The Sixteenth Conference of the International Society for Environmental Epidemiology (ISEE): Abstracts
Experimental evidence suggests that parental exposure to polycyclic aromatic hydrocarbons (PAH), which occurs primarily through tobacco smoke, occupational exposure and air pollution, could increase the risk of cancer during childhood. Several mechanisms have been proposed for this association: germ-cell mutation or epigenetic modification occurring before conception, transplacental carcinogenesis, or direct toxicity during childhood.
Population-based case-control studies in seven countries compared data for 1218 children with brain tumors and 2223 controls. Parental occupational exposure to PAH during the five-year period before birth was estimated with a job-exposure matrix separately for preconceptional and pregnancy periods. Risk estimates were adjusted for child’s age, sex and center.
Paternal preconceptional occupational exposure to PAH was associated with an increased risk of all childhood brain tumors (odds ratio (OR)=1.3 95% confidence interval (CI): 1.1, 1.6) and of astroglial tumors (OR=1.4 95% CI: 1.1,1.7). However, there was no trend of increasing risks with the predicted level of exposure. Paternal smoking alone (OR=1.4) was associated with the risk of astroglial tumors compared with non-smoking, non-occupationally exposed fathers. Risks for paternal occupational exposure were higher, with (OR=1.6) or without smoking (OR=1.7). Maternal occupational exposure to PAH before conception or during pregnancy was rare and this exposure was not associated with any type of childhood brain tumor.
Our large study supports the hypothesis that paternal preconceptional exposure to PAH increases the risk of brain tumors in children.