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Health Determinants
- Interaction between health determinants

 Recently, many studies have been published on the role of genetics in specific population health risk issues particularly identifying polymorphism in genes that could substantially alter the risk, for example, N-acetyltransferase 2 (NAT 2) slow acetylator phenotype increasing the risk of bladder cancer and the glutationne S-transferase µ1 (GSTM1) deficiency increasing lung cancer risk. Various reports have identified genetic-environment interactions including an increased lung cancer risk due to passive smoking in women who were GSTM1-deficient. Mutations in BRCA1 or BRCA2 contribute to breast cancer and ovarian incidence. Therefore, the identification of genetically susceptible population subgroups at which risk management strategies need to be targeted will definitely help in identifying gene-environment interactions.

It is now well-recognized that environmental determinants of risk interact with social and
genetic determinants. For example, synergistic interactions between asbestos and tobacco smoke and between radon and tobacco smoke have been clearly demonstrated in epidemiological studies of lung cancer risks in miners, raising questions about health risks in non-occupational groups exposed to these agents. Genetic susceptibility to environmental carcinogens has also been established, with the risk of radiation induced cancer of the eye greatly enhanced in individuals carrying the retinoblastoma gene. Complex mixtures of environmental contaminants, such as mixtures of pollutants in ambient air associated with cardio-respiratory morbidity and mortality, also present opportunities for interaction among the components of the mixture. For example, gene-diet interactions such as the adiponectin gene polymorphism (+10211T - G) may contribute to insulin resistance and diabetes and can be exaggerated when higher glycemic loads are consumed.

Social and environmental factors often interact in determining population health risks: social circumstances influence personal exposures to occupational and environmental hazards through education. This is then reinforced if the resulting ill-health leads to loss of income and resulting decline in social status. Similarly, associations between genetic and socio-economic factors are known: physical stature increases with social class and with upward social mobility, such that social circumstances limit the realization of the individual’s genetic potential. We therefore need to exploit health risk science to clarify the manner in which genetic, cultural and social circumstances interact to determine population health risks, both to enhance our ability to characterize disease risk, and to identify the optimal points for intervention.


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