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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Person-years at risk in occupational cohort mortality studies may be defined as "active" (when a person is working) or "inactive" (after a person has left employment at the plant under study). To investigate the effects of employment status (active/inactive) both across studies and within them, we have analyzed ten large cohort studies conducted by the National Institute for Occupational Safety and Health in which no occupational risk had been observed. These ten data sets included 89,376 workers, 1,984,505 person-years, and 18,840 deaths. In these ten studies, the SMR for all causes was positively correlated with the percentage of inactive person-years in the study (r = 0.57, p = 0.08). Considering only inactive person-years, the all-causes SMR was 1.12 (approximately 1.25 before age 65, dropping to 1.00 after age 65). Stratification of inactive person-years by time-since-last-employment showed markedly increased mortality during the first year following employment. The all-causes SMR during active person-years was 0.40 and was fairly constant across age categories. With active and inactive person-years combined, a strong negative trend in SMRs with duration of employment was observed for all causes and for heart disease. These trends were not apparent when person-years were stratified by employment status. These results indicate that investigators should evaluate the effects of employment status when comparing SMRs between multiple cohorts or when interpreting trends in rate ratios within cohorts.
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PMID:The importance of employment status in occupational cohort mortality studies. 179 Jan 93

We conducted a follow-up study to evaluate mortality among 14,861 workers employed in five facilities producing or using phenol and formaldehyde. More than 360,000 person-years of follow-up accrued. Mortality rates from all causes of death combined were similar to those in the general U.S. population. We observed excesses of cancer of the esophagus, cancer of the kidney, and Hodgkin's disease among workers exposed to phenol, but none of these excesses showed a dose-response relation with exposure to phenol. Excess lung cancer mortality (SMR = 1.2) showed no consistent pattern by any exposure index. Workers exposed to phenol had lower mortality ratios for cancer of the buccal cavity and pharynx, cancer of the stomach, cancer of the brain, arteriosclerotic heart disease, emphysema, disease of the digestive system, and cirrhosis of the liver. Of these, arteriosclerotic heart disease, emphysema, and cirrhosis of the liver were inversely related to duration of phenol exposure and to cumulative phenol exposure levels. Although these inverse associations may be due to chance or uncontrolled confounders, the ability of phenol to interfere with the generation of oxidants in experimental systems suggests that the pattern may have biologic plausibility.
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PMID:Mortality among industrial workers exposed to phenol. 205

An epidemiological study was undertaken to determine whether the animal carcinogen, epichlorohydrin (ECH), produces cancer in man. A total of 863 workers with probable exposure to ECH at two chemical plants during 1948-65 were followed up for deaths up to 1983. Twenty years or more after first exposure the all cancer SMR was 112.2 (22 deaths) and the SMR for leukaemia was 500.0 (three deaths), which is statistically significant. All cancer, leukaemia, and most other causes of death were related to estimated levels of exposure to ECH, except violence. The most consistent (both plants) relation was between exposure level and heart disease. Overall, the heart disease SMR 20 years or more after first exposure was 39.2 (five deaths) for low exposure and 105.4 (17 deaths) for high exposure. Limited evidence of a cardiovascular disease relation to ECH production in one other epidemiological study is supported by this study. Allyl chloride used in the production of ECH may play a part. The relation of heart disease and exposure does not appear to be an artifact, although the fact that many other causes of death were also related to exposure argues against a causal relation.
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PMID:Mortality of workers potentially exposed to epichlorohydrin. 224 92

Cause specific mortality was investigated among 36,622 members of a national furniture workers' union who were first employed in unionised shops between 1946 and 1962. Overall mortality for each race and sex group was less than expected when compared with United States death rates (white men SMR = 0.8, black men SMR = 0.7, white women SMR = 0.8, black women SMR = 0.5); however, raised risks were observed among white men employed in specific types of furniture industries and followed up for 20 or more years after first employment. Lymphatic and haematopoietic cancers were significantly raised (SMR = 1.8) among wood furniture workers followed up for at least 20 years due to excess deaths from leukaemia (SMR = 2.0) and non-Hodgkin's lymphoma (SMR = 2.0). Mortality from acute myeloid leukaemia was particularly high in this group (SMR = 4.7) based on six observed cases. Metal furniture workers followed up for at least 20 years experienced a significant excess of all cancers combined (SMR = 1.6), with non-significant increases in cancers of the lung, stomach, and colorectum. This group also had non-significant excesses of liver cirrhosis, arteriosclerotic heart disease, and cerebrovascular disease. Nasal cancer was not found to be significantly raised in this cohort, though the average follow up period may not have been sufficient to detect an excess risk for this uncommon tumour.
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PMID:Cancer and other mortality patterns among United States furniture workers. 277 70

