U.S. Environmental Protection Agency
Hazard Characterization Document

December 2012

SCREENING-LEVEL HAZARD CHARACTERIZATION

SPONSORED CHEMICAL

Trimethyl Phosphite	CASRN 121-45-9

SUPPORTING CHEMICALS

Dimethyl Phosphonate	CASRN 868-85-9

Methanol	CASRN 67-56-1

The High Production Volume (HPV) Challenge Program1 was conceived as a voluntary initiative
aimed at developing and making publicly available screening-level health and environmental
effects information on chemicals manufactured in or imported into the United States in quantities
greater than one million pounds per year. In the Challenge Program, producers and importers of
HPV chemicals voluntarily sponsored chemicals; sponsorship entailed the identification and
initial assessment of the adequacy of existing toxicity data/information, conducting new testing if
adequate data did not exist, and making both new and existing data and information available to
the public. Each complete data submission contains data on 18 internationally agreed to "SIDS"
(Screening Information Data Setl1'2) endpoints that are screening-level indicators of potential
hazards (toxicity) for humans or the environment.

The Environmental Protection Agency's Office of Pollution Prevention and Toxics (OPPT) is
evaluating the data submitted in the HPV Challenge Program on approximately 1400 sponsored
chemicals by developing hazard characterizations (HCs). These HCs consist of an evaluation of
the quality and completeness of the data set provided in the Challenge Program submissions.

They are not intended to be definitive statements regarding the possibility of unreasonable risk of
injury to health or the environment.

2 3

The evaluation is performed according to established EPA guidance ' and is based primarily on
hazard data provided by sponsors; however, in preparing the hazard characterization, EPA
considered its own comments and public comments on the original submission as well as the
sponsor's responses to comments and revisions made to the submission. In order to determine
whether any new hazard information was developed since the time of the HPV submission, a
search of the following databases was made from one year prior to the date of the HPV
Challenge submission to the present: (ChemID to locate available data sources including
Medline/PubMed, Toxline, HSDB, IRIS, NTP, AT SDR, IARC, EXTOXNET, EPA SRS, etc.),
STN/CAS online databases (Registry file for locators, ChemAbs for toxicology data, RTECS,
Merck, etc.), Science Direct and ECHA4. OPPT's focus on these specific sources is based on
their being of high quality, highly relevant to hazard characterization, and publicly available.

1	U.S. EPA. High Production Volume (HPV) Challenge Program; http://www.epa.gov/chemrtk/index.htm.

2	U.S. EPA. HPV Challenge Program - Information Sources; http://www.epa.gov/chemrtk/pubs/general/guidocs.htm.

3	U.S. EPA. Risk Assessment Guidelines; http://cfpub.epa.gov/ncea/raf/rafguid.cfm.

4	European Chemicals Agency, http://echa.europa.eu.


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OPPT does not develop HCs for those HPV chemicals which have already been assessed
internationally through the HPV program of the Organization for Economic Cooperation and
Development (OECD) and for which Screening Initial Data Set (SIDS) Initial Assessment
Reports (SIAR) and SIDS Initial Assessment Profiles (SIAP) are available. These documents are
presented in an international forum that involves review and endorsement by governmental
authorities around the world. OPPT is an active participant in these meetings and accepts these
documents as reliable screening-level hazard assessments.

These hazard characterizations are technical documents intended to inform subsequent decisions
and actions by OPPT. Accordingly, the documents are not written with the goal of informing the
general public. However, they do provide a vehicle for public access to a concise assessment of
the raw technical data on HPV chemicals and provide information previously not readily
available to the public.

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Chemical Abstract Service Registry Number

Sponsored Chemical

(CASRN)

121-45-9

Supporting Chemicals

868-85-9
67-56-1

Chemical Abstract Index Name

Sponsored Chemical
Phosphorus acid, trimethyl ester

Supporting Chemicals

Phosphorus acid, dimethyl ester
Methanol

Structural Formula

Sponsored Chemical

H3C-0^ ,0-CH3

0

1

ch3

SMILES: 0(P(0C)0C)C

Supporting Chemicals

0

ii

A

ch3 ch3
SMILES: 0=P(0C)0C

CH3-OH
SMILES: CO

Summary

TMP is a colorless liquid with high vapor pressure that reacts rapidly with water. It would be
expected to have moderate mobility in soil, and volatilization would be moderate based on its
Henry's Law constant; however, the rapid rate of hydrolysis suggests that these and other
environmental fate pathways are not applicable for this substance. The rate of atmospheric
photooxidation is slow. TMP is expected to have low persistence (PI) and low bioaccumulation
potential (Bl).

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The acute oral toxicity of TMP to rats and mice is low; acute inhalation toxicity to rats is low
and the acute dermal toxicity to rabbits is moderate. In a 90-day oral (gavage) repeated-dose
toxicity study in rats, TMP resulted in mortality at 160 mg/kg-day. The surviving animals at
this dose showed effects on liver and male reproductive organs. The NOAEL is 80 mg/kg-day.
In a 4-week oral (gavage) toxicity study in rats, effect on body weight and food consumption
was seen at 164 mg/kg-day. The NOAEL is 32.8 mg/kg-day. In three separate four-week
repeated-inhalation toxicity studies in rats, ocular effects were observed, including formation of
irreversible cataracts at 0.53 mg/L-day in two studies and at 0.26 mg/L-day in one study. The
NOAEC values in two studies are not established; the NOAEC for the third study is 0.051
mg/L-day. (In a limited study of employees of a TMP manufacturing plant showed no clinical
cataracts in either exposed or non-exposed employee groups.) In a 21-dy dermal toxicity study
in rabbits, TMP resulted in mortality and effects on liver at > 300 mg/kg-day; the NOAEL is not
established.

