifically occupational problems that this best measure of the effect upon mortality is also the best measure in relation to aetiology. In this respect the ratios of 8, 20 and 32 to 1 are far more informative. It does not, of course, follow that the differences revealed by ratios are of any practical importance. Maybe they are, maybe they are not; but that is another point altogether.
We may recall John Snow's classic analysis of the opening weeks of the cholera epidemic of 1854 (Snow 1855). The death rate that he recorded in the customers supplied with the grossly polluted water of the Southward and Vauxhall Company was in truth quite low--71 deaths in each 10,000 houses. What stands out vividly is the fact that the small rate is 14 times the figure of 5 deaths per 10,000 houses supplied with the sewage-free water of the rival Lambeth Company.
In this putting emphasis upon the strength of an association we must, nevertheless, look at the obverse of the coin. We must not be too ready to dismiss a cause-and-effect hypothesis merely on the grounds that the observed association appears to be slight. There are many occasions in medicine when this is in truth so. Relatively few persons harbouring the meningococcus fall sick of meningococcal meningitis. Relatively few persons occupationally exposed to rat's urine contract Weil's disease.
(2) Consistency: Next on my list of features to be specially considered I would place the consistency of the observed association. Has it been repeatedly observed by different persons, in different places, circumstances and times?
This requirement may be of special importance for those rare hazards singled out in the Section's terms of reference. With many alert minds at work in industry today many an environmental association may be thrown up. Some of them on the customary tests of statistical significance will appear to be unlikely to be due to chance. Nevertheless whether chance is the explanation or whether a true hazard has been revealed may sometimes be answered only by a repetition of the circumstances and the observations.
Returning to my more general example, the Advisory Committee to the Surgeon-General of the United States Public Health Service found the association of smoking with cancer of the lung in 29 retrospective and 7 prospective inquiries (us Department of Health, Education & Welfare 1964). The lesson here is that broadly the same answer has been reached in quite a wide variety of situations and techniques. In other words we can justifiably infer that the association is not due to some constant error or fallacy that permeates every inquiry. And we have indeed to be on our guard against that.
Take, for instance, an example given by Heady (1958). Patients admitted to hospital for operation for peptic ulcer are questioned about recent domestic anxieties or crises that may have precipitated the acute illness. As controls, patients admitted for operation for a simple hernia are similarly quizzed. But, as Heady points out, the two groups may not be in pari materia. If your wife ran off with the lodger last week you still have to take your perforated ulcer to hospital without delay. But with a hernia you might prefer to stay at home for a while--to mourn (or celebrate) the event. No number of exact repetitions would remove or necessarily reveal that fallacy.
We have, therefore, the somewhat paradoxical position that the different results of a different inquiry certainly cannot be held to refute the original evidence; yet the same results from precisely the same form of iniquity will not invariably greatly strengthen the original evidence. I would myself put a good deal of weight upon similar results reached in quite different ways, e.g. prospectively and retrospectively.
Once again looking at the obverse of the coin there will be occasions when repetition is absent or impossible and yet we should not hesitate to draw conclusions. The experience of the nickel refiners of South Wales is an outstanding example. I quote from the Alfred Watson Memorial Lecture that I gave in 1962 to the Institute of Actuaries:
"The population at risk, workers and pensioners, numbered about one thousand. During the ten years 1929 to 1938, sixteen of them had died from cancer of the lung, eleven of them had died from cancer of the nasal sinuses. At the age specific death rates of England and Wales at that time, one might have anticipated one death from cancer of the lung (to compare with the 16), and a fraction of a death from cancer of the nose (to compare with the 11). In all other bodily sites cancer had appeared on the death certificate 11 times and one would have expected it to do so 10-11 times. There had been 67 deaths from all other causes of mortality and over the ten years' period 72 would have been expected at the national death rates. Finally division of the population at risk in relation to their jobs showed that the excess of cancer of the lung and nose had fallen wholly upon the workers employed in the chemical processes.
More recently my colleague, Dr. Richard Doll, has brought this story a stage further. In the nine years 1948 to 1956 there had been, he found, 48 deaths from cancer of the lung and 13 deaths from cancer of the nose. He assessed the numbers expected at normal rates of mortality as, respectively 10 and 0.1.
In 1923, long before any special hazard had been recognized, certain changes in the refinery took place. No case of cancer of the nose has been observed in any man who first entered the works after that year, and in these men there has been no excess of cancer of the lung. In other words, the excess in both sites is uniquely a feature in men who entered the refinery in, roughly, the first 23 years of the present century.
No causal agent of these neoplasms has been identified. Until recently no animal experimentation had given any clue or any support to this wholly statistical evidence. Yet I wonder if any of us would hesitate to accept it as proof of a grave industrial hazard?" (Hill 1962).
In relation to my present discussion I know of no parallel investigation. We have (or certainly had) to make up our minds on a unique event; and there is no difficulty in doing so.
(3) Specificity: One reason, needless to say, is the specificity of the association, the third characteristic which invariably we must consider. If, as here, the association is limited to specific workers and to particular sites and types of disease and there is no association between the work and other modes of dying, then clearly that is a strong argument in favour of causation.
We must not, however, over-emphasize the importance of the characteristic. Even in my present example there is a cause and effect relationship with two different sites of cancer--the lung and the nose. Milk as a carrier of infection and, in that sense, the cause of disease can produce such a disparate galaxy as scarlet fever, diphtheria, tuberculosis, undulant fever, sore throat, dysentery and typhoid fever. Before the discovery of the underlying factor, the bacterial origin of disease, harm would have been done by pushing too firmly the need for specificity as a necessary feature before convicting the dairy.
Coming to modern times the prospective investigations of smoking and cancer of the lung have been criticized for not showing specificity--in other words the death rate of smokers is higher than the death rate of non-smokers from many causes of death (though in fact the results of Doll & Hill, 1964, do not show that). But here surely one must return to my first characteristic, the strength of the association. If other causes of death are raised 10, 20 or even 50% in smokers whereas cancer of the lung is raised 900-1,000% we have specificity--a specificity in the magnitude of the association.
We must also keep in mind that disease may have more than one cause. It has always been possible to acquire a cancer of the scrotum without sweeping chimneys or taking to mule-spinning in Lancashire. One-to-one relationships are not frequent. Indeed I believe that multi-causation is generally more likely than single causation though possibly if we knew all the answers we might get back to a single factor.
In short, if specificity exists we may be able to draw conclusions without hesitation; if it is not apparent, we are not thereby necessarily left sitting irresolutely on the fence.
(4) Temporality: My fourth characteristic is the temporal relationship of the association--which is the cart and which the horse? This is a question which might be particularly relevant with diseases of slow development. Does a particular diet lead to disease or do the early stages of the disease lead to those peculiar dietetic habits? Does a particular occupation or occupational environment promote infection by the tubercle bacillus or are the men and women who select that kind of work more liable to contract tuberculosis whatever the environment--or, indeed, have they already contracted it? This temporal problem may not arise often but it certainly needs to be remembered, particularly with selective factors at work in industry.
(5) Biological gradient: Fifthly, the association is one which can reveal a biological gradient, or dose-response curve, then we should look most carefully for such evidence. For instance, the fact that the death rate from cancer of the lung rises linearly with the number of cigarettes smoked daily, adds a very great deal to the simpler evidence that cigarette smokers have a higher death rate than non-smokers. That comparison would be weakened, though not necessarily destroyed, if it depended upon, say, a much heavier death rate in light smokers and a lower rate in heavier smokers. We should then need to envisage some much more complex relationship to satisfy the cause-and-effect hypothesis. The clear dose-response curve admits of a simple explanation and obviously puts the case in a clearer light.
The same would clearly be true of an alleged dust hazard in industry. The dustier the environment the greater the incidence of disease we would expect to see. Often the difficulty is to secure some satisfactory quantitative measure of the environment which will permit us to explore this dose-response. But we should invariably seek it.
(6) Plausibility: It will be helpful if the causation we suspect is biologically plausible. But this is a feature I am convinced we cannot demand. What is biologically plausible depends upon the biological knowledge of the day.
To quote again from my Alfred Watson Memorial Lecture (Hill 1962), there was
"...no biological knowledge to support (or to refute) Pott's observation in the 18th century of the excess of cancer in chimney sweeps. It was lack of biological knowledge in the 19th that led a prize essayist writing on the value and the fallacy of statistics to conclude, amongst other "absurd" associations, that "it could be no more ridiculous for the stranger who passed the night in the steerage of an emigrant ship to ascribe the typhus, which he there contracted, to the vermin with which bodies of the sick might be infected". And coming nearer times, in the 20th century there was no biological knowledge to support the evidence against rubella."
In short, the association we observe may be one new to science or medicine and we must not dismiss it too lightheartedly as just too odd. As Sherlock Holmes advised Dr. Watson, "when you have eliminated the impossible, whatever remains, however improbable, must be the truth."
(7) Coherence: On the other hand the cause-and-effect interpretation of our data should not seriously conflict with the generally known facts of the natural history and biology of the disease--in the expression of the Advisory Committee to the Surgeon-General it should have coherence.
Thus in the discussion of lung cancer the Committee finds its association with cigarette smoking coherent with the temporal rise that has taken place in the two variable over the last generation and with the sex difference in mortality--features that might well apply in an occupational problem. The known urban/rural ratio of lung cancer mortality does not detract from coherence, nor the restriction of the effect to the lung.
Personally, I regard as greatly contributing to coherence the histopathological evidence from the bronchial epithelium of smokers and the isolation from cigarette smoke of factors carcinogenic for the skin of laboratory animals. Nevertheless, while such laboratory evidence can enormously strengthen the hypothesis and, indeed, may determine the actual causative agent, the lack of such evidence cannot nullify the epidemiological observations in man. Arsenic can undoubtedly cause cancer of the skin in man but it has never been possible to demonstrate such an effect on any other animal. In a wide field John Snow's epidemiological observations on the conveyance of cholera by the water from the Broad Street pump would have been put almost beyond dispute if Robert Koch had been then around to isolate the vibrio from the baby's nappies, the well itself found the gentleman in delicate health from Brighton. Yet the fact that Koch's work was to be awaited another thirty years did not really weaken the epidemiological case though it made it more difficult to establish against the criticisms of the day - both just and unjust.
(8) Experiment: Occasionally it is possible to appeal to experimental, or semi-experimental evidence. For example, because of an observed association some preventive action is taken. Does it in fact prevent? The dust in the workshop is reduced, lubricating oils are changed, persons stop smoking cigarettes. Is the frequency of the associated events affected? Here the strongest support for the causation hypothesis may be revealed.
(9) Analogy: In some circumstances it would be fair to judge by analogy. With the effects of thalidomide and rubella before us we would surely be ready to accept slighter but similar evidence with another drug or another viral disease in pregnancy.
Here then are nine different viewpoints from all of which we should study association before we cry causation. What I do not believe--and this has been suggested--is that we can usefully lay down some hard-and-fast rules of evidence that must be obeyed before we accept cause and effect. None of my nine viewpoints can bring evidence for or against the cause-and-effect hypothesis and none can be required as a sine qua non. What they can do, with greater or less strength, is to help us to make up our minds on the fundamental question--is there any other way of explaining the set of facts before us, is there any other answer equally, or more, likely than cause and effect?
No formal tests of significance can answer those questions. Such tests can, and should, remind us of the effects that the play of chance can create, and they will instruct us in the likely magnitude of those effects. Beyond that they contribute nothing to the "proof" of our hypothesis.
Nearly forty years ago, amongst the studies of occupational health that I made for the Industrial Health Research Board of the Medical Research Council was one that concerned the workers in the cotton-spinning mills of Lancashire (Hill 1930). The question that I had to answer, by the use of National Health Insurance records of that time, was this: Do the workers in the cardroom of the spinning mill, who tend the machines that clean the raw cotton, have a sickness experience in any way different from that of other operatives in the same mills who are relatively unexposed to the dust and fibre that were features of the cardroom? The answer was an unqualified "Yes". From age 30 to age 60 the cardroom worker suffered over three times as much from respiratory causes of illness whereas from non-respiratory causes their experience was not different from that of the other workers. This pronounced difference with the respiratory causes was derived not from abnormally long periods of sickness but rather from an excessive number of repeated absences from work of the cardroom workers.
All this has rightly passed into the limbo of forgotten things. What interests me today is this: My results were set out for men and women separately and for half a dozen age groups in 36 tables. So there were plenty of sums. Yet I cannot find that anywhere I thought it necessary to use a test of significance. The evidence was so clear-cut, the differences between the groups were mainly so large, the contrast between respiratory and non-respiratory causes of illness so specific, that no formal tests could really contribute to anything of value to the argument. So why use them?
Would we think or act that way today? I rather doubt it. Between the two world wars there was a strong case for emphasizing to the clinician and other research workers the importance of not overlooking the effects of the play of chance upon their data. Perhaps too often generalities were based upon two men and a laboratory dog while the treatment of choice was deduced from a difference between two bedfuls of patients and might easily have no true meaning. It was therefore a useful corrective for statisticians to stress, and to teach the need for, tests of significance merely to serve as guides to caution before drawing a conclusion, before inflating the particular to the general.
I wonder whether the pendulum has not swung too far--not only with the attentive pupils but even with the statisticians themselves. To decline to draw conclusions without standard errors can surely be just as silly? Fortunately, I believe we have not yet gone so far as our friends in the usa where, I am told, some editors of journals will return an article because tests of significance have not been applied. Yet there are innumerable situations in which they are totally unnecessary--because the difference is grotesquely obvious, because it is negligible, or because, whether it be formally significant or not, it is too small to be of any practical importance. What is worse the glitter of the t table diverts attention from the inadequacies of the fare. Only a tithe and an unknown tithe, of the factory personnel volunteer for some procedure or interview, 20% of patients treated in some particular way are lost to sight, 30% of a randomly-drawn sample are never contacted. The sample may, indeed, be akin to that of the man who, according to Swift, "had a mind to sell his house and carried a piece of brick in his pocket, which he showed as a pattern to encourage purchasers'. The writer, the editor and the reader are unmoved. The magic formulae are there.
Of course I exaggerate. Yet too often I suspect we waste a deal of time, we grasp the shadow and lose the substance, we weaken our capacity to interpret data and to take reasonable decisions whatever the value of P. And far too often we deduce "no difference" from "no significant difference". Like fire, the x2 test is an excellent servant and a bad master.
Finally, in passing from association to causation I believe in "real life" we shall have to consider what flows from that decision. On scientific grounds we should do no such thing. The evidence is there to be judged on its merits and the judgement (in that sense) should be utterly independent of what hangs upon it -or who hangs because of it. But in another and more practical sense we may surely ask what is involved in our decision. In occupational medicine our object is usually to take action. If this be operative cause and that be deleterious effect, then we shall wish to intervene to abolish or reduce death or disease.
While that is commendable ambition it almost inevitably leads us to introduce differential standards before we convict. Thus on relatively slight evidence we might decide to restrict the use of a drug for early-morning sickness in pregnant women. If we are wrong in deducing causation from association no great harm will be done. The good lady and the pharmaceutical industry will doubtless survive.
On fair evidence we might take action on what appears to be an occupational hazard, e.g. we might change from a probably carcinogenic oil to a non-carcinogenic oil in a limited environment and without too much injustice if we are wrong. But we should need very strong evidence before we made people burn a fuel in their homes that they do not like or stop smoking the cigarettes and eating the fats and sugar that they do like. In asking for very strong evidence I would, however, repeat emphatically that this does not imply crossing every "t", and swords with every critic, before we act.
All scientific work is incomplete--whether it be observational or experimental. All scientific work is liable to be upset or modified by advancing knowledge. That does not confer upon us a freedom to ignore the knowledge we already have, or to postpone the action that it appears to demand at a given time.
Who knows, asked Robert Browning, but the world may end tonight? True, but on available evidence most of us make ready to commute on the 8.30 next day.
Doll R (1964) In: Medical Surveys and Clinical Trials. Ed. L. J. Witts, 2nd ed. London: p333
Doll R & HILL A B (1964)Brit. med. J., i,1399, 1460
Heady J A (1958) Med. World, Lond. 89, 305
Hill A B (1930) Sickness amongst Operatives in Lancashire Spinning Mills. Industrial Health Research Board Report No. 59. Hmso, London (1962), J. Inst. Actu 88, 178
Snow J (1855) On the Mode of Communication of Cholera, 2nd ed. London (Reprinted 1936, New York)
Us Department of Health, Education & Welfare (1964) Smoking and Health. Public Health Service Publication No. 1103, Washington
Document Number 04-04-08
Policy Primary cancer of the trachea, bronchus or lung is acceptable as an industrial disease under sections 1(1)n and 122 of the Workers' Compensation act as characteristic of gold mining in Ontario.
