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Träfflista för sökning "L773:0300 5771 OR L773:1464 3685 ;lar1:(umu);srt2:(2005-2009)"

Search: L773:0300 5771 OR L773:1464 3685 > Umeå University > (2005-2009)

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1.
  • Capella, Gabriel, et al. (author)
  • DNA repair polymorphisms and the risk of stomach adenocarcinoma and severe chronic gastritis in the EPIC-EURGAST study
  • 2008
  • In: International Journal of Epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 37:6, s. 1316-1325
  • Journal article (peer-reviewed)abstract
    • Background The contribution of genetic variation in DNA repair genes to gastric cancer (GC) risk remains essentially unknown. The aim of this study was to explore the relative contribution of DNA repair gene polymorphisms to GC risk and severe chronic atrophic gastritis (SCAG). Method A nested case control study within the EPIC cohort was performed including 246 gastric adenocarcinomas and 1175 matched controls. Controls with SCAG (n 91), as defined by low pepsinogen A (PGA) levels, and controls with no SCAG (n 1061) were also compared. Twelve polymorphisms at DNA repair genes (MSH2, MLH1, XRCC1, OGG1 and ERCC2) and TP53 gene were analysed. Antibodies against Helicobacter pylori were measured. Results No association was observed for any of these polymorphisms with stomach cancer risk. However, ERCC2 K751Q polymorphism was associated with an increased risk for non-cardial neoplasm [odds ratio (OR) 1.78; 95 confidence interval (CI) 1.023.12], being ERCC2 K751Q and D312N polymorphisms associated with the diffuse type. ERCC2 D312N (OR 2.0; 95 CI 1.093.65) and K751Q alleles (OR 1.82; 95 CI 1.013.30) and XRCC1 R399Q (OR 1.69; 95 CI 1.022.79) allele were associated with an increased risk for SCAG. Conclusion Our study supports a role of ERCC2 in non-cardial GC but not in cardial cancer. A concordant result was observed for subjects with low PGA levels. XRCC1 allele was associated also with SCAG. This is the first prospective study suggesting that individual variation in DNA repair may be relevant for gastric carcinogenesis, a finding that will require further confirmation validation in larger independent studies.
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  • Götschi, Thomas, et al. (author)
  • Air pollution and lung function in the European Community Respiratory Health Survey.
  • 2008
  • In: International journal of epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 37:6, s. 1349-58
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: The association of long-term air pollution and lung function has not been studied across adult European multi-national populations before. The aim of this study was to determine the association between long-term urban background air pollution and lung function levels, as well as change in lung function among European adults. METHODS: Forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and the ratio thereof (FEV1/FVC) were assessed at baseline and after 9 years of follow-up in adults from 21 European centres (followed-up sample 5610). Fine particles (PM(2.5)) were measured in 2000/2001 using central monitors. RESULTS: Despite sufficient statistical power no significant associations were found between city-specific annual mean PM(2.5) and average lung function levels. The findings also do not support an effect on change in lung function, albeit statistical power was insufficient to significantly detect such an association. CONCLUSIONS: The inability to refuse the null hypothesis may reflect (i) no effect of urban air pollution on lung function or (ii) inherent biases due to the study design. Examples of the latter are lack of individual-level air quality assignment, not quantified within-city contrasts in traffic-related pollution, or the heterogeneity of the studied populations and their urban environments. Future studies on long-term effects of air pollution on lung function could increase statistical power and reduce potential misclassification and confounding by characterizing exposure on the level of individuals, capturing contrasts due to local sources, in particular traffic.
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  • Hassler, Sven, et al. (author)
  • Causes of death in the Sami population of Sweden, 1961-2000.
