CARBON BLACK
EXPLANATION
Activated carbon (synonyms, activated charcoal and decolorizing
carbon), that is carbon black derived from vegetable material or
lignites, was evaluated under the name "activated vegetable carbon
(food grade)" at the fourteenth meeting of the Committee (Annex 1,
reference 22). An ADI "not limited", except that good manufacturing
practice be followed, was established. This refers to its use as a
clarifying agent, not as a food colour. A toxicological monograph was
published (Annex 1, reference 23), and new data evaluated at the
present meeting are included in this monograph addendum.
BIOLOGICAL DATA
Four recent reviews have been published on carbon black
(NCI, 1985; IARC, 1984; Rivin & Smith, 1982; NIOSH, 1978).
Biochemical aspects
Absorption, distribution, and excretion
Inhaled carbon black is retained in the lungs. Clearance is by
macrophage uptake, retrograde mucociliary movement, and possibly
secondary gastrointestinal ingestion. Absorption into the blood stream
for systemic distribution evidently does not occur. There have been no
reports of gastrointestinal absorption and carbon black is probably
cleared in the faeces (Nau et al., 1962, 1976; NCI, 1985).
Toxicological studies
Special studies on the bioavailability of polynuclear hydrocarbons
adsorbed on carbon blacks
In vitro studies
Samples of 3 different carbon blacks (rubber-grade oil furnace
blacks, ASTM designation N-234, N-351, and N-375) were extracted with
the following tissue fluids and cellular components: human plasma,
swine serum, the supernatant of swine lung homogenates, and swine lung
washings. All tissue fluids were poor eluters of benzo(a)pyrene (less
than 0.005% of the absorbed benzo(a)pyrene content of the carbon black
as determined by toluene extraction was extracted by the tissue
fluids). Swine serum was a less efficient extractant than human
plasma. Swine lung homogenate and lung washings were equally effective
(Buddingh et al., 1981).
The extent of the elution of benzo(a)pyrene depends on the
benzo(a)pyrene content of the carbon black and surface area of the
particles, e.g. soot particles of 100 nanometers or less adsorb free
benzo(a)pyrene from a protein medium (Falk & Steiner, 1952).
In vivo studies
Groups of 5 male and 5 female outbred CIGR mice were fed diets
containing 0, 0.0082, 0.20, or 2.0% of 3 different carbon blacks
(N-234, N-351 and N-371) for 3 successive generations. Litters from
the F0, F1, and F2 generations were killed at day 28, breeders
from the F2 generation were killed, and arylhydrocarbon hydroxylase
activities of the liver and lungs were determined. Dietary exposure to
carbon black had no effect on enzyme activity, suggesting that the
elution of benzo(a)pyrene was not sufficient to induce increased
enzyme activity in this system (Buddingh et al., 1981).
Special studies on carcinogenicity
Mice
Groups of 10-50 CFW white and/or CH3 brown mice in a series of
feeding experiments were administered, for periods of 12 to 18 months,
either: (1) 10% carbon black; (2) 10% benzene-extracted carbon black;
(3) benzene extract from carbon black; (4) 3-methyl-cholanthrene (MCA)
or MCA adsorbed to flour; or (5) MCA adsorbed to benzene-extracted
carbon black. The test material was dispersed in the basal diet by use
of either a water-base mixture containing carboxy-methyl cellulose or
an oil-base mixture containing cotton seed oil. For the control
groups, the basal diet was supplemented with either the water-base
mixture or oil-base mixture. At termination of the study, all the mice
were killed and complete gross and microscopic examinations were made
of all organs and tissues. No significant effects were observed in
either the control groups or the groups given the unextracted carbon
black. Mice fed extracted carbon black in the water-base diet
developed a number of rumours (10/100). Nine of these tumours
(3 intracutaneous fibrosarcomas, 3 begnin squamous papillomas, and 3
squamous metaplasas with malignancy) were considered to be due to
benzene-extractive material that had not been completely removed from
the benzene-extracted carbon black. No significant effects were
reported in the group fed extracted carbon black in the oil-base
mixture. Mice fed the benzene extract of carbon black in diets
containing either the water-base or oil-base mixture developed tumours
of the gastrointestinal tract and carcinomas of the stomach. In the
groups of mice fed MCA, there was a high incidence of adenocarcinomas
or squamous-cell carcinomas of the gastrointestinal tract. However, in
the groups of mice fed MCA that was adsorbed to extracted carbon
black, only 1 of 190 developed fibrosarcoma of the gastrointestinal
tract (Nau et al., 1958).
