Investigating changes in mortality attributable to heat and cold in Stockholm, Sweden.
Ontology highlight
ABSTRACT:
SUBMITTER: Oudin Astrom D
PROVIDER: S-EPMC6132879 | biostudies-other | 2018 Sep
REPOSITORIES: biostudies-other
Publications
Investigating changes in mortality attributable to heat and cold in Stockholm, Sweden.
Oudin Åström Daniel D Ebi Kristie L KL Vicedo-Cabrera Ana Maria AM Gasparrini Antonio A
International journal of biometeorology 20180511 9
Projections of temperature-related mortality rely upon exposure-response relationships using recent data. Analyzing long historical data and trends may extend knowledge of past and present impacts that may provide additional insight and improve future scenarios. We collected daily mean temperatures and daily all-cause mortality for the period 1901-2013 for Stockholm County, Sweden, and calculated the total attributable fraction of mortality due to non-optimal temperatures and quantified the cont ...[more]
Similar Datasets
Project description:Aims: The present study aimed to investigate if set thresholds in the Swedish heat-wave warning system are valid for all parts of Sweden and if the heat-wave warning system captures a potential increase in all-cause mortality and coronary heart disease (CHD) mortality. An additional aim was to investigate whether neighbourhood deprivation modifies the relationship between heat waves and mortality. Methods: From 1990 until 2014, in 14 municipalities in Sweden, we collected data on daily maximum temperatures and mortality for the five warmest months. Heat waves were defined according to the categories used in the current Swedish heat-wave warning system. Using a case-crossover approach, we investigated the association between heat waves and mortality in Sweden, as well as a modifying effect of neighbourhood deprivation. Results: On a national as well as a regional level, heat waves significantly increased both all-cause mortality and CHD mortality by approximately 10% and 15%, respectively. While neighbourhood deprivation did not seem to modify heat wave-related all-cause mortality, CHD mortality did seem to modify the risk. Conclusions: It may not be appropriate to assume that heat waves in Sweden will have the same impact in a northern setting as in a southern, or that the impact of heat waves will be the same in affluent and deprived neighbourhoods. When designing and implementing heat-wave warning systems, neighbourhood, regional and national information should be incorporated.
| S-EPMC6713612 | biostudies-literature
Project description:BackgroundThe relationship between statin treatment and Coronavirus Disease 2019 (COVID-19) mortality has been discussed due to the pleiotropic effects of statins on coagulation and immune mechanisms. However, available observational studies are hampered by study design flaws, resulting in substantial heterogeneity and ambiguities. Here, we aim to determine the relationship between statin treatment and COVID-19 mortality.Methods and findingsThis cohort study included all Stockholm residents aged 45 or older (N = 963,876), followed up from 1 March 2020 until 11 November 2020. The exposure was statin treatment initiated before the COVID-19-pandemic, defined as recorded statin dispensation in the Swedish Prescribed Drug Register between 1 March 2019 and 29 February 2020. COVID-19-specific mortality was ascertained from the Swedish Cause of Death Registry. Hazard ratios (HRs) were calculated using multivariable Cox regression models. We further performed a target trial emulation restricted to initiators of statins. In the cohort (51.6% female), 169,642 individuals (17.6%) were statin users. Statin users were older (71.0 versus 58.0 years), more likely to be male (53.3% versus 46.7%), more often diagnosed with comorbidities (for example, ischemic heart disease 23.3% versus 1.6%), more frequently on anticoagulant and antihypertensive treatments, less likely to have a university-level education (34.5% versus 45.4%), and more likely to have a low disposable income (20.6% versus 25.2%), but less likely to reside in crowded housing (6.1% versus 10.3%). A total of 2,545 individuals died from COVID-19 during follow-up, including 765 (0.5%) of the statin users and 1,780 (0.2%) of the nonusers. Statin treatment was associated with a lowered COVID-19 mortality (adjusted HR, 0.88; 95% CI, 0.79 to 0.97, P = 0.01), and this association did not vary appreciably across age groups, sexes, or COVID-19 risk groups. The confounder adjusted HR for statin treatment initiators was 0.78 (95% CI, 0.59 to 1.05, P = 0.10) in the emulated target trial. Limitations of this study include the observational design, reliance on dispensation data, and the inability to study specific drug regimens.ConclusionsStatin treatment had a modest negative association with COVID-19 mortality. While this finding needs confirmation from randomized clinical trials, it supports the continued use of statin treatment for medical prevention according to current recommendations also during the COVID-19 pandemic.
