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The 1891-1920 birth cohort of Quebec chrysotile miners and millers: development from 1904 and mortality to 1992.

https://arctichealth.org/en/permalink/ahliterature210233
Source
Ann Occup Hyg. 1997 Jan;41(1):13-36
Publication Type
Article
Date
Jan-1997
Author
F D Liddell
A D McDonald
J C McDonald
Author Affiliation
Department of Epidemiology and Biostatistics, McGill University Montreal, Canada.
Source
Ann Occup Hyg. 1997 Jan;41(1):13-36
Date
Jan-1997
Language
English
Publication Type
Article
Keywords
Aged
Air Pollutants, Occupational - adverse effects
Asbestos, Serpentine - adverse effects
Asbestosis - etiology - mortality
Cause of Death
Cohort Studies
Environmental monitoring
Epidemiological Monitoring
Humans
Male
Mesothelioma - etiology - mortality
Mining - statistics & numerical data
Neoplasms - etiology - mortality
Quebec - epidemiology
Abstract
This paper draws together the mortality experience for a cohort of some 11000 male Quebec Chrysotile miners and millers, reported at intervals since 1971 and now again updated. Of the 10918 men in the complete cohort, 1138 were lost to view, almost all never traced after employment of only a month or two before 1935; the other 9780 men were traced into 1992. Of these, 8009 (82%) are known to have died: 657 from lung cancer, 38 from mesotheliona, 1205 from other malignant disease, 108 from pneumoconiosis and 561 from other non-malignant respiratory diseases (excluding tuberculosis). After early fluctuations. SMRs (all causes) against Quebec rates have been reasonably steady since about 1945. For men first employed in Asbestos, mine or factory, they were very much what might have been expected for a blue collar population without any hazardous exposure. SMRs in the Thetford Mines area were almost 8% higher, but in line with anecdotal evidence concerning socio-economic status. At exposures below 300 (million particles per cubic foot) x years, (mpcf.y), equivalent to roughly 1000 (fibres/ml) x years-or, say, 10 years in the 1940s at 80 (fibres/ml)-findings were as follows. There were no discernible associations of degree of exposure and SMRs, whether for all causes of death or for all the specific cancer sites examined. The average SMRs were 1.07 (all causes), and 1.16, 0.93, 1.03 and 1.21, respectively, for gastric, other abdominal, laryngeal and lung cancer. Men whose exposures were less then 300 mpcf.y suffered almost one-half of the 146 deaths from pneumoconiosis or mesothelioma; the elimination of these two causes would have reduced these men's SMR (all causes) from 1.07 to approximately 1.06. Thus it is concluded from the viewpoint of mortality that exposure in this industry to less than 300 mpcf.y has been essentially innocuous, although there was a small risk or pneumoconiosis or mesothelioma. Higher exposures have, however, led to excesses, increasing with degree of exposure, of mortality from all causes, and from lung cancer and stomach cancer, but such exposures, of at least 300 mpcf.y, are several orders of magnitude more severe than any that have been seen for many years. The effects of cigarette smoking were much more deleterious than those of dust exposure, not only for lung cancer (the SMR for smokers of 20+ cigarettes a day being 4.6 times higher than that for non-smokers), but also for stomach cancer (2.0 times higher), laryngeal cancer (2.9 times higher), and-most importantly-for all causes (1.6 times higher).
Notes
Comment In: Ann Occup Hyg. 1997 Jan;41(1):3-129072948
Comment In: Ann Occup Hyg. 2001 Jun;45(4):329-35; author reply 336-811414250
PubMed ID
9072947 View in PubMed
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The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-88.

