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O25-4 Parental occupational exposure and risk of childhood central nervous system tumours: a pooled analysis of case–control studies from germany, france, and the uk
  1. Ann Olsson1,2,
  2. Chatherine Huoi1,
  3. Olivia Febvey1,
  4. Tracy Lightfoot3,
  5. Eve Roman3,
  6. Jacqueline Clavel4,5,6,
  7. Brigitte Lacour4,5,7,
  8. Hans Kromhout8,
  9. Roel Vermeulen8,9,
  10. Susan Peters8,10,
  11. Helen Bailey1,4,5,
  12. Joachim Schüz1
  1. 1International Agency for Research on Cancer, Lyon, France
  2. 2The Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
  3. 3Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, York, UK
  4. 4Institut National de la Santé (INSERM) U1153, Epidemiology and Biostatistics Sorbonne Paris Cité Centre (CRESS), Epidemiology of Childhood and Adolescent Cancers Team (EPICEA), Villejuif, France
  5. 5Paris-Descartes University, UMRS-1153, Epidemiology and Biostatistics Sorbonne Paris Cité Centre (CRESS), Paris, France
  6. 6RNCE – National Registry of Childhood Cancers, Villejuif, France
  7. 7RNCE – National Registry of Childhood Cancers, Nancy, France
  8. 8Institute for Risk Assessment Sciences (IRAS), Department of Environmental Epidemiology, Utrecht University, Utrecht, The Netherlands
  9. 9Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, Utrecht, The Netherlands
  10. 10Occupational Respiratory Epidemiology, School of Population Health, University of Western Australia, Perth, Australia

Abstract

Background Central nervous system (CNS) tumours are the commonest childhood solid malignancy. We assessed the risk of childhood CNS tumours associated with parental occupational exposure to pesticides, polycyclic aromatic hydrocarbons (PAH), diesel motor exhaust (DME), asbestos, crystalline silica, and metals.

Methods We pooled three population-based case-control studies from France, Germany and the UK. Cases were children below 15 years of age diagnosed with CNS tumours; controls were matched to cases by gender and age. Socio-demographic and parental occupational information was collected using study-specific standardised interviews, either face-to-face or by telephone. Each study provided occupational data coded according to their national schemes; which were harmonised into ILO’s International Standard Classification of Occupations 1968 and 1988. Two general population job-exposure matrices (DOM-JEM, ALOHA+) were used to estimate parental occupational exposures. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using logistic regression.

Results The study included 1,361 children with CNS tumours and 5,500 controls. ORs for paternal exposure (yes/no) around conception were as follows: PAH 1.22 (95% CI: 0.98–1.52); metals 1.18 (95% CI: 0.96–1.46); and asbestos 1.12 (95% CI: 0.95–1.32). Asbestos was the only potentially hazardous exposure were the point estimate increased at higher levels; OR 1.42 (95% CI: 0.87–2.32). Paternal exposure to pesticides, DME and silica showed no increased risk. The prevalence of maternal occupational exposures to pesticides, PAH, DME, asbestos, silica, and metals was low; and no increased ORs were observed either around the time of conception or during pregnancy.

Conclusion Our large pooled study provided little evidence of an association between paternal occupational exposure to PAH, metals, and asbestos around conception and CNS tumour risk in the offspring. Previous studies have reported inconsistent results for PAH, while no studies have reported significant associations for asbestos and metals.

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