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PubMed2006

Interaction of maternal protein and carbon monoxide on pup mortality in mice: implications for global infant mortality.

BACKGROUND: The United States Surgeon General declared 2005 as the "Year of Healthy Child." To improve the health of all children, we need to start before pregnancy, with their mothers. Unfortunately, protein deficiency in the diets of poor pregnant mothers in developing countries is widespread. Carbon monoxide (CO) pollution is serious public health problem in developed and developing countries. METHODS: A two-way factorial experimental design was used. Mice were maintained on 27%, 16%, 8%, or 4% protein diets. Dams were exposed to 0 ppm (control), 65 ppm, or 125 ppm CO in air, in environmental chambers for 6 hr/day during the first 2 weeks of pregnancy. Controls were also subjected to environmental chamber conditions. Food and water were available at all times. Animals were allowed to deliver, and data on pup mortality was recorded. RESULTS: Litter size was not affected by CO exposure, but was directly related to the dietary protein levels. Pup weight was inversely related to the CO exposure level, and directly related to the dietary protein levels. Pup mortality on date of birth was increased by CO exposure and was inversely related to the dietary protein levels. Pup mortality at 1 week of age was increased by CO exposure and 55% of all pups died in 125 ppm CO exposed group. Pup mortality at 1 week of age was inversely related to dietary protein levels. All pups in the 4% dietary protein and in all concentrations of CO died. All pups in the 8% protein group and in all CO concentrations died except in 125 ppm CO group. Pup mortality in the 16% dietary protein group ranged from 14.8% in 0 ppm to 36.8% in 65 ppm CO groups. Pup mortality in the 27% dietary protein group ranged from 14.3% in the 0 ppm to 41.1% in the 125 ppm CO groups. CONCLUSIONS: DATA suggest that protein deficiency and CO exposure enhance pup mortality. The protein and CO also interact to increase pup mortality in 16% and 27% protein groups. Carbon monoxide exposure, along with protein deficiency during gestation, may be contributing factors for high rates of infant mortality in developing countries. The results of the study also suggest that un-vented combustion for heating and cooking, ambient pollution, and biomass smoke may have a major impact on the health of children worldwide; and may explain the causes of high infant mortality in poor countries and some sections of the United States population.

Analysis of Variance↗
PubMed2000

Maternal mortality in New York City: excess mortality of black women.

To assess maternal mortality in New York City, birth certificates and mortality records for New York City from 1988 through 1994 were linked and examined. During these 7 years, maternal mortality in New York City (defined by the International Classification of Diseases, 9th edition [ICD-9], as 630-676) per 100,000 live births significantly exceeded that of the country as a whole (20.2 vs. 8.2, respectively). Within New York City, an even greater variation of maternal mortality by race/ethnicity was noted, with the mortality ratio of whites, blacks, and Hispanics being 7.1, 39.5, and 14.4 per 100,000 live births, respectively. Socioeconomic characteristics such as educational attainment, marital status, and income influenced maternal mortality more in non-blacks than blacks. Analyses of cause-specific mortality revealed that, overall, ectopic pregnancy, embolism, and hypertension were the leading causes of death. However, the major factors explaining the excess maternal mortality among blacks were hypertension (mortality ratio of blacks to whites 5.57, 95% confidence interval 2.30-13.39), ectopic pregnancy (4.78, 95% confidence interval 2.40-9.51), and abortion (4.58, 95% confidence interval 1.72-12.22). These findings confirm a persisting gap in maternal death between black and white women. Indeed, if all New Yorkers who became pregnant enjoyed the survival of the city's non-Hispanic white residents, the difference in maternal mortality between the city and the nation would be eliminated.

Adolescent↗
PubMed2004

The metabolic syndrome and mortality from cardiovascular disease and all-causes: findings from the National Health and Nutrition Examination Survey II Mortality Study.

