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J Epidemiol Community Health 64:A36 doi:10.1136/jech.2010.120477.6
  • Society for Social Medicine abstracts
  • Diabetes

P06 The epidemiology of type 1 diabetes in children from Northeast England

  1. T D Cheetham3
  1. 1Institute of Health and Society, Newcastle University, Newcastle upon Tyne, UK
  2. 2School of Biological Sciences, Liverpool University, UK
  3. 3Institute of Human Genetics, Newcastle University, Newcastle upon Tyne, UK

Abstract

Objective Environmental factors are involved in the aetiology of type 1 diabetes. A particular role for infectious exposures has been postulated. Temporal and spatial variation in incidence would be consistent with this hypothesis. We aimed to test predictions of increasing incidence and spatial variation occurring among cases of type 1 diabetes in children (aged 0–14 years) that might arise as a result of environmental mechanisms.

Design Population-based descriptive analysis of type 1 diabetes data.

Setting Northeast England.

Participants The study analysed 545 cases of type 1 diabetes diagnosed in children who were resident in a geographically defined region of northeast England during the period 1990–2007.

Main Outcome Measures Age-specific and age-standardised incidence rates were calculated. Temporal trends were analysed using Poisson regression. Relationships between incidence rates and small area (census ward) population density and Townsend deprivation index (and its components) were analysed using negative binomial regression.

Results Age-standardised incidence rates increased from 15.7 per 100 000 population in 1990–1995 to 27.9 per 100 000 population in 2002–2007. Furthermore, there was a regular 6-year cyclical pattern of plus or minus 25% in incidence rates (RR 1.25; 95% CI 1.11 to 1.41) and an overall increase of 4.8% per annum (95% CI 3.1 to 6.6). Lower incidence was associated with residence in wards that had higher levels of unemployment (RR per one percent increase in unemployment 0.97; 96% CI 0.95 to 0.99).

Conclusions The results are consistent with the involvement of one or more environmental exposures in aetiology. A possible role for a specific infectious agent should be considered.