By producing about 158,000 tons of nickel (Ni) per year, New Caledonia is one of the largest producers of Ni in the world, with soils rich in trace metals (Ni; chromium, Cr; cobalt, Co; manganese, Mn and iron, Fe). This ...
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By producing about 158,000 tons of nickel (Ni) per year, New Caledonia is one of the largest producers of Ni in the world, with soils rich in trace metals (Ni; chromium, Cr; cobalt, Co; manganese, Mn and iron, Fe). This massive Ni exploitation is a major economic issue for the country (8 to 17% of annual GDP) to the detriment of potential environmental and health impacts. Indeed, the exploitation of these open-pit nickel laterite mines leads to the emission of ultrafine particles of Ni and nickel oxide (NiO) disseminated in the environment, by the wind, or via run-off from watercourses but also of other metals present in these soils. These particles can be inhaled by mine workers and the surrounding population, raising questions relating to human toxicology, and can also be transported along freshwater streams close to the mines, to be deposited or washed downstream as far as the lagoon, thus impacting aquatic organisms, the study of which is a matter of ecotoxicology.From an environmental point of view, few studies have been conducted in New Caledonia. However, initial work on freshwater rivers near mines has shown very high levels of Ni accumulated in organisms under the mining influence, particularly in Pacific eels. In order to document the significance of the toxic impacts potentially inflicted on eels present at these sites, different types of approaches have been conducted: (i) Analysis of the toxic impacts of metals on Anguilla marmorata collected in situ during a mission (morphometric measurements, metal levels in organs, transcriptomic); (ii) Impact of exposure to NiO nanoparticles (NPs) on eel hepatocytes in vitro, the liver being a prime target of metal toxicity and an essential organ for eels. These approaches made it possible to early identify the cellular and molecular mechanisms of cytotoxic impact, oxidative stress, inflammation and mitochondrial dysfunction following this exposure.In parallel, human exposure to NPs is a public health concern. NPs can thus cross the alveolar-capillary barrier, find their way into the general circulation and exert deleterious effects through direct interactions with the cardiovascular system and, in particular, the endothelial cells (HPAEC) lining the lumen of the vessels and controlling vascular reactivity, which is modified after Ni NPs exposure. These effects could thus be amplified in cardiovascular pathologies. People suffering from pathologies of the pulmonary circulation (pulmonary hypertension, PH) could therefore constitute populations at risk. Thus, it is necessary to better characterize, in exposed populations, the toxic mechanisms induced by Ni-rich dusts and by NiO NPs on the cardiovascular system. For this purpose, we studied, on HPAEC, the effects induced by NiO NPs on calcium signaling , the pro-inflammatory response and the role of oxidative stress in the observed modifications, as well as the impacts of these NPs in a pathological conditions by using an in vitro model mimicking the vascular dynamics observed during PH with the STREX® stretching system. Our results show that exposure to NiO NPs induces oxidative stress, a pro-inflammatory response as well as alterations in calcium homeostasis and that these effects are amplified when the cells are under pathological conditions. This work therefore suggests that exposure to NiO NPs could aggravate some pathophysiological events in patients suffering from pre-existing cardiovascular diseases such as PH, and that these patients would be more sensitive to these particulate pollutants.
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