| 1. |
- Kassebaum, Nicholas J., et al.
(författare)
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Global, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990-2015 : a systematic analysis for the Global Burden of Disease Study 2015
- 2016
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Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 388:10053, s. 1603-1658
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Tidskriftsartikel (refereegranskat)abstract
- Background Healthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs). We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development. Methods We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015. We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year. We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita. We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate. Findings Total global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs off set by increased DALYs due to non-communicable diseases (NCDs). Much of this epidemiological transition was caused by changes in population growth and ageing, but it was accelerated by widespread improvements in SDI that also correlated strongly with the increasing importance of NCDs. Both total DALYs and age-standardised DALY rates due to most Group 1 causes significantly decreased by 2015, and although total burden climbed for the majority of NCDs, age-standardised DALY rates due to NCDs declined. Nonetheless, age-standardised DALY rates due to several high-burden NCDs (including osteoarthritis, drug use disorders, depression, diabetes, congenital birth defects, and skin, oral, and sense organ diseases) either increased or remained unchanged, leading to increases in their relative ranking in many geographies. From 2005 to 2015, HALE at birth increased by an average of 2.9 years (95% uncertainty interval 2.9-3.0) for men and 3.5 years (3.4-3.7) for women, while HALE at age 65 years improved by 0.85 years (0.78-0.92) and 1.2 years (1.1-1.3), respectively. Rising SDI was associated with consistently higher HALE and a somewhat smaller proportion of life spent with functional health loss; however, rising SDI was related to increases in total disability. Many countries and territories in central America and eastern sub-Saharan Africa had increasingly lower rates of disease burden than expected given their SDI. At the same time, a subset of geographies recorded a growing gap between observed and expected levels of DALYs, a trend driven mainly by rising burden due to war, interpersonal violence, and various NCDs. Interpretation Health is improving globally, but this means more populations are spending more time with functional health loss, an absolute expansion of morbidity. The proportion of life spent in ill health decreases somewhat with increasing SDI, a relative compression of morbidity, which supports continued efforts to elevate personal income, improve education, and limit fertility. Our analysis of DALYs and HALE and their relationship to SDI represents a robust framework on which to benchmark geography-specific health performance and SDG progress. Country-specific drivers of disease burden, particularly for causes with higher-than-expected DALYs, should inform financial and research investments, prevention efforts, health policies, and health system improvement initiatives for all countries along the development continuum.
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| 2. |
- Knutsen, Helle Katrine, et al.
(författare)
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Risk for animal and human health related to the presence of dioxins and dioxin-like PCBs in feed and food.
- 2018
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Ingår i: EFSA journal. European Food Safety Authority. - : Wiley. - 1831-4732. ; 16:11
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Tidskriftsartikel (refereegranskat)abstract
- The European Commission asked EFSA for a scientific opinion on the risks for animal and human health related to the presence of dioxins (PCDD/Fs) and DL-PCBs in feed and food. The data from experimental animal and epidemiological studies were reviewed and it was decided to base the human risk assessment on effects observed in humans and to use animal data as supportive evidence. The critical effect was on semen quality, following pre- and postnatal exposure. The critical study showed a NOAEL of 7.0pg WHO2005-TEQ/g fat in blood sampled at age 9years based on PCDD/F-TEQs. No association was observed when including DL-PCB-TEQs. Using toxicokinetic modelling and taking into account the exposure from breastfeeding and a twofold higher intake during childhood, it was estimated that daily exposure in adolescents and adults should be below 0.25 pg TEQ/kg bw/day. The CONTAM Panelestablished a TWI of 2 pg TEQ/kg bw/week. With occurrence and consumption data from European countries, the mean and P95 intake of total TEQ by Adolescents, Adults, Elderly and Very Elderly varied between, respectively, 2.1 to 10.5, and 5.3 to 30.4pg TEQ/kg bw/week, implying a considerable exceedance of the TWI. Toddlers and Other Children showed a higher exposure than older age groups, but this was accounted for when deriving the TWI. Exposure to PCDD/F-TEQ only was on average 2.4- and 2.7-fold lower for mean and P95 exposure than for total TEQ. PCDD/Fs and DL-PCBs are transferred to milk and eggs, and accumulate in fatty tissues and liver. Transfer rates and bioconcentration factors were identified for various species. The CONTAM Panelwas not able to identify reference values in most farm and companion animals with the exception of NOAELs for mink, chicken and some fish species. The estimated exposure from feed for these species does not imply a risk.