https://arctichealth.org/en/permalink/ahliterature219707
Source
Br J Ind Med. 1993 Dec;50(12):1073-81
Publication Type
Article
Date
Dec-1993
Author
J C McDonald
F D Liddell
A. Dufresne
A D McDonald
Author Affiliation
School of Occupational Health, McGill University, Montreal, Canada.
Source
Br J Ind Med. 1993 Dec;50(12):1073-81
Date
Dec-1993
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Asbestos, Serpentine
Asbestosis - mortality
Cause of Death
Cohort Studies
Humans
Lung Neoplasms - mortality
Male
Mesothelioma - mortality
Middle Aged
Mining
Occupational Exposure
Quebec - epidemiology
Smoking - mortality
Time Factors
Abstract
A cohort of some 11,000 men born 1891-1920 and employed for at least one month in the chrysotile mines and mills of Quebec, was established in 1966 and has been followed ever since. Of the 5351 men surviving into 1976, only 16 could not be traced; 2508 were still alive in 1989, and 2827 had died; by the end of 1992 a further 698 were known to have died, giving an overall mortality of almost 80%. This paper presents the results of analysis of mortality for the period 1976 to 1988 inclusive, obtained by the subject-years method, with Quebec mortality for reference. In many respects the standardised mortality ratios (SMRs) 20 years or more after first employment were similar to those for the period 1951-75--namely, all causes 1.07 (1951-75, 1.09); heart disease 1.02 (1.04); cerebrovascular disease 1.06 (1.07); external causes 1.17 (1.17). The SMR for lung cancer, however, rose from 1.25 to 1.39 and deaths from mesothelioma increased from eight (10 before review) to 25; deaths from respiratory tuberculosis fell from 57 to five. Among men whose exposure by age 55 was at least 300 million particles per cubic foot x years (mpcf.y), the SMR (all causes) was elevated in the two main mining regions, Asbestos and Thetford Mines, and for the small factory in Asbestos; so were the SMRs for lung cancer, ischaemic heart disease, cerebrovascular disease, and respiratory disease other than pneumoconiosis. Except for lung cancer, however, there was little convincing evidence of gradients over four classes of exposure, divided at 30, 100, and 300 mpcf.y. Over seven narrower categories of exposure up to 300 mpcf.y the SMR for lung cancer fluctuated around 1.27 with no indication of trend, but increased steeply above that level. Mortality form pneumoconiosis was strongly related to exposure, and the trend for mesothelioma was not dissimilar. Mortality generally was related systematically to cigarette smoking habit, recorded in life from 99% of survivors into 1976; smokers of 20 or more cigarettes a day had the highest SMRs not only for lung cancer but also for all causes, cancer of the stomach, pancreas, and larynx, and ischaemic heart disease. For lung cancer SMRs increased fivefold with smoking, but the increase with dust exposure was comparatively slight for non-smokers, lower again for ex-smokers, and negligible for smokers of at least 20 cigarettes a day; thus the asbestos-smoking interaction was less than multiplicative. Of the 33 deaths from mesothelioma in the cohort to date, 28 were in miners and millers and five were in employees of a small asbestos products factory where commercial amphiboles had also been used. Preliminary analysis also suggest that the risk of mesothelioma was higher in the mines and mills at Thetford Mines than in those at Asbestos. More detailed studies of these differences and of exposure-response relations for lung cancer are under way.
Notes
Cites: Br J Ind Med. 1980 Feb;37(1):11-247370189
Cites: Br J Cancer. 1982 Jan;45(1):124-357059455
Cites: Biometrics. 1983 Mar;39(1):173-846871346
Cites: Br J Ind Med. 1987 Jun;44(6):396-4013606968
Cites: Ann N Y Acad Sci. 1979;330:91-116294225
Cites: Br J Ind Med. 1992 Aug;49(8):566-751325180
Cites: Arch Environ Health. 1971 Jun;22(6):677-865574010
Cites: Arch Environ Health. 1972 Mar;24(3):189-975059627
Cites: Br J Ind Med. 1991 Aug;48(8):543-71878311
PubMed ID
8280638 View in PubMed
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Cancer occurrence among European mercury miners.