Mice and rats
Groups of 24 or 48 Swiss mice or Harlan stock rats were
administered, for more than 15 months, *para-dimethylaminoazobenzene
(DMAB), methyl cholanthrene, or 3,4-benzo(a)pyrene, either free or
adsorbed onto various carbon blacks; carbon black alone was
administered to other groups of mice and rats. The level of carbon
black in the diet ranged from 9 to 18%. All animals were killed and
necropsied, and selected tissues were examined histologically. No
tumours were observed in the groups of mice or rats receiving carbon
black only. In the group receiving free DMAB, 14/24 mice (58%)
developed hepatic tumours. Of the groups receiving DMAB adsorbed onto
carbon black, only one group developed tumours. The time to first
rumour in this group was 10.25 months compared to 6 months in positive
controls. None of the other groups treated with the adsorbed
carcinogens developed rumours, although high incidences were observed
in the test animals fed the carcinogens alone. Test animals treated
with acetone suspensions of carbon black plus 3,4-benzo(a)pyrene
developed a high incidence of tumours (54-69%); however, the onset of
rumours was delayed when compared to positive controls
(von Haam et al., 1958).
Groups of female 26-31 CF1 mice and female 29-45 Sprague-Dawley
rats were fed either 0 or 2.0 g carbon black (ASTM N-375) per kg of
ground lab chow diet for 2 years. This dietary level was calculated to
amount to an average consumption of 100 g/kg b.w./year for the mice
and 38 g/kg b.w./year for the rats. (The average fat content of this
rodent chow was later reported by these authors (1986) to be
approximately 5% by weight.) Simultaneously, groups of mice and rats
were exposed to carbon black for 52 weeks with or without the
administration of 1,2-dimethylhydrazine (DMH) via 16 weekly i.p.
injections at dose levels of 10 mg/kg b.w. in rats and 20 mg/kg b.w.
in mice. Control animals were given the solvent (lmM EDTA) by
injection. After 52 weeks or 2 years, the animals were killed, gross
necropsies performed, and all lesions examined microscopically. The
survival of all groups of animals was comparable; there was no
apparent effect of carbon black ingestion on tumour incidence. A small
non-significant incidence in colon tumours was seen in the group not
treated with DMH in the 2-year study. In the 52-week groups in which
carbon black plus DMH was administered, there were no enhancements in
gastrointestinal, respiratory, mammary, or urinary tumours. However,
groups given carbon black and DMH had an increased mortality (Pence &
Buddingh, 1985).
Rats
Groups of 25 female Sprague-Dawley rats were administered carbon
black (ASTM N-375) at a level of 0 or 2.0 g/kg diet. The study
utilized a high-fat diet and consisted of 20% (w/w) corn oil added to
a ground commercial chow diet. The average carbon black consumption
was calculated to be 38 g/kg b.w./year. Colonic tumours were induced
in the test groups by 16 weekly i.p. injections of DMH at 10 mg/kg
b.w. All groups were maintained on test diets for 52 weeks, killed,
subjected to necropsy, and all lesions were examined microscopically.
Weight gain and food intake were not affected by any of the four
regimens. DMH-treated rats had decreased survival due to intestinal
tumours, and this effect was most prominent in the group also
receiving carbon black. There were no colonic tumours in animals not
treated with DMH. In the DMH group maintained on a high-fat diet, 60%
of the females had colonic tumours. This was significantly different
(P < 0.05) from the 76% seen in the DMH group maintained on the same
high-fat diet which contained 2.0 g/kg carbon black (Pence & Buddingh,
1986).
Special studies on mutagenicity
Commercially produced furnace carbon black (rubber grade, CAS
No. 1333-86-4) containing 194 ppm polynuclear aromatic hydrocarbons
(PAHs) (determined on a benzene extract) showed limited toxicity but
no mutagenetic activity in the following assays; (1) Salmonella
assay, 5 tester strains of Salmonella typhimurium (TA98, TA100,
TA1535, TA1537 and TA1538), with or without metabolic activation, at
levels up to 7,500 µg/plate; (2) sister-chromatid exchange in Chinese
hamster ovary cells, with or without metabolic activation, at test
levels up to 1000 µg/ml; (3) mouse lymphoma cell L5178 assay, with or
without metabolic activation, at test levels up to 15,000 µg/ml; (4)
C3H/10 T1/2 cell transformation assay at test levels up to
16,384 µg/ml; and (5) the Drosophila assay (Kirwin et al., 1981).
Short-term studies
No information available.
Long-term studies
Mice
Groups of 8-week old C3H mice were fed diets containing either
0 or 10% thermal black for as long as 72 weeks. No significant gross
or microscopic changes from normal were seen. This was a summary
report and did not give any details (Nau et al., 1976).
Observations in man
No reports on oral ingestion of carbon black by humans were
available. The available information relates to occupational exposure
through inhalation. Three reviews have been published which examined
the toxicity of carbon black to humans under these conditions
(NIOSH, 1978; Rivin & Smith, 1982; IARC, 1984).
The major effect of carbon black in humans is on lung function.
Other effects in humans attributed to carbon black are dermatological
lesions, skin irritation, acute gastrointestinal diseases, myocardial
dystrophy, and cardiovascular changes. In both of the reports on heart
effects, there was concomitant exposure to carbon monoxide (Komarova,
1965, 1973, as cited by NIOSH, 1978).
