2 

Aluminum sulfate has use as a food additive, and is also used in consumer products including 

cosmetics and pharmaceuticals such as antacids and buffered aspirin.

The toxicology database for aluminum sulfate is complete, Aluminum sulfate has low acute toxicity 

by the oral route. No dermal or inhalation acute toxicity studies are available for aluminum sulfate. 

Aluminum sulfate is not a skin irritant, however, it is irritating to the eye. No skin sensitization 

studies are available Since ingested aluminum sulfate will readily dissociate in the stomach to 

aluminum (as will many other aluminum compounds), toxicology data on aluminum compounds and 

aluminum sulfate are considered as part of this assessment. Aluminum compounds have been 

evaluated by the Agency for Toxic Substances and Disease Registry (ASTDR, 2008) and as part of 

the toxicological profile of aluminum, ASTDR notes that “There is a rather extensive database on the 

oral toxicity of aluminum in animals. These studies clearly identify the nervous system as the most 

sensitive target of aluminum toxicity and most of the animal studies have focused on neurotoxicity 

and neurodevelopmental toxicity. Other adverse effects that have been observed in animals orally 

exposed to aluminum include impaired erythropoiesis in rats exposed to 230 mg Al/kg/day and 

higher, erythrocyte damage (as evidenced by decreases in hemoglobin, hematocrit, and erythrocyte 

osmotic fragility, and altered erythrocyte morphology) in rats exposed to 230 mg Al/kg/day and 

higher, increased susceptibility to infection in mouse dams exposed to 155 mg Al/kg/day, delays in 

pup maturation following exposure of rats to 53 mg Al/kg/day, and decreases in pup body weight 

gain in rats and mice exposed to 103 mg Al/kg/day and higher. . . Oral studies in rats and mice have 

not found significant histopathological changes in the brain under typical exposure conditions; 

however, altered myelination was found in the spinal cord of mouse pups exposed to 330 mg 

Al/kg/day on gestation day 1 through postnatal day 35. Overt signs of neurotoxicity are rarely 

reported at the doses tested in the available animal studies ( ≤330mg Al/kg/day for bioavailable 

aluminum compounds); rather, exposure to these doses is associated with subtle neurological effects 

detected with neurobehavioral performance tests. Significant alterations in motor function, sensory 

function, and cognitive function have been detected following exposure to adult or weanling rats and 

mice or following gestation and/or lactation exposure of rats and mice to aluminum lactate, aluminum 

nitrate, and aluminum chloride. The most consistently affected performance tests were forelimb 

and/or hindlimb grip strength, spontaneous motor activity, thermal sensitivity, and startle 

responsiveness. Significant impairments in cognitive function have been observed in some studies, 

although this has not been found in other studies even at higher doses. Adverse neurological effects 

have been observed in rats and mice at doses of 100–200 mg Al/kg/day and neurodevelopmental 

effects have been observed in rats and mice at doses of 103–330 mg Al/kg/day. 

. The toxicological data for aluminum is complicated by the variety of test materials, various 

species of animals, study durations, study endpoints, experimental designs, and methods of 

computation of the total dose of aluminum from test material as well as from the diet and water. The 

majority of the studies were not conducted under Good Laboratory Practice (GLP) Standards and 

were not conducted in accordance with any international testing guideline. The approach used for this 

analysis was to tabulate the NOAEL/LOAEL evaluations for the most relevant published studies but 

give greater weight and emphasis to the GLP guideline studies. Using this approach, the NOAEL 

from the two generation rat oral reproduction study of 41 mg/kg/bw/day aluminum sulfate (equivalent 

to 8.06 mg Al/kg bw/day) based on the decreased body weight from pups and parents and delay in 

vaginal opening. The similar effects seen in the two separate two generation rat oral reproduction 
3 

studies, both of which were conducted under GLPs and in compliance with OECD 416 guidelines, 

gives a high level of confidence and certainty in the data. There are no gaps in the database leading to 

uncertainty in the risk assessment for infants and children and there are no qualitative differences in 

sensitivity of offspring and adults. Therefore, the FQPA safety factor can be reduced to 1x. 

The chronic dietary exposure from food and water to aluminum sulfate is % of the cPAD for 

the U.S. population (adults) and 6.7% of the cPAD for children 1-2 years old, the most highly 

exposed population subgroup. There are no current residential uses for registered pesticide products 

containing aluminum sulfate as an inert ingredient and the proposed use would result in negligible 

residential exposures to aluminum sulfate, therefore a residential exposure and risk assessment was 

not performed. 

Ecological effects of concern are not expected from the proposed use of aluminum sulfate in 

antimicrobial pesticide formulations applied to food contact surfaces at a concentration not to exceed 

50 ppm in the pesticide formulation. 

Potential areas of environmental justice concerns, to the extent possible, were considered in 

this human health risk assessment, in accordance with U.S. Executive Order 12898, “Federal Actions 

to Address Environmental Justice in Minority Populations and Low-Income Populations,” 

http://www.eh.doe.gov/oepa/guidance/justice/eo12898.pdf. 

EPA has determined that there are no human health risk concerns that would preclude 

establishing the proposed exemption from the requirement of a tolerance for aluminum sulfate under 

40 CFR 180.940(a), for use as an inert ingredient in antimicrobial pesticide formulations applied to 

food-contact surfaces in public eating places, dairy-processing equipment, and food-processing 

equipment and utensils at a concentration not to exceed 50 parts per million (ppm). 

I. BACKGROUND 

Ecolab, Inc., submitted a petition to the U.S. Environmental Protection Agency (EPA), 

pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), to amend 40 CFR 

part 180 with respect to establishing an exemption from the requirement of a tolerance for aluminum 

sulfate (CAS Reg. No. 10043-01-3) under 40 CFR 180.940(a) for use as an inert ingredient in 

antimicrobial pesticide formulations applied to food-contact surfaces in public eating places, dairyprocessing equipment, and food-processing equipment and utensils] at a maximum concentration not 

to exceed 50 parts per million (ppm). 

II. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES 

Table 1 lists common synonyms and other identification information for aluminum sulfate. 

Table 2 lists important physical and chemical properties of aluminum sulfate. 
4 

Table 1. Nomenclature and Structure 

Identity Information 

Chemical structure: 

Chemical formula Al2(SO4)3

Synonyms: Aluminum sulphate; aluminum sulfate anhydrous; 

sulfuric acid, aluminum salt (3:2) 

CAS Registry Number: 10043-01-3 

Chemical Family: Inorganic salt 

Table 2. Physical and Chemical Properties 

Physical Chemical Property Result 

Color1,2,5 White 

Molecular Weight 342.15 

Physical Form1,2 Solid, white granule or powder chunks 

Odor1,4,5 Odorless 

pH5 2 

Stability to normal and elevated 

temperatures, metals, and metal ions1,2

Contact with alkalis and water-reactive materials causes 

exothermic reactions. 

