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PubMed2001

Observations on mortality during the 1918 influenza pandemic.

The original purpose of our study was to examine the unusual W-shaped mortality curve associated with the 1918 influenza pandemic and possibly explain the peak in mortality among individuals aged 20-40 years. We plotted age-specific excess mortality instead of total mortality for the 1918 pandemic using a 5-year baseline. For comparison, we also graphed excess mortality curves for the 1957 and 1968 pandemics using 5-year baselines. The 1957 and 1968 curves exhibited the usual U-shaped curve, with high excess mortality among infants and the elderly population relative to young adults. The 1918 curve, however, presented unexpected results. A peak in excess mortality among infants and young adults was seen, but the expected W shape did not result. We instead found negative excess mortality among elderly individuals, suggesting that this group was exposed, at an earlier date, to an influenza strain similar to the so-called Spanish influenza (H1N1) strain.

Adolescent↗
PubMed1998

Toward a broader definition of heat-related death: comparison of mortality estimates from medical examiners' classification with those from total death differentials during the July 1995 heat wave in Chicago, Illinois.

The classification of heat-related deaths solely according to body temperatures underestimates the magnitude of heat-related mortality during heat waves. Broader classifications are often used, but their utility in defining the mortality and identifying at-risk populations has not been evaluated. Using death data from the July 1995 heat wave in Chicago, the authors compared heat-related mortality rates based on the classification of heat-related deaths by the Cook County Medical Examiner's Office (CCMEO), with excess mortality rates based on total mortality differentials during and before the heat wave. In July 1995, the overall mortality in Chicago was 19 deaths per 100,000 population for heat-related mortality and 24 to 26 deaths per 100,000 population for excess mortality. Across Chicago community areas, the two mortality rates were closely related (r = 0.73-0.79; p < .01), but heat-related mortality rates were lower than excess mortality rates in community areas where excess mortality rates were higher (slope < 1; p < .01), a finding indicating an underestimation of heat-related deaths in such areas. The underestimation could not be explained by uncertainties in estimating excess mortality rates or by differences in socioeconomic and demographic characteristics among communities. These results support using the broader CCMEO classification of heat-related deaths as a relative indicator to target communities for prevention and relief efforts, but not as an adequate measure of actual heat-related mortality in a high-risk neighborhood.

Aged↗
PubMedDate not supplied

The GAME estimate of reduced life expectancy.

The Declining Exponential Approximation of Life Expectancy (DEALE) is a simple method of estimating the impact of excess mortality on life expectancy, but it can lead to considerable bias due to the implicit constant baseline and excess mortality rates. This article presents a new method that does not use constant mortality rates. The variability of the baseline mortality is modeled using gamma (GA) distributions. Excess mortality rates are modeled using mixed-exponential (ME) distributions, which is appropriate if the excess mortality rate is nonincreasing, convex, and smooth. The new gamma mixed-exponential (GAME) estimate is convenient enough to replace the DEALE in formal decision analyses. The error from assuming gamma distributions for the Dutch baseline mortality was shown to be less than 2 months and typically about 1 month. Therefore, the GAME estimate is accurate enough to replace more elaborate methods, provided the mixed-exponential model is an appropriate model for the excess mortality.

Age Factors↗
PubMed2006

Surveillance of the colorectal cancer disparities among demographic subgroups: a spatial analysis.

OBJECTIVE: The literature suggests that colorectal cancer mortality in Texas is distributed inhomogeneously among specific demographic subgroups and in certain geographic regions over an extended period. To understand the extent of the demographic and geographic disparities, the present study examined colorectal cancer mortality in 15 demographic groups in Texas counties between 1990 and 2001. METHODS: The Spatial Scan Statistic was used to assess the standardized mortality ratio, duration and age-adjusted rates of excess mortality, and their respective p-values for testing the null hypothesis of homogeneity of geographic and temporal distribution. RESULTS: The study confirmed the excess mortality in some Texas counties found in the literature, identified 13 additional excess mortality regions, and found 4 health regions with persistent excess mortality involving several population subgroups. CONCLUSION: Health disparities of colorectal cancer mortality continue to exist in Texas demographic subpopulations. Health education and intervention programs should be directed to the at-risk subpopulations in the identified regions.

