During the last decade, advances in analytical methods, an avalanche of information available over the Internet and a creation of international collaborations, have greatly increased our understanding of the role of trace elements in humans. Today, morbidity and mortality related to trace element deficiencies or toxicities affect more than half of the world's population. Research on both essential and toxic trace elements runs the gamut, from studies of dietary intake, requirements, and standards to optimal homeostasis and threshold values to genetic, molecular, and biochemical investigations of mechanisms of action. Specifically, trace elements are known to be involved in receptor, hormone, and enzyme functions, as well as genetics and derangements in disease.Disorders of trace element metabolism represent an important class of human diseases. The best known of these reflect abnormalities in iron, copper, or zinc metabolism. These diseases can lead to a deficiency of the metal in the tissues (e.g., matriptase-2 deficiency for iron, Menkes disease for copper, acrodermatitis enteropathica for zinc) or an excess (e.g., hemochromatosis for iron, Wilson's disease for copper). The adverse health effects resulting from trace element malnutrition have been almost completely solved in affluent countries with the exception of marginalized population groups, but deficiencies of trace element are still quite prevalent in less developed countries. Similarly, acute and chronic toxicity due to overexposure/pollution is a much more extensive problem in less developed countries than those that are affluent. Subclinical conditions of toxicity may be associated with a chronic low level occupational, environmental toxic exposure, or food toxicology and lead to insidious biological effects that indirectly affect health and disease risk.The propensity of a metal to be accumulated by living organisms depends on the affinity of the element for biological surfaces and its ability to cross external cell membranes, which, in turn, depends on its speciation. Once incorporated inside cells, the fate of the metal and its effects will depend on the ability of the organism to detoxify, and ultimately, eliminate the metal. Metals inappropriately bound to sensitive subcellular components, such as mitochondria or metabolic enzymes, can lead to oxidative stress and substantial metabolic costs. Each species within a food web possesses its own capacity for metal accumulation, storage, detoxification, and elimination. This species-specific response, combined with behavioral and ecological considerations of predator-prey interactions, greatly affects the capacity of metals to efficiently transfer along food webs and to induce toxicity.The present issue of ESPR contains selected articles contributed by speakers at the International Seminar BEcotoxicology and toxicology: problems and decisions.T he meeting was held in Rovaltain, Alixan, France, on 26 November 2015 and was organized by Trace ElementInstitute for UNESCO (TEU) and Foundation Rovaltain, in...