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Biomedical subjects

T Partanen

Publications and source records attributed to T Partanen.

At least 37 records · Page 2Linked to original sources
PubMed1997

Socioeconomic differences in cancer incidence and mortality.

This chapter summarizes accumulated data on the presence, magnitude and consistency of socioeconomic differentials in mortality and incidence of all malignant neoplasms and 24 individual types of neoplasms in 37 populations in 21 countries. More or less consistent excess risks in men in lower social strata were observed for all respiratory cancers (nose, larynx and lung) and cancers of the oral cavity and pharynx, oesophagus, stomach, and, with a number of exceptions, liver, as well as for all malignancies taken together. For women, low-class excesses were consistently encountered for cancers of the oesophagus, stomach, cervix uteri and, less consistently, liver. Men in higher social strata displayed excesses of colon and brain cancers and skin melanoma. In the two Latin American populations for which data were available, lung cancer was more frequent in higher social strata. Excesses in high female socioeconomic strata were seen in most populations for cancers of the colon, breast and ovary and for skin melanoma. Longitudinal data from England and Wales suggested widening over time of social class differences in men for all cancers combined and for cancers of the lung, larynx and stomach, and in women for all cancers combined and for cervical cancer.

Adolescent↗
PubMed1996

Exposure to styrene and mortality from nervous system diseases and mental disorders.

Chronic low-dose exposure to solvents has been associated in epidemiologic studies with chronic neurotoxicity, but the evidence is not consistent. Styrene causes acute disturbances in the central and peripheral nervous systems. To determine if exposure to styrene may contribute to chronic diseases of the central nervous system, the authors examined mortality from nervous system diseases, mental disorders, and suicide in relation to styrene exposure in an international historical cohort study. The cohort involved 35,443 workers employed during 1945-1991 in the reinforced plastics industry, where high exposures to styrene occur. Indicators of exposure were reconstructed through job histories and environmental and biologic monitoring data. Poisson regression was used for internal comparisons. Mortality from diseases of the central nervous system (27 deaths) increased with time since first exposure, duration of exposure, average level of exposure, and cumulative exposure to styrene. A quadratic model described best the dose-response shape for cumulative exposure and duration of exposure with the highest risks at around 300 ppm-years and 5 years, respectively, and a subsequent decrease in risk in the highest exposure categories. Mortality from epilepsy increased monotonically with all styrene exposure indicators, while associations for degenerative diseases of the central nervous system were generally weaker. Mortality from mental disorders and suicide decreased with increasing duration of exposure and cumulative exposure, while there was no trend with time since first exposure and average exposure to styrene. These findings suggest that, in addition to the known acute effects, exposure to styrene may contribute to chronic diseases of the central nervous system.

Cause of Death↗
PubMed1996

Exposure to styrene and mortality from nonmalignant respiratory diseases.

A cohort of 34,560 men and 6128 women employed in 660 European factories manufacturing reinforced plastic products, followed up originally to assess the risk of cancer, was used to assess the risk of non-malignant respiratory diseases associated with exposure to styrene. Mortality from pneumonia was associated with intensity of exposure to styrene, but this may have been due to chance. Mortality from bronchitis, emphysema, and asthma was not associated with styrene exposure.

Cohort Studies↗
PubMed1996

Exposure to styrene and mortality from nonmalignant diseases of the genitourinary system.