Storage Stability1,3 Stable at room temperature in closed containers under 

normal storage and handling conditions 

Corrosion Characteristics1 Corrosive to steel when wet 

Melting Point2,4,5 770 °C/1418 °F (decomposes) 

Boiling Point1 117 °C/242 °F 

Density1 varies, <98lb/cu ft 

Flammability1,5 May burn, will not ignite 

n-octanol water partition coefficient6 P = 9.33 X 10-02

Solubility in water1,5 Complete, 313 g/L at 0°C, 891 g/L at 100°C 

Vapor Pressure2,5 3.35x10-05 mmHg at 25°C, Essentially zero 

1

http://www.deltachemical.com/PDFS/DeltaAlumSolid.pdf

2

ChemSpider-http://www.chemspider.com/RecordView.aspx?rid=c14d2cf7-36b3-42f0-8338-

e16af3fa38ad
5 

3

Sigma Aldrich MSDS - http://www.sigmaaldrich.com/catalog/DisplayMSDSContent.do

4

http://www.inchem.org/documents/icsc/icsc/eics1191.htm

5 http://www.inchem.org/documents/ukpids/ukpids/ukpid34.htm

6 http://sitem.herts.ac.uk/aeru/footprint/en/Reports/26.htm

III. USE PATTERN 

Aluminum sulfate is currently used as an inert ingredient in nonfood and food use pesticide 

formulations, with food uses being in conformance with an existing exemption from the requirement 

of a tolerance under 40 CFR 180.920 for use as a solid diluent and carrier. An evaluation of existing 

product registrations that contain aluminum sulfate as an inert ingredient identify no residential uses 

and maximum use on growing crops of less than 1% (w/w). The proposed use of aluminum sulfate is 

as an inert ingredient in food-contact surface antimicrobial sanitizing solutions at a maximum 

concentration not to exceed 50 ppm. 

IV. HAZARD CHARACTERIZATION AND DOSE-RESPONSE ASSESSMENT 

A. Summary of Toxicological Effects 

The toxicology database for aluminum sulfate is complete, Aluminum sulfate is of low acute 

toxicity by the oral and dermal routes. No dermal or inhalation acute toxicity studies are available for 

aluminum sulfate. Aluminum sulfate is not a skin irritant, however, it is severely irritating to the eye. 

No skin sensitization studies are available Since ingested aluminum sulfate will readily dissociate in 

the stomach to aluminum (as will many other aluminum compounds), toxicology data on aluminum 

compounds and aluminum sulfate are considered as part of this assessment. Aluminum compounds 

have been evaluated by the Agency for Toxic Substances and Disease Registry (ASTDR, 2008) and 

as part of the toxicological profile of aluminum ASTDR notes that “There is a rather extensive 

database on the oral toxicity of aluminum in animals. These studies clearly identify the nervous 

system as the most sensitive target of aluminum toxicity and most of the animal studies have focused 

on neurotoxicity and neurodevelopmental toxicity. . Other adverse effects that have been observed in 

animals orally exposed to aluminum include impaired erythropoiesis in rats exposed to 230 mg 

Al/kg/day and higher, erythrocyte damage (as evidenced by decreases in hemoglobin, hematocrit, and 

erythrocyte osmotic fragility, and altered erythrocyte morphology) in rats exposed to 230 mg 

Al/kg/day and higher, increased susceptibility to infection in mouse dams exposed to 155 mg 

Al/kg/day, delays in pup maturation following exposure of rats to 53 mg Al/kg/day, and decreases in 

pup body weight gain in rats and mice exposed to 103 mg Al/kg/day and higher. . . Oral studies in 

rats and mice have not found significant histopathological changes in the brain under typical exposure 

conditions; however, altered myelination was found in the spinal cord of mouse pups exposed to 330 

mg Al/kg/day on gestation day 1 through postnatal day 35. Overt signs of neurotoxicity are rarely 

reported at the doses tested in the available animal studies ( ≤330mg Al/kg/day for bioavailable 

aluminum compounds); rather, exposure to these doses is associated with subtle neurological effects 

detected with neurobehavioral performance tests. Significant alterations in motor function, sensory 

function, and cognitive function have been detected following exposure to adult or weanling rats and 

mice or following gestation and/or lactation exposure of rats and mice to aluminum lactate, aluminum 

nitrate, and aluminum chloride. The most consistently affected performance tests were forelimb 
6 

and/or hindlimb grip strength, spontaneous motor activity, thermal sensitivity, and startle 

responsiveness. Significant impairments in cognitive function have been observed in some studies, 

although this has not been found in other studies even at higher doses. Adverse neurological effects 

have been observed in rats and mice at doses of 100–200 mg Al/kg/day and neurodevelopmental 

effects have been observed in rats and mice at doses of 103–330 mg Al/kg/day” 

The lowest-observed-adverse-effect level (LOAEL) for these effects range from 13–330 mg 

Al/kg/day with no-observed-adverse-effect levels ranging from 5-100 mg Al/kg/day. The ASTDR 

aluminum toxicity profile notes that “[a]nimal bioassays have found no conclusive evidence for 

carcinogenicity of aluminum.” 

 The most sensitive effect identified in the toxicology database for aluminum sulfate is based on a 

multi-generational rat reproduction study with a LOAEL of 188 mg/kg/day for aluminum sulfate 

based on decreased body weights of pups and parents and a delay in vaginal opening. The NOAEL 

for this study is 41 mg/kg/day for aluminum sulfate (equivalent to 8.06 mg/kg/day of aluminum). A 

10 uncertainty factor for inter- and intra-species variation and a 1X FQPA Safety Factor results in a 

chronic population adjusted dose (cPAD) of 0.41 mg/kg/day. The use of this endpoint for risk 

assessment purposes is health-protective of the effects of aluminum (such as neurotoxicological 

effects) observed in studies of other aluminum compounds. 

B. Absorption, Distribution, Metabolism and Elimination (ADME) 

Aluminum present in food and drinking water is poorly absorbed through the gastrointestinal 

tract. Bioavailability in rabbits following a single maximum safe dose was estimated by comparing 

areas under the plasma concentration-time curves after oral and intravenous dosing (Yokel and 

McNamara (1988)). The estimated bioavailability of the water-soluble compounds aluminum chloride 

(333 mg Al/kg), aluminum nitrate (934 mg Al/kg), aluminum citrate (1,081 mg Al/kg), and aluminum 

lactate (2,942 mg Al/kg) in rabbits was 0.57, 1.16, 2.18, and 0.63%, respectively. Aluminum occurs 

normally in all body tissues of humans (Ganrot 1986). Metabolism of aluminum does not occur 

(Ganrot 1986). As an element, aluminum is always found attached to other chemicals, and these 

affinities can change within the body. In living organisms, aluminum is believed to exist in four 

different forms: as free ions, as low-molecular-weight complexes, as physically bound 

macromolecular complexes, and as covalently bound macromolecular complexes (Ganrot 1986). The 

free ion, Al+3, is easily bound to many substances and structures; therefore, its fate is determined by 

its affinity to each of the ligands and their relative amounts and metabolism. 

