Documentation of work ability data in occupational health records.

BACKGROUND: In Finland, patient health records are structured in the same way. Patient data entries are grouped using national headings and each data entry must have at least one heading. AIMS: To determine the use of national headings for the documentation of work ability data and to gather the experience of professionals on usefulness, ease of use and usability of national headings in occupational health services (OHSs). METHODS: An electronic questionnaire and a semi-structured themed interview were used to collect data. Data were analysed using SPSS Statistics 24 and interview material was analysed by deductive content analysis using ATLAS.ti. RESULTS: A total of 359 people completed the questionnaire. Most of the work ability data were documented using the headings history, plan and current status. More than half of respondents felt that using national headings improved quality and allowed greater control. Almost all respondents thought that learning to use national headings was easy. During the interviews (n = 19), all respondents felt that use of national headings improved the quality of documentation. However, more than half stated that national headings were not well suited to documentation of work ability data. CONCLUSION: These results can be used to develop national documentation standards, as well as electronic health records, to support healthcare professionals' interactions with working-age patients. Earlier studies of national headings in OHSs were not found.

Multisite musculoskeletal pain predicts medically certified disability retirement among Finns.

BACKGROUND: Musculoskeletal pain at several sites (multisite pain) is more common than single-site pain. Little is known on its effects on disability pension (DP) retirement. METHODS: A nationally representative sample comprised 4071 Finns in the workforce aged 30 to 63. Data (questionnaire, interview, clinical examination) were gathered in 2000-2001 and linked with national DP registers for 2000-2011. Pain during the preceding month in 18 locations was combined into four sites (neck, upper limbs, low back, lower limbs). Hazard ratios (HR) of DP were estimated by Cox regression. RESULTS: The HR of any DP (n = 477) was 1.6 (95% confidence interval 1.2-2.1) for one, 2.5 (1.9-3.3) for two, 3.1 (2.3-4.3) for three and 5.6 (4.0-7.8) for four pain sites, when adjusted for age and gender. When additionally adjusted for clinically assessed chronic diseases, the HRs varied from 1.4 (1.0-1.8) to 3.5 (2.5-4.9), respectively. When further adjusted for physical and psychosocial workload, education, body mass index, smoking, exercise and sleep disorders, the HRs were 1.3 (0.9-1.7), 1.6 (1.2-2.2), 1.8 (1.3-2.5) and 2.5 (1.8-3.6). The number of pain sites was especially strong in predicting DPs due to musculoskeletal diseases (HRs in the full model; 3.1 to 4.3), but it also predicted DPs due to other somatic diseases (respective HRs 1.3 to 2.3); pain in all four sites was also predictive of DPs due to mental disorders (full model HR 2.2). CONCLUSIONS: The number of pain sites independently predicted DP retirement. Employees with multisite pain may need specific support to maintain their work ability.

Persistent asthma, comorbid conditions and the risk of work disability: a prospective cohort study.

BACKGROUND: This study examined whether asthma alone or together with chronic comorbidity is associated with an increased risk of long-term work disability. METHODS: We examined data from 2332 asthmatic and 66 354 nonasthmatic public sector employees in Finland who responded to a survey between 1997 and 2004. Respondents were coded as persistent asthmatics based on the special reimbursement for continuous asthma medication by the Social Insurance Institution. Data on long-term work disability (sickness absences or disability pensions > 90 days) were obtained from national registers. The risk of work disability was examined by Cox proportional hazard models adjusted for age, gender, socioeconomic status, type of employment contract, and type of employer. RESULTS: Asthma increased the risk of all-cause long-term work disability with hazard ratio (HR) 1.8 (95% CI 1.62-2.09) compared with controls (no asthma). Asthma and one other chronic comorbidity increased the risk of long-term all-cause work disability with HR 2.2 (95% CI 1.78-2.83). Asthma together with two or more other chronic conditions increased the risk with HR 4.5 (95% CI 2.98-6.78). Asthma and depression increased the risk with HR 3.6, and the risk was especially high for permanent work disability (HR 6.8). Among those with asthma, there were more women, obese individuals (BMI ≥ 30), ex-smokers, and lower-grade nonmanual workers. CONCLUSIONS: Asthma is associated with an increased risk of long-term all-cause work disability. The risk increases further with chronic comorbidities and is especially high in patients with asthma and depression.