Guidelines The following sets out categories of persuasive evidence to establish work-relatedness. In assessing entitlement, the decision-maker weighs all the work and non-work factors and determines the individual merits of the case.
|The worker has worked in an
Ontario gold mine.
|Substantiated occupational history.|
|The gold miner has been
diagnosed with primary cancer of
the trachea, bronchus or lung.
|Medical evidence establishing the presence of primary cancer of the trachea, bronchus or lung.|
|A biologically plausible latency
period is present.
|Latency can vary with intensity and type of exposure. Usually
it is biologically plausible that the disease occurs
15 years after first employment in a "dusty occupation"
5 years between first employment in mines with radon
progeny and the diagnosis of the disease.
|The gold miner has worked during
the dustiest years of gold mining.
|Evidence of "dusty gold mining"** experience in Ontario
prior to December 31, 1945.
Evidence of "dusty gold mining" experience in Ontario in
|Sufficient and consistent evidence
of occupational exposure must be
|To satisfy this condition, the gold miner has
1) a chest x-ray rating of 4 or more as rated by the Ontario
WCB chest x-ray classification system and a weighted
dust exposure index of 60 or more. Weighted dust
exposure is the sum of years worked in "dusty gold
mining" in Ontario
pre-1936 x 4
from 1936 to 1944 x 3
from 1945 to 1954 x 2
after 1954 x 1.
2) a chest x-ray rating of 4 or more as rated by the Ontario
WCB chest x-ray classification system and was first
employed in "dusty gold mining" in Ontario before
attaining the age of 30.
3) worked in mines which were dusty and had significant
Note: The duration of mining in such mines which
would constitute sufficient exposure depends on arsenic
levels in the mines. The most current scientific
information is used to assess whether the exposure to
arsenic is sufficient to establish work-relatedness.
4) worked in mines which had significant levels of radon
Note: The policy on lung cancer and uranium mining
(see 04-04-10) and the Ontario Miners Study is consulted
to determine whether the exposure is sufficient to
5) the equivalent of 5 years of "dusty gold mining" and was
first employed in an Ontario gold mine before attaining
30 years of age, if no arsenic or radon exposure is present.
6) the equivalent of 10 years of "dusty gold mining" if no
arsenic or radon exposure is present.
The above guidelines identify persuasive evidence which
would indicate that the conditions for work-relatedness are
met. All decisions are made in accordance with the real
merits and justice of the case, and all available evidence of
work and non-work factors is considered to make a
determination of work-relatedness in each individual case.
|"dusty occupation" and
"Dusty gold mining" is defined by the Ontario wcb
coding system which follows.
Dust Exposure Defined By Occupation Codes (Based on wcb Codes)
|11||Full time in dust exposure - mill|
|12||Full time in dust exposure - other surface|
|13||Full time in dust exposure - shaft sinking|
|14||Full time in dust exposure - other underground|
|15||Full time in dust exposure - surface and
|16||Full time in dust exposure - open pit|
|21||Part time in dust exposure - mill (including mill
in open pit)
|22||Part time in dust exposure - other surface|
|25||Part time in dust exposure - surface and
|26||Part time in dust exposure - open pit|
|97||Dust exposure, specifics unknown|
Workers' Compensation Act
Sections 1(1)n,86p, 122
Board of Directors
#5,August 29, 1991, Page 5471
Long Term Exposures (Industrial Diseases)
Lung Cancer - Gold Dust Exposure
Document Number 04-04-08
Primary cancer of the trachea, bronchus or lung is accepted as an industrial disease under sections 1(1)n and 122 of the Workers' Compensation Act as characteristic of gold mining in Ontario prior to 1945.
In order for a gold miner to qualify for compensation for cancer, a number of conditions must be met. Each condition, and the nature of the evidence required for meeting that condition is stated below.
|The worker must have worked in an Ontario Gold mine.||Substantiated occupational history.|
|The gold miner must have primary cancer of the trachea, bronchus or lung.||Medical evidence establishing the presence of primary cancer of the trachea, bronchus or lung.|
|A biologically plausible latency period must be present.||A minimum of 15 years between first employment in a "dusty occupation" (as defined by the wcb coding system) in an Ontario gold mine and the diagnosis of primary lung cancer of the trachea, bronchus or lung.|
|The gold miner must have worked during the dustiest years of gold mining.||Evidence of "dusty gold mining"* experience in Ontario prior to 1945.|
|Sufficient and consistent evidence of occupational exposure must be present.||To satisfy this condition, the gold miner must meet at least one of the following conditions:|
|1) a chest x-ray rating of 4 or more as rated by the Ontario WCB chest x-ray classification system and have a weighted dust exposure index of 60 or more, where weighted dust exposure is the sum of:
years worked in "dusty gold mining"* in Ontario pre-
1936, multiplied by 4;
years worked in "dusty gold mining" in Ontario from
1936 to 1944, multiplied by 3;
years worked in "dusty gold mining" in Ontario from
1945 to 1954, multiplied by 2;
years worked in "dusty gold mining" in Ontario after
1954, multiplied by 1.
2) a chest x-ray rating of 4 or more as rated by the Ontario
WCB chest x-ray classification system and have been first
employed in "dusty gold mining" in Ontario before
attaining the age of 30 years.
3) over 5 years of "dusty gold mining" experience prior to
1945 and have been first employed in an Ontario gold
mine before attaining the age of 30 years.
|* "Dusty gold mining" is defined by the Ontario WCB coding system.|
Workers' Compensation Act
Sections 1(1)n, 86p, 122
#3, January 8, 1988, Page 5216
Long Term Exposures (Industrial Diseases)
Lung Cancer - Radon and Radon Progeny Exposure
Document Number 04-04-10
Primary lung cancer caused by exposure to radon gas and radon progeny in industry is accepted as an industrial disease under Schedule 3, item 9 for the purposes of section 122 of the Act.
Radon gas is one of the natural substances produced as a result of the radioactive decay of uranium.
Radon progeny are natural radioactive substances produced by the radioactive decay of radon gas.
The following factors are considered in lung cancer claims where the latency period is at least 10 years:
Claims which fail to meet these criteria are considered on their own merits, having regard for all factors
Workers' Compensation Act
#14, August 14, 1979, Page 4806
A Literature Review and Discussion Paper
1. Background: Context of the Review
2. Epidemiological Evidence Regarding Lung Cancer Risks and Underground Mining
2.1 Radon and Radon Progeny
2.2 Arsenic and Gold Mining
2.3 Silica and Silicosis
2.4 Diesel Emissions
2.5 Nickel Mining
3. Exposures to Carcinogens in Ontario Mines
1. Context of this Discussion Paper
The last decade has seen a proliferation of reports linking a wide variety of exposures in the mining industry to an increased incidence of lung cancer. The Ontario Workers' Compensation Board (wcb) has historically played a leading role in recognizing such associations; adjudicative guidelines have been developed over the years with respect to uranium mining, gold mining and nickel mining. An extensive database has been developed that allows for ongoing studies of the mining industry (Muller, 1983,1989; Kusiak, 1991, 1991b and others.) The wcb has continued to refine understanding on these issues and alter guidelines accordingly (cf. Idsp, 1989).
Workers' compensation boards are entrusted with the responsibility of providing compensation for injuries or illnesses that arise out of employment. The goal of workers' compensation is to provide compensation in all cases in which the workplace caused or contributed to the outcome; cases that do not arise out of the workplace are left to be compensated from other programs, private insurance, etc.
The scientific literature illustrates that there is likely some marginal increase in risk of cancer even at very low levels of exposure to carcinogens, with the general consensus now being that there is no "safe" level of exposure. Moreover, the latency period between commencement of exposure and diagnosis of cancer may be widely variable depending on a large variety of factors including dose, dose rate, age, concomitant exposures, etc. The general purpose of guidelines is to define the criteria delineating the conditions wherein it becomes more probable than not that any one cancer is due to workplace exposure. In principle, that point is reached when the excess risk is double the normal background risk. It is important to appreciate, however, that while the question of whether a particular cancer stems from the workplace is scientific in character, often the answer cannot yet be derived from science. At best, epidemiology can indicate that an excess exists in a certain workforce with specific exposures and time frame; epidemiology cannot indicate which cancers are the "occupational" cases versus those which are "non-occupational". The ideal epidemiological study is one conducted on workers in the actual setting in question, with a sizeable group of subjects, with known and measured exposures, matched against a valid control group, and then followed long enough to detect all cancers occurring in both groups. The results for the cohort as a whole as well as its sub-cohorts with varying ages, years and duration of exposure, have to satisfy standard tests of statistical significance, and must have had adequate power to do so. Some of the studies conducted on Ontario miners come close to approximating this scenario. Yet limitations still exist. Before accepting an exposure situation as truly increasing the risk of a given outcome, scientists prefer to answer that we do not have enough data to make this connection. However, the claimant, and/or his or her surviving spouse, do not have the luxury of awaiting more studies.
It is in this context that this review is being undertaken. The intent is not to reanalyse raw data collected by the highly competent epidemiologists in Ontario who have studied this matter extensively. Rather it is to provide an independent perspective on the findings in these Ontario-based epidemiological studies in the context of world literature. The perspective is one of assessing the adequacy of data with respect to policy setting in workers' compensation in this area. As such, this report is entirely a secondary review of the literature. While attempting to be broad in scope, discussing many carcinogens likely to be found in many Ontario hardrock mines, it does not pretend to be an exhaustive review in these areas. It is noteworthy that several of the substances to be discussed in this report have already been subject to full Industrial Disease Standards Panel reviews.
2. Epidemiological Evidence Regarding Lung Cancer Risk and Underground Miners
Lung cancer among underground miners has been known for centuries. A high incidence of fatal pulmonary disease among miners in the Erzebirge Mountains was documented as early as the 1500s by Agricola. In the late 19th century it had been determined that these miners had developed respiratory malignancy, and in 1913, it was documented that this was indeed primary lung cancer. In 1929, underground miners in Joachimsthal were also shown to have a similar lung cancer problem. During the late 1940s and into the 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). Since then, many other groups of underground miners have been documented to have increased risk of lung cancer. This is generally thought to be related to the radon contamination in the mines. The role of other carcinogenic exposures in mines, however, is also being actively explored.
Archer (1988) summarized the results of 14 cohort and 7 case control studies regarding lung cancer risks of underground miners. Several interesting generalizations were drawn from this review. First, Archer noted that the longer the follow-up the greater the attributable risk (even though relative risk remains relatively constant). Secondly, he noted that the induction-latent period is quite variable, but is shortened by high exposure rate, cigarette smoking and increased age at the start of mining. Thirdly, and most importantly, he observed that lung cancer cases which would have been considered non-compensable a decade ago, would now be generally accepted to be compensable, or, at least, related to workplace exposures.
Three factors were specifically noted in this regard. First, with respect to cell type, Archer (1988) correctly observed that earlier studies (eg. Saccomanno, 1964) found a predominance of small cell undifferentiated cancers, leading to the conclusion that small cell cancer was characteristic of radiation-induced lung cancer. He noted that the frequency of small cell lung cancers among uranium miners declined sharply from about 60% in 1960 to 20% in 1980, with epidermal types correspondingly increasing in percentage during this time period. This shift was readily apparent when the data were analyzed by age or by time after start of mining (Saccomanno et al., 1982, as cited by Archer, 1988). This proved to be simply an artifact of the fact that radiation induced several types of cancer with the small cell type simply being the one that appeared first.
The second area of earlier misleading data discussed by Archer (1988) was regarding smoking. In the earlier studies, the vast majority of lung cancer cases identified in uranium miners also occurred in cigarette smokers. This was erroneously interpreted by some to mean that smoking was much more important than radiation in causing lung cancer among miners, with one scientist even declaring that if uranium miners would not smoke they would not get lung cancer. This too has been subsequently re-analyzed and found to be related to age. Archer noted that if data are collected on men mostly 35-65 years of age, a high proportion of the lung cancer will be among smokers, and the radon-smoking relationship will appear to be more multiplicative. He noted that data collected on miners from 60-70 years of age will find roughly equal lung cancer rates amongst smokers and non-smokers, whereas if lung cancer rates are collected mainly on men 65-85 years of age, lung cancer will appear predominantly among the non-smokers, and one might conclude that smoking is protective. If one collected data over the full life span, the smoking and radiation effects would appear to be little more than additive. He cited several studies to support this hypothesis (Sevc et al., 1987; Bradford et al., 1984; Edling, 1982).
The third observation of considerable interest offered by Archer (1988) was that the lung cancer risk per working level month (WLM) is now thought to be greater than it was in earlier reports (eg. Hornung and Meinhardt, 1987). He noted the Swedish studies, for example Radford and Reynard (1984), notable for its long follow-up and low average exposure, indicated a higher lung cancer risk per WLM than studies with shorter follow-up periods. He attributed the differences in lung cancer risk per WLM as relating to errors in estimation of average worker exposure, differences in length of follow-up and variations in cigarette smoking (noting that smoking was much less prevalent among Swedish miners than among US miners, yet the lung cancer risk per WLM found amongst Swedish miners had been consistently higher than among US miners). He also commented on the supralinearity that has been observed with respect to the exposure-response curve. He noted that this might be an artifact resulting from misclassification of the exposure of some miners, although noting that this explanation cannot apply to animal studies. The other more accepted explanation is that this may be an expression of the lower dose rate received by the men with low WLM. Lower dose rate is thought to be associated with increased risk per WLM. Thus supralinearity may be of considerable significance for individuals who receive low levels of exposure to radon, such as in those non-uranium mines where the radon levels are not thought to be very high, or radon exposure in homes. The theme of Archer's critique, namely that as research advances, it becomes increasingly apparent that occupational risks were greater than previously thought, constitutes the primary theme of this report as well.
Another recent report which has stirred the interest in lung cancer as a risk associated with hardrock mining generally, is that by Burns and Swanson (1991). This was an occupational lung cancer incidence surveillance study by usual occupational and industry in the Detroit Metropolitan area. 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). Mine machine operators were found to be at particularly high risk (OR=5.01). The strengths and limitations of this type of study are well known. By way of strengths, however, it should be noted that this type of study provides more accurate assessment of occupational lung cancer risks than many other types of studies in that it utilizes complete life-time employment histories and cigarette smoking habits to investigate the association between lung cancer and work. The explanation for the increased lung cancer risk found in mining and related occupations that was advanced by the authors was that this was probably due to exposure to diesel exhaust. This relationship is discussed further below as are the other carcinogens potentially responsible for the increase in lung cancer in hardrock miners. Thus the second theme of this report is that the increased lung cancer risk experienced by miners may be more generalized, attributable to etiological agents only now beginning to be explored, or to a combination of factors still poorly understood.
2.1 Lung Cancer and Radon Progeny
The Industrial Disease Standards Panel has extensively studied the relationship between uranium mining and lung cancer. In 1989, based on a thorough evaluation of existing literature, the Panel recommended that any uranium miner with a diagnosis of primary cancer of the trachea, bronchus and lung for which the latency period was at least 10 years, and who has a cumulative exposure of at least 40 WLM, receive workers compensation benefits. Acknowledging the magnitude of uncertainty in WLM estimates, the Panel formulated a second eligibility role wherein an individual whose cumulative WLM exposure was between 20 and 40 WLMs is compensated if the total WLM exposure in the time period 10-14 years prior to diagnosis of the primary cancer is at least 20 WLM, or total WLM exposure in the time period 10-14 years prior to diagnosis of the primary cancer plus 0.5 (or 50%) of the WLM exposure in the time period 15 or more years prior to the diagnosis of the primary cancer is at least 20 WLM. They concluded that the 5-9 years prior to diagnosis was not significant in the risk of producing lung cancer. They recommended that in adjudicating claims on a case-by-case basis additional factors such as possible exposure to other radiation types or other unidentified carcinogenic substances be taken into consideration, noting the possible roles of silica, radon exposure in non-uranium mines, arsenic and diesel emissions as possible agents in the production of lung cancer.
In reaching their decision the panel reviewed the epidemiological studies of miners exposed to radon both in uranium mines as well as in non-uranium mines. They noted that a causal relationship between lung cancer and exposure to radon is uncontested, but that disagreement exists on aspects of radon carcinogenesis.
