Mercury (Hg) in children has multiple exposure sources and the toxicity of Hg compounds depends on exposure routes, dose, timing of exposure, and developmental stage (be it prenatal or postnatal). Over the last decades, Hg was widely recognized as a threat to the children’s health and there have been acknowledgements at the international level of the need of a global policy intervention—like the Minamata treaty—aimed at reducing or preventing Hg exposure and protecting the child health. National human biomonitoring (HBM) data has demonstrated that low levels of exposure of Hg are still an important health concern for children, which no one country can solve alone. Although independent HBM surveys have provided the basis for the achievements of exposure mitigation in specific contexts, a new paradigm for a coordinated global monitoring of children’s exposure, aimed at a reliable decision-making tool at global level is yet a great challenge for the next future. The objective of the present review is to describe current HBM studies on Hg exposure in children, taking into account the potential pathways of Hg exposure and the actual Hg exposure levels assessed by different biomarkers.

In the assessment of human health risk, the obtainment of reference values in biological tissues and/or fluids is crucial to estimate the type and magnitude of occupational and environmental exposure. In this context, urine is the major excretion route for many noxious substances that have entered the organism and can be viewed as one of the most useful materials for biomonitoring campaigns. In this study, reference concentration ranges for Cr, Ni and V in urine were achieved in a sub-population of 131 youngsters, aged 6–10, attending primary schools in the urban area of Rome. Subjects under drug therapy or affected by any pathological diseases were not included in this investigation. Strict precautions against contamination or loss of the analytes of interest were adopted for all steps. Determinations were performed by means of high resolution inductively coupled plasma mass spectrometry. In general, the natural log-transformed concentration data for the three elements investigated conformed to a satisfactorily normal distribution. The estimated reference ranges were as follows (µg g⁻¹ creatinine): Cr, 0.07–0.76; Ni, 0.20–1.23; V, 0.02–0.22. The sex of the youngsters was tentatively treated as a statistical explanatory variable using the Fischer F-test on variance.

Cadmium (Cd) is a toxic heavy metal that is considered an environmental contaminant. Several sources of human exposure to Cd, including employment in primary metal industries, production of certain batteries, foods, soil and cigarette smoke, are known. Its inhalation has been related to different respiratory diseases and toxic effects, among which alterations of the physiological redox state in individuals exposed to the metal have been described. Host-cell redox changes characteristic of oxidative stress facilitate the progression of viral infection through different mechanisms. In this paper, we have demonstrated that pre-treatment with CdCl₂ of MDCK cells increased influenza virus replication in a dose-dependent manner. This phenomenon was related to increased viral protein expression (about 40% compared with untreated cells). The concentration of CdCl₂, able to raise the virus titer, also induced oxidative stress. The addition of two antioxidants, a glutathione (GSH) derivative or the GSH precursor, N-acetyl-L-cysteine, to Cd pre-treated and infected cells restored the intracellular redox state and significantly inhibited viral replication. In conclusion, our data demonstrate that Cd-induced oxidative stress directly increases the ability of influenza virus to replicate in the host-cell, thus suggesting that exposure to heavy metals, such as this, could be a risk factor for individuals exposed to a greater extent to the contaminant, resulting in increased severity of virus-induced respiratory diseases.