Reaction products of decanoic acid and lauric acid with glycerol and polyglycerol

Direct observations: clinical cases, poisoning incidents and other

Administrative data

Endpoint:

direct observations: clinical cases, poisoning incidents and other

Type of information:

experimental study

Adequacy of study:

supporting study

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

study well documented, meets generally accepted scientific principles, acceptable for assessment

Data source

Reference

Reference Type:

publication

Title:

Human Studies on Polyglycerol Polyricinoleate (PGPR)

Author:

R. WILSON and M. SMITH

Year:

1998

Bibliographic source:

Food and Chemical Toxicology 36 (1998) 743±745

Materials and methods

Study type:

study with volunteers

Endpoint addressed:

repeated dose toxicity: oral

Principles of method if other than guideline:

During 1964 and 1965, PGPR was fed to 19 human volunteers whose diet contained constant levels of fat and protein. Up to 10 g/day PGPR was fed to each volunteer in soups, cakes and toffee bars for 2 weeks. Pre-exposure normal values of biochemical parameters were established. Fat balance tests confirmed that digestion and absorption of PGPR took place.

GLP compliance:

no

Test material

Test material information

Constituent 1

Reference substance name:

9-Octadecenoic acid, 12-hydroxy-, (9Z,12R)-, polymer with 1,2,3-propanetriol

Cas Number:

29894-35-7

IUPAC Name:

9-Octadecenoic acid, 12-hydroxy-, (9Z,12R)-, polymer with 1,2,3-propanetriol

Test material form:

liquid

Details on test material:

Hydroxyl value 85±100
Acid value 2.0 max.
Iodine value 80±90
Refractive index at 658C 1.4635±1.4665

"the polyglycerol moiety shall be composed of not less than 75 percent of the di-, tri- and tetraglycerols and shall contain not more than 10 percent of polyglycerols equal to or higher than heptaglycerol'' (FAO, 1992).

Method

Type of population:

general

Ethical approval:

not specified

Route of exposure:

oral

Reason of exposure:

intentional

Exposure assessment:

measured

Details on exposure:

PGPR was introduced into three items: (1) soups (5 g/pint); (2) cakes (10 g/cake or 2.5 g/portion); (3) toffee bars (5 g/bar). The soups and cakes were supplied to the hospital in the form of a dry mix which
was freshly prepared each day in the hospital kitchens. The toffee bars were prepared at the Unilever Research Laboratory, Colworth House. The amount of PGPR fed to the volunteers was carefully regulated over a 3-wk period as follows: wk 1: none; wk 2: 5 g PGPR/day; wk 3:10 g PGPR/day.
The diet was designed to maintain constant intakes of fat (150 g/day, excluding PGPR) and protein (75 g/day) with a flexible level of carbohydrates to suit individual requirements.

Examinations:

Blood samples were taken at twice-weekly intervals throughout the study. The following serum clinical chemistry parameters were determined:
albumin, globulin, serum electrophoresis, thymol turbidity, bilirubin, cholesterol, alanine aminotransferase, cholinesterase and creatine clearance.
Faeces and urine samples were collected throughout the study and pooled for individuals as weekly samples. The faeces samples were analysed for fat and faecal nitrogen, while the urine samples were analysed for creatinine. The means and standard deviations were calculated.

Results and discussion

Results of examinations:

While some individuals occasionally deviated from the normal ranges for the liver function parameters, none of these deviations were attributable to the consumption of PGPR.
Creatinine clearance was included as a relatively simple test of kidney function which establishes the glomerular filtration rate. The consumption of PGPR was not associated with any detectable disruption of renal function.
Cholesterol levels were monitored and, once again, although there were individual variations, none were attributable to the consumption of PGPR.
The level of faecal fat was determined to investigate whether there was any evidence of interference with fat digestion. Most of the results were within the normal limits. Where there were deviations from normal, these could not be ascribed to the consumption of PGPR. Nitrogen determinations on the faeces provide an indicator of digestion and absorption in the alimentary tract. Analysis of randomly selected samples did not indicate any consistent effect produced by PGPR.

Applicant's summary and conclusion

Conclusions:

The range of clinical chemistry parameters measured as part of these human studies on PGPR is not as extensive as that which would be available for such an investigation today. The range of analyses were simply not available within an automated system at that time. However, the tests still are considered as appropriate indicators of any abnormalities in liver and renal function induced by PGPR as well as changes in fat balance.
The fat balance tests confirmed that the digestion and absorption of fat took place without any interference from PGPR. There was no consistent effect of PGPR on the clinical chemistry parameters or creatinine clearance and hence no indication of renal or kidney dysfunction.
PGPR was consumed at quantities of up to 10 g/day or 167 mg/kg/day for a 60-kg person. This amount is approximately 63 times the estimated maximum per capita mean daily intake by man of 2.64 mg/kg body weight/day. It is therefore concluded from this study that the consumption of PGPR has no adverse effects in man.