https://arctichealth.org/en/permalink/ahliterature21128
Source
Cancer Causes Control. 1998 Dec;9(6):591-9
Publication Type
Article
Date
Dec-1998
Author
P. Boffetta
M. Garcia-Gómez
V. Pompe-Kirn
D. Zaridze
T. Bellander
M. Bulbulyan
J D Caballero
F. Ceccarelli
D. Colin
T. Dizdarevic
S. Español
A. Kobal
N. Petrova
G. Sällsten
E. Merler
Author Affiliation
Unit of Environmental Cancer Epidemiology, International Agency for Research on Cancer, Lyon, France. boffetta@iarc.fr
Source
Cancer Causes Control. 1998 Dec;9(6):591-9
Date
Dec-1998
Language
English
Publication Type
Article
Keywords
Carcinogens - adverse effects
Cohort Studies
Europe - epidemiology
Female
Follow-Up Studies
Humans
Male
Mercury - adverse effects
Mining
Neoplasms - chemically induced - mortality
Occupational Diseases - chemically induced - mortality
Occupational Exposure - adverse effects
Research Support, Non-U.S. Gov't
Abstract
OBJECTIVES: To study the carcinogenicity of inorganic mercury in humans. METHODS: We studied the mortality from cancer among 6784 male and 265 female workers of four mercury mines and mills in Spain, Slovenia, Italy and the Ukraine. Workers were employed between the beginning of the century and 1990; the follow-up period lasted from the 1950s to the 1990s. We compared the mortality of the workers with national reference rates. RESULTS: Among men, there was no overall excess cancer mortality; an increase was observed in mortality from lung cancer (standardized mortality ratio [SMR] 1.19, 95 percent confidence interval [CI] 1.03-1.38) and liver cancer (SMR 1.64, CI 1.18-2.22). The increase in lung cancer risk was restricted to workers from Slovenia and the Ukraine: no relationship was found with duration of employment or estimated mercu ry exposure. The increase in liver cancer risk was present both among miners and millers and was stronger in workers from Italy and Slovenia: there was a trend with estimated cumulative exposure but not with duration of employment, and the excess was not present in a parallel analysis of cancer incidence among workers from Slovenia. No increase was observed for other types of cancer, including brain and kidney tumours. Among female workers (Ukraine only), three deaths occurred from ovarian cancer, likely representing an excess. CONCLUSIONS: Exposure to inorganic mercury in mines and mills does not seem strongly associated with cancer risk, with the possible exception of liver cancer; the increase in lung cancer may be explained by co-exposure to crystalline silica and radon.
PubMed ID
10189044 View in PubMed
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Carcinoma of the lung in Ontario gold miners: possible aetiological factors.

https://arctichealth.org/en/permalink/ahliterature225366
Source
Br J Ind Med. 1991 Dec;48(12):808-17
Publication Type
Article
Date
Dec-1991
Author
R A Kusiak
J. Springer
A C Ritchie
J. Muller
Author Affiliation
Health and Safety Studies Unit, Ontario Ministry of Labour, Toronto, Canada.
Source
Br J Ind Med. 1991 Dec;48(12):808-17
Date
Dec-1991
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - etiology - mortality
Arsenic - adverse effects
Canada
Carcinoma, Non-Small-Cell Lung - etiology - mortality
Carcinoma, Squamous Cell - etiology - mortality
Cohort Studies
Geological Phenomena
Geology
Gold
Humans
Lung Neoplasms - etiology - mortality
Male
Middle Aged
Mining
Nickel
Occupational Diseases - etiology - mortality
Occupational Exposure - adverse effects
Radon - adverse effects
Smoking - adverse effects
Time Factors
Abstract
A cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.
Notes
Cites: J Natl Cancer Inst. 1988 Nov 2;80(17):1404-73172266
Cites: Am J Ind Med. 1987;11(1):15-263028136
Cites: Br J Ind Med. 1979 Aug;36(3):199-205315411
Cites: Cancer. 1977 Apr;39(4):1647-55192433
Cites: Am Rev Respir Dis. 1979 Nov;120(5):1025-9228572
Cites: Am J Public Health. 1980 Dec;70(12):1261-87435743
Cites: Biometrics. 1983 Sep;39(3):665-746652201
Cites: Cancer. 1981 Mar 1;47(5):1042-66261919
Cites: Am J Ind Med. 1982;3(4):423-406301270
Cites: Br J Ind Med. 1989 Dec;46(12):881-62611163
Cites: Toxicol Ind Health. 1989 Dec;5(6):975-932626765
Cites: Br J Ind Med. 1989 Aug;46(8):529-362550048
Cites: Br J Ind Med. 1989 May;46(5):289-912546576
Cites: Am J Ind Med. 1985;7(4):285-942986455
PubMed ID
1663386 View in PubMed
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[Changes in the blood concentrations of interleukins and electrolytes in miners working in deep coal mines]