The complexes are metabolically active, particularly the nonpolar ones. Because aluminum 

has a very high affinity for proteins, polynucleotides, and glycosaminoglycans, much of the 

aluminum in the body may exist as physically bound macromolecular complexes with these 

substances. Metabolically, these macromolecular complexes would be expected to be much less 

active than the smaller, low-molecular-weight complexes. Aluminum may also form complexes with 

macromolecules that are so stable that they are essentially irreversible. For example, evidence 

suggests that the nucleus and chromatin are often sites of aluminum binding in cells (Crapper 

McLachlan 1989; Dyrssen et al. 1987; Ganrot 1986; Karlik et al. 1980). Following ingestion in 

humans, absorbed aluminum from the blood is eliminated in the kidney and excreted in the urine 
7 

(Gorsky et al. 1979; Greger and Baier 1983; Kaehny et al. 1977; Recker et al. 1977; Sutherland and 

Greger 1998). The unabsorbed aluminum is excreted primarily in the feces. 

C. Dermal Absorption 

There were no appropriate dermal absorption or toxicity studies available to allow an 

estimation of the dermal absorption by a route-to-route comparison of toxicity. For the purposes 

of this risk assessment 100% dermal absorption is assumed. 

D. Safety Factor for Infants and Children (FQPA Safety Factor) 

The toxicity database is complete, there is no evidence of increased qualitative or quantitative 

susceptibility in the young, and the endpoint selected for risk assessment purposes is protective 

of any potential neurotoxicological effects. No immunotoxicological effects were observed in 

the available aluminum database.and exposure estimates are unlikely to underestimate risk; 

therefore the 10-fold FQPA Safety Factor can be reduced to 1x. 

E. Completeness of the Toxicology Database 

The toxicology database for aluminum sulfate is complete and adequate to support risk 

assessments. 

F. Evidence of Neurotoxicity 

While there are no available neurotoxicity studies on aluminum sulfate, available studies 

with aluminum compounds with neurotoxicity endpoints demonstrate adverse effects at dose 

levels ranging from 30-130 mg Al/kg/day and NOAELs for these effects ranging from 25.7 to 75 

mg Al/kg/day. The adult neurotoxicity study with the NOAEL of 25.7 mg Al/kg/day has a 

LOAEL of 54.5 mg Al/kg/day based on reduction in vestibular-ocular reflex (Marneli et al. 

2006). The lowest LOAEL for an adult neurotoxicity study with an aluminum compound is 30 

mg Al/kg/day (Bilkei-Gorzo et al. 1993) based on neurobehavioral effects in maze performance, 

A NOAEL for this study was not reported as dose levels below 30 mg Al/kg/day were not 

tested. Standard neuropathology and functional observations battery (FOB) evaluations were 

included in a study on aluminum chloride by Beekhuijen, 2007 that was conducted in accordance 

with OECD 422 guidelines and no adverse effects were reported on those parameters at does 

levels up to 90 mg Al/kg/day. In a study of developmental neurological effects (Poirier et al. 

2011) in which rats were chronically exposed throughout all life stages to aluminum citrate via 

drinking water, a NOAEL of 30 mg Al/kg/day was identified with a LOAEL of 100 mg 

Al/kg/day based on impaired grip strength and foot splay. 

 G. Evidence of Sensitivity/Susceptibility in the Developing or Young Animal 

There is no evidence of increased quantitative or qualitative susceptibility of rat fetuses to in 

utero exposure to aluminum chloride (Beekhuijen, 2007). In a 12-month neurodevelopmental 

toxicity study conducted at dose levels of 0, 30, 100 and 300 mg Al/kg bw/day, rats were 

administered aluminum salts via drinking water throughout all life-stages. In this robust 
8 

study (Poirer et al. 2011), a NOAEL of 30 mg Al/kg bw/day was identified with a 

LOAEL of 100 mg Al/kg bw/day. Rats were exposed chronically via drinking water to 

aluminum citrate in utero, during lactation through dams, as juveniles and as older adult 

animals. Motor, sensory, and learning and memory tests were conducted according to 

OECD 426 guidelines for developmental neurotoxicity testing in pups and adults. 

Neuropathology evaluations on perfusion fixed brains were evaluated at postnatal days 

23, 64, 120 and 364 and no treatment -related effects were reported. Effects on 

neurobehavioral endpoints (e.g. auditory startle, motor activity, functional observational 

battery) were noted primarily at the highest dose level which caused severe systemic 

toxicity including mortality, although there was evidence of increased excitability, and 

impaired grip strength and foot splay at the mid dose as well also in the presence of 

· systemic toxicity. There were no effects on learning and memory at any dose level 

tested based on a Morris water maze test. 

H. Residual Uncertainty in the Exposure Database 

In conducting the chronic dietary exposure assessment for existing food uses of aluminum 

sulfate. Application of the Dietary Exposure Evaluation Model DEEM–FCIDTM, Version 3.18, 

EPA used food consumption information from the U.S. Department of Agriculture’s (USDA’s) 

2003-2008 National Health and Nutrition Examination Survey, What We Eat in America 

(NHANES/WWEIA). As to residue levels in food, no residue data were submitted for aluminum 

sulfate. In the absence of specific residue data, EPA has developed an approach which uses 

surrogate information to derive upper bound exposure estimates for the subject inert ingredient. 

Upper bound exposure estimates are based on the highest tolerance for a given commodity from 

a list of high-use insecticides, herbicides, and fungicides. A complete description of the general 

approach taken to assess inert ingredient risks in the absence of residue data is contained in the 

memorandum entitled “Alkyl Amines Polyalkoxylates (Cluster 4): Acute and Chronic Aggregate 

(Food and Drinking Water) Dietary Exposure and Risk Assessments for the Inerts.” (D361707, 

S. Piper, 2/25/09) and can be found at http://www.regulations.gov in docket ID number EPAHQ-OPP-2008-0738. 

In the dietary exposure assessment, the Agency assumed that the residue level of the inert 

ingredient would be no higher than the highest tolerance for a given commodity. Implicit in this 

assumption is that there would be similar rates of degradation (if any) between the active and 

inert ingredient and that the concentration of inert ingredient in the scenarios leading to these 

highest of tolerances would be no higher than the concentration of the active ingredient. 

The Agency believes the assumptions used to estimate dietary exposures lead to an extremely 

conservative assessment of dietary risk due to a series of compounded conservatisms. First, 

assuming that the level of residue for an inert ingredient is equal to the level of residue for the 

active ingredient will overstate exposure. The concentration of active ingredient in agricultural 

products is generally at least 50 percent of the product and often can be much higher. Further, 

pesticide products rarely have a single inert ingredient; rather there is generally a combination of 

different inert ingredients used which additionally reduces the concentration of any single inert 

ingredient in the pesticide product in relation to that of the active ingredient. 
9 

Second, the conservatism of this methodology is compounded by EPA’s decision to assume 

that, for each commodity, the active ingredient which will serve as a guide to the potential level 

of inert ingredient residues is the active ingredient with the highest tolerance level. This 

assumption overstates residue values because it would be highly unlikely, given the high number 

of inert ingredients, that a single inert ingredient or class of ingredients would be present at the 

level of the active ingredient in the highest tolerance for every commodity. Finally, a third 

compounding conservatism is EPA’s assumption that all foods contain the inert ingredient at the 

highest tolerance level. In other words, EPA assumed 100 percent of all foods are treated with 

the inert ingredient at the rate and manner necessary to produce the highest residue legally 

possible for an active ingredient. In summary, EPA chose a very conservative method for 

estimating what level of inert residue could be on food, then used this methodology to choose the 

highest possible residue that could be found on food and assumed that all food contained this 

residue. No consideration was given to potential degradation between harvest and consumption 

even though monitoring data shows that tolerance level residues are typically one to two orders 

of magnitude higher than actual residues in food when distributed in commerce. 

