TOXICITY OF NEODOL<"> SURFACTANTS
by
Anna S. Mammons
C. Donald Powers
Science Applications International Corporation
Oak Ridge, TN 37831
May 1987
Prepared for
Office of Toxic Substances
U.S. Environmental Protection Agency
Washington, DC 20460
Task Officer
Terry O'Bryan
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TABLE OF CONTENTS
1.0 INTRODUCTION 1
2.0 DESCRIPTION OF NEODOlW PRODUCTS 2
2.1 NEODOL Alcohols 2
2.2 NEODOL Ethoxylates 2
2.3 NEODOL Sulfates 3
2.4 NEODOL Ethoxysulfates 4
3.0 EFFECTS ON NON-MAMMALIAN ORGANISMS 5
3.1 Acute Effects LCcn 5
3.1.1 Alcohols 5
3.1.2 Alcohol Ethoxylates 7
3.1.3 Alcohol Sulfates 7
3.1.4 Alcohol Ethoxysulfates 8
3.2 Sublethal Effects 9
3.2.1 Aquatic Animals 9
3.2.2 Plants 10
3.3 Chronic Effects 12
4.0 ENVIRONMENTAL FACTORS INFLUENCING AQUATIC TOXICITY 13
4.1 Water Hardness 13
4.2 Biodegradablllty 13
4.3 Exposure 14
5.0 MAMMALIAN TOXICITY 15
5.1 Acute Effects 15
5.2 Subchronic Effects 16
5.3 Chronic Effects 17
5.4 Carclnogenlcity 17
5.5 Mutagenldty 18
5.6 Teratogenlcity/Reproduction 18
5.7 Studies In Humans 19
11
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TABLE OF CONTENTS
5.8 Metabolism jg
6.0 CONCLUSIONS 20
6.1 Toxicity to Non-Mammalian Organisms 20
6.2 Mammalian Toxicity 21
6.3 1,4-Dioxane Contamination 25
7.0 REFERENCES 26
APPENDIX A - Acute Toxicity (LC50) of Alcohol
Surfactants to Aquatic Animals 38
iii
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LIST OF TABLES
Table 1 General direction of toxicity and rate of bio-
degradation of linear primary alcohols and deriva-
tive surfactants in an aquatic environment as a
function of alkyl or ethoxylate (EO) chain length ... 6
Table 2 Effects of NEODOl products in laboratory mammals .... 22
iv
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TOXICITY OF NEODOL(R) SURFACTANTS
1.0 INTRODUCTION
This report is the result of Work Assignment #3 of IAG #DW-89930405.
Toxicity data from a voluntary submission (FYI-AX-0685-0410 Sequence A) by
Shell Chemical Company to EPA's TSCA Existing Chemicals Program and two
published reports by Arthur D. Little, Inc. ("Human Safety and Environmental
Aspects of Major Surfactants," May, 1977; "Supplement," by Goyer et al.
February, 1981) were reviewed to evaluate the toxicity and structure-activity
relationships of NEODOlW chemicals for which data are available and to
identify gaps in the toxicity database. TSCA 8(e) submission 8EHQ-0580-0326
Sequence C was also reviewed for its applicability to NEODOL toxicity.
Today's dishwashing and laundry agents are superior to those of the past
because they thoroughly clean man-made fibers, tolerate hard water, form
little foam, and are readily biodegraded. These improvements are due largely
to the extensive use of three classes of surfactants (NEODOL products) in
cleaning formulations. Derived from primary alcohols, these compounds are
classified according to the chemical group(s) attached to the alkyl chain:
alkyl sulfates, if sulfated; alkyl or alcohol ethoxylates, if ethylene oxides
are present; and alkyl or alcohol ethoxysulfates, if ethylene oxides are
sulfated.
In addition to the widespread use of NEODOL products as household
cleaning agents (primarily the ethoxysulfates), they are extensively used in
personal care products such as shampoos, bubble baths, and cosmetics, and also
have many industrial applications. NEODOL ethoxylates are also used as
analgesic.s and anesthetics. While recent product/consumption figures have not
been provided, a review of the values reported by Arthur D. Little (1977,
Goyer et al. 1981) indicates the considerable use of these surface-active
agents. Comparing data from 1973 and 1978, annual use of ethoxylates in the
United States increased from 188,000 tons to 238,000 tons during the five-year
period. Similarly, the use of ethoxysulfates rose from 53,000 tons to 64,000
tons during those same years. As for alkyl sul fates, 90,000 tons were used
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worldwide in 1976. Shell Chemical Company is the world's largest producer of
linear primary alcohols and alcohol-based surfactants, exceeding 450 million
pounds per year in the United States. In England and Japan certain NEODOL
products are produced under the name DOBONOl(R).
2.0 DESCRIPTION OF NEODOl(R) PRODUCTS
NEODOL products include:
o NEODOL alcohols (ROH)
o NEODOL ethoxylates [RO(CH2CH20)XH]
o NEODOL sulfates (ROS03-Na+ or NH4+)
o NEODOL ethoxysulfates [RO(CH2CH20)xS03-Na+ or NH4+]
2.1 NEODOL Alcohols
Linear primary alcohols (ROH) included in NEODOL products consist
essentially of two groups: chains of Cg to GU carbon atoms and chains of q2
to C15 carbon atoms. Nomenclature is based on the length of the alkyl chain.
For example, NEODOL 91 indicates that this product is a mixture of mostly Cg
to Cn alcohols; NEODOL 25 is a mixture of mostly C12 - Ci5 alcohols (Shell b,
P. 1).
2.2 NEODOL Ethoxvlates
NEODOL ethoxylates are mainly produced from the reaction of ethylene
oxide (CH2CH20 or EO) with linear primary alcohols, although some branched-
chain alcohols are used (Satkowski et al. 1967, as reported in Arthur D.
Little, Inc. 1977, p. 240).
Examples:
Primary
CH3-(CH2)X CH2-0-(CH2-CH2-0)yH
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Secondary
CH3-(CH2)z-CH-(CH2)ziCH3
0-(CH2-CH2-0)yH
x - usually 05 to Cje
y - usually £63 to E02Q
z + zj - usually €5 to
NEODOL 25-3 or Cj2-l5 ^03 indicates that the product is comprised mostly
of Cj2 to Cj5 alcohols reacted with an average of 3 molecules of EO to form a
3-unit EO chain (Shell b, p. 2).
2.3 NEODOL Sul fates
NEODOL sul fates (alcohol or alkyl sul fates or AS) are produced by
sulfation of the parent alcohol with either sulfur trioxide or chlorosulfonic
acid and subsequent neutralization of the product with an appropriate base as
follows:
S03 or NaOH
R-OH ....... > R-OS03-H+ ...... > R-OS03'Na+
C1S03H
(R usually averages between 12 and 18 carbons).
To produce secondary AS, the parent alkene is reacted with sulfuric acid.
H2S04
C-C-C-C-C-C-C-C=C ...... >C-C-C-C-C-C-C-C-C
OS03-H+
A complex mixture of isomers can occur because the sulfate ester group can add
at any position along the chain, except at the terminal carbon atoms (Higgins
and Burns 1975; Kerfoot and Flammer 1975; Swisher 1970, p. 36; as reported in
Arthur D. Little, Inc. 1977, p. 171).
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NEODOL 91 -S Indicates that the alkyl chain is Cg to Cu carbons in
length, and that the sulfated alcohol has been neutralized with NaOH to
produce a sodium (S) salt of the sulfate. NEODOL 23-A specifies the ammonium
(A) salt of the sulfate (Shell b, p. 1).
AS are used in many specialty products such as shampoos, cosmetics,
dentifrices, antacids, and depilatories (Gleason et al. 1969 as reported in
Arthur D. Little, Inc. 1977, p. 170), and are extensively used in heavy duty
laundry products (Kerfoot and Flammer 1975, as reported in Arthur D. Little,
Inc. 1977, p. 170).
2.4 NEODOL Ethoxvsulfates
Walker et al. (1973, as reported in Arthur D. Little, Inc. 1977, p. 346)
described the following procedures for production of NEOOOL ethoxysulfates
(EOS).
"(1) ethoxylation of a fatty alcohol (prepared from either
vegetable oil or petroleum hydrocarbons)
/ \ KOH
R-OH + / CH2-CH2 > R-0-(CH2CH20)X H
I \ / J catalyst
\ 0 J x (usually x = 2-4)
(2) sulfation of the product with either sulfur trioxide
(S03) or chlorosulfonic acid (C1S03H),
S03
R-0-(CH2CH20)X H > R-0-(CH2CH20)X S03 H
(3) and neutralization to form either the sodium or
ammonium salt
OH-
R-0-(CH2CH20)X S03 H > R-0-(CH2CH20)X S03'Na+(or NH4+)B
EOS can be designated as, for example, NEODOL 25-3A or Ci2.15E03A,
signifying a mixture of 12 to 15 carbon alcohols, an average of three mole-
cules of EO to form a three-unit chain, sulfation of the ethoxylate, and
neutralization to form the ammonium salt (Shell b, p. 1).