No reproductive toxicity studies were available for TMP, however, adverse effects on
spermatogenesis and testes were observed in the 90-day oral repeated-dose toxicity study in rats.
In an oral (gavage) combined reproduction/developmental toxicity screening test in rats with the
supporting chemical, DMHP, effects on mating and fertility indices were seen at
270 mg/kg-day; the NOAEL for reproductive toxicity is 90 mg/kg-day. The systemic toxicity
NOAEL is 90 mg/kg-day based on mortality and severe body weight effects at 270 mg/kg-day.
In the same study, the NOAEL for maternal and developmental toxicity is 90 mg/kg-day, based
on no effects at the highest dose at which females survived to term. In a two-generation
reproductive toxicity study in rats via inhalation, the supporting chemical, methanol, showed no
systemic or reproductive toxicity at 1.3 mg/L-day, highest dose tested. In the same study, the
earlier time of descensus testis in pups was seen at 0.013 mg/L-day; the NOAEC for
developmental toxicity is not established. In an oral prenatal developmental toxicity study in
rats with TMP, decreased body weights were seen in dams at 164 mg/kg-day; the NOAEL for
maternal toxicity is 49 mg/kg-day. In the same study, skeletal and soft tissue abnormalities
were seen in pups at 164 mg/kg-day; the NOAEL for developmental toxicity is 49 mg/kg-day.

TMP induced gene mutation in mammalian cells but not in bacteria in vitro, induced
micronuclei in bone marrow in vivo, induced DNA damage in bacteria in vitro and produced
point mutations, chromosomal aberrations and chromosome loss in fruit flies in vivo. TMP is
irritating rabbit skin and eyes.

For aquatic toxicity, all values are based on the supporting chemical DMHP. The 96-hour LC50
of supporting chemical DMHP for fish is > 15.6 mg/L. The 48-hour EC50 of supporting
chemical DMHP for aquatic invertebrates is 24.8 mg/L. The 72-hour EC50 of supporting
chemical DMHP for aquatic plants is >25 mg/L (growth rate).

No data gaps were identified under the HPV Challenge Program.	

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The sponsor, Rhodia Inc., representing a consortium with United Phosphorus Inc. and Sabero
Organic Gujarat Ltd., submitted a Test Plan and Robust Summaries to EPA for trimethyl
phosphite (TMP; CAS No. 121-45-9; CA name: phosphorous acid, trimethyl ester) on December
21, 2005. EPA posted the submission on the ChemRTK HPV Challenge website on February 7,
2006 (http://www.epa.gov/HPV/pubs/summaries/viewsrch.htm). EPA comments on the original
submission were posted to the website on August 11, 2008

(http://www.epa.gov/HPV/pubs/summaries/trimtphs/cl6139tc.htm). Public comments were also
received and posted to the website.

Justification for Supporting Chemicals

Dimethyl phosphonate (DMHP; CASRN 868-85-9; CA name: phosphonic acid, dimethyl ester)
is used as a supporting chemical for trimethyl phosphate. TMP hydrolyses to form DMHP and
methanol. Both hydrolysis products were assessed in the OECD HPV program, and their data
sets can be viewed at the following link: http://cs3-hq.oecd.org/scripts/hpv/. The first stage
hydrolysis reaction occurs in minutes over a range of pH values. EPA agrees that the using
DMHP and/or methanol data for addressing data gaps for human health and ecotoxicity
endpoints for TMP is appropriate.

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1. Chemical Identity

1.1	Identification and Purity

TMP is a colorless liquid with high vapor pressure that reacts rapidly with water. Where
indicated in robust summaries, the purity of the tested substance is >98%. Since TMP
hydrolyzes rapidly, it was protected from hydrolysis with nitrogen during the studies.

1.2	Physical-Chemical Properties

The physical-chemical properties of TMP (CASRN 121-45-9) and DMHP (CASRN 868-85-9)
are summarized in Table 1. The structures are provided in the Appendix.

Table 1. Physical-Chemical Properties of Trimethyl Phosphite and Dimethyl Phosphonate1

Property

Trimethyl Phosphite
(TMP)

Dimethyl Phosphonate
(DMHP)

CASRN

121-45-9

868-85-9

Molecular Weight

124.08

110.05

Physical State

Clear, colorless, water-like liquid

Colorless liquid2

Melting Point

-78°C (measured)

29°C (measured)2

Boiling Point

111-112°C (measured)

170.5°C (measured)2

Vapor Pressure

24.1 mm Hg at 25°C (measured)

1.5 mm Hg at 20°C (measured)

Dissociation Constant
(pKa)

Not applicable

Not applicable

Henry's Law Constant

Not applicable due to hydrolysis

2.2><10"6 atm-m3/mole (estimated)3

Water Solubility

Not applicable due to hydrolysis

100,000 mg/L at 20°C (measured)2

Log Kow

Not applicable due to hydrolysis

-1.13 (estimated)3

'The Trimethyl Phosphite Consortium. 2005. Test Plan and Robust Summary for Trimethyl Phosphite. Available online at
http://www.epa.gov/oppt/chemrtk/pubs/summaries/trimtphs/cl6139tc.htm as of June 4, 2012.

2Hazardous Substance Databank (HSDB). 2012. Available online at http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen7HSDB as of
June 1,2012.

3U.S. EPA. 2012. Estimation Programs Interface Suite™ for Microsoft® Windows, v4.10. U.S. Environmental Protection
Agency, Washington, DC, USA. Available online at http://www.epa.gov/opptintr/exposure/pubs/episuitedl.htm as of June 4,
2012

2. General Information on Exposure

2.1 Production Volume and Use

CASRN 121-45-9 had an aggregated production and/or import volume in the United States
between 1 to 10 million pounds during calendar year 2005.

Trimethyl phosphate is used as a solvent for aromatic halogenations and nitrations as required for
the preparation of pesticides and pharmaceuticals.

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2.2 Environmental Exposure and Fate
Environmental Fate Characterization

TMP is expected to have moderate mobility in soil, and volatilization is expected to be moderate;
however, the rapid rate of hydrolysis indicates that volatilization, mobility in soil and
biodegradation will not be important environmental fate processes. The hydrolysis half-life of
TMP is reported <5 minutes at pH 6 at 0°C. Its hydrolysis product, DMHP was degraded 50%
as measured by dissolved organic carbon (DOC) loss after 28 days using the modified OECD
(OECD 301E) test. DMHP achieved 48% of its theoretical biochemical oxygen demand (BOD)
using an activated sludge inoculum and the MITI (OECD 301C) test after a 28 day incubation
period. It also undergoes hydrolysis to produce monomethyl phosphonate which slowly
hydrolyzes to phosphorous acid and methanol. The rate of atmospheric photooxidation of TMP
is slow. TMP is expected to have low persistence (PI) and low bioaccumulation potential (Bl).

