Water Quality Guidelines For Diisopropanolamine (Dipa)

KOMEX INTERNATIONAL LTD.
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E N V I R O N M E N T AN D W AT E R R E S O U R C E S
WATER QUALITY GUIDELINES FOR

DIISOPROPANOLAMINE (DIPA)
Prepared for:
British Columbia Ministry of Water, Land and Air Protection
Water Management Branch
3rd Floor, 2975 Jutland Road
Victoria, B.C. V8T 5J9
Prepared by:
Komex International Ltd.
Suite 100
4500 16th Avenue NW
Calgary, Alberta T3B 0M6
C52330100 6 August 2003

KOMEX
CANADA, USA, UK AND WORLDWIDE
National Library of Canada Cataloguing in Publication Data
Water quality guidelines for diisopropanolamine (DIPA)
[electronic resource]. -– [Rev.] –-
Available on the Internet.

Cover title.
Running title: DIPA water quality guidelines.
“6 August 2003”
“C52330100”
Previously issued Aug. 15, 2002.
Technical report; an overview is published separately
under title: Ambient water quality guidelines for
diisopropanolamine (DIPA).
Includes bibliographical references: p.
ISBN 0-7726-5102-7
1. Water quality – Standards - British Columbia.

2. Diisopropanolamine – Environmental aspects - British
Columbia. 3. Diisopropanolamine – Toxicology.
I. British Columbia. Water Management Branch. II. Komex
International Ltd. III. Title: DIPA water quality
guidelines. IV. Title: Water quality guidelines for DIPA.
V. Title: Ambient Water quality guidelines for
diisopropanolamine (DIPA)
TD226.B7W37 2003 363.739’462’09711 C2003-960264-8

TABLE OF CONTENTS
EXECUTIVE SUMMARY ............................................................................................................. i
1. INTRODUCTION.......................................................................................................................1
1.1 Scope of Work....................................................................................................................1
1.2 Background ........................................................................................................................1
1.3 Protocols.............................................................................................................................1
1.4 Toxicity Data......................................................................................................................2
2. BACKGROUND INFORMATION............................................................................................2
2.1 Physical and Chemical Properties ......................................................................................2
2.2 Analytical Methods ............................................................................................................3
2.3 Production and Uses...........................................................................................................4
2.3.1 Production ..............................................................................................................4
2.3.2 Uses ........................................................................................................................4
2.3.2.1 Gas Treating ............................................................................................5
2.3.2.2 Cosmetics and Personal Care Products ...................................................5
2.3.2.3 Detergents and Cleaners..........................................................................5
2.3.2.4 Metal Working Fluids .............................................................................6
2.3.2.5 Coatings...................................................................................................6
2.3.2.6 Corrosion Inhibitors ................................................................................6
2.3.2.7 Cement Applications ...............................................................................6
2.3.2.8 Miscellaneous Uses .................................................................................6
2.4 Levels in the Canadian Environment .................................................................................6
2.5 Existing Guidelines and Criteria in Various Media ...........................................................7
2.6 Environmental Fate and Behavior......................................................................................7
2.6.1 Adsorption and Mobility ........................................................................................8
2.6.2 Aqueous-Phase Solubility ......................................................................................8
2.6.3 Leaching and Lateral Movement............................................................................9
2.6.4 Biodegradation .......................................................................................................9
2.6.5 Volatilization ........................................................................................................10
2.6.6 Photolysis .............................................................................................................11
2.7 Behavior and Effects in Terrestrial Biota.........................................................................11
2.7.1 Terrestrial Plants ..................................................................................................11
2.8 Behavior and Effects in Aquatic Biota.............................................................................12
2.8.1 Freshwater Aquatic Life.......................................................................................12
2.8.1.1 Aquatic Vertebrates...............................................................................12
2.8.1.2 Aquatic Invertebrates ............................................................................13
2.8.1.3 Aquatic Plants........................................................................................13
2.8.1.4 Other Aquatic Biota...............................................................................13
2.8.2 Marine Life...........................................................................................................13
2.8.2.1 Marine Vertebrates ................................................................................13
2.8.2.2 Marine Invertebrates .............................................................................13
2.8.2.3 Marine Plants.........................................................................................13
2.8.2.4 Other Marine Biota................................................................................14
2.9 Behavior and Effects in Mammalian Species and Humans .............................................14
2.9.1 Mammalian Species .............................................................................................14
2.9.1.1 Acute Toxicity Studies ..........................................................................14
2.9.1.2 Subchronic Toxicity Studies .................................................................15
2.9.1.3 Chronic Toxicity and Oncogenicity Studies .........................................16
2.9.1.4 Genetic Toxicology Studies ..................................................................17
2.9.1.5 Reproduction and Developmental Studies ............................................19
2.9.1.6 Absorption, Tissue Distribution, Biotransformation, and Excretion ....19
2.9.2 Humans.................................................................................................................20
2.9.2.1 Acute Toxicity Studies ..........................................................................20
2.9.2.2 Subchronic Toxicity Studies .................................................................21
2.9.2.3 Chronic Toxicity and Oncogenicity Studies .........................................21
2.9.2.4 Genetic Toxicology Studies ..................................................................21
2.9.2.5 Reproduction and Developmental Studies ............................................21
2.9.2.6 Absorption, Tissue Distribution, Biotransformation, and Excretion ....21
3. DERIVATION OF ENVIRONMENTAL AND HUMAN HEALTH WATER QUALITY
GUIDELINES ...........................................................................................................................21
3.1 Freshwater Aquatic Life...................................................................................................21
3.1.1 Data Quality .........................................................................................................22
3.1.2 Data Quantity .......................................................................................................22
3.1.3 Guideline Derivation ............................................................................................23
3.2 Marine Life.......................................................................................................................23
3.2.1 Data Quality .........................................................................................................23
3.2.2 Data Quantity .......................................................................................................24
3.3 Irrigation...........................................................................................................................24
3.4 Livestock Watering ..........................................................................................................26
3.4.1 Data Quality .........................................................................................................26
3.4.2 Data Quantity .......................................................................................................27
3.5 Source Water for Drinking ...............................................................................................28
3.5.1 Tolerable Daily Intake (TDI) ...............................................................................29
3.5.1.1 Human Tolerable Daily Intake (TDI)....................................................30
3.5.1.2 Bioavailability .......................................................................................30
3.5.2 Guideline Development........................................................................................30
3.5.3 Dermal Contact Check .........................................................................................31
3.6 Data Gaps .........................................................................................................................32
3.6.2 Marine Aquatic Life .............................................................................................33
3.6.3 Irrigation...............................................................................................................33
3.6.4 Livestock Watering ..............................................................................................33
3.6.5 Source Water for Drinking ...................................................................................33
3.7 Summary of Water Quality Guidelines ............................................................................34
3.7.2 Marine Life...........................................................................................................34
3.7.3 Irrigation...............................................................................................................34
3.7.4 Livestock Watering ..............................................................................................34
3.7.5 Source Water for Drinking ...................................................................................35
4. CLOSURE.................................................................................................................................35
5. REFERENCES..........................................................................................................................36
LIST OF TABLES
Table 2.1 Common Synonyms and Trade Names for Diisopropanolamine

Table 2.2 Physical and Chemical Properties for Diisopropanolamine
Table 2.3 Biodegradation Studies for Diisopropanolamine
Table 2.4 Toxicity of Diisopropanolamine to Terrestrial Plants
Table 2.5 Toxicity of Diisopropanolamine to Aquatic Species
Table 2.6 Toxicity of Diisopropanolamine to Mammalian Species
Table 3.1 Water Quality Guidelines for Diisopropanolamine
British Columbia Ministry of Water, Land and Air Protection DIPA Water Quality Guidelines
EXECUTIVE SUMMARY
Introduction
Diisopropanolamine (DIPA) is an organic chemical used for a wide variety of commercial,

industrial, and household applications. The primary uses of DIPA include natural gas
processing, cosmetics, detergents, and corrosion inhibition. Environmental quality guidelines
have not been developed for DIPA by federal or provincial agencies in Canada.
This report presents water quality guidelines for DIPA for the province of British Columbia.
This work was completed by Komex International Ltd. under contract # WMB 02-060 (the
“Contract”) to the British Columbia Ministry of Water, Land and Air Protection, Water
Management Branch. The guidelines were developed using protocols published by the Canadian
Council of Ministers of the Environment (CCME), where applicable, referred to herein as “the
Protocol”. The guidelines are numerical limits for contaminants in water intended to maintain,
improve, or protect environmental quality and human health. Water quality guidelines were
developed for freshwater aquatic life, irrigation, livestock watering, and source water for
drinking.
Diisopropanolamine Water Quality Guidelines
DIPA is a white solid at room temperature with a mild ammoniacal odour. It is hygroscopic,
completely miscible in water, and a polar, basic solvent. DIPA has a wide variety of
commercial, industrial, and household applications. Based on its physical and chemical
properties, DIPA applications include gas treating, cosmetics and personal care products,
detergents, metalworking fluids, coatings, corrosion inhibitors, and cement applications. DIPA
sorbs strongly to the clay mineral montmorillonite, and hence its mobility in the subsurface is
highly dependent on the amount and type of clay minerals in the aquifer. Biodegradation of
DIPA under typical aquifer conditions can be very slow. An extensive review of existing and
new toxicity studies in mammals, and vertebrates, invertebrates and plants from aquatic and
terrestrial environments was undertaken to assess the toxicity of DIPA to various biota.
Water quality guidelines for DIPA were calculated, using the Protocol, for four water uses:
source water for drinking, freshwater aquatic life, irrigation, and livestock watering. The
recommended guidelines are summarized in Table 3.1 of this report.
Source Water for Drinking

Interim source water for drinking guidelines were calculated for children (21 mg L-1) and adults
(37 mg L-1). The guideline protective of children is recommended.
Komex International Ltd. (C52330100) 6 August 2003 Page i

Freshwater Aquatic Life

The Interim guideline for freshwater aquatic life was calculated to be 1.6 mg L-1.
Marine Life
A guideline for marine life could not be calculated due to insufficient data quality and data
quantity.
Irrigation
Four Interim guidelines were calculated for irrigation. Based on the Protocol, guidelines were
calculated for 1) cereals, tame hays, and pasture crops, and 2) other crops. For each of these two
groups of plants, guidelines were calculated for two soil types: 1) loam and 2) the soil that gave
the most sensitive response from any plant in the toxicity testing (“poor soil”). The guidelines for
cereals, tame hays, and pasture crops were 91 mg L-1 (loam), and 78 mg L-1 (poor soil). For
other crops the irrigation guidelines were calculated to be 36 mg L-1 (loam), and 3.9 mg L-1 (poor
soil).
Livestock Watering
Preliminary guidelines for livestock watering were calculated for dairy cattle, beef cattle, and
deer, to represent likely agricultural and wild animals. The most sensitive species was the dairy
cow, for which a guideline of 38 mg L-1 was calculated. It should be noted that these guidelines
were based on studies on laboratory animals using appropriate safety factors, and no
toxicological information was available for livestock species (either mammalian or avian).
Should such data become available in the future, this guideline could be refined.
Data Gaps
Data gaps were identified in the toxicological dataset for DIPA, and are discussed in the main
text. Overall the data gaps for this compound are relatively minor, and it is felt that the presently
available toxicological dataset and the guidelines presented in this document provide a consistent
picture of the toxicity of this compound.
Komex International Ltd. (C52330100) 6 August 2003 Page ii

1. INTRODUCTION
This report presents water quality guidelines for diisopropanolamine (DIPA) for the province of
British Columbia. This work was completed by Komex International Ltd. (Komex) under
contract # WMB 02-060 (“the Contract”) to the British Columbia Ministry of Water, Land and
Air Protection Water Management Branch.
1.1 Scope of Work
The scope of work for this document included the following tasks:
• review and summarize relevant available background information on DIPA;

• review and summarize the environmental fate and behaviour of DIPA;
• review and summarize available information on the toxicity of DIPA;
• conduct additional toxicity testing on four species of plant and one species of terrestrial
invertebrate (Scientific Information Services (SIS));
• develop tolerable daily intakes (TDIs) of DIPA for humans and livestock (CanTox Inc.);
• derive water quality guidelines for DIPA using applicable (CCME) protocols for freshwater
aquatic life, irrigation, livestock watering, and source water for drinking.
1.2 Background
DIPA is an organic chemical used for a wide variety of industrial purposes. Synthesis of DIPA
was first reported in the 19th century (Siersch, 1868; Van der Zande, 1889). DIPA is not known
to occur in nature. DIPA has a wide variety of commercial, industrial, and household
applications. The primary uses of DIPA include natural gas processing, cosmetics, detergents,
and corrosion inhibition. Environmental quality guidelines have not been developed for DIPA
by federal or provincial agencies in Canada.
1.3 Protocols
Environmental quality guidelines for DIPA were developed using the following protocols
developed by CCME:
A Protocol for the Derivation of Water Quality Guidelines for the Protection of Aquatic Life.
(CCME, 1999).
Protocols for Deriving Water Quality Guidelines for the Protection of Agricultural Water Uses.
(CCME, 1999).
Komex International Ltd. (C52330100) 6 August 2003 Page 1

