Mapping the environment.

Research Many elements and compounds present in the environment pose significant health risks to exposed individuals, and contribute to the burden of disease for society. For any exposed person the outcome may be affected by factors such as the degree of exposure, age, and genetically determined differences in uptake, elimination, or sensitivity to the toxic effects of the substance. Investigation of such genetic differences has been called toxicogenetics (Orphanides and Kimber 2003), and although most work has been done on toxic reactions to therapeutic drugs, the approach is equally applicable to the study of environmental pollutants. There has long been concern about chronic toxic effects of the elements lead, cad-mium, arsenic, and mercury, and an extensive literature exists on their associations with a range of conditions. For lead, the main community concerns are about impaired intellectual development in infancy and childhood There is also some evidence that higher lead values are associated with increased adult mortality (Lustberg and Silbergeld 2002, Schober et al. 2006), and cognitive decline in older people (Weisskopf et al. 2004). Environmental exposure is a precondition for accumulation of these potentially toxic elements, and major changes in exposure (such as reduction in the lead content of petrol) have produced changes in indices of within the general population of a particular country or region and at a particular time, variation in exposure is probably only one of several factors influencing accumulation and body burden. There is evidence that blood lead concentrations are quite stable within people who are exposed to sources of lead only in the general environment , and that there are significant between-individual differences (Brody et al. 1994; Delves et al. 1984). Individual differences in risk from lead may be caused by differences in behavior (such as the known effects of smoking and drinking) or by genetic differences in metabolic or transport processes. A number of attempts have been made to test for effects of genetic poly-morphisms on blood or bone lead values. To date the results are mixed, with allelic associations both reported and denied for ALAD (aminolevulinate, delta-, dehydratase; HGNC ID 395) [all gene names, symbols, and ID numbers are from the Human Gene Nomenclature Committee (HGNC) available at Because of the clinical association between iron deficiency and lead toxicity, an association with iron status, which may up-or down-regulate intestinal divalent cation transporters, and specifically with HFE (hemochromatosis; HGNC ID 4886) genotype has been …