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EC number: 219-147-9 | CAS number: 2373-38-8
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
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Exposure related observations in humans: other data
Administrative data
- Endpoint:
- exposure-related observations in humans: other data
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Remarks:
- Case study Docusate sodium
- Adequacy of study:
- supporting study
Cross-reference
- Reason / purpose for cross-reference:
- read-across source
Reference
- Endpoint:
- exposure-related observations in humans: other data
- Type of information:
- other: Case study
- Adequacy of study:
- supporting study
- Reliability:
- 4 (not assignable)
- Rationale for reliability incl. deficiencies:
- secondary literature
- Endpoint addressed:
- other: Neonatal hypomagnesaemia secondary to maternal hypomagnesaemia
- Details on study design:
- Case study
- Exposure assessment:
- estimated
- Details on exposure:
- TYPE OF EXPOSURE: “Jitteriness” in a baby, and low blood magnesium levels in both baby and mother, were seen when the mother took 100-200 mg DSS or more daily for most of her pregnancy and after delivery. This had resulted in intermittent diarrhoea, which was thought to have been the cause of the low magnesium levels
EXPOSURE LEVELS: The mother said that she had been using a stool softener (docusate sodium 100-200 mg or more daily) during most of her pregnancy and after delivery. She decreased her use of docusate when she had diarrhoea. She had also been taking a multivitamin preparation which contained docusate (50 mg per dose).
EXPOSURE PERIOD: during most of her pregnancy and after delivery
POSTEXPOSURE PERIOD: When docusate was discontinued, the mother’s serum Mg++ increased to 1 - 4, 1 - 7, 1 - 6, and 1 - 8 mg/dL on the 5th, 6th, 8th, and 42nd post-partum days, respectively. A sample of breast milk on the 6th post-partum day had a normal Mg++ concentration (38 8 mg/dL).
- Results:
- During pregnancy Mg++ is transported against a gradient from mother to fetus. Animal studies suggest that the mother will retain Mg++ at the expense of the fetus.Postnatally, it is absorbed primarily in the proximal small bowel, but it can be absorbed anywhere in the small intestine and in some parts of the large intestine. Excretion is regulated by the kidney, with reabsorption of Mg++ in the thick ascending loop of Henle.
In the newborn magnesium deficiency may be due to a rare familial (possibly X-linked) absorption defect specific for magnesium, malabsorption secondary to small bowel surgery, transient hypomagnesaemia in small-for-gestational age infants, and excess administration of calcium or of vitamin D. In these conditions hypomagnesaemia does not occur in the first hours of life and, by the time it is manifest, other metabolic or nutritional disturbances are apparent. Neonatal hypomagnesaemia may also be secondary to maternal hypomagnesaemia. In adults magnesium deficiency has many causes, including the chronic use of laxatives.
In our case isolated hypomagnesaemia was discovered by chance in a jittery baby. Maternal overuse of stool softeners, to the extent of producing diarrhoea, provided a plausible explanation for hypomagnesaemia in both mother and infant. - Conclusions:
- Neonatal hypomagnesaemia may be secondary to maternal hypomagnesaemia. In adults magnesium deficiency has many causes, including the chronic use of laxatives.
In our case isolated hypomagnesaemia was discovered by chance in a jittery baby. Maternal overuse of stool softeners, to the extent of producing diarrhoea, provided a plausible explanation for hypomagnesaemia in both mother and infant. - Executive summary:
Neonatal hypomagnesaemia is usually associated with factors producing hypocalcaemia. In isolation it is rare, but has been associated with neurological dysfunction.2
A 3110 g male was delivered by elective caesarean section at term to a 34-year-old gravida 2, para 2 mother. The pregnancy was uncomplicated and delivery was uneventful. At 12 h the infant was jittery; the blood glucose was 90 mg/dL. The jitteriness resolved spontaneously. At 22 h his serum calcium was normal (8 - 4 mg/dL) but his serum magnesium (Mg++) was low (1 - 0 mg/dL). Mg++ concentrations at 32 and 48 h were 1.1 and 0.9 mg/dL, respectively.
The baby was treated with two intramuscular doses of magnesium sulphate, after which his serum Mg++ was 2.9 mg/dL. Concentrations on day 4, 5, 6, 8, and 42 were 1.9, 1.6, 1.5, 1.7, and 2.2 mg/dL, respectively. The baby was exclusively breast-fed.