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EOS, high foaming anionic surfactants, are principally used in light-duty
dishwashing products and laundry detergent formations. They are also used in
shampoos and other household specialty products (Arthur D. Little Inc 1977
p. 345).
3.0 EFFECTS ON NON-MAMMALIAN ORGANISMS
3 . 1 Acute Effects
Anionic surfactants are less acutely toxic to aquatic organisms than are
nonionic surfactants. However, anionics cause more permanent damage to the
gill structure of fish than do nonionics (Shell a, p. 4). Aquatic organisms
are better able to recover after exposure to nonionic surfactants than after
exposure to anionic surfactants. For example, 50% of the barnacle larvae
exposed for 30 minutes to the LC50 concentration of a nonionic surfactant
completely recovered within 20 minutes after removal to clean water. By
contrast, barnacle larvae tested under similar conditions recovered no
swimming ability within 48 hours after exposure to anionic surfactants ended
(Wright 1976, as reported in Shell a, p. 16).
Acute toxicities, expressed as LC50s, of NEODOL surfactants are compared
in Appendix A for those aquatic organisms for which sufficient data are
available. Chemicals are arranged in order of decreasing toxicity. Results
are discussed in the following subsections.
3.1.1 Alcohols
Alcohols are the NEODOL products least toxic to aquatic organisms
Toxicity decreases with increases in the length of the carbon chain (Table 1)
because water solubility eventually decreases so that the alcohol floats on
the water surface (Shell a, p. 11). This is demonstrated by studies with
rainbow trout (Salmp. gairdneri) showing an increase in 96 hour LC50 values
from 6 to 10 mg/L for Dobanol 91 (Shell Internal Report TLGR. 0166.78, as
reported in Shell a, p. 11) to a non-toxic response at saturation for Dobanol
45 (Shell Internal Report TLGR. 0162.78, as reported in Shell a, p. 11).
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TABLE 1. General direction of toxicity and rate of biodegradation of linear primary alcohols and derivative
surfactants in an aquatic environment as a function of alkyl or ethSiyfate (EO) chain" length
Chain Lenatfi
Alkyl EO
Class (No. of carbon atoms) (No. of units)
Alcohols | up
Alkyl sul fates . up
(AS) f
10
Alkyl ethoxylates I
(EO) t or .
I
19
1C
12
/o -
20
2
t
Alkyl ethoxy- 16
sul fates (EOS)
16
t
1 6
2
6
2
^^^^^^^^^^™B^^^^=a^^B1^^^^^^^^^^^«B™wa^^^^s^^B^«a^MB^^^^^^-^^^a5^
Rate of
Toxicity Biodegradation
I —
t — A.
.
v Reports range from "no
effect" to "very
slight decrease" as
complexity of the
molecule increases.
1
1
1
T
xLess
toxic Same as for EO com-
Ithan pounds.
parent
r
t
Key: | = increase
I = decrease
-no change
NP = not prese
= moderate or
gradual decrease
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3.1.2 Alcohol Ethoxylates
The toxicity of alcohol ethoxylates varies according to both the length
of the alkyl chain and the number of EO units present. Generally, when the
length of the alkyl chain remains the same, increases in the number of EO
units decrease the toxicity (Table 1), as shown in Appendix A by the one-hour
LC50 studies with goldfish (Carassius auratus) (Gloxhuber et al. 1968, as
reported in Shell a, p. 14) and the 96-hour LC50 studies with rainbow trout
(summarized by Shell a, p. 13, Figure 5) and Daohnia (U.S. Food and Drug
Administration, as reported in Shell a, p. 15). Shell (a, p. 4) suggests that
the toxicity is decreased because the molecule becomes less fat-soluble and,
therefore, penetrates the gill membrane less readily. If, however, the number
of EO units is unchanged and the length of the alkyl chain is increased,
toxicity increases (Shell a, p. 13).
Invertebrates (except Daohnia) are relatively tolerant to alcohol
ethoxylates, with most LC50 values ranging from 500 to 5,000 mg/L (Shell a, p.
13) compared to bluegill sunfish (Laoomis macrochirus). with LC50 values
ranging from 1.8 mg/L (C12-i5E03) to 11.0 mg/L (C12.i5E09, 98% linear pri-
mary), and rainbow trout, with LC50 values ranging from 0.8 mg/L (C14.15E07)
to 8-9 mg/L (C9.10E05) (Appendix A). Less active species are perhaps more
tolerant to surfactants than the more active species because lower respiratory
rates cause less surfactant to pass over their gills (Shell a, p. 4).
3.1.3 Alcohol Sulfates
Alcohol sulfates do not appear to be as acutely toxic to aquatic
organisms as are the ethoxylates. According to Kikuchi et al. (as reported in
Goyer et al. 1981, p. 100), 24-hour LC50 values reported for Japanese killi-
fish (Oryzias latipes) ranged from 0.78 mg/L for NaC16AS to 70 mg/L for
NaC12aveAS- The variation was attributed to the difference in the length of
the alkyl chain (Table I). However, close examination of the limited LC50
data presented in Appendix A does not clarify whether chain length affects
toxicity.
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3.1.4 Alcohol Ethoxysulfates
Sulfation of ethoxylates appears to reduce their toxicity by a factor of
21 to 23 compared to the parent products (Shell a 1985, p. 16). According to
studies using fathead minnows (Pimeohales promelas). the most important factor
influencing the toxicity of these surfactants is the number of EO units
present rather than the number of carbon atoms present (Monsanto Co., un-
published data, as reported in Arthur D. Little, Inc. 1977, p. 363). In-
creasing the number of EO units when the number of carbon atoms was kept
constant and less than 16 decreased toxicity (Table 1); however, when the
number of carbon atoms was equal to or more than 16, increasing the number of
EO units drastically increased toxicity (see Appendix A). The most toxic
surfactant tested was CjsEOsS, producing a 24-hour LC$Q value of 0.8 mg/L.
The peak toxicity at Cie changed very little with EO units decreasing to £03.
The least toxic ethoxysulfate tested was CisE02S at an LC$Q of 80 mg/L.
Contrary to Monsanto's results with minnows, Gafa (1974, as reported in Arthur
D. Little* Inc. 1977, p. 363) found CjeEOa^S to be one of the least toxic
surfactants to goldfish. Shell d (unpublished data, as reported in Goyer et
al. 1981, p. 199) demonstrated substantial differences in 96-hour LC$Q values
for rainbow trout when the numbers of carbon atoms were changed and the
numbers of EO units were only slightly different. The LC50 for C^-isEOsS was
8.9 mg/L compared to an LC5Q of 400-450 mg/L for Cg.ioE02.5S. These results
indicate that data are insufficient to generalize about the factors in-
fluencing the toxicities of various alcohol ethoxysulfates.
/
The few data available for invertebrates suggest that they may be
slightly less susceptible to EOS than are fish. LC$Q values (24-hour) ranged
from 5 mg/L (C12E03S) to 37 mg/L (C12E03S, Ziegler or natural fatty alcohol-
derived) in Daohnia (Lundahl et al. 1972, as reported in Arthur D. Little,
Inc. 1977, p. 364).
8
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3.2 Sublethal Effects
3.2.1 Aquatic Animals
Surfactants have been shown to cause a variety of sublethal effects In
aquatic organisms, such as changes In ventilation rates, Inhibition of larval
development, and Immobilization. Alcohol ethoxylates and ethoxysulfates
affect the ventilation rates of blueglll sunfish. For example, forty-eight
hour tests by Makl (1979a, as reported In Goyer et al. 1981, p. 158} demon-
strated that concentrations ranging from 0.26 mg/L to 1.2 mg/L of C^.sEO
suppress ventilation rates In bluegills by 30 to 50% compared to controls. To
a lesser extent, similar effects were also caused by C^^EO. However, 48
hours of exposure to 0.39 mg/L ^£03$ significantly increased the ventilation
rate of bluegills (Maki 1979a, as reported in Goyer et al. 1981, p. 198).
Larval development was inhibited in the Eastern oyster (Crassostrea viralnical
after 48 hours exposure to a 0.11 mg/L concentration of Ci^EO (Maki 1979b,
as reported in Goyer et al. 1981, p. 159), in the Pacific oyster (Crassostrea
ojflas) after 48 hours exposure to a 0.84 mg/L (average) concentration of
NaC^AS (Cardwell et al. 1977, as reported in Goyer et al. 1981, p. 104), and
in the horse clam (Tresus cajjax) after 48 hours exposure to a 0.4 mg/L
concentration of NaC^AS (Cardwell et al. 1978, as reported in Goyer et al.
1981, p. 104). Immobilization of barnacle nauplii occurred after 30 minutes
exposure to 580 mg/L of a concentration of CjoEt^o (Wright 1976, as reported
in Goyer et al. 1981, p. 159). Daohnia were immobilized by concentrations of
sulfates ranging from 42 mg/L for C^AS to 8200 mg/L for CsAS indicating a
trend of increasing AS toxicity with increasing numbers of carbon atoms
(Lundahl and Cabridenc 1978, as reported in Goyer et al. 1981, p. 97).