Black People↗
PubMed1996

Ventilator-associated pneumonia due to Pseudomonas aeruginosa.

OBJECTIVE: Ventilator-associated pneumonia (VAP) caused by Pseudomonas aeruginosa has been associated with higher case fatality rates than VAP caused by other bacterial etiologies. The causes of this excess mortality are unclear. DESIGN: Retrospective review of 38 consecutive ventilated patients with Pseudomonas pneumonia, documented by highly reliable methods. Charts of five additional patients were unavailable for review. SETTING: Medical ICUs of a university-affiliated Veterans Affairs Medical Center and a university-affiliated municipal hospital. MEASUREMENTS: Prospectively collected hospital admission acute physiologic and chronic health examination (APACHE) II scores and cause of ICU admission. Retrospectively calculated organ failure and APACHE scores, VAP score. Clinical and microbiologic variables. Antibiotic treatment and outcome. Direct cause of death by standard definitions. RESULTS: Overall mortality was 69% (26/38), significantly higher than the APACHE II predicted mortality of 42.6% (p=0.037). At least 38% (10/26) of deaths were directly attributable to Pseudomonas VAP. Multivariate analysis of factors associated with death found infectious cause for ICU admission (odds ratio [OR]=8.67; 95% confidence interval [CI], 0.86 to 85.94) and number of organ dysfunctions on the day of diagnosis (OR=1.73, 95% CI, 1.02 to 2.92) were significant. Septic shock from Pseudomonas VAP, septic shock from subsequent infection, and multiple organ dysfunction syndrome were the most common immediate causes of death. Mortality increased linearly with increasing APACHE III score on the day of diagnosis. Of initial antibiotic regimens, 67% (26/36) were considered failures. Persistent pneumonia occurred in 35% of patients while recurrent pneumonia was unusual (1/38). CONCLUSIONS: Development of Pseudomonas pneumonia results in a mortality rate in excess of that due to the presenting illness. The attributable mortality determined by several means appears to approach 40%. The excess mortality appears to be related to the host defense response to the pneumonia rather than any characteristic of the pneumonia. Even standard antibiotic regimens fail frequently and do not prevent the excess mortality. Since at least 38% of deaths can be directly attributable to the Pseudomonas pneumonia, improvement in therapy is needed.

APACHE↗
PubMed1999

Does the work environment contribute to excess male mortality?

It is sometimes assumed that male jobs are on average more unhealthy than female jobs. The aim of the present study is to examine whether work-related factors contribute to excess male mortality. All Swedish deaths during 1970-80 and 1980-86 were analysed with Poisson regressions--for all individuals and for labour force participants--in order to estimate gender mortality rate ratios for all causes, circulatory diseases and external causes. Results for all men and women, as well as results restricted to those in full-time employment, revealed that no work-related factors contribute to excess male mortality. For the period 1980-86, a more detailed analysis was performed, and work environment exposures were aggregated from a secondary data source. In accordance with previous studies, it was found that men experience unhealthier physical work environments than women and that women experience unhealthier psychosocial work environments than men. Among labour force participants, men's greater exposure to hazardous work contributed to men's excess of external causes of death. This finding however, applied only to part-time workers. In conclusion, when factors such as women's greater likelihood of having a low socioeconomic status, their poor psychosocial work environment (low levels of work control and workplace social support), and the fact that women working full-time are more likely than men to be unmarried, were taken into account, the work environment did not appear to contribute to excess male mortality. It is suggested that the lack of reduction in excess male mortality during the 1970 s could be a consequence of the following: women commonly took jobs with low mortality rates; the rapid increase in the numbers of Swedish women in paid employment probably lowered their mortality; other social, behavioural and bio-genetical factors are more important than work in determining excess male mortality. Causality considerations are also discussed.