Based on an evaluation of all registered pesticide products containing aluminum sulfate and 

registered for use on food, it was determined that the concentration of aluminum sulfate did not 

exceed 1% by weight. This effective functional use limitation was included in the dietary 

exposure assessment of aluminum sulfate. 

A dietary exposure assessment of proposed use in antimicrobial food contact surface 

sanitizing solutions was also performed in which it is conservatively assumed that 100% of the 

diet results from food treated with food contact surface sanitizers and that 100% of the sanitizing 

solution is transferred into food. A highly conservative model based on FDA assumptions 

regarding transfer of food contact sanitizing solution residues to food is utilized. The dietary 

exposure values derived from both the conservative model used to estimate residues from 

application to growing crops and raw agricultural commodities after harvest are then summed 

with the exposures estimated from the antimicrobial food contact sanitizer uses. 

Accordingly, although sufficient information to quantify actual residue levels in food and 

drinking water is not available, the compounding of these conservative assumptions will lead to a 

significant exaggeration of actual exposures. EPA does not believe that this approach 

underestimates exposure in the absence of residue data 

V. Toxicity Endpoint and Point of Departure Selections 

A. Dose-Response Assessment 

Acute Dietary Endpoint No appropriate endpoint was identified from any of the studies in 

the database, including developmental toxicity studies in the rat, consequently it was determined 

that there was no basis for selecting a dose and endpoint for an acute point of departure (POD) 

for the general population or females 13-49 . 
10 

. 

Chronic Dietary Endpoint for the General Population A two generation reproduction study of 

aluminum sulfate in rats was considered critical in establishing the PoD for chronic dietary risk 

assessment. The study supports a NOAEL of 41 mg/kg/day and a LOAEL of 188 mg/kd/day for 

decreased body weight in parents and pups and a delay in vaginal opening and should be used as the 

POD for all durations and exposure scenarios. A UF of 100x (10x for interspecies extrapolation and 

10x for intraspecies variation is applied to obtain a chronic reference dose (cRfD) of 0.41 mg/kg/day. 

The FQPA factor is reduced to 1x. The chronic population adjusted dose (cPAD) is 0.41 mg/kg/day. 

Incidental Oral Exposure (Short- and Intermediate-Term. A two generation reproduction study in rats 

was considered critical in establishing the PoD for incidential oral exposure (all durations). The 

study supports a NOAEL of 41 mg/kg/day and a LOAEL of 188 mg/kg/day for decreased body 

weight in parents and pups and a delay in vaginal opening and should be used as the POD for all 

durations and exposure scenarios. 

Dermal Exposure (Short-, Intermediate-, and Long-Term. Due to uncertainties in the dermal toxicity 

database, an oral toxicity study was selected for this exposure scenario. The same rationale as stated 

in the incidental oral exposure section is applied to this exposure scenario. The study supports a 

NOAEL of 41 mg/kg/day and a LOAEL of 188 mg/kg/day for decreased body weight in parents and 

pups and a delay in vaginal opening and should be used as the POD for all durations and exposure 

scenarios. Additionally for risk assessment purposes a default dermal absorption factor of 100% is 

used since these assessments for the routes of exposure are derived from POD selected from oral 

studies 

Inhalation Exposure, Short-, Intermediate- and Long-Term. There were no reliable inhalation studies 

available in the existing toxicity database, therefore an oral toxicity study was used for this exposure 

scenario . The same rationale as stated in the incidental oral exposure section is applied to this 

exposure scenario. The study supports a NOAEL of 41 mg/kg/day and a LOAEL of 188 mg/kg/day 

for decreased body weight in parents and pups and a delay in vaginal opening and should be used as 

the POD for all durations and exposure scenarios. Additionally for risk assessment purposes a default 

inhalation absorption factor of 100% is used since these assessments for the routes of exposure are 

derived from POD selected from oral studies. 

Recommendation for Combining Routes of Exposures for Risk Assessment 

Since the same studies were used to select endpoints and doses for risk assessment for dietary, dermal 

and inhalation routes of exposure (all durations), the risks from these exposure routes should be 

aggregated. 

Cancer Classification and Risk Assessment Recommendation 

 There are no available carcinogenicity studies with aluminum sulfate, however, in a cancer 

study with aluminum potassium sulfate there were no exposure-related increased incidences of 
11 

tumors, other proliferative lesions ornonneoplastic lesions in 60 male or 60 female B6C3F1 mice that 

ingested ≤979 mg Al/kg/day as aluminum potassium sulfate in the diet for 20 months (Oneda et al. 

1994). The level of aluminum in the base diet was not reported. Based on this information, 

aluminum sulfate is not expected to be a carcinogen and a cancer aggregate risk assessment is not 

required 

As required by FIFRA and FFDCA, EPA reviews numerous studies to assess potential 

adverse outcomes from exposure to chemicals. Collectively, these studies include acute, subchronic 

and chronic toxicity, including assessments of carcinogenicity, neurotoxicity, developmental, 

reproductive, and general or systemic toxicity. These studies include endpoints which may be 

susceptible to endocrine influence, including effects on endocrine target organ histopathology, organ 

weights, estrus cyclicity, sexual maturation, fertility, pregnancy rates, reproductive loss, and sex 

ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests and chronic studies 

that assess growth, developmental and reproductive effects in different taxonomic groups. As part of 

its most recent re-registration decision for pendimethalin, EPA reviewed these data and selected the 

most sensitive endpoints for relevant risk assessment scenarios from the existing hazard 

database. However, as required by FFDCA section 408(p), pendimethalin is subject to the endocrine 

screening part of the Endocrine Disruptor Screening Program (EDSP). 

EPA has developed the EDSP to determine whether certain substances (including pesticide 

active and other ingredients) may have an effect in humans or wildlife similar to an effect produced 

by a “naturally occurring estrogen, or other such endocrine effects as the Administrator may 

designate.” The EDSP employs a two-tiered approach to making the statutorily required 

determinations. Tier 1 consists of a battery of 11 screening assays to identify the potential of a 

chemical substance to interact with the estrogen, androgen, or thyroid (E, A, or T) hormonal 

systems. Chemicals that go through Tier 1 screening and are found to have the potential to interact 

with E, A, or T hormonal systems will proceed to the next stage of the EDSP where EPA will 

determine which, if any, of the Tier 2 tests are necessary based on the available data. Tier 2 testing is 

designed to identify any adverse endocrine-related effects caused by the substance and establish a 

dose-response relationship between the dose and the E, A, or T effect. 

Under FFDCA section 408(p), the Agency must screen all pesticide chemicals. Between 

October 2009 and February 2010, EPA issued test orders/data call-ins for the first group of 67 

chemicals, which contains 58 pesticide active ingredients and 9 inert ingredients. A second list of 

chemicals identified for EDSP screening was published on June 14, 2013, and includes some 

pesticides scheduled for registration review and chemicals found in water. Neither of these lists 

should be construed as a list of known or likely endocrine disruptors. 