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| 3. |
- Stockfelt, Leo, 1981, et al.
(författare)
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Long term effects of residential NOx exposure on total and cause-specific mortality and incidence of myocardial infarction in a Swedish cohort.
- 2015
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Ingår i: Environmental research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 142, s. 197-206
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: Exposure to air pollution has been linked to total and cardiopulmonary mortality. However, few studies have examined the effects of exposure over decades, or which time windows of long term exposure are most relevant. We investigated the long term effects of residential air pollution on total and cause-specific mortality and incidence of myocardial infarction in a well-characterized cohort of men in Sweden. METHODS: A cohort of 7494 men in Gothenburg was examined in 1970-1973 and followed subsequently to determine predictors of cardiovascular disease. We collected data on residential address and cause-specific mortality for the years 1973-2007. Each individual was assigned yearly nitrogen oxides (NOx) exposure based on dispersion models. Using multivariable Cox regression and generalized additive models with time-dependent exposure, we studied the association between three different time windows of residential NOx exposure, and selected outcomes. RESULTS: In the years 1973-2007, a total of 5669 deaths, almost half of which were due to cardiovascular diseases, occurred in the cohort. Levels of NOx exposure decreased during the study period, from a median of 38µg/m3 in 1973 to 17µg/m3 in 2007. Total non-accidental mortality was associated with participants' NOx exposure in the last year (the year of outcome) (HR 1.03, 95% CI 1.01-1.05, per 10µg/m3), with the mean NOx exposure during the last 5 years, and with the mean NOx exposure since enrolment (HR 1.02, 95% CI 1.01-1.04 for both). The associations were similar (HR 1.01-1.03), but generally not statistically significant, for cardiovascular, ischemic heart disease, and acute myocardial infarction mortality, and weaker for cerebrovascular and respiratory mortality. There was no association between NOx exposure and incident myocardial infarction. DISCUSSION AND CONCLUSIONS: Long term residential exposure to NOx at these relatively low exposure levels in Gothenburg was associated with total non-accidental mortality. The association was as strong for NOx exposure in the last year as for longer exposure windows. The effect was near linear, and only marginally affected by confounders and effect modifiers. The improved air quality in Gothenburg has by these estimates led to a 6% decrease in excess non-accidental mortality during the study period.
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| 4. |
- Stockfelt, Leo, 1981, et al.
(författare)
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Long-Term Exposure to Particulate Air Pollution, Black Carbon, and Their Source Components in Relation to Ischemic Heart Disease and Stroke
- 2019
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Ingår i: Journal of Environmental Health Perspectives. - Durham : National Institute of Environmental Health Sciences. - 0091-6765 .- 1552-9924. ; 127:10
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources.OBJECTIVES: We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities.METHODS: ), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models.RESULTS: exposure from residential heating.DISCUSSION: Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations.
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| 5. |
- Vos, Theo, et al.
(författare)
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Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013
- 2015
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Ingår i: The Lancet. - 1474-547X .- 0140-6736. ; 386:9995, s. 743-800
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Tidskriftsartikel (refereegranskat)abstract
- Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2.4 billion and 1.6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537.6 million in 1990 to 764.8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114.87 per 1000 people to 110.31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21.1% in 1990 to 31.2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries.
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| 6. |
- Andersson, Eva M., 1968, et al.