The one-year outcome of syncope and transient loss of consciousness was studied prospectively in 188 patients aged over 65 admitted to internal medicine departments. Thirty-seven patients (19.6 p. 100) died. This mortality rate at one year was 2.34 times higher than that of a non-hospitalized french population of the same age group (standardized mortality ratio, SMR = 2.34, P less than 0.001). The frequency of sudden death (7 cases) was much higher than that observed in the reference population (0.05 expected deaths, P less than 0.0001). Overmortality was clearly apparent in groups with an initial diagnosis of heart disease (SMR = 2.36, P less than 0.01) or neurological disease (SMR = 4.25, P less than 0.001). The relapse rate was 28 p. 100 globally and up to 43 p. 100 in cardiac patients. In the group with iatrogenic symptoms treatment was appropriately corrected in 86 p. 100 of the patients, and none of these relapsed. One year after the initial episode 11 p. 100 of the surviving patients had been institutionalized.
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PMID:[1-year prognosis of syncope and brief loss of consciousness in patients over 65. A multicenter study of 188 cases]. 296 36

Very little is known about the long-term health risks associated with the high stress police officer occupation. We report here on a retrospective cohort of 2,376 ever-employed white male police officers employed between January 1950 and October 1979. Vital status was obtained for 96%, the officers accumulating a total of 39,462 person-years. Six-hundred sixty-one deaths were observed. Total mortality from all causes was comparable to that of the overall U.S. white male population (standardized mortality ratio [SMR] = 106). Significantly increased mortality was seen for all malignant neoplasms combined (SMR = 127), cancer of the esophagus (SMR = 286), and cancer of the colon (SMR = 180). Significantly lower than expected mortality was seen for infectious diseases (SMR = 26), respiratory diseases (SMR = 64), and accidents (SMR = 60). Internal cohort comparisons revealed that policeman exhibited significantly higher mortality from suicide compared to all other municipal employees (rate ratio = 2.9). Analysis of mortality by length of service as a police officer showed that those employed 10-19 years were at significantly increased risk of digestive cancers and cancers of the colon and lymphatic and hematopoietic tissues and decreased risk for all diseases of the circulatory system. Policeman employed more than 40 years had significantly elevated SMRs for all causes, all malignant neoplasms combined, digestive cancers, cancers of the bladder and lymphatic and hematopoietic tissues, and arteriosclerotic heart disease. Risk of mortality from arteriosclerotic heart disease tended to increase with increasing years employed. These findings are discussed in light of the police stress literature. The hypotheses generated in this study must be tested through study of the role of important confounders including reactions to stress on the job.
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PMID:Mortality of a municipal worker cohort: III. Police officers. 378 83

This retrospective cohort study examines mortality and cancer incidence among 3,686 men and 75 women who were employed as chemists in 1959. During the period 1964 to 1977, the male chemists experienced lower overall mortality than other salaried employees of the chemical company (198 deaths observed, 241.0 expected, SMR = 82). Large deficits are seen in lung cancer and arteriosclerotic heart disease death. The chemist appear to be at slightly higher risk for death from malignancies of the colon (12 observed, 6.7 expected, SMR = 178) and from cerebrovascular disease (15 observed, 10.8 expected, SMR = 138). The low overall mortality resulted in a larger than expected proportion of deaths due to cancer. Fewer than expected cases were diagnosed of cancer of all sited combined (61 observed, 86.5 expected, SIR = 71) and of the lung (8 observed, 20.0 expected, SIR = 40). The incidence rates of melanoma and of cancer of the prostate are slightly higher than expected, relative to the Third National Cancer Survey and the experience of nonchemists, respectively. Among female chemists, deaths due to all causes and suicide occurred more frequently than expected. Possible explanations for the lack of anticipated excess risks and for the observed deficits are presented.
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PMID:A retrospective cohort study of mortality and cancer incidence among chemist. 725 10