For further information on the status of the EDSP, the policies and procedures, the lists of 

chemicals, future lists, the test guidelines and the Tier 1 screening battery, please visit our website, 

www.epa.gov/endo/ 
12 

Dietary Exposure and Risk Assessment 

Dietary Risk Assessment 

 Since there were no endpoints of concern identified for acute dietary risk assessments, a 

acute dietary risk assessment was not performed. A chronic dietary risk assessment was conducted 

for the existing uses of aluminum sulfate as an inert ingredient in pesticide formulations applied to 

growing crops or to raw agricultural commodities after harvest. The risk assessment considers food 

consumption from growing crops and raw agricultural commodities treated with pesticides that 

contain aluminum sulfate as an inert ingredient. As to residue levels in food, no residue data were 

submitted for aluminum sulfate. In the absence of specific residue data, EPA has developed an 

approach which uses surrogate information to derive upper bound exposure estimates for the subject 

inert ingredient. Upper bound exposure estimates are based on the highest tolerance for a given 

commodity from a list of high-use insecticides, herbicides, and fungicides. A complete description of 

the general approach taken to assess inert ingredient risks in the absence of residue data is contained 

in the memorandum entitled “Alkyl Amines Polyalkoxylates (Cluster 4): Acute and Chronic 

Aggregate (Food and Drinking Water) Dietary Exposure and Risk Assessments for the Inerts.” 

(D361707, S. Piper, 2/25/09) and can be found at http://www.regulations.gov in docket ID number 

EPA-HQ-OPP-2008-0738. 

In the dietary exposure assessment, the Agency assumed that the residue level of the inert 

ingredient would be no higher than the highest tolerance for a given commodity. Implicit in this 

assumption is that there would be similar rates of degradation (if any) between the active and 

inert ingredient and that the concentration of inert ingredient in the scenarios leading to these 

highest of tolerances would be no higher than the concentration of the active ingredient. 

Drinking water exposures are based on worst-case modeled estimates and are incorporated 

directly into the DEEMTM model. 

Additionally, a dietary exposure assessment of proposed use in antimicrobial food contact 

surface sanitizing solutions was also performed in which it is conservatively assumed that 100% 

of the diet results from food treated with food contact surface sanitizers and that 100% of the 

sanitizing solution is transferred into food. A highly conservative model based on FDA 

assumptions regarding transfer of food contact sanitizing solution residues to food is utilized. 

The dietary exposure values derived from both the conservative model used to estimate residues 

from application to growing crops and raw agricultural commodities after harvest are then 

summed with the exposures estimated from the antimicrobial food contact sanitizer uses. 

The chronic dietary risk estimate for the highest exposed population subgroup, children 1-2 years 

old is 6.7% of the chronic population adjusted dose (cPAD) and for the general U. S. population is 

1.6% of the cPAD. EPA is concerned when estimated dietary risk exceeds 100%. There are no 

chronic dietary risks of concern (Appendix 1). 

Residential (Non-Occupational) Exposure/Risk Characterization 
13 

There are no proposed new residential uses for aluminum sulfate; based on an evaluation of the 

currently registered products containing aluminum sulfate, there are no products with residential uses, 

therefore a residential exposure assessment and risk assessment was not performed. 

Aggregate Exposure/Risk Characterization 

In accordance with the FQPA, EPA must consider and aggregate (add) pesticide exposures 

and risks from three major sources: food, drinking water, and residential exposures. In an aggregate 

assessment, exposures from relevant sources are added together and compared to quantitative 

estimates of hazard (e.g., a NOAEL or PAD), or the risks themselves can be aggregated. When 

aggregating exposures and risks from various sources, EPA considers both the route and duration of 

exposure. For aluminum sulfate pendimethalin, potential exposures from food and drinking water 

from both the existing uses of aluminum sulfate on growing crops and raw agricultural commodities 

after harvest, and the proposed use as an inert ingredient in antimicrobial food contact sanitizing 

solutions were aggregated. 

Acute Aggregate Risk 

The aggregate acute risk estimates include exposure to residues of pendimethalin in food and 

water, and does not include dermal, inhalation or incidental oral exposure. Since there were no 

endpoints of concern identified for acute dietary risk assessments, an acute dietary risk assessment 

was not performed and there no acute aggregate risks of concern. 

Short-Term Aggregate Risk 

There is potential short-term exposure to pendimethalin via dietary (which is considered 

background exposure). However sine there are no residential exposure pathways, the short-term 

aggregate risk would be equivalent to the chronic dietary exposure estimate. Refer to Section xxor 

the chronic dietary (food and drinking water) exposure assessment. There are no short-term aggregate 

risks of concern. 

Table Short-Term Aggregate Risk Calculations for Aluminum Sulfate 

Life stage 

Short-Term Scenario 

NOAEL 

mg/kg/day LOC1 

Max Allowa

Exposure2

mg/kg/day 

Average Food

and Water 

Exposure 

Crop uses 

(mg/kg/day) 

Average Food

and Water 

Exposure 

Food contact u

use 

(mg/kg/day)

Total 

Exposure 

mg/kg/day4 

Aggregate 

MOE (food, 

 water, and 

residential)5 

Adult 41 100 0.41 0.003787 0.00286 0.00665 6170 

Child 41 100 0.41 0.014125 0.0133 0.0275 1490 1 Intraspecies factor= 10x; Interspecies factor = 3x 2 Maximum Allowable Exposure (mg/kg/day) = NOAEL (10 mg/kg/day)/LOC (100). 3 Child Residential Exposure = [Oral exposure (0.042 

mg/kg/day) + Dermal exposure (0.060 mg/kg/day) = 0.102 mg/kg/day (Table 6.1). 4 Total Exposure = (Avg (Food & Water) Exposure + Residential Exposure). 5 Adult Aggregate MOE = [NOAEL (10 

mg/kg/day)/ (Total Exposure (0.08 mg/kg/day)]; Child Aggregate MOE= [NOAEL (10 mg/kg/day)/ (Total Exposure (0.107 mg/kg/day)] 
14 

Intermediate-Term Aggregate Risk 

Intermediate-term exposures to aluminum sulfate are not likely because of the intermittent nature of 

applications by homeowners. Therefore the intermediate-term ggregate risk would be equivalent to 

the chronic dietary exposure estimate. Refer to Section xx for the chronic dietary (food and drinking 

water) exposure assessment. There are no intermediate-term aggregate risks of concern. 

Chronic Aggregate Risk 

Chronic exposure is not expected for the residential (dermal and inhalation) exposure pathways. 

Therefore, the chronic aggregate risk would be equivalent to the chronic dietary exposure estimate. 

Refer to Section xx for the chronic dietary (food and drinking water) exposure assessment. There are 

no chronic aggregate risks of concern. 

Cancer Aggregate Risk 

Based on the lack of concern for carcinogenicity a cancer aggregate risk assessment was not 

performed. 