Similarly, Wright (1976, as reported in Goyer et al. 1981, p. 97) found CjnAS
to be approximately ten times as toxic as CsAS in barnacle larvae (Elininius
modestus). However, Bode et al. (1978, as reported in Goyer et al. 1981, p.
101) found toxicity decreased with increasing chain length when budding Hvdra
attenuata were exposed to CJQ, C^, C^, and C^AS. The decrease was attri-
buted to reduced water solubility at the assay temperature of 20°C.
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Most data indicate that increasing the length of the alkyl chain of
alcohol sulfates tends to increase toxicity (Table 1). Insufficient data are
available on sublethal effects to make such generalizations about ethoxylates.
Another type of effect was detected in whitefish fCareaonus clupeaformisl
by Hara and Thompson (1978, as reported in Goyer et al. 1981, p. 103). The
olfactory bulbar electric response was suppressed with 0.1 mg/L Ci2aveAS, the
lowest concentration at which sublethal effects were observed. The authors
considered this an adverse effect because feeding and migrating behavior could
be impaired by reduced olfactory sensitivity.
Feather oils of ducks were dissolved after 30 minutes exposure to a
solution of 19 mg/L C12AS in distilled water (Choules et al. 1978, as reported
in Goyer et al. 1981, p. 110). Such an effect could obviously place water-
fowl at increased risk of hypothermia in waters polluted with detergents.
3.2.2 Plants
Surfactants are toxic to aquatic plants. Alcohol ethoxylates have been
shown to inhibit the growth of algae. C^.^AEs was algistatic to populations
of the diatom (Navicula seminuluml at concentrations of 5-10 mg/L and to the
green algae (Selenastrum capricornutuml at concentrations of 50 mg/L. The
same surfactant was algicidal to the diatom at 100 mg/L and to the green algae
at 1000 mg/L (Payne and Hall 1979, as reported in Goyer et al. 1981, p. 156).
The growth of 12 species of marine phytoplankton (chlorophyceae) was
completely inhibited by MgC12aveAS at concentrations of 100 and 1000 mg/L.
Nannochloris sp. and Stichococcus sp. were completely inhibited by this
surfactant at 10 mg/L (Ukeles 1965, as reported in Arthur D. Little, Inc.
1977, p. 194). Rockstroh (1967, as reported in Arthur D. Little, Inc. 1977,
p. 196) demonstrated the toxicity of Na-C12aveAS to ciliates fCvrtolophosisl.
Exposures of 4 and 15 minutes to concentrations of 0.1 and 0.2 mg/ml caused
autolysis of the cytoplasm, fissures in the mitochondrial membrane, and
formation of a diffuse mitochondrial edema.
10
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An unusual relationship between toxicity of a coconut-alcohol-derived
ethoxysulfate and a red tide dinoflagellate (Gvmnodinium breve) was reported
by Kutt and Martin (1974, as reported in Goyer et al . 1981, p. 201). Mor-
tality decreased with increasing concentrations of the surfactant (87% with
2.5 ug/L, 63% with 12.5 mg/L, and 44% with 50 ug/L). No explanation was given
for these abnormal results.
Surfactants also affect the growth and developmnt of higher plants.
Aquatic duckweed (Lemna minor) was adversely affected by exposures to C^^AE.
On the basis of frond count, the 7-day £650 was 21 mg/L and on the basis of
root length, it was 1.9 mg/L (Bishop and Perry 1979, as reported in Goyer et
al. 1981, p. 166). Of ten AE surfactants tested on rye and barley grasses by
Valores and Letez (1978, as reported in Goyer et al . 1981, p. 166), n-pri-Ci2-
15AE3 and n-pri-Cj2-i5AE3 were the most toxic to both grasses. Barley growth
was reduced 25% and 20%, respectively, and rye growth was reduced 50% and 80%,
respectively. All surfactants tested inhibited growth in both grasses at
concentrations of 100 mg/L. The least phytotoxic compounds were n-pri
15AE20» n-pri Cg.nAEe, and n-
Grain yield was reduced in paddy rice plants watered with 50 mg/L AS.
Water absorption by the roots was markedly inhibited, photosynthesis was
inhibited, and considerable yellowing of the leaf blade also occurred
(Taniyama and Nomura 1978, as reported in Goyer et al. 1981, p. 109).
However, a stimulatory effect was demonstrated with corn seeds watered with
0.01, 0.1, or 1 g/L Cj2aveAS (Nadasy et al. 1972, as reported in Arthur D.
Little, Inc. 1977, p. 197). Seeds weighed 97%, 130%, and 136% of controls,
respectively. Similar increases also occurred in length and dry weight of the
corn plants. Treatment of barley seeds (Hordeum vulaare L.) with 100% active
NaCi2aveAS (10~3M) for 24 hours before germination resulted in significant
growth inhibition as determined by shoot length (Antonielli and Lupatteli
1977, as reported in Goyer et al. 1981).
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3.3 Chronic Effects
Few data are available on the chronic effects of NEODOL products. Much
of the data that are available are "no observed effect concentrations" (NOEC)
for ethoxylates derived by Maki from studies with fathead minnows and Daohnia.
For example, a chronic toxicity test emphasizing egg production and spawning
rate in minnows resulted in a NOEC of 0.32 mg/L, the highest concentration
tested for C12-5EO (Maki 1979c, as reported in Goyer et al. 1981, p. 160).
For Daphnia, a similar NOEC, 0.27 mg/L, was obtained with a chronic exposure
to C13.67E02.25S (Mak1 1979d, as reported in Goyer et al. 1981, p. 200).
Growth was inhibited, however, in the fathead minnow after a one-year exposure
to 0.22 mg/L concentration of Cj3.7E02.2sS (Maki, 1979d, as reported in Arthur
D. Little, Inc. p. 200). Maki (1979a, as reported in Shell a, p. 18) demon-
strated that chronic exposure to low levels of alcohol ethoxylates decrease
respiratory rates in fathead minnows, whereas the rates are increased by
exposures to ethoxysulfates. The mode of action is unknown.
Other studies have shown that egg fertilization can be inhibited in
crustaceans by exposure to surfactants. Grammo and Jorgensen (1975, as
reported in Goyer et al. 1981, p. 160 and Shell a, p. 19) caused almost
complete inhibition of egg fertilization by exposing mussels fMvtilus edulisl
to 2 mg/L TAE10 (ethoxylated tallow alcohol) for five months. Some inhibition
occurred at concentrations as low as 0.1 mg/L. Arthur D. Little, Inc. (1977)
reviewed the results of a chronic toxicity test on clam (Mercenaria
mercenaria) and oyster (Crassostrea virainical larvae. At 1 mg/L AS, ferti-
lized egg development was significantly retarded compared to controls, while
complete inhibition of development occurred at 2.5 mg/L. After a 10-day
exposure to 5 mg/L, clam mortality was 68%; oyster mortality was 82% after 12
days exposure.
More studies are needed before conclusions can be reached about the long-
term toxicity of surfactants to aquatic systems. The limited data available
indicate that, generally, concentrations exceeding 0.2 mg/L can cause adverse
effects in aquatic organisms when exposures last for several months.
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4.0 ENVIRONMENTAL FACTORS INFLUENCING AQUATIC TOXICITY
4.1 Water Hardness
Water hardness appears to play a role in the toxicity of at least the
alcohol sulfates. WUh an Increase In water hardness, the toxicity (and
uptake) of AS increases (Arthur D. Little, Inc. 1977, p. 165; Goyer et al.
1981, p. 85 and 106). The effect of water hardness on ethoxylate and ethoxy-
sulfate toxicity is less certain, however. Studies by Maki and Bishop (1979)
and Maki et al. (1979) using Daohnia and Cj^EOy suggest a slight decrease in
EO toxicity with increased water hardness (as reported in Goyer et al. 1981,
p. 161). However, no such trends were apparent in similar studies by Procter
and Gamble Company (unpublished data, as reported in Goyer et al. 1981). No
intra-species, water hardness data were available for EOS.
4.2 Biodearadabilitv
It is generally agreed in all reports reviewed (Shell a and b; Arthur D.
Little, Inc. 1977, Goyer et al. 1981) that" the linear primary alcohol-based
surfactants do not persist in laboratory or field tests. Even slightly
branched or secondary structures are easily degraded, albeit at a somewhat
slower rate (Table 1). Concentrations of EO as high as 1000 mg/L in shake
flask tests simulating spills, were 70 to 80% degraded in three days (Kravetz
et al. 1979, as reported in Shell a, p. 5). Goyer et al. (1981, p. 143)
suggests, however, that a study using an atmosphere containing 70% oxygen to
enable "complete surfactant oxidation to C02n may not be indicative of
degradation rates occurring in the same time period under natural conditions.
Ethoxysulfates added to activated sludge were completely metabolized to carbon
dioxide and water within five to ten days (Mlura et al. 1979 and Itoh et al.