The environmental fate characteristics of TMP (CASRN 121-45-9) and DMHP
(CASRN 868-85-9) are summarized in Table 2.

Table 2. Environmental Fate Characteristics of Trimethyl Phosphite and DMHP1

Property

Trimethyl phosphite
(TMP)

Dimethyl phosphonate
(DMHP)

CASRN

121-45-9

868-85-9

Photodegradation Half-life

1.3 days (estimated)2

1.9 days (estimated)2

Hydrolysis Half-life

21 minutes at pH 10 and 25°C;
<5 minutes at pH 6 and 0°C

10 days at 25 °C and 19 days at 20°C at
an unspecified pH3

Biodegradation

Not applicable due to hydrolysis

50% after 28 days

(not readily biodegradable);

48% after 28 days

(not readily biodegradable)3

Bioaccumulation Factor

Not applicable due to hydrolysis

BAF = 0.9 (estimated)2

Log Koc

Not applicable due to hydrolysis

3.7 (estimated)2

Fugacity

(Level III Model)2'4

Air (%)
Water (%)
Soil (%)
Sediment (%)

98.7
0.6
0.6
<0.1

3.7
42.8
53.5
<0.1

Persistence5

PI (low)

PI (low)

Bioaccumulation5

Bl (low)

Bl (low)

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'The Trimethyl Phosphite Consortium. 2005. Test Plan and Robust Summary for Trimethyl Phosphite. Available online at
http://www.epa.gov/oppt/chemrtk/pubs/summaries/trimtphs/cl6139tc.htm as of June 1,2012.

2U.S. EPA. 2012. Estimation Programs Interface Suite™ for Microsoft® Windows, v4.10. U.S. Environmental Protection
Agency, Washington, DC, USA. Available online at http://www.epa.gov/opptintr/exposure/pubs/episuitedl.htm as of June 1,
2012

3Hazardous Substance Databank (HSDB). 2012. Available online at http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen7HSDB as of
June 1,2012.

4Half-lives of 0.08 hours were used for the water, soil, and sediment compartments while a half-life of 15 hours was used for the
atmosphere compartment.

'Federal Register. 1999. Category for Persistent, Bioaccumulative, and Toxic New Chemical Substances. Federal Register 64,
Number 213 (November 4,1999) pp. 60194-60204.

Conclusion: TMP is a colorless liquid with high vapor pressure that reacts rapidly with water.
It would be expected to have moderate mobility in soil, and volatilization would be moderate
based on its Henry's Law constant; however, the rapid rate of hydrolysis suggests that these and
other environmental fate pathways are not applicable for this substance. The rate of atmospheric
photooxidation is slow. TMP is expected to have low persistence (PI) and low bioaccumulation
potential (Bl).

3. Human Health Hazard

A summary of health effects data are provided in Table 3.

Acute Oral Toxicity

Trimethyl phosphite (CAS No. 121-45-9)

(1)	Sprague-Dawley rats (2/sex/dose) were administered TMP (purity not stated) via gavage at
900, 1350, 2025 or 3038 mg/kg and observed for 14 days. Mortality was 0/4, 2/4, 4/4 and 4/4 at
900, 1350, 2025 or 3038 mg/kg, respectively.

LD50 = 1350 mg/kg

(2)	In seven studies, Wistar rats (5/sex/dose for each study) were administered TMP
(purity 98.5-99%) via gavage at five doses (in each study) between 500 and 3000 mg/kg and
observed for 14 days. Mortality was observed at > 1000 mg/kg.

LD50 = 1500 - 2240 mg/kg

(3)	ICR mice (5/sex/dose) were administered TMP (purity 98.5%) via gavage at 3000, 3500,
4000, 4500 or 5000 mg/kg and observed for 14 days. Mortality was 2/10, 2/10, 3/10, 7/10 and
8/10 at 3000, 3500, 4000, 4500 or 5000 mg/kg, respectively.

LD50 = 4280 mg/kg

Acute Inhalation Toxicity

Trimethyl phosphite (CAS No. 121-45-9)

Male rats (5/concentration, strain not stated) were exposed via whole body inhalation to TMP
(purity not stated) at 9000 ppm (45.7 mg/L) for 4 hours. The observation period is not stated in
the robust summary. There was no mortality.

LC50 > 45.7 mg/L

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Acute Dermal Toxicity

Trimethylphosphite (CAS No. 121-45-9)

(1)	New Zealand White rabbits (minimum of 2/sex/dose) were administered TMP (purity not
stated) via the dermal route on intact and abraded sites at 266.7, 400, 600, 900, 1350, 2025, 3000
or 4556 mg/kg under occluded conditions for 24 hours. All residual test substance ewas
removed following the exposure period. The animals were observed for a total of 14 days.
Mortality occurred at > 400 mg/kg.

LD5o = 934 mg/kg

(2)	Male New Zealand White rabbits (4/dose) were administered TMP (purity 98.5%) via the
dermal route at 6000, 7500 or 9200 mg/kg and observed for up to 14 days. Exposure duration,
abrasion and occlusion conditions were unspecified. Mortality occurred at > 7500 mg/kg.
LD50 = 7500 mg/kg

Repeated-Dose Toxicity

Trimethyl phosphite (CAS No. 121-45-9)

Oral

In a subchronic study, Sprague-Dawley rats (15/sex/dose) were administered TMP (purity
98.5%, protected from hydrolysis with Nitrogen) by gavage (as 10% solution in corn oil) at 0,
40, 80 or 160 mg/kg-day for 90 consecutive days. At 160 mg/kg-day, treatment-related mortality
was seen (4 males and 3 females). In two animals tremors were seen in week 11. Body weight
and food consumption was significantly decreased (significance not provided); no consistent
pattern was seen in food utilization. No differences were observed in hematology, clinical
chemistry or urinalyses parameters. Significantly increased (significance not provided) absolute
weights of adrenal, brain and kidneys (both sexes) and significantly increased (significance not
provided) relative (to body) weights of heart and spleen were seen in females. At gross
pathology examination, irregular thickening of the stomach (one animal) and decreased spleen
size (two animals) were seen at 160 mg/kg-day. Histopathological examination at
160 mg/kg-day revealed minor fatty changes in the liver of both sexes and occasional
hepatocytes containing eosinophilic material in males. Hypoplasia of gonads, seen in 11 of 11
males at 160 mg/kg-day, was characterized by reduced spermatogenesis and reduction in size
and number of spermatogonia and other spermatogenic cells. However, density of sperm in the
epididymis was "not greatly or uniformly reduced" at 160 mg/kg-day. No significant effects
were seen at lower doses.

