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Partner 1B - Karolinska Insitutet, Institute of Environmental Medicine

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University and research group information

Karolinska Institutet (KI), founded in 1810, is Sweden’s only university to focus exclusively on the field of medicine. Situated in Stockholm, it is Sweden’s largest medical research centre, and accounts for roughly 45% of the country’s university based medical research. It is also home to the country’s largest medical school. 2500 postgraduate students and 2800 research staff (57% women) work in over 600 research units of KI.

 

KI is responsible for awarding the annual Nobel Prize in Medicine or Physiology. Research at KI has a strong European dimension, with around 400 contracts within EU Framework Programmes. Of these contracts, about 100 are or have been coordinated from KI.

 

The Institute of Environmental Medicine (IMM), a department at Karolinska Institutet, is an interdisciplinary research organization within the field of Environmental Medicine. The purpose of IMM is to carry out research and education, and perform investigations and analyses, pertaining to physical and chemical aspects of environmental medicine and health protection. Within IMM, internationally competitive research in the fields of toxicology, environmental medicine and epidemiology is conducted. IMM also provides assistance to public authorities and others through consulting and training personnel in the field of environmental medicine. Scientists from three research units as well as the Scientific Secretariat of IMM are engaged in CASCADE.

 

Partner 1B, the unit for Environmental Health Risk Assessment at IMM, has competence in experimental and regulatory toxicology of persistent organic pollutants and other endocrine disrupting compounds. The experimental research focuses on aryl hydrocarbon (Ah)-receptor- and estrogen receptor (ER)-mediated toxicity and retinoid (vitamin A) disruption as well as crosstalk between these systems. Disease areas addressed include adverse effects on bone, impaired reproduction and development, early heart malformations, and neurotoxicity. Development and application of quantitative methods on exposure and toxicological data to improve quantitative health risk assessment evaluations is also performed. In addition, research directed towards the development of novel concepts in hazard assessment is ongoing and focus is on the integration of genomic, proteomic and bioinformatics knowledge in the assessment of receptor-mediated toxicology during pre- and postnatal development.

Contribution to CASCADE

Partner 1B is the work package (WP) leader of WP10 – Risk Assessment Integration and WP11 - Risk Assessment Development, and is involved in the experimental work packages 17 - Mechanisms of Disease Development and 19 – Chemical Contaminants in Food.

 

The work carried out by Partner 1B within WP10 consists of:

  • Integration of risk assessment activities within CASCADE as well as with external organisations, stakeholders etc.
  • Development, organisation of and teaching in the CASCADE Research Education Programme in Environmental Health Risk Assessment.
  • Dissemination of health risk assessment information about the CASCADE model compounds as well as other selected compounds acting via nuclear receptors.

Within WP11, Partner 1B conducts:

  • Exposure assessment methodology development
  • Mathematical modelling of toxicological effect data with emphasis on benchmark dose (BMD) methodology
  • Analysis of methodological concepts and assumptions in risk assessment of toxicity involving nuclear receptor interaction(s) with emphasis on dioxin-like compounds.  

Partner 1B contributes to the experimental WP17 and WP19 with projects concerning:

  • The role of estrogen receptor subtypes in neural function and neurodegeneration
  • The Aryl hydrocarbon (Ah) receptor-mediated toxicity in the reproductive system and central nervous system (CNS).

Representative scientific articles as relevant to CASCADE

Berglund M, Elinder C-G, Järup LHuman Exposure Assessment. An Introduction. World Health Organization, Geneva and Institute of Environmental Medicine, Karolinska Institutet, Stockholm, pp. 196, 2001.


Falk Filipsson A, Sand S, Nilsson J, Victorin K: The Benchmark dose method - Review of available models, and recommendations for application in health risk assessment. Crit Reviews in Toxicology, 35, 505-542, 2003.

 

Fattore E, Trossvik C, Håkansson H: Relative potency values derived from hepatic vitamin A reduction in male and female Sprague Dawley rats following subchronic dietary exposure to individual polychlorinated dibenzo p dioxin and dibenzofuran congeners, and a mixture thereof. Toxicol Appl Pharmacol, 165, 184-194, 2000.


Nilsson CB, Håkansson H: The retinoid signaling system - a target in dioxin toxicity. Crit Rev Tox, 32, 211-232, 2002.


Smith-Warner SA, Spiegelman D, Yaun SS, Adami HO, Beeson WL, van den Brandt PA, Folsom AR, Fraser GE, Freudenheim JL, Goldbohm RA, Graham S, Miller AB, Potter JD, Rohan TE, Speizer FE, Toniolo P, Willett WC, Wolk A, Zeleniuch-Jacquotte A, Hunter DJ: Intake of Fruits and Vegetables and Risk of Breast Cancer: A Pooled Analysis of Cohort Studies. JAMA, 285, 769-776, 2001.


Öberg M: Health risk assessment of dioxin-like compounds in complex samples. Doctoral thesis, Karolinska Institutet, Sweden, 2003.