For ease of reference in this document, the phrase “the Protocol” refers to whichever of the
above documents is applicable. For instance, in the section on developing freshwater aquatic life
guidelines, “the Protocol” would refer to CCME (1999) A Protocol for the Derivation of Water
Quality Guidelines for the Protection of Aquatic Life. Note the Aquatic Life, and Agricultural
Water Uses Protocols listed above were originally published as CCME (1991), and CCME
(1993), respectively, and were reproduced with minor changes in CCME (1999).
Source water for drinking guidelines were developed using standard risk assessment algorithms
and protocols (US EPA, 1989; CCME, 1996).
1.4 Toxicity Data
An extensive literature search was conducted to identify toxicity data for DIPA to mammals, and
aquatic, terrestrial, and microbial organisms. Critical data gaps were identified, and two pieces
of work were commissioned. 1) DIPA toxicological testing of earthworms and four plant species
in four soil types was undertaken by Scientific Information Services (SIS). 2) A comprehensive
review of mammalian toxicology studies for DIPA, and derivation of tolerable daily intakes
(TDIs) was undertaken by Cantox Inc. (Cantox). As a result of data gaps identified in the
Cantox report, a subchronic study of the oral toxicity of DIPA to rats was commissioned.
2. BACKGROUND INFORMATION
2.1 Physical and Chemical Properties
DIPA [CAS#110-97-4], C6H15NO2, is known under a variety of synonyms and trade names
(Table 2.1).
DIPA belongs to the group of alkanolamines. Alkanolamines are organic derivatives of

ammonia and are classified based on the number of substituent groups attached to the nitrogen
atom. Substitution of one organic alcohol group, ROH, for one of the hydrogen atoms of
ammonia (NH3) forms a primary alkanolamine (ROHNH2). Similarly, substitution of two and
three organic groups yield secondary (ROH)2NH and tertiary (ROH)3N alkanolamines,
respectively (Solomons and Graham, 1988). DIPA is a secondary alkanolamine. The synthesis
of DIPA was first reported in the chemical literature in the late 19th century (Siersch, 1868; Van
der Zande, 1889).
Published physical and chemical properties of DIPA are summarized in Table 2.2. At room
temperature, DIPA is a white solid. Alkanolamines, including DIPA, have a basicity similar to

aqueous ammonia, are completely miscible in water, and are polar solvents. They are
characterized by a mild ammoniacal odour and are extremely hygroscopic. The subgroup of
isopropanolamines results from the reaction of propylene oxide (C3H6O) with ammonia and
comprises monoisopropanolamine (MIPA), diisopropanolamine (DIPA), and
triisopropanolamine (TIPA), with the general formula NH3-n(CH2CHOHCH2CH3)n.
2.2 Analytical Methods
There are currently no recommended methods for DIPA analysis published by CCME or
US EPA. Generally, DIPA can be analyzed by gas chromatography, high performance liquid
chromatography (HPLC), ion chromatography (IC), or wet test methods (Kirk-Othmer, 1999).
Methods using derivatization, gas chromatograph (GC) separation, and flame ionization
detection (FID) were described by Bachelor (1976) and Langvardt and Melcher (1980). GC
methods without derivatization using packed or capillary columns were reported by Salanitro
and Langston (1988) using direct injection and a nitrogen-phosphate detector and Dawodu and
Meisen (1993) using a flame ionization detector.
GC methods for DIPA analysis were summarized by Witzaney and Fedorak (1996) and
evaluated by CAPP (1997). Direct injection using a flame ionization or nitrogen-selective
detector in combination with a capillary column did not yield satisfactory results. Problems
were attributed to contamination of the injection port liner. Similarly, DIPA analysis using a
packed stainless steel column and a flame ionization detector was associated with carryover
(“ghosting”) and required that the column was conditioned. DIPA analysis using a non-polar,
megabore, thick-filmed capillary column which had been base-deactivated and using a nitrogen-
selective detector were more successful. However, the matrix of the samples studied contained
NH4Cl and chloroform, which interfered with the nitrogen-selective detector.
Methods for DIPA analysis employing high performance liquid chromatography were discussed
by Einarsson et al. (1986), Nasholm et al. (1987), and Serbin and Birkholz (1995).
Headley et al. (1999) described a method for analysis of vegetation samples collected from a
DIPA-contaminated wetland. Sample preparation included grinding and homogenizing frozen
vegetation samples under liquid nitrogen. Ground samples were transferred into centrifuge tubes
and allowed to warm to room temperature. Following addition of deionized water and
equilibration for 45 minutes, samples were centrifuged for 45 minutes at 2,500 rpm. DIPA
supernatants were analyzed using ion chromatography-electrospray ionization-tandem mass
spectrometry.

Analytical methods used by two commercial laboratories that routinely conduct environmental
DIPA analysis of water and soil samples are summarized below:
The first laboratory performs DIPA analysis based on the method described by Einarsson et al.
(1986) and Serbin and Birkholz (1995). Water samples or aqueous extracts of soil samples are
derivatized to 9-fluorenylmethyl formides. Analysis is then performed by HPLC. Detection
limits are 1 mg L-1 and 2.5 mg kg-1 for water and soil, respectively.
The second laboratory uses an IC method for DIPA analysis. Water samples are filtered prior to
analysis. Soil samples are extracted with deionized water and the extract is also filtered. Water
samples or extracts are analyzed by IC using a specialized column for separation and a two-
solvent gradient. DIPA detection is achieved with an electrochemical detector using pulsed
amperometry. Detection limits are 0.005 mg L-1 and 0.05 to 0.1 mg kg-1 for water and soil,
respectively.
2.3 Production and Uses
2.3.1 Production
Isopropanolamines have been commercially available for over 40 years (Kirk-Othmer, 1999).
DIPA is synthesized by a reaction of propylene oxide (C3H6O) with ammonia (NH3). The
reaction path is shown below:
2C 3H 6 O + NH3 → C 6 H15 NO 2
In North America, the Dow Chemical Company (Dow) is the dominant DIPA producer. In 1995,
the US production was estimated by Dow to be approximately 7,000 tons per year
(approximately 3,200 L). Commercially, DIPA is available as commercial grade compound
(98% pure, containing a maximum of 0.5% water) and as low freezing grade DIPA (containing
10 or 15% (wt.) deionized water).
2.3.2 Uses
DIPA has a wide variety of commercial, industrial, and household applications. Based on its
physical and chemical properties, DIPA applications include gas treating, cosmetics and personal
care products, detergents, metalworking fluids, coatings, corrosion inhibitors, and cement
applications. Commercial and industrial uses of DIPA summarized by Dow (1999) and Kirk-
Othmer (1999) are provided below.

2.3.2.1 Gas Treating
DIPA is used as solvent in the Sulfinol process to remove acid gases from natural gas streams.
The Sulfinol process was introduced by Shell in 1963 and consists of passing the natural sour gas
stream through a mixture of sulfolane, DIPA, or methyldiethanolamine, and water (e.g., Dunn,
1964; Fisch, 1977; Yogish, 1990; MacGregor and Mather, 1991; Murrieta-Guevarra et al.,
1994). Acid gases including hydrogen sulphide (H2S), carbon dioxide (CO2), carbonyl sulphide
(COS), carbon disulphide (CS2), and mercaptans (thiols) are physically absorbed by sulfolane
and chemically absorbed by DIPA thereby “sweetening” the gas stream.
DIPA is also used in alkanolamine-based acid gas removal (AGR) or “sweetening” processes
(Sorensen et al., 1996). In the AGR process, the weakly basic alkanolamines react with acid
gases to form salts that are thereby removed from the gas stream. Amine salts are subsequently
decomposed by thermal regeneration. DIPA is used in gas sweetening processes based on an
H2S selectivity (Goar and Arrington, 1979).
2.3.2.2 Cosmetics and Personal Care Products
Alkanolamine salts, including DIPA salts, are used as raw materials in the manufacture of
creams (Jellinke, 1970; Balsam and Sagarin, 1972; Navarre, 1975), lotions, shampoos, soaps,
and cosmetics based on their high foaming properties and low skin irritation. DIPA and MIPA
may comprise up to 10% of emulsifying agents for cosmetic lotions, bath preparations, and
neutralizers in cosmetics (Beyer et al., 1987). Chemistry similar to that used in soluble oils and
other emulsifiers is applicable to cleansing creams and lotions (Otomo et al., 1989; Sukai et al.,
1989). Isopropanolamines, including DIPA, neutralize acidic components, and provide a
balanced pH and suitable surfactant properties for hair sprays, hair wave lotions, skin lotions,
and moisturizers.
2.3.2.3 Detergents and Cleaners
DIPA is used extensively in soaps, cleaning products, and detergents as an emulsifying and
wetting agent, a foam stabilizer, and a rinse improver (Dow, 1999). Alkanolamines (including
DIPA) are also used in phosphate-free liquid detergents (Kirk-Othmer, 1999). In non-enzyme
products, they contribute alkalinity, pH control, and enhancement of product stability. In
enzyme products, alkanolamines contribute to the stability of the enzyme in water solutions (e.g.,
Hughes, 1985).

2.3.2.4 Metal Working Fluids
Isopropanolamines (DIPA, MIPA, and TIPA) are widely used in the metal working industry for
corrosion protection, lubrication, foam suppression, and reduction of friction in metal cutting
operations.
2.3.2.5 Coatings
In metal-coating preparations, alkanolamines (including DIPA) are used as metal-complexing

agents, neutralizers, promoters, modifiers, corrosion inhibitors (Brangs and Heinrich, 1969), and
in electrocoating (Wehrmann, 1972; Obana and Miyagawa, 1979). DIPA further assists in
improving curing resins, improving storage stability, and improving both fresh and salt water
resistance for some types of coatings (e.g., Takahashi et al., 1974; Vassiliou, 1976; Butler,
1978). In water-borne coatings, DIPA is used for acid neutralization, improvement of water
solubility, and reduction of water sensitivity and discoloration (Dow, 1999).
2.3.2.6 Corrosion Inhibitors
Alkanolamines (including DIPA) inhibit corrosion of ferrous metals (Brangs and Heinrich,
1969). Applications include coolant systems, lubricating oils (Stanik et al., 1988; De Jong et al.,
1989), metal working fluids, petroleum anti-fouling (Forester, 1989), and drilling needs (Mukhin
et al., 1989). Corrosion inhibitors for aluminum that contain alkanolamines have also been
discussed in the literature (Imai et al., 1988).
2.3.2.7 Cement Applications
Among other alkanolamines (e.g., MIPA and TIPA), DIPA is often used in cement admixtures as
an accelerator to reduce set time (Kobayashi and Fukazawa, 1989; Dow, 1999).
2.3.2.8 Miscellaneous Uses
Additional applications for DIPA include herbicides, pesticides, insecticides, paint strippers, wax
removers, polishes, paper and paperboard, photographic intermediates, plastics and polymers,
and as polyurethane additive.
2.4 Levels in the Canadian Environment
The occurrence of DIPA in the environment has been reported in groundwater, surface water,
soil, and plants in the vicinity of facilities where it has been used. It is anticipated, however, that
in environments located away from such facilities (i.e., most of Canada), DIPA will not be
present at measurable concentrations.

Reports on the presence of anthropogenic DIPA in the environment are limited to data collected
at three sour gas processing facilities in Alberta and British Columbia (CAPP, 1997; Wrubleski
and Drury, 1997). At these facilities, a maximum soil DIPA concentration of 1,480 mg kg-1 was
measured in clay-rich till. Maximum measured DIPA concentrations in groundwater collected
from contaminated aquifers beneath the gas processing facilities were 6 mg L-1 in a sand aquifer
and 590 mg L-1 in a shallow till aquifer (Greene et al., 1999). At one of the facilities, DIPA-
impacted groundwater discharged via a wetland into a creek. Levels within the wetland and the
creek were significantly reduced compared to the discharging groundwater. Maximum DIPA
concentrations reported in groundwater and creek water were 590 and 0.07 mg L-1, respectively
(Greene et al., 1999).
DIPA uptake by wetland vegetation was studied as part of a CAPP research program to evaluate
natural attenuation processes in contaminated wetlands (CAPP, 1998; 1999; 2000). Roots,
stems, leaves, flower heads, seed heads, and berries of cattail, dogwood, sedge, marsh reed grass,
cow parsnip, and smooth brome growing in a DIPA-impacted wetland were included in the study
(CAPP, 1999 and 2000; Headley et al., 1999). Analytical results indicated highly variable DIPA
concentrations for different parts of the same species (e.g., roots versus leaves), between
different plant species (e.g., cattail leaves versus sedge leaves), and even between different
samples of the same part of the same species. The maximum measured DIPA concentration in
plants from the wetland was 208 mg kg-1. The maximum measured DIPA concentration in water
within the wetland was 13 mg L-1.
No studies were found that had detected DIPA as naturally-occurring compound in the
environment.
2.5 Existing Guidelines and Criteria in Various Media
Federal or provincial environmental quality guidelines have not been developed for DIPA.
2.6 Environmental Fate and Behavior
The fate and behavior of a compound released to the subsurface environment is determined by
the physical and chemical properties of the compound and the attenuation processes (e.g.,
biodegradation) to which it is subjected. The relationship between compound properties, and
fate and behavior can be used to predict the potential for the persistence and transport of DIPA.
Physical and chemical properties of DIPA (Table 2.2) in combination with recently published
sorption studies and an alkanolamine fate and transport study conducted by Sorensen et al.

(1996) are discussed in the sections below to evaluate the environmental fate and behavior of
DIPA.
The environmental fate and behavior of DIPA is affected by its physical and chemical properties
and susceptibility to biodegradation, as well as the hydrogeological and geological properties of
the aquifer material.
2.6.1 Adsorption and Mobility
Luther et al. (1998) investigated DIPA sorption parameters in batch equilibration studies.
Sorbent materials included aquifer sediments from DIPA-contaminated sour gas treatment
facilities, reference soils of pure montmorillonite and kaolinite, and six soils of various clay and
organic matter contents. DIPA sorption isotherms were found to be curvilinear, and the slope
decreased with increasing concentration. X-ray analysis of DIPA-saturated montmorillonite
showed that DIPA enters the interlayer space of the mineral. Sorption by aquifer materials was
interpreted to be relatively independent of organic carbon content, but a strong function of
montmorillonite content. The DIPA distribution coefficient (Kd) for montmorillonite (16 to
42 L kg-1) was higher than for humus-rich soil (2.0 L kg-1). Cation exchange capacity (CEC)
was found to be a reasonable predictor of DIPA sorption by soils and aquifer materials with low
organic carbon content (i.e., <1%).
DIPA retardation coefficients calculated by Luther et al. (1998) for aquifer sediments were
reported to be 3.2 (weathered sandstone), 5.3 (weathered shale/sandstone), and 12 (clay-rich till).
These values indicate that, particularly in the presence of clay-rich sediments, DIPA migration is
significantly retarded relative to groundwater flow velocity.
The organic carbon-water partition coefficient (Koc) and the n-octanol-water partition coefficient
(Kow) represent the equilibrium ratio of DIPA sorbed by organic carbon or octanol to its
concentration in water, respectively. The low Koc, low Kow, pKa (negative logarithm of the acid
dissociation constant), and high water solubility of DIPA (Table 2.2) are consistent with the
findings of the sorption study, summarized above, that there is a low potential for DIPA to sorb
to sediments or soils, unless montmorillonite-rich clay comprises a significant fraction of aquifer
sediments.
2.6.2 Aqueous-Phase Solubility
DIPA is highly water soluble and considered miscible at 25º C (Verschueren, 1996; Kirk-
Othmer, 1999). Its pKa of 8.9 indicates that DIPA exists in an increasingly protonated form at
pH values less than 8.9, and acts as a weak base in water (Kim et al., 1987).

