From the aDepartment of Public Health and Clinical Medicine, Division of Occupational and Environmental Medicine, Umeå University, Umeå, Sweden; bAgeing and Living Conditions Programme, Umeå University, Umeå, Sweden; cCentre for Population Studies, Umeå University, Umeå, Sweden; and dDepartment of Public Health and Clinical Medicine, Division of Epidemiology and Global Health, Umeå University, Umeå, Sweden.
Climate change is projected to increase the frequency of extreme weather events. Short-term effects of extreme hot and cold weather and their effects on mortality have been thoroughly documented, as have epidemiologic and demographic changes throughout the 20th century. We investigated whether sensitivity to episodes of extreme heat and cold has changed in Stockholm, Sweden, from the beginning of the 20th century until the present.
We collected daily mortality and temperature data for the period 1901-2009 for present-day Stockholm County, Sweden. Heat extremes were defined as days for which the 2-day moving average of mean temperature was above the 98th percentile; cold extremes were defined as days for which the 26-day moving average was below the 2nd percentile. The relationship between extreme hot/cold temperatures and all-cause mortality, stratified by decade, sex, and age, was investigated through time series modeling, adjusting for time trends.
Total daily mortality was higher during heat extremes in all decades, with a declining trend over time in the relative risk associated with heat extremes, leveling off during the last three decades. The relative risk of mortality was higher during cold extremes for the entire period, with a more dispersed pattern across decades. Unlike for heat extremes, there was no decline in the mortality with cold extremes over time.
Although the relative risk of mortality during extreme temperature events appears to have fallen, such events still pose a threat to public health.
Despite robust evidence on the inverse relationship between socioeconomic status (SES) and mortality, deviations from expected results have been observed likely due to school achievement and psychosocial resources, termed as "reserve capacity." Since adolescence is a critical period in developing sound psychological and behavioural patterns and adolescent markers of SES were seldom used, we determine if family SES in adolescence predicts later mortality. We also study how reserve capacity (perceived health, health-promoting behaviour and social support) and school achievement modify this relationship and reduce the negative effects of low SES.
A longitudinal study was designed by linking baseline data on 12 to 18 year-old Finns in 1985-95 (N =?41,833) from the Adolescent Health and Lifestyle Surveys with register data on mortality and SES from Statistics Finland. Average follow-up time was 18.4 years with a total of 770,161 person-years. Cox regression models, stratified by sex, were fitted to determine the effects of variables measured during adolescence: family SES, reserve capacity and school achievement on mortality risk.
All reserve capacity dimensions significantly predicted mortality in boys. Perceived health and social support predicted that in girls. Adolescents with the lowest school achievement were more than twice at risk of dying compared to those with better school performance. Low SES increased the risk of death in boys (Hazard ratios: 1.6, 95% CI 1.1-2.4) but not in girls. Reserve capacity and school achievement weakened the effects of low SES on boys' risk of death.
High reserve capacity and good school achievement in adolescence significantly reduce the risk of mortality. In boys, these also mitigate the negative effect of low SES on mortality. These findings underscore the roles of reserve capacity and school achievement during adolescence as likely causal or modifying factors in SES-health inequalities.
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Younger age groups account for proportionally more mortality in influenza pandemics than in seasonal influenza epidemics. Mechanisms that might explain this include young people suffering from an over-reactive immune system ("cytokine storm"), older people benefiting from cross-immunity from a wider variety of previous influenza infections ("antigenic history"), and lifetime immune responses in all people being shaped by their first influenza A infection ("antigenic imprinting" or "original antigenic sin"). We examined whether these mechanisms can explain age-specific influenza mortality patterns, using the complete database of individual deaths in Canada from 1951 to 1999. The mortality pattern during the 1957 pandemic indicates that antigenic imprinting plays an important role in determining age-specific influenza virulence and that both shift years and major drift years contribute significantly to antigenic imprints. This information should help pandemic planners to identify age groups that might respond differently to novel influenza strains.
OBJECTIVES: This study compares mortality patterns for the Alaska Native population and the U.S. white population for 1989-1998 and examines trends for the 20-year period 1979-1998. METHODS: The authors used death certificate data and Indian Health Service population estimates to calculate mortality rates for the Alaska Native population, age-adjusted to the U.S. 1940 standard million. Data on population and mortality for U.S. whites, aggregated by 10-year age groups and by gender, were obtained from the National Center for Health Statistics, and U.S. white mortality rates were age-adjusted to the U.S. 1940 standard million. RESULTS: Overall, 1989-1998 Alaska Native mortality rates were 60% higher than those for the U.S. white population for the same period. There were significant disparities for eight of 10 leading causes of death, particularly unintentional injury, suicide, and homicide/legal intervention. Although declines in injury rates can be documented for the period 1979-1998, large disparities still exist. Alaska Native death rates for cancer, cerebrovascular disease, chronic obstructive pulmonary disease, and diabetes increased from 1979 to 1998. Given decreases in some cause-specific mortality rates in the U.S. white population, increased rates among Alaska Natives have resulted in new disparities. CONCLUSIONS: These data indicate that improvements in injury mortality rates are offset by marked increases in chronic disease deaths.
