Increasing societal dependence on manmade chemicals and lack of knowledge about their potential adverse effects is a major threat to wildlife and human health. Evidence show that exposure to air pollution or the over 140,000 chemicals that contaminate our environment are main risk factors for many chronic diseases. Understanding what environmental contaminants we are exposed to, their properties and the interactions with biological systems are therefore essential.
There has been a rapidly increasing interest in whether environmental factors modulate the establishment and maintenance of epigenetic modifications, and thereby affect gene expression and phenotype in humans and wildlife. We combine experimental model systems, omics tools, computational toxicology and molecular epidemiological research to study gene-environment interactions and epigenetic basis of disease. In particular, our research focuses on developmental origins of health and disease with an emphasis on the exposome and underlying molecular mechanisms. The projects concern the effects of environmental exposures such as endocrine disrupting chemicals, flame retardants, per- and polyfluoroalkyl substances (PFAS), pesticides, metals, as well as drugs, particulate air pollution, temperature changes, psycho-social stress and ethnical disparities. Ongoing efforts include studies of paternal epigenetic inheritance, funded by an European Research Council (ERC) Starting Grant, and environmental pollution in Bangladesh. Our research is also supported by grants from the Swedish Research Council (VR), the Swedish Research Council for Sustainable Development (Formas), and several private research foundations.
We are physically located at Science for Life Laboratory (SciLifeLab) in Solna, a national center for molecular biosciences. SciLifeLab provides infrastructure for state-of-the-art high-throughput molecular technologies and serves as a collaboration hub for Stockholm University, Karolinska Institute, KTH Royal Institute of Technology, and Uppsala University.