(författare)
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Partial Mediation by Cadmium Exposure of the Association Between Tobacco Smoking and Atherosclerotic Plaques in the Carotid Artery
- 2018
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Ingår i: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 187:4, s. 806-816
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to cadmium confers increased cardiovascular risk. Tobacco smoke contains cadmium, which, hypothetically, may mediate parts of the tobacco-associated risk of developing atherosclerotic plaques. Baseline data from the Swedish Malmo Diet and Cancer cohort (1991-1996) were used to test this hypothesis. Mediation analysis was used to examine associations between smoking and blood cadmium levels and the prevalence of ultrasound-assessed carotid atherosclerotic plaques. The total association with smoking status (never smokers, 2 categories of former smokers, and current smokers) was split into direct and indirect association, and the proportion mediated was estimated. The adjusted estimated plaque prevalence was approximately 27% among never smokers. We identified both a direct and an indirect pathway between smoking and carotid plaques; the indirect association, through cadmium, was observed among current smokers and former smokers who had quit smoking less than 15 years before. For current smokers, the prevalence ratio for plaque was 1.5, with 60%-65% of the association with smoking being mediated through cadmium. Recent former smokers had a prevalence ratio of 1.3, and 40%-45% was mediated through cadmium. Long-time former smokers had a prevalence ratio of 1.2, but none of the association was mediated through cadmium. In conclusion, about two-thirds of the proatherosclerotic association with smoking was mediated by cadmium.
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| 7. |
- Axelsson, Gösta, 1950, et al.
(författare)
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Lung cancer risk from radon exposure in dwellings in Sweden: how many cases can be prevented if radon levels are lowered?
- 2015
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Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 26:4, s. 541-547
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Tidskriftsartikel (refereegranskat)abstract
- Residential exposure to radon is considered to be the second cause of lung cancer after smoking. The purpose of this study was to estimate the number of lung cancer cases prevented from reducing radon exposure in Swedish dwellings. METHODS: Measurements of indoor radon are available from national studies in 1990 and 2008 with 8992 and 1819 dwellings, considered representative of all Swedish dwellings. These data were used to estimate the distribution of radon in Swedish dwellings. Lung cancer risk was assumed to increase by 16 % per 100 becquerels per cubic meter (Bq/m(3)) indoor air radon. Estimates of future and saved cases of lung cancer were performed at both constant and changed lung cancer incidence rates over time. RESULTS: The arithmetic mean concentration of radon was 113 Bq/m(3) in 1990 and 90 Bq/m(3) in 2008. Approximately 8 % of the population lived in houses with >200 Bq/m(3). The estimated current number of lung cancer cases attributable to previous indoor radon exposure was 591 per year, and the number of future cases attributable to current exposure was 473. If radon levels above 100 Bq/m(3) are lowered to 100 Bq/m(3), 183 cases will be prevented. If levels >200 Bq/m(3) are lowered to 140 Bq/m(3) (mean in the present stratum 100-200 Bq/m(3)), 131 cases per year will be prevented. CONCLUSIONS: Although estimates are somewhat uncertain, 35-40 % of the radon attributed lung cancer cases can be prevented if radon levels >100 Bq/m(3) are lowered to 100 Bq/m(3).
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| 8. |
- Bar, Yael, et al.
(författare)
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Quantitative and semi-quantitative histopathological examination of renal biopsies in healthy individuals, and associations with kidney function
- 2016
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Ingår i: Apmis. - : Wiley. - 0903-4641. ; 124:5, s. 393-400
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Tidskriftsartikel (refereegranskat)abstract
- This study assesed the prevalence of histopathological changes in renal biopsies from healthy individuals, and the association with age, sex and smoking. Donor biopsies from 109 subjects were obtained from living kidney donors, and blood and urine samples were collected together with medical history. All biopsies were scored according to the Banff 97 classification with some modifications. The parameters included in this study were tubular atrophy, interstitial fibrosis, glomerulosclerosis, arteriosclerosis, arteriolohyalinosis and a sclerosis score. An alternative scoring system for tubular atrophy was examined (using 5% rather than <1% as a cut-off for grade 0). Glomerular filtration rate was measured in most cases as chromium ethylenediaminetetra-acetic acid (Cr-EDTA) clearance. Age was a significant predictor for tubular atrophy, fibrosis and sclerosis. Pack-years of smoking increased the risk of tubular atrophy, fibrosis and arteriolohyalinosis. The alternative scoring of tubular atrophy showed a stronger association with smoking, but a weaker association with age, compared with the original one. Limited histopathological changes are common in healthy kidney donors around 50 years of age with normal kidney function. We propose that a cut-off of 5% yields a better definition of grade 0 tubular atrophy compared with the established cut-off of >0%.