2.6.3 Leaching and Lateral Movement
The leaching and lateral movement potential of DIPA is determined by its relatively strong
affinity for sorption to montmorillonite, low retardation coefficients in DIPA-contaminated
aquifer sediments (except for montmorillonite), and high solubility. CAPP (1997) used the
classification system of McCall et al. (1980) to classify DIPA mobility as very high to medium.
The mean retardation factor estimated from the data for DIPA at three sour gas facilities was 6.8
(Luther et al., 1998). Thus, DIPA is predicted to partition between water and montmorillonite in
the vadose (i.e., unsaturated) zone. Once in the saturated zone, the migration rate of DIPA is a
function of the clay content (i.e., montmorillonite) of the aquifer material, the hydraulic
conductivity of the aquifer material, the hydraulic gradient, and the susceptibility of DIPA to
biological attenuation processes (i.e., biodegradation).
2.6.4 Biodegradation
The biodegradation of DIPA has been investigated in acclimated sewage sludge, refinery
wastewater, laboratory microcosm studies using contaminated aquifer sediments, and as part of a
natural attenuation study in natural wetlands. Most studies have demonstrated that DIPA
biodegrades in aerobic microcosms from a variety of DIPA-contaminated environmental
samples. Reported DIPA biodegradation rates and lag times (i.e., time required before
degradation starts) are highly variable. Biodegradation rates range from 0 to 70 mg L-1 day-1.
Lag times range from <1 to 220 days (Table 2.3).
Witzaney and Fedorak (1996) reviewed previous work conducted on DIPA biodegradation. The
review indicated that some studies provided evidence of DIPA degradation (Bridié et al., 1979a;
Salanitro and Langston, 1988; Chong, 1994), whereas results of Rothkopf and Bartha (1984)
suggested that DIPA did not support microbial growth.
In recent studies, DIPA biodegradation using nutrient-amended and -unamended microcosms,

under aerobic and anaerobic conditions, and at temperatures ranging from 8° to 28° C has been
examined. Microcosm studies were conducted using sediments and soils from DIPA-
contaminated aquifers. Microcosm materials included sandstone, till, sand, and wetland
sediments. Materials, conditions, lag-times, and biodegradation rates reported in microcosm
studies are summarized in Table 2.3.
Gieg et al. (1998) conducted aerobic and anaerobic microcosm studies at 8° and 28° C using a
variety of sediments from contaminated aquifers. Shake flask cultures were incubated at 8º and
28º C under addition of the appropriate nutrients such as nitrogen and phosphate. This study

documented the presence of aerobic and anaerobic microbial DIPA degraders in contaminated
aquifer sediments from three sour gas treatment facilities. Under aerobic conditions at 28° C,
DIPA was completely removed. DIPA removal was significantly slower at 8° C and complete
DIPA removal was not achieved. Refeeding of microcosms with additional DIPA led to faster
and complete DIPA removal at 8° and 28° C. Kinetic analyses indicated that DIPA degradation
is best described by first-order kinetics. Under anaerobic conditions, DIPA biodegradation was
confirmed to occur at 28º C under NO3-, Mn4+, and Fe3+ reducing conditions. At 8º C, evidence
of anaerobic degradation under NO3-, Mn4+, and Fe3+ reducing conditions was observed in a
limited number of microcosms.
Gieg et al. (1999) used radio-labelled 14C-DIPA to investigate the microbial mineralization of
DIPA. They demonstrated the release of 14CO2 from 14C-DIPA and the reduction of the
respective electron acceptors in aerobic and anaerobic microcosm studies at 8° and 28° C. In
anaerobic cultures, DIPA degradation was observed under NO3- and Mn4+ reducing conditions at
8° and 28° C, whereas DIPA-degrading activity was difficult to sustain under Fe3+ reducing
conditions. In aerobic cultures, between 30 and 50% of the nitrogen from DIPA was found as
ammonium-nitrogen.
West (1995) suggested that the DIPA biodegradation pathway occurs via the metabolites
N-(2-oxopropyl)-isopropanolamine to MIPA and methylglyoxal. MIPA has been identified as
an intermediate metabolite in soil microcosms (CAPP, 1997). The aerobic microbial metabolism
of MIPA was studied by Jones and Turner (1973). The aerobic pathway occurred via initial
activation to 1-aminopropan-2-ol O-phosphate to propionaldehyde, which was subsequently
oxidized to propanoic acid. Propanoic acid was hypothesized to be further metabolized.
Anaerobic biodegradation of MIPA was investigated by Chou et al. (1978), who documented
that MIPA can be biodegraded under methanogenic conditions.
2.6.5 Volatilization
Volatilization potential is commonly expressed using the Henry’s law constant and the vapour
pressure of a compound. The Henry’s law constant is the equilibrium ratio of the concentration
in the gas phase to the concentration in the aqueous phase. This value is closely related to the
vapour pressure of a compound but is also dependent on its aqueous solubility and molecular
weight and, therefore, can be used to make a more accurate prediction of volatility than one
based on solely on vapour pressure.
Lyman et al. (1982) used Henry’s law constants to classify volatilization potential as follows:

• values less than 10-7 atm m3 mol-1 indicate that the substance is less volatile than water and
can be considered essentially non-volatile;
• values between 10-7 and 10-5 atm m3 mol-1 indicate that the substance may volatilize slowly
but the compound will still tend to partition into the aqueous phase;
• values between 10-5 and 10-3 atm m3 mol-1 indicate that volatilization is significant; and,
• values greater than 10-3 atm m3 mol-1 indicate that the majority of the mass of the compound
will tend to partition into the gas phase.
The vapour pressure of a compound is the pressure that the vapour phase of a compound exerts
at equilibrium with its aqueous phase. Vapour pressures are reported for a given temperature
and increase with increasing temperature. Compounds with high vapour pressures are more
likely to volatilize than those with lower vapour pressures. Thus, the potential of vapour-phase
transport of a compound increases with increasing vapour pressures.
The low Henry’s law constant of DIPA (1.72 x 10-7 atm m3 mol-1), combined with a low vapour
pressure (i.e., 0.02 mm Hg at 41°C) (Table 2.2), suggest that DIPA can be considered essentially
non-volatile. Thus, vapour-phase transport in the vadose zone is not expected to be significant.
2.6.6 Photolysis
No information on the susceptibility of DIPA to phototransformation reactions was available at

the time this report was prepared.
2.7 Behavior and Effects in Terrestrial Biota
2.7.1 Terrestrial Plants
The toxicity of DIPA to terrestrial plants is summarized in Table 2.4. Two toxicity studies have
been completed. Data for both studies is provided in CAPP (2001).
The first study (Komex, 1999) conducted on lettuce (Lactuca sativa), consisted of a five day
seed germination/root elongation test. This is a widely-used and accepted short-term test for
plants (e.g., Ratsch and Johndro, 1986; Wang, 1987; Wang and Williams, 1988; ASTM, 1990).
For lettuce (Lactuca sativa) grown in a fine-textured soil, Komex (1999) reported NOEC values
of 140 and 6,300 mg kg-1, for root elongation and seed germination, respectively (Table 2.4).
The second plant toxicity study (CAPP, 2001), was conducted using an Environment Canada
(1998) draft protocol, four plant species (lettuce (Lactuca sativa), carrot (Daucus carota), alfalfa
(Medicago sativa), and timothy (Phleum pratense)), and four soils with differing texture, organic

carbon content, and cation exchange capacity. The endpoints measured were emergence,
biomass, root length, and shoot length (Table 2.4). For all four plant species, the most sensitive
endpoint was root length. The lowest LOEC for this endpoint was 424 mg kg-1 (lettuce and
carrot in sand). The highest LOEC was 43,700 mg kg-1 for timothy emergence in loam. Plants
were generally most sensitive in sand and least sensitive in loam.
2.8 Behavior and Effects in Aquatic Biota
Available data on the toxicity of DIPA to freshwater and marine aquatic species are presented in
Table 3.6. Toxicological studies on rainbow trout (Oncorhynchus mykiss) and the sideswimmer
(Hyalella azteca) were commissioned for this report. A full report on this work is included in
CAPP (2001). Note that ERAC (1998) included a review of previous published and unpublished
freshwater aquatic toxicological data, and a report on freshwater toxicological studies, which
were commissioned for the ERAC (1998) report. References to ERAC (1998) in the following
sections refer only to the new data commissioned for the report. Original references are used for
other studies referenced in the ERAC (1998) report.
DIPA has a pKa of 8.9 (Table 2.2), which means that below a pH of 8.9, DIPA is present
predominantly in its charged, protonated form. Conversely, above pH 8.9, DIPA is
predominantly unprotonated (Section 2.6.2). This behaviour has the potential to affect DIPA’s
toxicity to freshwater aquatic life. Moreover, adding DIPA to water with a low buffering
capacity will result in an alkaline pH, which may preclude the survival of certain organisms, due
to pH alone. Accordingly, pH was included in Table 2.5, where available.
2.8.1 Freshwater Aquatic Life
2.8.1.1 Aquatic Vertebrates
Data were available for seven species of aquatic vertebrates (Table 2.5). An acute lethality study
on rainbow trout (Oncorhynchus mykiss) was completed for CAPP (2001). ERAC (1998)
completed a 7 day survival and growth test on fathead minnows (Pimephales promelas). The
results of acute lethality studies on clawed toad (Xenopus laevis), goldfish (Carassius auratus),
ide (Leuciscus idus), mosquito fish (Gambusia sp.), and stickleback (species not specified) were
also available. Reported LC50 values for the acute tests ranged from 42 mg L-1 (stickleback) to
7,698 mg L-1 (rainbow trout). The LOEC for the 7 day growth endpoint for the fathead minnow
was 1,000 mg L-1 at both test pHs.

2.8.1.2 Aquatic Invertebrates
Four studies considered the toxicity of DIPA to three species of aquatic invertebrates (Table 2.5).
An acute lethality study on a sideswimmer (Hyalella azteca) was completed at two pH values
(CAPP, 2001). Two studies reported the acute lethality of DIPA to Daphnia magna, and one
study investigated the 7 day reproduction and survival endpoints in Ceriodaphnia dubia.
Reported LC50 values for the acute tests ranged from 278 mg L-1 (D. magna) to 1,128 mg L-1 (H.
azteca, pH 7.5). The LOECs for the non-lethal (reproduction) endpoints for C. dubia were 31
mg L-1 at the lower pH (7.7 to 8.4) and 250 mg L-1 at the higher pH (8.2 to 9.4).
2.8.1.3 Aquatic Plants
Only one study for an aquatic vascular plant was available. SRC (1994) reported the EC50 for
duckweed (Lemna minor) growth to be 1,500 to 2,300 mg L-1. Two studies on the green alga
Selenastrum capricornutum and one study on the green alga Scenedesmus suspicatius were
available for various endpoints. The EC50/LC50 values ranged from 7 mg L-1 to 270 mg L-1.
2.8.1.4 Other Aquatic Biota
Other aquatic biota include all aquatic organisms not included in the animal or plant kingdoms.
This covers organisms from the kingdoms Monera, Protista, and Fungi. A study by SRC (1994)
measured 14C uptake and nitrogen fixation by the cyanobacteria Aphanizomenon flos-aquae and
14
C uptake by the diatom Cyclotella meneghiana. The reported EC50 values ranged from
110 mg L-1 to 200 mg L-1.
2.8.2 Marine Life
2.8.2.1 Marine Vertebrates
Literature data were not available for marine vertebrates
2.8.2.2 Marine Invertebrates
Literature data were not available for marine invertebrates
2.8.2.3 Marine Plants
Literature data were not available for marine plants

2.8.2.4 Other Marine Biota
Other marine biota include all marine organisms not included in the animal or plant kingdoms.
This covers organisms from the kingdoms Monera, Protista, and Fungi. Two studies examined
the effect of DIPA on the luminescence of the marine bacterium Vibrio fischerii (SRC, 1994;
ERAC, 1998). The reported EC50 values ranged from 50 to 9,202 mg L-1.
2.9 Behavior and Effects in Mammalian Species and Humans
2.9.1 Mammalian Species
Literature studies on the toxic effects of DIPA to mammals are presented in Table 2.6. This
section represents a summary of the review of mammalian DIPA toxicology undertaken by
Cantox for the CAPP (2001) report. The complete Cantox report is available in CAPP (2001).
2.9.1.1 Acute Toxicity Studies
Animal studies summarizing the acute lethality of DIPA using single dose exposures (LD50) are
summarized in Table 2.6. Test animals have included rat, mouse, guinea pig, and rabbit.
Oral Studies
A 30% aqueous solution of DIPA was administered orally to two groups of rats (two animals per
group). The first group received a total dose of 2,000 mg kg-1 bw without observable effect. A
second group received a dose of 3,980 mg kg-1 bw, and both died within 24 hours (Dow, 1954).
The acute toxicity of two sunscreen formulations containing DIPA (1%) was determined in male
and female albino rats, or Sprague Dawley rats. When administered by gavage, the LD50 for one
of the sunscreen preparations was 5,000 mg kg-1 bw in one instance, but this dose was tolerated
in the second study. At lower doses, there were no toxicological effects up to 14 days after
treatment (Biosearch, 1981a; Springborn, 1982a).
In another study, rats given 5,000 mg kg-1 bw day-1 for seven days produced no evidence of toxic
effect (BIBRA, 1991).
Dermal and Ocular Studies

