Niklas Berglind

Summary

Affiliation: Karolinska Institutet
Country: Sweden

Publications

  1. ncbi Air pollution exposure--a trigger for myocardial infarction?
    Niklas Berglind
    Institute of Environmental Medicine, Karolinska Institutet, SE 171 77 Stockholm
    Int J Environ Res Public Health 7:1486-99. 2010
  2. ncbi Ambient air pollution and daily mortality among survivors of myocardial infarction
    Niklas Berglind
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Epidemiology 20:110-8. 2009
  3. ncbi Interactions between glutathione S-transferase P1, tumor necrosis factor, and traffic-related air pollution for development of childhood allergic disease
    Erik Melen
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Environ Health Perspect 116:1077-84. 2008

Detail Information

Publications3

  1. ncbi Air pollution exposure--a trigger for myocardial infarction?
    Niklas Berglind
    Institute of Environmental Medicine, Karolinska Institutet, SE 171 77 Stockholm
    Int J Environ Res Public Health 7:1486-99. 2010
    ..No evidence of susceptible subgroups was found. This study provides no support that moderately elevated air pollution levels trigger first-time myocardial infarction...
  2. ncbi Ambient air pollution and daily mortality among survivors of myocardial infarction
    Niklas Berglind
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Epidemiology 20:110-8. 2009
    ..Certain subgroups in the general population, such as persons with existing cardiovascular or respiratory disease, may be more likely to experience adverse health effects from air pollution...
  3. ncbi Interactions between glutathione S-transferase P1, tumor necrosis factor, and traffic-related air pollution for development of childhood allergic disease
    Erik Melen
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    Environ Health Perspect 116:1077-84. 2008
    ..Air pollutants may induce airway inflammation and sensitization due to generation of reactive oxygen species. The genetic background to these mechanisms could be important effect modifiers...