Biomedical subjects

T J Partanen

Publications and source records attributed to T J Partanen.

16 recordsLinked to original sources

PubMed2000

Occupational exposures and pancreatic cancer: a meta-analysis.

OBJECTIVES: Consolidation of epidemiological data on pancreatic cancer and worksite exposures. METHODS: Publications during 1969-98 were surveyed. Studies without verified exposures were excluded. Meta-analyses were conducted on data from 92 studies covering 161 populations, with results for 23 agents or groups of agents. With a standard format, five epidemiologists extracted risk estimates and variables of the structure and quality of each study. The extracted data were centrally checked. Random meta-models were applied. RESULTS: Based on 20 populations, exposure to chlorinated hydrocarbon (CHC) solvents and related compounds was associated with a meta-risk ratio (MRR) of 1.4 (95% confidence interval (95% CI) 1.0 to 1.8). Nickel and nickel compounds were considered in four populations (1.9; 1.2 to 3.2). Excesses were found also for chromium and chromium compounds (1.4; 0.9 to 2.3), polycyclic aromatic hydrocarbons (PAHs) (1.5; 0.9 to 2.5), organochlorine insecticides (1.5; 0.6 to 3.7), silica dust (1.4; 0.9 to 2.0), and aliphatic and alicyclic hydrocarbon solvents (1.3; 0.8 to 2.8). Evidence on pancreatic carcinogenicity was weak or non-positive for the following agents: acrylonitrile (1.1; 0.0 to 6.2); arsenic (1.0; 0.6 to 1.5); asbestos (1.1; 0.9 to 1.5); diesel engine exhaust (1.0; 0.9 to 1.3); electromagnetic fields (1.1; 0.8 to 1.4); formaldehyde (0. 8; 0.5 to 1.0); flour dust (1.1; 0.3 to 3.2); cadmium and cadmium compounds (0.7; 0.4 to 1.4); gasoline (1.0; 0.8 to 1.2); herbicides (1.0; 0.8 to 1.3); iron and iron compounds (1.3; 0.7 to 2.5); lead and lead compounds (1.1; 0.8 to 1.5); man-made vitreous fibres (1.0; 0.6 to 1.6); oil mist (0.9; 0.8 to 1.0); and wood dust (1.1; 0.9 to 2.5). The occupational aetiological fraction of pancreatic cancer was estimated at 12%. In a subpopulation exposed to CHC solvents and related compounds, it was 29%; to chromium and chromium compounds, 23%; to nickel and nickel compounds, 47%; to insecticides, 33%; and to PAHs, 33%. CONCLUSION: Occupational exposures may increase risk of pancreatic cancer. High quality studies are called for on interactions between occupational, environmental, and lifestyle factors as well as interactions between genes and the environment.

Air Pollutants, Occupational↗

PubMed1999

Collaboration between developing and developed countries and between developing countries in occupational health research and surveillance.

Collaborative occupational health and safety studies between counterparts in developing and developed countries and between developing countries have demonstrated their potential for improving occupational health and safety. Such collaboration in occupational health and safety is encouraged in the development of infrastructure in research empowerment and capacity building. This action includes the setting of priorities, the identification and documentation of problems, sponsorship, data bases and surveillance systems, technical support, methodology, publishing, research and training programs, controlled intervention, information exchange, and networking. Examples of priorities in occupational health and safety in the developing world include the informal sector (informally hired and independent workers), temporary work, pesticides, accidents, dusts, carcinogens, solvents, ergonomics, women and child labor, human immunodeficiency virus/acquired immunodeficiencey syndrome (HIV/AIDS), and transfer of hazardous materials and technologies. The sustainability of occupational health and safety structures and functions in the developing countries is a primary concern. Socioethical principles emphasize local, national, mutual and global gains. Examples of collaboration are given. Pervasive problems and strategies toward their solution are highlighted.

Developed Countries↗

PubMed1998

Environmental risk factors of breast cancer.

Breast cancer is women's most ubiquitous cancer. The role of dietary factors is controversial, but there is limited evidence for such occupational risk factors as employment in the pharmaceutical industry and as a beautician. Ionizing radiation probably increases the risk. Exposure to chlorinated hydrocarbon pesticides, chlorinated solvents, and polychlorinated biphenyls may be risk factors, although the evidence is insufficient. Data on low-frequency electromagnetic fields are inconclusive. Tobacco smoking may be a risk factor, but the effect may depend on N-acetyltransferase 2 genetic polymorphisms. There are yet unidentified determinants, probably environmental, that may act via estrogenic activity or through other mechanisms. The etiology may vary according to the joint estrogen and progesterone receptor status of the tumor. P53 mutation frequency varies considerably in breast cancer populations, which may reflect variation in exogenous exposures. Epidemiology research on breast cancer needs to consider subtypes of the disease, lifetime exposure assessment, host susceptibility, and adjustment for reproductive and menstrual history.

Breast Neoplasms↗

PubMed1998

Epidemiology of occupational and environmental risk factors related to ovarian cancer.