LOAEL = 160 mg/kg-day (based on mortality and histopathological changes in liver and male
reproductive tissues)

NOAEL = 80 mg/kg-day

(2) In a sub-acute study, Sprague-Dawley rats (5/sex/dose) were TMP (purity 98.5%, protected
from hydrolysis with Nitrogen) by gavage at 0, 32.8, 164 or 328 mg/kg-day for 21 consecutive
days. Treatment-related mortality was seen at 328 mg/kg-day (4 males and 4 females). At

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328 mg/kg-day, clinical signs included decreased locomotor activity, abnormal gait and rough
coat in all animals. Decreased locomotor activity was also seen in animals at 164 mg/kg-day.
Body weights in females were significantly decreased (significance not provided) at >164
mg/kg-day during weeks 2 and 3. Food consumption was significantly decreased (significance
not provided) in females at 164 (week 3) and 328 (weeks 2 and 3) mg/kg-day. Food utilization
was also decreased at these doses. There were no effects on hematology, clinical chemistry and
urinalyses parameters. Gross pathology examination showed congestion of stomach in all
animals and loss of mucosal surface (2 animals) at 328 mg/kg-day. Histopathological
examination was not conducted.

LOAEL = 164 mg/kg-day (based on mortality and effect on body weight and food
consumption)

NOAEL = 32.8 mg/kg-day
Inhalation

(1)	In a 4-week study, Sprague-Dawley rats (10/sex/concentration) were exposed via whole-body
inhalation to TMP at 0, 104, 292 or 581 ppm (equivalent to 0, 0.53, 1.48 or 2.95 mg/L—effective
inhaled concentrations) 6 hours/day, 5 days/week. Treatment-related deaths (not reported by
sex) occurred in 2/20 rats at 292 ppm and 7/20 rats at 581 ppm. Clinical observation showed
yellow perianal staining at all concentrations, labored breathing, excessive lacrimation and
chromodacryorrhea at 292 and 581 ppm and reduced activity, coldness of body, general poor
condition and closed eyes at 581 ppm. Lower body weight and body weight gain occurred in
both sexes at 581 ppm. Increased kidney-to-body weight and kidney-to brain weight ratios were
seen at 292 and 581 ppm in females; absolute kidney weights in females were increased at

292 ppm and decreased at 581 ppm. Decreased absolute and relative brain weights (to body
weight) were also seen at 581 ppm. Red blood cell count was elevated in males at 581 ppm.
Gross pathology revealed scattered lung abnormalities in all treated groups and increased lung
discoloration and stomach abnormalities at 581 ppm. Ophthalmic examination at study
termination, showed corneal opacity at 104 ppm, corneal opacity and cloudy eyes at 292 ppm
and corneal opacity, cloudy eyes and film covering one or both eyes at 581 ppm. Histological
examination revealed cataracts at 292 and 581 ppm (incidences not given). Based on the ocular
effects seen in this study, the same laboratory conducted two follow-up studies that focused on
examination of the eyes more frequently, in greater detail and with more animals/group [see
summaries (2) and (3) below]. In the follow-up studies only mortality, clinical signs, body
weight, lung weight, ophthalmoscopy and histological examination of lungs, eyes and gross
lesions were conducted.

LOAEC = 0.53 mg/L-day (based on ocular effects)

NOAEC = Not established

(2)	Sprague-Dawley rats (20/sex in control and low-concentration groups; 36/sex in high-
concentrations group) were exposed via whole-body inhalation to TMP at 0, 105 or 600 ppm
(equivalent to 0, 0.53 or 3.04 mg/L) 6 hours/day, 5 days/week, for 28 days followed by 8 weeks
of post-exposure observation. Deaths occurred in 31 males and 20 females at 600 ppm. No
relevant non-ocular clinical signs were recorded. Mean body weights and body weight gains
were lower at 600 ppm throughout weeks 1- 5. Absolute and relative lung weights were
increased at 600 ppm, accompanied by a high incidence of lung abnormalities at gross
observation. Histopathology associated the deaths at 600 ppm with bronchopneumonia in

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23 of the males and 14 of the females—pulmonary granulomatous foci were seen in many of
these animals (22 males and 10 females). Ophthalmoscopy showed reversible striate opacities in
7/30 animals at 105 ppm and irreversible cataracts in almost all animals at 600 ppm.
Histopathology confirmed the presence of irreversible cataracts at 600 ppm.

LOAEC = 0.53 mg/L-day (based on ocular effects)

NOAEC = Not established

(3) Sprague-Dawley rats (20/sex/group) were exposed via whole-body inhalation to TMP at
measured concentrations of 0, 10, 51 or 101 ppm (equivalent to 0, 0.051, 0.26 or 0.51 mg/L,
respectively), 6 h/day, 5 days/week, for 4 weeks followed by 8 weeks of post-exposure
observation. No treatment-related deaths occurred and no non-ocular clinical signs were
recorded. Treatment did not affect body weight, lung weight or findings at gross observation.
Using ophthalmoscopy, ocular lesions (irregularities of the corneal surface) were first observed
at 4 weeks at 51 ppm (3/15 males and 7/17 females) and 101 ppm (5/15 males and 7/17 females).
Lenticular opacities in females were seen at 51 and 101 ppm at week 2 post-exposure and at 101
ppm at weeks 4 and 8 post-exposure. Histopathology showed mild inflammatory changes in
corneas of approximately 60% of males and females sacrificed after 4 weeks of exposure to 51 or
101 ppm; these effects were not observed in animals sacrificed at 2 or 8 weeks post-exposure.
The robust summary concluded that TMP is cataractogenic and a corneal irritant at 51 and 101
ppm.