https://arctichealth.org/en/permalink/ahliterature74962
Source
Lik Sprava. 2001 Sep-Dec;(5-6):178-80
Publication Type
Article
Author
Belkina, EB
Rebrov, BA
Rebrova, OA
Stroilo, NG
Voloshinovich, AR
Source
Lik Sprava. 2001 Sep-Dec;(5-6):178-80
Language
Russian
Publication Type
Article
Keywords
Adult
Coal Mining
Cohort Studies
Comparative Study
Electrolytes - blood
English Abstract
Health status
Humans
Interleukin-6 - blood
Interleukins - blood
Male
Middle Aged
Occupational Diseases - blood
Potassium - blood
Sodium - blood
Ukraine
Work - physiology
Abstract
Miners working in deep coal mines, engaged in hard physical work under most harsh mine conditions demonstrate a striking imbalance between pro- and antiinflammatory cytokines and a rise in the blood levels of electrolytes K+ and Na+ as well. The analysis performed revealed a direct correlation between the level of blood concentration of IL-6 and that of K+, Na+.
PubMed ID
11881367 View in PubMed
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Chrysotile, tremolite, and mesothelioma.

https://arctichealth.org/en/permalink/ahliterature215812
Source
Science. 1995 Feb 10;267(5199):776-7
Publication Type
Article
Date
Feb-10-1995

Classification of chest radiographs for pneumoconiosis: a comparison of two methods of reading.

https://arctichealth.org/en/permalink/ahliterature222647
Source
Br J Ind Med. 1992 Dec;49(12):869-71
Publication Type
Article
Date
Dec-1992
Author
D C Muir
C D Bernholz
W K Morgan
J O Roos
J. Chan
W. Maehle
J A Julian
A. Sebestyen
Author Affiliation
Occupational Health Program, McMaster University, Hamilton, Ontario, Canada.
Source
Br J Ind Med. 1992 Dec;49(12):869-71
Date
Dec-1992
Language
English
Publication Type
Article
Keywords
Cohort Studies
Humans
Lung - pathology - radiography
Mining
Observer Variation
Ontario - epidemiology
Pneumoconiosis - epidemiology - pathology - radiography
Technology, Radiologic - methods
Notes
Cites: Am J Ind Med. 1989;16(1):5-112750750
Cites: J Clin Epidemiol. 1988;41(10):949-583057117
Cites: Am J Epidemiol. 1987 Aug;126(2):161-93300279
Cites: Br J Ind Med. 1951 Jul;8(3):138-4914858773
Cites: Ann Occup Hyg. 1982;26(1-4):401-96295243
Cites: Br J Ind Med. 1960 Oct;17:279-9213698433
Cites: Arch Environ Health. 1966 Mar;12(3):314-305904510
PubMed ID
1472446 View in PubMed
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Clinical measures, smoking, radon exposure, and risk of lung cancer in uranium miners.