Adult↗
PubMedDate not supplied

Mortality in the years following bacterial meningitis.

During the years 1966-1976, 875 patients were treated for bacterial meningitis at the University Clinic for Infectious Diseases, Copenhagen. By about January 1, 1980, all 782 surviving patients had been traced. 87 had died in the observation period of four to 15 years. Mortality in the years following meningitis was studied by means of a comparison with the expected mortality in a matched normal population, using a computer program for the determination of late excess mortality. Late excess mortality was significantly increased during the first two years following discharge after meningitis and was of the same magnitude in the major etiological groups. The cumulative five-year late excess mortality rate was higher in the group of patients between 30 and 60 years, in those transferred from other hospitals, in those in coma or somnolence on admission and in those developing convulsions during hospitalization. In the group of patients aged 30 to 60 years, 11 patients died during the first two years after discharge. In nine of these cases, the main cause or the concomitant causes of death were conditions predisposing to infections or bacterial meningitis. The frequency of the causes of death in the 87 patients who died was not significantly different from that among the general Danish population.

Adolescent↗
PubMed1991

[Influenza and death. High mortality not only due to the great epidemics].

Excess mortality in a population is one of the hallmarks of an influenza epidemic. Apart from the pandemic years, 1918-1919, 1957 and 1968-1969, annual excess mortality has occurred 16 times in Sweden during the period 1911-1988. An unusually high mortality was caused by Influenza A Sichuan 2/87 (H3N2), the unexpected appearance of which at the beginning of November 1988 started an intensive epidemic in Sweden, while other European countries had a relatively mild influenza season. Swedish deaths in December totalled 10,500-2,200 more than expected; age groups over 65 years accounted for 95 per cent of the mortality, and those over 80 (N = 350,000 in Sweden) for 1,400 deaths. 0.4 percent of those over 80 died. The excess mortality is to be explained by the high proportion of the elderly in the Swedish population and the very low rate of influenza vaccination before the outbreak. As the increase in the proportion of the very elderly can be expected to continue, future influenza epidemics will result in even higher mortality unless adequate prophylactic measures are taken.

Adult↗
PubMed1981

Differences among hospitals as a source of excess neonatal mortality: the District of Columbia, 1970-1978.

Between 1970 and 1978 the neonatal mortality rate for black infants in the District of Columbia remained essentially constant while the national rate declined steadily. This report examines adjusted hospital-specific neonatal mortality rates in order to determine the extent to which the District's lack of improvement can be explained by excess mortality in a few hospitals. The indirect method of adjustment utilizing standardized morality ratios (SMRs) is used to control for the effect of the birth weight distribution on hospital-specific neonatal mortality rates. A generalized least squares approach is used to model the changes in the SMRs over time. No change was found in the SMRs for any hospital between 1970-72 and 1973-75, and four hospitals experienced no change in the 1973-75 to 1976-78 period (although one of these hospitals had very low SMRs initially). The remaining four hospitals experienced a 37% decline in their SMR's during the second interval (1973-75 to 1976-78). If the three hospitals that had high initial rates and showed no change in mortality rates from 1973-75 to 1976-78 had experienced the 37% decline, the District's SMR in 1976-78 would have been reduced by 20%.

Black or African American↗
PubMed1982

Increased mortality in rheumatoid arthritis.

A mortality study was performed on all patients treated in hospitals in Stockholm County who were diagnosed during 1971 as having rheumatoid arthritis. The group consisted of 1165 patients. They were followed up through 1978. The mortality was about 2.5 times higher than for the general Stockholm population, and the females had the highest excess mortality. The excess mortality was particularly high in cases of infection, and of gastrointestinal, urogenital and rheumatic disease. The mortality in cancer was no different from that of the general population, and there was also no excess mortality regarding any particular site or type of cancer. 20% of the deceased had RA as the underlying cause of death and 18% as contributory cause of death.

Adolescent↗
PubMed1990

Critical assessment of epidemiologic studies on the human carcinogenicity of 1,3-butadiene.

