1. |
- Wang, Meng, et al.
(författare)
-
Long-term exposure to elemental constituents of particulate matter and cardiovascular mortality in 19 European cohorts : Results from the ESCAPE and TRANSPHORM projects
- 2014
-
Ingår i: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 66, s. 97-106
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Associations between long-term exposure to ambient particulate matter (PM) and cardiovascular (CVD) mortality have been widely recognized. However, health effects of long-term exposure to constituents of PM on total CVD mortality have been explored in a single study only. Aims: The aim of this study was to examine the association of PM composition with cardiovascular mortality. Methods: We used data from 19 European ongoing cohorts within the framework of the ESCAPE (European Study of Cohorts for Air Pollution Effects) and TRANSPHORM (Transport related Air Pollution and Health impacts Integrated Methodologies for Assessing Particulate Matter) projects. Residential annual average exposure to elemental constituents within particle matter smaller than 2.5 and 10 pm (PM2.5 and PM10) was estimated using Land Use Regression models. Eight elements representing major sources were selected a priori (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc). Cohort-specific analyses were conducted using Cox proportional hazards models with a standardized protocol. Random-effects metaanalysis was used to calculate combined effect estimates. Results: The total population consisted of 322,291 participants, with 9545 CVD deaths. We found no statistically significant associations between any of the elemental constituents in PM2.5 or PM10 and CVD mortality in the pooled analysis. Most of the hazard ratios (HRs) were close to unity, e.g. for PM10 Fe the combined HR was 0.96 (0.84-1.09). Elevated combined HRs were found for PM2.5 Si (1.17, 95% Cl: 0.93-1.47), and S in PM2.5 (1.08,95% Cl: 0.95-1.22) and PM10 (1.09,95% Cl: 0.90-132). Conclusion: In a joint analysis of 19 European cohorts, we found no statistically significant association between long-term exposure to 8 elemental constituents of particles and total cardiovascular mortality.
|
|
2. |
- Fall, Tove, et al.
(författare)
-
The Role of Adiposity in Cardiometabolic Traits : A Mendelian Randomization Analysis
- 2013
-
Ingår i: PLoS Medicine. - : Public Library of Science (PLoS). - 1549-1277 .- 1549-1676. ; 10:6, s. e1001474-
-
Tidskriftsartikel (refereegranskat)abstract
- Background: The association between adiposity and cardiometabolic traits is well known from epidemiological studies. Whilst the causal relationship is clear for some of these traits, for others it is not. We aimed to determine whether adiposity is causally related to various cardiometabolic traits using the Mendelian randomization approach. Methods and Findings: We used the adiposity-associated variant rs9939609 at the FTO locus as an instrumental variable (IV) for body mass index (BMI) in a Mendelian randomization design. Thirty-six population-based studies of individuals of European descent contributed to the analyses. Age-and sex-adjusted regression models were fitted to test for association between (i) rs9939609 and BMI (n = 198,502), (ii) rs9939609 and 24 traits, and (iii) BMI and 24 traits. The causal effect of BMI on the outcome measures was quantified by IV estimators. The estimators were compared to the BMI-trait associations derived from the same individuals. In the IV analysis, we demonstrated novel evidence for a causal relationship between adiposity and incident heart failure (hazard ratio, 1.19 per BMI-unit increase; 95% CI, 1.03-1.39) and replicated earlier reports of a causal association with type 2 diabetes, metabolic syndrome, dyslipidemia, and hypertension (odds ratio for IV estimator, 1.1-1.4; all p<0.05). For quantitative traits, our results provide novel evidence for a causal effect of adiposity on the liver enzymes alanine aminotransferase and gamma-glutamyl transferase and confirm previous reports of a causal effect of adiposity on systolic and diastolic blood pressure, fasting insulin, 2-h post-load glucose from the oral glucose tolerance test, C-reactive protein, triglycerides, and high-density lipoprotein cholesterol levels (all p<0.05). The estimated causal effects were in agreement with traditional observational measures in all instances except for type 2 diabetes, where the causal estimate was larger than the observational estimate (p = 0.001). Conclusions: We provide novel evidence for a causal relationship between adiposity and heart failure as well as between adiposity and increased liver enzymes.
|
|
3. |
|
|
4. |
- Sjöstrand, Johan, 1936, et al.
(författare)
-
The decline in visual acuity in elderly people with healthy eyes or eyes with early age-related maculopathy in two Scandinavian population samples
- 2011
-
Ingår i: ACTA OPHTHALMOLOGICA. - 1755-375X. ; 89:2, s. 116-123
-
Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: This study aimed to analyse the decline in visual acuity (VA) during normal ageing in two Scandinavian population samples of subjects aged ≥ 70 years and to study the age-specific decline in VA in eyes with early age-related maculopathy (ARM). METHODS: We carried out a cross-sectional analysis of data pertaining to VA in the better eye in one population sample from Oulu (OU), Finland (aged 70-82 years) and a second population sample from Gothenburg (GG), Sweden (aged 82 or 88 years). The change in VA with age was evaluated in healthy eyes (OU, n = 119; GG, n = 40) and in eyes with early ARM (OU-ARM, n = 22; GG-ARM, n = 114) using linear regression or logistic regression. The results were compared with those of previous reports. RESULTS: Our population samples showed a significant decrease with age in VA in healthy eyes in subjects aged ≥ 44 years using both statistical models. Comparisons with previous reports demonstrated a homogeneity in the decline in VA with age. On average, 0.3 logMAR are lost from middle age up to 88 years, presumably as a result of physiological ageing. In early ARM, the rate of age-specific decline in VA more than doubled and the prevalence of VA < 0.5 markedly increased. CONCLUSIONS: Visual acuity in healthy eyes declines with age from middle age onwards. The decrease in VA possibly accelerates in subjects aged > 70 years, although no significant evidence for this was found. An age-specific decline in VA is shown in eyes with early ARM. These results are important for the evaluation of age-specific treatment results.
|
|