| S-EPMC8516243 | biostudies-literature
Project description:BackgroundMany studies have linked weather to mortality; however, role of such critical factors as regional variation, susceptible populations, and acclimatization remain unresolved.MethodsWe applied time-series models to 107 US communities allowing a nonlinear relationship between temperature and mortality by using a 14-year dataset. Second-stage analysis was used to relate cold, heat, and heat wave effect estimates to community-specific variables. We considered exposure timeframe, susceptibility, age, cause of death, and confounding from pollutants. Heat waves were modeled with varying intensity and duration.ResultsHeat-related mortality was most associated with a shorter lag (average of same day and previous day), with an overall increase of 3.0% (95% posterior interval: 2.4%-3.6%) in mortality risk comparing the 99th and 90th percentile temperatures for the community. Cold-related mortality was most associated with a longer lag (average of current day up to 25 days previous), with a 4.2% (3.2%-5.3%) increase in risk comparing the first and 10th percentile temperatures for the community. Mortality risk increased with the intensity or duration of heat waves. Spatial heterogeneity in effects indicates that weather-mortality relationships from 1 community may not be applicable in another. Larger spatial heterogeneity for absolute temperature estimates (comparing risk at specific temperatures) than for relative temperature estimates (comparing risk at community-specific temperature percentiles) provides evidence for acclimatization. We identified susceptibility based on age, socioeconomic conditions, urbanicity, and central air conditioning.ConclusionsAcclimatization, individual susceptibility, and community characteristics all affect heat-related effects on mortality.
| S-EPMC3366558 | biostudies-literature
Project description:Climate change affects human health; however, there have been no large-scale, systematic efforts to quantify the heat-related human health impacts that have already occurred due to climate change. Here, we use empirical data from 732 locations in 43 countries to estimate the mortality burdens associated with the additional heat exposure that has resulted from recent human-induced warming, during the period 1991-2018. Across all study countries, we find that 37.0% (range 20.5-76.3%) of warm-season heat-related deaths can be attributed to anthropogenic climate change and that increased mortality is evident on every continent. Burdens varied geographically but were of the order of dozens to hundreds of deaths per year in many locations. Our findings support the urgent need for more ambitious mitigation and adaptation strategies to minimize the public health impacts of climate change.
| S-EPMC7611104 | biostudies-literature
Project description:Preliminary evidence points to higher morbidity and mortality from coronavirus disease 2019 (COVID-19) in certain racial and ethnic groups, but population-based studies using microlevel data are lacking so far. We used register-based cohort data including all adults living in Stockholm, Sweden, between January 31, 2020 (the date of the first confirmed case of COVID-19) and May 4, 2020 (n = 1,778,670) to conduct Poisson regression analyses with region/country of birth as the exposure and underlying cause of COVID-19 death as the outcome, estimating relative risks and 95% confidence intervals. Migrants from Middle Eastern countries (relative risk (RR) = 3.2, 95% confidence interval (CI): 2.6, 3.8), Africa (RR = 3.0, 95% CI: 2.2, 4.3), and non-Sweden Nordic countries (RR = 1.5, 95% CI: 1.2, 1.8) had higher mortality from COVID-19 than persons born in Sweden. Especially high mortality risks from COVID-19 were found among persons born in Somalia, Lebanon, Syria, Turkey, Iran, and Iraq. Socioeconomic status, number of working-age household members, and neighborhood population density attenuated up to half of the increased COVID-19 mortality risks among the foreign-born. Disadvantaged socioeconomic and living conditions may increase infection rates in migrants and contribute to their higher risk of COVID-19 mortality.