Cumulative Exposure/Risk Characterization 

Unlike other pesticides for which EPA has followed a cumulative risk approach based on a common 

mechanism of toxicity, EPA has not made a common mechanism of toxicity finding as to aluminum 

sulfate and any other substances and pendimethalin does not appear to produce a toxic metabolite 

produced by other substances. For the purposes of this tolerance action, therefore, EPA has not 

assumed that aluminum sulfate has a common mechanism of toxicity with other substances. For 

information regarding EPA’s efforts to determine which chemicals have a common mechanism of 

toxicity and to evaluate the cumulative effects of such chemicals, see the policy statements released 

by EPA’s Office of Pesticide Programs concerning common mechanism determinations and 

procedures for cumulating effects from substances found to have a common mechanism on EPA’s 

website at http://www.epa.gov/pesticides/cumulative/. 

IX. ENVIRONMENTAL JUSTICE STATEMENT 

Potential areas of environmental justice concerns, to the extent possible, were considered in 

this human health risk assessment, in accordance with U.S. Executive Order 12898, "Federal Actions 

to Address Environmental Justice in Minority Populations and Low-Income Populations," 

http://www.eh.doe.gov/oepa/guidance/justice/eo12898.pdf. 
15 

As a part of every pesticide risk assessment, OPP considers a large variety of consumer 

subgroups according to well-established procedures. In line with OPP policy, RD estimates risks to 

population subgroups from pesticide exposures that are based on patterns of that subgroup’s food and 

water consumption, and activities in and around the home that involve pesticide use in a residential 

setting. Extensive data on food consumption patterns are compiled by the USDA under CSFII and 

are used in pesticide risk assessments for all registered food uses of a pesticide. These data are 

analyzed and categorized by subgroups based on age, season of the year, ethnic group, and region of 

the country. Additionally, OPP is able to assess dietary exposure to smaller, specialized subgroups 

and exposure assessments are performed when conditions or circumstances warrant. Whenever 

appropriate, non-dietary exposures based on home use of pesticide products and associated risks for 

adult applicators and for toddlers, youths, and adults entering or playing on treated areas 

postapplication are evaluated. Further considerations are currently in development as OPP has 

committed resources and expertise to the development of specialized software and models that 

consider exposure to bystanders and farm workers as well as lifestyle and traditional dietary patterns 

among specific subgroups 

X. ENVIRONMENTAL FATE 

 Aluminium occurs ubiquitously in the environment in the form of silicates, oxides and 

hydroxides, combined with other elements such as sodium and fluorine and as complexes with 

organic matter. It is not found as a free metal because of its reactivity. It has only one oxidation 

state (+3) in nature; therefore, its transport and distribution in the environment depend only upon its 

coordination chemistry and the chemical-physical characteristics of the local environmental system. 

At pH values greater than 5.5, naturally occurring aluminium compounds exist predominantly in an 

undissolved form such as gibbsite (Al(OH)3) or as aluminosilicates, except in the presence of high 

amounts of dissolved organic material, which binds with aluminium and can lead to increased 

concentrations of dissolved aluminium in streams and lakes. Several factors influence aluminium 

mobility and subsequent transport within the environment. These include chemical speciation, 

hydrological flow paths, soil-water interactions, and the composition of the underlying geological 

materials. The solubility of aluminium in equilibrium with solid phase Al(OH)3 is highly dependent 

on pH and on complexing agents such as fluoride, silicate, phosphate and organic matter. The 

chemistry of inorganic aluminium in acid soil and stream water can be considered in 

terms of mineral solubility, ion exchange and water mixing processes. 

 Upon acidification of soils, aluminium can be released into solution for transport to streams. 

Mobilization of aluminium by acid precipitation results in more aluminium being available for plant 

uptake. 

Transport and Distribution Across Media 

 Aluminium occurs ubiquitously in silicates such as feldspars and micas, complexed with 

sodium and fluoride as cryolite, and in bauxite rock composed of hydrous aluminium oxides, 

aluminium hydroxides, and impurities such as free silica (ATSDR, 1992). Aluminium is not found as 

a free metal because of its reactivity. It has only one oxidation state (+3); therefore, its transport and 
16 

distribution in the environment depend upon its coordination chemistry and the characteristics of the 

local environmental system. Aluminium partitions between solid and liquid phases by reacting and 

complexing with water molecules and electron-rich anions, such as chloride, fluoride, sulfate, nitrate, 

phosphate and negatively charged functional groups on humic materials and clay. 

 At a pH greater than 5.5, naturally occurring aluminium compounds exist predominantly in 

an undissolved form such as gibbsite (Al(OH)3) or as aluminosilicates, except in the presence of high 

amounts of dissolved organic material such as fulvic acid, which binds with aluminium and can cause 

an increase in dissolved aluminium concentrations in streams and lakes (ATSDR, 1992). Several 

processes influence aluminium mobility and its subsequent transport within the environment; these 

include chemical speciation, hydrological flow paths, other spatial and temporal factors related to 

soil-water interactions, and the composition of the underlying geological materials (Grant et al., 

1990). Watersheds with shallow, acidic soils and poorly buffered surface waters mobilize aluminium 

when exposed to acidic deposition (Driscoll et al., 1988). 

Air 

 Aluminium enters the atmosphere as a major constituent of a number of atmospheric 

particulates, such as soil-derived dusts from erosion and particulates from coal combustion (Grant et 

al., 1990). Eisenreich (1980) studied the atmospheric loading of aluminium to Lake Michigan, USA. 

It was found that aluminium was generally associated with large particles (> 2 μm diameter) and that 

these were deposited near the source. 

Freshwater 

Dissolved aluminium 

In groundwater or surface water systems an equilibrium is formed that controls the extent 

to which aluminium dissolution can occur. The solubility of aluminium in equilibrium with solid 

phase Al(OH)3 is highly pH-dependent. Aquo complex Al(H2O)6

3+ predominates at low pH 

values (e.g., pH < 4), but as the pH of the solution increases (e.g., pH 4-6) and/or the temperature 

rises, the positive charge of aluminium forces hydrolysis of a water ligand producing the 

Al(OH)(H2O)5

2+ ion. The degree of hydrolysis increases as the solution pH increases, resulting 

in a series of Al-OH complexes such as Al(OH)2+, Al(OH)2

+

, Al(OH) 4 - (Schecher & Driscoll, 

1987). 

 

Aluminium Adsorbed on Particles 

 The adsorption of aluminium by particles was found to increase with total aluminium, pH 

and particle concentration. Calculations using an adsorption equation, and taking competition by 

dissolved humic substances into account, suggest that adsorbed aluminium may commonly account 

for a significant proportion (> 10%) of total monomeric aluminium in such water. 

 

 Seawater 
17 

 In contrast to fresh water, seawater (salinity > 32%) has a constant pH of approximately 8.2. 

Hydes (1977) found that bottom and suspended clay sediments probably act as a source of dissolved 

aluminium to seawater. However, removal below predictions of clay solubility is probably the result 

of biological activity. 

 Soil 

 In soil, aluminium is released into solution for transport to streams upon acidification. The 

chemistry of inorganic aluminium in acid soil and, in particular, the solubility controls are very 

similar to those given in section 4.1.2 for fresh water (Furrer, 1993). However, the extrapolation of 

stream water chemistry to soil is difficult because of the complexity of hydrological pathways and 

chemical reactivity during water mixing (Neal, 1988). 

