DIETHYLSTILBESTROL

MEDICAL USES: Diethylstilbestrol has been used for various cancers including prostatic cancer. It was previously used extensively in the treatment and prevention of conditions known or presumed to be associated with low levels of endogenous estrogen. It was used extensively between 1940 and 1970 to prevent fetal loss in pregnancy, to alleviate symptoms associated with natural menopause, to prevent osteoporosis (bone calcium loss), to alter the hormonal cycle in various menstrual disorders, to stimulate development of female sex characteristics and suppress masculine characteristics in male-to-female transsexuals, and in female ovarian dysgenesis (Turner's syndrome; a genetic condition in females associated with absent secondary sex characteristics).
DES was also used in estrogen replacement therapy following surgical removal of the ovaries. Estrogens were used in the late 1960s for prevention of ischemic heart disease in men; this was discontinued because of feminizing side effects. DES and other estrogens were previously prescribed to suppress lactation and reduce breast engorgement after childbirth (Varga et al, 1972; Brett et al, 1971; Stirrat et al, 1968; Hodge, 1967). This indication was withdrawn by the FDA in 1989 because of increased risk of puerperal thromboembolism. In addition, estrogens are excreted in breast milk and potential effects in the nursing infant are unpredictable (USPDI, 1992).
POST-COITAL CONTRACEPTION: DES was prescribed in the past for post-coital contraception ("morning after pill"). It is effective in preventing conception; however, its use will not terminate pregnancy (HSDB). Although approved for "emergency use," for example, in cases of rape (AMA, 1990), other drugs are preferred because of lower incidence of side effects. The pharmaceutical manufacturer (Lilly) cautions that DES SHOULD NOT BE USED AS A POST-COITAL CONTRACEPTIVE (PDR , 1995). The possible increased risk of cancer and teratogenesis following contraception failure is not known; however, ectopic pregnancy is possible in cases of contraception failure.
USE IN PREGNANCY: DES was synthesized in 1938 and came into extensive use as a pharmaceutical during the 1940s-50s in the US and other countries to prevent complications of pregnancy, including spontaneous abortion, toxemia, premature delivery, postmaturity, and stillbirth (Underwood & Kreutner, 1978). The benefit of prescribing DES in pregnancy was never proven (PDR , 1995), and publication of studies showing lack of efficacy in the 1950s led to a decline in use by 1960 (Mansi, 1989; Malone, 1993). PREGNANCY IS CONSIDERED AN ABSOLUTE CONTRAINDICATION FOR ANY ESTROGEN TREATMENT.
CARCINOGENICITY/REPRODUCTIVE EFFECTS: In 1970, Herbst et al published the first report of clear cell adenocarcinoma of the vagina and cervix among daughters of women who had taken DES during pregnancy (see CARCINOGENIC EFFECTS). In 1972, the FDA required a package insert warning of the possible association of DES and vaginal adenocarcinoma in girls exposed in utero.
DES IS A RECOGNIZED HUMAN TERATOGEN AND TRANSPLACENTAL CARCINOGEN, AND SHOULD

NOT BE USED FOR ANY PURPOSE DURING PREGNANCY. The manufacturer of Stilphostrol (DES-diphosphate; used in chemotherapy for prostate cancer) further cautions that DES-DIPHOSPHATE IS NOT INDICATED IN THE TREATMENT OF ANY DISORDER IN WOMEN (PDR , 1995).