The prospective associations between the metabolic syndrome as defined by the National Cholesterol Education Program (NCEP/ATP III) expert panel and mortality from cardiovascular disease and all-causes has not been extensively examined. Using data from the National Health and Nutrition Examination Survey II Mortality Study (1976-1992), the author examined the association between the metabolic syndrome and mortality from all-causes and cardiovascular disease among 2431 US adults aged 30-75 years. The NCEP/ATP III criteria were modified to substitute body mass index >/=25 kg/m(2) for waist circumference for women and >/=30 kg/m(2) for men. After multiple-adjustment, the hazard ratios for participants with the metabolic syndrome were 1.37 (95% confidence interval (CI): 1.02, 1.85) for mortality from cardiovascular disease, 1.29 (95% CI: 0.92, 1.82) for mortality from coronary heart disease, 1.68 (95% CI: 0.86, 3.27) for mortality from stroke, 1.23 (95% CI: 0.95, 1.59) for mortality from diseases of the circulatory system, and 1.15 (95% CI: 0.92, 1.45) for all-cause mortality compared with participants without the syndrome. The association between the number of metabolic syndrome criteria and mortality from cardiovascular disease was near linear (P = 0.007). Three criteria of the syndrome-excess weight, hypertriglyceridemia, and low high-density lipoprotein cholesterol concentration-were not independently associated with any of the outcomes. Additional prospective studies are needed to examine the association between the metabolic syndrome and the incidence of cardiovascular disease and mortality from cardiovascular disease and all-causes.

Adult↗
PubMed2004

Income and mortality: the shape of the association and confounding New Zealand Census-Mortality Study, 1981-1999.

OBJECTIVE: To determine the shape of the income-mortality association, before and after adjusting for confounding by other socioeconomic variables. METHODS: Poisson regression analyses were conducted on 11.7 million years of follow-up of 25-59 year old New Zealand census respondents spanning four separate cohort studies (1981-1984, 1986-1989, 1991-1994, and 1996-1999). RESULTS: Mortality among low-income people was approximately two times that among high-income people. Adjustment for potential socioeconomic confounders (marital status, education, car access, and neighbourhood socioeconomic deprivation) halved the strength of the income-mortality association, but did not appreciably change the shape of the association. Further adjustment for labour force status largely removed the income-mortality association. The association of non-transformed income with mortality was non-linear, with a flattening out of the slope at higher incomes. Both the logarithm and rank of income appeared to have a better linear fit with the mortality rate, although the association of mortality with the logarithm of income flattened out notably at low incomes. CONCLUSIONS: Much, but not all, of the crude association of income with mortality could be due to confounding. Adjusting income-mortality associations for labour force status (also a proxy for health status) is problematic: on the one hand, it over-adjusts the association as poor health will be on the pathway from income to mortality; on the other hand, it appropriately adjusts for both confounding by labour force status and reverse causation whereby income changes as a result of poor health. Both logarithmic and rank transformations of income have a reasonable linear fit with income.

Censuses↗
PubMed2003

The effect of publicly reporting hospital performance on market share and risk-adjusted mortality at high-mortality hospitals.

BACKGROUND: It is unclear whether publicly reporting hospitals' risk-adjusted mortality affects market share and mortality at outlier hospitals. OBJECTIVES: To examine hospitals' market share and risk-adjusted mortality from 1991 to 1997 at hospitals participating in Cleveland Health Quality Choice (CHQC). RESEARCH DESIGN: Time series. SUBJECTS: Changes in market share were examined for all patients hospitalized with acute myocardial infarction, heart failure, gastrointestinal hemorrhage, obstructive pulmonary disease, pneumonia, or stroke at all 30 nonfederal hospitals in Northeast Ohio. Patients insured by Medicare were used to examine changes in mortality. MEASURES: Trends in market share (proportion of patients with the target conditions discharged from a given hospital) and risk-adjusted 30-day mortality. RESULTS: CHQC identified several hospitals with consistently higher than expected mortality. The five hospitals with the highest mortality tended to lose market share (mean change -0.6%, 95% CI -1.9-0.6), but this was not significant. The only outlier hospital with a large decline in market share had declining volume for 2 years before being declared an outlier. Risk-adjusted mortality declined only slightly at hospitals classified by us as "below average" (-0.8%; 95% CI, 2.9-1.8%) or "worst" (-0.4%; 95% CI -2.3-1.7). However, risk-adjusted mortality at one hospital changed from consistently above expected to consistently below expected shortly after first being declared an outlier. CONCLUSION: Despite CHQC's strengths, identifying hospitals with higher than expected mortality did not adversely affect their market share or, with one exception, lead to improved outcomes. This failure may have resulted from consumer disinterest or difficulty interpreting CHQC reports, unwillingness of businesses to create incentives targeted to hospitals' performance, and hospitals' inability to develop effective quality improvement programs.