1979, as reported in Goyer et al. 1981, p. 195). Numerous other studies using
sludge or river, estuarine or ocean waters have demonstrated the rapid
breakdown of these compounds. Degradation of ethoxylates has been shown to be
generally faster in saltwater than in freshwater, and faster in freshwater at
high temperatures than at lower temperatures (Schoberl and Mann, 1976, as
reported in Goyer et al. 1981, p. 142). The degradation rate of ethoxylates
13
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is also influenced by the length of the EO chain; increased length of the
chain caused degradation to be slower, especially in freshwater at low
temperature. Ethoxylates having 100 EO units/mole of alcohol biodegrade
considerably slower (20% ultimate biodegradation in 21 days) than those having
up to 30 EO units/mole of alcohol (90% or more in 21 days) (Kravetz et al.
1979, as reported in Shell p. 5; Goyer et al. 1981, p. 144). Shell claims to
market only products having a maximum of 13 EO units/mole (NEODOL 45-13).
Biodegradation was essentially complete 10 days after DOBONOL 45-7, simulating
a spill condition, was added to an activated sludge medium (Cook 1979, as
reported in Shell a, p. 5).
Degradation results In a rapid loss of toxicity of surfactants to aquatic
organisms. Products resulting from EO biodegradation were much less toxic to
rainbow trout and goldfish than were the parent compounds (Reiff 1976 and
Kurata et al. 1977, as reported in Goyer et al. 1981, p. 153). Maki et al.
(1979, as reported in Goyer et al. 1981, pp. 151 and 152) concluded that
initial concentrations of 3 mg/L or less of C14.5 E07 in stream water effluent
was non-toxic to fathead minnows within 24 hours. • At 10 mg/L, toxicity was
observed for five days in stream water and for two to three days in secondary
effluent. NEODOL-type surfactants are readily utilized as a carbon (energy)
source by bacteria present in activated sludge and natural waters (Shell a p
5).
4.3 Exposure
By comparing an organism's sensitivity to a chemical with the concentra-
tion of that chemical likely to be present in the environment, one can often
predict with reasonable accuracy the potential threat posed by the chemical to
the organism. Modeling techniques have been used to estimate surfactant
concentrations in 20 estuarine locations (Maki 1979b, as reported in Goyer et
al. 1981, pp. 163 and 164). Estimated maximum EO concentrations ranged from
0.2 ug/L in Penobscot Bay, Maine to 19.8 ug/L in the Hudson River; the
geometric mean for all estuaries was 3.2 ug/L. It should be noted that these
values are probably high because the model was provided with an elevated
14
-------
estimate of inflow from sewage treatment plants. Further, degradation was not
factored in.
Comparing these estimated concentrations with the acute sensitivities of
test species, it appears unlikely that, short of a direct spill, concentra-
tions of surfactants acutely dangerous to aquatic organisms will be attained
in the environment.
5.0 MAMMALIAN TOXICITY
5.1 Acute Effects
All LDso data reviewed indicate that, at their worst, NEODOL surfactants
are moderately toxic (0.5 to 5 g/kg) when rated according to Gosselin et al .
(1976, as reported in Shell b, p. 10). LDsgs for all types of surfactants
generally exceed 1.0 g/kg. Alcohols appear to be the least toxic (oral 1050$
>5 g/kg), becoming more so with either sulfation or ethoxylation. Sulfation,
however, decreases the toxicity of alcohol ethoxylates (Shell b, pp. 9-11).
Acute oral toxicity studies with rats indicate that the degree of
ethoxylation has some influence on toxicity. For example, NEODOL 91-2.5
produced LDsgs ranging from 2.7 to 10 g/kg (Shell Internal Reports HSE-78-
0156, TLGR.124.79, and TLGR. 088.80, as reported in Shell b, p. 11), whereas
NEODOL 91-8 was more toxic, exhibiting LDsgs of 1.0 or 2.7 g/kg (Shell
Internal Reports TLGR. 088. 80 and TLGR. 0024. 76, as reported in Shell b, p. 4).
The length of the alkyl chain does not appear to influence the acute toxicity
of alcohol ethoxylates (Shell b, Table V, p. 12).
Skin and eye irritation tests with rabbits have demonstrated that NEODOL
surfactants, except the alcohols, are generally severe irritants at high or
undiluted concentrations (Shell b, pp. 17 and 20). Shell b (p. 21), however,
reports that when directions are followed, actual use concentrations for
NEODOL products are <0.04%. At 0.1% dilutions, NEODOL products tested ranged
from non-irritating for alcohols and alcohol sul fates to non-irritating to
mildly irritating for alcohol ethoxylates (Shell b, p. 21).
15
-------
Most NEODOL products produced negative results in skin sensitization
tests (Shell b, p. 25, Table XIV). Most exceptions showed some, weak or
moderate, sensitivity in one type of test but none in other tests. By
contrast, NEODOL 25-3 was found to be a very weak sensitizer in the Maximiza-
tion Test (Shell b, p. 25). Results of repeated-insult patch tests of NEODOL
products in human volunteers agree with most observations in animal studies
that NEODOL products are not skin sensitizers (Shell b, pp. 25 and 27).
5.2 Subchronic Effects
Available data indicate that effects of subchronic exposures to surfac-
tants mainly involve changes in organ and body weights. Studies exposing rats
for 16 weeks to a diet containing C12 sulfate (4% of the total diet) resulted
in reduced body weights (Arthur D. Little, Inc. 1977 and 1981 and Fitzhugh and
Nelson 1948, as reported in Shell b, p. 29). Compared to controls, ethoxy-
lates (C13E06 and C14E07) produced elevated.liver weights in rats exposed to
concentrations equivalent to 1% of the total diet (Brown and Benke 1977,
Arthur D. Little, Inc. 1977, and Goyer et al. 1981, as reported in Shell b, p!
29). Lower body weight was also observed with exposure .to C13E06. Other
subchronic feeding studies exposing rats to sulfates and ethoxysulfates
produced no major biological effects at concentrations up to 0.1% of the diet
for 13 weeks (Shell Internal Report R(T)-12-66 and Walker et al. 1967, as
reported in Shell b, p. 29). Increases in serum urea or protein concentra-
tions and increases in some organ weights occurred at concentrations of 0.5%
of the diet. Because histopathology was normal, these effects were considered
minor.
Another type of effect observed was slight inhibition of the progression
of cholesterol-induced atherosclerosis in rabbits (Kivak et al. 1975 as
reported in Goyer et al. 1981). The mechanism of action is not known,
although a reduction in accumulation of cholesterol esters in aortic tissue
was suggested as a possibility (Morin et al. 1974, as reported in Goyer et al
1981).
16
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5.3 Chronic Effects
The few data available on the chronic effects of surfactants do not
demonstrate any alarming effects. One or two year studies using 1.0% alcohol
sulfate (Goyer et al. 1981, p. 118) or 0.5% alcohol ethoxysulfate (Arthur D.
Little, Inc. 1977, p. 377), respectively, in the diets of rats have produced
no adverse effects. However, 1% alcohol ethoxylate, C^-is £05.5, added to
the diets of rats for two years resulted in reduced body weight, elevated
organ to body weight ratios for liver, kidney, brain, and heart in females and
for liver in males and increased incidence of focal myocarditis, a common
spontaneous lesion found in aging populations of rats (Procter and Gamble,
unpublished data, as reported in Goyer et al. 1981, p. 174). Food consumption
was also reduced in groups having reduced body weights, and was attributed to
poor palatability of the diet. Reduced body weights and increased organ to
body weight ratios also occurred in females at the 0.5% treatment level. A
second feeding study using as much as 1.0% Ci4_15 EO; in the diets of rats for
two years resulted in reduced body weight gains for females and males, and in
decreased absolute organ weights for liver, kidney, heart, and thyroid/
parathyroid glands in females and for brain and adrenals in males in the 1%
treatment groups. Gross incidences of focal myocarditis increased with
increasing treatment levels for all groups of rats at 12 months, but severity
of lesions was not treatment-related (Proctor and Gamble, unpublished data, as
reported in Goyer et al. 1981, p. 175). Eighteen months exposure to repeated
dermal applications of up to 5.0% C^-iaEOe^ produced no notable results in
ICR Swiss mice (Procter and Gamble Company, unpublished data, as reported in
Goyer et al. 1981, p. 176).
5.4 Carcinoaenicitv
No evidence for carcinogenic potential of NEODOL products has emerged
from the limited data available from long-term oral or dermal studies exposing
rats or mice to C12_i3 E06<5 or C14.15 E07 (Proctor and Gamble Company,
unpublished data, as reported in Goyer et al. 1981, pp. 174-176); C^S (Goyer
et al. 1981, p. 119); or C12E03S (Tusing et al. 1962, as reported in Arthur D.
Little, Inc. 1977, p. 378).
17
-------
5.5 Mutaqenicltv
Mutagenicity has not been demonstrated for any NEODOL product tested with
in vitro or jn vivo mammalian systems or in bacterial or yeast systems. The
following NEODOL products have been tested for mutagenicity: C12ave AS (Hope
1977, as reported in Goyer et al. 1981, p. 120); n-pri-C12_13E03 (Shell
Toxicology Laboratory unpublished data, as reported in Goyer et al. 1981, p.