Risk of pancreatic cancer in workers exposed to chlorinated hydrocarbon solvents and related compounds: a meta-analysis.

This is a meta-analysis of occupational exposures to chlorinated hydrocarbon (CHC) solvents and pancreatic cancer, based primarily on studies that addressed exposure directly (agent studies) and secondarily on studies that reported data without verification of individual CHC exposures (job title studies), all of which were listed in databases for the period January 1969 to May 1998. Standardized extraction of data and double-checking of consistency of data extraction by five extractors were done. Simple random models estimated meta-relative risks. Suggestive weak excesses were found for trichloroethylene (meta-relative risk (MRR) = 1.24, 95% confidence interval (CI): 0.79, 1.97), polychlorinated biphenyls (MRR = 1.37, 95% CI: 0.56, 3.31), methylene chloride (MRR = 1.42, 95% CI: 0.80, 2.53), and vinyl chloride (MRR = 1.17, 95% CI: 0.71, 1.91) but not for carbon tetrachloride. One study addressed tetrachloroethylene (MRR = 3.08, 95% CI: 0.63, 8.99); another investigated chlorohydrin production (MRR = 4.92, 95% CI: 1.58, 11.4). Exposure-response meta-analyses for trichloroethylene and methylene chloride failed to reveal trends. Job title studies on metal degreasing and dry cleaning revealed significant MRRs (2.0 and 1.4, respectively). Publication bias was unlikely. Confounding may have remained insufficiently controlled. Unless the results are seriously biased by exposure or endpoint misclassification or by confounding, strong causal associations between CHC compounds and pancreatic cancer can be judged unlikely. Interactions between environmental and occupational agents, lifestyle factors, and genetic susceptibility remain a possibility, but the data for this meta-analysis did not address interactions.

Lung cancer and past occupational exposure to asbestos. Role of p53 and K-ras mutations.

Studies on somatic mutations in lung cancers associated with cigarette smoking and asbestos exposure are few. We investigated prevalence of mutations in the p53 and K-ras genes in lung tumors from smokers with and without asbestos exposure at work. For K-ras mutations, the study was an extension of an earlier analysis. Nearly all of the 105 consecutive patients examined were smokers and had non-small-cell carcinoma of the lung with squamous-cell carcinoma or adenocarcinoma histology. Exposure to asbestos was estimated by pulmonary fiber counts and occupational histories. A pulmonary burden of >/= 1 x 10(6) asbestos fibers per gram of lung tissue, indicating work-related exposure, was found in 32% of the patients for whom fiber-analysis data were available (33 of 102 patients, all men). The statistical analysis showed pulmonary fiber count as the only significant predictor of adenocarcinoma histology, in contrast to squamous-cell carcinoma (smoking-adjusted odds ratio [OR] 3.0, 95% confidence interval [CI] 1.1 to 8.5). The frequency of p53 mutations was 39% (13 of 33) among the asbestos-exposed cases, as compared with 54% (29 of 54) among the nonexposed cases; the difference was not significant, however. In male ever-smokers, a long duration of smoking was associated with p53 mutation (OR 3.2, 95% CI 1.2 to 8.8). In adenocarcinoma, p53 mutations were less prevalent (10 of 30, 33%) as compared with squamous-cell carcinoma (28 of 46, 61%; P = 0.02), whereas a strong and significant association was found between adenocarcinoma and K-ras mutation (OR 37, 95% CI 5.8 to 232, adjusted for smoking and asbestos exposure). Asbestos exposure alone was not significantly associated with increased occurrence of K-ras mutations. In conclusion, the results may primarily reflect the observed excess of adenocarcinoma in the asbestos- exposed patients, and hence the decrease in p53 mutations and increase in K-ras mutations.