| S-EPMC7989658 | biostudies-literature
Project description:BackgroundPrevious studies have shown that the experience of parental death during childhood is associated with increased mortality risk. However, few studies have examined potential pathways that may explain these findings. The aim of this study is to examine whether familial and behavioural factors during adolescence and socioeconomic disadvantages in early adulthood mediate the association between loss of a parent at age 0 to 12 and all-cause mortality by the age of 63.Methods and findingsA cohort study was conducted using data from the Stockholm Birth Cohort Multigenerational Study for 12,615 children born in 1953, with information covering 1953 to 2016. Familial and behavioural factors at age 13 to 19 included psychiatric and alcohol problems in the surviving parent, receipt of social assistance, and delinquent behaviour in the offspring. Socioeconomic disadvantage in early adulthood included educational attainment, occupational social class, and income at age 27 to 37. We used Cox proportional hazard regression models, combined with a multimediator analysis, to separate direct and indirect effects of parental death on all-cause mortality. Among the 12,582 offspring in the study (men 51%; women 49%), about 3% experienced the death of a parent in childhood. During follow-up from the age of 38 to 63, there were 935 deaths among offspring. Parental death was associated with an elevated risk of mortality after adjusting for demographic and household socioeconomic characteristics at birth (hazard ratio [HR]: 1.52 [95% confidence interval: 1.10 to 2.08, p-value = 0.010]). Delinquent behaviour in adolescence and income during early adulthood were the most influential mediators, and the indirect associations through these variables were HR 1.03 (1.00 to 1.06, 0.029) and HR 1.04 (1.01 to 1.07, 0.029), respectively. After accounting for these indirect paths, the direct path was attenuated to HR 1.35 (0.98 to 1.85, 0.066). The limitations of the study include that the associations may be partly due to genetic, social, and behavioural residual confounding, that statistical power was low in some of the subgroup analyses, and that there might be other relevant paths that were not investigated in the present study.ConclusionsOur findings from this cohort study suggest that childhood parental death is associated with increased mortality and that the association was mediated through a chain of disadvantages over the life course including delinquency in adolescence and lower income during early adulthood. Professionals working with bereaved children should take the higher mortality risk in bereaved offspring into account and consider its lifelong consequences. When planning and providing support to bereaved children, it may be particularly important to be aware of their increased susceptibility to delinquency and socioeconomic vulnerability that eventually lead to higher mortality.
| S-EPMC7951838 | biostudies-literature
Project description:BACKGROUND:An increased mortality risk associated with mental disorder has been reported for patients, but there are few studies are based on random samples with interview-based psychiatric diagnoses. Part of the increased mortality for those with mental disorder may be attributable to worse somatic health or hazardous health behaviour - consequences of the disorder - but somatic health information is commonly lacking in psychiatric samples. This study aims to examine long-term mortality risk for psychiatric diagnoses in a general population sample and to assess mediation by somatic ill health and hazardous health behaviour. METHOD:We used a double-phase stratified random sample of individuals aged 18-65 in Stockholm County 1970-1971 linked to vital records. First phase sample was 32 186 individuals screened with postal questionnaire and second phase was 1896 individuals (920 men and 976 women) that participated in a full-day examination (participation rate 88%). Baseline examination included both a semi-structured interview with a psychiatrist, with mental disorders set according to the 8th version of the International Classification of Disease (ICD-8), and clinical somatic examination, including measures of body composition (BMI), hypertension, fasting blood glucose, pulmonary function and self-reported tobacco smoking. Information on vital status was obtained from the Total Population Register for the years 1970-2011. Associations with mortality were studied with Cox proportional hazard analyses. RESULTS:A total of 883 deaths occurred among the participants during the 41-year follow-up. Increased mortality rates were found for ICD-8 functional psychoses (hazard ratio, HR = 2.22, 95% confidence interval (95% CI): 1.15-4.30); psycho-organic symptoms (HR = 1.94, 95% CI: 1.31-2.87); depressive neuroses (HR = 1.71, 95% CI: 1.23-2.39); alcohol use disorder (HR = 1.91, 95% CI: 1.40-2.61); drug dependence (HR = 3.71, 95% CI: 1.80-7.65) and psychopathy (HR = 2.88, 95% CI: 1.02-8.16). Non-participants (n = 349) had mortality rates similar to participants (HR = 0.98, 95% CI: 0.81-1.18). In subgroup analyses of those with psychoses, depression or alcohol use disorder, adjusting for the potential mediators smoking and pulmonary function, showed only slight changes in the HRs. CONCLUSIONS:This study confirms the increased risk of mortality for several psychiatric diagnoses in follow-up studies on American, Finnish and Swedish population-based samples. Only a small part of the increased mortality hazard was attributable to differences in somatic health or hazardous health behaviour measured at baseline.