177); CJ2-15EOS (Hope 1977, as reported in Goyer et al. 1981, p. 209); C12_
13E02.5S (53:43) (Inoue et al. 1980, as reported in Goyer et al. 1981, p.
210); and n-pri-C12-i5E03S (Shell Research Limited, unpublished data, as
reported in Goyer et al. 1981, p. 210).
5.6 Teratooeni ci tv/Reproducti on
Few teratogenesis/reproduction studies have been performed with NEODOL
products; no teratogenesis studies have been performed with AES administered
alone. However, formulations containing AES administered orally to mice,
rats, or rabbits have produced no teratogenie effects (limori et al. 1973,
Iseki 1972, Nolan et al. 1975, and Palmer et al. 1975 as reported in Arthur D.
Little, Inc. 1977, p. 379). Results from testing the following chemicals have
shown no cause for concern: C14.15 E07 and C12E06 (Proctor and Gamble
unpublished data, as reported in Arthur D. Little, Inc. 1977, p. 322) and
C12E03S (Tusing et al. 1962, as reported in Arthur D. Little, Inc. 1977, p.
378).
An alcohol sulfate whose chain length was not identified has also been
tested .(Nomura et al. 1980, as reported in Goyer et al. 1981, p. 119). Dermal
applications of 10 to 20% concentrations of the alcohol sulfate to pregnant
mice on days 1 to 10 of gestation interfered with embryonic development at the
cleavage stage. Applications of 2% on days 1 through 17 also reduced the
number of pregnancies, but the number of animals compared was too small to be
statistically significant. Dermal applications of 10% alcohol sulfate twice a
day prior to implantation (days 0 to 3) resulted in an elevated incidence of
deformed embryos, compared to controls (29.1% vs 4.9 of 0 in controls) (Nomura
18
-------
et al. 1980, as reported in Goyer et al. 1981, p. 120). Dermal application of
the alcohol sulfate during late pregnancy did not interfere with gestation.
More tests, especially with AES products, are necessary before conclu-
sions can be reached about the teratogenic potential or reproductive effects
of surfactants.
5.7 Studies in Humans
Studies using human volunteers have demonstrated the skin irritation
properties of NEODOL products (Shell b, p. 27). In most cases, 1% dilutions
caused very slight to mild Irritation with repeated exposures. Alcohol
ethoxylates appear to be the least irritating, with only non-to-mild irrita-
tions caused by repeated exposures to dilutions up to 25%. Use of certain
alcohol ethoxylates as analgesics and anesthetics have caused no adverse
reactions in humans (Goyer et al. 1981, p. 130).
5.8 Metabolism
Alcohol sulfates, short-chain ethoxylates, and ethoxysulfates (Goyer et
al. 1981, pp. 121, 178, and 211, respectively) are readily absorbed when
administered orally to rats, and are primarily excreted in urine. Increasing
the alkyl chain length of an ethoxylate decreases its excretion in urine and
feces, and increases the amount in expired air (Goyer et al. 1981, p. 178).
Increasing the length of the EO unit of an ethoxysul fate causes it to be
poorly absorbed and excreted primarily unchanged in the feces (Arthur D.
Little, Inc. 1977, p. 381).
Cutaneous absorption of alcohol ethoxylates (about 50%) is somewhat
slower than absorption after oral administration (>75%) (Drotmann 1977 and
1980, as reported in Shell b, p. 33). Dermal absorption of similar alcohol
ethoxylates is greater than dermal absorption of alcohol sulfates or ethoxy-
sul fates (Black and Howes 1979, as reported in Shell b, p. 33). Maximum
absorption of alcohol sulfates on human callus occurred with a chain length of
12 carbons (Dominguez et al. 1977, as reported in Goyer et al. 1981, p. 123).
19
-------
After application of 100 mg of an alcohol ethoxylate (C12E06) to human skin,
most (81% average) was recovered from swabbing the skin after 144 hours
(Drotman 1980, as reported in Goyer et al. 1981, p. 180).
6.0 CONCLUSIONS
6.1 Toxicitv to Non-Mammalian Organisms
Certain structure-activity relationships have been delineated for the
alcohol-derived surfactants in aquatic systems (see Table 1). As the number
of carbon atoms in the alkyl chain of straight-chain alcohols increases, the
toxicity of the alcohol decreases. When the (EO) chain length of alkyl
ethoxylates remains the same, an increase in the alkyl chain length increases
toxicity. Conversely, when the alkyl chain remains the same, an increase in
the EO chain length decreases toxicity (as opposed to the response of labora-
tory rodents). The sulfation of the end EO group reduces the acute toxicity
of these compounds by a factor of more than 20 compared to the parent ethoxy-
late compound. Alcohol sulfates also appear to be less acutely toxic to
aquatic organisms than are the alcohol ethoxylates. Although anionic surfac-
tants are less acutely toxic than nonionic surfactants, fish have a greater
ability to recover after exposure to nonionic surfactants than to anionic
surfactants.
Surfactants have been shown to cause a variety of sublethal effects in
aquatic organisms, such as changes in ventilation rates, inhibition of larval
development and immobilization.
The limited data available on the chronic effects of surfactants (mainly
the ethoxylates) indicate that growth inhibition and altered respiratory rates
in crustaceans can be caused by long-term exposures. In general, exposure for
several months to concentrations exceeding 0.2 mg/L can cause adverse effects
in aquatic animals.
Surfactants have been shown to inhibit the growth and development of
aquatic microflora and higher plants such as barley and rye.
20
-------
Due to dissolution of the waterproofing oils on their feathers, waterfowl
may be at increased risk of hyperthermia if exposed to surfactants.
NEODOLs and the other alcohol-based surfactants do not persist in aquatic
environments, and are readily biodegraded to apparently non-toxic inter-
mediates, then to carbon dioxide and water. Short of a direct spill, concen-
trations of surfactants reaching waterways would be substantially lower than
those that are acutely toxic to aquatic organisms.
Effects of repetitive exposures to surfactants have not been adequately
studied. Additional toxicity tests should focus on the effects of continuous
exposure of early life stages of test organisms to low concentrations of
surfactant, a situation such as might exist near a sewage outfall or drainage/
overflow conduit.
The effects of 1,4-dioxane contamination of ethoxysulfates on aquatic
organisms cannot be determined from available data.
6.2 Mammalian Toxicitv
In general, NEODOL products exhibit a low order of toxicity to mammals in
toxicity tests (see Table 2). At worst, acute toxicity can only be labeled
moderate, except in the cases of skin or eye irritations which are often
severe for undiluted derivitized NEODOL products. However, dilutions of 0.1%
are generally non-irritating, and according to Shell, use concentrations are
only <0.04%.
NEODOL alcohols, which are the least acutely toxic to mammalian systems,
become more toxic with either sulfation or ethoxylation. Sulfation of an
ethoxylate, however, decreases toxicity. Length of the alkyl chain does not
appear to play a significant role in acute toxicity of alcohol ethoxylates.
Subchronic and chronic dietary tests resulted in reduced body weights and
increased organ to body weight ratios for some organs. There was no evidence
of carcinogenicity or mutagenicity for any NEODOL product tested.
21
-------
TABLE 2. Effects of NEODOl(R) products In laboratory mammals
Alcohol Sulfates
Alcohol Ethoxylates
Alcohol Ethoxysulfates
ro
ro
Acute LOcn
(g/kg)
Skin irrita-
tion (rabbits)
Eye irritation
(rabbits)
Subchronic
Oral or dermal, rats, or
rabbits, >1; commercial
use dilutions between 5
and 15.
0.1% dilution, non-
irritating; >10% dilution,
severe.
Undiluted, severe to
extreme.
4% given in diet for 16
weeks reduced body weight
of rats; cumulative skin
irritation; daily inges-
tion of 250 mg/kg for two
months slightly inhibited
progression of choles-
terol-induced athero-
sclerosis in rabbits.
Oral, rats, 0.87 to >10;
dermal, rats or rabbits,
>2; inhalation (4 hrs.
exposure) rats, between
1.5 and 3 mg/L.
0.1%, non-irritating to
mild; >10%, mild to
severe.
>10%, practically non-
irritating to extreme;
0.1% non-irritating.
1% given in diet for 13
weeks reduced body weight,
increased liver weight of
rats.
Oral, rats, 1.7 to 5;
dermal, rabbits, 4.7 to
12.9.
0.1%, non-irritating to
minimal; undiluted, mild
to severe.
Undiluted, severe; 0.1%
non-irritating.
0.5% given in diet for 13
weeks increased kidney,
liver, and heart weights
in female and kidney
weights in male rats;
repeated skin (guinea pigs
and rabbits) exposure to
10% dilutions, severe
irritation; 1% no reac-
tion.
-------
TABLE 2. Effects of NEODOlW products In laboratory mammals (Continued)
Alcohol Sulfates
Alcohol Ethoxylates
Alcohol Ethoxysulfates
Chronic
Carcinogenic
ro
Mutagenic
1% in diet, rats, one
year, no adverse effects.