Occurrence, trends and environment etiology of pancreatic cancer.

This review summarizes data on the occurrence, the trends, and the life-style, environmental, occupational and genetic determinants of pancreatic cancer. Epidemiologic evidence implicates tobacco smoking as one cause. The evidence regarding alcohol consumption is inconsistent. Although both positive and inconclusive findings are encountered, the bulk of the evidence on coffee consumption is negative. Fat intake is linked with obesity and diabetes mellitus, which are risk factors for pancreatic cancer. Fruit and vegetable consumption appears to be protective. No occupational or environmental agent has been confirmed to increase the risk, but epidemiologic evidence is inconsistent, Little is known about the role of genetic polymorphisms of metabolic enzymes in pancreas carcinogenesis. Pancreatic cancer shows high rates of mutations of Ki-ras and losses or mutations of tumor suppressor genes (p53, p16INK4A, and SMAD4/DPC-4). Ki-ras mutations have been associated with life-style factors in relation to pancreatic cancer, but the evidence is still scant and inconsistent.

Molecular analysis of occupational cancer: infrequent p53 and ras mutations in renal-cell cancer in workers exposed to gasoline.

Occupational exposure to gasoline has been identified in several studies as a risk factor for renal-cell cancer. Cases of renal-cell cancer with and without work-related exposure to gasoline or gasoline and diesel fuel were studied for the presence of mutations in the tumour-suppressor gene p53 (n = 23 exposed and 30 non-exposed cases studied) and ras oncogene (n = 30 exposed and 36 non-exposed cases studied). An average cumulative exposure was estimated at 10 ppm-years benzene among the exposed. Three p53 mutations were detected by denaturing-gradient gel electrophoresis (DGGE) among the 23 exposed cases (3/23, 13%). Of the non-exposed referent cases, 4 had a mutation (4/30, 13%). All but one of the cases with a p53 mutation had smoked. A ras gene (K-ras or N-ras) mutation was found in 3 (3/66, 4.5%) cases, all of whom were smoker referents. We conclude that p53 and ras mutations are infrequent in renal-cell cancer associated with occupational exposure to gasoline. However, the majority of the mutations (6/7 for p53, and 3/3 for ras genes) were seen in smokers.

Cancer incidence and mortality among Finnish asbestos sprayers and in asbestosis and silicosis patients.

Cohorts of Finnish asbestos sprayers and of asbestosis and silicosis patients were followed for cancer with the aid of the Finnish Cancer Registry in the period 1967-1994. Compared with the cancer incidence of the total Finnish population, asbestos sprayers had an increased risk for total cancer (standardized incidence ratio [SIR] 6.7, 95% confidence interval [95% CI] 4.2-10); lung cancer (SIR 17.95% CI 8.2-31); and mesothelioma (SIR 263, 95% CI 85-614). The SIR of the asbestosis patients was 3.7 (95% CI 2.8-5.0) for all sites, 10 (95% CI 6.9-14) for lung cancer, and 65 (95% CI 13-188) for mesothelioma. The silicosis patients also had significantly high SIR values for all sites (1.5, 95% CI 1.0-2.1) and lung cancer (2.7, 95% CI 1.5-4.5). The values for the SIR and the standardized mortality ratio for all sites and lung cancer were very similar, and therefore it seems that both are reliable indicators of the occurrence of occupational cancer. It was concluded that pneumoconioses patients and asbestos-exposed workers have a markedly elevated risk for cancer. Asbestos-induced occupational cancers are not only diseases of the elderly, since the relative risk is high also for middle-aged people.

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.

Role of GSTT1 and GSTM1 genotypes in determining individual sensitivity to sister chromatid exchange induction by diepoxybutane in cultured human lymphocytes.

