Based upon a previous qualitative study a questionnaire ascertaining adolescents' awareness of gambling advertisements and their impact upon their behavior was developed and administered to 1,147 youth between the ages of 12 and 19. The findings suggest that almost all youth report being exposed to advertising with many individuals indicating being bombarded with messages, especially through pop-up ads viewed on the Internet. Sixty-one percent of youth reported receiving spam gambling advertisements by e-mail and 96% had seen TV advertisements for gambling. The underlying perceived message is that winning is easy, the chance of winning is high and that gambling is an easy way to become wealthy. While most youth are dismissive of the messages and are aware of the risks associated with gambling, a large percentage of youth report that these messages prompt them to gamble. Rather than inciting non-gamblers to begin gambling, advertisements appear to serve the function of maintaining established gambling habits and were particularly problematic to youth with gambling problems. Gender and developmental trends were noted.

Problem gambling has recently emerged as a significant public health issue. While most efforts target adult pathological gamblers, there is growing concern that adolescents and young adults represent the highest risk group for gambling problems. Prevailing public health initiatives addressing youth problem gambling are only beginning to be examined. Drawing upon the Ottawa Charter for Health Promotion as a guiding framework, a prevention model and framework for action are presented to better understand and address problem gambling from a population-based perspective. This framework applies denormalization, protection, prevention, and harm-reduction principles to youth gambling problems and describes primary, secondary and tertiary prevention objectives. A foundation for the development, implementation and evaluation of comprehensive, multi-level health promotion and prevention strategies for youth problem gambling is provided.

Purpose Despite accumulating evidence from experimental animal studies showing that paternal environmental exposures induce genetic and epigenetic alterations in sperm which in turn increase the risk of adverse health outcomes in offspring, there is limited epidemiological data on the effects of human paternal preconception exposures on children’s health. We summarize animal and human studies showing that paternal preconception environmental exposures influence offspring health. We discuss specific approaches and designs for human studies to investigate the health effects of paternal preconception exposures, the specific challenges these studies may face, and how we might address them. Recent Findings In animal studies, paternal preconception diet, stress, and chemical exposures have been associated with offspring health and these effects are mediated by epigenetic modifications transmitted through sperm DNA, histones, and RNA. Most epidemiological studies have examined paternal preconception occupational exposures and their effect on the risk of birth defects and childhood cancer; few have examined the effects of low-level general population exposure to environmental toxicants. While the design and execution of epidemiological studies of paternal preconception exposures face challenges, particularly with regard to selection bias and recruitment, we believe these are tractable and that preconception studies are feasible. Summary New or augmented prospective cohort studies would be the optimal method to address the critical knowledge gaps on the effect of paternal preconception exposures on prevalent childhood health outcomes. Determining if this period of life represents a window of heightened vulnerability would improve our understanding of modifiable risk factors for children’s health and wellbeing.

C.M. was supported by a Canadian Institutes of Health Research doctoral research award at the time of this study. No competing interests are declared.

Work supported by grants ES009718, ES022955, ES000002, and T32ES007069 from the National Institute of Environmental Health Sciences (NIEHS) and grant T32 DK007703-16 from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). C.M. was supported by a post-doctoral training award from the Canadian Institutes of Health Research. There are no competing interests to declare.