There are several studies that have examined the skin irritation and dermal toxicity of DIPA.
Undiluted DIPA was applied to intact, or abraded skin on the abdomens of rabbits (Dow, 1954).
Moderate hyperemia to severe necrosis were observed at the intact sites, and slight hyperemia,
oedema, and moderate denaturation were observed where DIPA was applied to abraded skin. A

10% aqueous solution of DIPA applied to rabbit ears had no observable effect. When applied to
either normal or abraded skin on the abdomens of rabbits, however, this dose of DIPA produced
moderate hyperemia and blistering, oedema, and moderate denaturation (Dow, 1954).
Undiluted DIPA is a severe eye irritant in rabbits. Application of 50 mg DIPA directly to the
eye caused burns of the eyelid, eyeball and corneal mucosa (Toropkov, 1980a). Recovery
occurred in 22 days, but ocular burns that produced cataracts or opaque corneas remained. A
dilute solution (1% DIPA) was tested in a sunscreen formulation on New Zealand rabbits to
evaluate skin irritation. The application of 0.2 mL of undiluted product produced evidence of
mild primary irritation (Springborn, 1982b).
The ocular irritation produced by a sunscreen containing DIPA (1%) was evaluated in two
studies in albino rabbits. Eyes were treated briefly with the solution and immediately rinsed, or
were treated and then left unattended for up to seven days. The product was deemed not to be an
ocular irritant (Biosearch, 1981b; Springborn, 1982c).
2.9.1.2 Subchronic Toxicity Studies
DIPA has been tested in rats for responses to subchronic exposures in drinking water. Groups of
five male and five female CFD Fischer 344 rats (ten animals per dose) were given doses of 0,
100, 300, 600, 1,200, or 3,000 mg kg-1 bw day-1 in their drinking water for a period of two
weeks. Observations of activity and physical characteristics were recorded during the exposure
period, at the end of which animals were examined for gross pathological changes, or changes in
organ weights. Histological studies were performed on liver, kidney, and urinary bladder (Dow,
1984).
The 3,000 mg kg-1 bw day-1 dose of DIPA was not well-tolerated by either sex. Two of five
male rats died before the completion of the two week study. Other animals demonstrated
marked weight loss, reductions in body fat, organ sizes and weights, and altered clinical
biochemical parameters. These changes were partially attributed to emaciated states from
marked decreases in food and water consumption. At the highest dose, rats suffered acute
inflammation and degeneration of kidney and urinary bladder. There was evidence of
generalized liver atrophy, but no clear evidence of hepatotoxicity (Dow, 1984).
Animals dosed at 1,200 mg kg-1 bw day-1 were observed to have lower dietary and water intake
which accounted for a small weight decrease in males, but the rate of weight gain for females
was unaffected. Kidney weights (relative to control animals) were slightly increased in this
group. The type of kidney alterations observed in the high-dose animals was observed on
histological examination of only one animal at this dose. All other rats of either sex showed no
treatment related effects in any of the organs examined.

No toxicological effects were observed among animals that received 600 mg kg-1 bw day-1 or
less in this study (Dow, 1984). As such, this dose rate could be considered the study no-
observable-adverse-effect-level (NOAEL).
Wistar rats that received 1% DIPA mixed with their powdered diet from age 6 weeks to 24
weeks showed no evidence of renal toxicity. There was no evidence of endogenously produced
N-nitrosobis(2-hydroxypropyl)amine detected in urine collected from these animals (detection
limit 50 nmol per 200 mL) (Konishi et al., 1991).
In another study, rats given 5,000 mg kg-1 bw day-1 for seven days produced no evidence of toxic
effect (BIBRA, 1991). In the guinea pig, a threshold for toxic effects for less than chronic
exposures was given at 0.22 mg kg-1 bw day-1 (Toropkov, 1980b).
2.9.1.3 Chronic Toxicity and Oncogenicity Studies
There was no increase in the incidence of tumors observed in target organs of Wistar rats fed 1%
DIPA (w/v) for a period of 94 weeks (Yamamoto et al., 1989; Konishi et al., 1991). The dosage
of DIPA was 391 ± 35 mg kg-1 bw day-1.
The lung, oesophagus, urinary bladder and kidney, as well as the nasal cavity, are recognized
target tissues for nitrosated diisopropanolamine. Among 16 treated rats that survived the full 94
week exposure period, there were no tumors of the nasal cavity, none in the lung, oesophagus,
liver, urinary bladder, or kidney. There were also no thyroid adenomas in any of the treated
animals, while one rat of 19 control animals had thyroid adenomas (Konishi et al., 1991). These
are sites known to be susceptible to tumor formation in rats exposed to N-nitrosobis(2-
hydroxypropanol)-amine. In addition, the spontaneous tumor frequency in adrenal gland, testis,
and pituitary gland was lower in DIPA treated animals than the controls. This indicates that
chronic (lifetime) exposure to 391 ± 35 mg kg-1 bw day-1 of DIPA was not carcinogenic
(Yamamoto et al., 1989).
When fed a similar diet in conjunction with a source of nitrite in the drinking water (0.3% but
not 0.15%), tumors appeared in every expected target organ. This was taken as evidence of
endogenous production of N-nitrosobis(2-hydroxypropanol)amine in conditions of simultaneous
exposure to DIPA and nitrite. Analysis of urine from animals chronically exposed to both
substances for a period of 24 weeks also showed evidence of N-nitrosobis(2-hydroxy-
propanol)amine from endogenous enzymatic activity. In conditions where the animals’ diet had
no source of excess nitrite, exposure to DIPA produced none of this carcinogenic material based
on the detection limit of the assay. Animals treated with DIPA at a dose of 448 ± 36 mg kg-1
bw day-1 with a daily nitrite intake of 151 ± 16 mg kg-1 bw day-1 developed significant numbers

of tumors at all sites examined. These were similar in type and location to tumors induced by
exposure to N-nitrosobis(2-hydroxypropanol)amine alone (Yamamoto et al., 1989). Among
animals that received similar doses of DIPA, but reduced nitrite (0.15% instead of 0.3% in
drinking water), tumor frequency in target tissues was not significantly different from control
animals. This suggests a threshold of tumor response in the rat, even though there is evidence
for production of the carcinogenic substance most likely responsible for tumor production. This
cannot be taken to mean that a combination of high nitrite exposure with DIPA is essential for
carcinogenic initiation in tissues.
Yamamoto et al. (1989) suggest that their results provide evidence that endogenous nitrosations
of environmental nitrosatable amines can be potential risk factors for human cancer
development.
2.9.1.4 Genetic Toxicology Studies
When evaluating data for genotoxicity, primary goals are to determine (1) the likelihood of
occurrence of a key event and (2) whether that event might lead to heritable changes associated
with any adverse effect in vivo, including cancer. The basis upon which a weight-of-evidence
evaluation can be constructed include the following:
• any statistically significant observations should be reproducible and biologically significant;

• a dose-response relationship should exist for effects;
• the effects should be permanent and progressive, as opposed to reversing upon cessation of
chemical dosing;
• the nature of DNA effects should be characterized;
• the database should be consistent or inconsistencies adequately explained; and,
• the effects produced in the assay should be relevant to humans.
A central objective of the weight-of-evidence approach is to balance experimental test data with
experience, and not to accord greater weight to any single result. For purposes of human hazard
assessment, greater confidence is placed in those test systems that examine possible genetic
effects from chemical exposure of animals, rather than in tests that rely on selected homogeneous
cell populations raised and tested in vitro. Chemical exposures of biological systems carried out
in vitro are much less realistic, and results of such tests can be determined by the effects of
toxicity. Such toxicity can occur at unusually high exposure concentrations and/or be dependent
on metabolic and detoxification capabilities. Finally, a weight-of-evidence evaluation seeks to
establish a dose-response relationship. Greater attention should be given wherever there is a
clear association between increased exposure and a genetic effect.
The consideration of the carcinogenic potential of DIPA can be assessed in a number of ways.

Short-term tests for mutation, or for other evidence of genotoxic activity, allow identification of
alterations in the genome. A primary purpose of such tests is to provide information on the
production of heritable changes (mutations) that could lead to further adverse biological
consequences. An initial and prominent question that genotoxicity tests are designed to answer,
is whether the chemical (or any derivative) interacts directly with and mutates DNA (Williams,
1989). Such interactions are known to bring about changes in gene expression or to affect other
key biological processes. However, there is clear evidence that some short-term tests
demonstrate effects of toxicity that may or may not support direct interaction with DNA.
Finally, some chemical exposures show no effect at low dosages, and can be shown to be
dependent on a threshold of exposure to produce an effect. The production of such indirect
effects is often limited to conditions of high dose, which may be irrelevant to health risk
assessment.
The genotoxicity of DIPA has not been extensively investigated. One study in Salmonella was
negative (at doses up to 10 mg plate-1) in several standard tester strains including TA100, TA98,
TA 1535, and TA1537 with or without microsomal activation using rat or hamster liver S9
(Mortelmans et al., 1986). An unpublished report (Dow, 1994) has examined DIPA in the in
vitro chromosomal aberration test (OECD Guideline 473). The purpose of the in vitro
chromosome aberration test is to identify agents that cause structural (chromosome or chromatid
type) chromosome aberrations in cultured mammalian cells. Chromosome mutations and related
events are the cause of many human genetic diseases and there is substantial evidence that
chromosome mutations and related events causing alterations in oncogenes and tumor suppressor
genes of somatic cells are involved in cancer induction in humans and experimental animals.
DIPA did not produce chromosomal aberrations in rat lymphocytes with and without metabolic
activation at exposures of 313 to 5,000 µg mL-1 (Dow, 1994 in BASF, 1994). There were no
other published reports in the literature.
While DIPA may not be genotoxic, a related nitroso-derivative that can be produced in the
environment and endogenously in certain conditions does have genotoxic potential. Commercial
DIPA prepared by chemical synthesis from propylene oxide and ammonia has been reported to
contain between 20 and 1,300 ppb of N-nitrosobis(2-hydroxypropyl)amine (Issenberg et al.,
1984). Older samples (>5 years storage) exhibited the highest concentration of this contaminant.
Recent commercial synthetic practice (Dow, 1985a) produces product with no evidence of
N-nitrosobis(2-hydroxypropyl)amine at a detection limit of 20 ppb. Therefore, it is likely any of
this product found in the environment would be the result of biological or direct chemical
reactions.
N-nitrosobis(2-hydroxypropyl)amine has genotoxic properties. It is rapidly absorbed through the

skin of hamsters, and topical application produced neoplasms of the lip, cheek pouch, and
vaginal epithelium (Pour et al., 1977; 1980). N-nitrosobis(2-hydroxypropyl)amine has been

identified as a potent pancreatic carcinogen in hamsters (Pour et al., 1974). Oral ingestion
(drinking water) in rats, induced neoplasms of the colon, respiratory tract, esophagus, and liver
(Lijinsky et al., 1978; Pour et al., 1979). In mice, it induced neoplasms in the lung, liver, and
nasal cavity. In rabbits and guinea pigs, it induced neoplasms in the liver.
There is no evidence that DIPA is either genotoxic in short-term assays or carcinogenic in a

94 week bioassay conducted in Wistar rats. DIPA, therefore, does not pose a genetic hazard as a
result of exposure. There is, on the other hand, ample evidence that DIPA may undergo
nitrosation reactions either in the environment, or after ingestion by endogenous mechanisms,
when sources of nitrite are available. Since DIPA undergoes biodegradation in the environment
primarily by oxidative metabolism, DIPA from groundwater sources would likely remain
unaltered. In the event that elevated levels of nitrite were concurrently available in drinking
water contaminated by DIPA, there is a possibility for endogenous generation of N-nitrosobis(2-
hydroxypropyl)amine.
Results of a long-term bioassay in rats suggest that relatively high levels of nitrite were required
to initiate the production of sufficient quantities of this carcinogenic substance to produce tumors
in tissues. No tumors developed, and no dose-response was observed when 0.15% soluble nitrite
was given to rats that consumed DIPA in their diet. At 0.3% nitrite in drinking water, animals
that received DIPA in the diet responded with significant increases in the number of tumors in
several target tissues. Thus, there is a clear dose-response relationship between the consumption
of DIPA and the amount of nitrite in drinking water.
The risk of developing genotoxic products endogenously is clearly related to the concentrations
of key substances in the environment. The relationship between nitrite and DIPA in the
environment will control the likelihood of the occurrence of a key event, or mutation in target
tissues.
2.9.1.5 Reproduction and Developmental Studies
According to a Russian source, a study carried out in rats at a dose of 0.055 mg kg-1 bw day-1
revealed no effects on a number of markers of reproductive toxicity (BIBRA, 1991). This was
based on an English language abstract of a paper in Russian. Since there is only one study, and
it is unclear whether GLP criteria were used, we conclude there is insufficient data to assess
whether DIPA exposure could produce adverse effects in reproductive endpoints.
2.9.1.6 Absorption, Tissue Distribution, Biotransformation, and Excretion
One study was available on the absorption, tissue distribution, and excretion of DIPA in
mammals. A 19.5 mg-1 kg bw dose of 14C-DIPA was dissolved in acetone and applied to the

skin of four female Fischer 344 rats (Dow, 1985b). After solvent evaporation, the DIPA
remained in direct contact with the skin for 48 hours. At 48 hours, 25% of the DIPA had
penetrated the skin and was absorbed. Approximately 12% of the applied dose was excreted
unaltered by metabolism in the urine, 12.5% remained in tissues, and less that 1% was either
eliminated in expired air or found in the feces. There was no evidence of DIPA accumulation in
fatty tissues. Approximately 50% of the applied material was recovered from the skin, and about
23% was recovered from the skin at and around the site of application.
In the same study, a 19 mg kg-1 bw dose of aqueous 14C-DIPA was administered intravenously to
four female Fischer 344 rats. Greater than 70% of the radioactivity was cleared from the blood
within the first six hours. Approximately 90% of the dose was recovered unchanged in urine
within twelve hours. No metabolites of DIPA were characterized in urinary excretions (Dow,
1985b).
Metabolism studies of DIPA in animals indicate that it is poorly metabolized in mammals. Dow
(1985b) concluded that DIPA, either ingested or absorbed through skin, would be eliminated
rapidly and almost entirely in the urine.
2.9.2 Humans
2.9.2.1 Acute Toxicity Studies
Oral Studies
Acute oral studies on humans were not available in toxicity literature for DIPA.
Dermal and Ocular Studies

Responses to pure DIPA, or to a 1% aqueous solution in a patch test demonstrated variable skin
irritation responses (BIBRA, 1991). A test of a sunscreen containing 1% DIPA on 24 human
subjects that required 15 separate applications to skin over a 21 day period concluded the
substance had minimal irritation qualities. However, in two other studies on human skin that
required repeated application of a cream containing 1% DIPA, there was evidence of
sensitization reactions. A number of dermal exposures were followed by a challenge to
determine whether any subject responded with evidence of sensitization. It was concluded that
the sunscreen product that contained DIPA was not a strong irritant, but that it may be capable of
inducing contact sensitization (ACT, 1987).
Acute ocular studies on humans were not available in toxicity literature for DIPA.