Alaska Native Epidemiology Center, Office of Alaska Native Health Research, Division of Community Health Services, Alaska Native Tribal Health Consortium, 4000 Ambassador Dr., C-DCHS, Anchorage, AK 99508, USA. email@example.com
OBJECTIVES: This article compared mortality data (1999-2003) for Alaska Natives (AN), U.S. white residents (USW), and Alaska white residents (AKW), and examined changes in mortality rates from 1979 to 2003. METHODS: We used SEERStat* software from the National Cancer Institute to calculate age-adjusted mortality rates. RESULTS: The AN all-cause mortality rate was 40% higher (rate ratio [RR]=1.4) than the rate for both the USW and AKW populations. Based on comparisons with USW, the largest disparities in AN mortality were found for unintentional injuries (RR=3.0), suicide (RR=3.1), and homicide (RR=4.4). Disparities were also found for eight of the 10 leading causes of death, including cancer (AN/USW RR=1.3), cerebrovascular disease (RR=1.3), chronic obstructive pulmonary disease (RR=1.4), pneumonia/influenza (RR=1.6), and chronic liver disease (RR=2.0). In contrast, the mortality rate for heart disease among AN was significantly lower (RR=0.9) than for USW, and lower-though not significantly lower-for diabetes. Findings were quite similar when rates for AN were compared with AKW. AKW also had high rates of unintentional injury mortality and suicide compared with USW, but the magnitude of the difference was much less for AKW. From 1979 to 2003, mortality rates among AN declined 16% for all causes, similar to the USW decline of 15%. CONCLUSIONS: Monitoring mortality rates and their trends is essential not only to understand the health status of a population but also to target areas for prevention and evaluate the impact of policy change or the effect of interventions over time.
We examined children hospitalised for invasive meningococcal disease, a leading cause of paediatric sepsis, in Troms County, North Norway, from 1973 to 2016, including the epidemic in the 1970s and 1980s.
This study was a retrospective review of children under the age of 15 years who were hospitalised for meningococcal disease at the University Hospital of North Norway and Harstad Hospital. We studied hospital and bacteriological records to determine the incidence rates and phenotypes involved.
There were 300 cases under 15 years and an incidence rate of 17 per 100,000 cases for 1973-2016. This was broken down into the following: 1973-1980 (n = 130, 49), 1981-1990 (n = 129, 39), and 1991-2016 (n = 41, 4.7), respectively. There were 21 (7%) deaths. Phenotype B:15:P1.7,16 was more common than the other phenotypes in the epidemic period before 1990 than after 1990 (p = 0.02) and had a significantly lower mortality rate than the other phenotypes (p = 0.04). Later years showed a more heterogenous phenotype distribution. Serogroup B was the dominant serogroup.
The B:15:P1.7,6 strain was more prevalent during the Norwegian epidemic of invasive meningococcal disease, but had a significantly lower mortality rate. The phenotype distribution was more heterogeneous after 1990. The dominant serogroup was B.
The author emphasizes that the mortality phenomenon is heterogeneous, integrating many components with different impact, with different methodological approaches to their evaluation. This paper presents an integrative approach to analysis of mortality. The following components are analyzed: total and age-associated mortality, violent deaths, perinatal mortality, hospital mortality, and deaths at home.
Research comparing mortality by socioeconomic status has found that inequalities are not the smallest in the Nordic countries. This is in contrast to expectations given these countries' policy focus on equity. An alternative way of studying inequality has been little used to compare inequalities across welfare states and may yield a different conclusion.
We used average life expectancy lost per death as a measure of total inequality in mortality derived from death rates from the Human Mortality Database for 37 countries in 2006 that we grouped by welfare state type. We constructed a theoretical 'lowest mortality comparator country' to study, by age, why countries were not achieving the smallest inequality and the highest life expectancy. We also studied life expectancy as there is an important correlation between it and inequality.
On average, Nordic countries had the highest life expectancy and smallest inequalities for men but not women. For both men and women, Nordic countries had particularly low younger age mortality contributing to smaller inequality and higher life expectancy. Although older age mortality in the Nordic countries is not the smallest. There was variation within Nordic countries with Sweden, Iceland and Norway having higher life expectancy and smaller inequalities than Denmark and Finland (for men).
Our analysis suggests that the Nordic countries do have the smallest inequalities in mortality for men and for younger age groups. However, this is not the case for women. Reducing premature mortality among older age groups would increase life expectancy and reduce inequality further in Nordic countries.
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This study investigates the relationship between business cycle fluctuations and health in the Canadian context, given that a procyclical relationship between mortality rates and unemployment rates has already been well established in the U.S. literature. Using a fixed effects model and provincial data over the period 1977-2009, we estimate the effect of unemployment rates on Canadian age and gender specific mortality rates. Consistent with U.S. results, there is some evidence of a strong procyclical pattern in the mortality rates of middle-aged Canadians. We find that a one percentage point increase in the unemployment rate lowers the predicted mortality rate of individuals in their 30s by nearly 2 percent. In contrast to the U.S. data, we do not find a significant cyclical pattern in the mortality rates of infants and seniors.