Animal studies show that antimony may cause lung cancer and heart and lung disease in rodents. In exposed humans, ECG abnormalities and heart and lung disease have been reported. This mortality study of 1,014 men employed between 1937 and 1971 in a Texas antimony smelter consisted primarily of workers of Spanish ancestry (n = 928, 91.5%). Hispanics are known to smoke at much lower rates than non-Hispanics, and their lung cancer and heart disease mortality is generally low. When ethnic-specific Texas lung cancer death rates were used for comparison, mortality from lung cancer among antimony workers was elevated (SMR) 1.39, 90% CI 1.01-1.88), and we observed a significant positive trend in mortality with increasing duration of employment. When ischemic heart disease death rates from three different Spanish-surnamed populations were used for comparison, the rate ratios for mortality from ischemic heart disease were 0.91 (90% CI 0.84-1.09), 1.22 (90% CI 0.78-1.89), and 1.49 (90% CI 0.84-2.63). Pneumoconiosis/ other lung disease death rates for Spanish-surnamed men were unavailable and so calculation of rate ratios used white males as a comparison population (SMR 1.22; 90% CI 0.80-1.80). These data suggest some increased mortality from lung cancer and perhaps nonmalignant respiratory heart disease in workers exposed to antimony. However, conclusions are limited by possible confounders and the difficulty of identifying appropriate referent groups.
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PMID:Mortality in a cohort of antimony smelter workers. 761 10

The long-term mortality experience of California agricultural workers who filed workers' compensation claims for respiratory diseases, pesticide illnesses, and injuries between 1946 and 1975 was observed until 1991 and compared to U.S. death rates. The respiratory disease claimants had an elevated relative risk of 3.27 (95% CI 2.09-4.86) for mortality from nonmalignant respiratory diseases (NMRD). Emphysema mortality was particularly high, with a relative risk of 5.94 (95% CI 2.56-11.70). NMRD mortality peaked 5 to 9 years after the claims were filed (relative risk 9.83, 95% CI 4.47-18.57) and was most strongly associated with exposure to wood, rice, coffee, and flour dusts. Among the pesticide illness claimants, mortality from heart disease was slightly elevated in the subcohort with systemic pesticide illness (SMR = 1.32, 95% CI 0.86-1.94). Among the injury claimants, risk was increased for motor vehicle deaths (relative risk 1.62, 95% CI 0.74-3.08). It was concluded that respiratory disease claimants in agriculture have a significantly elevated risk of mortality from respiratory diseases and that the risk is highest (10-fold) 5-9 years after claims are filed.
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PMID:Mortality in agricultural workers after compensation claims for respiratory disease, pesticide illness, and injury. 765 57

Previous studies of mortality among white males employed in a Charleston, South Carolina asbestos textile plant using chrysotile demonstrated significant excess mortality due to asbestos-related disease and a steep exposure-response relationship for lung cancer. This cohort was further studied by adding 15 years of follow-up and including mortality among white female and black male workers. Nested case-control analyses were undertaken to further explore possible differences in lung cancer risk by textile operation as well as possible confounding by mineral oil exposures. Preliminary data for white males have been previously published. White males experienced statistically significant excess mortality due to lung cancer (standardized mortality ratio [SMR] = 2.30; confidence interval [CI] = 1.88-2.79), all causes (SMR = 1.48; CI = 1.38-158), all cancers (SMR = 1.50; CI = 1.29-1.72), diabetes mellitus (SMR = 2.05; CI = 1.18-3.33), heart disease (SMR = 1.41; CI = 1.26-1.58), cerebrovascular disease (SMR = 1.50; CI = 1.08-2.02), pneumoconiosis and other respiratory diseases (SMR = 4.10; CI = 3.10-5.31), and accidents (SMR = 1.49; CI = 1.15-1.91). Among white females, statistically significant excesses occurred for lung cancer (SMR = 2.75; CI = 2.06-3.61), all causes (SMR = 1.21; CI = 1.11-1.32), pneumoconiosis and other respiratory diseases (SMR = 2.40; CI = 1.53-3.60), and other respiratory cancers (SMR = 14.98; CI = 4.08-38.7). Among the total cohort of black males, the only statistically significant excess observed was for pneumoconiosis (SMR = 2.19; CI = 1.23-3.62). Based on historical exposure measurements at the plant, there was a positive exposure-response relationship for both lung cancer and pneumoconiosis. Data for the entire cohort demonstrate an increase in the lung cancer relative risk of 2-3% for each fiber/cc-year of cumulative chrysotile exposure. This relationship was more consistent for the white male workers. The excess risk for lung cancer among white males and females appeared to occur at cumulative exposures lower than those for black males. Possible reasons for the lesser lung cancer risk among black males include less smoking and differences in airborne fiber characteristics experienced by black males as a result of plant job placement patterns. The case-control analysis found employment in preparation and carding operations (where most of the black males worked) to be associated with a slightly reduced lung cancer risk, although not statistically significant, whereas spinning and twisting employment was associated with a statistically significant increased lung cancer risk compared to other plant operations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Follow-up study of chrysotile asbestos textile workers: cohort mortality and case-control analyses. 781 May 43


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