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Oral Session 8 – Mortality studies: cancer and cardiovascular

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B. H. Alexander1, G. W. Olsen2, J. M. Burris2, J. H. Mandel2, J. S. Mandel3.1Division of Environmental Health Sciences, School of Public Health, University of Minnesota, Minneapolis, MN, USA; 23M Company, St. Paul, MN, USA; 3Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA

Introduction: Ammonium perfluorooctanoate (APFO), a synthetic surfactant used in industrial applications, dissociates in biological media to perfluorooctanoate (PFOA). APFO is a peroxisome proliferator and is associated with lipid metabolism interference and frequency of liver, Leydig cell, and pancreatic acinar tumours in laboratory animals. We present the results of a cohort mortality study of APFO production workers.

Methods: A retrospective cohort mortality study followed 3992 employees of an APFO production site. Cohort members were assigned to one of three exposure groups based on their work history: no, probable, and definite exposure to PFOA. Standardised mortality ratios (SMR) with 95% confidence intervals were calculated for all cause and cause specific mortality for the entire study cohort and the three exposure groups.

Results: A total of 607 deaths from all causes (SMR 0.85; 95% confidence interval (CI) 0.78 to 0.92) and 172 deaths from cancer (SMR 0.84; 95% CI 0.72 to 0.98) were observed in the cohort. No association was observed between PFOA exposure and all cause mortality or all cancer mortality. Workers with definite or probable PFOA exposure did not have elevated rates of mortality from liver cancer (SMR 0.59; 95% CI 0.01 to 3.27) or pancreatic cancer (SMR 1.44; 95% CI 0.53 to 3.13). A modest increased risk of death from cerebrovascular disease was observed in the subcohort with definite PFOA exposure (five observed, 1.94 expected; SMR 2.58; 95% CI 0.84 to 6.03).

Conclusion: In this study occupational exposure to PFOA was not associated with cancer mortality, including liver or pancreatic cancer; however, these findings are based on few cases. The basis for the observed PFOA-CVD association remains to be elucidated, and the possibility of a chance finding cannot be ruled out. Additional follow up of this cohort will clarify potential health effects of APFO and PFOA exposure.


A. ’t Mannetje1, D. McLean1,2, S. Cheng1, P. Boffetta2, D. Colin2, N. Pearce1.1Centre for Public Health Research, Research School of Public Health, Massey University, Wellington, New Zealand; 2International Agency for Research on Cancer, Unit of Environmental Cancer Epidemiology, Lyon, France

Introduction: Chlorophenoxy herbicides have been produced and used extensively in New Zealand from the late 1950s until 1987. During production, 2,4,5-T and its intermediates, such as chlorophenols, are contaminated with the highly toxic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Studies in occupationally or accidentally exposed populations have reported an increased risk of cancer related to chlorophenoxy herbicides and TCDD. Here we evaluate mortality in New Zealand phenoxy herbicide producers and sprayers.

Methods: Producers (n = 1025) and sprayers (n = 703) were followed up from 1 January 1969 and 1 January 1973, respectively, to 31 December 2000. Of these, 813 producers and 699 sprayers were classified as exposed to dioxin and phenoxy herbicides. Standardised mortality ratios (SMR) were calculated using national mortality rates.

Results: At end of follow up, 164 producers and 91 sprayers had died. Cancer mortality was reduced for sprayers (SMR 0.82; 95% confidence interval (CI) 0.57 to 1.14) and increased in exposed production workers (SMR 1.24; 95% CI 0.90 to 1.67), especially for synthesis workers (SMR 1.69), formulation and laboratory workers (SMR 1.64), and maintenance/waste treatment/cleaning workers (SMR 1.46). Lymphohaematopoietic cancer mortality was elevated in exposed production workers (SMR 1.65; 95% CI 0.53 to 3.85), especially for multiple myeloma (SMR 5.51; 95% CI 1.14 to 16.1). Among sprayers, there was a higher incidence of mortality from colon cancer (SMR 1.94; 95% CI 0.84 to 3.83).

Conclusions: We observed a non-significant excess cancer mortality of 24% in phenoxy herbicide producers, with a significant excess for multiple myeloma. Associations were stronger for those exposed to multiple agents including dioxin during production. Overall cancer mortality was not increased for producers and sprayers mainly handling final technical products, although they were likely to have been exposed to TCDD levels far higher than those currently in the general New Zealand population.


R. R. Habib1, S. M. Abdallah2, M. Law3, J. Kaldor3.1Faculty of Health Sciences, American University of Beirut, Lebanon; 2Faculty of Engineering and Architecture, American University of Beirut, Lebanon; 3National Centre in HIV Epidemiology and Clinical Research, UNSW, Sydney, Australia

Introduction: The retrospective cohort study at LHSTC assessed workers’ levels of cancer incidence and mortality, studied the association between external exposure to chronic low level ionising radiation and cancer occurrence, and contributed to an international study coordinated by the International Agency for Research on Cancer.

Methods: Data on workers were abstracted from company records. Deaths and cancer registrations were identified through electronic linkage of records with New South Wales and national case registers. Three inception cohorts, reflecting the coverage of follow up achieved, and comprising 4717 workers in employment between 1972–98, 4523 between 1972–96, and 3543 between 1980–98, were used to examine cancer mortality, cancer incidence, and all cause mortality respectively.