OBJECTIVES: A historical cohort study was carried out to investigate mortality from nonmalignant diseases of the genitourinary system among workers in the reinforced plastics industry, where high workroom concentrations of styrene are encountered. METHODS: The external comparisons in this report were based on an average of 12.6 years of retrospective follow-up of 35 443 workers who were first employed in the reinforced plastics industry during 1945-1991 and were known to have been exposed to styrene in their work. For the internal comparisons, 2641 subjects with incomplete occupational histories were excluded, leaving 32 802 subjects. Previous individual exposure histories to styrene were reconstructed through job histories and environmental and biological monitoring data. RESULTS: Mortality from nonmalignant diseases of the genitourinary system (N = 20) was associated with average exposure to styrene (P for trend 0.05). Weaker increasing trends in risk were seen for time since first exposure and cumulative exposure, while no increase was identified for duration of exposure. There was a significant increasing trend in mortality from nephritis and nephrosis (N = 5), associated with an increasing average level of exposure to styrene (P for trend 0.03). No clear trend was observed for time since first exposure, duration of exposure, or cumulative exposure. CONCLUSIONS: In this large cohort study of workers exposed to styrene, mortality from nonmalignant diseases of the genitourinary system increased as the average intensity of exposure increased. This finding indicates that other data should be scrutinized.

Air Pollutants, Occupational↗
PubMed1996

A molecular and epidemiological study on bladder cancer: p53 mutations, tobacco smoking, and occupational exposure to asbestos.

In this study, we found an unexpected association (crude odds ratio = 2.8; 95% confidence interval = 0.9-8.4) between definite work-related exposure to asbestos and carcinoma of the urinary bladder in a small group of patients (n = 28) initially recruited as referents for an epidemiological feasibility study on the occupational causes of lung cancer. We extended the study by using molecular methods to examine mutations in the p53 tumor suppressor gene in the same cases of bladder cancers. The same number of archival samples of transitional cell carcinoma, mainly of grade 3, were added to the analysis. We failed to show any association between occupational exposure to asbestos and p53 mutations among bladder cancer patients. We observed an increasing occurrence of p53 mutations in nonsmokers (5 of 17, 29%), former smokers (8 of 21, 38%), and current smokers (9 of 16, 56%) in that order; however, this was not statistically significant. The most prevalent type of mutation was G:C to A:T transition. Tumor grade was not associated with the frequency of mutations, but the higher stage (T3-T4) tumors appeared to have mutations more frequently than did the less invasive tumors (T1-T2).

Adult↗
PubMed1995

Coffee consumption not associated with risk of pancreas cancer in Finland.

BACKGROUND: Coffee consumption has been brought to focus as a possible risk factor for pancreas cancer. After having reviewed the available evidence, an International Agency for Research on Cancer working group concluded in 1991 that the evidence in humans that coffee drinking is carcinogenic in the pancreas is "inadequate," since the available data were considered suggestive of a weak relationship with high levels of coffee consumption, but the possibility that this was due to bias or confounding was judged tenable. METHODS: The association between coffee consumption and pancreas cancer risk was examined in a case-referent study in Finland. Data on coffee consumption 20 years prior to the diagnosis of cancer were obtained from the next of kin of 662 cases of pancreas cancer and 1,770 referent (stomach, colon, and rectum) cancers. The results were expressed as crude and age-, gender-, and tobacco smoking-adjusted odds ratios and 95% confidence intervals for three daily coffee dose categories 20 years prior to cancer diagnosis. RESULTS: The data failed to demonstrate any association between coffee consumption and risk for pancreas cancer. The crude odds ratios varied between 0.7 (95% confidence interval 0.3-1.5) and 1.3 (0.7-2.6), the adjusted ones between 0.5 (0.2-1.2) and 1.1 (0.6-2.1) in the different daily dose categories of coffee and between contrasts with the three referent cancers. The highest odds ratios were associated with the contrast between pancreas and colon cancer, the lowest between pancreas and rectum cancer. Adjustment for gender, age, and tobacco smoking slightly decreased the values of the odds ratios. The power of the study was low, however, to detect possible weak increases associated with coffee consumption. CONCLUSIONS: The results are unlikely to be negatively biased, and are compatible with the majority of epidemiologic results advanced, suggesting no positive association between coffee consumption and the risk of pancreas cancer.

Case-Control Studies↗
PubMed1995

Pancreatic cancer and occupational exposures.