This paper reviews articles published during 1970-1997 from 48 epidemiologic studies on occupational and environmental risk factors of ovarian cancer. Current evidence is characterized by poorly focused data for occupational and environmental agents, vulnerability to biases, and an almost complete lack of quantitative exposure-response data. The moderate amount of data on nurses, teachers, professionals, dry cleaning employees, women in agriculture, the pharmaceutical industry, pharmacists, waitresses, and cooks show very little, if any, evidence of excess risk. Hairdressers, beauticians, and women employed in the printing industry may be at increased risk, but the data are insufficient for strong conclusions. Some case-referent studies suggest a modest-to-moderate excess in association with genital talc application. Few high-quality studies have been carried out, and no chemical agents have been studied extensively, with the exception of exposure to talc. Ovarian cancer may have occupational and environmental etiologies intertwined with cultural, behavioral, and life-style factors and genetic susceptibility, but current knowledge is insufficient to quantify occupational and environmental etiologies reliably. Well-designed analytic epidemiologic studies with sufficient power are needed.

Adolescent↗

PubMed1997

Pancreas cancer, tobacco smoking and consumption of alcoholic beverages: a case-control study.

A population-based case-control study investigated pancreas cancer in relation to consumption of alcoholic beverages, tobacco smoking and pancreatitis, utilizing historical proxy data for 662 decedent Finnish pancreas cancer cases and 1770 cancer controls. Tobacco smoking increased the risk, with an attributable case fraction of 0.27. The data are consistent with a joint effect of early and late stage carcinogens in tobacco smoke. Consumption of distilled beverages did not increase risk, but heavy drinking of wine or beer did. History of pancreatitis was a strong risk factor.

Adult↗

PubMed1995

Cancer risk for European asphalt workers.

OBJECTIVES: The feasibility of a European epidemiologic study of cancer risk among asphalt workers was examined in Western Europe. The study was motivated by occupational and public health concern about possible health risk from exposure to bitumen fumes. METHODS: Information on the accessibility and quality of epidemiologic resources, retrospective worker records, mortality and cancer incidence records, and exposures was requested from research institutes and road paving and asphalt mixing companies in 15 European countries. RESULTS: Research institutes and asphalt companies in 12 countries responded. It was found that at least 44 companies in seven countries can be included in a retrospective mortality study of a minimum of 32,000 employees with 356,000 person-years (over 100 lung cancers). Coal tar will be an important confounder for these data. The power of a cohort study of workers who have never worked with tar-containing materials remains insufficient. Even in an ambispective study extending to the year 2005, the expected lung cancer deaths in a tar-free cohort would be only four. CONCLUSIONS: The results suggest that a case-referent study of lung cancer, nested in an international cohort of asphalt workers, represents the design of choice, conditionally on the possibility of assessing relevant individual life-time exposures. A cross-sectional determination of relevant biomarkers of exposure such as adducts in lymphocytes or the presence of metabolites of polycyclic aromatic compounds in urine in a group of workers exposed to bitumen fumes will provide further relevant information.

Adult↗

PubMed1993

Chemical exposures and respiratory cancer among Finnish woodworkers.

A case-control study of respiratory cancer, nested within a cohort of male woodworkers, was updated in Finland. The update extended the initial follow up of 3805 workers from 19 plants to 7307 workers from 35 plants. Each case of respiratory cancer (n = 136) diagnosed between 1957 and 1982 within the cohort was matched by year of birth with three controls (n = 408) from the cohort. Chemical exposures were assessed for the cases and the controls by a plant and period specific job exposure matrix. An excess of respiratory cancer was associated with phenol. Concomitant exposures to several other agents occurred as well, however, and no exposure-response relation for phenol was seen. An excess risk and an increasing exposure-response relation were found for engine exhaust from petrol and diesel driven factory trucks. The excess risk associated with pesticides was lower than in our previous study, an indication of qualitative and quantitative differences in exposure between the initial and augmented cohorts. Slightly increased risks were found for terpenes and mould spores, which may be due to chance although the contribution of occupational exposure cannot be ruled out. Exposure to wood dust, mainly from pine, spruce and birch, at a level of about 1 mg/m3, was not associated with lung cancer, upper respiratory cancer, or adenocarcinoma of the lung.

Case-Control Studies↗

PubMed1986

Respiratory cancers and chemical exposures in the wood industry: a nested case-control study.

A cohort of 3805 men who had worked for at least one year in the particleboard, plywood, sawmill, or formaldehyde glue industries between 1944 and 1965 was followed up until 1981. From within the cohort the 57 patients with verified "respiratory" cancer (ICD 7 codes: 160-162.1, 141, 143-8) were defined as "cases," and 171 men without respiratory cancer from within the cohort were matched on birth year and used as controls. The comparison of exposures was carried out according to work histories and job exposure matrices for each plant. The odds ratio for exposure to wood dust was 1.03 (32 exposed cases) without provision for any latent period, and 0.97 (27 exposed cases) when provision for a minimum latent period of ten years was applied. The odds ratios were 1.60 and 1.68, respectively, when smoking was controlled by stratification. These results did not differ significantly from unity. The estimated average level of exposure to wood dust among the exposed was 1-2 mg/m3 and the mean duration of exposure about ten years. Significantly (one sided test, 5% level) raised odds ratios were observed for exposure to pesticides and phenol. No single pesticide could be identified as "causative" because of frequent multiple exposures. The raised odds ratios for phenol were partly explained by smoking and exposure to pesticides which confounded the observed associations for phenol exposure. Exposure to terpenes and other heating products of coniferous woods was significantly associated with a risk of respiratory cancer when the duration of exposure exceeded five years.

Adult↗

PubMed1971