The individual genotoxic response of cultured human lymphocytes to diepoxybutane (DEB), an epoxide metabolite of 1,3-butadiene, shows a bimodal distribution. Blood donors can be classified as either DEB-sensitive or DEB-resistant on the basis of the frequency of sister chromatid exchanges (SCEs) induced by DEB in whole-blood lymphocyte cultures. The genetic basis of this phenomenon has thusfar been unknown. To investigate if differences in the ability of individuals to detoxify DEB could explain the bimodal response, sister chromatid exchanges (SCEs) induced by a 48-h treatment with DEB (2 and 5 microM) were analyzed in whole-blood lymphocyte cultures of 20 human donors with known genotypes of two polymorphic glutathione S-transferases (GSTs), GSTT1 and GSTM1. Both polymorphisms include a homozygous null genotype lacking the respective GST gene and isozyme. The mean frequency of SCEs/cell was 1.6 times higher among GSTT1 null donors (n = 8) than GSTT1 positive donors (n = 12) at both 2 microM DEB (mean 67.3 versus 40.9) and 5 microM DEB (mean 123.2 versus 77.5), with no overlapping in DEB-induced individual SCE frequencies between the two genotypes. Thus, all DEB-sensitive individuals were of the GSTT1 null genotype, while all DEB-resistant persons had a detectable GSTT1 gene. A significant (P < 0.05) negative correlation (r = -0.65 at 5 microM, r = -0.56 at 2 microM) was obtained in the GSTT1 positive donors between DEB-induced individual SCE frequency and RBC GSTT1 activity, measured by formaldehyde formation from dichloromethane; the GSTT1 null individuals showed no GSTT1 activity. At 5 microM DEB, the lymphocyte cultures of the GSTT1 null donors also had a significantly decreased replication index, indicating an impact of GSTT1 genotype on the cytotoxicity of DEB. No influence on DEB-induced SCEs or cytotoxic effects was observed for GSTM1 genotype. It is concluded that sensitivity to in vitro SCE induction by DEB is explained by the lack of GSTT1.

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.

Renal cell cancer and occupational exposure to chemical agents.

A case-referent study of occupational risk indicators of renal cell adenocarcinoma was conducted. Each incident case in Finland in 1977-1978 was matched with two population referents. Lifelong job histories were collected and translated into indicators of industry, occupation, and occupational exposures. The analyses of 338 sets of cases and referents revealed elevated risks for a history of employment in white-collar occupations; the printing industry; the chemical industry; the manufacturing of metal products; mail, telephone, and telegraph services; and iron and metalware work. A decreased risk was observed for male farmers. An elevated risk and an exposure-response relationship were found for gasoline exposure. The excess risk was highest at a latency period of approximately 30 years. The findings support the hypothesis that exposure to some constituent(s) of gasoline increases the incidence of renal adenocarcinoma in humans. Suggestions of elevated risks appeared for exposures to inorganic lead, cadmium, and nonchlorinated solvents.

Cytogenetic surveillance of workers exposed to genotoxic chemicals: preliminary experiences from a prospective cancer study in a cytogenetic cohort.

Cytogenetic endpoints, conventionally chromosomal aberrations, and later sister chromatid exchanges and micronuclei have long been used to assess exposure of human populations to genotoxic agents. Although the adverse nature of somatic chromosome damage is recognized at the group level, no ill-health manifestations have been causally related to cytogenetic damage at the individual level. In work-related exposures, e.g., ethylene oxide, styrene, benzene, vinyl chloride, and alkylating anticancer agents have been shown to induce somatic chromosomal damage in several studies. For all of these, a carcinogenic risk to humans has also been documented. The possible association of somatic chromosome damage and cancer will be elucidated in a Nordic prospective study. The objective is to find out the significance of a high or low score in any of the cytogenetic parametres to risk of cancer. In the Finnish part of the cohort of 806 individuals, 10 cases of cancer were observed during the first follow-up period. Although the cohort is young and the numbers small, a slightly significant (P = 0.04) trend was observed for individuals with cancer and a score of chromosomal aberrations. No trend was observed for sister chromatid exchanges. The application of cytogenetic surveillance is still not routine methodology, but it is useful and informative in carefully controlled study designs. Special efforts should be directed toward combining different disciplines, i.e., cytogenetics, adduct monitoring, and end-effect epidemiology, in order to reach quantitativeness in risk assessment.