LOAEC = 0.26 mg/L (based on ocular effects)

NOAEC = 0.051 mg/L

Dermal

New Zealand white rabbits (6/sex/dose) were administered undiluted TMP (purity 98.5%)
dermally at 0, 300, 600 or 1200 mg/kg-day 6 hours/day for 21 days. The test substance was
applied to the clipped trunks of the animals; the skin of half of the animals was abraded. After
the exposure period each day, the test substance was removed by gentle washing with warm
water. Mortality was 0/12 1/12, 2/12 and 11/12 at 0, 300, 600 or 1200 mg/kg-day, respectively.
Vocalization, decreased locomotor activity (at 300 and 600 mg/kg-day) and loss of righting
reflex was seen at 600 mg/kg-day. Treated animals showed dose-related irritation (edema and
Erythema) with severity increasing in animals with abraded skin with increasing time. Body
weights were significantly lower (significance not provided) at 1200 mg/kg-day. At necropsy, a
dose-related increased incidence of light-colored spots on lungs was seen. Histopathology
examination showed lung congestion and edema and advanced parenchymatious degeneration
with chronic round cell infiltration in liver at 600 mg/kg-day. At 300 mg/kg-day, lung
congestion and edema was seen at same degree as that for 600 mg/kg-day animals; effect on liver
was less marked than for 600 mg/kg-day.

LOAEL = 300 mg/kg-day (based on mortality and histopathology of liver and lungs)

NOAEL = not established

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Reproductive Toxicity

Trimethylphosphite (CAS No. 121-45-9)

No reproductive toxicity study data were submitted for TMP, but it produced adverse effects on
spermatogenesis and testes histology in the 90-day repeated-dose oral study in rats described
above. These data alone are inadequate to satisfy the reproductive toxicity endpoint.
Reproductive toxicity data for the hydrolysis products of TMP, DMHP and methanol, are used to
address the reproductive toxicity endpoint for TMP.

Dimethylphosphonate (CAS No. 868-85-9, supporting chemical)

In a combined reproduction/developmental toxicity screening study, Wistar rats (12/sex/dose)
were administered DMHP by gavage at 0, 30, 90 or 270 mg/kg-day from 2 weeks before mating
to the end of gestation and up to 4 - 5 days of lactation. Males were sacrificed after at least
28 days of treatment. Females and pups were sacrificed on days 4-5 postpartum. At
270 mg/kg-day, animals of both sexes exhibited clear clinical signs of systemic toxicity (poor
general state, apathy, high stepping gait, squatting position, bloody muzzle, piloerection,
emaciation, tremor and/or desiccation of skin) and severe body weight loss. Two males of this
group were found dead with discolored liver and/or lungs, and all females of this group had to be
sacrificed in moribund condition during mating or gestation. At 90 mg/kg-day, soft feces and/or
diarrhea were noted in both sexes more frequently than in the control group. No treatment-
related effects were noted at 30 mg/kg-day. At 270 mg/kg-day, relative testis weight was
increased and absolute epididymidis weight was decreased; however, no pathological changes
were found at macroscopic and microscopic examinations of these organs. No treatment-related
histological changes were reported for ovaries.

At 270 mg/kg-day, the number of females with corpora lutea and implantation sites and the
frequency and severity score of "large corpora lutea" and of granular luteal cells were decreased
and mating and fertility indices were reduced. At 30 and 90 mg/kg-day, no effects were found
on reproductive endpoints (mating parameters, fertility index, gestation indices, gestation length,
prenatal loss, number of implantation sites, macroscopically visible corpora lutea, live birth
index, sex ratio, pup birth weight, litter size, pup weight development, viability and lactation of
F1 rats). Sex ratio, mortality and weights of F1 pups were not affected by treatment up to and
including 90 mg/kg-day, while evaluation was not possible at higher doses as there were no
surviving pups. No externally malformed pups were observed. Summarized from "Dimethyl
Phosphonate", OECD SIDS, "868859.pdf' at http://cs3-hq.oecd.org/scripts/hpv/.

LOAEL (systemic toxicity) = 270 mg/kg-day (based on mortality and severe body weight loss)
NOAEL (systemic toxicity) = 90 mg/kg-day

LOAEL (reproductive toxicity) = 270 mg/kg-day (based on reduced insemination and fertility
indices)

NOAEL (reproductive toxicity) = 90 mg/kg-day

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Methanol (CAS No. 67-56-1, supporting chemical)

In a two-generation reproductive toxicity study, Sprague-Dawley rats (30/sex/group for F0
animals) were exposed 20 hours/day via whole-body inhalation to methanol at concentrations of
0 (untreated control), 0.013, 0.13 or 1.3 mg/L. For F0 animals, the premating exposure period
was 60 days. Exposure durations were as follows: F0 males, age 8 weeks through mating;
F0 females, age 8 weeks through end of lactation; F1 males, from birth through end of mating;
F1 females, from birth through weaning of F2 pups; and F2 males and females, from birth to day
21. Mating periods were up to 21 days. No treatment-related alterations of reproductive
endpoints, including sexual cycle, mating time, fertility and pregnancy rate, were seen in F0 or
F1 animals. The developmental parameter descensus testis occurred 0.5 tol day earlier than
control in F1 and F2 pups at 1.3 mg/L and occurred 0.5 days earlier than control in F2 pups at
0.13 mg/L. At 1.3 mg/L, absolute and relative (to body) brain weights were decreased in F1 and
F2 pups, but this was not accompanied by histological changes. Summarized from "Methanol",
OECD SIDS, "38958562.zip" at http://cs3-hq.oecd.org/scripts/hpv/.

NOAEC (F0 parental toxicity) = 1.3 mg/L-day (highest concentration tested)

NOAEC (reproductive toxicity) = 1.3 mg/L-day (highest concentration tested)

LOAEC (developmental toxicity) = 0.013 mg/L-day (based on earlier time of descensus testis)
NOAEC (developmental toxicity) = Not established

Trimethylphosphite (CAS No. 121-45-9)

In the 90-day gavage study of trimethyl phosphite in Sprague-Dawley rats described previously,
hypoplasia of gonads, seen in 11 of 12 males at 160 mg/kg-day, was characterized by reduced
spermatogenesis and reduction in size and number of spermatogonia and other spermatogenic
cells. However, density of sperm in the epididymis was "not greatly or uniformly reduced" at
160 mg/kg-day. No adverse effects on male reproductive organs were seen at the other doses
tested (40 and 80 mg/kg-day).

