Sorptive equilibrium profile of fluoride onto aluminum olivine [(FexMg1-x)2SiO4] composite (AOC): Physicochemical insights and isotherm modeling by non-linear least squares regression and a novel neural-network-based method.

A novel aluminum/olivine composite (AOC) was prepared by wet impregnation followed by calcination and was introduced as an efficient adsorbent for defluoridation. The adsorption of fluoride was modeled with one-, two- and three-parameter isotherm equations by non-linear regression to demonstrate the adsorption equilibrium. The FI was the best-fitted model among the two-parameter isotherms with a R2 value of 0.995. The three-parameter models were found to have better performance with low values of the error functions and high F values. The neural-network-based model was applied for the first time in the isotherm study. The optimized model was framed with eight neurons in hidden layer with a mean square of error of 0.0481 and correlation coefficient greater than 0.999. The neural-based model has the better predictability with a higher F value of 9484 and R2 value of 0.998 compared to regression models, exhibiting the F value and the R2 in the range of 86-3572 and 0.835-0.995, respectively. The material characterization established the formation of the aluminum oxide, silicate, etc. onto the olivine which is conducive of the removal of fluoride by the formation of aluminum fluoride compounds, such as AlF3 in the spent material after defluoridation.

Total allowable concentrations of monomeric inorganic aluminum and hydrated aluminum silicates in drinking water.