2.9.2.2 Subchronic Toxicity Studies
Subchronic studies on humans were not available in toxicity literature for DIPA.
2.9.2.3 Chronic Toxicity and Oncogenicity Studies
Chronic toxicity and oncogenicity studies on humans were not available in toxicity literature for
DIPA.
2.9.2.4 Genetic Toxicology Studies
Genetic toxicology studies on humans were not available in toxicity literature for DIPA.
2.9.2.5 Reproduction and Developmental Studies
Reproduction and developmental studies on humans were not available in toxicity literature for
DIPA.
2.9.2.6 Absorption, Tissue Distribution, Biotransformation, and Excretion
Absorption, tissue distribution, biotransformation, and excretion studies on humans were not
available in toxicity literature for DIPA.
3. DERIVATION OF ENVIRONMENTAL AND HUMAN HEALTH

WATER QUALITY GUIDELINES
Environmental and human health water quality guidelines for DIPA are presented in Table 3.1.
3.1 Freshwater Aquatic Life
Freshwater aquatic life guidelines for DIPA were developed using the Protocol (A Protocol for
the Derivation of Water Quality Guidelines for the Protection of Aquatic Life; CCME, 1999).
The following sections summarize the requirements of the Protocol and discuss the available
dataset in terms of these requirements. The toxicological dataset was summarized in Table 2.5,
and discussed in Section 2.8.
The Protocol defines (1) the requirements for a toxicological study to be acceptable for guideline
derivation (data quality requirement), (2) the minimum required dataset for Full and Interim
guideline development (data quantity requirement), and (3) the process for deriving guidelines.

The following paragraphs provide a summary of the requirements of the Protocol, and assess the
toxicological dataset.
3.1.1 Data Quality
The data quality requirement in the Protocol may be summarized as follows. For a toxicological
study to be considered “Secondary Data”, all relevant environmental variables (e.g., temperature,
pH, hardness, dissolved oxygen, etc.) should be measured and reported, and the survival of
controls must be reported. In addition, for data to be considered “Primary Data”, tests must
employ currently acceptable practices, concentrations must be measured at the beginning and
end of a test, and, in general, dynamic (i.e., flow-through) tests are required. Data that do not
conform to the requirements for Primary or Secondary Data are “Unacceptable Data”.
The toxicological dataset is summarized in Table 2.5 and classified as Primary, Secondary, and
Unacceptable. Only the work completed for this report conformed to all the requirements for
Primary Data. The study by ERAC (1998) was classified as Secondary Data. All other studies
were classified as Unacceptable Data. It should be noted that studies classified as “Unacceptable
Data” may, in fact, represent acceptable (i.e., Primary or Secondary) data, but insufficient
information was available to confirm this. According to the Protocol only Primary or Secondary
Data can be used in the guideline derivation process.
3.1.2 Data Quantity
The Protocol requirement for the quantity of Primary and/or Secondary Data for Interim
freshwater aquatic life guidelines may be summarized as follows. At least two studies on
freshwater fish species, and at least two studies on freshwater invertebrate species are required.
The tests may be acute or chronic. One of the fish must be a cold water species, and two
different classes of invertebrates must be represented, one of which includes a planktonic species
resident in North America (e.g., daphnid).
The Protocol requirements were met by the Primary and Secondary Data in Table 2.5. The acute
tests on rainbow trout and fathead minnow fulfill the requirement for tests on two freshwater fish
species, with the rainbow trout fulfilling the requirement for a cold water species. Acceptable
test results are available for three species of invertebrate: Daphnia magna and Ceriodaphnia
dubia, represent the Class Branchiopoda and Hyalella azteca, represent the Class Malacostraca.
Thus, all the Protocol requirements for data quantity were met.

3.1.3 Guideline Derivation
Note that the ERAC (1998) data at pH “>9” were not used in the guideline derivation process.
See the end of this section for an explanation. The protocol defines procedures for deriving
guidelines from both chronic and acute data. Guidelines were calculated from both acute and
chronic data, and the lower value was adopted as the freshwater aquatic life guideline. A
guideline is calculated from chronic data, by using the lowest LOEC from the most sensitive
endpoint of the most sensitive lifestage of the most sensitive species, multiplied by a safety
factor of 0.1 to give the freshwater aquatic life guideline. The lowest chronic LOEC for Primary
or Secondary Data in this dataset is 16 mg L-1 for the 7 day reproduction endpoint for
Ceriodaphnia dubia. This yields a guideline value of 1.6 mg L-1.
A guideline can also be calculated from acute data, by using the lowest LC50 or EC50 value, and
multiplying by an “application factor” of 0.05 for non-persistent variables. (DIPA would be
considered a non-persistent variable because the majority of the data in Table 2.3 imply a
biodegradation half-life of less than 8 weeks.) The lowest LC50 in the acute Primary or
Secondary Data (excluding pH >9 data) in this dataset is 74 mg L-1 from the ERAC (1998) study
on the 72 hour growth endpoint for Selenastrum capricornutum. Multiplying this value by an
application factor of 0.05 gives a guideline of 3.7 mg L-1. This value is higher than the guideline
calculated from the chronic dataset, and thus the guideline of 3.1 mg L-1 from the chronic dataset
is used (Table 3.1).
3.2 Marine Life
A marine life guideline for DIPA could not be developed using the Protocol (“A Protocol for the
Derivation of Water Quality Guidelines for the Protection of Aquatic Life”; CCME, 1999) due to
insufficient data quality and data quantity. The following sections summarize the requirements
of the Protocol and discuss the available dataset in terms of these requirements. The
toxicological dataset was summarized in Table 2.5, and discussed in Section 2.8.
3.2.1 Data Quality
study to be considered “Secondary Data”, all relevant environmental variables (e.g., temperature,

pH, hardness, dissolved oxygen, etc.) should be measured and reported, and the survival of
controls must be reported. In addition, for data to be considered “Primary Data”, tests must
employ currently acceptable practices, concentrations must be measured at the beginning and
end of a test, and, in general, dynamic (i.e., flow-through) tests are required. Data that do not
conform to the requirements for Primary or Secondary Data are “Unacceptable Data”.
The toxicological dataset is summarized in Table 2.5 and all studies were classified as
Unacceptable. It should be noted that studies classified as “Unacceptable Data” may, in fact,
represent acceptable (i.e., Primary or Secondary) data, but insufficient information was available
to confirm this. According to the Protocol only Primary or Secondary Data can be used in the
guideline derivation process. Therefore, a marine life water quality guideline for DIPA could
not be developed.
3.2.2 Data Quantity
Since Primary or Secondary studies on marine life were not available in the toxicological
literature, the marine life guideline could not be developed. The Protocol requirement for the
quantity of Primary and/or Secondary Data for Interim marine life guidelines may be
summarized as follows. At least two studies on marine fish species, and at least two studies on
marine invertebrate species are required. The tests may be acute or chronic. One of the fish
must be a temperate species, and two different classes of invertebrates must be represented.
The Protocol data quantity requirements were not met by the data in Table 2.5.
A marine life guideline for DIPA could not be developed using the Protocol due to insufficient
data quality and data quantity.
3.3 Irrigation
Irrigation water quality guidelines for DIPA were developed using the Protocol (“Protocols for
Deriving Water Quality Guidelines for the Protection of Agricultural Water Uses”; CCME,
1999). The toxicological data set was sufficient to derive Interim guidelines (Table 2.4). Data in
Table 2.4 are classified as primary toxicological data by the Protocol. As laid out in the
Protocol, irrigation guidelines were calculated for (1) tame hay, cereal, and pasture crops (e.g.,
alfalfa and timothy) and (2) other crops (e.g., lettuce and carrot).

As can be seen in Table 2.4, the sensitivity of plants to DIPA varies strongly depending on soil
type. For most plant species and endpoints, plants were most sensitive to DIPA in sand or till,
and least sensitive in loam. Accordingly, guidelines were calculated for “poor soil” (i.e., sand or
till), and loam. The reason for this approach was to provide both an overall irrigation guideline,
which was protective of crop growth on any soil type, and guidance on tolerable levels of DIPA
when crops are being grown on typical, improved, agricultural soils.
Four guidelines are presented in Table 3.1, including the two soil types (poor soil and loam) and
two crop types (tame hay, cereal, and pasture crops and other crops) noted above. The overall
irrigation guideline is the lowest of these four guidelines. The detailed guideline derivation
process is described below.
The first step in the guideline derivation process was the calculation of the acceptable soil
concentration (ASC), which is an estimate of the soil concentration that would not result in
adverse effects on crops over the course of one growing season:
 LOEC × NOEC 
ASC (mg kg −1 ) =  
 UF 
 
Where: LOEC = lowest-observed-effect-concentration (mg kg-1 soil);

NOEC = no-observed-effect-concentration (mg kg-1 soil); and,
UF = uncertainty factor of 10.
The calculated ASCs were as follows:

• 56 mg kg-1 for cereals, tame hays, and pasture crops grown in loam, based on the root length
endpoint for alfalfa;
• 48 mg kg-1 for cereals, tame hays, and pasture crops grown in poor soil, based on the biomass
endpoint for timothy in sand;
• 224 mg kg-1 for other crops grown in loam, based on the root length endpoint for lettuce; and,
• 24 mg kg-1 for other crops grown in poor soil, based on the root length endpoint for lettuce
and carrot in sand.
The next step in the guideline derivation process is to calculate species maximum acceptable
toxicant concentration (SMATC), which is the maximum amount of contaminant allowed in a
1 ha (100 m x 100 m) plot. The SMATC is calculated as:
 ASC × ρ × L × W × D 
SMATC (mg L−1 ) =  
 IR 

Where: ASC = acceptable soil concentration (mg kg –1; calculated above);

ρ = soil bulk density (1,300 kg m-3);
L = length (100 m);
W = width (100 m);
D = depth (1.5 m for tame hays, cereals, and pasture crops, and 0.15 m for other
crops); and,
IR = irrigation rate per year (1.2 x 107 L ha-1).
The SMATC for cereals, tame hays, and pasture crops was 91 mg L-1 (loam), and 78 mg L-1
(poor soil). For other crops the SMATC was 36 mg L-1 (loam), and 3.9 mg L-1 (poor soil).
These values are proposed as Interim Irrigation water quality guidelines for DIPA (Table 3.1).
3.4 Livestock Watering
Livestock watering guidelines for DIPA were developed using the Protocol (“Protocols for
Deriving Water Quality Guidelines for the Protection of Agricultural Water Uses”, CCME,
1999). The following sections summarize the requirements of the Protocol and discuss the
available dataset in terms of these requirements. The toxicological dataset is summarized in
Table 2.6, and discussed in Section 2.9.
3.4.1 Data Quality
study to be considered “Secondary Data”, the dose, duration of exposure, and effects should be
reported, the response and survival of controls must be reported. Secondary Data may be for any
route of exposure (e.g., oral, inhalation, dermal). Secondary Data does not have to conform to
accepted laboratory practices as long as all necessary information is reported. For data to be
considered “Primary Data”, tests must employ currently acceptable laboratory practices, report
dose in standard units (i.e., mg kg-1 bw day-1 for chronic tests and mg kg-1 bw for acute tests),
report the response and survival of controls, report the scientifically valid statistics used. In
addition, it is preferred that Primary Data have (1) doses measured analytically, (2) be through a
simulated drinking water exposure (e.g., ad libitum, gavage, oesophageal cannula, or rumen

fistula of food and water), (3) be full life cycle studies, and (4) examine sensitive endpoints (e.g.,
development, growth, fecundity) and production parameters (e.g., milk yield, litter size, feed
conversion). Data that do not conform to the requirements for Primary or Secondary Data are
“Unacceptable Data”.
The toxicological dataset is summarized in Table 2.6 and classified as Primary, Secondary, or
Unacceptable. Primary and Secondary Data were available for the rat, mouse, guinea pig, and
rabbit. Eight acute, two subchronic, and two chronic Primary Data studies were available.
Acute effects ranged from 2,120 to 6,720 mg kg-1 bw. Subchronic and chronic NOAELs for
DIPA alone ranged from 0.22 to 600 mg kg-1 bw day-1.
3.4.2 Data Quantity
The Protocol requirement for the quantity of Primary and/or Secondary Data for an Interim
livestock watering guideline was two studies on two or more mammalian species, one of which
should be a livestock species, and one study on one or more avian livestock species. The tests
can be acute or chronic. The species must be raised in Canada.
According to the Protocol data quantity requirements, there is insufficient data to derive an
Interim guideline. However, the data quality was such that a “Preliminary” guideline was
developed. The Preliminary guideline was developed following the Protocol by using the non-
livestock mammalian toxicity data.
The TDI was based on acute toxicological data from laboratory animals (Table 2.6). The mean
and standard deviation for five acute studies on three species was 4,260 ± 1,920 mg kg-1 bw
day-1. The dermal study reported by Union Carbide (1973) was not included due the large LD50
resulting from lowered bioavailability.
The first step in the guideline derivation process was the calculation of the TDI, which was
based on an extrapolation of acute to chronic data (CCME, 1999):
 LD50 
TDI (mg kg −1 bw day −1 ) =  
 70 × UF 
Where: LD50 = lethal dose to 50% of the population (4,260 mg kg-1 bw day-l; Table 2.6);
70 = extrapolation factor from acute to chronic data (CCME, 1999); and,
UF = uncertainty factor (10; CCME, 1999).