Trimethyl phosphite reduced spermatogenesis and produced adverse histological changes
in the testes in this repeated-dose oral study.

Developmental Toxicity

Trimethyl phosphite (CAS No. 121-45-9)

In a prenatal developmental toxicity study, pregnant Sprague-Dawley rats (25/dose) were
administered TMP by gavage in corn oil at 0, 16, 49 or 164 mg/kg-day from day 6 through day
15 of gestation and were sacrificed on gestation day 21. No treatment-related maternal clinical
signs or mortalities occurred. At 164 mg/kg-day, maternal body weight was reduced during days
6 - 10 of gestation and at day 20; dam body weight minus gravid uterus weight was also reduced
at this dose. Developmental effects at 164 mg/kg-day included abnormalities of long bones,
increases in dilated ventricles and undescended testes and teratogenic effects including
exencephaly, spina bifida and scoliosis and cleft palate. No developmental effects were noted in
mid- and low-dose groups.

LOAEL (maternal toxicity) = 164 mg/kg-day (based on reduced body weight)

NOAEL (maternal toxicity) = 49 mg/kg-day

LOAEL (developmental toxicity) = 164 mg/kg-day (based on skeletal and soft tissue
abnormalities)

NOAEL (developmental toxicity) = 49 mg/kg-day

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Dimethylphosphonate (CAS No. 868-85-9, supporting chemical)

In a combined reproduction/developmental toxicity screening study described above, Wistar rats
(12/sex/dose) were administered DMHP by gavage at 0, 30, 90 or 270 mg/kg-day from 2 weeks
before mating to the end of gestation and up to 4 - 5 days of lactation. Males were sacrificed
after at least 28 days of treatment. Females and pups were sacrificed on days 4-5 postpartum.
At 270 mg/kg-day, the number of females with corpora lutea and implantation sites and the
frequency and severity score of "large corpora lutea" and of granular luteal cells were decreased
and mating and fertility indices were reduced. At 30 and 90 mg/kg-day, no effects were found
on reproductive endpoints (mating parameters, fertility index, gestation indices, gestation length,
prenatal loss, number of implantation sites, macroscopically visible corpora lutea, live birth
index, sex ratio, pup birth weight, litter size, pup weight development, viability and lactation of
F1 rats). Sex ratio, mortality and weights of F1 pups were not affected by treatment up to and
including 90 mg/kg-day, while evaluation was not possible at higher doses as there were no
surviving pups. No externally malformed pups were observed. Summarized from "Dimethyl
Phosphonate", OECD SIDS, "868859.pdf' at http://cs3-hq.oecd.ore/scripts/hpv/.

NOAEL (maternal/developmental toxicity) = 90 mg/kg-day (based on no effects at highest
dose in which females survived to term)

Genetic Toxicity — Gene Mutation
In vitro

Trimethylphosphite (CAS No. 121-45-9)

(1)	Salmonella typhimurium strains TA98, TA100, TA1535, TA1537 and TA1538 were exposed
to TMP at 0.5, 3, 15, 30 or 50 |iL/plate with and without metabolic activation. Positive and
negative controls were tested concurrently and responded appropriately. TMP was cytotoxic at
50 |iL/plate without activation and 30 |iL/plate with activation.

Trimethyl phosphite was not mutagenic in this assay.

(2)	Salmonella typhimurium strains TA98, TA100, TA1535, TA1537 and TA1538 and
Sacromyces cerevisiae D4 were exposed to trimethyl phosphite at 0.001, 0.01, 0.1, 1 or 5
|iL/plate with and without metabolic activation. Positive and negative controls were tested
concurrently and responded appropriately. No cytotoxicity was seen at any concentration tested.
Trimethyl phosphite was not mutagenic in this assay.

(3)	In three studies, mouse lymphoma cells (L5178Y/TK+/-) were exposed to trimethyl
phosphite at various concentrations (0.18 - 2.7 |iL/mL without metabolic activation and
0.24 - 3.2 |iL/mL with activation in the first study; 0.13-1.8 |iL/mL without metabolic
activation and 0.24 - 3.2 |iL/mL with activation in the second study; and 0.18 - 2.7 |iL/mL
without metabolic activation and 0.24 - 3.2 |iL/mL with activation in the third study). Positive
and negative controls were tested concurrently and responded appropriately. Trimethyl
phosphite was cytotoxic at 1 |iL/mL in the first study and 10 |iL/mL in the other two studies. In
all three studies, trimethyl phosphite induced increases in mutation with and without metabolic
activation.

Trimethyl phosphite was mutagenic in these assays.

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In vivo

Trimethylphosphite (CAS No. 121-45-9)

In three studies, fruit flies (Drosophila melanogaster) were exposed to TMP (purity 99.51%) at
multiple concentrations (0.07 mL as an aerosol in 25 mL flasks for 1 minute or 30 seconds,
respectively, in the first and second studies; 0.3 mL in a 50-mL volume for an unspecified
interval in the third study). Positive and negative controls were tested concurrently and
responded appropriately. In the first study (1-minute exposure), no effects occurred for the
point-mutation endpoints (induction of sex-linked lethals and white-ivory somatic reversions)
and the chromosome aberrations and loss endpoints (induction of dominant lethal mutations,
Y chromosome loss and bithorax test of Lewis) that were examined. Because levels of sterility
and mortality were unacceptable after 1 minute of exposure in the first study, the exposure period
was reduced to 30 seconds in the second study. In this study, TMP was positive in a test for
point mutations (induction of sex-linked lethals) and positive for two tests for chromosome
aberrations and loss (induction of dominant lethal mutations and the bithorax test of Lewis). In
the third study, TMP was positive for the same endpoints as in the second study and, in addition,
induced Y chromosome loss.

Trimethyl phosphite induced point mutations, chromosomal aberrations and chromosome
loss in these assays.