No evidence from long-term
feeding studies in rats or
skin-painting tests in
mice.
No effects on chromosomes
of rat bone marrow cells
from 90 day diet of
maximum tolerated dose
(1.13% active ingredient).
1% in diet, rats, two
years, reduced body
weight, elevated organ to
body weight ratios,
increased incidence of
focal myocarditis. 5%
dermal application to mice
for 1.5 years, no notable
results.
No evidence from long-term
feeding tests in rats or
from long-term percu-
taneous administration to
mice.
No evidence from in vitro
and host-mediated mutagen-
icity tests.
0.5% in diet, rats, two
years, no adverse effects.
No evidence from two-year
feeding (0.5%), drinking
water (0.1%), or skin-
painting (5.0%) studies.
No effects on choromosomes
of rat bone marrow cells
from 90 day diet of
maximum tolerated dose
(1.13% active ingredient).
No evidence from hamster
embryo cell culture or
yeast or bacteria studies.
-------
TABLE 2. Effects of NEODOlW products In laboratory mammals (Continued)
Teratogenic/
Reproductive
Alcohol Sulfates
No evidence from ingestion
of up to 300 mg/kg during
gestation. Daily skin
application of 20% to
pregnant mice on days 1 to
10 interfered with
embryonic development; 10%
2 times/day, pregnant
mice, days 0 to 3,
elevated incidence of
deformed embryos. Doses
severely toxic to dams
reduced litter size and
caused fetal loss in mice
but not in rats or
rabbits.
Alcohol Ethoxylates
No evidence from feeding
(up to 0.5%) studies in
rats or rabbits.
Alcohol Ethoxysulfates
No data on AES admini-
stered alone. No evidence
from oral administration
of formulations containing
AES to mice, rats, or
rabbits. No adverse
reproductive effects from
0.1% in the diets of rats
for two generations.
-------
Data are generally lacking on teratogenic/reproductive effects. Data
available from a limited number of feeding studies indicate no teratogenicity
for any of the NEODOL products tested. However, repeated dermal exposure of
mice to high concentrations of an alcohol sulfate during early gestation
interrupted cleavage of eggs and retarded fetal development. Further studies
should be performed to clarify the teratogenic potential and/or reproductive
effects of NEODOL products.
Animal studies show that, in general, NEODOL products administered orally
are readily absorbed, metabolized, and primarily excreted in the urine.
Cutaneous exposure, the usual route of exposure to most surfactants, results
in slower absorption of alcohol ethoxylates.
6.3 1.4-Dioxane Contamination
There is concern because 1,4-dioxane is a contaminant of some NEODOL
products. Shell (May 7, 1980 memorandum to G.T. Youngblood) claims that 1,4-
dioxane (OCH2CH20CH2CH2) is present only in their EOS products, and postulates
that it is formed during sulfation of the EO and that the presence of a
polyoxyethylene chain and a highly acidic agent, such as sulfur trioxide, are
required. The typical potential exposure for an adult female is estimated to
be 1.65 x 10'8g/kg/d from hair shampoo and 7.56 x 10"10 g/kg/d from light duty
liquid (Shell c 1980, Appendix B-3). Worst case estimates are 1.12 x 10"
7g/kg/d for shampoo and 6.68 x 10~9g/kg/d for light duty liquids.
It is impossible to determine from the data provided whether dioxane
contributes to the observed EOS toxicity. However, dioxane contamination does
not alter the significance of the toxicity of NEODOL products, for it appears
that it is often the dioxane-contaminated products (EOS) to which environ-
mental species are exposed. It would be useful to compare the toxicities of
contaminated samples with purified samples.
25
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Lundahl P., Cabridenc R. 1978. Molecular structure-biological properties
relationships in anionic surface-active agents. Water Res 12:25-30. (As
reported in Goyer et al. 1981).
Lundahl P., Cabridenc R., Xuereff R. 1972. Qualites biologiques de quelques
agents de surface anioniques, 6th International Congress on Surface Active
Agents. (As reported in Arthur D. Little, Inc. 1977).
Maki A.W. 1979a. Respiratory activity of fish as a predictor of chronic fish
toxicity values for surfactants. Special Technical Publ 667, ASTM,
Philadelphia, PA. pp. 77-95. (As reported in Goyer et al. 1981).
30
-------
Maki A.W. 1979b. An environmental safety evaluation of detergent chemicals
in estuarine ecosystems. Proceedings of the 14th International Marine
Biological Symposium--"Protection of Life in the Sea". Helgoland, Germany.
Sept 24-28. Biologische Anstalt Helgoland, Hamburg, Germany (in press). (As
reported in Goyer et al. 1981).
Maki A.W. 1979c. Correlations between Daohnia maana and fathead minnow
(Pimeohales promelas) Chronic toxicity values for several classes of test
substances. J Fish Res Board Can. 36:411-421. (As reported in Goyer et al.
1981).
Maki A.W. 1979d. Correlations between Daohnia maona and fathead minnow
(Pimephales oromelas). Chronic toxicity values for several classes of test
substances. J Fish Res Bd Can. 36:411-421. (As reported in Goyer et al.
1981).
Maki, A.W., Bishop, W.E. 1979. Acute toxicity studies of surfactants to
Daphnia magna and Daohnia oulex. Arch. Environ. Contarn. Toxicol. 8:599-612
(as reported in Goyer et al. 1981).
Maki A.W., Rubin A.J., Sykes R.M., Shank R.L. 1979. Reduction of nonionic
surfactant toxicity following secondary treatment. J Water Poll Control Fed
51(9):2301-2313. (As reported in Goyer et al. 1981).
Marchetti R. 1964. Toxicity of some surfactants to fish. La Rivista
Italiane Delle Sostanze Grasse (The Italian Journal of Oily Substances)
41:533-542. (Italian Publication). (As reported in Shell a).
Miura K., Yamanaka K., Sangai T., Yoshimura K., Hayashi N. 1979. Application
of biological oxygen consumption measurement technique to the biodegradation
test of surfactants. Yukagaku 28(5):351-355 (English translation). (As
reported in Goyer et al. 1981).
Monsanto Company, unpublished data. (As reported in Arthur D. Little, Inc.
1977).
31
-------
Morin R.J., Edralin G.G., Woo J.M. 1974. Esterification of cholesterol by
subcellular fractions from swine arteries and inhibition by amphiphatic and
polyanionic compounds. Atherosclerosis 20:27-39. (As reported in Goyer et
al. 1981).
Nadasy M., Dobozy O.K., Bartha B., Palfi D., Kolesei M. 1972. Anwendung von
Tensiden in der Landwirtochaft. Chemie, physikalische Chemie und
Anwendungstechnik der grenzflaechenaktive stoffe. Berichte vom VI. Intern.
Kongress fuer grenzflaechenaktive stoffe. Zurich. (As reported in Arthur D.
Little, Inc., 1977).
Nolan G.A., Klusman L.W., Patrick L.F., Geil, R.G. 1975. Teratology studies
of a mixture of tallow alkyl ethoxylate and linear alkylbenzene sulfonate in
rats and rabbits. Toxicology 4:231-243. (As reported in Arthur D. Little,
Inc. 1977).
Nomura T., Kimura S,, Hata S., Kanzaki T., Tanaka H. 1980. The synthetic
surfactants AS and LAS interrupt pregnancy in mice. Life Sci 26:49-54. (As
reported in Goyer et al. 1981).
Palmer A.K., Readshaw M.A., Neuff, A.M. 1975. Assessment of the teratogenic
potential of surfactants. Part I-LAS, ABS, and CLD. Toxicol 3:91-106. (As
reported in Arthur D. Little, Inc. 1977).
Payne A.G., Hall R.H. 1979. A method for measuring algal toxicity and its
application to the safety assessment of new chemicals. Spec. Tech. Pub. 667,
ASTM. (As reported in Goyer et al. 1981).
Procter and Gamble Company, unpublished data. (As reported in Arthur D.
Little, Inc. 1977).
Procter and Gamble Company, unpublished data (as reported in Goyer et al
1981).
32
-------
Reiff B. 1976. The effect of biodegradation of three nonionic surfactants on
their toxicity to rainbow trout. 7th International Congress on Surface Active
Substances. Moscow, USSR. September 12-18. (As reported in Shell a and
Goyer et al. W81).
Reiff B., Lloyd R., How M.J., Brown D., Alabaster J.S. 1979. The acute
toxicity of eleven detergents to fish: Results of an inter!aboratory exer-
cise. Water Res 13:207-210. (As reported in Shell a and in Goyer et al.
1981).
Rockstroth T. 1967. Uber die Wirkung von Detergent!en auf die Morphologic
einer Ziliatenzelle. Acta. Biol. Med. German. 19(1):161-184. (As reported in
Arthur D. Little, Inc. 1977).
Satkowski W.B., Huang S.K., Liss R.L. 1967. Polyoxyethylene alcohols.
Chapter 4. In. Nonionic surfactants. Surfactant Science Series, vol. 1.