On the third post-partum day the mother had normal serum calcium, phosphorus, and alkaline phosphatase levels; her Mg++ concentration was low (1.2 mg/dL). The mother said that she had been using a stool softener (docusate sodium 100-200 mg or more daily) during most of her pregnancy and after delivery. She decreased her use of docusate when she had diarrhoea. She had also been taking a multivitamin preparation which contained docusate (50 mg per dose). When docusate was discontinued, the mother’s serum Mg++ increased to 1.4, 1.7, 1.6, and 1.8 mg/dL on the 5th, 6th, 8th, and 42nd post-partum days, respectively. A sample of breast milk on the 6th post-partum day had a normal Mg++ concentration (3.8 mg/dL).3
During pregnancy Mg++ is transported against a gradient from mother to fetus. Animal studies suggest that the mother will retain Mg++at the expense of the fetus.4Postnatally, it is absorbed primarily in the proximal small bowel, but it can be absorbed anywhere in the small intestine and in some parts of the large intestine. Excretion is regulated by the kidney, with reabsorption of Mg++ in the thick ascending loop of Henle.
In the newborn magnesium deficiency may be due to a rare familial (possibly X-linked) absorption defect specific for magnesium, malabsorption secondary to small bowel surgery, transient hypomagnesaemia in small-for-gestational age infants, and excess administration of calcium or of vitamin D.1In these conditions hypomagnesaemia does not occur in the first hours of life and, by the time it is manifest, other metabolic or nutritional disturbances are apparent. Neonatal hypomagnesaemia may also be secondary to maternal hypomagnesaemia. In adults magnesium deficiency has many causes, including the chronic use of laxatives.5
In our case isolated hypomagnesaemia was discovered by chance in a jittery baby. Maternal overuse of stool softeners, to the extent of producing diarrhoea, provided a plausible explanation for hypomagnesaemia in both mother and infant.
1. Tsang RC. Neonatal magnesium disturbances.Am J Dis Child 1972; 126: 282-93.
2. Cockburn F, Brown JK, Belton NR, Forfar JO Neonatal convulsions associated with primary disturbance of calcium, phosphorus, and magnesium metabolism. Arch Dis Child 1973, 48: 99-108
3. Frannson GB, Lonnerdal B. Zinc, copper, calcium and magnesium in human milk J Pediatr 1982; 101: 505-08.
4 Dancis J, Springer D, Cohlan SA.Fetal homeostasis in maternal malnutrition. II Magnesium deprivation. Pediatr Res 1971; 55: 131-36
5. Rude RK, Singer FR. Magnesium deficiency and excess. Annu Rev Med 1981, 32: 245-59.
Data source
Materials and methods
Test material
- Reference substance name:
- Sodium 1,4-bis(1,3-dimethylbutyl) sulphonatosuccinate
- EC Number:
- 219-147-9
- EC Name:
- Sodium 1,4-bis(1,3-dimethylbutyl) sulphonatosuccinate
- Cas Number:
- 2373-38-8
- Molecular formula:
- C16H30O7S.Na
- IUPAC Name:
- sodium 1,4-bis[(4-methylpentan-2-yl)oxy]-1,4-dioxobutane-2-sulfonate
Constituent 1
Method
- Details on study design:
- Case study
- Exposure assessment:
- estimated
Results and discussion
- Results:
- During pregnancy Mg++ is transported against a gradient from mother to fetus. Animal studies suggest that the mother will retain Mg++ at the expense of the fetus.Postnatally, it is absorbed primarily in the proximal small bowel, but it can be absorbed anywhere in the small intestine and in some parts of the large intestine. Excretion is regulated by the kidney, with reabsorption of Mg++ in the thick ascending loop of Henle.
In the newborn magnesium deficiency may be due to a rare familial (possibly X-linked) absorption defect specific for magnesium, malabsorption secondary to small bowel surgery, transient hypomagnesaemia in small-for-gestational age infants, and excess administration of calcium or of vitamin D. In these conditions hypomagnesaemia does not occur in the first hours of life and, by the time it is manifest, other metabolic or nutritional disturbances are apparent. Neonatal hypomagnesaemia may also be secondary to maternal hypomagnesaemia. In adults magnesium deficiency has many causes, including the chronic use of laxatives.
