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EC number: 203-680-9 | CAS number: 109-55-7
- Life Cycle description
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- Ecotoxicological Summary
- Aquatic toxicity
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- Short-term toxicity to fish
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- Long-term toxicity to aquatic invertebrates
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- Endocrine disrupter testing in aquatic vertebrates – in vivo
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- Toxicological Summary
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- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
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- Specific investigations
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- Additional toxicological data

Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
No data available for the determination of toxicokinetics, metabolism and distribution. In general, lower primary aliphatic amines are metabolized to the corresponding carboxylic acid and urea.
Assessment of Toxicokinetic Behaviour
3-(Dimethylamino)propylamine (Cas-No. 109-55-7) is a colorless liquid with a molecular weight of 102.2 g/mol and a vapor pressure of 5.9 hPa (20°C). It is miscible in water and the log Po/w is -0.352.
Evidence for systemic availability of 3-(Dimethylamino)propylamine comes from acute (oral, dermal, inhalation) and subacute toxicity.
The LD50 for oral acute toxicity in rats was calculated as ca. 1600 mg/kg body weight (BASF, 1958). Main clinical signs observed were drowsiness and staggered gait. At necropsy, decomposition of abdominal cavity and haemorrhagic stomachs were observed. In three further studies the test substance caused likewise moderate toxicity after a single ingestion LD50 = 1037 mg/kg BW (Hoechst, 1979), LD50 = 922 mg/kg BW (Bayer, 1979), LD50=1870 mg/kg BW (Smyth et al. 1962).
The acute inhalation toxicity (BASF, 1991) showed no mortality and the LC50 was set to be over the applied dose of 4.31 mg/L air. Main clinical signs observed were immediately escape attempts, eyelid closure, accelerated respiration, irregular respiration and restlessness. No pathologic abnormalities were observed. Additional data were available from an inhalation risk test (IRT) which meets generally accepted scientific principles (BASF AG, 1979). The inhalation of a saturated vapor-air mixture for 2 hours caused mortality. Clinical signs were dyspnoea and eye closure, ruffled fur, apathy, crusted eyelids, corneal opacity. At necropsy, hyperemia of the renal medulla and decomposed organs.
In the acute dermal toxicity, both animals died on day 2 after administration of 2000 mg/kg. They showed no clinical signs before death. After administration of 1000 mg/kg, both rats showed sedation and tremors between day 2 and day 5 with severe cutaneous reactions (necrosis associated with edema on day 2). At 400 mg/kg, animals showed neither clinical signs nor irritation (CIT, 1993).
In a 28-day subchronic toxicity study, the no-observed-adverse effect-level (NOAEL) was 50 mg
/kg bw/day. In this oral toxicity study on Wistar rats, decreased spontaneous activity, stilted gait, swollen abdomen, and impaired respiration were observed between days 11 and 24, mainly in the females that died. In the four high-dose females that died, macroscopically visible changes such as discoloration of lungs with multiple red spots on its surfaces and foamy content were observed. Histopathological examinations revealed lesions which included congestion of organs, pulmonary hemorrhage, and edema, consistent with cardiorespiratory failure as cause of death. One of the females exhibited marked loss of lymphatic follicles of the spleen with massive marginal zone and periarteriolar lymphoid sheath atrophy. The one high-dose male rat that exhibited clinical signs had focal ballooning degeneration of the squamous epithelium of the forestomach found at necropsy (Hoechst 1996).In the available reproduction/developmental toxicity sreening test the no-observed-adverse effect-level (NOAEL) was 200 mg/kg bw/day.
DMAPA was not mutagenic in the Ames Test and in a mouse micronucleus assay.
Taken together, the corrosive property of the compound prompts workers to limit the potential exposure to this chemical.
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