Maximum contaminant levels are used to control potential health hazards posed by chemicals in drinking water, but no primary national or international limits for aluminum (Al) have been adopted. Given the differences in toxicological profiles, the present evaluation derives total allowable concentrations for certain water-soluble inorganic Al compounds (including chloride, hydroxide, oxide, phosphate and sulfate) and for the hydrated Al silicates (including attapulgite, bentonite/montmorillonite, illite, kaolinite) in drinking water. The chemistry, toxicology and clinical experience with Al materials are extensive and depend upon the particular physical and chemical form. In general, the water solubility of the monomeric Al materials depends on pH and their water solubility and gastrointestinal bioavailability are much greater than that of the hydrated Al silicates. Other than Al-containing antacids and buffered aspirin, food is the primary source of Al exposure for most healthy people. Systemic uptake of Al after ingestion of the monomeric salts is somewhat greater from drinking water (0.28%) than from food (0.1%). Once absorbed, Al accumulates in bone, brain, liver and kidney, with bone as the major site for Al deposition in humans. Oral Al hydroxide is used routinely to bind phosphate salts in the gut to control hyperphosphatemia in people with compromised renal function. Signs of chronic Al toxicity in the musculoskeletal system include a vitamin D-resistant osteomalacia (deranged membranous bone formation characterized by accumulation of the osteoid matrix and reduced mineralization, reduced numbers of osteoblasts and osteoclasts, decreased lamellar and osteoid bands with elevated Al concentrations) presenting as bone pain and proximal myopathy. Aluminum-induced bone disease can progress to stress fractures of the ribs, femur, vertebrae, humerus and metatarsals. Serum Al ≥100 µg/L has a 75-88% positive predictive value for Al bone disease. Chronic Al toxicity is also manifest in the hematopoietic system as an erythropoietin-resistant microcytic hypochromic anemia. Signs of Al toxicity in the central nervous system (speech difficulty to total mutism to facial grimacing to multifacial seizures and dyspraxia) are related to Al accumulation in the brain and these symptoms can progress to frank encephalopathy. There are four groups of people at elevated risk of systemic Al intoxication after repeated ingestion of monomeric Al salts: the preterm infant, the infant with congenital uremia and children and adults with kidney disease. There is a dose-dependent increase in serum and urinary Al in people with compromised renal function, and restoration of renal function permits normal handling of systemically absorbed Al and resolution of Al bone disease. Clinical experience with 960 mg/day of Al(OH)(3) (~5 mg Al/kg-day) given by mouth over 3 months to men and women with compromised renal function found subclinical reductions in hemoglobin, hematocrit and serum ferritin. Following adult males and females with reduced kidney function found that ingestion of Al(OH)(3) at 2.85 g/day (~40 mg/kg-day Al) over 7 years increased bone Al, but failed to elicit significant bone toxicity. There was one report of DNA damage in cultured lymphocytes after high AlCl(3) exposure, but there is no evidence that ingestion of common inorganic Al compounds presents an increased carcinogenic risk or increases the risk for adverse reproductive or developmental outcomes. A number of studies of Al exposure in relation to memory in rodents have been published, but the results are inconsistent. At present, there is no evidence to substantiate the hypothesis that the pathogenesis of Alzheimer's Disease is caused by Al found in food and drinking water at the levels consumed by people living in North America and Western Europe. Attapulgite (palygorskite) has been used for decades at oral doses (recommended not to exceed two consecutive days) of 2,100 mg/day in children of 3-6 years, 4,200 mg/day in children of 6-12 years, and 9,000 mg/day in adults. Chronic ingestion of insoluble hydrated Al silicates (in kg) can result in disturbances in iron and potassium status, primarily as a result of clay binding to intestinal contents and enhanced fecal iron and zinc elimination. Sufficiently high doses of ingested Al silicates (≥50 g/day) over prolonged periods of time can elicit a deficiency anemia that can be corrected with oral Fe supplements. There is essentially no systemic Al uptake after ingestion of the hydrated Al silicates. Rats fed up to 20,000 ppm Ca montmorillonite (equivalent to 1,860 ppm total Al as the hydrated Al silicate) for 28 weeks failed to develop any adverse signs. The results of dietary Phase I and II clinical trials conducted in healthy adult volunteers over 14 days and 90 days with montmorillonite found no adverse effects after feeding up to 40 mg/kg-day as Al. Since the Al associated with ingestion of hydrated Al silicates is not absorbed into the systemic circulation, the hydrated Al silicates seldom cause medical problems unless the daily doses consumed are substantially greater than those used clinically or as dietary supplements. A no-observable-adverse-effect-level (NOAEL) of 13 mg/kg-day as total Al can be identified based on histologic osteomalacia seen in adult hemodialysis patients given Al hydroxide for up to 7 years as a phosphate binder. Following U.S. EPA methods for calculation of an oral reference dose (RfD), an intraspecies uncertainty factor of 10x was applied to that value results in a chronic oral reference dose (RfD) of 1.3 mg Al/kg-day; assuming a 70-kg adult consumes 2 L of drinking water per day and adjusting for a default 20% relative source contribution that value corresponds to a drinking water maximum concentration of 9 mg/L measured as total Al. A chronic NOAEL for montmorillonite as representative of the hydrated Al silicates was identified from the highest dietary concentration (20,000 ppm) fed in a 28-week bioassay with male and female Sprague-Dawley rats. Since young rats consume standard laboratory chow at ~23 g/day, this concentration corresponds to 56 mg Al/kg-day. Application of 3x interspecies uncertainty factor and a 3x factor to account for study duration results in a chronic oral RfD of 6 mg Al/kg-day. Of note, this RfD is 5-10 fold less than oral doses of Al silicates consumed by people who practice clay geophagy and it corresponds to a maximum drinking water concentration of 40 mg Al/L. To utilize the values derived here, the risk manager must recognize the particular product (e.g., alum) or source (e.g., groundwater, river water, clay or cement pipe) of the Al found in tap water, apply the appropriate analytical methods (atomic absorption, energy dispersive X-ray diffraction, infrared spectral analysis and/or scanning transmission electron microscopy) and compare the results to the most relevant standard. The drinking water concentrations derived here are greater than the U.S. EPA secondary maximum contaminant level (MCL) for total Al of 0.05-0.2 mg/L [40 CFR 143.3]. As such, domestic use of water with these concentrations is likely self-limiting given that its cloudy appearance will be greater than the maximum permitted (0.5-5.0 nephalometric turbidity units; 40 CFR Parts 141 and 142). Therefore, the organoleptic properties of Al materials in water determine public acceptance of potable water as contrast to any potential health hazard at the concentrations ordinarily present in municipal drinking water.