Schick M.J., ed. New York, NY: Marcell Dekker, Inc. (As reported in Arthur
D. Little, Inc. 1977).
Schoberl P., Mann H. 1976. Temperature—Eisfluss auf des biologischen abbau
nicht-ionischer tenside in see-und susswasser. [The influence of temperature
on the degradation of nonionic tensides in sea-and freshwater]. Arch Fisch
Wiss 27(2):149-158. (As reported in Goyer et al. 1981).
Shell a. Shell Chemical Company (FYI-AX-0685-0410 Sequence A). Aquatic
safety of NEODOL(R) products. 37 pp.
Shell b. Shell Chemical Company (FYI-AX-0685-0410 Sequence A). Human safety
of NEODOL(R) products. 40 pp.
Shell c. Shell Chemical Company. 1980. (8EHQ-0580-0326 Sequence C). 1,4
Dioxane in alcohol ethoxysulfate products. 90 pp.
Shell d. Shell Chemical Company, unpublished data (as reported in Goyer et
al. 1981).
33
-------
Shell Chemical Company. 1980. Interoffice Memorandum from J.J. Coyle to G.T.
Youngblood.
Shell Internal Report. EC01 Program. Summer 1973-Spring 1974. (As reported
in Shell a).
Shell Internal Report. 1971. Toxicity of surfactants to fishes. (As
reported in Shell a).
Shell Internal Report EMGR.0138.71. Dispersants for dealing with oil spill-
ages. Development of a low toxicity product. Part 1. (As reported in Shell
a).
Shell Internal Report EMGR.0150.71. Dispersants for dealing with oil spill-
ages. Development of a low toxicity product. Part III. (As reported in
Shell a).
Shell Internal Report EMGR.0162.71. Dispersants for dealing with oil spill-
ages. Development of a low toxicity product. Part III. (As reported in
Shell a).
Shell Internal Report HSE-78-0156. Rat acute oral toxicity NEODOL 91-2.5 (as
reported in Shell b).
Shell Internal Report R(T)-12-66. The comparative toxicity of some biode-
gradable detergent materials (as reported in Shell b).
Shell Internal Report TLGR.0052.77. The acute toxicity of Dobanol 25 to
rainbow trout. (As reported in Shell a).
Shell Internal Report TLGR.0064.77. The acute toxicity of Dobanol 45-18 to
rainbow trout (as reported in Shell a).
Shell Internal Report TLGR.0066.77. The acute toxicity of Dobanol 91-5 to
rainbow trout. (As reported in Shell a).
34
-------
Shell Internal Report TLGR.0079.068. The acute toxicity of Dobanol 91-2.5 to
rainbow trout. (As reported in Shell a).
Shell Internal Report TLGR.0088.80. Toxicology of detergents: The acute
toxicity of Dobanol ethoxylates: 91-2.5, 91-5, 91-6, 91-8 (as reported in
Shell b).
Shell Internal Report TLGR.0124.79. Toxicology of detergent intermediates:
acute mammalian toxicity, skin and eye irritancy and skin sensitizing poten-
tial of Dobanol 91-2.5 (as reported in Shell b).
Shell Internal Report TLGR.0161.78. The acute toxicity of Dobanol 23 to
rainbow trout. (As reported in Shell a).
Shell Internal Report. TLGR.0162.78. .The acute toxicity of Dobanol 45 to
rainbow trout (as reported in Shell a).
Shell Internal Report TLGR.0166.78. The acute toxicity of Dobanol 91 to
rainbow trout. (As reported in Shell a).
Shell Research Limited, unpublished data (as reported in Goyer et al. 1981).
Shell Toxicology Laboratory, unpublished data (as reported in Goyer et al.
1981).
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vol. 3. New York, NY: Marcel Dekker, Inc. (As reported in Arthur D.
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studies on sodium lauryl sulphate, sodium lauryl ethoxysulphate and corre-
35
-------
spending surfactants derived from synthetic alcohols. Fd Cosmet Toxicol
5:763-769 (as reported in Arthur D. Little, Inc. 1977).
Ukeles R. 1965. Inhibition of unicellular algae by synthetic surface-active
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Unilever Research Laboratories, unpublished data. (As reported in Arthur D.
Little, Inc. 1977).
U.S. Department of the Interior. Letter to Shell Development Co. Subject:
Toxicity data for selected Neodol products. September, 1968. (As reported in
Shell a).
i
U.S. Food and Drug Administration/Master File (MFJ-122 Shell Drug Master File
on NEODOL alcohols and ethoxylates (as reported in Shell a).
Valoras N., Letez J. 1978. Screening of Neodal chemicals for potential use
in erosion control. Report of the University of California, Riverside, to
Shell Chemical Co., Houston, Texas, Manuscript. (As reported in Goyer et al
1981).
Walker A.P., Ashforth, 6.K., Davies, R.E., Newman, E.A. and Ritz, H.L. 1973.
Some characteristics of the sensitizer in alkyl ethoxy sulphate. Acta
Dermatovener 53:141-44 (as reported in Arthur D. Little, Inc. 1977).
Walker A.I.T., Brown V.K.H., Ferrigan L.W., Pickering R.G., Williams D.A.
1967. Toxicity of sodium lauryl sulfate, sodium lauryl ethoxysulfate, and
corresponding surfactants derived from synthetic alcohols. Food Cosmet
Toxicol 5:763-769. (As reported in Shell b).
Wright A. 1976. The use of recovery as a criterion for toxicity. Bull
Environ Contam Toxicol 15(6):747-749. (As reported in Goyer et al. 1981).
36
-------
APPENDIX A. Acute toxlclty
of alcohol surfactants to aquatic animals
Exposure
(hours)
Surfactant
LC50 (mg/L)
Reference
Daphnia maqna
24 C12_13E06.5
CO
C12-15E09
C14E08
C12-14E07.4
C12-14E06.3
(39%)
C12-14E011
NaC12-14AS
NaC^aveAS (Ziegler derivative)
C12-14E03S (Ammonium salt)
C12-14E03S (Sodium salt)
0.57
1.1
1.71
2.0
2.3
2.5
3.3
5.0
5.1
6.3
13.5
16.3
18.9
Shell Internal Report 1974. ECO 1
Program
Arthur D. Little, Inc. 1978
Shell Internal Report 1974. ECO 1
Program
Arthur 0. Little, Inc. 1978
Arthur D. Little, Inc. 1978
Arthur 0. Little, Inc. 1978
Shell Internal Report 1974. ECO 1
Program
Lundahl et al. 1972
Arthur D. Little, Inc. 1978
Arthur D. Little, Inc. 1978
Lundahl et al. 1972
Continental Oil Co., unpublished data
Continental Oil Co., unpublished data
-------
APPENDIX A. Acute toxldty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
LC5o (mg/L)
Reference
to
00
Daohnia maana
24 Cn.16E03S
48
96
C14.15E07
C12-14E02.2S (Natural alcohol
derived)
Ci2E03S (Ziegler derived)
C14E03
C14E02
C14E04
C14EOg
Blueaill sunflsh (Leooomis macrochirusl
24
19.6 (average)
0.36 (average)
21
37
0.73
0.83
1.53
1.76
4.17
10.07
0.3
1.8
Unilever Research Laboratories, unpub-
lished data
Goyer et al. 1981
Lundahl et al. 1972
Lundahl et al. 1972
U.S. Food and Drug Administration
U.S. Food and Drug Administration
U.S. Food and Drug Administration
U.S. Food and Drug Administration
U.S. Food and Drug Administration
U.S. Food and Drug Administration
Procter and Gamble Company, unpublished
data
U.S. Dept. of Interior 1968
-------
APPENDIX A. Acute toxlclty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
LC50 (mg/L)
Reference
Blueaill sunfish (Leooomis macrochirus)
C12-15E09
CO
vo
C12-13E°6.5
Ci4E03S
C12-15E09 (75% linear primary)
C14-18E09
1.87
2.4 (average)
1.9
<2.1; <2.4
2.45; 2.36
4.3
<5.7; <7.5
7.1
8.0
10
Shell Internal Report 1974. ECO 1
Program
U.S. Dept. of Interior. 1968
Procter and Gamble Co., unpublished
data
Procter and Gamble Co., unpublished
data
Shell Internal Report. 1974. ECO 1
Program
Procter and Gamble Co., unpublished
data
Procter and Gamble Co., unpublished
data
Procter and Gamble Co., unpublished
data
Cook Research Laboratories 1966
Cook Research Laboratories 1966
-------
APPENDIX A. Acute toxldty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Blued ill
24
Surfactant
sunflsh (Leopomls macrochlrus)
C17.9E°1.9S
C12-15E09 (98% linear primary)
C19.6E01.1S
Ci3E03S
C12-15E03A
Cl2-15E03S
C12E03S
C12E03S
C12E02.iS
C8E03S
LC50 (mg/L)
10.8
11.0
15
24
32
32
37
73
87
>250
Reference
Procter and Gamble Co., unpublished
data
Cook Research Laboratories 1966
Procter and Gamble Co., unpublished
data
Procter and Gamble Co., unpublished
data
Shell Internal Report 1971
Shell Internal Report 1971
Procter and Gamble Co., unpublished
data
Procter and Gamble Co., unpublished
data
Procter and Gamble Co., unpublished
data
Procter and Gamble Co., unpublished
data
-------
APPENDIX A. Acute toxlclty (1X50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours) Surfactant
Blueaill sunfish (Leopomis macrochirus)
C10E02tlS
96 NH4C15AS, branched
NH4C12.i4AS
NH4C15AS
NaC12AS
NaC12AS
NH4C15AS
NH^nAS, branched
NH4Ci3AS, branched
NH4C12AS
"50
375
2
3
3
4
4
5
16
18
20
.13
.2
.39
.5
.83
.19
.5
.4
.3
(«ng/L)
(1
(2.