Results: All cause mortality was 31% lower than the national rates; all cancer mortality and incidence were 19% and 15% below the NSW rates respectively. Statistically significant excesses relative to NSW rates were observed for pleural cancer mortality (SMR 21.11; 95% confidence interval (CI) 8.79 to 50.72) and incidence (17.71; 95% CI 7.96 to 39.43), and for incidence of cancer of the small intestine (4.34; 95% CI 1.40 to 13.46). Cancer cases unrelated to smoking were elevated in monitored relative to non-monitored workers (relative risk (RR) 1.52; 95% CI 1.00 to 2.31); 10 year lagged dose. Similar results were found in registrations of radiosensitive solid cancers when exposures were not lagged (RR 1.80; 1.02 to 3.19). A statistically significant (p⩽0.05) positive association was observed between 10 year lagged cumulative external radiation dose and lung cancer mortality (p = 0.054) and incidence (p = 0.011). Similar results were seen for incidence, but not for mortality, of both colon cancer (p = 0.024) and radiosensitive solid cancers (p = 0.020).

Conclusion: Given the lack of an established association with radiation exposure and the strong link to asbestos, the increased risk of pleural cancer was probably due to unmeasured exposures. Results for cancer of the small intestine were based on small numbers and were difficult to interpret. Results for lung cancer were compatible with other studies; those for colon cancer have not been previously reported. Results for radiosensitive solid cancers were largely influenced by lung and colon cancers, which made up 50% of all radiosensitive solid cancer cases. Confounding with other factors such as smoking habits could not be ruled out.


I. Burstyn1,2,3, H. Kromhout1, O. Svane4, S. Langård5, W. Ahrens6, T. Kauppinen7, I. Stücker8, J. Shaham9, D. Heederik1, P. Boffetta2,10, and the Asphalt StudyGroup.1Institute for Risk Assessment Sciences, Utrecht, The Netherlands; 2The International Agency for Research on Cancer, Lyon, France; 3The University of Alberta, Edmonton, Canada; 4Danish Working Environment Service, Copenhagen, Denmark; 5Rikshospitalet University Hospital, Oslo, Norway; 6Bremen Institute for Prevention Research and Social Medicine, Bremen, Germany; 7Finnish Institute of Occupational Health, Helsinki, Finland; 8INSERM U170, Villejuif, France; 9National Institute of Occupational and Environmental Health, Raanana, Israel; 10German Cancer Research Center, Heidelberg, Germany

Introduction: There is some evidence that occupational exposure to polycyclic aromatic hydrocarbons (PAH) is a risk factor for ischaemic heart disease (IHD), but exposure–response relationships have not been demonstrated.

Methods: We studied a relationship between mortality from IHD (418 cases) and exposure to PAH in a cohort of 12 367 male asphalt workers from Denmark, Finland, France, Germany, Israel, the Netherlands, and Norway. The earliest follow up (country specific) started in 1953 and the latest ended in 2000 (average duration 17 years). Exposures to benzo(a)pyrene (proxy for all 4–6 ring PAH) were assessed quantitatively using a measurement driven statistical model. Exposure to coal tar was assessed in a semi-quantitative manner on the basis of information supplied by company representatives. Sensitivity analyses were carried out to assess potential confounding by tobacco smoking.

Results: Both cumulative and average exposure to benzo(a)pyrene were positively associated with mortality from IHD, showing monotonic increase in risk. The highest relative risk (1.64; 95% confidence interval (CI) 1.13 to 2.38) was observed for average benzo(a)pyrene exposures in excess of 273 ng/m3. Similar results were obtained for coal tar exposure. In a realistic scenario of confounding by smoking, we would still observe an approximately 20–40% excess risk in IHD in the highest PAH exposure categories.

Conclusions: Our results lend support to the hypothesis that occupational PAH exposure causes fatal IHD and for the first time demonstrates consistent exposure–response relationships for this association.


B. Persson1, A. Magnusson2, H. Westberg3, E. Andersson4, K. Torén4, G. Wingren5.1Department of Occupational and Environmental Medicine, University Hospital, Linköping, Sweden; 2Center for Clinical Research and 3Department of Occupational and Environmental Medicine, University Hospital, Örebro, Sweden; 4Department of Occupational and Environmental Medicine, Sahlgrenska University Hospital, Göteborg, Sweden; 5Division of Occupational and Environmental Medicine, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping, Sweden

Introduction: Many diseases, not only malignant conditions but also cardiovascular and respiratory disorders and diabetes mellitus, have been associated with work in pulp and paper production. The present study focuses on cardiovascular mortality in relation to various exposures in this type of industry.

Methods: The present cohort encompasses workers from three major old mills in the middle of Sweden with at least 1 year of continuous employment. The cohort was followed up for mortality in the national Causes of Death Register. Deaths from diseases of the circulatory system (ICD8 390–458) were considered, along with ischaemic heart diseases (ICD8 410–414) and cerebrovascular diseases (ICD8 430–438).

Results: Only 18 workers were lost to follow up and 7107 workers (6350 men and 757 women), were included in the cohort, with a total of 635 deaths from diseases of the circulatory system. These observed cases were compared to numbers based on national death rates. A slightly increased risk (standardised mortality ratio (SMR) 109; 95% confidence interval (CI) 100 to 118) for death from diseases of the circulatory system was found for male workers. Further analyses focused on the different exposures occurring in the pulp and paper production. Increased risks for death in circulatory diseases were found for sulphate digestion (SMR 146; 95% CI 103 to 200), steam and power generation (SMR 159; 95% CI 101 to 238), and maintenance (SMR 124; 95% CI 101 to 150). For ischaemic heart diseases, the risks were most pronounced among those exposed to sulphate digestion and steam and power generation. For cerebrovascular diseases, the risks were increased for maintenance work and for work with paper and paperboard production and manufacture.

Conclusions: In a cohort of this type, a “healthy worker effect” is often prevalent. Therefore, our results might reflect work related cardiovascular effects. Dust and small particles along with sulphur compounds might be possible causes of the current effects.