USE IN CHEMOTHERAPY: DES is used as a chemotherapeutic agent in selected cases of advanced male and female breast and prostate cancer. Because suppression of testosterone (male sex hormone) is an effect of DES, it continues to be used as palliative treatment for advanced prostate cancer. An estimated 500,000 patients are treated with DES each year, primarily males with prostate cancer (USDHHS, 1991). Oral and injectable formulations are available as DES or DES-diphosphate.
OCCUPATIONAL EXPOSURE: Following licensure in the US in 1942, more than 100 pharmaceutical companies were engaged in DES production (Underwood & Kreutner, 1978). Despite this, epidemiologic studies of reproductive and other effects among occupationally exposed men and women are notably absent in the published literature. Sporadic case reports of occupational toxicity have appeared (see CHRONIC EXPOSURE).
USE IN LIVESTOCK: Until banned in 1979 by the FDA (Baselt, 1988), DES was used as a growth promotor in chickens and livestock intended for human consumption. Concern has been raised regarding a possible relationship between cancer and hormone residues in beef; however, the low levels of DES residuals in beef should present little cancer risk (Clayton & Clayton, 1982). Even heavy consumption of beef would most likely result in ingestion of no more than a few micrograms of DES per year, creating a hormone level less than physiologic levels of natural hormones and well below the amount of "natural" estrogens consumed by persons adding wheat germ to their diets (wheat germ and other plants contain natural estrogens).

FORMS

Diethylstilbestrol (DES) is a nonsteroidal, synthetic stilbene derivative with estrogenic activity used extensively in the past in human medicine and in livestock as a growth promoter for cattle, sheep, and chicken, and to prevent miscarriages in humans (Lewis, 1993; Budavari, 1996). DES was banned by the US FDA as a livestock growth promotor in 1979 (Budavari, 1996).
DES occurs as a nearly white, odorless, crystalline powder (JEF Reynolds , 1995; Lewis, 1993). It is practically insoluble in water, but is soluble in ethanol, chloroform, diethyl ether, acetone, dioxane, ethyl acetate, methyl alcohol, vegetable oils, and aqueous solutions of alkaline hydroxides (USDHHS, 1991; JEF Reynolds , 1995; Budavari, 1996; Lewis, 1993).
Diethylstilbestrol acts like other estrogens, but is highly effective when orally administered and is not degraded as easily as other estrogens, providing a longer duration of action (Gilman et al, 1990) Prod Info Stilphostrol(R), 1995).
Many of the adverse effects of DES in humans are related to augmentation or suppression of normal physiological hormonal responses/processes in the presence of excessive amounts of estrogen. Especially important is interference with hormone-mediated development.

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

Editor's Note: An ERG guide with information appropriate to this material does not exist.

ACUTE CLINICAL EFFECTS

WITH POISONING/EXPOSURE

DES is toxic by all exposure routes (inhalation, ingestion, dermal absorption) (HSDB). In contrast to natural estrogens, DES is highly active when given by mouth, and the duration of action of a single dose is longer (Gilman et al, 1990) Prod Info, 1991).
There are limited data regarding the toxicity of DES following a single administration, as medical uses have generally involved multiple doses. Toxicity following acute exposure to DES is generally limited to anorexia, nausea, vomiting, and abdominal cramps; withdrawal vaginal bleeding may be seen with large acute doses (PDR , 1995; Baselt, 1988).

WITH THERAPEUTIC USE

Acute side effects are common when high doses of DES are taken as a post-coital contraceptive, especially nausea, vomiting, headache, vaginal spotting, dizziness, bloating or swelling, weight gain, breast tenderness, and diarrhea (Kuchtera, 1973) 1974).
Among 63 rape victims treated with DES, 40 complained of nausea, vomiting, or both. At least 6 patients discontinued therapy because of these symptoms (Glover et al, 1976). Contraceptive doses of DES do not appear to affect time to menses or menstrual flow in the majority of patients (Kuchtera, 1973); when post-coital use of DES fails, there is some evidence of increased risk of ectopic pregnancy.

ANIMAL STUDIES - Tumors have developed in experimental animals given a single dose of DES pre- and neonatally.

