Effects of Aluminium Contamination on the Nervous System of Freshwater Aquatic Vertebrates: A Review

Aluminium (Al) is the most common natural metallic element in the Earth’s crust. It is released into the environment through natural processes and human activities and accumulates in aquatic environments. This review compiles scientific data on the neurotoxicity of aluminium contamination on the nervous system of aquatic organisms. More precisely, it helps identify biomarkers of aluminium exposure for aquatic environment biomonitoring in freshwater aquatic vertebrates. Al is neurotoxic and accumulates in the nervous system of aquatic vertebrates, which is why it could be responsible for oxidative stress. In addition, it activates and inhibits antioxidant enzymes and leads to changes in acetylcholinesterase activity, neurotransmitter levels, and in the expression of several neural genes and nerve cell components. It also causes histological changes in nerve tissue, modifications of organism behaviour, and cognitive deficit. However, impacts of aluminium exposure on the early stages of aquatic vertebrate development are poorly described. Lastly, this review also poses the question of how accurate aquatic vertebrates (fishes and amphibians) could be used as model organisms to complement biological data relating to the developmental aspect. This “challenge” is very relevant since freshwater pollution with heavy metals has increased in the last few decades.

Adsorption of Organosilanes on the Surface of Aluminium and the Formation of Organosilane Films to Protect It from Corrosion

Adsorption of diaminesilane (DAS), vinyltrimethoxysilane (VS) on the surface of thermally precipitated aluminium was examined. The use of different adsorption isotherms made it possible to calculate the adsorption heats for DAS and VS. It was determined that chemisorption of these organosilanes occurred on the surface of aluminium. Exposure of aluminium for 60 min to aqueous solutions of organosilanes led to the formation of organosilane films on the surface of the metal. The use of infrared spectroscopy and scanning electron microscopy in the work made it possible to assess the interactions of organosilanes with the metal surface, as well as to determine the structural features of the films and their thickness. Electrochemical and corrosion research methods made it possible to study the protective properties of organosilane films on aluminium.

Rapid recovery of normal gill morphology and blood physiology in brown trout (Salmo trutta) after short-term exposure to toxic concentrations of aqueous aluminium under non-steady state chemical conditions

Freshwater acidification is characterised by elevated concentrations of aqueous aluminium. Global emissions of acidifying agents are reduced due to international agreements, and freshwater acidification has shifted from chronic to a more episodic character. The recovery of fish populations in acidified areas is likely to depend on the individual’s ability to recover from short-time aluminium exposures. We exposed brown trout (Salmo trutta) to an Al-rich medium, nominal concentration 600 µg L–1, for 0.5, 2, 6, 8 and 11 hours, before transfer to circumneutral Al-poor water for recovery. As controls, fish were either exposed for 11 hours to an acidified Al-poor medium or to untreated water. Some mortality during the first 24 hours of the recovery period occurred in fish exposed for 11, 8 and 6 hours to aluminium. No mortality during recovery was observed in the remaining groups. Aluminium exposure led to increased haematocrit and plasma lactate concentration, decreased plasma chloride concentration, deposition of aluminium on gill surfaces, and morphological alteration of the gill structures. The responses depended on exposure time. Aluminium deposited on the gill disappeared and plasma lactate levels were at control levels after 1 day in the recovery water, while haematocrit and plasma chloride levels were at control levels after 14 days of recovery. Gills in fish exposed to aluminium for 11 hours were almost fully recovered after 14 days. We conclude that the toxic response in brown trout exposed to an acutely toxic aluminium challenge is reversible. Moreover, the first 24 hours after aluminium exposures is the most critical period for the fish recovery. Further, it takes no more than 14 days for brown trout to fully recover from an acute toxic aluminium exposure, and only 1 day if the aluminium challenge is moderate.

Aggregated aluminium exposure: risk assessment for the general population

Aluminium is one of the most abundant elements in earth’s crust and its manifold uses result in an exposure of the population from many sources. Developmental toxicity, effects on the urinary tract and neurotoxicity are known effects of aluminium and its compounds. Here, we assessed the health risks resulting from total consumer exposure towards aluminium and various aluminium compounds, including contributions from foodstuffs, food additives, food contact materials (FCM), and cosmetic products. For the estimation of aluminium contents in foodstuff, data from the German “Pilot-Total-Diet-Study” were used, which was conducted as part of the European TDS-Exposure project. These were combined with consumption data from the German National Consumption Survey II to yield aluminium exposure via food for adults. It was found that the average weekly aluminium exposure resulting from food intake amounts to approx. 50% of the tolerable weekly intake (TWI) of 1 mg/kg body weight (bw)/week, derived by the European Food Safety Authority (EFSA). For children, data from the French “Infant Total Diet Study” and the “Second French Total Diet Study” were used to estimate aluminium exposure via food. As a result, the TWI can be exhausted or slightly exceeded—particularly for infants who are not exclusively breastfed and young children relying on specially adapted diets (e.g. soy-based, lactose free, hypoallergenic). When taking into account the overall aluminium exposure from foods, cosmetic products (cosmetics), pharmaceuticals and FCM from uncoated aluminium, a significant exceedance of the EFSA-derived TWI and even the PTWI of 2 mg/kg bw/week, derived by the Joint FAO/WHO Expert Committee on Food Additives, may occur. Specifically, high exposure levels were found for adolescents aged 11–14 years. Although exposure data were collected with special regard to the German population, it is also representative for European and comparable to international consumers. From a toxicological point of view, regular exceedance of the lifetime tolerable aluminium intake (TWI/PTWI) is undesirable, since this results in an increased risk for health impairments. Consequently, recommendations on how to reduce overall aluminium exposure are given.