Since publication of the IDSP report of 1989 several follow-up studies have been completed, most importantly, the study of lung cancer in Ontario gold miners by Kusiak et al.,(1991) and the study of lung cancer mortality in Ontario uranium miners (Kusiak, et al., 1991b). A discussion of Kusiak and colleagues gold mining study is deferred to the next section. Kusiak's most recent draft report on uranium mining will be discussed further below.
It is important to recognize, however, that the risk of lung cancer associated with exposure to radon decay products has been investigated in approximately 20 different populations of underground miners, as again recently summarized by Samet (1991). Table 1, reproduced from Archer (1988), outlines 11 of the most important cohort studies. The various exposure-response models utilized by BEIR IV and other agencies were discussed by Samet (1991). As shown in Table 2, for a 30 year exposure (the likely maximum duration of time spent underground) each risk model projects a substantial increment of lung cancer risk at 4 WLM, and even at 1 WLM annually, or 30 WLM total. The lifetime risk of 8.4% for lung cancer represents a 25% increment over the baseline risk; at 4 WLM for 30 years, lifetime lung cancer risk is nearly doubled. As this level has been the allowable level for many years, this suggests that exposure in mines that met legal requirements was still associated with a substantial increase in lifetime risk of lung cancer.
In the most recent report from the historical prospective cohort mortality study of Ontario uranium miners (Kusiak et al., 1991b), it was found that an excess of lung cancer mortality existed in all uranium miners (SMR=169) as well as the sub-group of uranium miners who did not work in gold mines in Ontario (SMR=139), those who did work in cold mines before 1946 (SMR=224), uranium miners who began working in gold mines between 1946 and 1957 (SMR=188), and in uranium miners who began gold mining after 1959 (SMR=210). Thus, it was again found that the excess of lung cancer in uranium miners who mined gold was larger than the excess among other uranium miners and that this excess was larger than would be expected from their exposure to radon decay products alone. An excess of lung cancer among uranium miners who first mined nickel-copper after 1934 (SMR=145) was also found, an excess approximately similar to uranium miners who did not work in gold or nickel-copper mines.
Kusiak and colleagues (1991b) noted that in uranium miners who did not mine gold, the largest increase in the risk of developing lung cancer occurred 5-9 years after exposure to radon decay products began and declined as the time interval since first exposure to radon decay products increased. (Thus the time period that the IDSP  guidelines designated as irrelevant, proves now to be actually associated with greater risk.) In uranium miners who also mined gold, however, the excess of lung cancer mortality peaked 20-25 years after first exposure to radon decay products in Ontario uranium mines, according to their data. (One would have expected the reverse, as exposure to two carcinogens, namely radon decay products and gold mining, would have been expected to decrease the latency period, rather than increase it, as these data seem to imply.)
The authors noted that the relative excess of lung cancer mortality from a given amount of exposure to radon decay products may be higher in younger miners than in older miners. The investigators noted that in uranium miners who accumulated less than 40 WLM of exposure to radon decay products lagged 15 years, the relative excess of lung cancer mortality increased in proportion to the index of exposure to arsenic. They specifically noted that each year of employment in a mine containing 0.1% arsenic was associated with a 2.5% increase in lung cancer mortality rates. In contrast, in uranium miners who accumulated more than 40 WLM of exposure but incurred low levels of exposure to arsenic, each year of employment in mines containing 0.1% arsenic was associated with a 24.4% increase in lung cancer mortality rates 15 and more years after the exposure to arsenic occurred. This indicates that a considerably complex interaction seems to be occurring. The investigators also noted that while the lag interval of 15 years provided the best fit with the data, the approximate 95% confidence interval for the lag interval was 5-25 years.
The authors discuss the results of fitting various models. Comparing the deviances of two of their models, they conclude that the age-specific, time-since-exposure model that had recently been developed (BEIR IV) may fit better to the relative excess of lung cancer mortality than the five year lag model. (The fact that arguments can be made for different models highlights another source of uncertainty in these data, as discussed further below.)
The previous report presented by these authors (Muller et al., 1989) about lung cancer mortality in Ontario uranium miners who did not mine gold, found an association between the relative excess of lung cancer mortality and the amount of exposure to radon decay products received 10-14 years earlier but not more recently. This earlier report also failed to detect an association between the excess of lung cancer mortality and attained age. In the more recent report (Kusiak et al., 1991b), more lung cancer deaths were observed at older ages and at longer times after the exposures occurred, as well as in more recent years. Also, while no excess of lung cancer mortality had yet been detected between the ages of 65 and 74 years in Ontario uranium miners who did not mine gold, an association between lung cancer mortality and exposure to radon decay products 15 or more years earlier was now able to be detected in these miners. The relative excess of lung cancer mortality from the more recent exposures to radon decay products appeared to be larger than the risk of earlier exposures, but the differences did not reach statistical significance. Thus, not only are the weights which were applied by the IDSP to the "years since exposure" now known to be erroneous, but they can not be reliably replaced with new weights.
Kusiak et al.,(1991b) also investigated the relationship of cigarette smoking with these exposures, as well as pathological type. As consistent with other studies, they found that the association between the relative excess of lung cancer mortality and exposures to arsenic and radon decay products is not attributable to smoking. With respect to histology they noted that their data showed an association between the proportion of small cell cancers in uranium miners and the amount of exposure to radon decay products at a time interval 5-14 years before death. They felt that this explained the excess of lung cancer mortality which occurred shortly after exposure to radon decay products being larger than the excess of lung cancer mortality which occurred long after the exposure occurred.
The authors also noted that many miners in Ontario worked in nickel-copper bearing ores and that some or these nickel-copper mines contained up to 0.07% arsenic in the rock while other nickel-copper mines likely contained less than 0.001% arsenic in the rock. The levels of radon decay products in some of the nickel-copper mines ranged between 0.001 WLs and 0.2 WLs in active areas and up to 0.78 WLs in inactive areas. They felt that the recently noted excess of lung cancer among nickel-copper miners in Ontario (eg. Roberts et al., 1989) who began mining nickel-copper before the mid 1930s may be due to the combined exposure to arsenic and radon decay products in the nickel-copper mines. This is discussed further in Section 2.4 below, as it is noteworthy that Kusiak and colleagues felt that lung cancer mortality rates in Ontario uranium miners may also be increased because of the exposures some uranium miners received in the nickel-copper mines.
Although the most recent report by Kusiak et al.,(1991b) goes a long way in advancing understanding on the broad nature of the factors and conditions associated with increased lung cancer risk in Ontario miners, several short-comings of the report are noteworthy. With respect to definition of cohort, inclusion of all miners who had worked at least 2 weeks in a uranium mine would be expected to decrease the risk experienced by the total cohort. The fact that the total cohort still had a statistically significant increased risk of lung cancer, despite the dilution effect of including workers with very short exposure times, is noteworthy. It is also noteworthy that in the definition of the cohort, miners who had worked in uranium mills were excluded as were miners who worked in asbestos mines or uranium mines outside of Ontario. These exclusions were based on the lack of data regarding these exposures. However, by excluding these groups, the cohort may be depleted of its most highly at-risk populations. Again, the inclusion of workers with very short durations of exposures and elimination of groups of miners who may in fact have been at highest risk, served to underline the importance of the positive findings. (One would wonder how cases of lung cancer that occur in miners in these excluded groups would be adjudicated. Presumably, the assumption would be that all cancers that occur in these groups would be compensable as their exclusion was on the basis of confounding carcinogenic exposures. In fact, it is unclear how these cases are actually adjudicated.)
With respect to exposure to radon decay products, it is noted that even during periods after 1958-1960, when levels of radon decay products in the mines began to be measured, each miner's yearly exposure to radon decay products was determined from the average levels of radon decay products in the mines where he was employed rather than the actual levels of exposures. Inaccuracies in exposure estimation would also tend to underestimate risks, such that the positive results found are likely underestimates of the true relative risks. This also applies to inaccuracies in smoking habits due to the fact that miners smoking habits were only recorded beginning in 1976.
Another source of error leading to the risks reported being underestimates of true risks relates to the errors in the ascertainment of mortality. It is estimated that roughly 6% of deaths were not found. In addition, the validation exercise carried out at the Ontario Cancer Registry (IDSP, 1989) suggested that cancer risk estimates based on the Ontario population may have been approximately 4% too high in relation to the observed deaths among uranium miners. Together these observations suggest that lung cancer mortality risks may have been underestimated by roughly 10%.
It is noteworthy that these limitations led to a dissenting opinion in the IDSP 1989 report. The minority report indicated that the inaccuracies in exposure estimations were not properly addressed in the establishment of the eligibility rules, and that an individual miner's exposure in reality would be much higher if he had worked on a specific job. They felt that radon exposure incurred in service and mill workers should be recognized, and they highlighted the uncertainty in individual measurements before 1960 being approximately one order of magnitude (which would mean that an average WLM exposure of 15 WLM could be as high as 150 WLM).
The minority report also noted that the latency requirement referred only to latency with respect to uranium mining, noting that the period of actual radon exposure, or exposure to other potential carcinogens such as arsenic, silica etc., is not properly taken into consideration in the latency requirement either of the gold mining eligibility rule or the uranium mining rule. They felt that it is essential that eligibility rules, if applied, consider all potentially carcinogenic exposures.
The minority report concludes that compensation should not be limited to only those miners who fall within the statistical excess identified by latency and average WLM exposure, especially given the huge inaccuracies in individual exposure extrapolations from average mining readings and the failure to recognize latency before entering uranium mining. This recommendation will be discussed further in the conclusion of this report, in the context of the research results that have become available since the report was written.
2.2 Arsenic, Gold Mining and Lung Cancer
It is now well known that arsenic is capable of causing cancer (cf. IARC, 1980) Exposure to arsenic has been thought to be the cause of increased lung cancer mortality in gold miners in France; in China, the increased incidence of lung cancer in tin miners in Hunan Province is thought to be due to radon decay products and arsenic (Taylor et al., 1989). An excess of lung cancer also exists among gold miners in Western Australia, where the arsenic concentrations in the rocks mined have an average concentration of less than 0.005% and levels of radon decay products are at most 0.045 WL (Armstrong et al., 1979).
In an earlier report of Muller et al.,(1986), it was suggested that exposure to arsenic in the gold mines of Ontario was associated with the excess of mortality from lung cancer, but, as noted by Kusiak et al.,(1991) at that time little was known about exposure of the miners to radon decay products. In fact, several carcinogens have, at various times, been suggested as the cause of the increase in lung cancer in Ontario gold miners, including radon decay products (BEIR IV, 1988) and silica (Goldsmith and Guidotti, 1982) as well as arsenic. A recent study of South African gold miners suggested that silica is the causative agent (Hnizdo and Sluis-Cremer, 1991), as discussed in Section 2.3 below.
Kusiak et al.,(1991) recently published an update of the mortality study on a cohort of 54,128 Ontario miners for mortality between 1955 and 1986. These miners worked in nickel, gold or uranium mines; some also worked in silver, iron, lead/zinc, or other ore mines. Kusiak and colleagues found an excess of lung cancer among the 13,603 Ontario gold miners (SMR=129; 95% CI: 115-145) even when excluding mortality after a worker had started to mine uranium. Kusiak and colleagues provide an extensive review of exposures, exploring various etiological factors. These are discussed further in Section 3 below.
Lung cancer mortality among gold miners who had not mined nickel before 1936 were grouped according to degree of exposure to radon decay products in gold mines, lagged by 5 years. Indices of exposure to arsenic before 1945 and after 1945 each lagged by 20 years, and duration of employment in mines containing mineral fiber lagged by 20 years, were also derived to allow the investigators to calculate deaths from lung cancer in each category. They noted that although a statistically significant association between exposure to arsenic before 1946 and lung cancer mortality was found for each lag interval (15, 20, 25 and 30 years), the best fit was found for a lag interval of 20 years. In exploring the various categories, they concluded that lung cancer was increased in Ontario miners who began gold mining before the end of 1945 or nickel before the end of 1936. They were not able to confirm an excess of lung cancer in miners who began mining gold after 1945 or nickel after 1936 using their models. They felt that the increase in lung cancer in gold miners was probably due to exposure to arsenic and radon decay products.
It is noteworthy, however, that no measurements of the level of radon decay products were available for Ontario gold mines before 1961. The investigators noted that there was also considerable variability in arsenic concentration among mines, with larger mines tending to have larger concentrations but some mines being more arsenic enriched than others. They noted, for example, that the Red Lake Camp was well known for its high concentration of arsenic, whereas the Timmins and Kirkland Lake Camps contained less arsenic. With respect to silica exposure, a 1978 survey of the amount of airborne respirable dust and silica was used to estimate the percentage of free silica in airborne dust at several major gold mines. Thus, as with the vast majority of historical perspective studies, exposure indices for all potential etiological factors were essentially best-guess estimates for a major part of the study.
It should also be noted that by counting person-years at risk from the year of entry to the study up to the year where the miner began uranium mining in Ontario (or the year of death, or the end of the period of observation for mortality, whichever occurred first), would tend to falsely lower the result in gold miners who began mining uranium then died from their experience in gold mining. Also, the study found that over the age of 75 mortality from all causes combined was much lower than expected, suggesting a short-fall in ascertainment. The authors note that this was probably due to deaths outside Canada which are not always recorded in the Canadian Mortality Database.
The study noted no increase in lung cancer mortality in miners who began mining gold after 1945 and never mined nickel (SMR=95, 95% CI: 77-116), and no significant increase in lung cancer mortality was detected in miners who began nickel mining after 1935 and did not mine gold (SMR=101, 95% CI: 88-105). The death rate from lung cancer in miners who mined ore other than gold and nickel was not increased (SMR=97, 95% CI: 74-127). If mortality occurred in miners who began to work in a uranium mine are excluded and they are therefore assumed to be alive at the end of their follow-up period, this would artificially lower the risk for gold miners.
It was interesting that hospital records indicated 3 cases of mesothelioma among the miners, two of which occurring in men who had worked in the gold mines. While neither gold miner was known to be exposed to the rocks that sometimes contain fibrous amphiboles (asbestos), it would be difficult to explain these cases otherwise. Many of these issues are discussed further below.
2.3 Lung Cancer, Silica and Silicosis
In an editorial in the British Journal of Industrial Medicine (McDonald, 1989) it was noted that until recently epidemiologists had not given much thought to the possibility that exposure to silica may be linked with lung cancer. Indeed, McDonald noted, the World Health Organization (WHO) report of 1986 did not mention cancer. However, at that time evidence was beginning to suggest that indeed a link may exist. Goldsmith et al.,(1982), for example, had hypothesized that silica may be a carcinogen or co-carcinogen or that silicosis increased the risk of lung cancer. The International Agency for Research on Cancer (IARC, 1987), evaluating the literature at that time, stated that there was sufficient animal evidence for an association between silica and cancer, and there was "limited" human evidence for an association.
Several large cohorts of mining and quarry workers showed moderately raised SMRs for lung cancer, ranging from 127 to 156 (cf. McDonald, 1989). This included a mortality study in gold and coal miners in Western Australia (Armstrong et al., 1979), and the Ontario Miners Study of Muller et al.,(1983). However, as McDonald noted (McDonald, 1989), several large studies had produced negative conclusions (McDonald et al., 1978; Brown et al., 1986 as cited by McDonald, 1989). There have been several cohort studies of men with silicosis, all of which with SMRs for lung cancer substantially raised, by some 2-4 fold (Finkelstein et al., 1982, 1986; and Kurppa et al., 1986 Westerholm et al., 1986 and Zambon et al., 1986 (as cited by McDonald, 1989)). As McDonald (1989) noted, however, apart from the study of Zambon and colleagues, no account was taken of smoking habits and in none was consideration given to the possibility of other exposures. He therefore concluded that the increased lung cancer that occurred in underground miners may not be due to silica exposure but to exposure to radon daughters or other underground carcinogens.