Based on the acute to chronic extrapolation, the TDI for DIPA applicable to livestock is
6.1 mg kg-1 bw day-l. The chronic NOAEL reported by Yamamoto et al. (1989) was 391 mg kg-1
bw day-l which, after applying the 10-fold uncertainty factor recommended by CCME (1999),
yields a TDI of 39 mg kg-1 bw day-l. The TDI calculated using the acute to chronic extrapolation
method was an order of magnitude more protective and was used to develop the DIPA livestock
watering guideline.
The next step in the guideline derivation process was to calculate the reference concentration
(RC), which represents the livestock watering guideline. The reference concentration is
calculated using the body weight and water ingestion rate of particular species. Dairy cattle and
beef cattle were selected to represent livestock; deer were also considered to help assess possible
risks to other species. The equation used was:
 TDI × BW 
RC (mg L−1 ) =  
 WIR 
Where: TDI = tolerable daily intake for DIPA (6.1 mg kg –1 day-1; calculated above);
BW = body weight (862 kg for dairy cattle (CCME, 1999), 730 kg for beef cattle
(CCME, 1999), and 68 kg for deer (Smith, 1993); and,
WIR = daily water intake rate (137 L day-1 for dairy cattle, CCME (1999), data
for lactating cows at 21° C), 80 L day-1 for beef cattle (CCME, 1999), and
4.4 L day-1 for deer (Smith, 1993).
The RCs for dairy cattle, beef cattle, and deer were 38, 56, and 94 mg L-1 DIPA, respectively.
These values are recommend for the livestock watering guidelines (Table 3.1).
3.5 Source Water for Drinking
The generic scenario assumed to develop source water for drinking guidelines was the
“Agricultural Land Use” scenario defined by the Protocol. This scenario assumes a multi-
functional farm with a family with children resident on the property. The farm grows produce,
raises livestock, has a dairy herd and a large proportion of the produce (50%), meat (50%), and
milk (100%) consumed by the family is produced on the farm. It is assumed here that
groundwater is used for drinking water. For DIPA, the most sensitive human receptor would be
a child.
Humans could be exposed to DIPA in groundwater by (1) ingestion of drinking water and water
used for cooking and (2) dermal contact during bathing and washing. While individuals could be

exposed to DIPA in surface water through swimming and/or fishing, this exposure pathway will
be minimal relative to those noted above. A dermal contact check is provided to evaluate the
relative importance of this exposure pathway.
3.5.1 Tolerable Daily Intake (TDI)
The Protocol defines the Tolerable Daily Intake (TDI) as the intake to which it is believed a
receptor can be exposed over a lifetime without deleterious effects. The TDI represents the
combination of (1) real values for toxicological endpoints when no evidence of adverse effects
can be detected in experimental animals or humans and (2) safety factors that account for
anticipated differences between responses in the species tested and humans, sensitive individuals
in the human population, and other factors that contribute to the uncertainty of the toxicological
data.
The TDI is defined by the Protocol as:
 LOAEL or NOAEL 
TDI =  
 Safety Factor 
The conversion of toxicological data from the laboratory into values or rates of exposure
acceptable for human health assessment requires the introduction of safety factors. These factors
account for uncertainties that arise from differences between laboratory animals and humans,
sensitivity of populations, and experience. The introduction of safety factors is a concept that
has had wide acceptance in the scientific and regulatory communities around the world.
The Joint European Committee on Food Additives (JECFA) proposed principles for determining
a margin of safety, and has developed a methodology to establish an acceptable value for a factor
that would directly link animal toxicological data to human health and safety (FAO/WHO,
1958). The margin of safety allows for any interspecies differences in susceptibility, the
numerical differences between the test animals and the exposed human population, the greater
variety of complicating disease processes in the human population, the difficulty of estimating
the human intake, and the possibility of synergistic action. JECFA stated that the 100-fold
margin of safety applied to the maximum ineffective dosage (expressed in mg kg-1 body weight
day-1) was believed to be an adequate factor (FAO/WHO, 1958). The value of 100 has been
regarded as comprising two factors of ten to allow for interspecies and intraspecies variation
(WHO, 1994).
The validity and size of safety/uncertainty factors, and their application across many substances
including pesticides has undergone periodic reevaluation (Renwick and Lazarus, 1998). By and

large, the allocation of appropriate safety factors is considered on a case-by-case basis, relying
on analysis of the total weight of evidence including a consideration of data gaps (WHO, 1990).
WHO Scientific Groups have confirmed a 100-fold safety factor as an adequate and useful guide,
particularly when there are few toxicological data gaps (WHO, 1967; 1994).
The National Research Council report on Pesticides in the Diets of Infants and Children (NRC,
1993) indicated that the current 10-fold intraspecies factor is adequately protective of
socioeconomic, nutritional, and health status factors that influence the vulnerability of children
to environmental toxicants.
3.5.1.1 Human Tolerable Daily Intake (TDI)
The availability of toxicological data for DIPA would suggest that, for humans, application of a
10-fold safety factor for interspecies differences, and a 10-fold factor for variability in the
sensitivity of the human population is warranted. Because of the uncertainty associated with the
variable level of nitrite in the diet, and the possible endogenous production of genotoxic
substances, we recommend an additional five-fold safety factor to protect children and
developing infants (newborns and fetuses). Thus, a 500-fold safety factor was applied to the
Yamamoto et al. (1989) chronic NOAEL of 391 mg kg-1 bw day-1 to derive a tolerable daily
intake of 0.78 mg kg-1 bw day-1.
3.5.1.2 Bioavailability
Data were not available to derive an oral bioavailability factor for DIPA. As a result, a
bioavailability of 100% has been assumed for oral exposures. Dow (1985b) has established a
dermal bioavailability factor of 25%. This factor was used in guideline derivation.
3.5.2 Guideline Development
The absorbed dose from ingestion of DIPA in source water for drinking was calculated for
humans and livestock using (US EPA, 1989; CCME, 1996):
 C ⋅ IRW ⋅ BIOO ⋅ EF 
Dose (mg kg −1 bw day −1 ) =  W 
 BW ⋅ AT 
Where: CW = concentration of DIPA in water (mg L-1);

IRW = drinking water ingestion rate (0.6 L day-1 (child, 0.5 to 5 years) and
1.5 L day-1 (adult); CCME, 2000);
BIOO = oral bioavailability (1; assumed);

EF = exposure frequency (365 days; assumed);

BW = receptor body weight (16 kg (child, 0.5 to 5 years) and 70.7 kg (adult);
CCME, 2000); and,
AT = averaging time (365 days; assumed).
The above formula was re-arranged to yield the source water for drinking guidelines (US EPA,
1989; CCME, 1996):
 BW ⋅ TDI 
Drinking Water Guideline (mg ⋅ L−1 ) =  
 IRW ⋅ BIOO 
Where: BW = receptor body weight (16 kg (child, 0.5 to 5 years) and 70.7 kg (adult);
CCME, 2000);
TDI = tolerable daily intake (0.78 mg kg-1 bw day-1);
IRW = drinking water ingestion rate (0.6 L day-1 (child, 0.5 to 5 years) and
1.5 L day-1 (adult); CCME, 2000); and,
BIOO = oral bioavailability (1; assumed).
For a child and an adult, the proposed Interim source water for drinking guidelines are 21 mg L-1
and 37 mg L-1, respectively. The guideline protective of a child is reported in Table 3.1.
3.5.3 Dermal Contact Check
To determine if dermal contact was a significant exposure route relative to oral ingestion, dermal
exposure modelling was conducted following US EPA (1992, 1997). Dermal exposure
modelling is concerned with absorption and transport of chemicals through the outer skin layer
(stratum corneum) and into the viable epidermis. The stratum corneum is the primary barrier to
dermal absorption. This layer consists of a protein (keratin) and lipid matrix that channels
chemicals through transcellular (aqueous) and intercellular (lipid) pathways.
The absorbed dose from dermal contact with DIPA for a child during bathing was calculated
using (US EPA, 1992):
CW ⋅ SA ⋅ ET ⋅ PC ⋅ EF
Dose ( mg kg −1 bw day −1 ) =
BW ⋅ AT ⋅ 1000
Where: CW = concentration of DIPA in water (mg L-1);

SA = skin surface area exposed during bathing (7,640 cm2 95th percentile for
whole body for 3 to 4 year old child; US EPA, 1992);

ET = length of time the skin is in contact with water (0.5 hours day-1; assumed);
PC = chemical specific dermal permeability constant (0.0003 cm hour-1;
calculated);
EF = exposure frequency (365 days; assumed);
BW = receptor body weight (16 kg; CCME, 2000); and,
AT = averaging time (365 days; assumed).
The value of 1000 was used to convert from cm3 to L.
The chemical-specific dermal permeability constant (PC) for DIPA was estimated using
(US EPA, 1992):
Log PC (cm hour −1 ) = −2.72 + 0.71 log K OW − 0.0061 MW
Where: log Kow = n-octanol-water partition coefficient (-0.072, unitless); and,

MW = molecular weight (133.19 g mol-1).
Using the chemical/physical properties noted above (see also Table 2.2), the estimated dermal
permeability constant for DIPA was 0.0003 cm hour-1.
Assuming a DIPA concentration in water of 1 mg L-1, and assuming a 0.5-hour bath each day,
the calculated absorbed dermal dose for a child was 7 x 10-5 mg kg-1 bw day-1. The calculated
absorbed dose for a child drinking water was 0.038 mg kg-1 bw day-1, assuming 1 mg L-1 DIPA
concentration in the source water for drinking supply. Therefore, the dermal pathway accounts
for approximately 0.2% of the oral dose and can be safely ignored.
3.6 Data Gaps
The dataset for freshwater aquatic life was sufficient to derive Interim guidelines. For a Full
freshwater aquatic life guideline to be developed, the following additional studies would be
required:
• two chronic studies on freshwater fish species resident in North America;

• two chronic studies on two invertebrate species from different classes, one of which was a
planktonic species resident in North America (e.g., a daphnid); and,
• one study on a freshwater vascular plant or algal species resident in North America.
All the studies for a Full guideline must be of Primary data quality.

3.6.2 Marine Aquatic Life
The dataset for marine aquatic life guideline was not sufficient to derive Interim guidelines. The
following additional toxicity tests would be required:
• two acute or chronic studies on different marine fish species, including one temperate
species; and,
• two acute or chronic studies on temperate marine invertebrate species from two different
classes.
For a Full marine guideline to be developed, the following additional studies would be required:
• three studies on three species of temperate marine fish of which at least two are chronic;
• two chronic studies on two temperate marine invertebrate species from different classes; and,
• one study on a temperate marine vascular plant or algal species.
All the studies for a Full guideline must be of Primary data quality.
3.6.3 Irrigation
Sufficient data were available to meet the requirements for the Interim irrigation guideline.
3.6.4 Livestock Watering
To comply with the requirements of the Protocol for an Interim livestock watering guideline, the
following additional studies would be required:
• two acute or chronic studies on mammalian species raised in Canada, of which one is a
livestock species; and,
• one acute or chronic study on an avian livestock species.
In spite of this deficiency, a Preliminary livestock watering guideline was derived, based on
laboratory animal studies.
3.6.5 Source Water for Drinking
Sufficient data were available to calculate the Interim source water for drinking guideline for
DIPA.

3.7 Summary of Water Quality Guidelines
Water quality guidelines were calculated for four water uses: freshwater aquatic life, irrigation,
livestock watering, and source water for drinking. The recommended guidelines are summarized
in Table 3.1.
The Interim guideline for freshwater aquatic life was calculated to be 1.6 mg L-1.
3.7.2 Marine Life
A guideline for marine life could not be developed due to insufficient data quality and data
quantity.
3.7.3 Irrigation
Four guidelines were calculated for irrigation. Based on the Protocol, Interim guidelines were
calculated for 1) cereals, tame hays, and pasture crops, and 2) other crops. For each of these two
groups of plants, guidelines were calculated for two soil types: loam and poor soil. The
guideline for cereals, tame hays, and pasture crops was 91 mg L-1 (loam) and 78 mg L-1 (poor
soil). For other crops it was 36 mg L-1 (loam), and 3.9 mg L-1 (poor soil).
3.7.4 Livestock Watering
Preliminary guidelines for livestock watering were calculated for dairy cattle and beef cattle, to
represent likely agricultural animals. In addition, a Preliminary guideline was calculated for
deer, to assist in evaluating possible risks to other species. The most sensitive species was the
dairy cow, for which a guideline of 38 mg L-1 was calculated. The reason for the difference in
sensitivity between life stages or species is related to how water consumption relates to body
weight. In a situation where water was being used for the consumption of a single livestock
species other than cattle, typical water ingestion rates and body weight could be used to calculate
a species-specific guideline. It should be noted that this guideline was based on studies on
laboratory animals using appropriate safety factors, and no toxicological information was
available for either a mammalian or avian livestock species. Should sufficient data become
available in the future, this guideline could be refined.

