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Mortality studies

Spirtas R, Stewart PA, Lee JS, et al. 1991. Retrospective cohort mortality study of workers at an aircraft maintenance Facility 1. Epidemiological results. Br J Ind Med 515-530. [Pg.291]

Mortality studies for workers exposed occupationally to lead are available. These studies all report discrepant results, and all are limited with respect to study design. Therefore, no firm conclusions regarding cause and effect can be drawn from these studies relative to a minimum lethal dose. A cohort mortality study of employees at lead-producing facilities was conducted (Cooper 1988 Cooper et al. [Pg.37]

In summary, while no strong conclusions can be drawn based on these mortality studies, it is important to note that four of these studies (Fanning 1988 Malcolm and Barnett 1982 McDonald and Potter 1996 Michaels et al. 1991) reported some elevation in deaths due to cerebrovascular disease. No other studies reported increased mortality due to cerebrovascular disease caused by lead exposure. [Pg.49]

One cohort mortality study (Fanning 1988) has reported an increased mortality rate due to circulatory disease, but three others found no such correlation (Cooper 1988 Gerhardsson et al. 1986b, 1995a) as discussed in Section 2.2.1.1 (Table 2-1). An increased risk of death due to cerebrovascular disease was observed in a cohort of 1,261 white male newspaper printers (typesetters) (Michaels et al. 1991) (see Section 2.2.1.1). [Pg.52]

A cohort mortality study was conducted to compare the mortality rates due to chronic renal disease in 4,519 battery plant workers and 2,300 lead production or smelter workers from 1947 to 1980 (Cooper 1988 Cooper et al. 1985). The mortality data for these workers were compared with national mortality rates for white males. Environmental lead levels and PbB levels were available for only about 30% of all workers for varying time periods from 1947 to 1972. Statistically significant increases in mortality from "other hypertensive disease" and "chronic nephritis" were seen in both lead cohorts. Limitations of this study include the fact that various confounding factors, such as smoking, were not accounted for, and the workers were probably exposed to other toxic chemicals. [Pg.69]

In a historical cohort mortality study of 1,990 primary lead smelter workers, an SMR of 2.04 for mortality from renal cancer was calculated (Selevan et al. 1985). The cohort consisted of workers who had worked at least 1 year, with at least 1 day of employment at the smelter between 1940 and 1965. The cohort had been heavily exposed to lead and in 1976 the PbB levels averaged 56.3 pg/dL. Exposures to cadmium and arsenic were generally minor. A follow-up study of this cohort was conducted from 1977 through 1988 (Steenland et al. 1992). Analysis of the follow-up study revealed an excess of kidney cancer, particularly in the high-lead group (SMR 2.39). Although, as the authors indicate, the study is... [Pg.129]

FanningD. 1988. A mortality study of lead workers, 1926-1985. Arch Environ Health 43 247-251. [Pg.520]

Michaels D, Zoloth SR, Stem FB. 1991. Does low-level lead exposure increase risk of death A mortality study of newspaper printers. Int J Epidemiol 20 978-983. [Pg.549]

Nati onal Cancer Insti tute Mortality study of 25,316 workers potentially exposed to acrylonitrile in eight U.S. facilities between 1952 and 1965 NCI/NIOSH... [Pg.75]

Morrill Act of 1862, 24 353 Mortality studies, PCB-related, 13 141 Mortar cements, 5 500t Mortars, 5 467, 500t 21 482-483 citric acid application, 6 648 furan resins in, 12 274 slaked lime in, 15 64 Mortar substitute, sulfur coatings as, 23 593... [Pg.603]

Ditraglia D, Brown DP, Namekata T, et al. 1981. Mortality study of workers employed at organochlorine pesticide manufacturing plants. Scand J Work Environ Health 7 140-146. [Pg.170]

Ribbens PH. 1985. Mortality study of industrial workers exposed to aldrin, dieldrin and endrin. Int Arch Occup Environ Health 56 75-79. [Pg.186]

Cardiovascular Effects. In a cohort mortality study of workers in a large rubber and tire manufacturing plant, Wilcosky and Tyroler (1983) found a significant increase in mortality from ischemic heart disease in phenol exposed workers. Of the 25 solvents used in the plant, phenol exposure showed the strongest association with mortality from heart disease, greater even than that observed for exposure to carbon disulfide, the only known occupational cause of atherosclerosis. [Pg.44]

In a cohort-mortality study of workers from five phenol-formaldehyde resin plants, Dosemeci et al. [Pg.44]