Shortcomings of previous studies of lung cancer mortality in silicotics were addressed by a recent study of Amandus and Costello (1991) who studied lung cancer mortality during 1959-1975 in a cohort of silicotic metal miners who were diagnosed for silicosis in 1959-1961. Their study employed an internal reference group of non-silicotics, had chest x-rays for both silicotics and non-silicotics classified according to a standardized method, and individual data on cigarette smoking and exposure to radon and diesel were available. Their results indicated a slightly increased SMR in non-silicotics (1.15) who had worked in excess of 20 years in an underground metal mine and in silicotics (14.03) and non-silicotics (2.66) who had been employed at a mercury mine. After excluding mercury miners, SMRs were similar in silicotics (1.39) and non-silicotics (1.14). The increase in lung cancer mortality was observed regardless of cigarette smoking, years spent in underground jobs at a metal mine, and low radon exposure. The authors did note that the power of their study to detect an association in most sub-groups was low, suggesting the need for further follow-up. They noted that even if all silicotics had smoked cigarettes and all non-silicotics had never smoked, confounding from smoking would account for less than a 30% increase in cancer risk thus would not explain age-adjusted rate ratios of more than 1.3 which they found. They also felt that confounding carcinogenic metals or carcinogens that contaminate some metal ores, (eg. arsenic) was an unlikely explanation for the higher lung cancer mortality in silicotics. They excluded all coal mines from their study as diesel equipment had been used underground, which they felt posed a significant risk. They felt that their classifications of mines with respect to radon exposure was fairly accurate and they concluded that their results suggested that silica was indeed carcinogenic, as compatible with positive results in animals (IARC, 1987).
Amandus et al.,(1991) also studied silicosis and lung cancer in North Carolina dusty trades workers and found that age-adjusted lung cancer rates in silicotics who had no exposure to other known occupational carcinogens was 2.4 (95% CI: 1.5-3.9) times higher than in the reference group of non-silicotic metal miners. Age and smoking adjusted rates in silicotics were 3.9 (95% CI: 2.4-6.4) times higher than that in non-silicotic metal miners. They also concluded that their analysis effectively controlled confounding by age, cigarette smoking, and exposure to other non-occupational carcinogens, and that it was unlikely that other correlates of silica exposure could explain the excess of lung cancer mortality in the silicotics. A table of other studies showing increased lung cancer rates in silicotics was also produced, as shown in Table 3.
Of considerable importance is the recent study by Hnizto and Sluis-Cremer (1991) in which no association between lung cancer and silicosis of the parenchyma or pleura was found, but an association was found between silicosis of the hilar glands and lung cancer. Their results showed a significant dose-response relationship between death from lung cancer and silica dust particle-years and cigarette pack-years. The relative risk for lung cancer associated with the exposure to 1000 particle-years of silica dust standardized for smoking, year of birth, and age, was 1.03 (95% CI: 1.016-1.04). Thus the expected relative risk for the men in the highest exposure category with an average of exposure above 50,000 particle-years, relative to those with less than 15,000 but with more than 10 years of gold mining, was calculated to be 3.18 (95% CI: 1.34-7.45). Their data suggested a multiplicative model indicating synergy between dust and smoking for those with more than 35 pack-years of smoking and more than 30,000 particle-years of dust. They note that this was consistent with the findings of Goldsmith and Guidotti (1986).
The hypotheses advanced to explain the excess of lung cancer in silica exposed workers include the following:
1) Silica directly causes lung cancer; 2) Silica causes silicosis, which may be an intermediate state leading to lung cancer; and 3) silica combines with polycyclic aromatic hydrocarbons from cigarette smoke and other occupational exposures thus increasing the effective dose of carcinogens in the lung (Goldsmith and Guidotti, 1986; Hnizdo and Sluis-Cremer, 1991; and others). Guidotti et al.,(1986) also advanced the theory that silica may cause lymphatic obstruction, reduce clearance of lymphatic dust and thus increase residence time of active carcinogens. Archer et al., (1986) noted that silicosis among a group of miners usually reflects the presence of both a silicatious type of ore and poor ventilation, the latter also being associated with raised radon progeny concentrations which may in turn be responsible for the increased lung cancer mortality in miners.
Hnizdo and Sluis-Cremer (1991) do not support the hypothesis that silicosis is an intermediate state leading to lung cancer. As the intensity of exposure to dust was related to lung cancer, and not the actual duration of the underground exposure, they feel that the hypothesis that silica directly induces lung cancer cannot be rejected. However, they acknowledge that the increased intensity of dust exposure may be related to increased concentrations of radon progeny.
Thus it seems that silica exposure is associated with an increased risk of lung cancer. Whether this is due to the carcinogenicity of silica itself, silica acting as a co-factor or promotor, or merely silica exposure being a surrogate measure for some other or combination of other underground carcinogens, remains unanswered.
2.4 Lung Cancer and Diesel Emissions
Diesel exhaust is known to contain large quantities of carbonaceous particulates to which polycyclic aromatic hydrocarbons (PAH) are absorbed. Many of these PAHs are known to be mutagenic as well as carcinogenic both in animals and in humans (IARC, 1973). Evidence regarding the carcinogenic effect of diesel exhaust exposure per se has been accumulating rapidly over the last decade. These studies have been reviewed by several individuals and institutions (eg. Steeland, 1986; Fraser, 1986). As noted in the various critical reviews of this subject, quantitative assessment of exposure is a major problem in epidemiological studies on diesel exhaust. Many studies have simply compared workers in certain job categories presumed to be exposed to diesel fumes, to some presumably non exposed population. Even when diesel fumes have been measured, there is no standard method for such measurements, and there is even uncertainty as to the specific substances to measure when assessing occupational exposure. Thus results of the occupational-based studies have been conflicting and inconclusive. Moreover, negative studies often had insufficient power to detect any association, had insufficient latency periods, or compared incidence or mortality rates among workers to national rates only, resulting in possible biases caused by the healthy worker effect (cf. Boffetta et al., 1988). Also, positive studies often did not control for smoking or other occupational exposures.
Boffetta et al.,(1988) reported the interim results of a long-term prospective mortality study, in which death rates were determined for subjects in target occupations including diesel exposed subjects, controlling for smoking and other possibly confounding variables. Their results supported previously published occupationally-based studies linking diesel exhaust exposure to increased risk of lung cancer. Specifically, railroad workers, heavy equipment operators, miners, and truck drivers were found to have had a higher mortality from lung cancer when compared with subjects with no exposure to diesel exhaust. A dose-response effect was present for lung cancer mortality.
With respect to the animal evidence of carcinogenicity, as reviewed by Steenland (1986), while data from animals exposed to diesel exhaust via inhalation have yielded differing results, it appears that positive results will be obtained if rodents are exposed to high enough levels for long enough periods.
The introduction of diesel engines into metal mines dates from the early to mid-1960s. Although virtually all metal mines use diesel equipment, it is difficult to estimate how many miners are actually exposed to diesel fumes. Furthermore, the still relatively short latency period limits the usefulness of studying a cohort of metal miners to assess the effects of diesel exhaust. More extensive work has been done regarding truck drivers, bus company employees, railroad workers and heavy equipment operators, as summarized in the review articles cited above. There have also been several case-control studies of lung cancer, also described in the above review articles. As summarized by Fraser (1986), the evidence for the existence of excess lung cancer risk with exposure to diesel engine emissions includes the following findings:
1. carcinogenicity of diesel extracts to small animals;
2. the existence of sufficient evidence for carcinogenicity of soots, tars and oils in humans;
3. the consistent lung cancer excess in transport and transport-related occupations in geographically distant locations such as Singapore, the United Kingdom and the United States;
4. lung cancer excess found in occupational analyses in transportation operatives and other diesel related occupations which persist after controlling for smoking;
5. the excess lung cancer risk detected in studies of US vehicle workers;
6. the excess lung cancer risk found in studies of railroad workers, with a significantly increased excess in one study which remains after controlling for cigarette smoking;
7. the consistently detected increase in non-smoking lung cancer patients for employment in diesel-related occupations.
As all authors generally agree, the relative risk, when detected, is usually smaller than 1.5 and a long exposure period and/or a long latent period are required for it to become evident. However, the risk has been shown to increase with years of employment, to exhibit a dose-response relationship and to be unrelated to smoking and asbestos exposure. As such, it is highly likely that exposure to diesel exhaust increases risk of lung cancer.
2.5 Lung Cancer and Nickel Mining
The carcinogenicity of various nickel species has been known for decades and has been the subject of many reviews. Based on early epidemiological investigations and a host of animal experiments, the National Institute for Occupational Safety and Health (NIOSH) concluded that inhaled nickel was carcinogenic. While the majority of the animal data suggested that nickel subsulphide was the culprit, NIOSH concluded in its 1977 criteria document on nickel (NIOSH, 1977) that "in the absence of evidence to the contrary, nickel metal and all inorganic nickel compounds, when airborne, should be considered carcinogens". The International Agency for Research on Cancer reached a similar consensus regarding nickel's carcinogenic potential, concluding: "It is likely that nickel in some forms is carcinogenic to man." (IARC, 1976).
Since that time further epidemiological studies have been conducted. In 1985 an international committee was again specifically formed with the goal of identifying those nickel species that are carcinogenic and of deriving dose-response relationships for these species. This report (Doll et al., 1990) indicated that there was "strong evidence" that soluble nickel was associated with increased respiratory cancer risk and "some evidence" that oxidic nickel increased lung and nasal cancer risks, while "the role that sulphitic nickel exposure played ... was somewhat unclear". They were still unable to answer the question of the level at which nickel becomes a substantial hazard.
Several Ontario studies are worthy of specific commentary. Shannon and colleagues (Shannon et al., 1984) noted an excess of lung and laryngeal cancers in Ontario's Falconbridge Operations comprising mining, milling and smelting, however, the SMRs were not strong enough and the patterns by length of exposure were not sufficiently consistent for an occupational link to be established. In the extended follow-up of the cohort of 11,567 nickel workers to include the period 1977-1984 from the original 1950-1976 study, Shannon and colleagues (1991) found lung cancer to be significantly in excess in the mines (SMR=153, 95% CI:118-196). More detailed analysis by duration of exposure in the mines did not show a consistent or significant increase in SMRs with increasing duration of exposure, however, the numbers were small. Lung cancer by calendar year of first work in the mines also failed to show those who had begun earlier having higher mortality. Rather, those who began after 1960 had the highest SMR, although, again the numbers were relatively small. The investigators noted that diesel machines were first used underground in the 1960s and therefore this group deserves further follow-up. Thus the study showed that there was a significant excess in lung cancer in the mines, but not elsewhere in the Falconbridge operations. While the trend by duration of exposure was not significant, the power of the study was relatively low with sub-groups often containing very small numbers. This suggests that there may be actual risks which could not be detected in this study.
In the study of International Nickel Company (INCO) workers, Roberts et al.,(1989) also found a modest elevation in lung cancer deaths in nickel miners, but felt that this was not nickel-related. This study was commissioned by the Joint Occupational Health Committee of INCO following the publication of the NIOSH criteria document, is a historical prospective mortality study of approximately 54000 INCO workers with 6 months or more of service, followed for mortality during a 35 year period by computerized record linkage to the Canadian Mortality Database. Roberts et al., (1989) had observed that the NIOSH criteria document based its conclusion primarily on the mortality experience of nickel workers at INCO's Clydach Refinery in South Wales, and Falconbridges' Christians and Refinery in Norway. Both facilities had refined nickelmatte which consists mainly of cuprous sulphide and nickel subsulphide derived from sulphide ore deposit of the Sudbury basin. At Clydach, the early studies had suggested that an excess in respiratory cancer was associated with the dustier parts of the process. The observed SMRs for lung and nasal cancer declined in workers hired in later years due probably to lower concentrations of airborne dusts. Roberts et al., also observed that NIOSH had noted that nickel refinery workers in New Caledonia had also found increased respiratory cancers in workers chiefly exposed to non-sulphide forms of nickel, and that NIOSH also referenced the extensive body of information from animal experiments which showed that many forms of nickel can produce localized cancer at the site of implantation or injection in a variety of animal species. They therefore acknowledged that while it can be argued that the epidemiological evidence of increased respiratory cancer in nickel refinery workers could be attributable to other environmental contaminants associated with the ore and its processing (eg. arsenic), the animal data leave little doubt that some forms of nickel can cause some cancers.
The study of Roberts et al., indeed confirmed the existence of large excess risks of lung cancer associated with the Coppercliff and Coniston plants and with the leaching, calcining, and sintering department at Port Colburn. An epidemiologically modest excess of lung cancer mortality was however, also seen within the Sudbury area workers without sinter plant experience. Further analysis revealed that the excess of approximately 50 lung cancer deaths in Sudbury nonsinter workers appeared to be largely attributable to mining. Lung cancer risk in miners occurred most markedly in men with at least 25 years of experience who joined the company many years previously. For example, men with 25 years or more of mining experience who first started to work prior to 1930 showed a lung cancer SMR of 163, compared to an SMR of 125 for those first working between 1930 and 1949, and an SMR of 107 for men starting after 1950. Roberts et al., noted that the modest elevation in lung cancer risk is consistent with risks reported in Ontario gold miners and thus may be associated with hardrock mining rather than with the nickel-ore per se. One possible explanation they offer is that the carcinogen is quartz (silica), which appears in the underground airborne dust of both gold and nickel mines in Ontario (Roberts et al., 1989).
Thus, most internationally respected committees on cancer have consistently concluded that there is strong evidence that some types of nickel are carcinogenic. While the Ontario-based studies in both INCO and Falconbridge have confirmed increased cancer in some types of nickel exposure, and have also both found increased lung cancer in nickel miners, the carcinogenic agent is still the subject of controversy.
3. Exposure of Ontario Miners to Carcinogens
Various Ontario studies have attempted to characterize the potential exposures of Ontario miners to the various carcinogens discussed above.
With respect to gold mines, Kusiak et al.,(1991) noted that dust concentrations for some occupations in the 1930s and 40s were often above 1000 particles/millitre (p/ml) but that by 1959 the average dust concentration in Ontario gold mines was approximately 400 p/ml, and by 1967 the average was under 200 p/ml.
For radon decay products, as noted above, no measurements were taken in Ontario gold mines until the 1960s and most measurements were conducted in the 1980s. Kusiak et al.,(1991) noted that the highest levels of radon decay products usually occurred in inactive areas, where 0.3 WL or greater were found. They felt that this probably represented the maximum to which gold miners were exposed before 1945 when the ventilation in the mines was inferior.
For arsenic, as noted above, concentrations were quite high in gold mines, but varied substantially from one mine to another. In their cohort mortality study an index of arsenic exposure was calculated for each gold miner by weighting the duration of employment in dusty jobs up to the end of 1945 according to the arsenic content in the mine of employment and then applying a second arsenic index calculated in a similar fashion for each year subsequent to 1945.
For silica, the percentage of free silica in airborne dust at several major gold mines varied from 4.3-11.8%.
With respect to the nickel mines, Shannon et al.,(1991) felt that the exposure to nickel in these mines was relatively low and that there was relatively little free silica in the nickel mines as well. Kusiak et al.,(1991b) noted that some of the nickel-copper mines contained up to 0.07% arsenic in the rock, while other nickel-copper mines may have contained less than 0.001% arsenic. The levels of radon decay products in some of the nickel-copper mines ranged between 0.001 WLs and 0.2 WLs in active areas and up to 0.78 WL in inactive areas. They felt that the recently noted excess of lung cancer among nickel-copper miners in Ontario who began mining nickel-copper before the mid 1930s (Roberts et al., 1989), may be due to the combined exposure to arsenic and radon decay products in the nickel-copper mines. They felt that the lung cancer mortality rates in Ontario uranium miners may in fact also have been increased because of the exposures some uranium miners received in the nickel-copper mines.
With respect to radon levels it is noteworthy that in 1972 maximum permissible radon levels were reduced from 1-0.33 WLs which required an improvement in industrial hygiene since that time (IDSP, 1989). With respect to diesel fumes, it was noted (ibid), however, that until 1979 the problem of diesel fumes was often severe at mine headings due not only to the presence of too many machines in the area, but also due to ventilation design problems.
It was noted that the problem of diesel exhaust is a function of type and size of machines as well as their age and general condition of maintenance. No specific exposure data regarding diesel emissions were able to be obtained for this review.
That underground miners incur an increased risk of lung cancer has been known for centuries. There is now strong evidence that several substances to which miners are exposed are indeed carcinogenic. While there is considerable consensus that Ontario miners are indeed exposed to carcinogens, the specific types and levels of exposure still remain elusive. As it is extremely difficult to retrospectively estimate levels of past exposure, uncertainties regarding the extent of past exposure to the various carcinogens will likely always remain.
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. It has been noted that some subgroup analyses still lack the power to document statistically significant increases. It has also been acknowledged that for some substances, such as diesel exhaust, an insufficient latency period may exist to document increases linked to such exposures.