CHRONIC CLINICAL EFFECTS

WITH POISONING/EXPOSURE

DES is unlikely to accumulate in the body with repeated exposure. It is generally excreted within 3 days. The toxicity of DES has predominantly been described in association with chronic use as a pharmaceutical agent.
OCCUPATIONAL EXPOSURE - Although it was in large-scale production during the 1940s-70s, no epidemiological studies of occupational exposure to DES were identified at the time of this review. The size of the workforce potentially exposed to DES is now small, estimated at 827 individuals in the 1981-83 NIOSH survey (RTECS). Knowledge of health effects related to workplace exposure is thus limited to a small number of case reports. The symptoms and signs described in these cases parallel those observed in persons treated medically with DES.
Exposure in the occupational setting may occur through the percutaneous, inhalation, and oral routes. Workers most likely to have had significant occupational exposure include those engaged in pharmaceutical production, mixing DES into animal feed, handling feed, and (possibly) those handling livestock carcasses containing DES residues.
Air samples collected from inside the protective clothing of full-time workers in a DES manufacturing plant contained 0.4 to 1.8 mcg/m(3) of DES. Two sets of air samples collected in areas outside the main work room contained 0.2 and 12.8 mcg/m(3). An air sample from a finishing room contained 24 mcg/m(3). Ambient air samples in 3 plants where DES was mixed into animal feed contained 0.002 to 1.03 mcg/m(3) of DES (IARC, 1979).
In MALES, occupational exposure to estrogens has produced prominent gynecomastia with or without areolar pigmentation, decreased libido, impotence, tenderness of the pubic area, dizziness, and weakness (Gosselin et al, 1984; Harrington, 1978; Klorfin & Bartini, 1956). Prolactinoma (a benign pituitary tumor), high level of prolactin, bilateral breast swelling, nipple tenderness, intermittent episodes of impotence, diminished libido, and galactorrhea (milk secretion) were reported in a 61-year-old man exposed daily to estrogens (norethindrone and mestranol) in a pharmaceutical plant manufacturing oral contraceptives (Baron et al, 1983).
In FEMALES, occupational exposure has been reported to produce menstrual irregularities (intermenstrual bleeding; shorter but more frequent menses; hemorrhagic menstruation), breast enlargement and tenderness, increased libido, weight gain or obesity, headaches, and weakness. In addition, nodular uteri were found in 2/9 women with other symptoms and signs of occupational estrogen exposure (Pacynski & Robaczynski, 1968).
Health effects have been reported in CHILDREN OF PARENTS OCCUPATIONALLY EXPOSED to DES. Two boys (aged 8 and 10 years), one whose mother worked in DES tablet production and the other whose father was a pharmacist, had headaches, weakness, swollen breasts, and changes in breast color (Klorfin & Bartini, 1956).
Hyperestrogenic effects of occupational DES exposure were studied among 4 women and 7 of their children exposed during pregnancy in a Polish pharmaceutical plant (Budzynska et al, 1967a) 1967b). Six of the 7 children showed signs of hyperestrogenism; in three instances, mother and child had the same signs of hyperestrogenism. Effects included gynecomastia and pigmentation disorders. The mother of the one child without hyperestrogenic signs had discontinued work during pregnancy and herself showed no signs of estrogen hyperactivity.
Effects of occupational DES absorption in 9 women employed in a Polish pharmaceutical plant and 7 of their children were described in a separate report (Pacynski & Robaczynski, 1968). Duration of employment was from less than 1 year (3 women) to 6-16 years (6 women). All 9 complained of menstrual irregularities, obesity, hemorrhagic menstruation, and swollen breasts. Nodular uteri were found in two patients. Cytohormonal smears showed anovular, single phase cycles with excessive estrogenic activity and a lack of luteal phase. All had apparently disregarded safety and hygiene recommendations for DES exposure.
CHILDREN - Ingestion of vitamin capsules contaminated with estrogens resulted in breast enlargement and nodularity in both male and female children. Changes in secondary sexual characteristics were fully reversible on cessation of exposure (Gosselin et al, 1984) HSDB). No long-term effects have been observed following accidental ingestion of oral contraceptives by children; acute overdose toxicity is the same as for adults, with nausea the most common symptom. However, the stimulatory effects of estrogen on bone tissue may cause accelerated epiphyseal closure in children and adolescents chronically exposed to estrogens (USPDI, 1992).