We conducted a nationwide case-control study in Finland to identify occupational risk factors for pancreatic cancer. We constructed the occupational exposure histories for 595 incident cases of primary exocrinic cancer of the pancreas and of 1,622 cancer controls, using three different methods. We found elevated odds ratios (OR) for ionizing radiation [OR = 4.3; 95% confidence interval (CI) = 1.6-11.4], nonchlorinated solvents (OR = 1.6-1.8), and pesticides (OR = 1.7; 95% CI = 0.8-3.4). Asbestos, chromates, cleaning agents, waxes, polishes, and most other exposures were not meaningfully associated with pancreatic cancer. Inorganic dust containing crystalline silica (OR = 2.0; 95% CI = 1.2-3.5), heat stress (OR = 2.2; 95% CI = 0.8-6.6), and rubber chemicals including acrylonitrile (OR = 2.1; 95% CI = 0.9-4.7) emerged as previously unsuspected risk factors. Occupational exposure probably has a small role in the etiology of pancreatic cancer in the present-day industrialized or postindustrial work environment.

Adult↗
PubMed1995

Carbamazepine and its metabolites in human perfused placenta and in maternal and cord blood.

Placental transfer and metabolism of carbamazepine (CBZ) was studied in a dual recirculating placental cotyledon perfusion system and was also evaluated in 16 pairs of maternal venous and cord blood samples. Among the parameters studied as possible indicators of a successful perfusion, volume changes in perfusate divided the perfusions into two groups, whereas no significant differences between perfusions were noted in blood gas analysis or in antipyrine transfer. CBZ added into the maternal circulation crosses the placenta in the beginning quicker than antipyrine which is in agreement with the different lipid solubilities of these compounds. Because the transfer rates of antipyrine and CBZ were about the same, the mechanism of transfer of CBZ is probably similar to that of antipyrine (passive diffusion). No metabolites of CBZ could be detected in the perfusate by high-performance liquid chromatography (HPLC) or gas chromatography/mass spectrometry. With the improved HPLC methodology for CBZ metabolites, six metabolites were detected in clinical samples, including 10-hydroxy-10,11-dihydro-CBZ (10-OH-CBZ), which has been described earlier in only 1 uremic patient. Relative levels of metabolites showed significant individual differences. CBZ crosses perfused placenta rapidly, but this does not contribute to CBZ metabolites detected in maternal and fetal circulation.

Antipyrine↗
PubMed1995

Silica, silicosis and cancer in Finland.

Approximately 100 000 Finnish workers are currently employed in jobs and tasks that may involve exposure to airborne silica dust. The major industries involved are mining and quarrying; production of glass, ceramics, bricks and other building materials; metal industry, particularly iron and steel founding; and construction. Over 1500 cases of silicosis have occurred in Finland since 1935. Tuberculosis has been a frequent complication of silicosis. Results of studies from several countries strongly suggest that silica dust also causes lung cancer. The results of the relevant Finnish epidemiologic and industrial hygiene studies addressing cancer risk and exposure to quartz dust are summarized.

Confidence Intervals↗
PubMed1994

Pancreatic cancer in industrial branches and occupations in Finland.

An examination of the risk of pancreatic cancer associated with occupation, by industrial branch and job title, was undertaken in a nationwide case-referent study in Finland. The results are based on job history information from the next-of-kin of 625 incident cases of primary malignant exocrinic pancreatic neoplasms, and of 1,700 cancer referents (stomach, colon, and rectum). All cases and referents were between 40 and 74 years at diagnosis. The diagnoses were made in 1984-87, and both cases and referents were known to be dead by April 1, 1990. The source of the cases and referents was the Finnish Cancer Registry. Increases in risk of pancreatic cancer were suggested for a small number of industrial branches and job titles, including stone mining (odds ratio 3.7), cement and building materials (11.1), pharmacists and sales associates in pharmacies (12.9), male wood machinists (4.1), male gardeners (6.7), female textile workers (5.4), and male transport inspectors and supervisors (9.4). The exposures potentially implicated are discussed. In agreement with the overall results of epidemiologic studies conducted elsewhere, direct occupational determinants probably do not account for a substantial share of the etiology of pancreatic cancer, at least in conditions resembling Finnish working environments some 15-40 years ago.