Genetic Toxicity — Chromosomal Aberrations
In vivo

Dimethylphosphonate (CAS No. 868-85-9, supporting chemical)

(1)	In micronucleus assay, B6C3F1 mice were administered DMHP via intraperitoneal injection
at 0, 250 and 500 mg/kg-day once daily for three consecutive days. Twenty four hours after last
treatment, the polychromatic erythrocytes from bone marrow were analyzed for micronuclei.
The number of micronucleated polychromatic erythrocytes (PCEs) per 1000 PCEs score was
elevated in the first trial at 500 mg/kg-day. In the second trial, this result could not be
reproduced. The results were inconclusive.

Dimethyl phosphonate induced micronuclei in this assay.

(2)	In another micronucleus assay NMRI mice were administered a single dose of DMHP at
200 mg/kg. The incidences of micro-nucleated polychromatic erythrocytes (PCEs) per

1000 PCEs scored were measured 16, 24 and 48 hours after i.p. injection of DMP. There was a
statistically non-significant doubling of micro-nucleated PCEs after 48 hours (negative controls
1.3 ± 1.1, 16h0.8 ± 1.1, 24h 1.8 ± 1.5, 48 h 2.7 ± 3.1). Although statistically significant, the
values for the positive control group (cyclophosphamide) were unusually low (7.3 ± 5.5 as
compared to the laboratory's historical positive control range of 10.2 - 25.1). It is therefore not
certain, whether this test was sufficiently sensitive. The study authors concluded the results of
this assay as negative.

Dimethyl phosphonate did not induce micronuclei in this assay.

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Genetic Toxicity - Other
In vitro

Trimethylphosphite (CAS No. 121-45-9)

In DNA damage and repair studies, Escherichia coli WP2/WP100 and Salmonella typhimurium
TA1978/TA1538 strains were exposed to TMP at 0.3 - 50 |iL/plate in two studies and at
10 |iL/plate in a third study; all studies were conducted with and without metabolic activation.
Positive and negative controls were tested concurrently and responded appropriately.
Cytotoxicity occurred at 50 |iL /plate. Preferential killing of repair-deficient strains was
observed with and without activation in the two studies that tested up to 50 |iL/plate, whereas no
preferential killing was observed in the third study (maximum concentration of 10 |iL/plate).
Trimethyl phosphite induced DNA damage in these assays.

Additional Information
Skin Irritation

Trimethyl phosphite (CAS No. 121-45-9)

(1)	Six New Zealand albino rabbits were administered undiluted TMP (0.5 g 98.5% purity),
moistened with a minimal amount of water, via the dermal route on intact and abraded sites
under occluded conditions for 24 hours and observed at 24 and 72 hours following dosing. The
subtotals for mean scores for erythema and edema were 2.6 for abraded and 2.5 for unabraded
skin. The primary dermal irritation index (PDII) was 1.3.

Trimethyl phosphite was irritating to rabbit skin in this study.

(2)	Six New Zealand albino rabbits were administered undiluted TMP (0.5 g 98.5% purity),
moistened with a minimal amount of water and protected from hydrolysis by N2, via the dermal
route to intact and abraded sites under occluded conditions for 24 hours and observed at 24 and
72 hours following dosing. No erythema, edema or eschar formation was observed. The PDII
was 0.

Trimethyl phosphite was not irritating to rabbit skin in this study.

Eye Irritation

Trimethyl phosphite (CAS No. 121-45-9)

(1) Six New Zealand albino rabbits were administered undiluted TMP (0.1 mL, purity not
indicated) by instillation into the conjunctival sac of one eye of each rabbit. Ocular reactions
were graded after 1, 24, 48 and 72 hours and 7 days. Irritation was observed in the iris at 1 hour
and the conjunctiva at 1 and 24 hours. No reaction was noted in the cornea during the study or
the iris after 1 hour and the conjunctiva after 24 hours.

Trimethyl phosphite was irritating to rabbit eyes in this study.

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(2) Six New Zealand albino rabbits were administered undiluted TMP (0.1 mL of 98.5% purity,
protected from hydrolysis by N2) by instillation into the conjunctival sac of one eye of each
rabbit. Ocular reactions in cornea, iris and conjunctiva were graded after 1, 24, 48 and 72 hours
and 4 and 7 days.

Trimethyl phosphite was not irritating to rabbit eyes in this study.

Conclusion: The acute oral toxicity of TMP to rats and mice is low; acute inhalation toxicity to
rats is low and the acute dermal toxicity to rabbits is moderate. In a 90-day oral (gavage)
repeated-dose toxicity study in rats, TMP resulted in mortality at 160 mg/kg-day. The surviving
animals at this dose showed effects on liver and male reproductive organs. The NOAEL is 80
mg/kg-day. In a 4-week oral (gavage) toxicity study in rats, effect on body weight and food
consumption was seen at 164 mg/kg-day. The NOAEL is 32.8 mg/kg-day. In three separate
four-week repeated-inhalation toxicity studies in rats, ocular effects were observed, including
formation of irreversible cataracts at 0.53 mg/L-day in two studies and at 0.26 mg/L-day in one
study. The NOAEC values in two studies are not established; the NOAEC for the third study is
0.051 mg/L-day. (In a limited study of employees of a TMP manufacturing plant showed no
clinical cataracts in either exposed or non-exposed employee groups.) In a 21-dy dermal toxicity
study in rabbits, TMP resulted in mortality and effects on liver at > 300 mg/kg-day; the NOAEL
is not established.

No reproductive toxicity studies were available for TMP, however, adverse effects on
spermatogenesis and testes were observed in the 90-day oral repeated-dose toxicity study in rats.
In an oral 9gavage) combined reproduction/developmental toxicity screening test in rats with the
supporting chemical, DMHP, effects on mating and fertility indices were seen at
270 mg/kg-day; the NOAEL for reproductive toxicity is 90 mg/kg-day. The systemic toxicity
NOAEL is 90 mg/kg-day based on mortality and severe body weight effects at 270 mg/kg-day.
In the same study, the NOAEL for maternal and developmental toxicity is 90 mg/kg-day, based
on no effects at the highest dose at which females survived to term. In a two-generation
reproductive toxicity study in rats via inhalation, the supporting chemical, methanol, showed no
systemic or reproductive toxicity at 1.3 mg/L-day, highest dose tested. In the same study, the
earlier time of descensus testis in pups was seen at 0.013 mg/L-day; the NOAEC for
developmental toxicity is not established. In an oral prenatal developmental toxicity study in rats
with TMP, decreased body weights were seen in dams at 164 mg/kg-day; the NOAEL for
maternal toxicity is 49 mg/kg-day. In the same study, skeletal and soft tissue abnormalities were
seen in pups at 164 mg/kg-day; the NOAEL for developmental toxicity is 49 mg/kg-day.

