WATER QUALITY ADYISORY ALUMINUM CRITERIA FIND STRNDRRDS DIVISION OFFICE OF WATER REGULRTIONS AND STRNDRRDS UNITED STRTES ENVIRONMENT RL PROTECTION RGENCY JUNE 1 3 Q G ------- WATER QUALITY ADVISORY Number 10 ALUMINUM Criteria and Standards Division Office of Water Regulations and Standards United States Environmental Protection Agency Advisory: Aquatic Life No aquatic life advisory is given because publication of a final ambient water quality criterion document for aluminum is scheduled for September, 1986. Advisory: Human Health The advisory concentration for aluminum is ambient water for the protection of human health is estimated to be 4.07 mg/L, when exposure is assumed to include consumption of 6.5 g of contaminated fish and 2L of contaminated water per day, or 12.9 mg/L when exposure is assumed to include consumption of contaminated fish only. These concentrations do not take into account relative source contributions from other media. Care should be taken in the application of this advisory, with consideration of its derivation, as stated in the attached support document. ------- human health effects LITERATURE SEARCH AND DATA EVALUATION FOR - ALUMINUM U.S. ENVIRONMENTAL PROTECTION AGENCY OFFICE OF WATER REGULATIONS AND STANDARDS CRITERIA AND STANDARDS DIVISION WASHINGTON, D.C. 20460 ii ------- TABLE OF CONTENTS PAGE INTRODUCTION iv RELATIVE SOURCE CONTRIBUTION 1 TOXICOKINETICS 2 HEALTH EFFECTS 3 QUANTIFICATION OF TOXICOLOGICAL EFFECTS 4 REFERENCES 7 LIST OF TABLES Table l. Relative Media Contribution of Aluminum 2 Table 2. Water Quality Advisory for Aluminum (mg/L) 6 iii ------- INTRODUCTION Advisories have been developed to give the best available scientific information on the aquatic and human health effects of chemicals in surface waters. They are issued in cases when information is needed quickly, but where there is not sufficient data to calculate national ambient water quality criteria. An advisory concentration for the protection of human health can be derived from a number of sources. The office of Drinking Water Health Effects Advisories; Acceptable Daily Intake (ADI) values from EPA; Office of Pesticides and Toxic Substances risk assessment; Carcinogen Assessment Group (CAG) cancer risk estimates; risk estimates; risk estimates derived from the open literature; or other sources which will be given in the support document. The advisory concentrations derived from these sources will vary in confidence and usefulness, based on the amount and quality of data used as well as the assumptions behind the original estimates. The user is advised to read the background information carefully before using the advisory concentrations to determine the strengths or deficiencies of the values given in the advisory. iv ------- Human Health Section Water Quality Advisory (Aluminum) Identifying the most appropriate set of Advisory numbers (fish only, water only, fish plus water) requires an appreciation of several parameters: (1) Relative source contribution analysis or all sources of exposure expressed in percent (2) Toxicokinetics or the uptake, distribution, retention, and metabolism of the pollutant (3) Health effects including both non-carcinogenic and car- cinogenic bioeffects (4) Quantification of the toxicological effects A. Relative Source Contribution The average and average maximum concentrations of Aluminum (Al) at raw water are approximately 0.1 mg/L and 1.94 mg/L (ten EPA regions). The National Academy of Sciences (NAS) ('82) notes a concentration of 0.074 ug/ml and a value of 0.130 mg/L can be calculated from a paper by Miller et al. ('84). Surface water appears to have higher concentrations than groundwater. The Al concentration can exceed 100 mg/L when the pH is 5 and mining operations can encourage such conditions. The maximum ambient concentrations by EPA regions have been determined by Miller et al. ('84) where the average maximum was 1.94 mg/L and Region VII had the highest maximum of 5.35 mg/L. The Al detection limit was 0.014 mg/L. Using a conservative Bioconcentration Factor (BCF) of 10 and assuming that the average surface water concentra- tion is 100 ug/L and that an adult consumes 