SHELLAC
First draft prepared by
Dr K.B. Ekelman and Dr D. Benz
US Food and Drug Administration
Washington DC, USA
1. EXPLANATION
Shellac has not been previously evaluated by the Committee. It
has a long history of use in food coatings and there are no reports
attributing adverse effects to such uses.
2. BIOLOGICAL DATA
2.1 Biochemical aspects
2.1.1 Absorption, distribution, and excretion
Relative dissolution rates of shellac- and cellulose-acetate
phthalate-coated prednisolone tablets were studied in humans in a
double-blind, crossover clinical trial. Subjects were six volunteers
(5 males, 1 female; mean age 26 years) who were not receiving any
other medication at the time of the study. Plasma prednisolone
concentration was significantly lower after administration of
shellac-coated tablets than after administration of cellulose
acetate phthalate-coated tablets, and considerable inter-individual
variation was noted in plasma prednisolone levels after
administration of shellac-coated tablets (Lee et al., 1979).
Information on bioavailability, distribution and rate of
excretion of shellac are not available.
2.1.2 Biotransformation
No information available.
2.1.3 Effects on enzymes and other biochemical parameters
No information available.
2.2 Toxicological studies
2.2.1 Acute toxicity studies
The acute oral toxicity of four types of food-grade shellac was
determined in rats. Groups of ten rats were administered a single
gavage dose (5 g/kg) of one of four types of shellac in aqueous
suspension. No deaths were recorded (Levenstein, 1980). Table 1
summarizes the results of this study.
Table 1: Acute toxicity of shellac (Leberco Laboratories Data Summary)
Type of test material No. Fed/No. Dead
Regular Bleached Bone-Dry Shellac 10/0
Refined Wax-Free Bone-Dry Bleached Shellac 10/0
Orange with Wax Shellac 10/0
Orange Wax Free Shellac 10/0
The report did not supply information on the identity of the
rat strain used in this study.
2.2.2 Short-term studies
In a 90-day rat feeding study, 42 female SIV 50 rats (average
weight, 76 g) were divided into three groups. Groups 1 and 2 were
fed diets containing 2% shellac (each group was fed a different
brand of food-grade shellac) for 90 days; Group 3 rats served as
controls. The average feed consumption was 13.2 g/d, and average
weight gains for animals in Groups 1 and 2 (127 ± 11.4 g and 128.6 ±
12.7 g, respectively) did not differ significantly from the average
weight gain for animals in Group 3 (123.7 ± 9.9 g) The investigator
reported that shellac had no effect on the appetite of test animals,
and no residues of shellac were detected in the test animals'
faeces. At the end of the study four rats from each group were
examined histologically (liver, duodenum, ileum, caecum, colon, and
kidneys). Although animals fed shellac tended to have enlarged caeca
and swelling in the proximal region of the colon, gross examination
revealed no pathological changes in the intestinal tract, liver, nor
kidneys. Colons of control rats exhibited less intestinal
eosinophilia than those of shellac-fed rats and less oedema of the
lamina propria was detected in the caeca of control and Group 2 rats
than in Group 1 rats. Although this study did not identify
pathological changes associated with the consumption of shellac,
results were confounded by the failure of growth in both
experimental and control animals during the latter phase of the
study (Buchloch, 1979).
2.2.3 Long-term/carcinogenicity studies
No information available.
2.2.4 Reproduction/teratogenicity studies
Regular bleached shellac was evaluated in a 90-day toxicity
study with an in utero exposure phase. Twenty-five Sprague-Dawley
rats per sex (F0) were fed commercial diets containing 0
(control), 1000, 3000, and 10 000 ppm shellac for 28 consecutive
days. Animals within groups were mated after this period, and
females were allowed to deliver and wean a single litter. On day 4
of lactation, litters were culled to 5 male and 5 female rats, if
possible. Twenty-five weaned F1 animals per sex from each group
were randomly selected for the 90-day study, and were fed the same
diets as their parents had consumed. Animals were killed after 11
weeks (F0 males) or 13 weeks (F0 females, F1 animals) of
consumption of shellac-containing or control diets. The following
assessments were made for test and control groups of rats:
mortality; external physical, behavioural and developmental signs of
toxicity; body weight; feed consumption; reproduction and
developmental indices; haematology; clinical chemistry; urine
analysis; gross necropsy; and histopathological examination. There
was no evidence of treatment-related toxicological effects in
shellac-fed F0 and F1 animals (FDRL, 1984).
2.2.8 Special studies on mutagenicity
Food grade regular bleached shellac was evaluated for
mutagenicity in a series of in vitro microbial assays.
Mutagenicity evaluation of shellac using the Ames
Salmonella/microsome plate test was performed on concentrations
ranging from 1 to 10 000 œg/plate shellac in corn oil. These
in vitro microbial plate assays were performed in the absence and
in the presence of a metabolic activation system (S9 fraction from
Aroclor-induced rats). The negative control for both activation and
non-activation assays consisted of incubation of the strains with
corn oil alone. The positive control, 2-anthramine in DMSO at a
concentration of 2.5 µg/plate, was used in the activation assays
with all strains. No toxicity was observed in any of the indicator
strains used. No increase in the number of revertants was observed
in any strain either in the presence or in the absence of metabolic
activation. Results of these studies are summarized in Table 2.
Table 2: Summary of mutagenicity studies with shellac
Test material System Strain Results Reference
Food Grade Salmonella TA-1535 negative Jagannath &
regular bleached typhimurium TA-1537 Myln, 1981
Shellac TA-1538
TA-98
TA-100
Shellac Wax Salmonella TA-1535 negative Brusick, 1975
typhimurium TA-1537
TA-1538
Shellac Wax Saccharomyces D4 negative Brusick, 1975
cerevisiae
2.2.9 Special studies on immune responses
No information available.