1,3-Butadiene, a major ingredient of synthetic rubber, has been shown to be carcinogenic in two animal species. To assess the possible human carcinogenicity of 1,3-butadiene, a critical review was undertaken of the epidemiologic literature. An early retrospective study of 8017 males employed in tire manufacturing found excess mortality for lymphatic and hematopoietic neoplasms in production workers (standardized mortality ratio, SMR = 560); these workers were exposed to 1,3-butadiene as well as to styrene and possibly to benzene. A recently updated epidemiologic study of 2568 workers at a butadiene manufacturing plant in Texas reported low mortality overall (SMR = 84) but found excess deaths for lymphosarcoma and reticulum cell sarcoma (SMR = 229). A retrospective study of workers employed at two synthetic rubber plants in Texas found excess mortality for lymphatic and hematopoietic malignancies in the older of these facilities; the excesses for lymphosarcoma (SMR = 224) and leukemia (SMR = 278) were most significant in wartime workers. A large, recently updated retrospective study of 12,113 workers employed in eight synthetic rubber manufacturing plants in the United States and Canada found excess mortality for lymphatic and hematopoietic cancer in production workers; the SMR for other lymphatic cancers in white production workers was 230, and the SMR for all lymphatic malignancies in black production workers was 507. These updated epidemiologic results strongly suggest an etiologic association between occupational exposure to 1,3-butadiene and human cancer. It is reasonable, therefore, to conclude that there now exists at least limited evidence for the human carcinogenicity of 1,3-butadiene.

Butadienes↗
PubMed1997

The significance of ulcer disease on late mortality after partial gastric resection.

OBJECTIVE: To study the causes of long-term mortality after peptic ulcer surgery with special attention to the impact of underlying ulcer disease. DESIGN: Retrospective cohort investigation. PATIENTS: A cohort of 1305 patients who had surgery for gastric and duodenal ulcer disease 29 to 59 years ago. At the end of follow-up 80% of gastric ulcer patients, and 64% of duodenal ulcer patients were dead. RESULTS: Overall mortality was significantly higher among gastric ulcer patients: standardized mortality ratio (SMR) 1.17 (95% confidence interval (CI) 1.05-1.29); duodenal ulcer patients had an overall mortality comparable to the reference population: SMR 1.06 (CI 0.97-1.15). Excess mortality among gastric ulcer patients was found to be due to neoplasms in gastrointestinal organs (SMR 1.54 (CI 1.11-2.11) which developed more than 20 years postoperatively, and to respiratory diseases and suicide unrelated to time since surgery. An increased mortality due to malignant tumours, respiratory diseases and suicide was also found among duodenal ulcer patients but this increased mortality was offset due to a significantly decreased mortality in diseases of the heart and vascular system (SMR 0.86 (CI 0.75-0.97)), evident mainly after 20 years postoperatively. Excess mortality due to gastrointestinal cancers outnumbered excess mortality from carcinomas in the respiratory organs, and was due to cancers in the stomach, colon and pancreas. CONCLUSION: An increased mortality due to gastrointestinal carcinoma, especially gastric and pancreatic carcinoma, is apparent regardless of underlying ulcer disease. As preventive measures against these tumours have yielded little benefit in prospective trials, and as smoking-related diseases and tumours together with suicide constitute 75% of the excess mortality, measures to combat smoking and suicide might be more worthwhile to reduce mortality in this cohort.

Adolescent↗
PubMed2001

Association between premature mortality and hypopituitarism. West Midlands Prospective Hypopituitary Study Group.