0.0065 kg of fish/day, an Al intake via fish could be calculated to be 6.5 ug/day via 0.1 mg/L x 10 BCF x 0.0065 kg/day. In finished community water in the U.S., the average and average maximum concentration of Al can be calculated from Miller et al. ('84) to be 0.069 and 1.155 mg/L, respectively. The use of Al as coagulant appears to increase the Al concentration in the finished water. Since Al is a very abundant element and soil concentra- tions vary considerably, Al concentrations in foods vary widely. The average daily intake of Al via food is 3 0 mg/L (La 86, NAS 82 and ICRP 75). The intake via air- borne Al is approximately 0.10 mg/day (ICRP 75). A relative media contribution analysis for man via natural sources of Al (less medicines) indicates that ------- food is the major source of exposure (Table I). The intake of Al via food is responsible for some 99% while the remainder is due to air (0.3%) and water (0.5%). The contribution via water is primarily due to potable water and only a small amount is contributed by the consumption of fish. For the purpose of this Advisory, water will be assumed to be responsible for 1% of man's intake of Al. Table 1. Relative Media Contribution of Aluminum Water Human Intake Exposure Media Cone. (mg/L) mg/day % Food Air Water 30 99.2 0.1 0.3 0.15 0.5 O Fish 0.1 (0.0065) (0.02) o Potable 0.07 (0.14) (0.46) Total 30.25 100 Compromised individuals using antacid medicine containing Al, people suffering from kidney disorders and workers exposed to dust containing Al would be expected to receive Al doses that may be substantial!v higher than that specified for the normal ?ndividuliY nation-wide (NAS 82, EPA 84). aiviauai B. Toxicokinetics intake of Al is largely by ingestion and only minor amounts are inhaled (icrp 75). People normally take in some 30 mg/day, however, renal-failure * £ a?* 5_1n 9 Al/day via aluminum hydroxide, an antacid (NAS 82). Normal gastrointestinal absorption rates approximatelv threeU5fmic P^ients (8-9%) being approximately three (3) times greater (EPA 84) Th» normal plasma level of Al is 5 ug/L (EPA 84) Patient on antacids can have Al plasma levels significantly higher (40 mg/L) than the normal. According to EPA (84), neurological effects do not appear until serum levels exceed 100-200 ug/L. Aluminum gastrointestinal tract (GIT) absorption was reported to be enhanced by parathyroid hormone (PTH) (NAS 82). y -2- ------- Aluminum is virtually found in all tissues (EPA 84). Aluminum distributes to the skeleton, muscle, lungs, brain etc. Aluminum concentration in the brain and bone are important to the decisions made in this Advisory. An A1 balance study by the ICRP shows that excretion occurs mainly via the bile and feces with minor amounts via sweat, urine, and hair. While the biological half-life remains unclear, the human body burden of A1 is estimated by the NAS (82) to range from 50-150 mg where most soft tissues contain 0.2-0.6 ug/g. Uremic patients are often encouraged to take aluminum hydroxide to reduce the hyperphosphatemia (NAS 82, La 86). This is accomplished because of the A1 complexes with phosphate in the gastrointestinal tract, thereby reducing GIT phosphate absorption. Unfortunately the resolution of one problem (uremia) .causes a greater availability of A1 which may cause other potential health problems like hypercalciuria and osteromalacia. In 1984 EPA assumed that Aluminum in doses near 100 mg/day was more or less homeostatically controlled (EPA 84). However, some 4% of one's intake is retained and the* body burden obviously increases with age. The bioaccumulation of A1 in fish remains unclear (EPA 86). However, using a paper by Buergel and Wrenn (84), a BCF of ten (10) may be appropriate and will be used in this Advisory. C. Health Effects Aluminum has been associated with encephalopathies known as Alzheimer's disease and as dialysis dementia (NAS 82). Alzheimer's disease is a neurologic disorder which occurs in a substantial number of humans after age 40 years. It is slowly progressive and may be influenced by the ever-increasing A1 body burden. Symptoms include behavioral change, memory disturbances, spacial