It is particularly important to note, however, that as Archer (1988) had concluded, as the quality of studies improve by longer follow-up periods and more in-depth analyses, exposures previously thought to constitute low risk are increasingly found to have been, in fact, significant. With respect to Ontario miners, the recent study by Kusiak and colleagues (1991b) found that the IDSP (1989) conclusion that radon exposure in the 5-9 year period prior to diagnosis was irrelevant, was, in fact, wrong. There was indeed an excess in lung cancer (specifically small cell tumours) in the 5-9 year period following first exposure and that this period may be associated with the greatest risk of all. The period 15 or more years since exposure is also now known to be associated with greater risk than earlier thought. A third example demonstrating that increased risk becomes more apparent with time is that the previous report on gold miners who did not work in uranium mines (Muller et al., 1989), found no association between exposure to arsenic after 1945 and lung cancer mortality, whereas the most recent report (Kusiak et al., 1991b) found that some of the excess lung cancer in uranium miners did, in fact, relate to exposure to arsenic after 1946.
While there is still considerable uncertainty as to the relative role of arsenic, radon progeny, silica, diesel exhaust, nickel substances (and even asbestos, although not discussed here), as well as their interactions at various concentrations, ages, etc., the fact that exposure to such carcinogens occurs and the fact that lung cancer rates in miners have been consistently elevated remains.
The most recent studies by Kusiak et al., (1991, 1991b) served to confirm that a complex relationship exists between mining exposures and increased lung cancer rates, and has cast serious doubt on the adequacy of the existing compensation guidelines. The Minority Report of IDSP (1989) highlighted problems relating to inadequate exposure data and inappropriately handling the latency issue. Two further concerns can now be added, namely that the weighting of the exposure by years prior to diagnosis is now known to be incorrect, and secondly that some adjustments must be made for exposure to both gold and uranium mining in an interaction we now know to be important
What can be concluded is that, as an occupational group, miners are at some increased risk of lung cancer, although the extent of this increase varies considerably depending on a multitude of factors. If a policy decision was to be made that in all situations where occupational exposures played some (even small) role in increasing risk of a certain outcome, such that should this outcome occur it should be compensable, it would be difficult to argue against compensating all miners. In other words, as noted by numerous authorities investigating workers' compensation systems, the only way to ensure that all cases in which occupational factors played a role receive compensation is to compensate all cases that occur. (Equally, one may wish to argue that in most of these cases, some non-occupational factors are also present, particularly in the case of cigarette smokers.) The role of cigarette smoking, while unequivocally of major importance in lung cancer causation, also complicates the assessment of occupational factors.
As discussed at considerable length in my report to the Weiler Inquiry (Yassi, 1982) the most "fair" system is one in which an individual in need receives benefits without regard to meeting artificial tests of causation. As shown in this report, such tests of causation continue to change as research proceeds and are always clouded by complexities, uncertainty and controversy.
Cohort Radon-Mining Studies and Lung Cancer
|Senior Author||Year||Nation||Ore Type||Mean Follow-up Time (years)||Lung Cancer Deaths||Attributable LC/WLM/104 Person-Years||Lowest Group Mean withSignificant Excess (WLM)|
|Reference: Archer 1988|
Projected Lifetime Lung Cancer Risk by Different Risk Projection Models for 30-year Exposure
|NCRP||0.4%||1.6%||Attributable risk for exposure beginning at age 20|
|BEIR IV||8.4%||13.1%||Total lifetime risk for exposure beginning at age 20|
|NIOSH||1.0%||4.2%||Excess lifetime lung cancer risk|
|(BIER IV = biological effects of ionizing IV; NCRP=National Council on Radiation Protection
and Measurements; NIOSH=National Institute for Occupational Safety and Health;
WLM=woring level month)
Reference: Samet, 1991
Follow-Up and Case-Control Studies of Silicosis and Lung Cancer Mortality
|Lung cancer SMR by industrya|
|Principal author [year]||Source of silicosis records
|No. of siliotics||Year of silicosis||Year of follow-up||Only mining||Mining, quarry, tunnel, or stone||Foundry||Ceramic||Other||Totalb|
|Occupational registry dis.||49-69||69||3.8d||2.2d||2.9||1.0||2.8d|
|Gudbergsson ||Hospital med. record||331||64-74||75||3.0d|
|National insur. fund||(person-
|Schuler ||Medical examination||2,399||60-78||78||2.5d||1.2||3.9d||1.9||2.4d|
|Neuberger ||Pension fund||2,212||50-60||80||1.4d|
|Hessel ||Pneumocon. registry||Case-contl.||--||--||(1.1)c||(1.1)c|
|Westerholm ||Occupational registry dis.||712||59-77||79||5.4d||3.9d||4.4d|
|Forastiere [1986, 1987]||Compensation Case-contl.||--||--||2.1c,d||2.1c,d|
|Zambon ||Union death benefits||1,313||59-63||84||1.4d||1.8d||2.2||1.9d|
|Ng ||Medical examination||1,419||80||86||2.0d|
|a SMR computed from an external reference group; RR computed from an internal reference group (parentheses); MOR computed from an external reference group [brackets]
b Total: all workers in study combined
c Adjusted for cigarette-smoking status
d Significantly different from 1.0 (p value < .05).
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Amandus HE, Shy C, Wing S, Blair A and Heineman EF. Silicosis and lung cancer in North Carolina dusty trades workers. Am J Ind Med 1991;20:57-70.
Armstrong BK, McNulty JC, Levitt LJ, et al. Mortality in gold and coal miners in Western Australia with special reference to lung cancer. Br J Ind Med 1979;36:199-205.
Archer VE. Lung Cancer Risks of Underground Miners: Cohort and Case-Control Studies. Yale J Biology & Med 1988;61:183-193.
Boffetta P. Stellman SD, and Garfinkel L. Diesel exhaust exposure and mortality among males in the American Cancer Society prospective study. Am J Ind Med. 1988;14:403-415.
Burns PB and Swanson GM. The occupational cancer incidence surveillance study (OCISS): Risk of lung cancer by usual occupation and industry in the Detroit Metropolitan area. Am J Ind Med. 1991;19:655-671.
Doll R, Andersen A, Cooper WC, Cosmatos I, et al. Report of the International Committee on Nickel Carcinogenesis in Man. Scand J Work Environ Health. 1990;16:1-82(Supple).
Findelstein M, Liss GM, Krammer F, Kusiak RA. Mortality among workers receiving compensation awards for silicosis in Ontario 1940-85. Br J Ind Med 1987;44:588-594.
Fraser D. Lung cancer risk and diesel exhaust exposure. Public Health Reviews. 1986;14:139-71.
Goldsmith DF, Guidotti TL, Johnson Dr. Does occupational exposure to silica cause lung cancer? Am J Ind Med 1982; 3:423-40.
Hnizdo E, Sluis-Cremer GK. Silica exposure, silicosis, and lung cancer: a mortality study of South African gold miners. Br J Ind Med 1991;48:53-60.
Hornung RW, Meinhardt TJ. Quantitative risk assessment of lung cancer in U.S. Uranium miners. Health Physics 1987;52(4):417-430.
Industrial Disease Standards Panel (IDSP). Report to the Workers' Compensation Board on the Ontario Uranium Mining Industry. Report 6, Toronto, Ontario, February, 1989.
International Agency for Research on Cancer. Monographs on the evaluation of the carcinogenic risk of chemicals to humans. Vol 42. Silica and some silicates. Lyon: IARC, 1987.
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International Agency for Research on Cancer: Cadmium, nickel, some epoxides, miscellaneous industrial chemicals, and general considerations on volatile anesthetics. IARC monograph 11, World Health Organization, Geneva, 1976.
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Kusiak RA, Springer J, Ritchie AC, et al. Carcinoma of the lung in Ontario gold miners: possible etiological factors. Br J Ind Med. 1991;48:808-817.
Kusiak RA, Springer J, Ritchie AC, et al. Lung Cancer Mortality in Ontario Uranium Miners. Draft for comment: 15 October, 1991.
McDonald JC. Silica, silicosis and lung cancer. Editorial British Journal of Industrial medicine 1989;46:289-291.
McDonald JC, Gibbs GW, Liddell FDK, et al. Mortality after long exposure to cummingtonite-grunerite. Am Rev Respir Dis. 1978;118:271-7.
Muller J, Wheeler WC, Gentleman JF, Suranyi G, Kusiak RA. Study of Ontario miners, 1955-1977, part 1. Ontario: Ontario Ministry of Labour, Ontario Workers' Compensation Board, Atomic Energy Control Board, 1983.
Muller J, Kusiak RA, Suranyi G, Ritchie AC. Study of mortality of Ontario gold miners 1955-1977. Ontario: Ontario Ministry of Labour, Ontario Workers' Compensation Board, Atomic Energy Control Board, 1986.
National Institute for Occupational Safety and Health. Criteria for a recommended standard: Occupational exposure to inorganic nickel. U.S. Department of Health, Education and Welfare (NIOSH) Publication No. 77-164, 1977.
Radford EP, St.Clair Renard KG. Lung cancer in Swedish iron miners exposed to low doses of radon daughters. The New England Journal of Medicine 1984;311(23):1485-1494.
Roberts RS, Julian JA, Muir DCF, Shannon HS. A Study of Mortality in Workers Engaged in the Mining, Smelting, and Refining of Nickel. II. Mortality from Cancer of the Respiratory Tract and Kidney. Toxicology and Industrial Health;5:975-993, 1989.
Saccomanno G, Yale C, Dixon W, Auerbach O, Huth GC. An epidemiological analysis of the relationship between exposure to Rn progeny, smoking and bronchogenic carcinoma in the u-mining population of the Colorado Plateau - 1960-1980. Health Physics 1986;50(5):605-618.
Saccomanno G, Archer VE, Saunders RP, et al. Lung cancer of uranium miners on the Colorado Plateau. Health Phys. 1964;10:1195-1201.
Samet JM. Diseases of uranium miners and other underground miners exposed to radon. Occ Med. 1991:629-639.
Shannon HS, Walsh CC, Jadon N, et al. Mortality of 11,500 nickel workers - extended follow up and relationship to environmental conditions. Toxicol and Ind Hlth. 1991;7(4):277-294.
Shannon HS, Julian JA, Muir DCF, et al. A Mortality of Study of Falconbridge Workers. Nickel in the Human Environment. 1 984;117-23.
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Radon Progeny and Cigarette Smoking:
A Summary of World Literature Regarding the Effect of Cigarette Smoking and Lung Cancer Risk in Uranium Miners and Other Hardrock Miners Exposed to Radon
The following is a summary of scientific publications from investigators in Canada, United States, Western Europe and Japan. Original scientific publications were reviewed to the extent possible, although no reanalysis of primary data was conducted. As this topic has been extensively studied by the highly reputable National Research Council committee on the Biological Effects of Ionizing Radiation (BEIR), extensive citation of the analysis and conclusions reported in the most recent BEIR report addressing this issue (BEIR IV, 1988) is included. While other investigators have also reviewed this topic, as the highly regarded "neutral" reputation of BEIR is beyond reproach, it is the BEIR conclusions that are used extensively in this report.
The epidemiological studies of smoking and radiation reviewed in BEIR IV are shown in Table 1, reproduced in total from BEIR IV. It can be seen that the Ontario data are not included in this table. As noted in my cover letter Dr. Warner's specific request for analyzing the effect of smoking in the Ontario cohort would best be referred to the authors of the Ontario mining study.
There have been several studies among Swedish metal miners aimed at clarifying the role of radon exposure combined with tobacco use on the occurrence of lung cancer. In the case-control study by Damber and Larsson (1982), cases were ascertained in the years 1972-1977, and for each case, one deceased control and living control was sought. (The authors recognized that smoking-related risks that are based on deceased controls may be underestimated, since tobacco use is likely to have been greater by the deceased than by the general population. However, use of controls required to be alive until 1982 may overestimate relative risks, since their smoking rates may have been less than those of the general population. Thus having both controls allowed the authors to evaluate this concern. The results, interestingly, were generally comparable regardless of control group.) Smoking history was obtained through interviews with the index subject or the next of kin. Since no accurate measurements of direct radon exposure were available, the surrogate variable, years underground, was used for analysis. Results were tabulated by three categories of lifetime tobacco use, namely non-smoker, cumulative consumption of less than 150,000 cigarettes and consumption of greater than 150,000 cigarettes. As shown in Table 1, relative risks rose from the baseline 1.0 for non-smokers to 2.4 for low consumption above-groundworkers, to 8.4 for heavy smoking above-ground workers; for underground miners, however, the lung cancer risk was 5.4 for non-smokers, 21.7 for low cigarette consumption workers, and 69.7 for underground heavy smoking miners. These results suggested a multiplicative rather than additive relationship between radon exposure and smoking.
Another study of Swedish metal miners was the historical cohort study of 1,415 miners conducted by Radford and Renard (1984). Data on current smoking habits were reported from questionnaires administered in 1972-1973 to active miners and surface workers and from pensioners; smoking habits were thus obtained on approximately half the workers who were still living at the time of this study. Smoking histories for lung cancer patients were obtained from next of kin or the index subject. Smokers were defined as those who had stopped smoking within 10 years of the interview or were currently smoking, while non-smokers were defined as subjects who stopped smoking 10 years or more prior to the interview or who had never smoked. The smoking status of miners was then compared with a national smoking survey conducted in 1963. It was determined that the miners had a high proportion of smokers, although no adjustment was made for the different time periods in the two surveys. Moreover, as noted by the BEIR IV review, the evidence presented in their report did not adequately support their conclusion that mining and smoking-related risks combined additively. BEIR IV concluded that the Radford and Renard results seem to suggest, however, that the risks for the two exposures are sub-multiplicative.
A third Swedish study, that by Axelson and Sundell (1978), compared smoking and mining experiences in 29 lung cancer cases deceased between 1956 to 1976, with controls who died of causes other than lung cancer. For subjects with mining experience, smoking histories were derived through interviews with the foremen who were contemporaries of the subjects. Smoking status was not determined for non-miners. The authors concluded that smoking appeared to be protective for lung cancer, hypothesizing that smokers have a lower radiation-induced risk of lung cancer because of the thickened mucous layer in critical bronchial segments. BEIR IV concluded that because there was no smoking histories in non-miners and the duration of radon exposure in miners was not ascertained, the interaction between radon and smoke exposures could not be ascertained from this study.
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, that 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. The further analysis by Archer et al, reported in this same paper, also found that the induction-latent period was shorter for smokers than for non-smokers; the BEIR IV group, however, found flaws with the methodology used to reach this conclusion.
Another U.S. study, that by Lundin et al. (1979), also analyzed the effect of smoking in miners. The results suggested that a greater amount or radiation-induced lung cancer risk existed for smokers than non-smokers. However, no formal statistical testing was conduced in this study.
Whittmore and McMillan (1983) reappraised lung cancer mortality among 3,362 U.S. uranium miners using a nested case-control approach. They found substantial support for a multiplicative model. The data regarding radon progeny and cigarette use obtained by Whittmore and McMillan (1983) was reanalysed by the BEIR IV committee using a variety of models. They found that the best fitting model was sub-multiplicative, although noted that it did not provide a statistically significant improvement in fit over the multiplicative model. The National Institute for Occupational Safety and Health (NIOSH 1986) found synergistic effects between cigarette smoking and radon progeny exposure, ie. that the combined effects exceeded the sum of the separate effects. The data, however, suggested that the combined effect was less than multiplicative.
Saccomanno et al. (1986) studied 9,817 miners, underground and open pit, and millers who worked between 1960 and 1980 and who agreed to participate in the study. Cases were defined as men who had at least one sputum cytology specimen classified as moderate or worse atypical squamous metaplasia. Controls consisted of a random sample of the non-case members of the cohort. The results suggested a multiplicative association, although, again, BEIR IV noted several potential biasing factors in this study.
The studies among New Mexico uranium miners also suggest that a multiplicative combination of the two exposures is more compatible than is an additive model, although again there was no statistically significant difference between the models.
The one Canadian uranium miners study which was analyzed with respect with cigarette smoking and radon exposure among a group of miners was that by Band et al. (1980). The study group consisted of 249 underground miners and 123 male controls, all residents of Uranium City Saskatchewan. In a manner similar to that of Saccamanno et al. (1986) the outcome status was determined by degree of sputum cytology abnormalities. Information on smoking and occupational history was obtained by questionnaire. Based on work history, cumulative working level month (WLM)exposure to radon through 1977 was determined for each underground miner. There was an increased risk with radon exposure and with cigarette use. However, there were too few non-smokers with moderate or severe atypia to assess the interaction of these factors.