Consumer Behavior↗
PubMed2005

Hospital variation in mortality after first acute myocardial infarction in Denmark from 1995 to 2002: lower short-term and 1-year mortality in high-volume and specialized hospitals.

BACKGROUND: This study used linked data from the National Hospital Registry to determine the factors that contribute to differences between hospitals in all-cause mortality after first acute myocardial infarction (AMI) between 1995 and 2002. METHODS: The study included 64,321 patients with their first admission for AMI between 1995 and 2002 and surviving the day of admission. Multilevel logistic regression was used to determine the relationships between regional and hospital characteristics and 28-day and 365-day mortality after adjusting for individual characteristics, period, and medical history. RESULTS: Tertiary cardiac care centers (odds ratio [OR], 0.80; 95% confidence interval [CI], 0.67-0.96) and main regional hospitals (OR, 0.90; 95% CI, 0.80-0.99) had improved 28-day mortality compared with local hospitals. A 2-fold increase in annual total MI volume decreased 28-day mortality (OR, 0.91; 95% CI, 0.87-0.94) and 365-day mortality (OR, 0.95; 95% CI, 0.91-0.98). Differences between hospitals were more substantial for short-term mortality, such that patients were about twice as likely to die within 28 days in hospitals with the worst performance versus those with the best performance. Higher regional AMI incidence was associated with lower mortality before 2000; this disappeared after 2000. Other regional contextual characteristics had very modest effects on mortality. CONCLUSIONS: Type of hospital, and especially total MI volume at the hospital level, were significantly associated with mortality after AMI. Individual hospitals varied substantially in both short- and long-term mortality.

Adult↗
PubMed2007

Risk of non-AIDS-related mortality may exceed risk of AIDS-related mortality among individuals enrolling into care with CD4+ counts greater than 200 cells/mm3.

OBJECTIVE: To quantify cause-specific mortality risk attributable to non-AIDS-related and AIDS-related causes before and after the advent of highly active antiretroviral therapy (HAART). METHODS: Competing-risk methods were used to determine the cumulative AIDS-related and non-AIDS-related risk of mortality between 1990 and the end of 2003 in the Johns Hopkins HIV Clinical Cohort, a prospective cohort study. RESULTS: Beginning in 1997 with the introduction of HAART, all-cause mortality declined and has remained stable at approximately 39 deaths per 1000 person-years. AIDS-related mortality continued to decline in this period (P = 0.008), whereas non-AIDS-related mortality increased (P < 0.001). Using competing-risk methods, the risk of dying attributable to AIDS-related causes remains significantly higher than the risk of dying attributable to non-AIDS-related causes for patients with a CD4 count 200 cells/mm, however, non-AIDS-related mortality was greater than AIDS-related mortality, particularly among injection drug users. Other transmission categories had similar AIDS-related and non-AIDS-related cumulative mortalities. CONCLUSIONS: HAART has reduced mortality rates among HIV-infected individuals, but further efforts to reduce mortality in this population require increased attention to conditions that have not traditionally been considered to be HIV related.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Mortality predicted by APACHE II. The effect of changes in physiological values and post-ICU hospital mortality.