disorientation, agnosia, dysphasia and seizures (NAS 82). Aluminum has been associated with neurofibrillar tangles in the brain. Plaques and neurofibrillar degeneration obviously inhibit and prevent proper conduction of nerve impulses. Dialysis dementia or dialysis encephalopathy is a rather rapidly deteriorative neurological disorder which may cause death within a year (NAS 82). This relentless progressive neurological disease has often been found in chronic dialysis patients. Dialysis dementia is characterized by the onset of altered behavior, speech disturbances, dyspraxia, tre- mors, convulsions, personality changes and psychoses (NAS 82). An epidemiological study in Chicago in the -3- ------- 1970's demonstrated that Al in drinking water greatly- impacted 20 patients who had been maintained on long- term dialysis (Du 78). When Al levels were 300-400 mg/L, dementia occurred, and when the Al concentrations were <14 ug/L to 150 ug/L, dementia was absent. Both Al concentration and the natural progression of the disease itself, with or without Al, may be responsible for the sudden increase in this neurological disorder. From a conservative viewpoint, Al should be assumed, at this time, to be an associated etiological factor in this serious neurological disorder. A review of Al concentration in dialysis-type water suggests that 14 ug/L is that critical concentration with regard to uptake (Hodge 81 and Parkinson et al) suggested that when dialysis water exceeds 50 ug/L, the incidence of encephalopathy exceeds 5%. Aluminum may also be responsible for causing osteomala- cia (NAS 82). Aluminum may compete with calcium within the bone, leaving the bone soft and susceptible to fracturing. Excessive use of aluminum hydroxide could cause a phosphate absorption deficit which may interfere with bone mineralization and may lead to direct deposi- tion of Al in the skeleton (NAS 82). Claims have been made that Al blocks calcium uptake resulting in hyper- calcemia (NAS 82). Aluminum is used to prevent hyperphosphatemia in uremic patients. Al is used to control phosphorus absorption (EPA 84). However, reduced phosphorus metabolism results in significant decreases in serum ATP level. More ADP and AMP and less ATP could impact the functioning of other metabolic cycles. Aluminum does cause pulmonary fibrosis but has been primarily associated with inhalation exposures via occu- pational workplace (NAS 82). Pulmonary fibrosis probably is not caused by Al ingestion. Aluminum appears not to be mutagenic nor carcinogenic (EPA 84). One study has reported lymphoma leukemia in female mice but it would be premature to assume carcino- genicity in humans. There also has been a claim for interference with animal reproduction, but again it would be premature to assume any association with Al at this time (EPA 84). D. Quantification of Toxicological Effects Aluminum is not an essential element (La 86). The ideal suggested daily intake then obviously would be none. However, since Al is a very abundant element and people are exposed to some 30 mg/day, it--is important to identify that level of exposure where toxicity may ------- actually start occurring since it simply is not possible to exclude it. Therefore, a practical ADI must be determined. Since many people experience neurological and bone disorders that have been associated with Al, it rs entirely possible that the ADI is substantially below our natural level of exposure. Should this be the case, our only option would be to limit our exposure to the extent feasible. Two sensitive indicators of Al toxicity seem to be a reduction in serum ATP levels or increased serum Al levels (EPA 84). One may question how important it is to have reduced energy units or increased Al levels in the blood. The answers to those questions are uncertain but they may either serve as threshold markers or evidence that the speculated association of Al with Alzheimer's disease, dialysis dementia and osteomalacia are real. Utilizing the studies by Ondreick et al. (66) and by Krasovskii et al. (79) as reviewed by EPA (84), it seems apparent that 6 mg/kg oral exposure in animals is a NOAEL since higher acute doses (17,27 + 50 mg/kg) caused a decrease in ATP. Using the Krasovskii data, an ADI of 4.2 mg/day can be calculated: _(6 mg/kg/day) (70 kg) - 4.2 mg/day 100 S.F. Note: A safety factor (S.F.) of 100 was used because it was an animal experiment where the NOAEL was identified. Utilizing an Al balance study (20 days) by Greger and Baier (83) as described by EPA (84), a NOAEL of 125 mg Al/day or 1.79 mg/kg/day would seem appropriate since the gastrointestinal absorption of phosphorus appeared to begin to be noticeably inhibited and serum levels were 25 times the norm. The 1.79 mg/kg apparently would be expected to cause an Al serum level of 125 ug/L or 7 5 ug/L below the 200 ug Al/1 threshold specified within EPA ('84) Al criteria document. (Note that the normal serum level is 5 ug/L.) Using the Greger and Baier study then, an ADI of 12.6 mg/day could be calculated: 1.79 mg/kg/day) (70 kg) -1.3 mg/day 100 S.F. Note: A safety factor (S.F.) of 100 was used to reflect uncertainty associated with a short-term, human study where the NOAEL could be identified. To avoid having reference doses being dictated by a single experiment and experimented design, it is often appropriate to appreciate the dose/response results of -5- ------- more than one experiment. Therefore, averaging the two possible values suggests an ADI or RFD of 2.8 mg/day. Without consideration of other sources of exposure it is possible to calculate: ' a. Lifetime acceptable level in drinking water via ADI/2 b. Lifetime acceptable level in ambient water if only fish were consumed but the water was not consumed via ADI/RF c. Lifetime acceptable level in which the water was con- sumed and the fish living within the water were consumed at the rate of 0.0065 kg/day via ADI/2 plus 10 (0.0065). The three values for drinking water only, fish only water plus fish are 1.4 mg/L, 43 mg/L and 1.4 mg/L, ' respectively: o Drinking water only: ADI = 2.8 mg/day = l.4mg/L 2 2 1/day o Fish only: ADI 2.8 mg/day = 43 mg/L RF (10 BCF)(0.0065 kg/day) o Ambient water or fish plus drinking water: ADI 2.8 mg/d =1.4 mg/L 2+RF 2 1/d + (10 BCF)(0.0065 kg/d) Since water is only 1% of man's A1 intake, all initial Advisory levels should be modified by 100. However, since an ADI already has a 100-fold safety factor and there is a practical limit to which water alone can control the total Al intake, only an additional factor of 10 will be utilized to convert initial values to final water quality advisory levels (Table 2). Table 2. Water Quality Advisory For Aluminum (mg/L) Water Use Relative Source Contribution No Yes Fish plus potable 1.4 «—1 • o Fish only 43 4.3 Potable only 1.4 0.14 -6- ------- References Bu 84. Buergel & Wrenn. Health Effects. PB#84-178-44l. tf.S. EPA. Du 78. Dunea, Mahurkar, Mamdani Smith. Role of Aluminum in Dialysis Dementia. Ann. Intern. Med. 88:502-504. /EPA 84. U.S. EPA. Drinking Water Criteria Document for J Aluminum. ORD ECAO-Cincinnati, Ohio. EPA 86. U.S. EPA. Ambient Aquatic Life Water Quality Criteria for Aluminum. ORD-Duluth, Minn. Gr 83. Greger and Baier. Excretion and retention of low or moderate levels of aluminum by human subjects. Fd. Chem. Toxicol. 21:473-477. Hodge, Day, OHAIA Research, Ackrill Ralston. Critical concentration of aluminum in water use for dialysis. Lancet, pp. 802-803. ICRP 75. Int. Com. Rad. Prot. Reference Man. (#23), pp. 480. KR 79. Krasovskii et al. Experimental study of the biological effects of lead and aluminum following oral administration. Environ. Hlth. Perspect. 30:47-51. La 86. Lappenbusch. Contaminated Drinking Water and Your Health. Lappenbusch Environmental Health, 6480 Overlook Drive, Alexandria, Virginia 22312, pp. 192. Miller 84. Miller et al. The Occurrence of Aluminum in Drinking Water. J. AWWA 5 76(1):84-91. NAS 82. National Acad. Sci. (SDWC). Drinking Water and Health, Volume 4, pp. 299. On 66. Ondreick et al. Chronic toxicity of aluminum in rats and mice and its effects on phosphorus metabolism. Br. J. Ind. Med. 23:305-312. Parkinson, Ward and Kerr. Dialysis encephalopathy bone disease and anemia; The Aluminum Toxication Syndrome During Regular Hemodyalysis. Clinical Path., Vol. 34, pg. 1285-1294. -7- ------- |