BACKGROUND: Four retrospective studies have reported premature mortality in patients with hypopituitarism with standard mortality ratios (SMRs) varying between 1.20 and 2.17. Patients with hypopituitarism have complex endocrine deficiencies, and the mechanisms underpinning any excess mortality are unknown. Furthermore, the suggestion has emerged that endogenous growth-hormone deficiency might account for any excess mortality. We aimed to clarify these issues by doing a large prospective study of total and specific-cause mortality in patients with hypopituitarism. METHODS: We followed up 1014 UK patients (514 men, 500 women) with hypopituitarism from January, 1992, to January, 2000. 573 (57%) patients had non-functioning adenomas, 118 (12%) craniopharyngiomas, and 93 (9%) prolactinomas. SMRs were calculated as the ratio of observed deaths to the number of deaths in an age-matched and sex-matched UK population. FINDINGS: The number of observed deaths was 181 compared with the 96.7 expected (SMR 1.87 [99% CI 1.62-2.16], p<0.0001). Univariate analysis indicated that mortality was higher in women (2.29 [1.86-2.82]) than men (1.57 [1.28-1.93], p=0.002), in younger patients, in patients with an underlying diagnosis of craniopharyngioma (9.28 [5.84-14.75] vs 1.61 [1.30-1.99], p<0.0001), and in the 353 patients treated with radiotherapy (2.32 [1.71-3.14] vs 1.66 [1.30-2.13], p=0.004). Excess mortality was attributed to cardiovascular (1.82 [1.30-2.54], p<0.0001), respiratory (2.66 [1.72-4.11], p<0.0001), and cerebrovascular (2.44 [1.58-4.18], p<0.0001) causes. There was no effect of hormonal deficiency on mortality, except for gonadotropin deficiency, which, if untreated was associated with excess mortality (untreated 2.97 [2.13-4.13] vs treated 1.42 [0.97-2.07], p<0.0001). Multiple regression analyses identified age at diagnosis, sex, a diagnosis of craniopharyngioma, and untreated gonadotropin deficiency as independent significant factors affecting mortality. INTERPRETATION: Patients with hypopituitarism have excess mortality, predominantly from vascular and respiratory disease. Age at diagnosis, female sex, and above all, craniopharyngioma were significant independent risk factors. Specific endocrine-axis deficiency, with the exception of untreated gonadotropin deficiency, does not seem to have a role.

Adenoma↗
PubMed1989

Incidence of AIDS and excess of mortality associated with HIV in haemophiliacs in the United Kingdom: report on behalf of the directors of haemophilia centres in the United Kingdom.

OBJECTIVE--To estimate the cumulative incidence of AIDS by time since seroconversion in haemophiliacs positive for HIV and to examine the evidence for excess mortality associated with HIV in those who had not yet been diagnosed as having AIDS. DESIGN--Analysis of data from ongoing national surveys. SETTING--Haemophilia centres in the United Kingdom. PATIENTS--A total of 1201 men with haemophilia who had lived in the United Kingdom during 1980-7 and were positive for HIV. INTERVENTION--None. END POINTS--Diagnosis of AIDS; death in those not diagnosed as having AIDS. MEASUREMENTS AND MAIN RESULTS--Estimation of cumulative incidence of AIDS and number of excess deaths in seropositive patients not diagnosed with AIDS. Median follow up after seroconversion was 5 years 2 months. Eight five patients developed AIDS. Cumulative incidence of AIDS five years after seroconversion was 4% among patients aged less than 25 at first test positive for HIV, 6% among those aged 25-44, and 19% among those aged greater than or equal to 45. There was little evidence that type or severity of haemophilia or type of factor VIII or IX that had caused HIV infection affected the rate of progression to AIDS. Mortality was increased among those who had not been diagnosed as having AIDS, especially among those with "AIDS related complex." Thirteen deaths were observed among 36 patients diagnosed as having AIDS related complex against 0.65 expected, and 34 deaths in 1080 other patients against 22.77 expected; both calculations were based on mortality rates observed in haemophiliacs in the United Kingdom in the late 1970s. CONCLUSIONS--Rate of progression to AIDS depended strongly on age. There is a substantial burden of fatal disease among patients positive for HIV who have not been formally diagnosed as having AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1998

The development of sex differences in cardiovascular disease mortality: a historical perspective.