  • 2005
  • In: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 34:3, s. 623-629
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Indigenous people often have a pattern of mortality that is disadvantageous in comparison with the general population. The knowledge on causes of death among the Sami, the natives of northern Scandinavia, is limited. The aim of the present study was to compare gender and cause specific mortality patterns for reindeer herding Sami, non-herding Sami, and non-Sami between 1961 and 2000. METHODS: A Sami cohort was constructed departing from a group of index-Sami identified as either reindeer herding Sami or Sami eligible to vote for the Sami parliament. Relatives of index-Sami were identified in the National Kinship Register and added to the cohort. The cohort contained a total of 41 721 people (7482 reindeer herding Sami and 34 239 non-herding Sami). A demographically matched non-Sami reference population four times as large, was compiled in the same way. Relative mortality risks were analysed by calculating standardized mortality ratios (SMRs). RESULTS: The differences in overall mortality and life expectancy of the Sami, both reindeer herding and non-herding, compared with the reference population were relatively small. However, Sami men showed significantly lower SMR for cancers but higher for external causes of injury. For Sami women, significantly higher SMR was found for diseases of the circulatory system and diseases of the respiratory system. An increased risk of dying from subarachnoid haemorrhage was observed among both Sami men and women. CONCLUSIONS: The similarities in mortality patterns are probably a result of centuries of close interaction between the Sami and the non-Sami, while the observed differences might be due to lifestyle, psychosocial and/or genetic factors.
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  • Jacquemin, B., et al. (author)
  • Annoyance due to air pollution in Europe
  • 2007
  • In: Int J Epidemiol. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 36:4, s. 809-20
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Annoyance due to air pollution is a subjective score of air quality, which has been incorporated into the National Environmental monitoring of some countries. The objectives of this study are to describe the variations in annoyance due to air pollution in Europe and its individual and environmental determinants. METHODS: This study took place in the context of the European Community Respiratory Health Survey II (ECRHS II) that was conducted during 1999-2001. It included 25 centres in 12 countries and 7867 randomly selected adults from the general population. Annoyance due to air pollution was self-reported on an 11-point scale. Annual mean mass concentration of fine particles (PM(2.5)) and its sulphur (S) content were measured in 21 centres as a surrogate of urban air pollution. RESULTS: Forty-three per cent of participants reported moderate annoyance (1-5 on the scale) and 14% high annoyance (>/=6) with large differences across centres (2-40% of high annoyance). Participants in the Northern European countries reported less annoyance. Female gender, nocturnal dyspnoea, phlegm and rhinitis, self-reported car and heavy vehicle traffic in front of the home, high education, non-smoking and exposure to environmental tobacco smoke were associated with higher annoyance levels. At the centre level, adjusted means of annoyance scores were moderately associated with sulphur urban levels (slope 1.43 mug m(-3), standard error 0.40, r = 0.61). CONCLUSIONS: Annoyance due to air pollution is frequent in Europe. Individuals' annoyance may be a useful measure of perceived ambient quality and could be considered a complementary tool for health surveillance.
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  • Vilkuna-Rautiainen, T, et al. (author)
  • Serum antibody response to periodontal pathogens and herpes simplex virus in relation to classic risk factors of cardiovascular disease.
  • 2006
  • In: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 35:6, s. 1486-1494
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Increasing evidence links chronic infections, especially burden of several infections, with increased risk for cardiovascular diseases (CVD). We studied joint immune response against two major periodontal pathogens and herpes simplex virus (HSV) in relation to established risk factors of CVD. METHODS: Serum antibody levels to HSV, Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis were determined by ELISA. The study included 1107 subjects, 734 from Finland and 373 from Russia. RESULTS: Combined antibody response to periodontal pathogens was associated inversely (OR, 95% CI) with high-density lipoprotein (HDL) cholesterol concentration (beta = 0.35; 0.20, 0.60; P < 0.001) and directly with HSV antibody quartiles: compared with the first quartile, ORs (95% CI) for quartiles 2-4 were 1.43 (0.88-2.32), 1.74 (1.07-2.82), and 1.89 (1.18-3.02), respectively (P for trend <0.001), after adjusting for age, gender, area, education, smoking, BMI, alcohol, triglycerides, and number of teeth. In linear regression analysis, the 3-pathogen antibody score (comprising antibody levels against periodontal pathogens and HSV) was inversely associated with HDL cholesterol concentration (beta = -0.067/1 mmol/l; -0.235, -0.018; P < 0.05). CONCLUSIONS: HSV infection may promote infection by periodontal pathogens. Furthermore, the infectious burden comprising HSV and periodontitis may increase the risk for CVD by clearly decreasing HDL cholesterol concentrations.
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