(2
.37-3.
8-3.7)
.59-4.
3D
43)
Procter
data
Procter
data
Procter
data
Procter
data
Reference
and Gamble
and
and
and
Bishop and
(4
(3
(13
(15
(16
.06-5.
.97-6.
.1-21.
.2-22.
.0-25.
75)
77)
0)
2)
7)
Procter
data
Procter
data
Procter
data
Procter
data
Procter
and
and
and
and
and
Gamble
Gamble
Gamble
Perry
Gamble
Gamble
Gamble
Gamble
Gamble
Co.,
Co.,
Co.,
Co.,
1979
Co.,
Co.,
Co.,
Co.,
Co.,
unpublished
unpubl
ished
unpublished
unpubl
unpubl
unpubl
unpubl
ished
ished
ished
ished
unpublished
unpubl
ished
data
-------
APPENDIX A. Acute toxlclty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
ro
Blueaill sgnfi^ (LeoDomis macrochirus)
NH4C16AS
NH4CHAS
C16-18AS
NaCjAS
Rainbow trout (Salmo qalrdneri)
96 C14_15E07
C12-15E°9
C12-14E°10.5
C12.i5E03
C12-13E°2
C14-15E°11
LC50 (mg/L)
Reference
21.7 (16.7-28.1) Procter and Gamble Co., unpublished
data
26.0 (19.0-35.4) Procter and Gamble Co., unpublished
data.
76.0 (50-116) Procter and Gamble Co., unpublished
data.
1000
0.8
0.9
1.2
1.8 and 0.8
1.3 and 1.7
1 - 2
1.8 - 2.5
Procter and Gamble Co., unpublished
data.
Abram et al. 1977
Reiff 1976
U.S. Dept. of Interior. 1968
Reiff et al. 1979
Shell Internal Report, TLGR 113.78
Shell Internal Report, TLGR 0115.78
Reiff 1976
-------
APPENDIX A. Acute toxldty
of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
LC50 (mg/L)
Reference
Rainbow trout I Sal mo oairdneri)
C14-15E011
96
C12-i3
C14-15E018
C9-10E02.5
Cg-io
C9-10E05
C12-15
C9-10E02.5S
Fathead, minnow fPimeohales oromelasl
24 C16E06S
C16E04S
1.1
2.7
4 - 10
5 - 6.3
5 - 7
6 - 10
8 - 9
8.9 (7.3-10.3)
28 (23-35)
45
400 - 450
0.8
0.9
Abram et al. 1977
Arthur 0. Little, Inc. 1978
Shell Internal Report, TLGR 0161.78
Shell Internal Report, TLGR 0064.77
Shell Internal Report, TLGR 79.068
Shell Internal Report, TLGR 0166.78
Shell Internal Report, TLGR 0066.77
Shell Chemical Co., unpublished data
Shell Chemical Co., unpublished data
Shell Internal Report, TLGR 0052.77
Shell Chemical Co., unpublished data
Monsanto Co., unpublished data
Monsanto Co., unpublished data
-------
APPENDIX A. Acute toxlclty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
Reference
Fathead minnow (Plmeohales promelas)
Ci6E02S
C12E02S
C14E02S
24 C12_14E06.3
C12-14E°7.4
Ci8E06S
C14E04S
C14E06S
Ci8E04S
CnE04S
C18E02S
Goldfish (Carasslus auratus)
6 C12.14E08
C15E03.2S» branched
1.0
1.5
1.8
1.8
1.8
2.1
4.0
9.3
15
17
80
1.8
3.7
Monsanto
Monsanto
Monsanto
Arthur D
Arthur D,
Monsanto
Monsanto
Monsanto
Monsanto
Monsanto
Monsanto
Co., unpublished data
Co., unpublished data
Co., unpublished data
. Little, Inc. 1978
. Little, Inc. 1978
Co., unpublished data
Co., unpublished data
Co., unpublished data
Co., unpublished data
Co., unpublished data
Co., unpublished data
Reiff et al. 1979
Gafa 1974
-------
APPENDIX A. Acute toxlclty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
LC50 (mg/L)
Reference
U1
Goldfish fCarassius auratus)
C12-14E010.5
nC14AS (92.4% AI)
C12E04
C14E03S
nC14AS (94.3% AI)
C14AS (94% AI, branched)
nC12-15AS (95.8% AI)
C12-15AS
Cn.15AS
C14E03S (5% branched)
C13E05
nC12-16AS (94-3
nC13AS (94.8% AI)
C16E03.4S
4.3
5.0
5.2
6.0
6.3
7.8
7.8
7.8
8.1
8.1
8.5
12.0
18.3
41.0
Reiff et al. 1979
Gafa 1974
Marchetti 1964
Gafa 1974
Gafa 1974
Gafa 1974
Gafa 1974
Gafa and Lattanzi 1974
Gafa and Lattanzi 1974
Gafa 1974
Shell Internal Report, TLGR 79.068
Gafa 1974
Gafa 1974
Gafa 1974
-------
APPENDIX A. Acute toxlclty (LC50) of alcohol surfactants to aquatic animals (continued)
o»
Exposure
(hours) Surfactant
Goldfish I Carassius auratus)
C14AS (98% AI, branched)
Cl2E02.eS
nC12AS (93% AI)
C12E02.6S (5* branched)
nC16AS (95.3% AI)
1 C12E02
C12E04
Ci2E06
C12E08
C12E010
C12E012
C12E014
Cl2«>i6
C12E018
«-C50 (mg/L)
49.1
55.0
60.0
66.5
>300
2
4
5
7
10
20
30
40
100
Reference
Gafa 1974
Gafa 1974
Gafa 1974
Gafa 1974
Gafa 1974
Gloxhuber et al.
Gloxhuber et al.
Gloxhuber et al.
Gloxhuber et al.
Gloxhuber et al.
Gloxhuber et al.
Gloxhuber et al.
Gloxhuber et al.
Gloxhuber et al.
1968
1968
1968
1968
1968
1968
1968
1968
1968
-------
APPENDIX A. Acute toxlclty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
^^^^^^•^^•••M
Goldfish
48
Surfactant LC50 (mg/L)
fCarasslus auratus)
. C12-15E09 (oxo-9™) 1.4
Cl2-15E<>9 (LA-9™) 1.9
C12-14E07 3.3
C12-14E09 5.1
C12-14E012 12.0
Reference
Kurata et al. 1977
Kurata et al. 1977
Kurata et al. 1977
Kurata et al . 1977
Kurata et al. 1977
Hermit crab
48
C12-15E03 (30%, kerosene 85
solution)
C12E01 (30%, Isopropanol «1000
solution)
C12E03 (30%, Isopropanol <1000
solution)
C12E09 (30%, Isopropanol «1000
solution)
C14-15E03 (30%, Isopropanol <1000
Shell Internal Report,
U.S. Dept. of Interior
Shell Internal Report,
Shell Internal Report,
Shell Internal Reoort.
EMGR 0150.71
1968
EMGR 0162.71
EMGR 0162.71
EMGR 0162.71
solution)
-------
APPENDIX A. Acute toxlclty (1.650) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
LC50 (mg/L)
Reference
Hermit crab
00
Brown shrimp
48
(30%, kerosene
solution)
C14E03 (30*» isopropanol
solution)
C16E09 (30*» isopropanol
solution)
C14EOg (30% ?)
(30%, isopropanol
solution)
C14-15E01 (30%» isopropanol
solution)
C16-18E06 (30%» isopropanol
solution)
Cl6-18E09 (30%, isopropanol
solution)
C14-15E03 (30%t kerosene
solution)
<2000
1500
2000
2500
3500
3000-6000
4000
4000
50
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
-------
APPENDIX A. Acute toxldty (LC50) of alcohol surfactants to aquatic animals (continued)
Exposure
(hours)
Surfactant
Brown shrimp
• C12-15E03 (30%, kerosene
solution)
C12-15E03 (30%. Isopropanol
solution)
C14-15E03 (30%, Isopropanol
solution)
C14-15E01 (30%, Isopropanol
solution)
C12-15E09 (30%, Isopropanol
solution)
LC50 (mg/L)
20-30
200
200
500
>3300
Reference
Shell Internal Report, EMGR 0150.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0162.71
Shell Internal Report, EMGR 0138.71
------- |