The contribution of physiological values to the APACHE II score was determined by retrospective analysis of 11348 patients undergoing intensive care. Eleven physiological variables contributed a mean of 8.9 points, 54% of the total APACHE II score. The mortality ratio (observed hospital mortality/hospital mortality predicted by APACHE II) was 1.13. We altered the APACHE II scores and post-intensive care hospital mortality in order to examine the effect on the mortality ratio of these changes. Increasing scores by two or four points decreased mortality ratios to 1.00 and 0.89 respectively: decreasing scores by two or four points to a minimum of zero increased mortality ratios to 1.27 and 1.44 respectively. A 25% increase or decrease in post-intensive care hospital mortality changed mortality ratios to 1.21 and 1.05 respectively. Physiological values vary with the timing of collection and accuracy of recording. Small consistent differences in scores cause potentially important changes in the mortality ratio. Unless data collection and the effect of management before and after intensive care are standardised, using mortality ratios to compare intensive care units is likely to be inaccurate and misleading.

APACHE↗
PubMed2002

Persistent social class mortality differences in New Zealand men aged 15-64: an analysis of mortality during 1995-97.

OBJECTIVE: Social class mortality differences in New Zealand men aged 15-64 years have previously been examined for the periods 1975-77 and 1985-87 using the Elley-Irving social class scale. The objective was to repeat these analyses for 1995-97 in order to examine time trends, and to assess current social class patterns of mortality. METHODS: Age-standardised mortality rates were calculated for each social class and a weighted estimate of the social class mortality gradient was obtained. RESULTS: Male mortality declined 21% between 1985-87 and 1995-97, but the social class mortality differences have not diminished and may have even increased. The Relative Index of Inequality has increased from 1.8 in 1975-77 to 2.1 in 1985-87 and 2.3 in 1995-97. Unlike previous analyses, the relative social class mortality gradient was just as strong in the older age groups as in the younger age groups, indicating that the possible increase in social class gradient has largely occurred in the older age groups. CONCLUSIONS: These findings indicate that the potential to address the excess preventable mortality caused by socio-economic factors has not been fully realised in New Zealand. IMPLICATIONS: Social class analyses identify groups in the community that have an excess mortality that is potentially preventable. There are still major social class differences in mortality in New Zealand, and these differences may even have increased. It is important that these patterns are taken into account in public health planning and that further research is conducted to identify the mechanisms by which these differences occur.

Adolescent↗
PubMed2002

Added value of three-way methods for the analysis of mortality trends illustrated with worldwide female cancer mortality (1968-1985).

Trends in mortality rates are usually presented per tumour site or per country without an overall analysis of the complete data encompassing all three aspects (tumour sites, countries, trends). This paper presents a methodology for such an overall analysis using three-way methods applied to a data set on female mortality rates for 17 tumour sites of 43 countries for the years 1968-1985. Multivariate techniques like biplots and three-mode principal component analysis within an overall three-way analysis-of-variance framework were used. We confirmed the known patterns of comparatively high mortality for women due to cancer of the bladder, intestines, pancreas, rectum, breast, ovary, skin and leukaemia and the relatively low mortality rates for liver cancer in Western and Northern Europe, the USA, Australia and New Zealand. Also, the reverse pattern was observed for Middle and Southern Europe, Hong Kong, Singapore, and in Japan, and in some but not all Latin American countries. The relatively mortality due to cancer was high in the lungs, mouth, larynx and oesophagus in the British Isles, but was much less in other European countries. Mortality due to cancer of the thyroid, uterus, gall bladder and stomach was high in Middle European countries, as was the case in Japan, Chile and Costa Rica. Rates were low for Southern European countries, North America, Australia and New Zealand. Specific deviating patterns in the data were the more rapidly decreasing mortality rates for stomach cancer in Chile and Japan and the more rapidly increasing mortality rates for lung cancer in the USA, Scotland and Denmark. In conclusion, using three-way methods, it was feasible to analyse the cancer mortality data in their entirety. This enabled the simultaneous comparison of trends in relative mortality rates between all countries due to all tumour sites, as well as the identification of specific deviating trends for specific tumour sites in specific countries.

