Aluminum contamination in parenteral products :

Aluminum is one of the most common metal elements in the earth's crust. It is not an essential element for life and has commonly been thought of as a rather inert and insoluble mineral. Therefore, it has often been regarded as not posing a significant health hazard. In consequence, aluminum-containing agents been used in many food processing steps and also in removal by flocculation of particulate organic matter from water. In recent years, acid rain has tended to mobilize aluminum-containing minerals into a more soluble form, ionic Al(3+), which has found their way into many reservoirs that constitute residential drinking water resources. As a result, the human body burden of aluminum has increased. Epidemiological studies suggest that aluminum may not be as innocuous as was previously thought and that aluminum may actively promote the onset and progression of Alzheimer's disease. Epidemiological data is strengthened by experimental evidence of aluminum exposure leading to excess inflammatory activity within the brain. Such apparently irrelevant immune activity unprovoked by an exogenous infectious agent characterizes the aging brain and is even more pronounced in several neurodegenerative diseases. The causation of most of these age-related neurological disorders is not understood but since they are generally not genetic, one must assume that their development is underlain by unknown environmental factors. There is an increasing and coherent body of evidence that implicates aluminum as being one such significant factor. Evidence is outlined supporting the concept of aluminum's involvement in hastening brain aging. This acceleration would then inevitably lead to increased incidence of specific age-related neurological diseases. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Aluminum, a contaminant of commercial intravenous-feeding solutions, is potentially neurotoxic. We investigated the effect of perinatal exposure to intravenous aluminum on the neurologic development of infants born prematurely. We randomly assigned 227 premature infants with gestational ages of less than 34 weeks and birth weights of less than 1850 g who required intravenous feeding before they could begin enteral feeding to receive either standard or specially constituted, aluminum-depleted intravenous-feeding solutions. The neurologic development of the 182 surviving infants who could be tested was assessed by using the Bayley Scales of Infant Development at 18 months of age. The 90 infants who received the standard feeding solutions had a mean (+/-SD) Bayley Mental Development Index of 95+/-22, as compared with 98+/-20 for the 92 infants who received the aluminum-depleted solutions (P=0.39). In a planned subgroup analysis of infants in whom the duration of intravenous feeding exceeded the median and who did not have neuromotor impairment, the mean values for the Bayley Mental Development Index for the 39 infants who received the standard solutions and the 41 infants who received the aluminum-depleted solutions were 92+/-20 and 102+/-17, respectively (P=0.02). The former were significantly more likely (39 percent, vs. 17 percent of the latter group; P=0.03) to have a Mental Development Index of less than 85, increasing their risk of subsequent educational problems. For all 157 infants without neuromotor impairment, increasing aluminum exposure was associated with a reduction in the Mental Development Index (P=0.03), with an adjusted loss of one point per day of intravenous feeding for infants receiving the standard solutions. In preterm infants, prolonged intravenous feeding with solutions containing aluminum is associated with impaired neurologic development.

Metal pollutants are a global health risk due to their ability to contribute to a variety of diseases. Aluminum (Al), a ubiquitous environmental contaminant is implicated in anemia, osteomalacia, hepatic disorder, and neurological disorder. In this review, we outline how this intracellular generator of reactive oxygen species (ROS) triggers a metabolic shift towards lipogenesis in astrocytes and hepatocytes. This Al-evoked phenomenon is coupled to diminished mitochondrial activity, anerobiosis, and the channeling of α-ketoacids towards anti-oxidant defense. The resulting metabolic reconfiguration leads to fat accumulation and a reduction in ATP synthesis, characteristics that are common to numerous medical disorders. Hence, the ability of Al toxicity to create an oxidative environment promotes dysfunctional metabolic processes in astrocytes and hepatocytes. These molecular events triggered by Al-induced ROS production are the potential mediators of brain and liver disorders.