OBJECTIVES: Little is known about why males have higher cardiovascular disease (CVD) mortality rates than do females. An important factor that has hampered efforts in this regard is the lack of clarity about whether male excess mortality from CVD has existed throughout history. To answer this question, an investigation was conducted of trends in CVD mortality differences between the sexes from the time when data first became available until the present, including the full range of age groups. METHODS: Mortality statistics for CVD in England and Wales from 1861 through 1992 and in the United States from 1900 through 1991 were used. RESULTS: Three stages in the relationship between male and female CVD mortality were found: (1) An early stage of equal male and female mortality, (2) a stage of the appearance of sex differences in mortality, and (3) a stage with consistently present male excess mortality. CONCLUSION: Male excess mortality from CVD has not always been present in the historical record. Further research is needed to elucidate the causes of this excess mortality.

Cardiovascular Diseases↗
PubMed1989

Mortality in psychiatric inpatients.

The number of persons taken into psychiatric hospital care during 1982 in France was estimated using data on length of stay and analysing these by the person-year method. The number of observed deaths was compared by sex and age group with the number of deaths expected if the mortality in the general French population in 1982 were applied to the numbers of inpatients of the same sex and age group. The result of this comparison was that the mortality in mentally ill inpatients was found to be 3 times higher than that in the general population. This higher rate is further accentuated in younger age groups, especially women. This excess mortality has been observed with respect to natural causes of death as well as to unnatural causes, i.e. injury and suicide. Deaths from diseases of the circulatory system are overrepresented. As is true in the general population, these diseases account for the greatest number of deaths. Excess mortality is also high from diseases of the respiratory system. There is a high excess mortality due to signs, symptoms and ill-defined conditions, especially among women. Only in the case of neoplasms is there no excess mortality. Finally, excess mortality is found for deaths by injury and poisoning, especially for women, and suicides, particularly among men. Nevertheless, up to the age of 34, the female suicide rate is higher than that of men.

Adolescent↗
PubMed1999

Maternal predictors of perinatal mortality: the role of birthweight.

BACKGROUND: Many maternal characteristics increase the risk for perinatal death. To locate potential sites for intervention, it is important to identify these risk factors and examine how much of the excess mortality is explained by infants' low birthweight. METHODS: Data on all newborns in Finland born between 1991 and 1993 (N = 199,291, of which 1461 were perinatal deaths) were obtained from the Medical Birth Register. Logistic regression analysis was used to adjust for background variables, both including and excluding infants' birthweight. The percentage reduction in odds ratios after adjustment for infants' birthweight was used to estimate the contribution of infants' low birthweight to the excess mortality. RESULTS: After adjusting confounding factors, increased risk for perinatal death was found for eight maternal characteristics. In the following the increased risk is given as odds ratios and the proportions of the excess mortality explained by infants' low birthweight are in parentheses: in-vitro fertilization 4.12 (> 100%); earlier stillbirth 3.43 (87%); higher maternal age, from 1.21 to 3.08 (38-99%); maternal diabetes 2.87 (50%); lower socioeconomic status, from 1.30 to 1.70 (27-44%); smoking during pregnancy 1.45 (> 100%); single mother 1.44 (50%); first birth 1.36 (75%). CONCLUSIONS: Excess mortality due to maternal risk factors occurred mainly through their tendency to cause low birthweight. However, the excess mortality associated with low socioeconomic status, single motherhood, and diabetes was mediated by other mechanisms in addition to low birthweight.

Adult↗
PubMed1993

Marriage selection and mortality patterns: inferences and fallacies.

Researchers have long wondered whether marital-status differences in mortality arise largely from selection mechanisms or from causal processes typically known as marriage protection. Unfortunately, many investigators have relied on aggregate patterns of mortality differentials--such as age schedules of excess mortality in the single population or the relationship between the level of excess mortality and the relative size of the single population--to make inferences about the relative importance of selection and causal processes. In this paper, a simple mathematical simulation model is used to demonstrate that many inferences derived from observed patterns are simply not justified. This finding highlights the importance of prospective data for assessing the relative importance of selection and causal factors in accounting for the excess mortality of the unmarried.

Adult↗