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| 9. |
- Barregård, Lars, 1948, et al.
(författare)
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Blood Cadmium Levels and Incident Cardiovascular Events during Follow-up in a Population-Based Cohort of Swedish Adults: The Malmo Diet and Cancer Study
- 2016
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Ingår i: Environmental Health Perspectives. - : Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 124:5, s. 594-600
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Cadmium exposure may increase the risk of cardiovascular disease. The only published longitudinal study on cadmium and incident cardiovascular disease was performed in American Indians with relatively high cadmium exposure. OBJECTIVES: Our aim was to examine the association between blood cadmium at baseline and incident cardiovascular events in a population-based study of Swedish men and women with cadmium levels similar to those of most European and U.S. populations. METHODS: A Swedish population-based cohort (n = 6,103, age 46-67 years) was recruited between 1991 and 1994. After we excluded those with missing data on smoking, 4,819 participants remained. Acute coronary events, other major cardiac events, stroke, and cardiovascular mortality were followed until 2010. Associations with blood cadmium (estimated from cadmium in erythrocytes) were analyzed using Cox proportional hazards regression including potential confounders and important cardiovascular risk factors. RESULTS: Hazard ratios for all cardiovascular end points were consistently increased for participants in the 4th blood cadmium quartile (median, 0.99 mu g/L). In models that also included sex, smoking, waist circumference, education, physical activity, alcohol intake, serum triglycerides, HbA1c, and C-reactive protein, the hazard ratios comparing the highest and lowest quartiles of exposure were 1.8 (95%CI: 1.2, 2.7) for acute coronary events, and 1.9 (1.3, 2.9) for stroke. Hazard ratios in never-smokers were consistent with these estimates. CONCLUSIONS: Blood cadmium in the highest quartile was associated with incident cardiovascular disease and mortality in our population-based samples of Swedish adults. The consistent results among never-smokers are important because smoking is a strong confounder. Our findings suggest that measures to reduce cadmium exposures are warranted, even in populations without unusual sources of exposure.
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| 10. |
- Barregård, Lars, 1948, et al.
(författare)
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Impact on Population Health of Baltic Shipping Emissions
- 2019
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Ingår i: International Journal of Environmental Research and Public Health. - : MDPI AG. - 1660-4601. ; 16:11
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Tidskriftsartikel (refereegranskat)abstract
- Emission of pollutants from shipping contributes to ambient air pollution. Our aim was to estimate exposure to particulate air pollution (PM2.5) and health effects from shipping in countries around the Baltic Sea, as well as effects of the sulfur regulations for fuels enforced in 2015 by the Baltic Sulfur Emission Control Area (SECA). Yearly PM2.5 emissions, from ship activity data and emission inventories in 2014 and 2016, were estimated. Concentrations and population exposure (0.1 degrees x 0.1 degrees) of PM2.5 were estimated from a chemical transport mode, meteorology, and population density. Excess mortality and morbidity were estimated using established exposure-response (ER) functions. Estimated mean PM2.5 per inhabitant from Baltic shipping was 0.22 mu g/m(3) in 2014 in ten countries, highest in Denmark (0.57 mu g/m(3)). For the ER function with the steepest slope, the number of estimated extra premature deaths was 3413 in total, highest in Germany and lowest in Norway. It decreased by about 35% in 2016 (after SECA), a reduction of >1000 cases. In addition, 1500 non-fatal cases of ischemic heart disease and 1500 non-fatal cases of stroke in 2014 caused by Baltic shipping emissions were reduced by the same extent in 2016. In conclusion, PM2.5 emissions from Baltic shipping, and resulting health impacts decreased substantially after the SECA regulations in 2015.
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