https://arctichealth.org/en/permalink/ahliterature210925
Source
Occup Environ Med. 1996 Oct;53(10):697-702
Publication Type
Article
Date
Oct-1996
Author
M M Finkelstein
Author Affiliation
Ontario Ministry of Labour, Toronto, Canada.
Source
Occup Environ Med. 1996 Oct;53(10):697-702
Date
Oct-1996
Language
English
Publication Type
Article
Keywords
Air Pollutants, Radioactive - adverse effects
Cause of Death
Cohort Studies
Forced expiratory volume
Humans
Incidence
Lung Neoplasms - chemically induced - epidemiology
Mining
Occupational Exposure - adverse effects
Ontario - epidemiology
Radon - adverse effects
Regression Analysis
Silicosis - etiology
Smoking - adverse effects
Time Factors
Uranium
Abstract
Exposure to the radioactive daughters of radon is associated with increased risk of lung cancer in mining populations. An investigation of incidence of lung cancer following a clinical survey of Ontario uranium miners was undertaken to explore whether risk associated with radon is modified by factors including smoking, radiographic silicosis, clinical symptoms, the results of lung function testing, and the temporal pattern of radon exposure.
Miners were examined in 1974 by a respiratory questionnaire, tests of lung function, and chest radiography. A random selection of 733 (75%) of the original 973 participants was followed up by linkage to the Ontario Mortality and Cancer Registries.
Incidence of lung cancer was increased threefold. Risk of lung cancer among miners who had stopped smoking was half that of men who continued to smoke. There was no interaction between smoking and radon exposure. Men with lung function test results consistent with airways obstruction had an increased risk of lung cancer, even after adjustment for cigarette smoking. There was no association between radiographic silicosis and risk of lung cancer. Lung cancer was associated with exposures to radon daughters accumulated in a time window four to 14 years before diagnosis, but there was little association with exposures incurred earlier than 14 years before diagnosis. Among the men diagnosed with lung cancer, the mean and median dose rates were 2.6 working level months (WLM) a year and 1.8 WLM/year in the four to 14 year exposure window.
Risk of lung cancer associated with radon is modified by dose and time from exposure. Risk can be substantially decreased by stopping smoking.
Notes
Cites: J Occup Med. 1985 Sep;27(9):644-504045575
Cites: Int J Epidemiol. 1986 Mar;15(1):134-73754239
Cites: Int J Cancer. 1990 Jan 15;45(1):26-332404878
Cites: Am J Epidemiol. 1990 Aug;132(2):265-742372006
Cites: Am Rev Respir Dis. 1991 Aug;144(2):307-111859052
Cites: CMAJ. 1995 Jan 1;152(1):37-437804920
Cites: Br J Ind Med. 1993 Oct;50(10):920-88217852
Cites: Am J Epidemiol. 1994 Aug 15;140(4):323-328059767
Cites: Am J Epidemiol. 1994 Aug 15;140(4):333-98059768
Cites: BMJ. 1994 Oct 8;309(6959):901-117755693
Cites: J Natl Cancer Inst. 1993 Mar 17;85(6):422-38445662
PubMed ID
8943835 View in PubMed
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The combination of effects on lung cancer of cigarette smoking and exposure in quebec chrysotile miners and millers.

