Physicochemical Changes of Aluminium in Mixing Zones: Mortality and Physiological Disturbances in Brown Trout (Salmo Trutta L.)

Abstract

Abstract-A standardized laboratory setup, simulating field mixing zones that originate at the confluence of limed rivers with acidic, aluminium-rich, tributaries, has been developed. Detailed analyses of the chemical speciation of aluminium (Al) in relation to the biological response of brown trout were performed to identify the mechanism of unexpected high fish mortality in the above-mentioned mixing zones with pH levels above 6.0. Brown trout experienced an acute cumulative mortality (98% in 48 h) immediately after neutral and acidic, Al-rich, water had mixed. Mortality was only 60% within 48 h of exposure to the acid water with Al (pH 4.6 ϩ 6.8 mol Al/L), although the Al concentration in the mixing zone was less (2.8 mol Al/L) at a nonharmful pH level (pH 6.4). Chemical speciation and ultrafiltration studies demonstrated that the transformation of low-molecular weight Al (Ͻ10 kD) into high-molecular weight Al (Ͼ10 kD), defined as Al polymerization, could better be related to the toxic response of fish, than the total Al concentration. The aging of polymerized Al forms (for 480 s) resulted in reduced fish mortality and less pronounced physiological stress. Brown trout in the initial mixing zone showed significantly increased plasma glucose and cortisol levels. Light and electron microscopy studies demonstrated serious damage to the skin: increased mucous secretion, a high ratio of acid to neutral glycoprotein-containing mucous cells, increased apoptosis, and infiltration of leucocytes and macrophages between the epithelial cells. Ionoregulatory parameters, which showed minor changes in fish in the initial mixing zone, did not allow explanation of acute fish mortality. Data on the ventilation frequency and the blood hematocrit, which both increased, gave support for the hypothesis that acute fish mortality in mixing zones could be caused by respiratory dysfunction.

Chronic toxicity of aluminum, at a pH of 6, to freshwater organisms: Empirical data for the development of international regulatory standards/criteria

“…For example, toxicity has been observed under laboratory conditions when the test solutions were not aged and not at steady state, owing to the existence of more toxic transient Al species [12]. Preliminary tests in our laboratory and others [3,9,10] have shown that aging of test waters for a short period before testing was sufficient for stabilizing toxicity. Gensemer et al [3] concluded that approximately 3 h was sufficient.…”

“…Aluminum represents a challenge for toxicity testing because insoluble hydroxide species can form quickly when pH changes from acidic to relatively circumneutral pH conditions (minutes to a few hours) [9][10][11][12]. Aluminum species can be transformed quickly in ambient waters to more insoluble phases after Al introduction; nevertheless, toxicity has been observed.…”

“…In particular, newly formed insoluble Al hydroxides are significantly more toxic than polymeric hydroxide species in waters that have been allowed to age. These transitions from monomeric to polymeric species can occur over a few minutes to hours depending on water quality, and incorporating an aging period before organism exposure leads to substantial reductions in observed toxicity [1,2,9,10,13]. To reduce the impact of transient, short-lived toxic effects caused by rapid speciation changes, and because they are considered unrepresentative of Al exposures in most natural waters, we adopted an aging period of 3 h. Preliminary analytical measurements and toxicity tests of variously aged solutions showed that toxicity associated with speciation changes generally had stabilized by 3 h [3].…”

Evaluating the effects of pH, hardness, and dissolved organic carbon on the toxicity of aluminum to freshwater aquatic organisms under circumneutral conditions

“…During this transformation period, the formation of short-lived (i.e., transient) forms of precipitated Al, such as colloidal and amorphous forms, can exist on the scale of a few minutes to hours, whereas more stable crystalline forms can take days to fully form [8]. Studies have shown that the toxicity of test solutions prepared from an acidic Al stock solution decrease considerably the longer they are allowed to age prior to exposure of organisms [9][10][11][12]. Transient species responsible for toxicity of Al are, therefore, unlikely to exist long enough to be a chronic risk to aquatic organisms except in mixing zones, where Al-rich acidic or basic waters meet more neutral waters, leading to continual precipitation of Al [10].…”

Fish kill caused by aluminium and iron contamination in a natural pond used for fish rearing: a case report

“…Al accumulation, in addition to injury to the gill epithelium, causes apoptosis and necrosis of gill ion-transporting cells (Eeckhaoudt 1994), which is considered to be the main cause of ion-regulatory and osmoregulatory dysfunction (Witters et al 1996). Fish death following Al exposure is also associated with an inflammatory response to Al-hydroxides with excessive mucous production and subsequent disruption of O 2 and CO 2 diffusion Witters et al 1991).…”