Cross-Cultural Comparison↗
PubMed1988

Post-1950 mortality trends and medical care: gains in life expectancy due to declines in mortality from conditions amenable to medical intervention in The Netherlands.

In order to assess the impact of medical care innovations on post-1950 mortality in The Netherlands, we analysed trends in mortality from a selection of conditions suggested by Rutstein et al.'s lists of "unnecessary untimely mortality". This selection covers 11 types of innovation, and includes 35 conditions which have become amenable to medical care. Loglinear regression analysis shows that for most of these conditions mortality declined during each of two subperiods (1950-1968; 1969-1984). Mortality decline accelerated in the second subperiod for many conditions. Reductions in mortality from these conditions between 1950/54 and 1980/84 added 2.96 and 3.95 years to life expectancy at birth of Dutch males and Dutch females respectively. A priori evidence indicates that these mortality reductions are due to some extent to 'spontaneous' incidence declines. Although the exact contribution of medical care innovations to these changes in mortality thus cannot be determined, the impact of medical care on post-1950 mortality in The Netherlands could well have been substantial.

Cause of Death↗
PubMed2005

Does testing for prostate-specific antigen contribute to declining prostate cancer mortality? Estimating the broader economic influences on aggregate prostate cancer mortality rates.

Key variables associated with prostate cancer mortality were examined using Canadian province level time-series data over the period 1979-1999 in a multiple regression framework. The key variables driving the prostate cancer mortality rate are per capita income, per capita number of family physicians, rate of prostate cancer incidence, real per capita total health spending, and a time trend. As well, provincial dummy variables show that regional differences exist with higher rates of mortality in eastern Canada. Econometric results show a positive and significant relationship between incidence and mortality, suggesting that the increased amount of prostate-specific antigen (PSA) testing may not have been responsible for mortality declines. However, there is also a downward trend in mortality from prostate cancer when all other factors are controlled for that can be attributed partly to the onset of PSA testing given that the benefits should emerge over time. A 1% increase in incidence is associated with a 0.2% increase in mortality. A 1% increase in real per capita income is associated with a 0.5% increase in mortality when real per capita income is below Canadian dollars 20,054. A 1% increase in the per capita number of family physicians reduces the mortality rate by 0.5%. A 1% increase in real per capita total health expenditures is associated with a 0.7% decline in the mortality rate. Finally, by 1999 there were 4.74 fewer deaths per 100,000 population due to the effect of time after controlling for all other factors--a decrease of approx. 15%.

Aged↗
PubMed1991

Longitudinal Gompertzian analysis of primary malignant brain tumor mortality in the U.S., 1962-1987: rising mortality in the elderly is the natural consequence of competitive deterministic dynamics.

Age-adjusted mortality rates for primary malignant brain tumors (PMBT) in the United States from 1962 to 1987 were subjected to longitudinal Gompertzian analysis. Age-adjusted PMBT mortality rate distributions between age 25 and 65 years were determined by a variable environmental factor and a common intersect point. The environmental factor declined (improved) 1.58-fold for men and 2.34-fold for women in 1987 as compared to 1962. The age at the common intersect point was 68.4 years for men and 64.1 years for women. Between 1962 and 1987, non-age-standardized annual crude PMBT mortality rates increased 14.5% for men and 37.8% for women. However, PMBT mortality rates at age 77.5 years rose 259% for men and 409% for women between 1962 and 1987. Longitudinal Gompertzian analysis of PMBT mortality data suggests that rapidly rising PMBT mortality rates in the elderly are the natural consequence of competitive deterministic mortality dynamics and should not be attributed to environmental factors, past or present, that are directly contributing to PMBT mortality. Furthermore, longitudinal Gompertzian analysis demonstrates that PMBT mortality should not be studied in isolation, but rather should be examined in relation to other causes of death. When viewed from this perspective, the basis for the dramatic rise in PMBT mortality in the elderly becomes quite evident.