Studies of the home environment and studies among Japanese atomic bomb survivors were also reviewed by BEIR IV, the results of which are shown in Table 1.
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.
Effects of Cigarette Smoking on the Respiratory Tract as it Relates to Risk from Occupational Exposures
The effects of cigarette smoking on all levels of the respiratory tract have been extensively studied. Although it is well accepted that cigarette smoking affects the lung parenchyma, causing structurally altered cells, altered function of some cells, fibrosis and emphysema, it is the effects of cigarette smoking on the airways that is most relevant for the risk of lung cancer.
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 physiologic 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 by 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.
It has been argued that dose might be reduced in smokers by thickening of the mucosa and the increased mucous production in the airways of smokers. However, cigarette smoking induced diseases such as chronic bronchitis and chronic airway obstruction have been associated with increased lung cancer risk. Epidemiological studies have indeed shown that these diagnoses are associated with increased lung cancer even with adjustment for cigarette smoking. In an early case control study, Doll and Hill (1952) found that lung cancer cases had a history of chronic bronchitis significantly more often than the controls; in two subsequent case-control studies (Samet et al. 1986; and Van De Wal et al. 1966) this held true even when controlling for cigarette smoking. Davis (1976) also showed that the incidence of lung cancer was higher in individuals with smoking related non-malignant respiratory diseases. Two further studies, that by Rimington (1971) and Peto et al. (1983) also concurred with this finding. BEIR IV felt that the hypothesis that increased mucous production reduces penetration of alpha particles into the lining of the airways, thus protecting cellular damage, was inconsistent with the facts. The conclusion, therefore, is that smoking induces a series of changes which predispose workers to lung cancer from other carcinogenic exposures.
The Association Between Lung Cancer, Smoking and Radiation
As noted in the introductory component of this interim response, epidemiological studies will never provide the definitive answers to all the complicated questions regarding causation; it is particularly noted that no amount of study can determine the extent to which one factor or other caused cancer in an individual. However, much study has been done, and there is little point in the IDSP trying to commission studies to do that which can not be done. The most internationally acclaimed experts on the subject of the association between lung cancer, smoking and radiation have concluded the following:
"Cancer risk associated with exposure to radon progeny depends on cumulative dose, age, and time since exposure. The actual biological relationship is undoubtedly more complex than the statistical model that the committee has developed and may be influenced by other factors that cannot be fully evaluated with the available data. These factors might include age at first exposure, dose rate, sex, diet, and genetic predisposition. Moreover, the association of tobacco consumption with lung cancer is also complex and depends on duration and number of cigarette smoked per day, type of tobacco product, method of inhalation, and years since cessation of use for former smokers. Assessment of the combined effects of cigarette smoking and radon progeny should account for the individual patterns of effect from both insults. Other aspects of the combined exposure may also be important, for example, the effect of the sequencing of exposures and the degree of their overlap in time."
Thus, I conclude, as I did in my Literature Review and Discussion Paper on Hardrock Mining and Lung Cancer, that while cigarette smoking is probably the most important single cause of lung cancer in miners, the effect of occupational exposures is certainly not negligible. Moreover, there is no simple way of defining the relationship amongst the different carcinogenic exposures to which either a smoking or non-smoking miner is exposed, and thus no scientifically sound method of attributing causation in an individual case.
Archer VE, JK Wagoner, and FE Lundin. 1973. Uranium mining and cigarette smoking effects on man. J. Occup. Med. 15:204-211.
Axelson O, and L Sundell. 1978. Mining lung cancer and smoking. Scand. J. Work Environ. Health 4:46-52.
Band P, M Feldstein, G Saccomanno, L Watson, and O King. 1980. Potentation of cigarette smoking and radiation: Evidence from a sputum cytology survey among uranium miners and controls. Cancer 45:1273-1277.
Davis AL. 1976. Bronchogenic carcinoma in chronic obstructive pulmonary disease. J. Am. Med. Assoc. 235:612-622.
Doll R, and AB Hill. 1952. A study of the aetiology of carcinoma of the lung. Br. Med. J. 2:1271-1286.
Health risks of Radon and other internally deposited alpha-emitters. BEIR IV, 1988. National Academy Press, Washington, DC.
Lundin FE, Jr., VE Archer, and JK Wagoner. 1979. An exposure-time-response model for lung cancer mortality in uranium miners - effects of radiation exposure, age and cigarette smoking. p. 243-264 in Proceedings of the Work Group at the Second Conference of the Society for Industrial and Applied Mathematics, N.E. Breslow, and A. Whittemore, eds.
National Institute for Occupational Safety and Health (NIOSH), 1986. Evaluation of Epidemiologic Studies Examining the Lung Cancer Mortality of Underground Miners. Division of Standards Development and Technology Transfer. Cincinnati, Ohio: Centers for Disease Control, National Institute for Occupational Safety and Health.
Peto R, FE Speizer, AL Cochrane, F Moore, CM Fletcher, CM Tinker, IT Higgins, RG Gray, SM Richards, J Gilliland and B Norman-Smith. the relevance in adults of air-flow obstruction, but not mucus hypersecretion to mortality from chronic lung disease: Results from 20 years of prospective observation. Am. Rev. Respir. Dis. 128:491-501.
Damber L, and LG Larson. 1982. Combined effects of mining and smoking in the causation of lung carcinoma. Acta Radiol. Oncol. 21:305-313.
Radford EP and KG St. Clair Renard. 1984. Lung cancer in Swedish iron ore miners exposed to low doses of radon daughters. N. Engl. J. Med. 310(23):1485-1494.
Rimington J. 1971. Smoking chronic bronchitis and lung cancer. Br. Med. J. 2:373-375.
Saccomanno G, C Yale, W. Dixon, O Auerbach and GC Huth. 1986. An epidemiological analysis of the relationship between exposure to Rn progeny, smoking and bronchogenic carconoma in the U-mining population of the Colorado Plateau-1960-1980. Health Phys. 50:605-618.
Samet JM, CG Humble, and DR Pathok. 1986. Personal and family history of respiratory disease and lung cancer risk. Am. Rev. Respir. Dis. 134:466-470.
Van Der Wal AM, E Huizingav, NG Orie, HS Sliuter, and K de Vries. 1966. Cancer and chronic nonspecific lung disease (C.N.S.L.D.). Scand. J. Respir. Dis. 47:161-172.
Whittemore AS, and A. McMillan. 1983. Lung cancer mortality among U.S. uranium miners: A reappraisal. J. Natl. Cancer Inst. 71:489-499.
Relative Risk from Selected Studies of Cigarette Use, Radiation Exposure, and Lung-Cancer Risk
|Kiruna and Gallivare,
|Cases (69) from death register 1972-1982; two types of controls: alive from general population (60) and deceased from register (67)||Cigarette Usea||Smoking data from interviews of subjects or next-of-kin; results consistent with multiplicative, relative risk (RR) model, although formal testing not presented|
|Malmberget, Sweden||Cohort study of 1,415 miners, with 50 cases of lung cancer||Nonsmoker||Smoker||Results suggestive of submultiplicative model for RR, possibly additive; calculation of RRs not precisely described; formal model fitting not presented|
|Hammar, Sweden||Cases (29) listed in death register 1957-1976; controls (174) also from register, matched on year of death.||RR for mining 16.6 (90% confidence interval, 7.8-35.3); RR for smoking among miners 0.5 (90% confidence interval, 0.1-2.2)||Suggestive of a protective effect of
smoking among miners; results subjective to biases (see text)
|Colorado||Cohort study of uranium miners examined through 1960; followup from 1964-1967 with 39 cases of lung cancer||Cigarette Use||Multiplicative combination is suggested; analysis of cases shows shorter latency period for smokers|
|Lung Cancer Rate x 105||No||Yes|
|Colorado||Nested case control study from 3,362 miners followed from 1964-1977, with 194 cases and 776 controls; exposures lagged 10 years||Cigarette Use (pack yr)||Analyses formally reject additive RR model; data consistent with multiplicative model|
|Colorado||Cohort study of 3,362 miners followed through 1982, with 256 observed cases of lung cancer, exposures lagged 5 years||Cigarette Use (no./day)||Data fit well with multiplicative model (P=0.53), while additive was rejected (P=0.03); although not statistically superior to multiplicative model, best fitting power model was submuliplicative|
|Grand Junction, Colorado||Cases (489) and controls (992) drawn from cohort of 9,817 miners followed from 1960-1980, from whom sputum specimens were regularly obtained; cases defined as moderate or worst cell atypia||Cigarette Use ((pack yr)||Study is cell atypia; suggests multiplicative effects, although statistical testing not presented|
|New Mexico||Cases (52) and controls (222) extracted from cohort of uranium miners||Cigarette Use (no./day)||Both multiplicative and additive RR models consistent with data, although former exhibit better fit|
|Yr Mining Underground||<5||5-14||15-24||>25|
|Uranium City, Saskatchewan, Canada||Followup for 3 yr of underground miners and controls who participated in lung cancer screening program; cases defined as moderate or worst case atypia||Cigarette Use||Study is of cell atypia; few event among nonsmokers, data and analysis insufficient to assess interaction of exposures|
|Oeland, Sweden||Cases (22) and controls (178) drawn from death registry 1960-1978; smoking habits obtained from next-of-kin using mail questionnaire||Cigarette use||Data were sparse, and no formal models were fit, but RRs suggest multiplicative interaction, or at least greater than additive|
|Japan||Cohort study of 40,498 A-bomb survivors for whom smoking data are available; there were 281 lung-cancer deaths||Cigarette Use||Both multiplicative and additive RR models fit data equally well|
|Radiation exposure (rad)||No||Yes|
|Japan||Cases (485) and controls (1,089) identified during 1971-1980 from Life Span Study among A-bomb survivors||Cigarette Use (no./day)||Both multiplicative and additive RR models fit data equally well|
|Radiation exposure (rads)||0||1-10||11-20||>20|
|a Lifetime numbers in thousands
b Incidence based on rates in mountain states.
c Baseline category based 0.7 expected cases compared to 0 observed
d See text for category definitions
Data from Case Control Study of New Mexico Uranium Miners
|Years of Underground Mining|
|No of cigarettes/day||No. of Cases||No. of Controls||No. of Cases||No. of Controls||No. of Cases||No. of Controls||No. of Cases||No. of Controls|
|Regression Models||No. of Parameters||2xMLL||P-Value|
|1: 1+0(yr, n/d)||15||-121.8|
|a Relative risks from additive model, Equation VII-2
b Relative risks from multiplicative model, Equation VII-1
Observed Lung-Cancer Mortality and Calculated Lung-Cancer Mortality Rate as a Function of Cumulative Exposure and Cigarette Consumption for the Colorado Miner Cohorta
|Cumulative||No. of Cigarettes/day|
a Cumulative exposure limited to 2,000 WLM.
b Baseline rate per 100,000 computed expected number of cases, bases on U.S. white male mortality rates for lung cancer adjusted to nonsmokers
c Person years
Dr. J.P. Ashmore, National Dose Registry, Bureau of Radiation and Medical Devices, Health Protection Branch, Health and Welfare Canada, Ottawa.
Dr. Bernard C.K. Choi, Department of Preventive Medicine, and Biostatistics, University of Toronto, Toronto
Dr. Paul Corey, Department of Preventive Medicine, University of Toronto, Toronto
Dr. Sture Engdahl, Construction Division, National Board of Occupational Health and Safety, Sweden
Frank Hearl, Professional Engineer, Chief, Environmental Investigations Branch, National Institute for Occupational Safety and Health, Division of Respiratory Disease Studies, Morgantown, West Virginia
Cameron Hopkins, Professor of Chemistry in the Mining Technology Program at Cambrian College, Sudbury
Alan Jennings, Metallurgical Engineer, Professional and Specialized Services, Operations Division, Ministry of Labour, Sudbury.
Riitta-Sisko Koskela, Researcher, Institute of Occupational Health, Finland
Robert Kusiak, Supervisor, Biostatistics, Health and Safety Studies Unit, Ministry of Labour, Toronto
Dr. W.Maehle, Phyisician, Ontario Chest Clinics, Ministry of Labour, Toronto
Dr. John Patterson, Mining Engineering Department, Queen's University, Kingston
Ian Plummer, Provincial Co-ordinator, Occupational Health and Safety Branch, Mining Health and Safety Program, Ministry of Labour, Sudbury
Dr. Janet Springer, Geologist, Pre-Cambrian Geology Section, Ministry of Northern Development and Mines, Sudbury
John Vergunst, Mining Engineer, Provincial Specialist for the Mine Environment, Mining Health and Safety Program, Ministry of Labour, Sudbury
(a) Degrees of evidence for carcinogenicity to humans and in experimental animals and supporting evidence
It should be noted that these categories refer only to the strength of the evidence that these agents are carcinogenic and not to the extent of their carcinogenic activity (potency) nor to the mechanism involved. The classification of some agents may change as new information becomes available.
(i) Human carcinogenicity data
The evidence relevant to carcinogenicity from studies in humans is classified into one of the following categories:
Sufficient evidence of carcinogenicity: The Working Group considers that a causal relationship has been established between exposure to the agent and human cancer. That is, a positive relationship has been observed between exposure to the agent and cancer in studies in which chance, bias and confounding could be ruled out with reasonable confidence.
Limited evidence of carcinogenicity: A positive association has been observed between exposure to the agent and cancer for which a causal interpretation is considered by the Working Group to be credible, but chance, bias or confounding could not be ruled out with reasonable confidence.
Inadequate evidence of carcinogenicity: The available studies are of insufficient quality, consistency or statistical power to permit a conclusion regarding the presence or absence of a cause association.
Evidence suggesting lack of carcinogenicity: There are several adequate studies covering the full range of doses to which human beings are known to be exposed, which are mutually consistent in not showing a positive association between exposure to the agent and any studied cancer at any observed level of exposure. A conclusion of "evidence suggesting lack of carcinogenicity" is inevitably limited to the cancer sites, circumstances and doses of exposure and length of observation covered by the available studies. In addition, the possibility of a very small risk at the levels of exposure studied can never be excluded.
In some instances, the above categories may be used to classify the degree of evidence for the carcinogenicity of the agent for specific organs or tissues.
(ii) Experimental carcinogenicity data
The evidence relevant to carcinogenicity in experimental animals is classified into one of the following categories:
Sufficient evidence of carcinogenicity: The Working Group considers that a causal relationship has been established between the agent and an increased incidence of malignant neoplasms or of an appropriate combination of benign and malignant neoplasms (as described on p.23) in (a) two or more species of animals or (b) in two or more independent studies in one species carried out at different times or in different laboratories or under different protocols.
Exceptionally, a single study in one species might be considered to provide sufficient evidence of carcinogenicity when malignant neoplasms occur to an unusual degree with regard to incidence, site, type of tumour or age at onset.
In the absence of adequate data on humans, it is biologically plausible and prudent to regard agents for which there is sufficient evidence of carcinogenicity in experimental animals as if they presented a carcinogenic risk to humans.
Limited evidence of carcinogenicity: The data suggest a carcinogenic effect but are limited for making a definitive evaluation because, e.g., (a) the evidence of carcinogenicity is restricted to a single experiment; or (b) there are unresolved questions regarding the adequacy of the design, conduct or interpretation of the study; or (c) the agent increases the incidence only of benign neoplasms or lesions of uncertain neoplastic potential, or of certain neoplasms which may occur spontaneously in high incidences in certain strains.
Inadequate evidence of carcinogenicity: The studies cannot be interpreted as showing either the presence or absence of a carcinogenic effect because of major qualitative or quantitative limitations.
Evidence suggesting lack of carcinogenicity: Adequate studies involving at least two species are available which show that, within the limits of the tests used, the agent is not carcinogenic. A conclusion of evidence suggesting lack of carcinogenicity is inevitably limited to the species, tumour sites and doses of exposure studied.
(iii) Supporting evidence of carcinogenicity
The other relevant data judged to be of sufficient importance as to affect the making of the overall evaluation are indicated.
(b) Overall evaluation
Finally, the total body of evidence is taken into account; the agent is described according to the wording of one of the following categories, and the designated group is given. The categorization of an agent is a matter of scientific judgement, reflecting the strength of the evidence derived from studies in humans and in experimental animals and from other relevant data.
Group 1 - The agent is carcinogenic to humans.
This category is used only when there is sufficient evidence of carcinogenicity in humans.
This category includes agents for which, at one extreme, the degree of carcinogenicity in humans is almost sufficient, as well as agents for which, at the other extreme, there are no human data but for which there is experimental evidence of carcinogenicity. Agents are assigned to either 2A (probably carcinogenic) or 2B (possibly carcinogenic) on the a basis of epidemiological, experimental and other relevant data.