Adult↗
PubMed1994

Cancer risk in asphalt workers and roofers: review and meta-analysis of epidemiologic studies.

Twenty epidemiologic studies have described cancer risk in asphalt workers and roofers in various countries. A current concern for these workers is the potential carcinogenicity posed by inhalation of bitumen fumes or dermal exposure to bitumens. Bitumens are chemically different from many carcinogenic coal-tar based materials. Both have been employed in road paving and waterproofing. We examined and combined the results of the epidemiologic studies conducted on asphalt workers and roofers. We examined the cancer risk separately in three broad job categories: 1) roofers (exposed to bitumen fumes and previously often to coal-tar fumes); 2) highway maintenance workers (HMWs) and road pavers (exposed to bitumen fumes as well as possibly coal-tar fumes previously); and 3) miscellaneous and unspecified bitumen/asphalt workers. In roofers, an increased risk was suggested for cancers of the lung (aggregated relative risk 1.8, 95% confidence interval 1.5-2.1), stomach (1.7, 1.1-2.5), nonmelanoma skin (4.0, 0.8-12), and leukemia (1.7, 0.9-2.9). Some of the excesses may be attributable to polycyclic aromatic hydrocarbons (PAH) from coal-tar products. The aggregated relative risks in road pavers and HMWs were consistently lower than in roofers for cancers of the lung (0.9, 0.8-1.0), stomach (1.1, 0.8-1.5), bladder (1.2, 0.7-1.8), skin (2.2, 1.2-3.7), and leukemias (1.3, 0.9-1.8). Their risk of skin cancer was significantly increased, based on one study. Miscellaneous and unspecified workers had a significant excess (1.5, 1.2-1.8) of lung cancer. The data were poorly focused to address the carcinogenicity of bitumen fumes, as contrasted with tar-derived exposures. For the prospect of shedding more light on the bitumen-cancer controversy, the feasibility of a powerful multicenter cohort is currently being studied by the International Agency for Research on Cancer (IARC).

Air Pollutants, Occupational↗
PubMed1994

Increased incidence of lung and skin cancer in Finnish silicotic patients.

Cancer incidence during 1953 to 1991 in 811 Finnish silicotic patients diagnosed between 1936 and 1977 was evaluated. In comparison with the general population, excesses were observed for all cancers (standardized incidence ratio, 1.7 [95% confidence interval, 1.4 to 1.9]), all lung cancers (2.9 [2.4 to 3.5]), squamous cell lung cancers (3.3 [2.3 to 4.5]), and skin cancers: melanoma (3.0 [0.8 to 7.6]) and nonmelanoma (2.9 [1.2 to 6.1]). Confounding by tobacco smoking did not explain the lung cancer increment. The consistency of the association between silicosis and lung cancer across a large number of studies suggests that silicosis represents a direct or indirect lung cancer hazard. The skin cancer excess, a relatively novel finding, may be explained either by carcinogens in foundries, or silica-induced lowering of immunocompetence, which would lead to a more pronounced effect of solar ultraviolet radiation.

Adult↗
PubMed1993

K-ras mutations in human adenocarcinoma of the lung: association with smoking and occupational exposure to asbestos.