In our case isolated hypomagnesaemia was discovered by chance in a jittery baby. Maternal overuse of stool softeners, to the extent of producing diarrhoea, provided a plausible explanation for hypomagnesaemia in both mother and infant.
Applicant's summary and conclusion
- Conclusions:
- Neonatal hypomagnesaemia may be secondary to maternal hypomagnesaemia. In adults magnesium deficiency has many causes, including the chronic use of laxatives.
In our case isolated hypomagnesaemia was discovered by chance in a jittery baby. Maternal overuse of stool softeners, to the extent of producing diarrhoea, provided a plausible explanation for hypomagnesaemia in both mother and infant. - Executive summary:
Neonatal hypomagnesaemia is usually associated with factors producing hypocalcaemia. In isolation it is rare, but has been associated with neurological dysfunction.2
A 3110 g male was delivered by elective caesarean section at term to a 34-year-old gravida 2, para 2 mother. The pregnancy was uncomplicated and delivery was uneventful. At 12 h the infant was jittery; the blood glucose was 90 mg/dL. The jitteriness resolved spontaneously. At 22 h his serum calcium was normal (8 - 4 mg/dL) but his serum magnesium (Mg++) was low (1 - 0 mg/dL). Mg++ concentrations at 32 and 48 h were 1.1 and 0.9 mg/dL, respectively.
The baby was treated with two intramuscular doses of magnesium sulphate, after which his serum Mg++ was 2.9 mg/dL. Concentrations on day 4, 5, 6, 8, and 42 were 1.9, 1.6, 1.5, 1.7, and 2.2 mg/dL, respectively. The baby was exclusively breast-fed.
On the third post-partum day the mother had normal serum calcium, phosphorus, and alkaline phosphatase levels; her Mg++ concentration was low (1.2 mg/dL). The mother said that she had been using a stool softener (docusate sodium 100-200 mg or more daily) during most of her pregnancy and after delivery. She decreased her use of docusate when she had diarrhoea. She had also been taking a multivitamin preparation which contained read-across test item docusate (50 mg per dose). When docusate was discontinued, the mother’s serum Mg++ increased to 1.4, 1.7, 1.6, and 1.8 mg/dL on the 5th, 6th, 8th, and 42nd post-partum days, respectively. A sample of breast milk on the 6th post-partum day had a normal Mg++ concentration (3.8 mg/dL).3
During pregnancy Mg++ is transported against a gradient from mother to fetus. Animal studies suggest that the mother will retain Mg++at the expense of the fetus.4Postnatally, it is absorbed primarily in the proximal small bowel, but it can be absorbed anywhere in the small intestine and in some parts of the large intestine. Excretion is regulated by the kidney, with reabsorption of Mg++ in the thick ascending loop of Henle.
In the newborn magnesium deficiency may be due to a rare familial (possibly X-linked) absorption defect specific for magnesium, malabsorption secondary to small bowel surgery, transient hypomagnesaemia in small-for-gestational age infants, and excess administration of calcium or of vitamin D.1In these conditions hypomagnesaemia does not occur in the first hours of life and, by the time it is manifest, other metabolic or nutritional disturbances are apparent. Neonatal hypomagnesaemia may also be secondary to maternal hypomagnesaemia. In adults magnesium deficiency has many causes, including the chronic use of laxatives.5
In our case isolated hypomagnesaemia was discovered by chance in a jittery baby. Maternal overuse of stool softeners, to the extent of producing diarrhoea, provided a plausible explanation for hypomagnesaemia in both mother and infant.
1. Tsang RC. Neonatal magnesium disturbances.Am J Dis Child 1972; 126: 282-93.
2. Cockburn F, Brown JK, Belton NR, Forfar JO Neonatal convulsions associated with primary disturbance of calcium, phosphorus, and magnesium metabolism. Arch Dis Child 1973, 48: 99-108
3. Frannson GB, Lonnerdal B. Zinc, copper, calcium and magnesium in human milk J Pediatr 1982; 101: 505-08.
4 Dancis J, Springer D, Cohlan SA.Fetal homeostasis in maternal malnutrition. II Magnesium deprivation. Pediatr Res 1971; 55: 131-36
5. Rude RK, Singer FR. Magnesium deficiency and excess. Annu Rev Med 1981, 32: 245-59.
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