Group 2A The agent is probably carcinogenic to humans.
This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. Exceptionally, an agent may be classified into this category solely on the basis of limited evidence of carcinogenicity in humans or of sufficient evidence of carcinogenicity in experimental animals strengthened by supporting evidence from other relevant data.
Group 2B The agent is possibly carcinogenic to humans.
This category is generally used for agents for which there is limited evidence in humans in the absence of sufficient evidence in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans or when human data are nonexistent but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent for which there is inadequate evidence or no data in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
Group 3 The agent is not classifiable as to its carcinogenicity to humans.
Agents are placed in this category when they do not fall into any other group.
Group 4 The agent is probably not carcinogenic to humans.
This category is used for agents for which there is evidence suggesting lack of carcinogenicity in humans together with evidence suggesting lack of carcinogenicity in experimental animals. In some circumstances, agents for which there is inadequate evidence of or no data on carcinogenicity in humans but evidence suggesting lack of carcinogenicity in experimental animals, consistently and strongly supported by a broad range of other relevant data, may be classified in this group.
The following summarizes the laws and policies of other jurisdictions on matters that affect the compensation of miners with lung cancer. Omitted from the following discussion are any policies or laws that relate to other conditions of the lungs, such as asbestosis, mesothelioma, silicosis or tuberculosis.
In the Northwest Territories' Workers' Compensation Act, an industrial disease is defined as "a disease caused by conditions in a place where an industrial process, trade, industry or occupation is carried on".1 A provision in this statute provides that if a worker was employed in an industry that exposed him or her to conditions that may cause an industrial disease, and within 12 months the worker contracts the industrial disease, then the disease is presumed to be an industrial disease unless the contrary is proven.2
Policies of the Workers' Compensation Board of the Northwest Territories acknowledge that pulmonary or bronchogenic cancer are industrial diseases.3
At the Yukon Territory Workers' Compensation Board, claims are adjudicated on their own merits.4
Policies of the Yukon's Workers' Compensation Board list "arsenic poisoning" and "radiation" as examples of diseases that are to be charged to the "Reserve for Industrial Diseases".5
If a worker suffers from a disease listed on Schedule B to the British Columbia Workers' Compensation Act, and can show that at that time or immediately before the worker was employed in a manner that exposed him or her to the corresponding process listed on the Schedule, then it is presumed that the disease was caused by employment unless the contrary is proven.6
The British Columbia statute also states that if a worker dies before the age of 70, suffered from an industrial disease that impaired the function of his or her lungs and the death was caused by an ailment or impairment of the lungs or heart of a non-traumatic origin, then it shall be irrefutably concluded that the death was caused by an industrial disease.7
As well, it is presumed, unless proven to the contrary, that primary cancer of the lung is an industrial disease if the worker was exposed at work to "aerosols and gases containing arsenic, chromium, nickel or their compounds", to "bis (chloromethyl) ether", to "the dust of uranium, or radon gas and its decay products", or to "particulate polycyclic aromatic hydrocarbons".8
Moreover, it is presumed, unless proven to the contrary, that radiation injury or disease is an industrial disease if the worker was exposed to ionizing radiation.9
If a worker suffers from one of the diseases deemed to be an industrial disease by Schedule B of the regulations to Alberta's Workers' Compensation Act and the worker can show that during the preceding 12 months he or she was employed in a manner that exposed him or her to the corresponding process listed on the Schedule, then it is presumed that the disease was caused by employment unless the contrary is proven.10
If a worker in Alberta suffers from radiation injury or disease and can show that during the preceding 12 months he or she was employed in a workplace that exposed him or her to "sufficient occupational exposure to ionizing radiation," then it is presumed, unless the contrary is proven, that the disease is an occupational disease.11
Furthermore, the policies of the Alberta Workers' Compensation Board state that if a worker "suffers a disease of the respiratory system due in part to occupational factors and in part to non-occupational factors", then the disability is presumed to be related to employment.12
Saskatchewan has no statutory provision that explicitly recognizes that industrial diseases are to be compensated, nonetheless industrial diseases are compensated in Saskatchewan as "accidents".
Saskatchewan has no policies that explicitly address issues that have to do with the compensation of workers who suffer from lung cancer.
The Manitoba Workers' Compensation Act defines "accident" as including a disease caused by work13, and defines "industrial disease" as including any disease "that is peculiar to, or characteristic of, an industrial process, trade, or occupation".14
In Manitoba, a disease will be compensated only in the proportion that it is caused by the workplace.15 The policies of the Manitoba Board have interpreted this to mean that a disease will be compensated only if the workplace is the "dominant cause" of the disease.16 The Board has also promulgated a policy to assist in determining whether a disease is an "disease of ordinary life".17
If a worker suffers from a disease listed on Schedule I to the Quebec workers' compensation statute, and can show that at that at some time he or she was employed in a manner that exposed him or her to the corresponding process listed on the Schedule, then it is presumed that the disease was caused by employment unless the contrary is proven.18
If a worker suffers from a disease caused by ionizing radiation, and can show that at that at some time the worker was employed in a manner that exposed him or her to "any work involving exposure to ionizing radiations," then it is presumed that the disease was caused by employment unless the contrary is proven.19
In New Brunswick, a worker may be compensated if he or she suffers from an industrial disease.20 A disease is an occupational disease if it is declared as such by the regulations or if it is peculiar to or characteristic of a particular industrial process, trade or occupation.21
New Brunswick's list of industrial diseases includes any disease that results from workplace-induced mercury, phosphorus or arsenic poisoning.22
If a Nova Scotia worker suffers from a disease listed on Schedule A to the statute and was exposed to the corresponding risk listed on the Schedule, then it is presumed that the disease was caused by work unless the contrary is proved.23 However, compensation for the disease is payable only for the proportion of the disease "as may reasonably be attributed to the personal injury sustained".24
If a worker suffers from any disease that results from arsenic poisoning or from exposure to X-rays, radium or other radiative substances, then it is presumed that the disease is compensable unless the contrary is proven.25
The Nova Scotia Workers' Compensation Act states that a coal miner who suffers from loss of lung function will receive workers' compensation benefits for his or her disability.26
As well, policies enacted by the Nova Scotia Workers' Compensation Board indicate that lung cancer in coke oven workers will be treated as an industrial disease. This policy also discusses how these claims will be adjudicated if the injured worker was a smoker.27
Prince Edward Island
Prince Edward Island's workers' compensation statute establishes that compensation is available if a worker suffers from an industrial disease. As well, the statute defines "industrial disease" to include any of the diseases listed in the Schedule to the Act or any other disease declared by the regulations to be an industrial diseased.28 This Schedule indicates that any consequence of arsenic poisoning is an industrial disease.29
Newfoundland's workers' compensation statute establishes that workers suffering from industrial diseases are entitled to be compensated, and provides that for diseases listed on the schedule it shall be presumed, unless the contrary is proven, that the disease was caused by work.30
If a worker involved in fluorspar extraction suffers from lung cancer, then the disease is presumed to be due to employment in the mines unless the disease is traceable to another cause.31
As well, if a worker suffers from a "bronchopulmonary disease[s] caused by hard metal dust", a disease caused by cadmium, chromium or arsenic or their toxic compounds, or a disease caused by ionising radiations and the worker was exposed at work to the relevant risk, then it is presumed that the worker's disease was caused by work unless the contrary is proven.32
In Massachusetts, if a firefighter is afflicted with one of many different types of cancer, then it is presumed, unless the contrary is proven, that the cancer was due to employment. Added to this, however, is the condition that the firefighter must have been working as a firefighter and regularly attended fires for at least five years.33
Mr. Odoardo DiSanto
Workers' Compensation Board
2 Bloor Street East
Dear Mr. DiSanto:
Enclosed is a copy of the Panel's "Report to the Workers' Compensation Board on Lung Cancer in the Hardrock Mining Industry".
The Panel hopes that with the assistance of the Board staff that the rebuttal matrix can be developed as quickly as possible. We do, however, acknowledge that time will be required to develop a useful and effective matrix. More time will be added to the implementation of the report if the WCB agrees to endorse the IDSP recommendation and it is necessary for the Government to pass a regulation. In light of these delays, it is our view that on an interim basis it is important that the WCB continue to adjudicate all hardrock mining primary lung cancers under existing policies and on a case by case basis.
I would be pleased to discuss the Report with you. Please let me know when it would be convenient to do so.
1 Working Levels (WLs) and Working Level Months (WLMs) are estimated measurements of human exposure to radon progeny. One Working Level is equivalent to 1.3 x 105 mega electron volts (Mev) of alpha energy per litre of air emitted by any combination of short-lived radon decay products. One WLM is the amount of a person's exposure to radon progeny resulting from breathing air chat contains one WL for a 170 hour period.
1 Workers' Compensation Act General Regulations, R.R.O.1990, Reg. 1102, as amended by O.Reg. 276/92
2 Workers' Compensation Act, R.S.O. 1990, c. W.11, s. 134(10)
3 Workers' Compensation Act General Regulations R.R.O. 1990, Reg. 1102, Schedule 3
4 Workers' Compensation Act, R.S.O. 1990, c. W.11, s. 134(9)
5 "In dealing with questions of causation, the Appeals Tribunal has generally applied a significant contributing factor' test--i.e., when trying to decide whether employment caused' the disability, panels oftern ask: Was the employment a significant contributing factor to the disability?' This is essentially the material contribution' test posed in the case of Bonnington Castings v. Warsaw,  A.C. 613 (H.L.). ... Lord Reid's description of the material contribution' test appears at page 621 of that decision:
The medical evidence was that pneumoconiosis is caused by a gradual accumulation in the lungs of minute particles of silica inhaled over a period of years. That means, I think, that the disease is caused by the whole of the noxious material inhaled and, if that material comes from two sources, it cannot be wholly attributed to material from one source or the other. I am in agreement with much of the Lord President's opinion in this case, but I cannot agree that the question is: which was the most probable source of the respondent's disease, the dust from the pneumatic hammers or the dust from the swing grinders? It appears to me that the source of his disease was the dust from both sources, and the real question is whether the dust from the swing grinders materially contributed to the disease. What is a material contribution must be a question of degree. A contribution which comes within the exception de minimus no curat lex ["the law does not care for, or take notice of, very small or trifling matters"] is not material, but I think any contribution which does not fall withing that exception must be material. I do not see how there can be something too large to come within the de minimus principle but yet too small to be material."
Decision No. 276/92 (May 29, 1992, Strachan, Preston, Rao); see also Decision No. 894/88 (Nov. 15, 1990, McGrath, Guillemette, Fox) at p. 9; Decision No. 699/91 (June 19, 1992, Moore, Ferrari, Apsey); and Decision No. 47/91 (July 7, 1992, Sandomirsky, Lebert, Ronson).
A "significant contribution" may be found found where only 25% of the worker's disease was work-related. Decision No. 1006/88 (June 1, 1992; Kenny, Lebert (Jewell dissenting)) at pp. 21-22.
6 "According to s. 3(1) of the Workers' Compensation Act, benefits are payable when workers suffer personal injury by accident arising in and out of the course of their employment.
"Section 122 of the Act provides for the payment of benefits for the consequences of an industrial disease' as if the disease was a personal injury by accident'. Industrial diseases are diseases either listed in Schedule 3 of the Act or diseases which have been found to be peculiar to and characteristic of a specific industrial process.
"The legislation also includes the concept of disablement arising out of and in the course of employment within the definition of accident. Previous WCAT decisions, specifically 850 [now reported at (1988), 8 W.C.A.T.R. 73 (Thomas, Acheson, Seguin) at 89] and 559/87 [now reported at (1988), 9 W.C.A.T.R. 103 (Ellis, Lankin, Preston) at 147], have extensively analysed the interplay between the industrial disease section and the disablement provisions. The end result of that analysis is that compensation is payable if it can be established that the worker's disability arose from a recognized industrial disease as defined by the Act or was a disablement caused by an injuring process', as long as the work process was a significant contributing factor to the development of the disability."
Decision No. 94/87 (1989), 11 W.C.A.T.R. 20 (Catton, McCombie, Guillemette) at 32; approved of in the following cases: Decision No. 134/89I2 (Oct. 16, 1991, Moore, Sutherland, Fox) at pp. 3-4; Decision No. 407/91I (Nov. 25, 1991, Moore, Lebert, Meslin) at pp. 6-8; Decision No. 875/90F (Jan. 21, 1992, Bradbury, Clarke, Robillard) at pp. 6-7; Decision No. 665/89 (May 1, 1990, Bigras, Jewell, Fox) at pp. 4-5; Decision No. 681/89 (March 13, 1990, Moore, Klym, Nipshagen) at p. 2; Decision No. 1009/89 (Jan. 28, 1991, Bigras, Clarke, McCombie) at p. 8
7 Schedule 3
|COLUMN 1||COLUMN 2|
|Description of disease||Process|
7. Poisoning and its sequelae by
Any process involving the use of arsenic or its
preparations of compounds Any process involving the use of benzol
Any process involving the use of cadmium or
its preparations or compounds
General Regulations to the Workers' Compensation Act, R.R.O. 1990, Reg. 1102, Schedule 3
8 Schedule 3
|COLUMN 1||COLUMN 2|
|Description of disease
9. Any disease due to exposure to
X-rays, radium or other
[There is no corresponding entry on Column
2 for this item.]
General Regulations to the Workers' Compensation Act, R.R.O. 1990, Reg. 1102, Schedule 3
9 Workers' Compensation Board Operational Policy, document no. 04-04-08, effective Nov. 1, 1991. This policy is reprinted at Appendix B to this report.
10 Workers' Compensation Board Operational Policy, document no. 04-04-09, effective November, 1989.
11 Workers' Compensation Board Operational Policy, document no. 04-04-10, effective November 1989. This policy is reprinted at Appendix C to this report.
12 Workers' Compensation Board Operational Policy, document no. 04-04-11, effective November, 1989.
13 Workers' Compensation Board Operational Policy, document no. 04-04-12, effective November, 1989.
1 1. (1) In this Act,
"industrial disease" means a disease caused by the conditions in a place where an industrial process, trade, industry or occupation are carried on;
Workers' Compensation Act, R.S.N.W.T. 1988, c. W-6, s. 1(1)
2 14. ...
(5) Where a worker suffers disablement from or because of an industrial disease and at some time during the 12 months preceding the disablement, the worker was employed in an industry where the worker was exposed to conditions that might reasonably have caused that disease, the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved.
Workers' Compensation Act, R.S.N.W.T. 1988, c. W-6, s. 14(5)
3 "INDUSTRIAL DISEASE CAN BE SEPARATED INTO THREE AREAS:
1. Industrial noise-induced progressive hearing loss and tinnitus.
c. Pulmonary or bronchogenic cancer
3. Other industrial diseases, e.g. industrial dermatitis, fume toxicity, lead absorption, arsenic absorption, infectious diseases, radiation burns."
Policies of the Northwest Territories Workers' Compensation Board, Policy 20-13-01, page 1 (effective 12/81)
4 "Under the Workers' Compensation Act any disease as a result of employment is compensable and each case is adjudicated on its own merits."
Policies of the Yukon Territory Workers' Compensation Board, Policy no. 44, adopted July 21, 1983, and on April 30, 1987
5 No. 44 Reserve for Industrial Diseases
Without limiting adjudication, the following are examples of diseases which shall be charged to the Reserve for Industrial Diseases.
Arsenic, Lead and Mercury Poisoning
Policies of the Yukon Territories Workers' Compensation Board, Policy no. 44, approved April 30, 1987.
6 6. (1) Where
(a) a worker suffers from an industrial disease and is thereby disabled from earning full wages at the work at which he was employed or the death of a worker is caused by an industrial disease; and
(b) the disease is due to the nature or any employment in which the worker was employed, whether under one or more employments,
compensation is payable under this Part as if the disease were a personal injury arising out of and in the course of that employment. Medical aid may be paid although the worker is not disabled from earning full wages at the work at which he was employed.
(2) The date of disablement shall be treated as the occurrence of the injury.
(3) If the worker at or immediately before the date of the disablement was employed in a process or industry mentioned in the second column of Schedule B, and the disease contracted is the disease in the first column of the schedule set opposite to the description of the process, the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved.
(4) (a) The board may, on the terms and conditions and with the limitations the board deems adequate and proper, add to or delete from Schedule B a disease which the board deems to be an industrial disease, and may in like manner add to or delete from the said Schedule a process or industry.