Bioaccumulation 

Plants 

 Plants differ in their ability to take up aluminium; some accumulate aluminium whereas others 

are able to immobilize it at the root surface (Roy et al., 1988). Exposure to aluminium in nutrient 

solution leads to accumulation, especially in the roots (Lee, 1972; Boxman et al., 1991). 

 Invertebrates 

 Invertebrates have the ability to up take aluminum to varying degrees. Frick & Herrmann 

(1990) studied the accumulation of aluminium by nymphs of the mayfly (Heptagenia sulphurea) 

exposed to concentrations of 0.2 and 2 mg inorganic monomeric aluminium/ litre at pH 4.5 for up to 

4 weeks. The highest mean concentrations found in mayflies were 1.24 and 2.34 mg/g aluminium 

(dry weight) for the higher treatment groups, which did not undergo moulting. The major part of the 

aluminium was deposited on/in the exuviae of the nymphs, as aluminium determinations revealed a 

70% decrease in content after moulting. 

 Fish 

 Fish have the ability to up take aluminum to varying degrees depending mostly on the water pH. 

Other factors such as water temperature and minerals present may play a derminant role as well. 

Cleveland et al. (1986) exposed brook trout ( Salvelinus fontinalis) eggs, larvae and juveniles to 300 

μg/litre total aluminium at three pH levels. At 30 days post-hatch for larvae and for an exposure 

period of 30 days for juveniles (37 to 67 days), significantly more aluminium was accumulated at pH 

5.28 than at either pH 7.24 or 4.44. Aluminium levels at pH 5.28 were 398 and 112 mg/kg for the 

larvae and juveniles, respectively. At pH 7.24 residues were 12 and 33 mg/kg, and at pH 4.44, 71 and 

17 mg/kg, respectively. 

 Cleveland et al. (1991) maintained brook trout in water containing 200 μg/litre total 

aluminium at pH values of 5.0, 6.0 and 7.2 for 56 days. Estimated steady state ioconcentration 

factors for aluminium, which were inversely related to pH, were 215 at pH 5.3, 123 at pH 6.1 and 36 
18 

at pH 7.2. The estimated time to 90% steady state was 1.5 days at pH 5.3, 4.2 days at pH 6.1 and 1.7 

days at pH 7.2. Elimination during the 28-day depuration phase was more rapid at pH 5.3 than at pH 

6.1 or 7.2. 

 Karlsson-Norrgren et al. (1986b) found that brown trout ( Salmo trutta) accumulated 

significantly more aluminium in gill tissue at pH 5.5 than at pH 7.0 (60-160 μg/kg and 10-40 μg/kg 

dry weight, respectively) when exposed to 200-500 μg total aluminium/litre. 

 Segner et al. (1988) exposed young brown trout ( Salmo trutta) to total aluminium (230 

μg/litre) at pH 5.0 in high calcium water at a temperature of 12°C for 5 days. Whole body aluminium 

concentrations were 230 mg/kg dry weight in aluminium-exposed fish, as compared to 

75 mg/kg (pH 5.0) and 44 mg/kg (pH 7.2) for fish in aluminium-free water. 

 Wicklund Glynn et al. (1992) exposed minnows ( Phoxinus phoxinus) to acidic water (pH 

5.0) with and without total aluminium (150 μg/litre) at varying calcium (0, 0.07 and 2 mmol/litre) and 

humus (5 and 25 Pt) concentrations for 15 days. Aluminium concentrations in the gills were highest 

in the lower calcium level groups with or without humus. In the absence of calcium the median 

aluminium level in the gills was 109 mg/kg wet weight, and at 2 mmol/litre calcium the aluminium 

level was 50 mg/kg. 

Birds 

 There are bird studies that show a dose-related and significant increase in aluminum content 

of the femur and sternum. Carrière et al. (1986) fed ring doves ( Streptopelia risoria) on a diet 

containing 0.1% aluminium sulfate with reduced calcium and phosphorus (0.9% Ca; 0.5% P) for a 

period of 4 months. Analysis of the tissues of breeding adult doves revealed that there was no 

accumulation of aluminium in kidney, brain or male femurae; however, the femurae of female doves 

showed a significant increase from a mean of 7.42 mg/kg dry weight in controls to 15.87 mg/kg in 

treated birds. Juvenile doves fed on diets containing 500, 1000 and 1500 mg/kg aluminium sulfate 

did not accumulate aluminium in leg and wing bones but did show a significant tendency to 

accumulate in the sternum. 

 Sparling (1991) fed black ducks ( Anas rubripes) and mallard ( Anas platyrhynchos) on a diet 

containing 200, 1000 or 5000 mg aluminium/kg with varying amounts of calcium (3600 and 15 100 

mg/kg) and phosphorus (6200, 13 500 and 21 500 mg/kg) for a period of 10 weeks. All of the diets 

produced a dose-related and significant increase in the aluminium content of the femur. Black ducks 

maintained on normal calcium and phosphorus levels showed femur aluminium concentrations of 

5.42, 13.6 and 19.5 mg/kg after 10 weeks at the three dose levels, respectively. Mallard femurs 

contained aluminium levels of 9.49, 12.1 and 18 mg/kg, respectively. 

Photodegredation, Analytical Method Validation, Hydrolysis stability in water or Transport/distribution 

(fugacity model):
19 

 No studies have been found to address Photodegredation, Analytical Method Validation, 

Hydrolysis stability in water or Transport/distribution (fugacity model). Aluminum is the most 

abundant metal on Earth and constitutes 8.13% of the Earth’s crust (IPCS, 1997). Aluminum is found 

in many consumer products including antacids, astringents, buffered aspirin, food additives, 

antiperspirants and cosmetics (ATSDR Aluminum, 2008). 

Conclusion 

 Aluminum background must be accounted for based on its abundance in the earth’s crust. 

Although aluminum is shown to persist in the environment and bioaccumulate in wildlife the actual 

exposure to the environment as the result of the propose use pattern is expected to be minimal and 

therefore the proposed aluminum sulfate use as an inert ingredient is of low concern and risk to the 

environment and wildlife. 

Table 6. Bioaccumalation 

 Species Dose Duration Result (μg/L) Reference 

Invertebrate Mymphs & 

 mayfly (Heptageni

sulphurea) 

0.2 & 2 mg 

aluminum/ 

litre at pH 4.5

4 weeks 1.24 - 2.34 mg/g 

aluminum 

Frick & Herrman

(1990) 

Fish BrookTrout 

(Salvelinum 

fontinalis) 

300ug/litre 

aluminum 

30 days 398 &112 mg/kg 

for larvae and 

juveniles, 

 respectively 

at ph levels 5.28 

Cleveland et all. 

(1986) 

Brook Trout 

(Salvelinum 

fontinalis)

200ug/litre 

aluminum 

1.5, 4.2, 

6.1, 1.7 

days at 

varying 

pH levels 

aluminum 

concentration 

was inversely 

 related to pH 

Cleveland et all. 