3.7.5 Source Water for Drinking
Interim source water for drinking guidelines were calculated for children (21 mg L-1) and adults
(37 mg L-1). If further mammalian toxicological studies become available in the future, this
guideline could be refined.
4. CLOSURE
The information presented in this report was produced exclusively for the purposes stated in the
Scope of Work. Komex International Ltd. provided this groundwater derivation document for
British Columbia Ministry of Water, Land and Air Protection, solely for the purpose noted
above, and does not accept any responsibility for the use of this report for any purpose other than
intended or to any third party.
Komex International Ltd. has exercised reasonable skill, care, and diligence to assess the
information acquired during the preparation of this report. The methodology used deriving the
guidelines in this report is based on current regulatory protocols and current understanding of
biological systems, mechanisms of exposure, and toxicological properties of chemicals.
Questions concerning the derivation or use of the guidelines in this report should be directed to
Dr. James H. Sevigny, Mr. Miles Tindal, or Ms. Adele Houston.

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J:\50560000\BCMELP REVISIONS\DIPA WATER GUIDELINES 6 AUGUST 2003.DOC

TABLES
Table 2.1. Common Synonyms and Trade Names for Diisopropanolamine
Synonyms
Bis(2-hydroxypropyl)amine 1,1’-Iminodi-2-propanol
Bis(2-propanol)amine 1,1’-Iminodipropan-2-ol
DIPA 2-Propanol, 1,1’iminobis-
Dipropyl-2,2-dihydroxy-amine 2-Propanol, 1,1’-iminodi-
1,1’-Iminobis(2-propanol)
Source: NIST Chemistry WebBook (2000)
J:\50560000\BCMELP Revisions\DIPA Water Quality Tables 10 June 2003.doc

Table 2.2. Physical and Chemical Properties for Diisopropanolamine
Property Value Units Reference
CAS registry number 110-97-4 -

Molecular formula C6H15NO2 - Lide (1996)
Molecular weight 133.19 g/mole Lide (1996)
Melting point 44 ºC Kirk-Othmer (1999)
Boiling point 249 ºC Kirk-Othmer (1999)
Specific gravity
20º C (DIPA) /4º C (Water) 1.004 - Aldrich (1990)
40º C (DIPA) /4º C (Water) 0.992 - Dow (1999)
Flashpoint 126 (closed up) ºC Lenga, 1985
3
Density at 25º C 0.989 g/cm Lide (1996)
Vapour density (air=1) 4.6 g/L Verschueren (1996)
Vapour pressure
42º C 0.02 mm Hg Verschueren (1996)
50º C 0.035 mm Hg Dow (1999)
100º C 3 hPA Verschueren (1996)
n-Octanol-water partition coefficient (Kow) -0.072 log Dow (1995)
Organic carbon partition coefficient (Koc) 21.77 log Dow (1995)
-7 3
Henry’s law constant 1.72 x 10 atm x m /mol Dow (1995)
Solubility in water
25º C 1,200 g/100g Kirk-Othmer (1999)
25º C 870 g/L Verschueren (1996)
Water soil partition coefficient (Kd)
montmorillonite 16-42 L/kg Luther et al. (1998)
kaolinite 3.5 L/kg Luther et al. (1998)
humus-rich soil 2.0 L/kg Luther et al. (1998)
low carbon content surface soils 0.73 - 4.0 L/kg Luther et al. (1998)
till 3.2 L/kg Luther et al. (1998)
sandstone, shale/sandstone 0.54 - 1.1 L/kg Luther et al. (1998)
pKa 8.88 -log K Kim et al. (1987)
Viscosity
30º C 870 centipoise Sorensen et al. (1996)
54º C 86 centipoise Kirk-Othmer (1999)

Table 2.3. Biodegradation Studies for Diisopropanolamine
Biodegradation
Study Concentration (1) Microcosm Material Conditions Nutrients Temperature Lag Time
Rate
(mg L-1) (° C) (days) (mg L-1 day-1)
Salanitro and Langston (1988) 75 Sandy loam aerobic N, P 10 7 to 14 10 (2)

Chong (1994) 260 Activated sludge aerobic N, P 25 6 70
Gieg et al. (1998) 200 Sandstone aerobic N, P 8 na 6.3 (2)
Gieg et al. (1998) 200 Sandstone aerobic N, P 28 na 2.7 (2)
Gieg et al. (1998) 200 Till aerobic N, P 8 na 1.5 (2)
Gieg et al. (1998) 200 Sand aerobic N, P 8 na 1.7 (2)
Gieg et al. (1998) 200 Sand aerobic N, P 28 na 0.6 (2)
Greene et al. (1999) (3) 490 Till aerobic none 8 220 0
(3)
Greene et al. (1999) 490 Till aerobic P 8 na 5.3
(3)
Greene et al. (1999) 680 Till aerobic none 8 220 0
(3)
Greene et al. (1999) 680 Till aerobic P 8 15 3.6
(3)
Greene et al. (1999) 0.0024 Wetland sediment aerobic none 8 <1 1.4
(3)
Greene et al. (1999) 0.013 Wetland sediment aerobic none 8 14 0.5
(1) = minimum concentration reported. (2) = reported at half-life in days. (3)= data reported for 2.5 L microcosms. na = not available.
Nutrients: N = nitrogen; P = phosphorous

Table 2.4. Toxicity of Diisopropanolamine to Terrestrial Plants
Species Scientific Name Endpoint Soil Type NOEC LOEC EC25 EC50 Reference
(mg kg-1) (mg kg-1) (mg kg-1) (mg kg-1)
Lettuce Lactuca sativa root elongation Till 140 na na 600 Komex (1999)
Lettuce Lactuca sativa germination Till 6,300 na na 9,400 Komex (1999)
Lettuce Lactuca sativa emergence Artificial 1,750 3,490 1,310 3,840 CAPP (2001)
Lettuce Lactuca sativa emergence Loam 10,400 20,800 15,400 20,400 CAPP (2001)
Lettuce Lactuca sativa emergence Sand 1,700 3,390 1,700 2,260 CAPP (2001)
Lettuce Lactuca sativa emergence Till 3,480 6,970 4,830 6,210 CAPP (2001)
Lettuce Lactuca sativa biomass Artificial 3,490 6,980 4,530 >6,980 CAPP (2001)
Lettuce Lactuca sativa biomass Loam 10,400 20,800 15,800 >20,800 CAPP (2001)
Lettuce Lactuca sativa biomass Sand 1,700 >1,700 >1,700 >1,700 CAPP (2001)
Lettuce Lactuca sativa biomass Till 3,480 6,970 810 5,480 CAPP (2001)
Lettuce Lactuca sativa root length Artificial 873 1,750 1,220 3,750 CAPP (2001)
Lettuce Lactuca sativa root length Loam 2,600 5,200 5,660 14,000 CAPP (2001)
Lettuce Lactuca sativa root length Sand 212 424 635 1,391 CAPP (2001)
Lettuce Lactuca sativa root length Till 1,740 3,480 2,100 2,930 CAPP (2001)
Lettuce Lactuca sativa shoot length Artificial 3,490 6,980 5,820 >6,980 CAPP (2001)
Lettuce Lactuca sativa shoot length Loam 20,800 >20,800 >20,800 >20,800 CAPP (2001)
Lettuce Lactuca sativa shoot length Sand 1,700 >1,700 >1,700 >1,700 CAPP (2001)
Lettuce Lactuca sativa shoot length Till 3,480 6,970 5,230 >6,970 CAPP (2001)
Minimum Toxicity Values for Lettuce 140 424 635 600

na = not available
Page 1 of 4
Table 2.4. Toxicity of Diisopropanolamine to Terrestrial Plants (Cont’d)

Carrot Daucus carota emergence Artificial 3,490 6,980 4,280 6,980 CAPP (2001)
Carrot Daucus carota emergence Loam 5,460 10,900 8,700 24,600 CAPP (2001)
Carrot Daucus carota emergence Sand 1,700 3,390 2,280 2,870 CAPP (2001)
Carrot Daucus carota emergence Till 3,480 6,970 4,290 5,180 CAPP (2001)
Carrot Daucus carota biomass Artificial 6,980 >6,980 >6,980 >6,980 CAPP (2001)
Carrot Daucus carota biomass Loam 21,900 >21,900 >21,900 >21,900 CAPP (2001)
Carrot Daucus carota biomass Sand 3,390 >3,390 >3,390 >3,390 CAPP (2001)
Carrot Daucus carota biomass Till 3,480 >3,480 >3,480 >3,480 CAPP (2001)
Carrot Daucus carota root length Artificial 873 1,750 1,880 3,670 CAPP (2001)
Carrot Daucus carota root length Loam 5,460 10,900 8,510 12,000 CAPP (2001)
Carrot Daucus carota root length Sand 212 424 355 1,810 CAPP (2001)
Carrot Daucus carota root length Till 1,710 3,480 2,050 >3,480 CAPP (2001)
Carrot Daucus carota shoot length Artificial 3,490 6,980 4,890 >9,890 CAPP (2001)
Carrot Daucus carota shoot length Loam 10,900 21,900 17,000 >21,900 CAPP (2001)
Carrot Daucus carota shoot length Sand 1,700 3,390 2,140 3,360 CAPP (2001)
Carrot Daucus carota shoot length Till 3,480 >3,480 >3,480 >3,480 CAPP (2001)
Minimum Toxicity Values for Carrot 212 424 355 1,810

na = not available
Page 2 of 4

Alfalfa Medicago sativa emergence Artificial 6,980 14,000 7,310 9,540 CAPP (2001)
Alfalfa Medicago sativa emergence Loam 10,400 20,800 14,300 20,400 CAPP (2001)
Alfalfa Medicago sativa emergence Sand 1,700 3,390 2,000 2,460 CAPP (2001)
Alfalfa Medicago sativa emergence Till 3,480 6,970 3,620 4,740 CAPP (2001)
Alfalfa Medicago sativa biomass Artificial 6,980 >6,980 >6,980 >6,980 CAPP (2001)
Alfalfa Medicago sativa biomass Loam 10,400 20,800 14,200 >20,800 CAPP (2001)
Alfalfa Medicago sativa biomass Sand 1,700 >1,700 >1,700 >1,700 CAPP (2001)
Alfalfa Medicago sativa biomass Till 3,480 6,970 810 5,480 CAPP (2001)
Alfalfa Medicago sativa root length Artificial 873 1,750 1,590 2,780 CAPP (2001)
Alfalfa Medicago sativa root length Loam 650 1,300 1,580 9,240 CAPP (2001)
Alfalfa Medicago sativa root length Sand 424 848 718 >1,700 CAPP (2001)
Alfalfa Medicago sativa root length Till 871 1,740 1,410 2,780 CAPP (2001)
Alfalfa Medicago sativa shoot length Artificial 1,750 3,490 4,760 >6,980 CAPP (2001)
Alfalfa Medicago sativa shoot length Loam 20,800 >20,800 17,800 >20,800 CAPP (2001)
Alfalfa Medicago sativa shoot length Sand 1,700 >1,700 >1,700 >1,700 CAPP (2001)
Alfalfa Medicago sativa shoot length Till 3,480 >3,480 >3,480 >3,480 CAPP (2001)
Minimum Toxicity Values for Alfalfa 424 848 718 >1,700

na = not available
Page 3 of 4

Timothy Phleum pratense emergence Artificial 3,490 6,980 5,850 8,430 CAPP (2001)
Timothy Phleum pratense emergence Loam 21,900 43,700 25,600 32,200 CAPP (2001)
Timothy Phleum pratense emergence Sand 1,700 3,390 2,340 2,980 CAPP (2001)
Timothy Phleum pratense emergence Till 3,480 6,970 6,530 9,070 CAPP (2001)
Timothy Phleum pratense biomass Artificial 1,750 3,490 1,950 3,230 CAPP (2001)
Timothy Phleum pratense biomass Loam 10,900 21,900 9,680 >43,700 CAPP (2001)
Timothy Phleum pratense biomass Sand 424 847 606 1,680 CAPP (2001)
Timothy Phleum pratense biomass Till 6,970 >6,970 >6,970 >6,970 CAPP (2001)
Timothy Phleum pratense root length Artificial 1,750 3,490 4,080 5,290 CAPP (2001)
Timothy Phleum pratense root length Loam 10,900 21,900 1,820 20,900 CAPP (2001)
Timothy Phleum pratense root length Sand 424 874 1,590 2,260 CAPP (2001)
Timothy Phleum pratense root length Till na na na na CAPP (2001)
Timothy Phleum pratense shoot length Artificial 1,750 3,490 3,830 5,700 CAPP (2001)
Timothy Phleum pratense shoot length Loam 10,900 21,900 15,200 19,600 CAPP (2001)
Timothy Phleum pratense shoot length Sand 847 1,700 1,870 2,790 CAPP (2001)
Timothy Phleum pratense shoot length Till 3,480 6,970 4,490 6,090 CAPP (2001)
Minimum Toxicity Values for Timothy 424 874 606 1,680