(b) Notwithstanding paragraph (a), the board may designate or recognize a disease as being a disease peculiar to or characteristic of a particular process, trade or occupation on the terms and conditions and with the limitations the board deems adequate and proper.
Workers' Compensation Act, R.S.B.C. 1979, c. 437, s. 6
7 6. ...
(11) Where a deceased worker was, at the date of his death, under the age of 70 years and suffering from an industrial disease of a type that impairs the capacity of function of the lungs, and where the death was caused by some ailment or impairment of the lungs or heart of non-traumatic origin, it shall be conclusively presumed that the death resulted from the industrial disease.
Workers' Compensation Act, R.S.B.C. 1979, c. 437, s. 6
|Description of disease||Description of Process or Industry|
|(e) Primary cancer of the lung||Where there is prolonged exposure to|
|(1) aerosols and gases containing arsenic,
chromium, nickel or their compounds; or
|(2) his (chloromethyl) ether; or|
|(3) the dust of uranium, or radon gas and its
decay products; or
|(4) particulate polycyclic aromatic
Workers' Compensation Act, R.S.B.C. 1979, c. 437, Schedule B
|Description of disease||Description of Process or Industry|
|17. Radiation injury or disease:|
|(a) Due to ionizing radiation||Where there is exposure to ionizing radiation.|
|(b) Due to non-ionizing radiation... ...|
Workers' Compensation Act, R.S.B.C. 1979, c. 437, Schedule B
10 19. ...
(6) If a worker suffers disablement from or because of any occupational disease and at some time during the 12 months preceding the disablement was employed in the industry or process deemed by the regulations to have caused that disease, the disease is deemed to have been caused by that employment unless the contrary is shown.
Workers' Compensation Act, S.A. 1981, c. W-16, s. 19(6)
1. (1) In this Act,
(s) Occupational disease" means occupational disease as defined in the regulations;
Workers' Compensation Act, S.A. 1981, c. W-16, s. (19)(6)
20. (1) For the purposes of the Act and this regulation "occupational disease" means
(a) a disease or condition listed in Column 1 of Schedule B that is caused by employment in the industry or process listed opposite it is Column 2 of Schedule B, and
(b) any other disease or condition that the Board is satisfied in a particular case is caused by employment in an industry to which the Act applies.
(2) For the purposes of subsection (1)(a), employment in an industry or process
(a) listed in Column 2 of Schedule B, and
(b) in the manner and circumstances set out in Column 2 of Schedule B shall, unless the contrary is proven, be deemed to be the cause of the specified disease or condition listed opposite it in Column 1 of Schedule B.
Workers' Compensation Regulation, Alta. Reg. 427/81, as amended, s. 20.
|Column 1||Column 2|
9. Radiation injury or disease
|An industry or process|
|(a) due to ionizing radiation;||(a) where there is sufficient occupational
exposure to ionizing radiation.
Workers' Compensation Regulation, Alta. Reg. 427/81, as amended
12 "Where a person suffers a disease of the respiratory system due in part to occupational factors and in part to non-occupational factors, the overall disability will be presumed to be related to employment."
Claims Department Policy Manual, Policy statement OCC-4, page 1, effective Feb. 23, 1987.
13 1. (1) In this Act,
"accident" means a chance event occasioned by a physical or natural cause; and includes
(a) a wilful and intentional act that is not the act of the worker, and
(i) event arising out of, and in the course of, employment, or
(ii) thing that is done and the doing of which arises out of, and in the course of, employment, and
(c) conditions in a place where an industrial process, trade, or occupation is carried on, that occasion a disease, and as a result of which a worker is disabled;
Workers' Compensation Act, R.S.M. 1987, c. W200, s. 1(1)
14 1. (1) In this Act,
"industrial disease" means any disease that is peculiar to, or characteristic of, an industrial process, trade, or occupation to which Part I applies;
Workers' Compensation Act, R.S.M. 1987, c. W200, s. 1(1)
15 4. (4) Where the personal injury consists of a disease, in part due to the employment and in part due to causes other than the employment, the compensation paid shall be the same proportion of the whole of the compensation that would have been payable had the personal injury been wholly due to the employment as the part of the personal injury that is due to the employment is of the whole of the personal injury.
Workers' Compensation Act, R.S.M. 1987, c. W200, s. 4(4)
16 "Where an injury consists of an occupational disease that is, in the opinion of the board, due in part to the employment of the worker and in part to a cause or causes other than the employment of the worker and in part to a cause or causes other than the employment, the board may determine that the injury is the result of an accident arising out of and in the course of employment only where, in its opinion, the employment is the dominant cause of the occupational disease."
Policy Manual of the Manitoba Workers' Compensation Board, section 44.20, page 2, issued June 1992
"a. The WCB will determine:
1. the existence of a disease,
2. the nature of the disease in question,
3. the circumstances surrounding the manner in which the disease arose.
b. The WCB will then determine if the disease is an occupational disease by applying the criteria in the Workers' Compensation Act and this policy. To be an occupational disease the disease must be:
i) particular to or characteristic of a particular trade or occupation, or
ii) peculiar to the particular employment (of the worker)
As well the disease must be neither:
i) an ordinary disease of life, nor
ii) stress, unless that stress is an acute reaction to a traumatic event
If it is determined that the disease is not an occupational disease, but the claim should be adjudicated as an accident the claim will be subject to the WCB policy on pre-existing conditions and general policy on arising out of and in the course of employment.
c. If it is determined that the disease is an occupational disease the following steps apply:
1. if the WCB determines that there are multiple causes that contributed to the disease, compensability will be contingent upon the worker's employment, on the balance of probabilities, being the dominant cause of the disease. (The dominant cause requirement, in the Act, applies only to the compensability of occupational disease. It does not apply to the claims attributed to workplace accidents even when the accident involves a disease as a pre-existing condition or a disease as a result of an accident.)
2. the disease is not compensable if caused by any change in respect of employment, including promotion, transfer, demotion, lay-off, or termination.
3. Synergistic effects will be considered in the determination of dominant cause. If the synergy is between similar sources (work or non-work), the entire increased effect will be attributed entirely to work or non-work, as the case may be. If the synergy is a combination of work and non-work sources, the WCB will assess the case on the merits of available medical and scientific evidence."
Policy Manual of the Manitoba Workers' Compensation Board, section 44.20, pages 4-5, issued June 1992
"e. dominant cause of the occupational disease'
If the combined effect of the employment causes exceeds the combined effect of the non-employment causes then the work will be deemed to be the dominant cause of the disease."
Policy Manual of the Manitoba Workers' Compensation Board, section 44.20, page 3, issued June 1992
17 "c. ordinary disease of life'
An ordinary disease of life is a disease that can be commonly acquired from a variety of life situations. A disease will not be considered to be an ordinary disease of life if the risk of contracting the disease through the employment can be shown to be greater than the risk associated with ordinary living experience."
Poliy Manual of the Manitoba Workers' Compensation Board, section 44.20, page 3, issued June 1992
18 29. The diseases listed in Schedule I are characteristic of the work appearing opposite each of such diseases on the schedule and are directly related to the risks peculiar to that work.
A worker having contracted a disease contemplated in Schedule I is presumed to have contracted an occupational disease if he has done work corresponding to that disease according to the Schedule.
An Act respecting industrial accidents and occupational diseases, S.Q. 1985, c. 6, s. 29
DISEASES CAUSED BY PHYSICAL AGENTS
|Disease||Type of Work|
|(5) Disease caused by ionizing
|any work involving exposure to ionizing
An Act respecting industrial accidents and occupational diseases, S.Q. 1985, c. 6, Schedule I
20 85. (1) Where a worker suffers from an occupational disease and is thereby disabled or his death is caused by an occupational disease and the disease is due to the nature of any employment in which he was engaged, whether under one or more employments, the worker is or his dependents are entitled to compensation as if the disease was a personal injury by accident and the disablement was the happening of the accident, unless at the time of entering into the employment he wilfully and falsely represented himself in writing as not having previously suffered from the disease.
Workers' Compensation Act, S.N.B., c. W-13, s. 85
21 1. In this Part
"occupational disease" means any disease, which by the regulations, is declared to be an occupational disease and includes any other disease peculiar to or characteristic of a particular industrial process, trade or occupation;
22 13. The following diseases are hereby declared to be industrial diseases:
(c) mercury poisoning or its sequelae caused by any process involving the use of mercury or its preparations or compounds;
(d) phosphorus poisoning or its sequelae caused by any process involving the use of phosphorus or its preparations or compounds;
(e) arsenic poisoning or its sequelae caused by any process involving the use of arsenic or its preparations or compounds;
Workers Compensation Act Regulation, N.B. Reg. 84-66, s. 13.
23 84. ...
(2) If the worker at or immediately before the date of the disablement was employed in any process mentioned in the second column of Schedule A to this Act and the disease contracted is the disease in the first column of said Schedule set opposite to the description of the process, the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved.
Workers' Compensation Act, R.S.N.S. 1989, c. 508, s. 84(2)
24 9. ...
(2) Where the personal injury by accident results in injury or disease due in part to the employment and in part due to causes other than to the employment or here the personal injury aggravates, activates or accelerates a disease or disability existing prior to the injury, compensation shall be payable for such proportion of the disability and disablement as may reasonably be attributed to the personal injury sustained.
Workers' Compensation Act, R.S.N.S. 1989, c. 508, s. 9(2)
|Description of diseases||Description of process|
Arsenic poisoning or its sequelae
|Any process involving the use of arsenic or its preparations or compounds|
Any disease or disability due to exposure to X-rays, radium, or other radioactive substances
|Any process in the refining of radium or other radioactive substances or involving exposure to X-rays|
Workers' Compensation Act, R.S.N.S. 1989, c. 508, Schedule A
26 12. Any coal miner who has worked at the face of a mine or in similar conditions for twenty years or more and who suffers from a loss of lung function will be compensated according to his disability.
Workers' Compensation Act, R.S.N.S. 1989, c. 508, s. 12.
The Nova Scotia Workers' Compensation Board has defined this reference in section 12 to workers who have worked at the U face of a mine" to be a reference to "any coal miner who is/was employed by a coal company and works/worked underground for a period of twenty years or more." The Board has defined "similar conditions" as a reference to "coal miners who are/were employed by a coal company and works/worked at the wash plant, at or near the bankhead or on the shipping /coal piers": Policy Statement, Workers' Compensation Board of Nova Scotia, Code no. 10.11.1, page 1 (issued May 1, 1987).
Lung Cancer in Coke Oven Workers will be considered under the following guidelines.
1. Lung cancer in coke oven workers accepted as an industrial disease as peculiar to and characteristic of exposure to coke oven emissions in the steel industry.
2. Based on medical studies, lung cancer claims shall be favourably considered when the following appropriate combinations of circumstances regarding exposure, latency, and cessation factors apply:
2.1 Persons employed five or more years in full time topside exposure.
2.2 Persons employed for ten or more years in mixed side-oven/topside exposure.
2.3 Persons employed for fifteen or more years in side-oven exposure only.
2.4 The inception (latent) period between first exposure and the acceptance of lung cancer be at least ten years.
2.5 The cessation interval (CI) (time between cessation of occupational risk and appearance of lung cancer) in a smoker shall be fifteen years or less.
2.6 The cessation interval (CI) in a confirmed non-smoker or ex-smoker shall be twenty years or less (see definition below).
3. Claims which do not meet with criteria in (2.) above, be individually judged on their own merits, taking into consideration the variations in intensity and duration of exposure which would cause lung cancer. Where it seems reasonable that lung cancer resulted from exposure to coke oven emissions in the steel industry, consideration shall be given to these cases. The benefit of reasonable doubt applies.
Definition of Smoking
1. Non-Smoker -- A never smoker. A person who has never smoked even occasionally.
2. Ex-Smoker -- A person who has smoked during his lifetime but who has not smoked for the past ten or more years.
3. Smoker -- A person who currently smokes, or who has ceased smoking for less than the previous ten years."
Policy Statement, Nova Scotia Workers' Compensation Board, Code no. 20.15.2, pages 1-2 (issued April 21, 1989)
28 1. In this Act
(j) "industrial disease" means any of the diseases mentioned in the Schedule and any other disease which by the regulations is declared to be an industrial disease;
Workers' Compensation Act, R.S.P.E.I. 1988, Cap. W-7, s. 1(j)
|DESCRIPTION OF DISEASES||DESCRIPTION OF PROCESS|
Arsenic Poisoning or its Sequelae
|Any process involving the use of arsenic or its
preparations or compounds
Workers' Compensation Act, R.S.P.E.I. 1988, Cap. W-7, Schedule
30 78. ...
(3) If a worker referred to in subsection (1) at or immediately before the date of the disablement was employed in any process prescribed and the disease contracted is the prescribed disease associated with the description of the process, the disease shall be deemed to have been due to the nature of that employment unless the contrary is proved.
Workers' Compensation Act, 1983, S.N. 1983, c. 48, s. 78(3)
31 79. (1) Subject to subsections (2) and (3) but notwithstanding any other provision of this Act or the regulations, other than those regulations referred to in subsection (2), where
(a) a worker suffers from a chronic obstructive pulmonary disease or from silicosis or carcinoma and is thereby disabled from earning full wages at the work at which he was employed, or his death is or was, as the case may be, caused by such disease and such worker was employed at any time, whether before or after the first day of January, 1951, in fluorspar extraction, or both, at St. Lawrence; or
the disease or disability suffered by such worker or his death, as the case may be, shall be deemed to be due to the nature of the employment in the said mines unless it is traceable to other employment and the worker or, if the worker is dead or dies, his dependents are entitled to compensation
(c) from the date referred to in subsection (4); or
(d) from the date of disability or death, as the case may be,whichever is later, as if the disease were an injury arising out of and in the course of his employment in the said mines and the disablement or death, as the case may be, were the happening of the injury.
Workers' Compensation Act, R.S.N. 1983, c. 48, s. 79
32 28. Industrial Diseases. Pursuant to subsection (2) of section 78 of the Act the following sets out industrial diseases and associates descriptions of processes with the diseases:
|Industrial Disease||Description of process|
2. Bronchopulmonary diseases caused by hard metal dust.
|All work involving exposure to the risk concerned.|
7. Diseases caused by cadmium or its toxic compounds.
|All work involving exposure to the risk concerned.|
9. Diseases caused by chromium or its toxic compounds.
|All work involving exposure to the risk concerned.|
11. Diseases caused by arsenic or its toxic compounds.
|All work involving exposure to the risk concerned.|
25. Diseases caused by ionising radiations.
|All work involving exposure to the action of ionising radiations.|
Workers' Compensation Regulations, 1984, Nfld. Reg. 330/83, as amended.
33 94B. (1) Notwithstanding the provisions of any general or special law to the contrary, any condition of cancer affecting the skin or the central nervous, lymphatic, digestive, haematological, urinary, skeletal, oral or prostate systems, resulting in total disability or death to a uniformed member of a paid fire department, or to any permanent crash crewman, crash boatman, fire controlman or assistant fire controlman employed at the General Edward Lawrence Logan International Airport, shall, if he successfully passed a physical examination on entry into such service or subsequent to such entry, which examination failed to reveal any evidence of such condition, be presumed to have been suffered in the line of duty, unless it is shown by a preponderance of the evidence that non-service connected risk factors or non-service connected accidents or hazards undergone, or any combination thereof, caused such incapacity. The provisions of this section shall only apply if the disabling or fatal condition is a type of cancer which may, in general, result from exposure to heat, radiation, or a known or suspected carcinogen as determined by the International Agency for Research on Cancer, so called.
(2) The provisions of this section shall not apply to any person serving in such positions for fewer than five years at the time that such condition is first discovered, or should have been discovered. Any person first discovering any such condition within five years of the last date on which such person actively so served shall be eligible to apply for benefits hereunder, and such benefits, if granted, shall be payable as of the date on which the employee last received regular compensation. The provisions of this sections shall not apply to any person serving in such position unless such person shall first establish that he has regularly responded to calls of fire during some portion of the period of his service in such position.
(3) The provisions of this section shall also apply to any condition of cancer, other than those listed in subdivision (1), which, in general, may result from exposure to heat or radiation or to a known or suspected carcinogen as determined by said International Agency for Research on Cancer, so-called, and the incidence of which is found by regulation by the commissioner of the department of public health to have a statistically significant correlation with fire service.
General Laws of Massachusetts, c. 32, s. 94B, as amended by the 1990 statutes, c. 100.