Adult↗
PubMed1992

Rising mortality due to Parkinson's disease and amyotrophic lateral sclerosis: a manifestation of the competitive nature of human mortality.

Over the past 15 yr, a marked increase in crude mortality rates from Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS) has occurred in the U.S. This is often attributed to as yet undefined environmental factors. The deterministic risk of general mortality and mortality due to PD, ALS, ischemic heart disease (IHD), and stroke for the years 1963, 1977, and 1986 in the U.S., as defined by the method of longitudinal Gompertzian analysis, were calculated and compared. When the rise in PD and ALS mortality is viewed from the perspective of deterministic and competitive mortality dynamics, it becomes evident that the major force increasing mortality from these two neurologic diseases is the declining mortality from IHD and stroke. Consequently, there is no need to invoke intrinsic etiologic alterations in the environment to account for the observed increases in PD and ALS mortality. Recognition of the competitive nature of human mortality illustrates the inherent risk of making etiopathogenic conclusions based upon single disease mortality data.

Adult↗
PubMed1997

The effect of different sensitivity, specificity and cause-specific mortality fractions on the estimation of differences in cause-specific mortality rates in children from studies using verbal autopsies.

BACKGROUND: Verbal autopsies (VA) are increasingly being used in developing countries to determine causes of death, but little attention is generally given to the misclassification effects of the VA. This paper considers the effect of misclassification on the estimation of differences in cause-specific mortality rates between two populations. METHODS: The bias in the percentage difference in cause-specific mortality between two populations has been explored under two different models: i) assuming that mortality from all other causes does not differ between the two populations; ii) allowing for a difference in mortality from all other causes. The bias is described in terms of the sensitivity and specificity of the VA diagnosis and the proportion of mortality due to the cause of interest. Methods for adjustment of sample size and adjusting the estimate of effect are also explored. RESULTS: The results are illustrated for a range of plausible values for these parameters. The bias is more extreme as both sensitivity and specificity fall, and is particularly affected even by a small loss of specificity. The bias also increases as the proportion of all deaths due to the cause of interest decreases, and is affected by the size of the true change in mortality due to the cause of interest relative to the change in mortality from other causes. Calculations from existing data suggest prohibitively large sample sizes may often be required to detect important differences in cause-specific mortality rates in studies using existing VA. CONCLUSIONS: Highly specific VA tools are needed before observed differences in cause-specific mortality can be interpreted. Loss of power due to misclassification may obscure real differences in cause-specific mortality.

Autopsy↗
PubMed2004

How far are socioeconomic differences in coronary heart disease hospitalization, all-cause mortality and cardiovascular mortality among adult Swedish males attributable to negative childhood circumstances and behaviour in adolescence?

OBJECTIVES: Coronary heart disease (CHD) and mortality are unevenly distributed between social classes, the lower being disadvantaged compared with the higher. Adverse social circumstances in childhood have been related to an increased risk of CHD and mortality in adulthood. The present purpose was to investigate the effect of differences in social disadvantage in early life on later differences in risk of CHD, all-cause mortality, and cardiovascular mortality between socioeconomic groups among Swedish men aged 40-50. METHODS: Data on circumstances in childhood and adolescence, e.g. crowded housing and low social position of the father, measured at age 9-11, was collected among 49,323 men, born in 1949-51, and conscripted for compulsory military training in 1969/70. Data on adult socioeconomic position was obtained from the 1990 census, data on CHD from the Swedish In-patient Care register 1991-2000, and data on mortality from the Causes of Death register 1991-2000. RESULTS: A social gradient was found for all health outcomes. The relative risk of CHD, all-cause mortality, and cardiovascular mortality among unskilled workers compared with that among high-level non-manual employees was 1.82 (95% CI: 1.36, 2.44), 2.24 (95% CI: 1.72, 2.93), and 2.38 (95% CI: 1.47, 3.86) respectively. The early life risk indicators, such as crowded housing and low childhood social position (measured at age 9-11), short stature (measured at age 18-20), and low education (reported at age 18-20), were more common among those who in 1990 (i.e. at age 39-41) were manual workers than among those who were in non-manual occupations. In multivariate analyses, considering the indicators of childhood social disadvantage and adjusting for lifestyle factors established at age 18-20, (smoking, alcohol consumption, overweight) the increased relative risk of CHD hospitalization and cardiovascular mortality in the four categories of employed workers was reduced by 72-100%. CONCLUSION: Predictors of CHD measured in childhood and adolescence may explain a substantial part of the social gradient in CHD, cardiovascular mortality, and all-cause mortality among the 40-50 year old males studied.