na = not available
Page 4 of 4
Table 2.5. Toxicity of Diisopropanolamine to Aquatic Species
Type of Study
Type of Biota
Experimental
Temperature
Reference
Acceptable?
LC50/EC50
Common
Endpoint
Duration
Species
NOEC
LOEC
Name
Analysis?
Hardness
Chemical
Controls
Protocol
Design
DO
pH
(mg L-1) (mg L-1) (mg L-1) (mg L-1) (mg L-1)
Primary Freshwater Data
acute vertebrate rainbow trout Oncorhynchus mykiss 96 hours survival 7,698 15±1 7.5 na 255 S Y S ECP CAPP, 2001
acute vertebrate rainbow trout Oncorhynchus mykiss 96 hours survival 4,940 15±1 8.5 na 255 S Y S ECP CAPP, 2001
acute invertebrate sideswimmer Hyalella azteca 96 hours survival 1,128 23±1 7.5 na 255 S Y S (ECP) CAPP, 2001
acute invertebrate sideswimmer Hyalella azteca 96 hours survival 848 23±1 8.5 na 255 S Y S (ECP) CAPP, 2001
Secondary Freshwater Data
acute vertebrate fathead minnow Pimephales promelas 7 days survival 1,000 >1,000 >1,000 25 8 5.3-8.0 na S N S ECP ERAC, 1998
acute vertebrate fathead minnow Pimephales promelas 7 days growth 500 1,000 >1,000 25 8 5.3-8.0 na S N S ECP ERAC, 1998
acute vertebrate fathead minnow Pimephales promelas 7 days survival 500 1,000 788 25 >9 5.0-8.7 na S N S ECP ERAC, 1998
acute vertebrate fathead minnow Pimephales promelas 7 days growth 500 1,000 >1,000 25 >9 5.0-8.7 na S N S ECP ERAC, 1998
acute invertebrate daphnid Daphnia magna 48 hours survival - - 441 na 8 na na S N S ECP ERAC, 1998
acute invertebrate daphnid Daphnia magna 48 hours survival - - 289 na >9 na na S N S ECP ERAC, 1998
chronic invertebrate daphnid Ceriodaphnia dubia 7 days survival 125 250 188 25 8 6.3-9.2 na S N S ECP ERAC, 1998
chronic invertebrate daphnid Ceriodaphnia dubia 7 days reproduction <31 31 164 25 8 6.3-9.2 na S N S ECP ERAC, 1998
chronic invertebrate daphnid Ceriodaphnia dubia 7 days survival 125 250 180 25 >9 6.9-8.1 na S N S ECP ERAC, 1998
chronic invertebrate daphnid Ceriodaphnia dubia 7 days reproduction 125 250 179 25 >9 6.9-8.1 na S N S ECP ERAC, 1998
chronic plant/alga green alga Selenastrum capricornutum 72 hours growth 31 63 74 na 8 na na S N S ECP ERAC, 1998
chronic plant/alga green alga Selenastrum capricornutum 72 hours growth 7.8 16 63 na >9 na na S N S ECP ERAC, 1998
Unacceptable Freshwater Data
acute vertebrate clawed toad Xenopus laevis 48 hours survival - - 410 na na na na na na na na De Zwart and Sloof, 1987
acute vertebrate goldfish Carassius auratus 24 hours survival - - 1,100 na 9.7 na na na na na na Bridie et al 1979b
acute vertebrate goldfish Carassius auratus 24 hours survival - - >5,000 na 7.0 na na na na na na Bridie et al 1979b
acute vertebrate ide Leuciscus idus 96 hours survival 460 - - na 8.0 na na na na na na BASF AG, 1987a
acute vertebrate ide Leuciscus idus 48 hours survival 1,000 - - na na na na na na na na Huels AG, 1992
acute vertebrate mosquitofish Gambusia sp. 48 hours survival - - 1,350 na na na na na na na na Exxon, 1986
acute vertebrate mosquitofish Gambusia sp. 96 hours survival - - 1,350 na na na na na na na na Exxon, 1986
acute vertebrate stickleback na 48 hours survival - - 42 na na na na na na na na Exxon, 1986
acute vertebrate stickleback na 96 hours survival - - 42 na na na na na na na na Exxon, 1986
acute invertebrate daphnid Daphnia magna 48 hours survival - - 278 na 7.9 na na na na na na BASF AG, 1987b
acute invertebrate daphnid Daphnia magna 24 hours survival - - 354 na 7.9 na na na na na na BASF AG, 1987b
chronic plant/alga duckweed Lemna minor 4-7 days growth - - 1,500-2,300 na na na na na na na na SRC, 1994
chronic plant/alga green alga Scenedesmus suspicatus 72 hours survival - - 270 na 8.4 na na na na na na BASF AG, 1988
14
chronic plant/alga green alga Selenastrum capricornutum 24 hours C uptake - - 170 na na na na na na na na SRC, 1994
chronic plant/alga green alga Selenastrum capricornutum 72-96 biomass - - 7-30 na na na na na na na na SRC, 1994
hours
14
chronic other cyanobacteria Aphanizomenaon flos-aquae 24 hours C uptake - - 130 na na na na na na na na SRC, 1994
chronic other cyanobacteria Aphanizomenaon flos-aquae 24 hours nitrogen fixation - - 150-200 na na na na na na na na SRC, 1994
14
chronic other diatom Cyclotella meneghiana 24 hours C uptake - - 110 na na na na na na na na SRC, 1994
Unacceptable Marine Data
acute other bacterium (microtox) Vibrio fischerii na luminescence - - 50-60 na na na na na na na na SRC, 1994
acute other bacterium (microtox) Vibrio fischerii 15 minutes luminescence - - 9,202 na 8 na na na na na na ERAC, 1998
acute other bacterium (microtox) Vibrio fischerii 15 minutes luminescence - - 86 na >9 na na na na na na ERAC, 1998
Notes:
General: - = no data or not applicable; na = not available.
Chemical Analysis?: Y = yes; N = no
Controls Acceptable?: S = satisfactory; U = unsatisfactory.
Experimental Design: F = flow through; R = renewal; S = static.
Protocol: ECP = Environment Canada Protocol; (ECP) = Modified Environment Canada Protocol.
J:\50560000\BCMELP Revisions\DIPA Aquatic Tox Table 10 June 2003.doc

Table 2.6. Toxicity of Diisopropanolamine to Mammalian Species
Type of Exposure Mode of Carrier Test Animal Dosage Units Duration Effect Reference
Study Route Administration
Primary Data
acute oral ? ? Rat 6,720 mg kg-1 bw 1 dose LD50 NIOSH UB6600000
acute oral ? ? Rat 5,660 mg kg-1 bw 1 dose LD50 Toropkov (1980b)
acute oral gavage? water Rat 3,980 mg kg-1 bw 1 dose LD100 Dow (1954)
acute oral gavage? water Rat 2,000 mg kg-1 bw 1 dose LD0 Dow (1954)
acute oral ? ? Mouse 2,120 mg kg-1 bw 1 dose LD50 Toropkov (1980b)
acute oral ? ? Guinea pig 2,800 mg kg-1 bw 1 dose LD50 Toropkov (1980b)
acute oral ? ? Rat 5,000 mg kg-1 bw day-1 7 days NOAEL BIBRA (1991)
acute oral gavage sunscreen Rat 5,000 mg kg-1 bw 1 dose LD50 Biosearch (1981a)
(Albino)
acute oral gavage sunscreen Rat 5,000 mg kg-1 bw 1 dose NOAEL (mortality) Springborn (1982a)
(Sprague Dawley)
subchronic oral ad libitum water Rat 3,000 mg kg-1 bw day-1 2 weeks 2 of 5 males died, significant weight loss, reduction in body fat, organ sizes Dow (1984)
(CFD Fischer 344) and weights, and altered clinical biochemical parameters, decrease in food
and water consumption, acute inflammation and degeneration of kidney and
urinary bladder, generalized liver atrophy
subchronic oral ad libitum water Rat 1,200 mg kg-1 bw day-1 2 weeks Decrease in food and water consumption, weight loss in males, increased Dow (1984)
(CFD Fischer 344) kidney weight relative to control, acute inflammation and degeneration of
kidney and urinary bladder in only one animal (the other animals had no
treatment related effects in the organs examined)
subchronic oral ad libitum water Rat 600 mg kg-1 bw day-1 2 weeks NOAEL (activity, physical characteristics, gross pathology, organ weight, Dow (1984)
(CFD Fischer 344) histology of liver, kidney, and urinary bladder)
subchronic oral ? ? Guinea pig 0.22 mg kg-1 bw day-1 ? NOAEL (toxic effects) Toropkov (1980b)
chronic oral ad libitum food Rat 391 ± 35 mg kg-1 bw day-1 94 weeks NOAEL (no carcinogenic effects in nasal cavity, lung oesophagus, liver, Konishi et al. (1991)
(Wistar) urinary bladder, or kidney) Yamamato et al. (1989)
chronic oral ad libitum food Rat 448 ± 36 mg kg-1 bw day-1 94 weeks Carcinogenic effects in nasal cavity, lung oesophagus, liver, urinary bladder, Yamamato et al. (1989)
(nitrite in (Wistar) (DIPA) and kidney)
drinking water) 151 ± 16
(nitrite)
Secondary Data
acute dermal ? ? Rabbit 8,000 mg kg-1 bw 1 dose LD50 Union Carbide (1973)
Unacceptable Data
acute oral ? ? Rat 0.055 mg kg-1 bw day-1 7 days NOAEL (reproductive effects) BIBRA (1991)
acute dermal direct application to undiluted DIPA Rabbit 100 % ? Moderate hyperemia to severe necrosis Dow (1954)
intact skin (abdomen)
acute dermal direct application to undiluted DIPA Rabbit 100 % ? Slight hyperemia, oedema, and moderate denaturation Dow (1954)
abraded skin (abdomen)
acute dermal direct application to water Rabbit 10 % ? NOAEL for dermal effects Dow (1954)
intact skin (ears)
acute dermal direct application to water Rabbit 10 % ? Moderate hyperemia and blistering, oedema, and moderate denaturation Dow (1954)
intact skin (abdomen)
acute dermal direct application to water Rabbit 10 % ? Moderate hyperemia and blistering, oedema, and moderate denaturation Dow (1954)
abraded skin (abdomen)
acute dermal direct application to skin sunscreen Rabbit 1 % 1 dose Mild primary irritation Springborn (1982b)
(New Zealand) (0.2 mL)
acute ocular direct application to eye undiluted DIPA Rabbit 50 mg 1 dose Burns on eyelid, eyeball and corneal mucosa Toropkov (1980a)
acute ocular direct application to eye sunscreen Rabbit 1 % 7 days NOAEL (ocular irritation) Biosearch (1981b)
(Albino)
acute ocular direct application to eye sunscreen Rabbit 1 % 7 days NOAEL (ocular irritation) Springborn (1982c)
(Albino)
subchronic oral ad libitum food Rat 1 % Age 6 to NOAEL renal toxicity Konishi et al. (1991)
(Wistar) 24 weeks
? = data not available in CAPP (2001).

Table 3.1. Water Quality Guidelines for Diisopropanolamine
Water Use
Freshwater Aquatic Life Marine Life Irrigation Livestock Watering Source Water for Drinking
-1 -1 -1 -1
(mg L ) (mg L ) (mg L ) (mg L ) (mg L-1)
1.6 - 3.9 38 (2) 21
Limiting Guideline
Guidelines 1.6 - Loam: 38 (dairy cattle) 21
91 (tame hay, cereal, 56 (beef cattle)
pasture)
36 (other crops) 94 (deer)
Poor soil (1):

78 (tame hay, cereal,
pasture)
3.9 (other crops)
Guideline Status Interim Not Available Interim Preliminary (2) n/a
(1) The “poor soil” guideline is calculated using the species/endpoint/soil type combination that yielded the lowest guideline (see text). In practice, “poor soil” is either till or sand. The “poor soil”
guideline is protective of plants growing in all soil types.
(2) Insufficient data to satisfy Protocol requirements for an Interim guideline. Guideline generated from mean LC50 value of 16 data points included in 3 studies using 4 routes of administration on
4 species of laboratory animals. Guideline is designated “Preliminary”.

Water Quality Guidelines For Diisopropanolamine (Dipa)

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Water Quality Guidelines For Diisopropanolamine (Dipa)

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SUITE 100, 4500 – 16 AVENUE N.W.

WATER QUALITY GUIDELINES FOR

C52330100 6 August 2003

Available on the Internet.

1. Water quality – Standards - British Columbia.

TD226.B7W37 2003 363.739’462’09711 C2003-960264-8

Table 2.1 Common Synonyms and Trade Names for Diisopropanolamine

Diisopropanolamine (DIPA) is an organic chemical used for a wide variety of commercial,

Diisopropanolamine Water Quality Guidelines

Source Water for Drinking

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Freshwater Aquatic Life

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1.1 Scope of Work

• review and summarize relevant available background information on DIPA;

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1.4 Toxicity Data

2.1 Physical and Chemical Properties

DIPA belongs to the group of alkanolamines. Alkanolamines are organic derivatives of

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2.2 Analytical Methods

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2.3 Production and Uses

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2.3.2.1 Gas Treating

2.3.2.2 Cosmetics and Personal Care Products

2.3.2.3 Detergents and Cleaners

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2.3.2.4 Metal Working Fluids

In metal-coating preparations, alkanolamines (including DIPA) are used as metal-complexing

2.3.2.6 Corrosion Inhibitors

2.3.2.7 Cement Applications

2.3.2.8 Miscellaneous Uses

2.4 Levels in the Canadian Environment

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2.5 Existing Guidelines and Criteria in Various Media

2.6 Environmental Fate and Behavior

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2.6.1 Adsorption and Mobility

2.6.2 Aqueous-Phase Solubility

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2.6.3 Leaching and Lateral Movement

In recent studies, DIPA biodegradation using nutrient-amended and -unamended microcosms,

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No information on the susceptibility of DIPA to phototransformation reactions was available at

2.7 Behavior and Effects in Terrestrial Biota

2.7.1 Terrestrial Plants

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2.8 Behavior and Effects in Aquatic Biota

2.8.1 Freshwater Aquatic Life

2.8.1.1 Aquatic Vertebrates

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2.8.1.2 Aquatic Invertebrates

2.8.1.3 Aquatic Plants

2.8.1.4 Other Aquatic Biota

2.8.2 Marine Life

2.8.2.1 Marine Vertebrates

Literature data were not available for marine vertebrates

2.8.2.2 Marine Invertebrates

Literature data were not available for marine invertebrates

2.8.2.3 Marine Plants

Literature data were not available for marine plants

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2.8.2.4 Other Marine Biota

2.9 Behavior and Effects in Mammalian Species and Humans

2.9.1 Mammalian Species

2.9.1.1 Acute Toxicity Studies

Dermal and Ocular Studies

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2.9.1.2 Subchronic Toxicity Studies

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2.9.1.3 Chronic Toxicity and Oncogenicity Studies

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2.9.1.4 Genetic Toxicology Studies