https://arctichealth.org/en/permalink/ahliterature190229
Source
Ann Occup Hyg. 2002 Jan;46(1):5-13
Publication Type
Article
Date
Jan-2002
Author
F D K Liddell
B G Armstrong
Author Affiliation
Department of Epidemiology and Biostatistics, McGill University, Montreal, Canada.
Source
Ann Occup Hyg. 2002 Jan;46(1):5-13
Date
Jan-2002
Language
English
Publication Type
Article
Keywords
Air Pollutants, Occupational - adverse effects
Asbestos, Serpentine - adverse effects
Causality
Cause of Death
Cohort Studies
Humans
Lung Neoplasms - etiology
Male
Mining
Models, Statistical
Quebec
Risk assessment
Smoking - adverse effects
Abstract
Although it is well known that both cigarette smoke and microscopic airborne asbestos fibres can cause lung cancer, evidence as to how these two agents combine is nebulous. Many workers have believed in the multiplicative theory, whereby asbestos increases the risk in proportion to the risk from other causes. However, evidence against this theory is mounting: a recent review concluded that the multiplicative hypothesis was untenable, and that the relative risk of lung cancer from asbestos exposure was about twice as high in non-smokers as in smokers, a finding largely independent of type of asbestos fibre. The criteria for entry to the current study were met by 7279 men in the 1891-1920 birth cohort of Quebec chrysotile miners and millers. The data consisted of date of birth, place of employment, smoking habit, asbestos exposure accumulated to age 55 and, for those 5527 who died between 1950 and June 1992, date and cause of death; 533 of the deaths were from lung cancer. For the principal analyses, ex-smokers were excluded from the study cohort, which comprised 5888 men, of whom 473 died of lung cancer. The conventional form of analysis is simply of the double dichotomy: non-smokers of cigarettes, 'unexposed' and exposed; all others, 'unexposed' and exposed. The respective standardized lung cancer mortality ratios (SMRs) were 0.29 and 0.62; and 1.37 and 1.72. Thus, the differences in relative risk, due to exposure, were closely similar, 0.33 and 0.35. On the other hand, the effects of asbestos measured by the corresponding ratios, 2.12 and 1.25, did differ, being 1.7 times as high in non-smokers as in others. The principal analysis was much more penetrating: the method was to fit models to a 'disaggregated' 6 x 10 array, by smoking habit (excluding ex-smokers) and asbestos exposure, of lung cancer SMRs. Both linear and log-linear models were fitted: the former included the additive and linear-multiplicative; the latter embraced the more conventional multiplicative form. The additive model fitted much the best. The fit of each multiplicative model was improved by the introduction of an interaction term that implied a less than multiplicative relationship. Thus smoking and exposure to chrysotile appear to have acted independently in causing lung cancer, with 10 cigarettes a day having an effect roughly equivalent to exposure amounting to 700 million particles per cubic foot x years. The refutation of the multiplicative hypothesis in these data reinforces its inapplicability in general; but the additive hypothesis is not generally applicable either. Indeed, there seems to be no good reason to believe that interactions conform to any simple theory. The implications are important.
PubMed ID
12005133 View in PubMed
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Components and modifiers of the healthy worker effect: evidence from three occupational cohorts and implications for industrial compensation.

https://arctichealth.org/en/permalink/ahliterature232124
Source
Am J Epidemiol. 1988 Dec;128(6):1364-75
Publication Type
Article
Date
Dec-1988
Author
G R Howe
A M Chiarelli
J P Lindsay
Author Affiliation
National Cancer Institute of Canada Epidemiology Unit, University of Toronto, Ontario.
Source
Am J Epidemiol. 1988 Dec;128(6):1364-75
Date
Dec-1988
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Canada
Cohort Studies
Environmental Exposure
Female
Health
Health status
Humans
Male
Middle Aged
Mining
Mortality
Nuclear Energy
Occupations
Workers' Compensation
Abstract
The authors examined the components and modifiers of the healthy worker effect using mortality data from three occupational cohorts: the employees of Atomic Energy of Canada Limited followed between 1950 and 1981, a 10% sample of the Canadian labor force followed between 1965 and 1979, and workers at the Eldorado Resources Limited Beaverlodge uranium mine followed between 1950 and 1980. Two important components of the healthy worker effect have been identified in these cohorts, namely, initial selection of and continuing employment of healthy individuals. There is less evidence for a contribution from the existence of differential risk factors among employed individuals as compared with the general population. The healthy worker effect is, however, substantially modified by time since employment, sex, age, specific cause of death, and specific occupation. Because of this variation, it is inappropriate to account for the healthy worker effect by a single parameter, and all of the above factors must be taken into account in any appropriate analysis. When the only available comparison group for an occupational cohort is the general population, the healthy worker effect is unlikely to have any substantial influence on the process of assessing causality for any observed association or attributing cause in an individual case. This would be particularly true for cancer, and even more so for lung cancer, a disease often associated with industrial compensation cases.
PubMed ID
2973746 View in PubMed
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39 records – page 1 of 4.