Adolescent↗
PubMed1999

Update of the Texaco mortality study 1947-93: Part I. Analysis of overall patterns of mortality among refining, research, and petrochemical workers.

OBJECTIVE: To update information on the workers of the Texaco mortality study to determine if the patterns of mortality have changed with 16 additional years of follow up. SUBJECTS AND METHODS: All workers were employed for > or = 5 years at company refineries, petrochemical plants, and research laboratories from 1947-93. The cohort now consists of 28,480 employees with an average of > or = 20 years of follow up. RESULTS: The overall mortality, and most cause specific mortalities were lower than or similar to those for the general population of the United States. For white men (86% of the cohort), there were 8873 observed deaths and 11,181 expected resulting in a significantly lower standardised mortality ratio (SMR) of 79. There were significant deficits for all the leading causes of death in the United States including all cancers, cancer of the lung, stroke, heart disease, respiratory disease, and accidents. Slightly increased mortality was found for cancer of the pancreas, cancer of the brain and central nervous system, leukaemia, and cancer of other lymphatic tissue. For cancer of the bone, the SMR was 162 (95% confidence interval (95% CI) 86 to 278), and for benign and unspecified neoplasms, it was 152 (95% CI 109 to 206). Overall mortality patterns for non-white men and women were similar to those for white men. Mortality patterns for white men were also examined by duration of employment, time first employed, location, and by job and process unit. There were significantly increased SMRs for brain cancer for those people employed as laboratory workers and on units with motor oil and for cancer of other lymphatic tissue for people employed on the fluid catalytic cracking unit. CONCLUSIONS: The results of the updated study showed a favourable mortality experience for employees in the Texaco mortality study compared with the United States population. There were a few increases found consistently including, but not limited to, brain cancer and cancer of other lymphatic tissue. These increases led to additional analyses that will be discussed in the accompanying paper.

Brain Neoplasms↗
PubMed2006

International differences in dialysis mortality reflect background general population atherosclerotic cardiovascular mortality.

Existing national, racial, and ethnic differences in dialysis patient mortality rates largely are unexplained. This study aimed to test the hypothesis that mortality rates related to atherosclerotic cardiovascular disease (ASCVD) in dialysis populations (DP) and in the background general populations (GP) are correlated. In a cross-sectional, multinational study, all-cause and ASCVD mortality rates were compared between GP and DP using the most recent data from the World Health Organization mortality database (67 countries; 1,571,852,000 population) and from national renal registries (26 countries; 623,900 population). Across GP of 67 countries (14,082,146 deaths), all-cause mortality rates (median 8.88 per 1000 population; range 1.93 to 15.40) were strongly related to ASCVD mortality rates (median 3.21; range 0.53 to 8.69), with Eastern European countries clustering in the upper and Southeast and East Asian countries in the lower rate ranges. Across DP (103,432 deaths), mortality rates from all causes (median 166.20; range 54.47 to 268.80) and from ASCVD (median 63.39 per 1000 population; range 21.52 to 162.40) were higher and strongly correlated. ASCVD mortality rates in DP and in the GP were significantly correlated; the relationship became even stronger after adjustment for age (R(2) = 0.56, P < 0.0001). A substantial portion of the variability in mortality rates that were observed across DP worldwide is attributable to the variability in background ASCVD mortality rates in the respective GP. Genetic and environmental factors may underlie these differences.

Atherosclerosis↗