Preparation and characterization of nicotine-magnesium aluminum silicate complex-loaded sodium alginate matrix tablets for buccal delivery.

Nicotine (NCT) buccal tablets consisting of sodium alginate (SA) and nicotine-magnesium aluminum silicate (NCT-MAS) complexes acting as drug carriers were prepared using the direct compression method. The effects of the preparation pH levels of the NCT-MAS complexes and the complex/SA ratios on NCT release, permeation across mucosa, and mucoadhesive properties of the tablets were investigated. The NCT-MAS complex-loaded SA tablets had good physical properties and zero-order release kinetics of NCT, which indicate a swelling/erosion-controlled release mechanism. Measurement of unidirectional NCT release and permeation across porcine esophageal mucosa using a modified USP dissolution apparatus 2 showed that NCT delivery was controlled by the swollen gel matrix of the tablets. This matrix, which controlled drug diffusion, resulted from the molecular interactions of SA and MAS. Tablets containing the NCT-MAS complexes prepared at pH 9 showed remarkably higher NCT permeation rates than those containing the complexes prepared at acidic and neutral pH levels. Larger amounts of SA in the tablets decreased NCT release and permeation rates. Additionally, the presence of SA could enhance the mucoadhesive properties of the tablets. These findings suggest that SA plays the important role not only in controlling release and permeation of NCT but also for enhancing the mucoadhesive properties of the NCT-MAS complex-loaded SA tablets, and these tablets demonstrate a promising buccal delivery system for NCT.

Molecular interaction in alginate beads reinforced with sodium starch glycolate or magnesium aluminum silicate, and their physical characteristics.

Diclofenac calcium-alginate (DCA) beads were reinforced with different amounts of sodium starch glycolate (SSG) or magnesium aluminum silicate (MAS) and were prepared using ionotropic gelation method. Complex formation of sodium alginate (SA) and SSG or MAS in calcium-alginate beads was revealed using FTIR spectroscopy. Differential scanning calorimetric study indicated that diclofenac sodium (DS) in amorphous form was dispersed in the matrix of DCA beads. The thermal behavior of SSG-DCA and MAS-DCA beads was similar to the control bead. Both additives can improve the entrapment efficiency of DCA beads. The swelling and water uptake of the beads depended on the properties of incorporated additives. The SSG-DCA beads showed a higher water uptake and swelling than MAS-DCA beads. Moreover, the swelling of the beads showed a good correlation with the square root of time. The release kinetic of the beads in pH 6.8 phosphate buffer was swelling controlled mechanism, while that in distilled water followed Higuchi's model. The slower release rate and the longer lag time in pH 6.8 phosphate buffer was obtained from the SSG-DCA and MAS-DCA beads because of complex formation between SA and SSG or MAS. However, SSG in the beads could increase the release of DS from the beads in distilled water because it acted as a channeling agent. In contrast, MAS retarded the release of DS from the beads in distilled water due to the stronger matrix formation.

The absorption of iron, calcium, phosphorus, magnesium, copper and zinc in the jejunum-ileum of control and iron-deficient rats.

The effects of iron deficiency on the absorption of different dietary sources of iron were studied, together with the interactions between iron, calcium, phosphorus, magnesium, copper and zinc in the jejunum-ileum of control and iron-deficient rats. In this study, three perfusion solutions containing different iron sources: ferric citrate, haemoglobin, and equal parts of ferric citrate and haemoglobin were used. In addition, the same perfusion solutions were used with and without 2,4-dinitrophenol, an inhibitor of oxidative phosphorylation. Iron absorption in anaemic rats was greater than in the controls, except after perfusion with solutions containing haemoglobin. The absorption of calcium, copper and zinc in iron-deficient animals was not significantly affected, while the absorption of phosphorus and magnesium increased, with respect to animals in the control group. After perfusion with solutions containing haemoglobin, the absorption values of calcium, copper and zinc were lower than after ferric citrate in both groups (control and iron-deficient rats).