Similar to the findings of Kauppinen et al. (1986), a large (14,861) cohort mortality study of workers in the phenol-formaldehyde resin manufacturing industry found nondose-related increases in the risk of... [Pg.53]

Alavanja MCR, Blair A, Masters M. 1988. Mortality study of workers in the grain industry [Abstract]. Am J Epidemiol 128 900. [Pg.111]

A mortality study of a cohort of 3,827 licensed male pesticide applicators was conducted in Florida. This cohort did not exhibit the healthy worker effect, as the overall SMR was close to expected (Blair et al. 1983). Increased SMRs, although not statistically significant, were seen for leukemia, cancers of the brain, and lung cancer. Follow-up was achieved for over 95% of the identified cohort members, but no information was available for smoking history. [Pg.19]

An occupational mortality study conducted on a cohort of workers employed for at least 3 months between 1952 and 1979 at a Velsicol plant in Memphis, Tennessee, revealed no pattern of disease... [Pg.22]

Death. Occupational mortality studies of pesticide workers exposed to heptachlor have not revealed an excess number of deaths in these cohorts compared to the general U.S. population. This may possibly be explained as a healthy worker effect. The ERA has described human case reports in which convulsions and death were reported following suicidal ingestion of technical-grade chlordane, which typically contains 6-30% heptachlor, but these effects cannot be attributed to heptachlor or heptachlor epoxide. There are no controlled, quantitative human data for any route of exposure. Acute lethality data were located for animals exposed via the oral and dermal routes. Both heptachlor and heptachlor epoxide may be considered very toxic via the oral route on the basis of acute animal data in rats and mice. Intermediate oral exposure to these compounds also caused up to 40% and 100% mortality in rats and mice, respectively. There appear to be differences in sensitivity in males and females in some species with the males being most sensitive. Heptachlor epoxide is more toxic than heptachlor. Heptachlor may be considered very toxic to extremely toxic via the dermal route on the basis of acute lethality data in rats and mice. The severity of acute effects may possibly depend upon the extent of formation of heptachlor epoxide and the species tested. [Pg.53]

There are occupational mortality studies that have collected data appropriate for determining whether those engaged in the manufacture or application of heptachlor are at increased risk for dying of cancer. These studies have not shown an increased risk of cancer mortality (Infante et al. 1978 MacMahon et al. 1988). Occupational studies that collected cancer incidence data, rather than just mortality data, would be useful for further exploration of this issue. [Pg.71]

Los Angeles, California, mortality studies on oxidants in, 417-19 Los Angeles County Air Pollution Control District (laapcd)... [Pg.713]

Whorton MD, Amsel J, Mandel J Cohort mortality study of prostrate cancer among chemical workers. Am J Ind Med 33(3) 293-296, 1998... [Pg.16]

In a retrospective mortality study of over 900 workers exposed from 3 months to 23 years to median time-weighted acetone concentrations up to 1070 ppm there was no significant risk of death from any cause (all causes, malignant neoplasm, circulatory system disease, ischemic heart disease) compared with rates for the general population. ... [Pg.17]

In a human mortality study of 371 workers no increase in total malignant neoplasms or any specific cancers attributable to acrylamide exposure were found." Exposure levels reached l.Omg/m before 1957 and were between 0.1 and 0.6mg/m after 1970. However, this study was of such a limited sample size that only large excesses could have been detected. [Pg.25]

Rockette HE, Arena VC Mortality studies of aluminum reduction plant workers Potroom and carbon department. J Occup Med 25 549-557, 1983... [Pg.38]

A mortality study of 1014 men employed between 1937 and 1971 in a Texas antimony smelter found increased mortality from lung cancer (standardized mortality ratio 1.39) and a positive trend in mortality with increasing duration of exposure. The data also suggested some increased mortality from nonmalignant respiratory heart disease in these workers. [Pg.53]

A subsequent mortality study of this same cohort found significant increases for death due to lung cancer. (Mortality from noncarcino-genic respiratory diseases including bronchitis, emphysema, and asthma also occurred in excess.)... [Pg.62]

Sorahan T, Waterhouse JAH, Coke MA, et al A mortality study of workers in a factory... [Pg.78]


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Cohort mortality studies

Meta-analysis studies mortality

Mortality

Mortality retrospective studies

Mortality time-series studies

Proportional mortality ratio studies

Updated Mortality Study (Summary)

Worker population, mortality studies

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