IARC (1984) reviewed the available epidemiological data and
concluded that the data provide inadequate evidence to evaluate the
carcinogenicity of carbon black to humans.
COMMENTS
Carbon black used for colouring purposes falls within two main
groups, those derived from hydrocarbons and those derived primarily
from peat and plant materials, commercially described as vegetable
black.
The food colouring uses of carbon blacks derived from both
sources were evaluated by the Committee at the twenty-first meeting
(Annex 1, reference 44). No ADI was established for food colouring
uses from either source. A major concern of that Committee related to
the question as to how strongly and irreversibly PAHs are adsorbed
onto carbon black.
The present Committee considered data from studies involving
carbon black prepared from hydrocarbon sources. Benzene extracts of
certain carbon blacks were found to be carcinogenic to mice. These
carcinogenic extracts contain PAHs adsorbed to carbon black. Data were
available to show that only small amounts of PAHs (less than 0.005% of
the benzene-extractable PAHs) were eluted from carbon black by
biological fluids. Carbon black was not mutagenic in bacterial or
mammalian systems. Dietary carbon black was not carcinogenic in
limited lifetime studies in rats and mice at levels up to 10% of the
diet. Information was also presented to show that carbon black was
able to adsorb some chemical carcinogens and, under certain
experimental conditions, was shown to reduce their carcinogenic
potential.
No toxicological data were available on carbon black derived from
vegetable sources.
EVALUATION
Carbon black (hydrocarbon sources)
Food contact materials
The use of carbon black from hydrocarbon sources is provisionally
accepted in food contact materials, including wax coatings for cheese.
Future specifications should include figures relating to residual
PAHs.
Direct use in food
No ADI could be established (a) because carbon blacks from
hydrocarbon sources have been shown to contain different amounts of
known carcinogens and knowledge is lacking on the ability of man to
extract such carcinogens upon ingestion and (b) because of limited
feeding studies in experimental animals with defined carbon blacks.
Carbon black (vegetable black)
No ADI could be established because no toxicological data were
available.
REFERENCES
Buddingh, F., Bailey, M.J., Wells, B., & Haesemeyer, J. (1981).
Physiological significance of benzo(a)pyrene adsorbed to carbon
blacks: Elution studies; AHH determinations. Amer. Ind. Hyg.
Assoc. J., 42, 503-509.
Falk, H.L. & Steiner, P.E. (1952). The adsorption of 3,4-benzpyrene
and pyrene by carbon blacks. Cancer Res., 12, 40-43.
von Haam, E., Titus, H.L., Caplan, I., & Shinowara, G.Y. (1958).
Effect of carbon blacks on carcinogenic compounds. Proc. Soc. Exptl.
Biol. Med., 98, 95-98.
IARC (1984). Monographs on the evaluation of the carcinogenic risk of
chemicals to humans. International Agency for Research on Cancer.
WHO/IARC Monograph, vol. 33, pp. 35-85.
Kirwin, C.J., Le Blanc, J.V., & Thomas, W.C. (1981). Evaluation of the
genetic activity of industrially-produced carbon black.
J. Tox. Environ. Health, 7, 973-989.
Nau, C.A., Neal, J., & Stembridge, V.A. (1958). A study of the
physiological effects of carbon black - I. Ingestion. A.M.A. Arch.
Ind. Health, 17, 21-28.
Nau, C.A., Neal, J., Stembridge, V.A., & Cooley, R.N. (1962).
Physiological effects of carbon black - IV. Inhalation.
Arch. Environ. Health, 4, 415-431.
Nau, C.A., Taylor, G.T., & Lawrence, C.H. (1976). Properties and
physiological effects of thermal carbon black. J. Occup. Med.,
18, 732-734.
NCI (1985). Monograph on human exposure to chemicals in the workplace:
Carbon black. National Cancer Institute. NTIS publication
No. PB86-152048, Springfield, VA, USA.
NIOSH (1978). Criteria for a recommended standard. Occupational
exposure to carbon black. National Institute for Occupational Safety
and Health. DHEW publication No. 78-204. US Department of Health,
Education and Welfare, Washington, DC 20204, USA.
Pence, B.C. & Buddingh, F. (1985). The effect of carbon black
ingestion on 1,2-dimethylhydrazine induced colon carcinogenesis in
rats and mice. Tox. Letters, 25, 273-277.
Pence, B.C. & Buddingh, F. (1986). Co-carcinogenesis effect of carbon
black ingestion with dietary fat on the development of colon tumours
in rats. Manuscript submitted to Tox. Letters, September, 1986.
Rivin, D. & Smith, R.G. (1982). Environmental health aspects of carbon
black. Rubber Chem. Technol., 55, 707-761.
See Also:
Toxicological Abbreviations
Carbon black (ICSC)
Carbon Black (IARC Summary & Evaluation, Volume 65, 1996)