2.3 Observations in humans
2.3.1 Respiratory studies
The possible association between the inhalation of shellac in
hair sprays and respiratory disease has been studied. An acute
respiratory toxicity study was conducted using an unreported number
of women volunteers (Draize et al., 1959). Of the six hair spray
formulations tested in this study, one contained shellac. Exposure
in a test cubicle to each spray lasted 10 or 30 seconds with an
additional 5 min in the cubicle with the sprayed atmosphere. This
exposure to shellac was reported to be insufficient to produce
adverse effects. Non-volatile components of the sample atmosphere
were determined and considered to be negligible. No data on the
subjects' age, weight, and physical health were given. Exposures for
this study are summarized in Table 3, below.
Table 3: Human exposure to shellac type hair spray
Spray Released Nonvolatile Spray
sec g in air, g inspired, g
10 8.8 0.0024 0.00016
30 22.5 0.0038 0.0002
A paper by Gelfand (1963) documents allergies (particularly
bronchial asthma and allergic skin reactions) reportedly caused by
exposure to chemical compounds in the rubber, lacquer, shellac, and
beauty industries through reports of patients exposed to the
compounds as customers or workers in these industries. The author
suggested that respiratory allergies reported to be associated with
inhalation of shellac were not due to shellac but to other solvents.
2.3.2 Oral toxicity
No information on human oral dosing was available.
2.3.3 Long-term studies
Little is known about the effects of long-term exposure to
shellac on humans. A forensic autopsy of a 55-year old male cabinet
maker found a hardened mass of shellac (bezoar) in his stomach
(Janica, 1983). Cause of death was reported to be from trauma to the
skull caused by a fall. How the shellac was ingested remains
unclear.
3. COMMENTS
As evaluated by mirobial assays, shellac is not mutagenic. In a
90-day study, female rats fed diets containing shellac showed caecal
enlargement and swelling in the proximal region of the colon. There
were no hisopathological changes associated with the consumption of
shellac, although the results were confounded by the failure of both
experimental and control animals to grow during the latter part of
the study.
A recent 90-day study (including an in utero exposure phase)
produced no evidence of treatment-related toxic or pathological
effects in F0 or F1 rats fed diets containing up to 1% shellac
(equal to 660 mg/kg bw/day for female rats).
4. EVALUATION
The Committee concluded that the present functional uses of
shellac (as a coating, glazing and surface-finishing agent applied
externally to food) were of no toxicological concern.
5. REFERENCES
BRUSICK, D. (1975). Mutagenic evaluation of compound PM 90000593
shellac wax (73-51). Unpublished report from Litton Bionetics, Inc.,
Kensington, MD, USA. Submitted to Food and Drug Administration,
Rockville, MD, USA.
BUCHLOCH, G. (1979). Anatomical-histological examination: 42 rats
fed with shellac. Unpublished report from the American Bleached
Shellac Manufacturers Association, Inc., New York, USA. Submitted to
the Federation of American Societies for Experimental Biology,
Bethesda, MD, USA.
COSMETIC INGREDIENT REVIEW (CIR). (1986). Final report on the safety
assessment of shellac. J. Amer. Coll. Tox., 5: 309-327.
DRAIZE, J.H., NELSON, A.A., NEWBURGER, S.H., & KELLEY, E.A. (1959).
Non-toxicity of aerosol hair sprays. Drug & Cosmetic Ind., 84:
592-593, 644, 652.
FDRL (1984). Ninety-day (in utero) dietary toxicity study of regular
bleached shellac in Sprague-Dawley rats. FDRL study No. 7455. Report
from Food and Drug Research Laboratories, Waverly, New York, USA.
Submitted to WHO by the American Bleached Shellac Manufacturers
Association, Inc., New York, NY, USA.
FEDERATION OF AMERICAN SOCIETIES FOR EXPERIMENTAL BIOLOGY (FASEB).
(1981). Evaluation of the health aspects of Shellac and Shellac Wax
as food ingredients. Final Report for FDA.
Publication No. PB82-160383.
GELFAND, H.H. (1963). Respiratory allergy due to chemical compounds
encountered in the rubber, lacquer, shellac and beauty culture
industries. J. Allergy, 38: 374-381.
JAGANNATH, D.R. & MYLN, B.C. (1981). Mutagenicity evaluation of
regular bleached food grade shellac in the Ames
Salmonella/microsome plate test. Unpublished report from the
Litton Bionetics, Inc. Kensington, MD, USA submitted to Federation
of American Societies for Experimental Biology, Bethesda, MD, USA by
American Bleached Shellac Manufactures Association, Inc., New York,
NY, USA.
JANICA, J. (1983). Shellac bezoar of the stomach. Wiad. Lek., 36:
881-883.
LEE, D.A.H., TAYLOR, G.M., WALKER, J.G. & JAMES, V.H.T. (1979). The
effect of food and tablet formulation on plasma prednisolone levels
following administration of enteric-coated tablets. Br. J. Clin.
Pharmac., 7: 523-528.
LEVENSTEIN, I. (1980). Acute oral toxicity study on five types of
food grade Shellacs in rats. Unpublished report from Leberco
Laboratories submitted to Food and Drug Administration, Rockville,
MD, USA.
ROGERS, R. (1978). Monograph on shellac. FDA Publication No. PB 287
765.
See Also:
Toxicological Abbreviations