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Mortality data

If the probability of worker injury or death because of participation in a given work-related activity can be shown to be much less than the risk of injury or death associated with presently accepted activities under very similar circumstances (e.g., the same type of hazard), then you may feel more comfortable about accepting the status quo. Table 14 illustrates the types of public mortality data available for such comparisons. In the previous example, where the worker risk was calculated as 2 X 10 fatalities... [Pg.53]

Cardiovascular disease has been identified as one of the leading causes of death in organ transplant recipients.55 Posttransplant hypertension (HTN) is associated with an increase in cardiac morbidity and patient mortality in all transplant patients and is also an independent risk factor for chronic allograft dysfunction and loss.56 Based on all the available posttransplant morbidity and mortality data, it is imperative that posttransplant HTN be identified and managed appropriately. [Pg.846]

Cocco et al. (1997) evaluated cause-specific mortality among workers of a lead-smelting plant in Italy. The cohort consisted of 1,388 men whose vital status was followed from January 1950, or 12 months after the date of hiring, whichever was later, through December 1992. For this period, reference mortality rates of the Italian male population were available from the mortality data base of the World Health Organization (WHO). The deaths from all causes, all malignant neoplasms, diseases of the... [Pg.48]

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]

Oral LDlo values in a number of animal species are available for lead (see Table 2-3). Mortality data from longer-term studies in animals are often inconclusive. However, based on the information available in humans, it is apparent that high body burdens of lead can result in death, which is most often secondary to lead-induced encephalopathy. [Pg.280]

Table I. Comparative Mortality Data of Combustion Products of Polymers... Table I. Comparative Mortality Data of Combustion Products of Polymers...
The rather strong relationship between meat use and fatal diabetes was only recently discovered, and to our knowledge this relationship has not been reported by other investigators. Since most people with diabetes do not die from their disease, mortality data is not the preferable type of data to use in investigating a possible causative link between diabetes and meat use. However, the relationship is fairly strong and shows a dose-response pattern for both males and females despite a very limited number of diabetic deaths. There is a clear need for further studies to evaluate the relationship of meat and other dietary habits to the frequency of diabetes utilizing more direct methods of measuring diabetes risk. [Pg.172]

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]

Although it is generally accepted that mortality data are not sensitive indicators of morbidity factors, a consistent or significant effect of cotton exposure on health should display some manifestations in mortality indices. This is certainly not the case for textile workers. To date, every effort devoted to the identification of a measurable Influence of textile work on the mortality of its own operatives has failed to show any effect (35-38). Paradoxically, one of these surveys has concluded that more favorable mortality experience appears to characterize textile workers (38). [Pg.208]

Mortality data obtained from Office of Population and Statistics of England and Wales and Registrar-General of Scotland. Data for single drug or single drug+alcohol. [Pg.186]

Expected deaths are obtained from mortality tables, which are compiled from documented causes of death (usually death certificate) for the population of a nation or an area of a country. The usual sources of mortality data are mortality rates, commonly in five-year age groupings, published annually by vital records offices of a country or political subdivision (state, county, etc.). Some of the data sets are available through the World Health Organization tabulations of disease worldwide, which are based on the International Classification of Diseases. [Pg.145]

Young, J. L., C. L. Percy, A. S. Asire, eds. (1981). Surveillance, epidemiology and end results incidence and mortality data. 1973-1977. National Cancer Inst. Mono. No. 57. Bethesda, MD. [Pg.162]

Mortality data were also reported in intermediate-duration studies using rats, guinea pigs, and rabbits. In studies performed by Hollingsworth et al. (1956), rats, guinea pigs, and rabbits were exposed to... [Pg.33]

Conventionally this is interpreted as meaning that if NNT patients are treated with each treatment, one additional patient will benefit from being treated with the new treatment compared to the control. Applying this definition to the mortality data from the Hindle et al. study gives an NNTofl/(0.161—0.063) = 10.83. Conventionally this is interpreted as meaning that approximately 11 patients need to be treated intrathecally to save one life. [Pg.294]