TMP induced gene mutation in mammalian cells but not in bacteria in vitro, induced micronuclei
in bone marrow in vivo, induced DNA damage in bacteria in vitro and produced point mutations,
chromosomal aberrations and chromosome loss in fruit flies in vivo. TMP is irritating rabbit skin
and eyes.

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Table 3. Summary of the Screening Information Data Set under

the U.S. HPV Challenge Program - Human Health Data



Endpoint

SPONSORED
CHEMICAL
TMP
(121-45-9)

Supporting
Chemical
DMPH
(868-85-9)

Supporting
Chemical
Methanol
(67-56-1)

Acute Toxicity
Oral LD5o (mg/kg)

1350 - 4200

—

—

Acute Toxicity
Inhalation LC50 (mg/L)

>45.7





Acute Toxicity
Dermal LD50 (mg/kg)

934 - 7500

—

—

Repeated-Dose Toxicity
NOAEL/LOAEL
Oral (mg/kg-day)

(rat, 90 d)
NOAEL = 80
LOAEL = 160

(rat, 4 wk)
NOAEL = 32.8
LOAEL 164





Repeated-Dose Toxicity
NOAEC/LOAEC
Inhalation (mg/L-day)

(rat, 4 wk)
NOAEC = not

established
LOAEC = 0.53





Repeated-Dose Toxicity
NOAEL/LOAEL
Dermal (mg/kg-day)

(rabbit, 21 d)
NOAEL = not

established
LOAEL = 300





Reproductive Toxicity (oral)

N O AEL/N O AE C/LO AEL/LO AE C

(mg/kg-day/mg/L/day)

Systemic Toxicity

No data
NOAEL = 90
LOAEL = 270

NOAEL = 90
LOAEL = 270

—

Reproductive Toxicity

NOAEL = 90
LOAEL = 270
(RA)

In the 90-day
repeated-dose oral

toxicity study,
adverse effects on
spermiogenesis and
testes
histopathology

NOAEL = 90
LOAEL = 270



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were seen.





Reproductive Toxicity (Inhalation)

NOAEC/LOAEC

(mg/L/day)

Systemic Toxicity
Reproductive Toxicity

No data
NOAEC = 1.3
(highest conc.

tested)
NOAEC = 1.3
(highest conc.
tested)
(RA)



NOAEC = 1.3
(highest conc.

tested)
NOAEC = 1.3
(highest conc.
tested)

Developmental Toxicity
NOAEL/LOAEL
Oral (mg/kg-day)

Maternal Toxicity

NOAEL = 49
LOAEL = 164





Developmental Toxicity

NOAEL = 49
LOAEL = 164





Genetic Toxicity - Gene Mutation
In vitro

Negative
(bacteria)
Positive
(mammalian cells)





Genetic Toxicity - Chromosome

Aberrations

In vivo

(Drosophila)
Positive





Genetic Toxicity - Other
DNA Damage and Repair

In vitro

Positive





Additional Information

Skin Irritation
Eye Irritation

Irritating
Irritating





Bold-Indicates experimental data; RA = Read Across; - Data not needed/used for this assessment

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4. Environmental Effects - Aquatic Toxicity

A summary of ecotoxicity data for SIDS and other endpoints is provided in Table 4. The table
also indicates where data for the supporting chemical are read-across (RA) to the sponsored
substances.

Acute Toxicity to Fish

Trimethylphosphite (CAS No. 121-45-9)

No data.

Dimethylphosphonate (CASRN 868-85-9, supporting chemical)

(1)	Fathead minnows (Pimephalespromelas) were exposed to DMHP at unspecified
concentrations under static conditions for 96 hours.

96-h LC50 = 225 mg/L

(2)	Zebrafish (Brachydanio rerio) were exposed to DMHP at 100 mg/L (nominal concentration)
under static conditions for 96 hours. The mean measured concentration was 15.6 mg/L over

24 - 96 hours. No mortalities were observed.

96-h LC50 > 15.6 mg/L

Acute Toxicity to Aquatic Invertebrates

Trimethyl phosphite (CAS No. 121-45-9)

No data.

Dimethyl phosphonate (CASRN 868-85-9, supporting chemical)

Daphnia magna were exposed to DMHP at nominal concentrations of 0, 6.25, 12.5, 25, 50 or
100 mg/L under static conditions for 48 hours. Immobilization was seen at > 25 mg/L.
48-h EC50 = 24.8 mg/L

Toxicity to Aquatic Plants

Trimethyl phosphite (CAS No. 121-45-9)

No data.

Dimethyl phosphonate (CASRN 868-85-9, supporting chemical)

Green algae (Desmodesmus subspicatus) were exposed to DMHP at 0 or 100 mg/L (nominal
concentration) under static conditions for 72 hours. The measured concentration of monomethyl
phosphonate was -25 mg/L. Growth rate inhibition relative to controls did not occur.

72-h EC50 (growth rate) > 25 mg/L

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Conclusion: For aquatic toxicity, all values are based on the supporting chemical DMHP. The
96-hour LC50 of supporting chemical DMHP for fish is > 15.6 mg/L. The 48-hour EC50 of
supporting chemical DMHP for aquatic invertebrates is 24.8 mg/L. The 72-hour EC50 of
supporting chemical DMHP for aquatic plants is >25 mg/L (growth rate).

Table 4. Screening Information Data Set as Submitted under the U.S.
HPV Challenge Program—Aquatic Toxicity Data

Endpoints

SPONSORED
CHEMICAL
Trimethyl phosphite
(121-45-9)

SUPPORTING
CHEMICAL
Dimethyl phosphonate
(868-85-9)

Fish

96-h LC50 (mg/L)

No Data
>15.6
(RA)

> 15.6

Aquatic Invertebrates
48-h EC50 (mg/L)

No Data
24.8
(RA)

24.8

Aquatic Plants
72-h EC50 (mg/L)
(growth)

No Data
>25
(RA)

>25

Bold-Indicates experimental data; RA = Read Across

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