WITH THERAPEUTIC USE

Common adverse effects, which may occur soon after treatment is initiated, include: gastrointestinal disturbances (abdominal cramping, bloating), loss of appetite, and nausea. Less frequent adverse effects are diarrhea, dizziness, intolerance of contact lenses, increased libido in women, decreased libido in men, migraine or throbbing headaches, and vomiting.
Adverse effects associated with prolonged DES therapy in both men and women are breast pain or tenderness, gynecomastia, and peripheral edema (USPDI, 1992). Menstrual changes (cessation of menses; excessive menses; breakthrough bleeding or spotting), breast tumor or lumps, and galactorrhea may also occur.
EFFECTS IN MEN TREATED WITH DES FOR PROSTATE CANCER - Among men treated with DES for prostate cancer, the most frequent adverse effects are nausea, vomiting, gynecomastia, and peripheral edema. Effects are dose-related, with few effects noted at 1 mg/day, but with a high incidence of adverse effects at 5 mg/day (O'Brien & Lynch, 1988; DiPiro et al, 1989). Side effects are a common reason for withdrawal of treatment.
Severe adverse effects are less common, and include cardiovascular, hematologic and immunologic abnormalities, endocrine and metabolic disorders, and cancer.
EFFECTS ON THE MALE BREAST - In addition to gynecomastia, the male mammary gland can be modified by estrogen to a histological picture analogous to that of the female breast (Wolf et al, 1969; Hendrickson & Anderson, 1970; Gagnon et al, 1979). Florid papillomatosis of the nipple, bilateral gynecomastia, and nipple discharge occurred in a 83-year-old man treated with 5 mg of DES daily over a 10-year period (Waldo et al, 1975). Hyperkeratosis, hyperpigmentation, papillomatosis of the nipple, and bilateral gynecomastia occurred in a 72-year-old man who had received 3 mg DES per day for 8 months (Mold & Jegasothy, 1980).
HEMATOLOGIC EFFECTS - Hematologic effects have been associated with both short- and long-term treatment of prostate cancer. Pancytopenia (depression of all blood cellular elements), rash, and fever developed in a 66-year-old man being treated for metastatic prostate cancer with DES for 5 years. Withdrawal resulted in prompt resolution (Collins, 1989). These effects were considered to be both endocrine and immunologically mediated. A similar, but fatal, case of pancytopenia was reported in a 71-year-old man who had received large doses of DES for 7 years (150 mg per day) (Anderson & Lynch, 1980). Other reported effects of chronic exposure to DES include thrombocytopenia, fatal hemolytic anemia, decreased plasma antithrombin III levels, and hypocalcemia (Cooper & Bigelow, 1960; Rosenfeld et al, 1989; Harley et al, 1983; Emtage et al, 1988).
CARDIOVASCULAR TOXICITY - Thromboembolism and thrombus formation have been reported among male breast and prostate cancer patients treated with DES (Beaumont et al, 1980). Doses of 5 mg of DES per day to treat male breast or prostate cancer have also been associated with increased risk of myocardial toxicity and cardiovascular death (Byar & Corle, 1988). The cardiovascular hazard was reduced at 1 mg doses, and doses greater than 1 mg have not been found to increase therapeutic effectiveness (Byar & Corle, 1988).
Other effects reported among male prostate cancer patients are peliosis hepatitis (mottled blue liver, due to blood-filled lacunaein the parenchyma); porphyria or porphyria cutanea tarda with related symptomatology of bullous skin lesions, photosensitivity, skin erosion and blisters on hands, facial hypertrichosis (excessive facial hair), and hyperpigmentation of sun-exposed skin; and urethral stricture and dysuria (Copeman et al, 1966; Levere, 1966; Vail, 1967; McRae, 1974; Wiemar et al, 1978; Yokoyama et al, 1983; Puppala & Ro, 1979).
EFFECTS IN WOMEN TREATED WITH DES - In women, prolonged high levels of estrogens can cause redness and swelling of the laryngeal mucosa and hoarseness (Damste, 1967), throbbing headaches, changes in menstruation, changes in breasts, nausea, and other general signs and symptoms of estrogen excess (Gilman et al, 1990; PDR , 1995). Pancreatitis with abdominal pain and nausea was reported in a 48-year-old woman who received 3 mg of DES daily for 2 years following oophorectomy (removal of the ovaries) (Gluek et al, 1972).
Several cases of thrombosis and thromboembolism have been associated with DES for suppression of lactation after delivery (Daniel et al, 1968; Millar & Robertson, 1968). Typical doses given to women to suppress milk production and breast engorgement were 15-45 mg/day or more. Administration of DES or other estrogens to prevent post-partum breast engorgement is not currently recommended, due to the increased risk of puerperal thromboembolism (USPDI, 1992).
DES TREATMENT OF FEMALE BREAST CANCER - At various doses and treatment durations, the following effects have been associated with DES treatment of breast cancer: hypercalcemia and gastrointestinal disturbances including nausea, vomiting and increased thirst (Swaroop & Krant, 1973). These effects were observed in 2 women who received short-term treatment with DES for breast cancer (5 mg per day for 1-2 days). DES itself increases the risk of breast cancer (see CARCINOGENIC EFFECTS section).