Although life expectancy is the best available general measure of health outcomes, no life tables exist by disease. We constructed an alternative measure of disease-specific life expectancy by computing the proportion of deaths that occurred above certain ages, such as 65, using data on deaths by disease category from a time series of mortality data obtained from the Department of Health in Taiwan. ... [Pg.250]

Buckley NA, McManus PR (2002) Fatal toxicity of serotoninergic and other antidepressant drugs analysis of United Kingdom mortality data. BMJ 325 1332-1333 Buckley NA, Dawson AH, Whyte IM, O Connell DL (1995) Relative toxicity of benzodiazepines in overdose. BMJ 310 219-221... [Pg.496]

The mortality data were eompared for field and eultured heart urchins using two way ANO-VA. Survival data were statistically analyzed in ToxCalc using the Trimmed Spearman-Karber point estimate test to determine the lethal concentration LC i,. [Pg.60]

On the basis of an examination of toxicologic literature, case reports from Edgewood volunteers, and a review of mortality data conducted by the National Research Council Medical Follow-up Agency, the Committee found no evidence of chronic disease in animals or humans associated with single or repeated doses of the cholinesterase reactivators (oximes). [Pg.12]

Table 4-7 shows observed deaths in the three categories compared with age-specific expected numbers based on mortality data on U.S. white males born in 1891. In general, the observed expected ratios are lower than 1, apparently because the preinduction medical examinations excluded men not in good health. Deaths did increase sharply in the mustard-gas roster for 1930-1939. [Pg.121]

The oral LDso of isophorone was reported as 3450 mg/kg in male rats (Hazleton Labs 1964) and 2104-2150 mg/kg in female rats (Smyth et al. 1969, 1970). LDso values of 2700 200 mg/kg for male rats, 2100 200 mg/kg for female rats, and 2200 200 mg/kg for male mice also were reported by Dutertre-Catella (1976). The value reported by Hazleton Labs (1964) was estimated because the mortality data did not lend itself to statistical analysis. Furthermore, the doses were widely spaced, and the animals were fasted for only 3-4 hours before dosing, which could have interfered with gastrointestinal absorption of isophorone. Necropsy of rats that died revealed congestion of the lungs, kidneys, adrenals, and pancreas, and gastrointestinal inflammation. Necropsy of rats that survived the 14-day observation period revealed no effects. The studies by Smyth et al. (1969, 1970) were determinations of the joint toxic action of 27 pairs of industrial solvents (see Section 2.7 on Interactions with other chemicals), but the details of the individual LDs° determinations and the cause of death were not provided. Nevertheless, the values for isophorone were reproducible in the two studies by Smyth et al. (1969, 1970). The reason for the sex difference... [Pg.32]

A mortality study was conducted among 697 male employees (610 whites and 11 assumed to be white) at a chlorination plant in Tennessee (United States) (Wong, 1988). The cohort consisted of all employees at the plant between 1943 and 1980. Almost all of the cohort held jobs with potential exposure to benzotrichloride, benzyl chloride or benzoyl chloride, there being substantial overlap between these groups. The mortality data were compared with the United States national age- and cause-specific rates for five-... [Pg.460]

In the United Kingdom Prospective Diabetes Study a subgroup of patients taking sulfonylurea therapy to which metformin was added appeared to have had excess mortality. Data from 263 general practices in the UK were analysed 8488 patients took a sulfonylurea initially, to which metformin was added in 1868 (25). The crude mortality rates per 1000 person years were 59 and 40 respectively. Metformin was used initially in 3099 patients and a sulfonylurea was added in 867. The crude mortality rates per 1000 person years were 25 and 20 respectively. These results suggest there is no increased mortality risk with a combination of a sulfonylurea and metformin. [Pg.369]

Available in digital form for use on GIS so that they can be viewed interactively with other datasets, such as those for landuse and for animal and human morbidity and mortality data. [Pg.8]


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See also in sourсe #XX -- [ Pg.2 , Pg.4 , Pg.5 , Pg.72 ]




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Mortality

Mortality data defined

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