(19991) 

Brown Trout 

(Salmo trutta))

200-500 

aluminum/ 

litre 

n/a Aluminum - gill 

tissue – inversely 

 related to pH 

KarlssonNorrgren et al. 

(1986b) 

Brown Trout (Salm

trutta) 

230 ug/litre 5 days 230 mg/kg 

 aluminum 

Segner et al. 

(1988)) 

Minnows (Phoxinu

phoxinus) 

150 ug/litre 15 days 109 mg/kg 

aluminum in 

gills 

Wicklund 

Glynn et al. 

(1992) 

Bird Ring doves - 

adult(Streptopelia 

risoria) 

0.1% 

aluminum 

sulfate 

4 months 15.87 mg/kg in 

femurae of 

female doves 

Carriere et al. 

(1986) 

Ring doves – juven

(Streptopelia risoria

0.1% 

aluminum 

sulfate 

4 months Significant 

accumulation 

in the sternum 

Carriere et al. 

(1986) 
20 

Black ducks (Anas 

rubripes) 

200, 1000, 

5000 

aluminum / 

kg 

10 weeks 5.42, 13.6, 19.5 

mg/kg, 

respectivelyblack duck fem. 

Sparling (1991)

 Mallard ducks (Ana

platyrhyNchos)

200, 1000, 

5000 

aluminum / 

kg 

10 weeks 9.49, 12.1, 18 

mg/kg, 

respectivelyMallard femurs 

Sparling (1991)

XI. ECOLOGICAL EFFECTS 

Biotransformation 

Biodegradation and Abiotic Degradation 

 Elemental aluminium does not degrade in the environment. In the trivalent oxidation state, it can 

complex with electron-rich species (ATSDR, 1992). 

Inherent Biodegradation: 

No studies have been found to address inherent biodegradation. Biodegradation is typically 

identified for organic compounds and not inorganic salts such as aluminum sulfate. 

Aquatic Toxicity 

 The following table presents ecotoxicity data endpoints located in EPA’s ECOTOX database for 

aluminum sulfate. These data demonstrate that aluminum sulfate would be expected to have minimal 

aquatic toxicity, based on the typical dilution to 10 ppm or less, which is equivalent to 10,000 ug/L. 

Table 7. Aquatic Toxicity 

Species Study Result (μg/L) Tox. Category 

Invertebrates Daphnia magna 

(Water Flea)

24-hour LC50 7,000 - 16,000 Moderately Toxic 

Daphnia magna 

(Water Flea)

48-hour LC50 3,200 - 8,000 Moderately Toxic 

Ceriodaph niadubia

(Water Flea)

48-hour LC50 23,630 – 35,970 Slightly Toxic 

Fish Oncorhynchus mykiss 

(Rainbow Trout)

144-hour 

 (6 day) LC50

88 – 1,050 Very Highly Toxic 

Pimephales promelas 

(Fathead Minnow)

96-hour 

(4 day) LC50

4,400 – 36,100 Moderately Toxic 

Pimephales promelas

(Fathead Minnow)

192-hour 

(8 day) LC50

19,300 – 25,500 Slightly Toxic 
21 

Algae Aphanizomenon flos-aquae

(Blue-Green Algae)

1.5-hour EC50 >25,000 Practically Non-toxic

Acute and Chronic Toxicity to Invertebrates 

 A 336-Hour (14 day) Daphnia similis study (Sotero-Santos, et al., 2005) showed no acute 

toxicity after 48 hours and a mortality rate equivalent to the control after 14 days in untreated sludge 

from two water treatment plants located in neighboring cities in Brazil. 

US EPA Ver. 3.16, 03-08-d 

DEEM-FCID Chronic analysis for ALSULFATE NHANES 2003-2008 2-day 

Residue file name: J:\AlSulfate\INERTS_57ACTIVE_100PPBH2OREV1PCT.R08 

 Adjustment factor #2 used. 

Analysis Date 04-14-2015/11:26:38 Residue file dated: 04-14-2015/11:25:29 

Reference dose (RfD, Chronic) = .41 mg/kg bw/day 

COMMENT 1: Inert 57 active ingredients + drinking water (100ppb) @ 1% Formulation 

===================================================================

============ 

 Total exposure by population subgroup 

------------------------------------------------------------------------------- 

 Total Exposure 

 ----------------------------------- 

 Population mg/kg Percent of 

 Subgroup body wt/day Rfd 

-------------------------------------- ------------- ---------------- 

Total US Population 0.003787 0.9% 

Hispanic 0.004135 1.0% 

Non-Hisp-White 0.003716 0.9% 

Non-Hisp-Black 0.003519 0.9% 

Non-Hisp-Other 0.004467 1.1% 

Nursing Infants 0.004964 1.2% 

Non-Nursing Infants 0.009195 2.2% 

Female 13+ PREG 0.003305 0.8% 

Children 1-6 0.010933 2.7% 

Children 7-12 0.004548 1.1% 

Male 13-19 0.002675 0.7% 

Female 13-19/NP 0.002719 0.7% 

Male 20+ 0.002820 0.7% 

Female 20+/NP 0.003063 0.7% 

Seniors 55+ 0.003054 0.7% 

All Infants 0.007889 1.9% 

Female 13-50 0.002928 0.7% 
22 

Children 1-2 0.014125 3.4% 

Children 3-5 0.009713 2.4% 

Children 6-12 0.005011 1.2% 

Youth 13-19 0.002696 0.7% 

Adults 20-49 0.002895 0.7% 

Adults 50-99 0.003036 0.7% 

Female 13-49 0.002927 0.7% 

------------------------------------------------------------------------------- 

APPENDIX B 

 

Summary of Parameters used for Dietary Exposure Estimation for Food 

Contact Surface Sanitizing Uses for Aluminum Sulfate 

Parameter Definition Value/Units 

AR Application rate 50 ppm 

RS Residual solution 1 mg/cm2 

(worse case assumption) 

SA Treated surface area 

that comes into contact 

with food 

Assumed to be 2000 cm2 

for counter tops and 

cutting boards; 

assumed to be 4000 cm2 

for food utensils 

F % fraction of the inert 

(migration factor) 

No units; assume 100%, F=1 

CF1 Conversion Factor mg/day 10-6 (1/1,000,000) 

EDI Estimated Daily Intake 

DDD Daily Dietary Dose 

BW Body Weight (adult): 70 kg; 

(child): 15 kg 

Child = 3-1 yr. toddler 

DDD (adult) Daily Dietary Dose for adult EDI/BW (adult) 

DDD (child) Daily Dietary Dose for child EDI/BW (child) 

cPAD Chronic Dietary end point 1 mg/kg/day 

% cPAD Ratio of DDD and cPAD Exposure expessed as % of chronic 

population adjusted dose 

Food Contact Surface  Sanitizer Exposure:   

Formulas:

EDI=AR*RS*SA*F*CF1

DDD (adult)=EDI/BW (adult)

DDD (child)=EDI/BW (child)

Parameter Result Formula
23 

EDI 0.2 mg per day =50 mg*1 mg/cm 2

*4000 cm2 *

%*10-6

DDD(adult) 0.00286 mg/kg/day =0.2 mg/70 kg

DDD(child) 0.0133 mg/kg/ day =0.2 mg/15 kg
24