We investigated point mutational activation of the ras genes (K-ras codons 12, 13 and 61; N-ras codons 12, 13 and 61; H-ras codons 12 and 61) in primary, resected lung cancer by dot blotting and oligonucleotide hybridization. K-ras mutations were found in 14 (29%) of the 48 lung tumour specimens examined, but no N-ras or H-ras mutations were found. The highest frequency of K-ras mutation was observed in adenocarcinoma: 12 of the 21 samples studied (57%) had a mutation, which is one of the highest frequencies reported for lung adenocarcinoma. The commonest type of mutation in these lung tumour samples consisted of transversions: we observed 11, of which 8 (57% of all mutations) were G to T transversions. Most of the 48 patients studied had a history of heavy smoking, either with or without evidence of occupational exposure to asbestos. Statistical analysis revealed--in addition to the highly significant association between the adenocarcinoma type of lung cancer and K-ras mutation--a clear association of K-ras mutations with heavy life-time smoking (> or = 50 pack-years of cigarette smoking; odds ratio (OR) 4.9, 90% CI 1.2-19.5, multivariate analysis). In addition, occupational asbestos exposure showed an elevated, but non-significant, OR of 2.2 (90% CI 0.6-8.7) with the presence of K-ras mutation. We conclude that the occurrence of K-ras mutations in adenocarcinoma of the lung is frequent, and that such mutations are associated with heavy life-time exposure to tobacco smoke, possibly in combination with occupational exposure to asbestos fibres.

Adenocarcinoma↗
PubMed1993

Malignant lymphomas and leukemias, and exposures in the wood industry: an industry-based case-referent study.

Jobs and exposures in woodwork may entail an elevated risk of lymphomas and leukemias. Exposures occurring in woodwork were scrutinized in a small industry-based case-referent study of four cases of Hodgkin's disease, eight cases of non-Hodgkin's lymphoma, 12 cases of leukemia, and 152 matched referents, all from the Finnish wood industry. Past exposures to wood dust, chlorophenols, terpenes, and engine exhaust, individually reconstructed through plant- and period-specific job exposure matrices, were unrelated to lymphoma/leukemia risk. Exposures to various solvents were associated with an odds ratio (OR) of 5.6 (95% confidence interval 1.0-32.0). The OR for formaldehyde was 2.5 (nonsignificant). The results are interpreted as providing limited evidence of the role of exposure to some as yet unidentified organic solvents in increasing the risk of malignant lymphomas. Formaldehyde may be another woodwork-related risk factor for some lymphomas, but the power of the study was too low for empirical confirmation of this possibility. Leukemias did not seem to be associated with any of the exposures studied.

Air Pollutants, Occupational↗
PubMed1993

Interaction between smoking and asbestos in human lung adenocarcinoma: role of K-ras mutations.

To investigate the role of tobacco smoking and asbestos fibers in the etiology of human lung cancer, we examined the activating point mutations in the K-ras oncogene in DNA samples from 49 patients. Mutations were found more often in tissue from adenocarcinomas (12/21) than in tissue from tumors other than nonadenocarcinomas of the lung (3/28). Among the adenocarcinoma patients, asbestos exposure was predictive of K-ras mutation (odds ratio, 4.9; 95% confidence interval, 0.7-34.3); in patients with other types of lung cancer, the relation appeared to be an inverse one, but the numbers were small. The proportion of heavy smokers (over 50 pack-years) was 60% among people with K-ras mutations and 35% among the K-ras-negative subjects, suggesting that smoking causes K-ras mutations. If mutations in K-ras genes are caused by smoking, asbestos would act as a promoting agent by conferring selective growth conditions for clonal expansion on these mutated cells. Asbestos may favor recruitment of (initiated) K-ras mutation-positive cells in the multistage process of carcinogenesis by stimulating cellular growth.

Adenocarcinoma↗
PubMed1993

Formaldehyde exposure and respiratory cancer--a meta-analysis of the epidemiologic evidence.

A recent meta-analysis by Blair and his co-workers stimulated the undertaking of a reanalysis of the epidemiologic evidence of an association between formaldehyde and respiratory cancer. Emphasis was placed on extracting the maximal amount of relevant data from the source studies. In close agreement with the original analysis, the aggregated evidence did not indicate an excess risk or an exposure-response gradient for lung cancer. An exposure-response gradient was seen for both sinonasal and nasopharyngeal cancers. The risk for substantial exposure was significantly elevated (odds ratio 1.7 for sinonasal and 2.7 for nasopharyngeal cancer). It is suggested that at least substantial levels of occupational exposure to formaldehyde are associated with a risk of these cancers. The excess risk would be of the order of 100% or more over background rates.

Epidemiologic Methods↗