| S-EPMC7137603 | biostudies-literature
Project description:Investigators have examined whether heat mortality risk is increased in neighborhoods subject to the urban heat island (UHI) effect but have not identified degrees of difference in susceptibility to heat and cold between cool and hot areas, which we call acclimatization to the UHI.We developed methods to examine and quantify the degree of acclimatization to heat- and cold-related mortality in relation to UHI anomalies and applied these methods to London, UK.Case-crossover analyses were undertaken on 1993-2006 mortality data from London UHI decile groups defined by anomalies from the London average of modeled air temperature at a 1-km grid resolution. We estimated how UHI anomalies modified excess mortality on cold and hot days for London overall and displaced a fixed-shape temperature-mortality function ("shifted spline" model). We also compared the observed associations with those expected under no or full acclimatization to the UHI.The relative risk of death on hot versus normal days differed very little across UHI decile groups. A 1°C UHI anomaly multiplied the risk of heat death by 1.004 (95% CI: 0.950, 1.061) (interaction rate ratio) compared with the expected value of 1.070 (1.057, 1.082) if there were no acclimatization. The corresponding UHI interaction for cold was 1.020 (0.979, 1.063) versus 1.030 (1.026, 1.034) (actual versus expected under no acclimatization, respectively). Fitted splines for heat shifted little across UHI decile groups, again suggesting acclimatization. For cold, the splines shifted somewhat in the direction of no acclimatization, but did not exclude acclimatization.We have proposed two analytical methods for estimating the degree of acclimatization to the heat- and cold-related mortality burdens associated with UHIs. The results for London suggest relatively complete acclimatization to the UHI effect on summer heat-related mortality, but less clear evidence for cold-related mortality.Milojevic A, Armstrong BG, Gasparrini A, Bohnenstengel SI, Barratt B, Wilkinson P. 2016. Methods to estimate acclimatization to urban heat island effects on heat- and cold-related mortality. Environ Health Perspect 124:1016-1022;?http://dx.doi.org/10.1289/ehp.1510109.
| S-EPMC4937865 | biostudies-other
Project description: Not available
| S-EPMC6150471 | biostudies-literature
Project description:BackgroundMost of the epidemiological studies that have examined the detrimental effects of ambient hot and cold temperatures on human health have been conducted in high-income countries. In India, the limited evidence on temperature and health risks has focused mostly on the effects of heat waves and has mostly been from small scale studies. Here, we quantify heat and cold effects on mortality in India using a nationally representative study of the causes of death and daily temperature data for 2001-2013.Methods and findingsWe applied distributed-lag nonlinear models with case-crossover models to assess the effects of heat and cold on all medical causes of death for all ages from birth (n = 411,613) as well as on stroke (n = 19,753), ischaemic heart disease (IHD) (n = 40,003), and respiratory diseases (n = 23,595) among adults aged 30-69. We calculated the attributable risk fractions by mortality cause for extremely cold (0.4 to 13.8°C), moderately cold (13.8°C to cause-specific minimum mortality temperatures), moderately hot (cause-specific minimum mortality temperatures to 34.2°C), and extremely hot temperatures (34.2 to 39.7°C). We further calculated the temperature-attributable deaths using the United Nations' death estimates for India in 2015. Mortality from all medical causes, stroke, and respiratory diseases showed excess risks at moderately cold temperature and hot temperature. For all examined causes, moderately cold temperature was estimated to have higher attributable risks (6.3% [95% empirical confidence interval (eCI) 1.1 to 11.1] for all medical deaths, 27.2% [11.4 to 40.2] for stroke, 9.7% [3.7 to 15.3] for IHD, and 6.5% [3.5 to 9.2] for respiratory diseases) than extremely cold, moderately hot, and extremely hot temperatures. In 2015, 197,000 (121,000 to 259,000) deaths from stroke, IHD, and respiratory diseases at ages 30-69 years were attributable to moderately cold temperature, which was 12- and 42-fold higher than totals from extremely cold and extremely hot temperature, respectively. The main limitation of this study was the coarse spatial resolution of the temperature data, which may mask microclimate effects.ConclusionsPublic health interventions to mitigate temperature effects need to focus not only on extremely hot temperatures but also moderately cold temperatures. Future absolute totals of temperature-related deaths are likely to depend on the large absolute numbers of people exposed to both extremely hot and moderately cold temperatures. Similar large-scale and nationally representative studies are required in other low- and middle-income countries to better understand the impact of future temperature changes on cause-specific mortality.
| S-EPMC6057641 | biostudies-literature