ANIMAL STUDIES - DES has produced cancers, tumors, congenital abnormalities, and reproductive effects in a wide range of laboratory animal species. The carcinogenicity of DES has prompted research on its effects on the immune system. Decreased size of the thymus and spleen has been reported in rodents exposed to DES or steroidal estrogens administered after birth. Although the weight normalizes over time, abnormalities of lymphocytes and functional impairment of cell-mediated immunity persist throughout the rodent's lifetime (Noller, 1988).

-RANGE OF TOXICITY

MAXIMUM TOLERATED EXPOSURE

Carcinogenicity Ratings for CAS56-53-1 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
EPA (U.S. Environmental Protection Agency, 2011): Not Listed
IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 1 ; Listed as: Diethylstilboestrol

1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
MAK (DFG, 2002): Not Listed
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS56-53-1 (U.S. Environmental Protection Agency, 2011):

Not Listed

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS56-53-1 (American Conference of Governmental Industrial Hygienists, 2010):

Not Listed

AIHA WEEL Values for CAS56-53-1 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS56-53-1 (National Institute for Occupational Safety and Health, 2007):

Not Listed

OSHA PEL Values for CAS56-53-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS56-53-1 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS56-53-1 (U.S. Environmental Protection Agency, 2010):

Listed as: Phenol, 4,4[prime]-(1,2-diethyl-1,2-ethenediyl)bis-, (E)
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:
Listed as: Diethylstilbestrol
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS56-53-1 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS56-53-1 (U.S. Environmental Protection Agency, 2010b):

Listed as: Diethylstilbesterol
P or U series number: U089
Footnote:
Listed as: Phenol, 4,4[prime]-(1,2-diethyl-1,2-ethenediyl)bis-, (E)-
P or U series number: U089
Footnote:
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS56-53-1 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS56-53-1 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS56-53-1 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS56-53-1 (EPA, 2005):

Listed as: Phenol, 4,4'-[(1E)-1,2-diethyl-1,2-ethenediyl]bis-

LABELS

NFPA

NFPA Hazard Ratings for CAS56-53-1 (NFPA, 2002):

Not Listed

-PERSONAL PROTECTION

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 56-53-1.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS56-53-1 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

Editor's Note: An ERG guide with information appropriate to this material does not exist.

NFPA Extinguishing Methods for CAS56-53-1 (NFPA, 2002):

Not Listed

EVACUATION PROCEDURES

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

AIHA ERPG Values for CAS56-53-1 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS56-53-1 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Diethylstilbestrol; ((E)-4,4'-(1,2- Diethyl-1,2-ethenediyl)bisphenol)
TEEL-0 (units = mg/m3): 0.025
TEEL-1 (units = mg/m3): 0.075
TEEL-2 (units = mg/m3): 0.6
TEEL-3 (units = mg/m3): 15
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS56-53-1 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS56-53-1 (National Institute for Occupational Safety and Health, 2007):

Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

SMALL LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

LARGE LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

268.35

-REFERENCES

GENERAL BIBLIOGRAPHY

40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.

40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.

49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.

62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.

65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

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65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

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DIETHYLSTILBESTROL

Classification | Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents