CARBON BLAeK

1. Exposure Data

Carbon black was considered by previous Working Groups (lARe, 1984, 1987a).
New data have since become available, and these are incIuded in the present monograph
and have been taken into consideration in the evaluation.

1.1 Chernical and physical data

1.1.1 Nomenclature

The Chem. Abstr. Serv. Reg. No. for aIl carbon blacks is 1333-86-4.
Acetylene black
Chem. Abstr. Name: Carbon black, acetylene
¡UPAC Systematic Name: Carbon black, acetylene
Synonyms: CI 77266; CI Pigment Black 7; explosion acetylene black; explosion black
Trade Names: P68; P1250; Shawinigan Acetylene Black; Ucet
Channel black
Chem. Abstr. Name: Carbon black, channel
¡UPAC Systematic Name: Carbon black, channel
Synonym: CI 77266; CI Pigment Black 7; Impingement black
Trade Names: Aroflow; Arrow; Atlantic; Black Pearls; Carbolac; Carbomet; CK3;
Collocarb; Conductex, Continental; Croflex; Crolac; Degussa; Dixie; Dixiecell;
Dixiedensed; Elf; Excelsior; Farbruss; Fecto; Huber; Kosmink; Kosmobil; Kosmolak;
Kosmos; Kosmovar; Micronex; Mogul; Monarch; Neo-Spectra; Peerless; Printex;
Raven; Regent; Royal Spectra; Special Black IV & V; Spheron; Superba; Super-
Carbovar; Super-Spectra; Texas; Triangle; United; Witco; Wyex
Furnace black
Chem. Abstr. Name: Carbon black, furnace
¡UPAC Systematic Name: Carbon black, fumace
Synonyms: CI 77266; CI Pigment Black 7; gas-furnace black; oil-furnace black
Trade Names: Aro; Arogen; Aromex; Arovel; Arotone; Atlantic; Black Pearls;
Carbodis; ColIocarb; Conductex, Continex; Corax; Croflex; Dixie; Durex; Elftex;
Essex; Fumal; Futnex; Gastex; Huber; Humenegro; Kosmos; Metanex; Modulex;

-149-
150 IARC MONOGRAPHS VOLUME 65

Mogul; Molacco; Monarch; Neotex; Opal; Peerless; Pelletex; Philblack; Printex;

Rebonex; Regal; Special Schwarz; Statex; Sterling; Texas; Ukarb; United; Vulcan
Larnpblack
Chem. Abstr. Name: Carbon black, lamp
IUPAC Systematic Name: Carbon black, lamp
Synonyms: CI 77266; CI Pigment Black 6
Trade Names: Carbon Black BV and V; Durex; Eagle Germantown; Flamruss;
Magecol; Tinolite; Torch Brand
Therrnal black
Chem. Abstr. Name: Carbon black, thermal
IUPAC Systematic Name: Carbon black, thermal
Synonyms: CI 77266; CI Pigment Black 7; therma-atomic black
Trade Names: Atlantic; Cancarb; Croflex; Dixitherm; Huber; Kosmotherm; Miike 20;
P-33; Sevacarb; Shell Carbon; Statex; Sterling; Thermatomic; Thermax; Thermblack;
Velvetex

1.1.2 General description

Carbon black is sometimes confused with soot but it is a very different material
(Medalia et aL., 1981). Carbon black is a powdered form of elemental carbon
manufactured by the controlled vapour-phase pyrolysis of hydrocarbons. Different types
of carbon black have a wide range of particle sizes, high surface areas per unit mass,
quite low contents of ash and toluene-extractable materials and varying degrees of
particle aggregation. A carbon black with a high degree of aggregation is said to have a
high 'structure'. Structure is determined by the size and shape of the aggregated particles,
the number of primary particles per aggregate and their average mass.
The fundamental unit of a carbon black is the aggregate. This is a chain of roughly
spherical carbon particles that are permanently fused together in a random branching
structure. The aggregate may consist of a few or hundreds of spherical particles (or, as in
thermal black, primarily single spheres rather th an chains). The chains are open
structures and are used to absorb fluids and reinforce materials such as rubber. The
aggregates can bind together by van der Waals forces in more loosely associated
agglomerates, or they may be compressed in pelIets (up to 0.5 cm) held together by
means of binders (molasses/lignosulfonates) (Dannenberg et aL., 1992; Gardiner et al.,
1992a).
To describe a carbon black aggregate, two dimensions are necessary:
(l) Mean diameter of the component spheres in the chain. This is a measure of the
chain 'thickness'. This is calIed the primary particle size and generalIy is
inversely proportional to the surface area of the black.
(2) Extent of the branched chain aggregate. This is called the aggregate size and is
the dimension of the rigid framework that is the aggregate.
 CARBON BLACK 151

ln addition to these two dimensions, there is a pro

pert y or 'structure' which is the
volume of space that is 'reinforced' by the aggregate - essentially, the amount of fluid it
can absorb internally. A standard method of measuring this property is by the dibutyl
phthalate absorption of a black, in units of mL/l 00 g.
Also of importance for human exposure is the behaviour of carbon black in air and its
deposition in the respiratory tract upon inhalation. This is determined by the aerodynamic
diameter of the particles. The aerodynamic diameter can be measured by impactors and
is dependent upon the geometric diameter, material density and shape factor of the aggre-
gates. Most commonly, the size distribution of airborne particles is expressed as its mass
median aerodynamic diameter (MMAD) with its geometric standard deviation.
Carbon black is variously known as asetylene black, channel black, furnace black,
lampblack or thermal black, depending on the specific process by which it is manu-
factured (see Section 1.2.1). The properties of typical types of carbon black are presented
in Tables 1-6.
ln contrast to carbon black, soot is a material of varying and often unknown compo-
sition, which is an unwanted by-product of the incomplete combustion of aIl kinds of
carbon-containing materials, such as waste oil, coaL, paper, rubber, plastic, garbage and
also fuel oils or gasoline. Soots have a low available carbon surface area owing to their
large particle size and small carbon component. They typically contain large quantities of
dichloromethane- and toluene-extractable materials, and their ash content can be 50% or
more (European Committee for Biological Effects of Carbon Black, 1982).
Two other commercial carbonaceous products are activated carbon and bone black.
Activated carbon is a collective name for a group of porous carbons. These are manu-
factured either by the treatment of carbon with gases or by the carbonization of carbona-
ceous materials with simultaneous activation by chemical treatment. Activated carbon
possesses a porous structure, usually with small amounts of chemicalIy bonded oxygen
and hydrogen, and can contain up to 20% of mineraI matter, which is usualIy indicated as
ash or residue as a result of ignition. The nature of this mineraI material depends on the
raw materials used, and can consist of silica and compounds of alkali and alkaline-earth
metals, for example. X-Ray investigations show that the carbon is mainly in the form of
very small crystallites with a graphite-like structure (V ohler et al., 1986).
Bone black is a by-product of the bone char industry. Bone char is made by carbo-
nizing bones and is used principally in sugar refining. Bone black is a pigment derived
from bone char, used primarily as a colourant in artists' paint and for tinting vinyl fabrics
for upholstery and automotive interiors. The carbon content of bone black is usually
approximately 10% (Lewis, 1988, i 993).

1. i.3 Chemical and physical properties of the technical products

AlI commercially available types of carbon black are insoluble in water and organic
solvents, but various types differ in other chemical and physical properties. The ranges of
properties of each of the four types of carbon black are summarized in Table 1. Analyses
of samples of carbon tllack produced commercially in the United States of America and
152 IARC MONOGRAPHS VOLUME 65

Europe are given in Table 2, and those of the carbon black types produced in Japan are
given in Table 3.

Table 1. Typical ranges of properties for four types of carbon black

pigrnent

Property Acety lene Furnace Lampblack Thermal

black black black

Average aggregate diameter (nm) NR 80-500 NR 300-8 10"

Average primary parti cie 35-50 17-70 50- 1 00 150-500
diameter (niu)
Surface area", N, (m2/g) 60-70 20-200 20-95" 6-15
(17-25)'
Oil absorption (mL/g) 3.0-3.5 0.67-1.95 1.05-1.65 0.30-0.46
pH 5-7 5-9.5 3-7 7-8
Volatile matter (%) 0.4 0.3-2.8 0.4-9.0' 0.10-0.50
(0.5- 1.5)"
Hydrogen (%) 0.05-0.10 0.45-0.71 NR 0.3-0.5
Oxygen (%) 0.10-0.15 0.19-1.2 NR 0.00-0.12
Benzene extract (%) 0.1 0.01-0.18 0.00-1.4 0.02-1.7
Ash (%) 0.00 0.1-1.0 0.00-0.16 0.02-0.38
Sulfur (%) 0.02 0.05- 1.5 NR 0.00-0.25
Density (g/mL) NR 1.80 1.77" NR

From Garret (1973), Weast (1981) and Hess & Herd (1993)
NR, not reported
"Surface area ca1culated by the nitrogen adsorption method
"Value in the United States
'Value in Europe (data provided by European carbon black manufacturers (lARe,
1984) )

Extractable polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, and sulfur-

containing aromatics from carbon black are discussed in Section 1.1.4.
Acetylene black
Acetylene black is characterized by its high purity, low oxygen content and an
extremely high degree of aggregation or structure. X-Ray analysis indicates that
acetylene black is the most crystalline or graphitic of the commercial blacks. The levels
of ash content and benzene-extractable materials are very low, and acetylene black is not
readily wetted by water, since its surface is saturated with hydrogen atoms.
Channel black
Channel black is no longer produced in the United States but, in Europe, its
manufacture still continues and, in some operations, is expanding. ln the past, channel
black was characterized by its small particle size, low degree of aggregation or structure,
relatively high content of oxygen complexes on its surface and acidic pH. Natural gas
was used as the feedstock and 'water was not required for the quenching of the reaction,
 Table 2. Analyses of sarnples of several carbon blacks produced cornrnercially in the United States and Europe
Property Acetylene Fumace Fumace Lampblack Thermal Thermal
(HAFfN330) (FEFfN550) (FT/N880) (MTfN990)
USA Germany USA Europe
Average aggregate diameter (nm) NR NR 260 470 NR NR 300 400
Average particle diameter (nm) 40 35 28 42 65 95 200 400
Surface area (BET) (m'/g) 65 70 80 42 22 20 12 7
n
Toluene extract (%) ;p
0.1 0.05" 0.08 NR 0.2" 0.1" 0.8 0.3 ;;
pH 4.8 7.0 7.5 Cö
Volatile matter (%)
NR 3.0 7.0 9.0 8.5 0
0.3 0.05 1.0 1.0 1.5 1.0 0.5 0.5 Z
Ash (%) 0.0 0.05 0.3 Cö
0.2 0.02 0.05 0.1 0.3 l'
Composition (%)
Carbon 99.7 99.8 97.9 98.4
n;p
Hydrogen
98 98 99.2 99.3 ~
0.1 0.05 0.3 0.4 0.2 0.4 0.5 0.3
Sulfur 0.02 0.005 0.6 0.7 0.8 0.6 0.01 0.01
Oxygen 0.2 0.05 0.8 0.4 0.8 0.4 0.3 0.1
From Hoechst AktiengeseIIschaft (I979); Dannenberg (I978); lARC (I 984); Robertson & Smith (I 994)
NR, not reported; HAF, high-abrasion furnace; FEF, fast extrusion fumace; FT, fine thermal; MT, medium thermal; BET, the Brunauer,
Emmett and Teller procedure for caIculating sudace area
" Benzene extract (%)

Vl
W
154 lARC MONOGRAPHS VOLUME 65

and, therefore, channel black had a very low ash content. The volatile content of channel
black was about 5% but could be increased to as mu ch as 18% by after-treatments. The
surface of this channel black reportedly contained hydroxyl, carbonyl and carboxylic
acid groups (Garret, 1973; Claassen, 1978).

Table 3. Typical analyses of three types of carbon

black cornrnercially available in Japan

Property Acety lene Furnace Thermal

black black black

Average particle diameter (nm) 40 21 90

lodine adsorption (mg/g)" LOS 119 26
DBPA" (mL/IOOg) 125 115 27
pH 7.5 7.7 8.5
Volatile matter (%) 0.2 1.4 0.5
Ash (%) 0.1 0.25 0.4

From lARe ( 1984)

" lodine adsorption is reported as the milligrams of iodine adsorbed
per gram of carbon black under specified conditions established by
the American Society for Testing and Materials (American Society
for Testing and Materials, i 995a) and has been used to approximate
the surface area of carbon blacks (Johnson & Eberline, 1978)
" DB PA, the dibutyl phthalate absorption method, a standard pro-
cedure for measuring void volume, a characteristic related to struc-
ture

Channel black, when manufactured, was available as a dry chemical in either powder
or pelleted form. Three types were available for reinforcing rubber - easy, medium and
hard processing. These varied slightly in particle diameter, that with the largest particle
diameter (approximately 29 nm) being known as easy-processing channel and that with
the smallest (approximately 22 nm) as hard-processing channel (IARC, 1984).
The average diameters of the channel blacks used for colour and ink applications are
shown in Table 4. Medium-flow channel blacks and long-flow channel blacks received
an after-treatment with hot air to increase their volatile contents and thereby increase the
'flow' of the lithographic inks in which they were used.
Carbon black made in Germany by an impingement rolIer process from aromatic
hydrocarbon-containing coal-tar residues and coke-oven gases is said to have similar
properties to those of older channel black. lt has an acidic pH, a volatile content of about
5%, a surface area of about 100 m2/g and an average particle diameter of 10-30 nm
(Claassen, 1978; Dannenberg et al., 1992).
Furnace black
Furnace black consists of irregularly shaped aggregate structures of spherical
partic1es. Originally produced by the. gas-furnace process, it is now produced almost
entirely by the oil-furnace process. Gas-furnace black was characterized by a low degree
 CARBON BLACK 155

Table 4. Average diarneters of channel blacks

used in colours and inks

Channel black Symbol Average diameter

(nm)

High-colour channel HCC 12

Medium-colour channel MCC 16
Regular colour channel RCC 25
Medium-f1ow channel MFC 25
Long-f1ow channel LFC 25

From IARC (1984)

of structure and had properties that led to a low-to-medium reinforcing performance. Oil-
furnace blacks have a substantially higher degree of aggregation and structure and,
consequently, furnace black is now available with a wide range of characteristics
depending on the desired product performance. The quality of furnace black is controlIed
by variations of the raw materials, operating temperatures, atmospheric turbulence and
by alteration of furnace design. A very small percentage of the total quantity of furnace
blacks is subjected to after-treatment by various oxidation processes for particular
applications.
Furnace black is available in several grades. Those used in rubber products have been
classified by the American Society for Testing and Materials (ASTM) according to a
standard four-character nomenclature system. ln this system, the letter N indicates that
the product gives a normal curing rate, while the letter S indicates that it reduces the rate
of cure. The first digit is used to designate the typical average partic1e size (e.g.
1 indicates 11-19 nm and 9 indicates 201-500 nm) and the last two digits are assigned
arbitrarily. The NI00 series are super-abrasion furnace blacks; the N200 series are
intermediate super-abrasion furnace blacks; the N300 series are high-abrasion furnace
blacks; the N500 series are fast-extrusion furnace blacks; and the N700 series are semi-
reinforcing furnace blacks. The N900 series are thermal blacks (American Society of
Testing and Materials, 1995a).

Table 5 pro vides the ASTM designations for furnace blacks used in rubber, a
description of their types, the symbols used to designate the types, as weIl as three typical
measures of surface area (iodine adsorption, cet
yI trimethyl ammonium bromide
adsorption and nitrogen adsorption), one measure of the degree of aggregation (dibutyl
phthalate absorption) and one rough measure of partic1e size (tinting strength). Table 6
provides similar information for furnace blacks used in inks, paints and plastics.
Larnpblack
Lampblack is considered to be the forerunner of all carbon blacks. Essential and
typical properties of lampblack are its high degree of aggregation or structure and low
surface area. Formerly, lampblack was an oily product sold in the fluffy state or partialIy
l56 IARC MONOGRAPHS VOLUME 65
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:s g N 0 0 (V 'T N tr N 'T r- r- 00 0 ¡it)U)::U)üU)"OU)
:" ~ :s ¡: :: ., ;¿
:ë ¡. .g; 8 ~ (\¡.~E-~¡.
~
~ C/ (\
~ "0 zzzzzzzzzzzzzz
'T in \0 00 tr \0 \0 r- r- 00 0 0 Q" Q"
\0 \0 \0 \0 r- r- r- r- r- r- Q" Q" Q" Q" o ~ .. C/ ¡. cr .. C/
~:: r ~ u,,~ p~
 -
Ui
00

Table 6. Typical properties of furnace blacks for inks, paints, paper and plastics
Furnace black Surface Partic1e Aggregate DBPA Bulk density Nigro- Tinting Volatile
area" size size (mL/100 g) (g/L) me ter strength content
(m2/g) (nm) (nm) indexl' (%) (%)
Fluffy Pellets Fluffy Pellets
..
~
Normalfurnace grades ~
n
High coi our 250-300 14-15 60 70-75 60-65 50-300 400-550 65-76 Il 7 -124 1.2-2.0 S;
Medium colour 150-220 16-24 50-160 47-122 46-117 130-300 390-550 74-78 118-124 1.0-1.5 0
45-140 20-37 60-220 42-125 42-124 Z
Regular col

Low colour
our

24-45
176-420 350-600 84-93 73- 1 19 0.9-1.5 0
41-75 280-430 71 64-120 256 352-512 94-99 48-69 0.6-0.9 c:
~
Surface oxidized grades ~
""
High colour 400-600 10-20 - 121 105 - - 64 100-135 8.0-9.5
::
C/
Medium colour 100-138 23-24 - 49-60 55 240-360 530 83-84 112-135 3.5-5.0 ~
(long flow) 0l'
Medium co10ur 96- 1 10 25 - 49-72 70 225-360 480 84 112-114 2.5-3.5 c:
(medium flow) S;
rr
Low colour 30-40 50-56 - 48-93 - 260-500 - 92-100 64 3.5 0\
Ui

From Dannenberg et al. (1992)

DBP A, dibutyl phthalate absorption
" As ca1cu1ated by the Brunauer, Emmett and Teller (BET) procedures
b A method for measuring the diffuse reflectance from a black paste with a black tile standard. The low numbers represent the 'jettest', or
most intense, black grades
 CARBON BLACK 159

compressed; however, recent grades are essentially free of residual oil and sold as a dry
pigment or as a suspension in linseed oil.
The ASTM (American Society for Testing and Materials, 1995b) specifications for
the dry pigment are: moisture and other volatile matter, 3.0% max.; acetone extract, 1.0%
max.; ash, 0.5% max.; and coarse particles (residue on a No. 325 sieve), 0.5% max.
Specifications for the pas te in oil are: pigment, 25% min.; linseed oil, 75% max.;
moisture and other volatile matter, 0.7% max.; and coarse particles (residue on a No. 325
sieve), 1.0% max.

Therrnal black
Thermal black. exhibits the largest particle size and the lowest surface area of the
commercial carbon blacks. Consisting of discrete spherical particles, it also has the
lowest degree of aggregation or structure, and is also characterized by low oxygen
content.
Thermal blacks are available in several grades. Table 5 provides information on the
ASTM classification of these products, according to the system described above for
furnace black.

1.1.4 Extractable impurities in carbon black

Because of their source materials, the methods of their production and their large
surface areas and surface characteristics, commercial carbon blacks typically contain
varying quantities of adsorbed by-products from the production process, particularly
aromatic compounds. A number of methods have been developed and used to extract and
characterize the se adsorbed chemicals (see Section 1.1.5(b)). The classes of chemicals
most commonly identified in these ex tracts are P AHs, nitro derivatives of P AHs (nitro-
PAHs) and sulfur-containing PAHs. Examples of these three classes of chemicals
identified in carbon black extracts are given in Table 7.
The specific chemicals detected in carbon black extracts and their relative quantities
vary widely from sample to sample. Extraction method, type and grade of carbon black
and after-treatments aIl appear to be factors that affect the types and quantities or'
impurities obtained. However, substantial batch-to-batch variation is typical.
Among the P AHs frequently found at the highest levels in carbon black extracts are
benzoIghi)perylene, coronene, cyclopenta(cd)pyrene, fluoranthene and pyrene. For
example, in a study of five types of furnace black used in tyre manufacture, extraction
with hot benzene after 250 h yielded means of 252-1417 mg extract per kg carbon black.
The quantities of various P AHs found in the extracts were as folIows (mg/kg):
anthanthrene,.. 0.5-108; benzacridine derivative, .. 0.5; benzo(dej)dibenzothiophene and
benzo( e )acenaphthylene, .. 0.5; benzofluoranthenes (total), .. 0.5-17; benzo(ghi)fluo-
ranthene, 20-161; benzo(ghi)perylene, 23-336; benzopyrenes (total), 2-40; cyclopenta-
(cd)pyrene, .. 0.5-264; coronene and isomer, 13-366; dimethylcyclopentapyrene and/or
dimethylbenzofluoranthene, 2-57; fluoranthene, 10-100; indeno(1,2,3-cd)pyrene, 1-59;
phenanthrene and/or anthracene, .. 0.5-5; and pyrene, 46-432 (Locati et aL., 1979). The
160 IARC MONOGRAPHS VOLUME 65

Table 7. Sorne cornpounds identified in carbon black

extracts
Polycyclic aromatic hydrocarbons (PAHs) (see also rARC, 1983)
Acenaphthy lene
Anthanthrene
Anthracene
Benz( a )acenaphthy lene
Benz( a )anthracene
Benzo( b ) fl uoran the ne
Benzo(g hi) fluoranthene
BenzoU)fuoranthene
Benzo(k )fluoranthene
Benzo(a)pyrene
Benzo( elpyrene
Benzo(ghi)perylene
Chrysene
Coronene
4H -Cyc lopenta( def) phenanthrene
Cyclopenta( cd)pyrene
Dibenz( a, h )anthracene
Fluoranthene
rndeno( 1 ,2,3-cd)pyrene
Naphthalene
Perylene
Phenanthrene
Pyrene
Nitro derivatives of PAHs (nitro-P AHs) (see also rARC, 1987b, 1989)
1,3-Dinitropyrene
1,6-Dinitropyrene
1,8-Dinitropyrene
9- N itroanthracene
3- Nitro-9- fluorenone
1 -Nitronaphthalene
1 - Nitropyrene
1,3,6- Trinitropyrene
Sulfur-containing PAHs
Benzo( def)dibenzothiophene
Dibenzothiophene
Phenanthro( 4,5-bcd)thiophene
Triphenyleno( 4,5-bcd)thiophene

From Falk & Steiner (1952); Gabor et aL. (1969); Gold (1975); Qazi &
Nau (1975); Renes (1975); WalIcave et al. (1975); Lee & Hites
(1976); Fitch et al. (1978); Nakajima et al. (1978); Fitch & Smith
(1979); Locati et al. (1979); De Wiest (1980); Rosenkranz et al.
(1980); Taylor et al. (1980); Sanders (1981); Ramdahl et aL. (i 982);
Rivin & Smith (1982); Butler et al. (1983); Novrocik et al. (1983);
Nishioka et al. (i 986); Jin et al. (i 987); Agurell & Löfroth (i 993)
 CARBON BLACK 161

results of two similar studies, which used benzene to extract adsorbates from a number of
oil-furnace blacks and one thermal black are shown in Table 8 (Taylor et aL., 1980;
Zoccolillo et aL., 1984).

Table 8. Benzo(alpyrene concentrations in the benzene

extracts of 10 carbon blacks

ASTM Surface area Total extract Benzo(a)pyrene

designation " (m"/g) (mg/kg) concentration
(no. of samples) (mg/kg)
(no. of samples)

N220 118 250 (2) 0.29 (4)

N234 128 630 (2) 1.08 (5)
N326 80 225 (1) 0.18 (1)
N339 90 510 (4) 1.46 (2)
N347 90 343 (1) 0.50 (l )
N351 70 780 (3) 5.47 (5)
N375 101 1020 (5) 3.81 (2)
N550 42 610(1) 0.14 (1)
N660 36 653 (6) 4.8 (6)
N990 lO 8020 (1 ) 35.00 (1)

From Taylor et al. (1980) and ZoccolilIo et aL. (1984)

" For American Society for Testing and Materials designations of
types, see Table 5

PAH fractions from six different batches of the same furnace black (ASTM desi-
gnation N660) were analysed and ranged from 200 to 736 mglkg; benzo(a)pyrene
concentrations ranged from 1.2 to 9.7 mglkg in benzene extracts (ZoccolilIo et al., 1984).
Seven types of carbon black used in tyre production in Poland (domestic: JAS-220,
JAS-330, JAS-530; imported: HAF-N-326, HAF-N-330, SRF-N-762 and Durex-O) were
analysed. The toluene-soluble extractable compounds, including P AHs, were determined
by the gravimetric method, and benzo(alpyrene by high-performance liquid chroma-
tography (HPLC) with a spectrometric detector. Toluene-soluble compounds were found
to amount to 0.12-0.25% (by weight). Benzo(a)pyrene, at a range of 1.44-3.07 ppm
(mglkg), was detected in five of the seven carbon blacks examined (Rogaczewska et aL.,
1989).
Agurell and Löfroth (1993) studied the variation of impurities in a furnace carbon
black (N330) manufactured in Sweden over a three-year period. The folIowing P AHs
were determined at the following ranges of concentration in benzene extracts (mglkg
carbon black): phenanthrene, 0.9-15; fluoranthene, 4.5-72; pyrene, 26-240; benzo(ghi)-
fluoranthene, 7.2-72; cyclopenta(cd)pyrene, 6.6-188; chrysene, 0.1-1.3; benzo(b )fluo-
ranthene, benzoU)fluoranthene and benzo(k)fluoranthene, 0.4-18; benzo(e)pyrene, 0.9-
19; benzo(a)pyrene, 0.9-28; perylene, 0.1-3.5; indeno(I,2,3-cd)pyrene, 2-43; benzo-
(ghi)perylene, 14-169; and coronene, 14-169.
162 IARC MONOGRAPHS VOLUME 65

Somewhat higher totallevels of P AH were found in extracts of thermal blacks. A 24-

h benzene extract of an N990-type thermal black yielded approximately 4000 mg extract
per kg carbon black. Individual PARs included (mglkg): benzo(ghi)perylene, 1217;
coronene, 800; pyrene, 603; anthanthrene, 299; fluoranthene, 197; benzo(a)pyrene, 186;
tract
and benzo(e )pyrene, 145 (De Wiest, 1980). The totallevel of P AH in the benzene ex

of another N990 thermal black sample was 2140 mglkg, which included 35 mg/kg
benzo(a)pyrene (Zoccolillo et al., 1984).
Nitro-P AHs were identified in extracts of sorne samples of channel black and furnace
black that had been subjected to an oxidative treatment using nitric acid. Discovery of
these by-products in a photocopy toner in the late 1970s led to modifications in this
oxidative treatment process, and these steps have reportedly eliminated nItro-PAHs from
commercial furnace black produced since 1980 (Fitch et al., 1978; Fitch & Smith, 1979;
Rosenkranz et al., 1980; Sanders, 198 i; Ramdahl et aL., 1982; Butler et al., 1983).
A number of oxidized PAHs (e.g. ketones, quinones, anhydrides, carboxylic acids)
were also identified in carbon black samples that had undergone oxidative treatment
(Fitch et al., 1978; Fitch & Smith, 1979; Rivin & Smith, 1982), and one study reported
that 3-nitro-9-fluorenone was detected in a nitric acid-treated carbon black used for
making carbon ink in China (Jin et al., 1987).
Carbon black made from high-sulfur feedstocks frequently contains detectable
quantities of extractable sulfur-containing aromatic compounds such as benzothiophene
derivatives (Lee & Hites, 1976; Nishioka et al., 1986).
Trace amounts of a variety of inorganic elements (e.g. calcium, iron, potassium, lead,
arsenic, chromium, selenium) also have been identified in sorne analyses of carbon black
samples (Collyer, 1975; Sokhi et al., 1990).

i .1.5 Analysis
This section briefly reviews methods of analysis to detect the presence of carbon
black in various matrices, as weIl as methods used to isolate and analyse surface conta-
minants (see Section 1.1.4).

(a) Carbon black in various matrices

Because of the difficulty of separating carbon black from other airborne particulates
in the workplace, total dust is usu?lly measured as a surrogate for airborne concentration
of carbon black in facilities producing or using carbon black. Both personal membrane-
filter and static high-volume sampling techniques are used to collect carbon black in the
work environment, folIowed by gravimetric analysis to arrive at the total dust
concentration. Free carbon has been determined by predigestion of a sample with nitric
acid to destroy organic matter followed by weighing of the residue and ignition between
140 and 700°C. The amount of free carbon is determined by the loss of weight upon
ignition (United States National Institute for Occupational Safety and Health, 1978). The
gravimetric method (Method 5000) of the United States National Institute for Occupa-
tional Safety and Health for determining total dust has a working range of 1.5-10 mg/m'
 CARBON BLACK 163

for a 200-L sample of air and an estimated limit of detection of 0.03 mg/sample (Eller,
1994) .
The American Society for Testing and Materials (1995a) has published similar
methods for the analysis of carbon black in several natural and synthetic rubbers. it has
been reported that thermogravimetric analysis is accurate for determining the carbon
black content of rubbers in the range of 0.1 to 30% by weight (Charsley & Dunn, 1981).

(b) Adsorbates on carbon blacks

Several methods have been reported for the extraction and analysis of adsorbates on
carbon black. Soxhlet extraction with various organic sol vents has been the primary
method used to remove the adsorbed chemicals from the carbon black samples, but
vacuum sublimation or extraction combined with sonification have also been used
(Zoccolilo et al., 1984). The efficiency of the Soxhlet extraction de pends on the
extraction time and solvent, the type of carbon black, the relationship between sample
weightlsolvent volume and the amount of extractable material. Sorne sol
vents can react
with the surface groups of carbon black and form artifacts during the extraction (Fitch
et aL., 1978).
Locati et al. (1979) found that in five furnace blacks a Soxhlet extraction time of
150 h was necessary to remove 95% of the benzene-extractable matter and 250 h for
exhaustive extraction. They also observed that the lower the relative molecular mass was,
the shorter the time necessary to obtain extraction was.
Taylor et al. (1980) examined the solvent efficiency of three solvents (24-h Soxhlet)
as measured by benzo(a)pyrene extractability from five furnace blacks. They found that
toluene and benzene had quite similar efficiencies, but that cyclohexane cou
Id not
remove more than 10% of the benzene-extractable benzo(a)pyrene from any of the
furnace blacks. Toluene was, however, clearly the best extractant when the adsorbate
content of the carbon black was low (Jess than 1 mg/kg).
Giammarise et al. (1982) found that benzene, toluene, monochlorobenzene and ortho-
dichlorobenzene were aIl effective extraction solvents for nitropyrenes from an old
carbon black sample with a high level of nitropyrene impurities (approximately
70 mg/kg). Monochlorobenzene was the best extractant. When a CUITent carbon black
with only traces of nitropyrene impurities (approximately 0.5 mg/kg) was extracted,
monochlorobenzene removed more than 90% of the nitropyrenes within 24 h, while
toluene extracted only 60% in that time.
, Analytical methods used to determine the components of the carbon black extracts
produced by Soxhlet extraction of carbon black with various solvents have been
summarized (Jacob & Grimmer, 1979). Common methods inc1ude gas chromatography
(GC) with packed and capilIary columns and HPLC with spectrophotometric and
spectrofluorimetric detection.
Zoccolillo et al. (1984) reported the determination of P AHs in carbon black by
Soxhlet extraction with benzene, purification by silica gel thin-layer chromatography and
analysis by GC and/or HPLC.
 164 IARC MONOGRAPHS VOLUME 65

Colmsjö and Östman (i 988) reported a method to isolate and fingerprint some high-
molecular-weight P AHs in carbon black. The P AH fraction of a carbon black extract
(Soxhlet-extracted with dichloromethane) was isolated with a backflush technique and
applied to an amino-bonded stationary phase for HPLC. This fraction was further sepa-
rated by reverse-phase HPLC and each subfraction was analysed by low-temperature
fluorescence.
Sigvardson and Birks (1984) reported that selective detection of nitro-P AHs in carbon
black was achieved by Soxhlet extraction wIth toluene, evaporation to dryness, disso-
lution in dichloromethane and direct injection into the HPLC column. The nitro-PAHs
were reduced online to the corresponding amino-PAHs and detected by peroxyoxalate
chemiluminescence.
Jin et al. (1987) described a method for the analysis of nitroarenes in carbon black.
The method involved the Soxhlet extraction of the sample with organic solvents (the use
of chlorobenzene resulted in the highest overalI yield), pre-separation by column
chromatography on silica gel and separation and determination by reverse-phase HPLC
with ultraviolet detection.
The bioavailability of the P AHs adsorbed onto the surface of the carbon black has
been assessed by means of quantifying the concentration of the major adsorbed P AH,
pyrene, by use of its urInary metabolite, I-hydroxypyrene. The urine was adjusted to pH
5.0 and incubated with 50 ¡.L ß-glucuronidase/aryl sulfatase for 4 h at 37°C. After
extraction and washing, the hydrolysed urine was injected into a HPLC unit with a fluo-
rescence detector. The limit of detection was approximately 0.075 nmol/L (16 ng/L)
(Gardiner et al., 1992b).

1.2 Production and use

i .2.1 Production
The early Chinese and Hindus produced carbon black for their inks and lacquers by a
simple lampblack process. Lampblack supplied the needs of the pigment industry until
the opening of the natural gas fields in the United States in i 872 and the establishment of
the channel process. At that time, annual worId consumption of carbon black was less
than i 000 tonnes. Consumption increased rapidly folIowing the discovery in 1904 of
carbon black's usefulness in the reinforcement of rubber; the needs of the growing world
rubber industry were met by supplies of channel black and lampblack from the United
States. ln i 922, the gas-furnace process was introduced in the United States (Garret,
1973). The increasing cost of natural gas led to a switch to the oil-furnace process in the
early 1940s and to the final closure of channel black manufacture in the United States in
1976. Since oil feedstock is readily transported, the oil-furnace process can be located
close to the user industries, and, following the end of the Second World War, carbon
black manufacture was established in many industrialized countries (Dannenberg et al.,
i 992).
W orldwide production of carbon black in 1993 was about six milion tonnes (estimate
based on demand for carbon black; see Table 1 i). Production data on carbon black in
 CARBON BLACK 165

several countries from 1987 to 1994 are presented in Table 9, and production data on
carbon black by grade in the United States, western Europe and Japan in 1988 are
presented in Table 10.

Table 9. Production of carbon black in several countries frorn

1987 to 1994 (thousand tonnes)

Country 1987 1988 1989 1990 1991 1992 1993 1994

Canada in 181 190 178 157 161 166 167

China 290 290 320 327 334 NA NA NA
France 232 241 270 252 224 232 204 235
Germany 361 379 401 393 380 375 334 297
Italy 190 200 202 180 185 182 171 187
J apan 635 740 779 783 793 771 702 698
Republic of NA NA NA NA 232 248 300 311
Korea
USA 1355 1324 1320 1302 1234 1370 1462 1503

From Anan. (1989, 1991 a); Dannenberg et aL. (1992); Anon. (1993); China
National Chemical Information Centre (1993); Anon. (1995)
NA, not available

Table 10. Production of carbon blacks for rubber in

1988 in the United States, western Europe and Japan
(thousand tonnes)

Grade USA Western Japan

Europe

Tread grades
NlOO 35 28 37
N200 158 161 118
N300 555 528 300
Total 748 (55.2%) 717 (63.8%) 455 (61.5%)"
Non-tread grades
N500 120 153 136
N600 326 137 87
N700 129 103 29
N900 (thermal) 23 9
Total 598 (44.1 %) 393 (35.0%) 261 (35.3%)"
Other grades
Acetylene 9 14 24
Total carbon black 1355 1124 740"

Adapted from Dannénberg et al. (1992)

"Calculated by the Working Group
 166 IARC MONOGRAPHS VOLUME 65

Carbon black is produced by many companies in Russia, 12 companies in China, six

companies each in India, Japan and the United States, three companies each in Canada,
France, ltaly and the Netherlands, two companies each in Australia, Brazil, Germany, the
Republic of Korea, Poland, Spain, Thailand and the United Kingdom, and one company
each in Chile, Colombia, the Czech Republic, Estonia, Hungary, Iran, Malaysia, Mexico,
the Philippines, Portugal, Romania, South Africa, Sweden, Taiwan and Turkey
(Chemical Information Services, 1994; Cabot Co., 1995).

Acetylene black
Acetylene black was first made commercially in Germany in 1928, in Canada in the
1930s, in Japan in 1942 and in the United States in 1964. lt is currently estimated to
comprise substantially less than 1 % of total carbon black production (Dannenberg et al.,
1 992).
The dissociation of acetylene into carbon and hydrogen was achieved as early as
1861, and the first commercial process was based on the partial combustion of acetylene
(Bean, 1964). Subsequently, a process based on the explosion of an electric arc was
developed in Germany. The process currently in use - continuous thermal decompo-
sition - is covered by a series of patents going back to 1938 and was reported in 1964 to
have been in commercial use for some years in continental Europe, Asia and Canada
(Bean, 1964; Claassen, 1978).
ln the continuous thermal decomposition process for acetylene black, the reaction is
initiated by burning the acetylene feedstock with a controlIed amount of air. When the
reaction temperature is sufficiently high (e.g. 800°C), the air supply is shut off, oxidation
ceases and an exothermic self-sustained dissociation of acetylene to form hydrogen and
acetylene black occurs at temperatures of up to 1000 °C (Dannenberg et aL., 1992).

Channel black
The channel process for making carbon black was first used commercially in the
United States in 1872 (Garret, 1973). From the First World War to the Second World
War, the channel black process accounted for most of the carbon black used worldwide
for rubber and pigment applications. However, rising priees of natural gas, smoke
pollution, low yield and the rapid development of the furnace-process grades of carbon
black have been given as reasons for this process being abandoned in 1976 in the United
States; operations still exist and are being expanded in Europe (Dannenberg, 1978;
Dannenberg et al., 1992).
ln the channel or impingement process, smalI natural-gas flames were impinged on
channel irons that colIected the deposited carbon black (Garret, 1973). This process gave
only very low yields (5%); however, in Germany, a plant making carbon black by an
impingement process, sometimes called 'gas black', is reported to give yields of 60%
using coal-tar residues containing naphthalene or anthracene as the carbon feedstock. ln
this process, the molten material is evaporated by a stream of hot coke-oven gas and
heated to about 370°C prior to reaching the burners. The flames are directed onto
 CARBON BLACK 167

revolving water-cooled pipes and the carbon black, which forms on impingement, is
continuously scraped from the pipes. For the production of finer-particle black for use as
pigments, the amount of oil carried by the gas is decreased and the vapours to the burner
are diluted with air (Claassen, 1978).
Production of channel black in the United States reached a peak of 307 000 tonnes in
1948, but it had fallen to 132 000 tonnes by 1960 and showed a steady decline until
production stopped in 1976. The quantity of carbon black made by the manufacturer in
Germany using the impingement process is believed to constitute less than 1 % of total
world production of carbon black.

Furnace black
The gas-furnace process for making carbon black was first introduced in the United
States in 1922, and the oil-furnace process in 1943 (Garret, 1973). Furnace black was
first produced commercially in Japan around 1950. The gas-furnace process, which is
based on the partial combustion of natural gas, was carried out using refractory-lined
retorts or furnaces at a temperature of 1200-1500 °C. The process achieved onl y low
yields of carbon black and has not been used in the United States since the 1960s
(Dannenberg, 1978). ln the oil-furnace process, which is now used to produce over 95%
of total output of aIl carbon black, a heavy aromatic feedstock from a petroleum refinery
or petrochemical operation is injected by atomization into a high-velocity stream of
combustion gases produced by the complete burning of an auxiliary fuel (such as natural
gas) with excess air. Although sorne of the feedstock is burned at 1200-1850 °C, most is
converted to hydrogen and carbon black with high yields. Downstream, the reaction
gases are cooled by spraying with water. The carbon black particles are then separated
from the gases and pelletized. A very small percentage of furnace black is subjected to
after-treatment by various oxidation processes, sorne of which have involved nitration. ln
the United States, about 95% of feedstocks are decant oils (c1arified heavy distilIates
from the catalytic cracking of gas oils); European feedstock sources are 50% decant oils
and 50% ethylene tars and creosote oils (Dannenberg et al., 1992).

Larnpblack
Lampblack was first produced commercially in the United States in the 1840s
(Patterson, 1980). It is made principalIy by burning aromatic petroleum oils and coal-tar
products, such as creosote and anthracene oils, in open, shalIow pans using a restricted
air supply (Smith, 1964). This is carried out at temperatures lower than those for other
carbon black processes. The lampblack is separated from the gases and pelletized.
Currently, only a few plants located mostly in western and eastern Europe still produce
these rather coarse blacks (mean partic1e diameter, approximately 100 nm) which have
special properties (V ohler et al., 1986; Dannenberg et aL., 1992). Lampblack is not
produced in Japan.
Lampblack is produced on a small scale; total production is believed to constitute less
than 1 % of total world productíon of carbon black.
 168 lARC MONOGRAPHS VOLUME 65

Therrnal black

ber filled with checkered

ln the thermal process, which dates back to 1922, a cham

brickwork is heated to about 1300°C by injecting a burning mixture of gas and air.
When the required tempe rature has been reached, the flow of burning gas is stopped and
the hydrocarbon feedstock (usually gas) is injected. Contact with the hot bricks causes
the feedstock to crack, forming carbon black and hydrogen. This process is run cyclically
using two chambers, one being heated while the other produces carbon black. ln one
plant in the United Kingdom, medium thermal black is produced from oil rather than
using natural gas as the raw material (Johnson & Eberline, 1978; Dannenberg et aL.,
1992).
Total production of thermal black is estimated to be about 2% of total carbon black
production of North America, western Europe and Japan.

1.2.2 Use
The primary use of carbon black (for example, approximately 90% in the United
States) is in rubber products (see IARC, 1982), incIuding tyres (69% in the United
States), tubes, treads and other automotive products (about 10% in the United States) and
other industrial rubber products (Il % in the United States). Miscellaneous non-rubber
uses (approximately 10%) include applications as pigments in paints, plastics, paper, inks
and ceramics. These levels of use have been steady for the past 10 years (Anon., 1985,
1988, i 991 b, 1994). W orld demand for carbon black by region is presented in Table 11.
Western Europe consumes 74% in tyres and other automotive products and almost 20%
in other industrial rubber products. Applications as pigments in western Europe and
Japan account for 5-6% of consumption (Dannenberg et al., i 992).

Table Il. World carbon black dernand

by region (thousand tonnes)
Region 1983 1993

North America 1387 1664

Central and South America 221 336
Western Europe 1058 1102
Eastern Europe 1022 556
Africa and the Middle East 107 147
Asia and Oceania 1139 2173
World 4934 5978

From The Freedonia Group (1 994a)

Information on the quantities of carbon black used in various applications is very

seldom presented in a form that provides separate data on the individual types of carbon
black. However, it can be inferred that the major carbon black used is furnace black,
since this is the predominant item in commerce, and that thermal black follows as a
distant second place; minor quantities of the other carbon blacks are used in highly
 CARBON BLACK 169

specialized applications. Most carbon black is supplied as wet or dry pellets, but very
small amounts are still shipped in bags as fluffy black.

Carbon black is an intense black pigment, but its principal industrial use today is
based on its ability to reinforce natural and synthetic rubbers (for a description of the
rubber manufacturing processes in which carbon blacks are used, see IARC, 1982).
Addition of carbon black in quantities in the range 10-150 parts per 100 parts by weight
of rubber polymer results in very marked improvements in the properties of vulcanized
rubbers, particularly in terms of resistance to abrasion, tear strength, tensile strength,
stiffness and hardness. Addition of carbon black also changes the properties of rubbers in
the unvulcanized condition, so improving handling and shaping in the manufacture of aIl
types of rubber products. Carbon black is particularly useful in its ability to reinforce
rubber. The world rubber industry is thus dependent on the use of carbon black.

The most important product of the rubber industry is the pneumatic tyre and this
represents the single largest application of carbon black. For every 100 parts by weight of
rubber used in the manufacture of a tyre, there are about 60 parts by weight of carbon
black. Since tyres also contain steel and textile materials, carbon black represents about
25% of the total weight of a finished pneumatic tyre. The consumption of the various
grades of carbon black can be divided into 'tread grades' for tyre reinforcement and
'non-tread grades for non-tread tyre use and other applications. ln the United States,
55% of carbon black produced for rubber is for tread grades; tread-grade production is
64% in western Europe and 60% in Japan (Dannenberg et al., 1992).

Many of the non-tyre applications of carbon black in rubber are also for the auto-
motive industry - for example, in hoses, weatherstrips, sponge seals and engine
mountings. OveralI, about 80% of total carbon black consumption is for automotive
applications.

For more than a thousand years before the discovery in 1904 of its reinforcing effect
in rubber, carbon black was used as a pigment. Today, although pigments represent less
than 10% of the total usage, it is used in inks, paints, lacquers, cements, paper, coatings
and in plastics, where it is also used as an ultraviolet absorber.

Acetylene black

Acetylene black is used primarily for speciality applications because of its relatively
high cost. Approximately 95% of worldwide use of acetylene black is in the manufacture
of dry-celI batteries. Because of its ability to absorb large quantities of electrolyte,
acetylene black impars greater capacity, longer shelf-life and lower resistance to dry
cells than any other filler. lts high thermal and electrical condl!ctivity also imparts
desirable properties to certain rubber and plastic products, such as thermal insiilators, belt
drives, cable sheathing, hoses and shoe soles (Bean, 1964; Union Carbide Corp., 1964;
Claassen, 1978; Gulf Oil Chemicals Company, 1982; V ohler et al., 1986).
 170 IARC MONOGRAPHS VOLUME 65

Channel black
Channel black has been used for rubber reinforcement and as a pigment. ln rubber
reinforcement, it was reported to yield products with high tensile strength, high elon-
gation and high tear resistance. With the smallest particle size, channel black gave high
colour intensity when used as a pigment in paint, ink and plastics. The carbon black
made by the impingement process in Germany also reportedly finds limited use in rubber
reinforcement and more extensive use in pigment applications in printing inks, plastics,
lacquers and coatings. High-quality oxidized black from this process is particularly
useful in deep black lacquers and coatings (Claassen, 1978; V ohler et al., 1986).

Furnace black
Over 95% of the carbon black in the rubber industry is produced by the furnace
process (Garret, 1973), and furnace black is also used in printing inks, plastics and
paints. For the se different purposes, a wide variety of specially tailored grades possessing
the necessary properties are available (for example, different grades are used in tyre
sidewalls ).
The furnace black process has the advantage of being continuous and carried out in
closed reactors, which means that aIl parameters and inputs can be controlIed. Properties
of carbon black, such as surface area, particle size, structure, absorptivity, abrasion
resistance, tint strength and others, can systematicalIy be varied in the furnace black
process by adjusting the operating parameters. Thus, most semi-reinforcing rubber blacks
(SRF, GPF, FEF) with specific surface areas of 20-60 m2/g, and active reinforcing blacks
(HAF, SAF, ISAF) (see Table 5 for definition of these terms) with specifie surface areas
of 65-150 m2/g are manufactured by this process, as are, tó an increasing extent,
pigment-grade types of carbon black with much larger surface areas and smaller partic1e
sizes (V ohler et al., 1986).

The major application of furnace black in the rubber industry is in the manufacture of
tyres, retread rubber and inner tubes. Other automotive uses in elastomers include belts,
hose, motor mounts, O-rings and wire and cable covers. Non-automotive uses in
elastomers include coated fabrics, conveyor belts, floor mats, footwear, gaskets, gloves,
hard rubber products, hose, packaging, pontoons, toys and wire and cable covers.
The majority of the furnace black used in printing inks is for newspaper inks, with the
remainder divided among lithographic/offset, gravure, letterpress, flexographic and other
inks. Furnace black is also used as a colourant in alkyd and acrylic enamels, industrial
finishes, lacquers and a variety of other paints.
Furnace black is used in plastics principally for the following purposes: as an anti-
static agent, colourant, filer (sometimes to impart strength) and ultraviolet radiation
stabilizer and as an additive to increase or decrease electrical conductivity. End-uses
se-
include appliances, automotive accessories, extrusion and calender coatings, film, hou

wares, phonograph records, pipe and conduit, and wire and cable (Dannenberg, 1978;
Dannenberg et aL., 1992).
 CARBON BLACK 171

Larnpblack
Most of the lampblacks produced currently are coarse particulates with special
properties (V ohler et al., 1986). They are used mainly as non-reinforcing or semi-
reinforcing blacks in rubber goods. Lampblacks are used to a lesser extent as pigments
for tinting and shading cosmetics, enamels, inks, lacquers, paints and plastics. Lamp-
black pigments are readily dispersible and have little tendency to float in paint or ink
formulations (Claassen, 1978). The principal use of lampblack in the pigmentation of
artists' paints is in water colours; it has a more minor role in oil colours (Levison, 1973).
The physical and electrical properties of lampblack make it useful in the production
of arc carbons, brushes and resistors. Its high tinting strength and hiding power has led to
its use in blackboards, cement, crayons and leather (Garret, 1973).

Therrnal black

Thermal black is used principally in mechanical rubber goods with high filer content
(V ohler et aL., 1986). Thermal black is used in non-tyre rubber when low reinforcement
is required, and it is used in speciality polymers and in neoprene, nitrile and ethylene-
propylene elastomers (Patterson, 1980). End-product applications include belts, foot-
wear, gaskets, hose, mechanical goods, V -belts, O-rings and seals, tyre innerliners and
wire insulation (Dannenberg, 1978).

1.3 Occurrence
1.3.1 Naturaloccurrence

Carbon black is not known to occur as natural product.

1.3.2 Occupational exposure

Occupational exposure by any route to carbon black has been reduced markedly in the
last 30-35 years, mainly by technological improvements, increases in the proportion of
the product that is bulk loaded (by trucks and trains) and legislative enforcement. Until
recently, very few reliable data on occupational exposure to carbon black were available,
but two major prospective cross-sectional studies in the United States and Europe
(France, Germany, Italy, the Netherlands, Spain, Sweden and the United Kingdom) have
se workforces. These data and those from the
characterized exposure accurately in the

previous studies have been reviewed (Gardiner, 1995a) but a further summary of the
more important data is given below.
The majority of the studies of occupational exposure do not report adequately the
sampling strategies with which the data were collected. Only in one study were the
measurements taken specifically for the purpose of an epidemiological study and hence
used techniques such as person/day randomization. Rarely were the type (personal/-
static), duration or rationale for the number of samples stated. lt is possible to measure a
variety of aerosol fractions, but usually respirable and total inhalable dust are measured.
Respirable dust is that fraction of an aerosol with an aerodynamic diameter suitable for
 172 IARC MONOGRAPHS VOLUME 65

penetration into the alveoli/gas exchange region of the lung (typically .c 10 /-m). Total
inhalable dust is that fraction of an aerosol with an aerodynamic diameter suitable for
inspiration into the respiratory system (typicalIy .c 100 /-m). Differences in definitions of
these fractions and in the methodologies by which they are measured require that inter-
study comparison should be undertaken with care.
KolIo (1960) took 160 measurements in a Russian channel black plant where airborne
dust levels ranged from 44 to 407 mg/m' in the factory area, 25.3 to 278.6 mg/m' in the
working aisles, 9.3 to 972 mg/m' in the pelletizing area and 26.7 to 208.6 mg/mJ in the
packing area.
Sands and Benitez (1961) used a static high- volume sampler to measure total dust in
various areas of three factories processing rubber (one in Uruguay and two in the United
States). The range in the three factories was 0.14-4.59 mg/m', 1.06-17.66 mg/m'and
1.06-38.84 mg/m', with the range being 1.77-38.84 mg/m' by the Banbury mixer loading
area, 1.41-13.42 mg/m' during milling and 0.14-4.24 mg/m' in the general air of the
miling rooms. It was suggested by the authors that 3.5 mg/m' represented a safe and
achievable air standard which prompted the American Conference of Governmental
lndustrial Hygienists (ACGIH) to propose a threshold limit value (TL V) of 3.5 mg/m' in
1965, which was adopted in 1967 (American Conference of Governmental Industrial
Hygienists,1993).
Komarova (1965) measured exposure to carbon black in the packaging departme'nt of
two Russian factories manufacturing lampblack and furnace black. The number of
measurements was not specified, but the ranges were 166-1000 mg/m' (lampblack) and
60-78 mg/m' (furnace black). Slepicka et al. (1970) found exposures ranging from 8.4 to
29.0 mg/m' in two Czechoslovakian channel black factories between 1960 and 1968,
although neither the number of samples nor their location was quoted.
A survey found a range of concentrations of 90-196 mg/m' (from an unspecified
number of samples) in a Russian furnace black factory (Spodin, 1973). The lowest and
highest average concentrations recorded by another Russian study were 1.53 :t 0.4 mg/m'
for workers by the hatches of the electrostatic filter and 34.5 :t 8.9 mg/m' for workers
inv()lved in cleaning the production areas; in total, 109 samples were taken. It was noted
that throughout the 1960s and 1970s, workers packing carbon black were exposed to two
to seven times the maximal permissible concentration (10 mg/m' in 1975) for 60-70% of
their working shifts (Troitskaya et aL., 1975, 1980).
Between July 1972 and January 1977, the United States Occupational Safety and
Health Administration conducted 85 workplace investigations to determine compliance
with the occupation al exposure limit for carbon black of both manufacturers and users.
Approximately 20% of the workplaces inspected were in violation of the total inhalable
exposure limit of 3.5 mg/m', and about 60% of these were one to two times above the
limit (United States Occupational Safety and Health Administration, 1977).
A number of Health Hazard Evaluations have been conducted by the United States
National lnstitute of Occupational Safety and Health in facilities either producing or
using carbon black(Belanger & Elesh, i 979; HolIett, 1980; Salisbury, 1980; Boiano &
Donohue, 1981). ln general, these measurements were less than 3.5 mg/m', although
 CARBON BLACK 173

these studies involved a limited number of samples and a limited number of days over
which the measurements were taken.
ln the rubber industry, employees are exposed to carbon black mainly in the com-
pounding and Banbury mixing areas. It has been reported that for total dust (in which
carbon black was one compone nt) the median levels in 14 tyre and tube manufacturing
plants in the United States were 1.7 mg/m' for the compounding area samples (individual
plant means ranged up to 3.9 mg/m') and 1.3 mg/m' for the Banbury mixing-area
samples (for which the highest plant mean was 4.2 mg/m') The values for personal
samples were 3.1 mg/m' for the compounding area (highest plant mean, 5.0 mg/m') and
1.9 mg/m' for the Banbury area (highest plant mean, 5.8 mg/m') (WilIiams et a!., 1980).
A United States National Institute for Occupation
al Safety and Health study (Heitbrink &
McKinnery, 1986) evaluated the effect of control measures at Banbury mixers and the
mills beneath the mixers in tyre factories and found lower exposures than those found by
Williams et aL. (1980). The geometric means of mixer operators' exposures at five
factories ranged from 0.08 to 1.54 mg/m'and the geometric means of miling operators'
exposures at three factories ranged from 0.20 to 1.22 mg/m'.
Over a six-month period, beginning in October 1979, a total of 1951 personal samples
(1564 total dust, 387 respirable dust) were colIected from 24 carbon black production
facilities in the United States (Smith & Musch, 1982). A summary of the results are
provided in Table 12. Workers involved in filIing and stacking bags of carbon black
(material handling) håd the highest me an total dust exposures up to 2.2 mg/m'. Samples
were not taken from aIl employment areas in every factory and the numbers of samples
taken differed from area to area. These data were subsequently used in the first cross-
sectional analyses of the American respiratory morbidity study (Robertson et aL., 1988)
and the update of the American cohort study examining circulatory, respiratory and
malignant diseases (Robertson & IngalIs, 1989).

Table 12. Surnrnary of average dust exposure by employrnent area in

United States carbon black production facilities (1979-80)
Area of employment Total dust Respirable dust

No. of No. of Geometric No. of No. of Geometrie

plants samples mean plants samples mean
(mg/m') (mg/m')

Administration 8 72 0.01 2 28 0.00

Laboratory 17 133 0.04 LA 35 0.01
Production 22 480 0.44 14 III 0.13
Maintenance 19 386 0.59 Ii 89 0.12
Material handling 20 493 1.45 13 124 0.35

From Smith & Musch (1982)

ln a mortality study conducted in the United Kingdom (Hodgson & Jones, 1985), the
authors used a limited amount of exposure data collected by Her Majesty's Factory
 174 IARC MONOGRAPHS VOLUME 65

lnspectorate in 1976. Personal samples were taken of 47 people in five 'Carbon black
factories, 24 (51 %) of these being above 3.5 mg/m'. The highest exposure recorded for
routine work was 79 mg/m', but workers engaged in filter-bag replacement may have
been exposed to even higher levels, although exposure measurements were not reported.
The United States particulate sampling survey of 1979-80 (Smith & Musch, 1982)
was repeated twice, once in 1980-82 and then again in 1987 (Musch & Smith, 1990).
The number of participating companies decreased from seven to six and the number of
plants decreased from 24 to 17. ln 1980-82, 973 total dust samples were taken; the
number feIl to 577 in 1987. The data are summarized in Table 13. A drop of approxi-
mately 50% in exposure was evident in maintenance and material handling parts of the
factories. Of the job categories in the maintenance section, the folIowing reduction was
seen between the second and third surveys: utility, 0.89 to 0.55 mg/m'; in plant, 0.79 to
0.52 mg/m"'; shop, 1.00 to 0.07 mg/m'; instrument, 0.47 to 0.17 mg/m'; and foreman,
0.35 to 0.18 mg/m'. Of the job categories in the material handling section, the following
reduction was seen between the second and third surveys: stack and bag, 1.92 to
0.77 mg/m'; bagger, 2.67 to 0.85 mg/m'; bulk loader, 2.07 to 0.82 mg/m'; stacker, 1.15 to
0.70 mg/m'; fork-lift truck driver, 0.53 to 0.34 mg/m'; and foreman, 0.18 to 0.02 mg/m3.

Table 13. Surnrnary of average total dust exposure by

ernployrnent area in United States carbon black pro-
duction facilties in 1980-82 and 1987
Area of 1980-82 1987
employment
No. of Geometric No. of Geometrie
samples mean samples mean
i
(mg/m) (mg/m')

Administration 4 0.06 2 0.02

Laboratory 85 0.51 23 0.20
Production 273 0.45 164 0.45
Maintenance 363 0.71 181 0.36
Material handling 248 1.63 207 0.71

From Musch & Smith (1990)

The most recent and comprehensive data come from the exposure assessment element
of the trans-European respiratory morbidity study (Gardiner et al., 1993). The first data
published from this study were from a pilot study assessing the bioavailability of the
adsorbed P AHs. Five individuals packing carbon black into 25-kg bags were assessed
over the period of a week; their weekly personal mean dust exposures were 1.53, 5.30,
9.56,9.99 and 13.21 mg/m3 (Gardiner et al., 1992b).
The first cross-sectional phase of the prospective European study was conducted
between 1987 and 1989 with the second extending from 1990 to 1992. A fully rando-
mized, epidemiologicalIy based sampling strategy was used to minimize the inherent
biases of worker selection, and a statisticalIy relevant proportion of aIl job categories in
 CARBON BLACK 175

aIl 18 plants was taken. ln addition, both respirable and total inhalable dust fractions
were measured. ln the first phase, 1278 respirable and 1288 total inhalable dust samples
were taken (Gardiner et al., 1992a). The use of a unique multiplication factor derived
from the variability of the phase L data (Gardiner, 1995b) means that, in phase II,
significantly more samples were taken - 2941 respirable and 3433 total inhalable dust
samples (Gardiner et al., 1996). The respirable dust data for both phases are presented in
Table 14 and the data for total inhalable dust are summarized in Table 15.
As with the data presented by Musch and Smith (1990), it is evident that in the three
years between the two surveys exposure had decreased by approximately 50% (total
inhalable dust, 49.9%; respirable dust, 42%) (Gardiner et aL., 1996).
The National Occupational Exposure Survey conducted by the United States National
Institute for Occupation al Safety and Health (1995) between 1981 and 1983 indicated
that about 1 729000 employees in the United States were potentially exposed ta carbon
black. The estimate is based on a survey of companies and did not involve measurements
of actual exposure, and might, for man y workers, involve very low levels and/or inci-
dental exposure to carbon black.
No data were available on exposure to carbon black in the non-automotive rubber,
paint, printing or printing ink (i.e. 'user') industries. Operators iti these user industries
who handle the fluffy or pelIetized carbon black during rubber, paint and ink production
are expected to have significantly lower exposures to carbon black than workers in
carbon black production. Other workers in user industries have little opportunity for
exposure. End users of these products (rubber, ink or paint) are not exposed ta carbon
black per se, since it is bound within the product matrix.

1.3.3 Ambient air

ln 1978, it was estimated that 1240 tonnes of carbon black were emitted during
carbon black manufacture in the United States (Rawlings & Hughes, 1979). Table 16
summarizes typical particulate carbon black emissions into the air during various stages
of manufacture by the oil-furnace process prior to 1979. The particulate matter was
reported to comprise carbon black (McBath, 1979).
Rivin and Smith (1982) reviewed the literature on emissions of carbon black into the
atmosphere during its manufacture. Modern carbon black plants generalIy employ bag
filters to reduce emissions; discharge from a bag filter in good condition during this
process (under normal conditions) reportedly contains carbon black (wet basis) at less
th an 50 mg/m', a concentration that is not visible (Johnson & Eberline, 1978).
Tyre dust, of which carbon black is a component, was estimated, in a 1969 study, to
account for approximately 0.8% of the aerosol above an urban area in California. An
estimated 0.2% of the particulates in the aerosol consisted of elemental carbon
contributed by tyre dust (Friedlander, 1973).

Carbon black was not detected in the atmosphere around a factory in Germany where
it was manufactured (Deimel & Dulson, 1980).
176 IARC MONOGRAPHS VOLUME 65
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Table 15. Total inhalable dust data frorn phase 1 and II of the European respira
tory rnorbidity study
Job title Phase L Phase II

No. of Geometrie %?3.5 Maximum No. of Geometrie %? 3.5 Maximum

samples mean mg/ml (mg/ml) samples mean mg/ml (mg/ml)
(mg/ml) (mg/ml)
Administrative staff 289 0.18 0.0 2.77 302 0.12 0.0 1.71
(office bound, phase 1) n
Administrative staff - - - - 186 0.19 0.0 2.56 ;:
~
(non-office bound, phase II) t:
Laboratory assistant 143 0.38 2.1 9.66 326 0.24 0.0 2.44 0
Process control room operator 50 0.29
Z
0.0 2.19 157 0.17 0.0 1.40 t:
Instrument mechanIc 59 0.55 8.5 22.67 257 0.40 1.6 8.61 L'
Electrician ;:
58 0.65 lO.3 31.12 193 0.33 0.0 3.33 n
Process foreman 70 0.37 0.0 3.42 296 0.25 0.7 5.03 ~
Furnaee operator 56 0.54 5.4 9.21 156 0.44 1.9 9.48
FItter 95 1.28 11.6 22.77 270 0.53 2.6 6.87
Welder 41 1.18 7.3 9.56 75 1.06 lO.7 8.75
Process operator 179 0.96 16.8 30.75 420 0.44 1.4 16.92
Conveyor operator 59 0.53 5.1 4.20 127 0.64 4.7 8.97
Warehouse/paeker 151 1.96 35.1 41.11 490 0.96 12.0 19.95
Cleaner 38 1.24 21.1 21.17 178 0.58 8.4 18.04

From Gardiner et al. (1996)

-
--
--
178 IARC MONOGRAPHS VOLUME 65

Table 16. Typical particulate ernissions during the

rnanufacture of carbon black by the oIl-furnace process
Source Range Average
(kg/tonne) (kg/tonne)
Main process vent (uncontrolIed) 0.1-5 3.27
Flare 1.2-1.5 1.35
Carbon monoxide boiler and incinerator - 1.04
Dryer vent:
Uncontrolled 0.05-0.40 0.23
Bag filter 0.01-0.40 0.12
Scrubber 0.01-0.70 0.36
Pneumatic system vent:
Bag filter 0.06-0.70 0.29
Vacuum dean-up system vent:
Bag filter 0.01-0.05 0.03
Fugitive emissions 0.10
Solid waste incinerator (where used) 0.12
From McBath (1979)

Becaiise the production of carbon black often involves the combustion of aromatic
residual oils from petroleum refining and coal tar, the carbon black industry miist also
consider potential ambient air emissions of sulfur and nitrogen oxides, hydrogen sulfide,
volatile hydrocarbons and carbon monoxide (The Freedonia Group, 1994b).

1.4 Regulations and guidelines

Occupational exposure limits and guidelines for carbon black are presented in
Table 17. The use of carbon black from hydrocarbon sources in food contact materials is
provisionally accepted by FAO (Food and Agriculture Organization of the United
Nations)/WHO (World Health Organization) (United Nations Environment Programme,
1995).
The United States Food and Drug Administration (1976, 1994a) has banned the use of
carbon black (prepared by the impingement or channel process) for direct use in food,
drugs and cosmetics (21 CFR 81.10). The United States Food and Drug Administration
(1 994b) has approved the folIowing uses of carbon black:
- Carbon black (channel process) is permitted as an indirect food additive as a com-
ponent of adhesives that come in contact with food (21 CFR 175.105);
- Carbon black (channel process, prepared by the impingement process from
stripped natural gas) is permitted as a colourant (21 CFR 178.3297) in resinous
and polymeric coatings that come in contact with food (21 CFR 175.300) and in
rubber articles intended for repeated use that come in contact with food (21 CFR
177.2600);
 CARBON BLACK 179

Table 17. Occupational exposure lirnits and guidelines

for carbon black
Country Year Concentration Interpretation
J
(mg/m )

Argentina 1991 3.5 TWA

Australia 1993 3 TWA
Belgium 1993 3.5 TWA
Bulgaria" 1995 3.5 TWA
Canada 1991 3.5 TWA
Colombia" 1995 3.5 TWA
Denmark 1993 3.5 TWA
Finland 1993 3.5 TWA
7 STEL (15 min)
France 1993 3.5 TWA
Germany 1995 None
Jordan " 1995 3.5 TWA
Mexico 1991 3.5 TWA
Netherlands 1994 None
New Zealand" 1995 3.5 TWA
Philippines 1993 3.5 TWA
Republic of Korea" 1995 3.5 TWA
Russia 1993 4 MAC
Singapore " 1995 3.5 TWA
Sweden 1993 3 TWA
United Kingdom 1995 3.5 TWA
7 STEL (l5-min)
USA
ACGIH (TLV) 1995 3.5" TWA
NIOSH (REL) 1994 35 (Ca) TWA
OS HA (PEL) 1994 3.5 TWA
Viet Nam " 1995 3.5 TWA

From US National Institute for Occupational Safety and Health

(NIOSH) (1 994a,b); US Occupational Safety and Health Admi-
nistration (OS HA) (1994); American Conference of Governmental
Industrial Hygienists (ACGIH) (1995); Deutsche Forschungs-
gemeinschaft (1995); Health and Safety Executive (1995); United
Nations Environment Programme (1995)
TW A, time-weighted average; STEL, short-term exposure limit;
MAC, maximal allowable concentration; TL V, threshold limit
value; REL, recommended exposure Ii mit; Ca; potential occupa-
tional carcinogen; PEL, permissible exposure limit
"Follows ACGIH TLVs
"Substance identified by other sources as a suspected or confirmed
human carcinogen
, ln the presence of polynuclear aromatic hydrocarbons (PAHs), the
limit for PAHs is 0.1 mg/mJ TW A, determined as cyclohexane-
extractable fraction
 180 IARC MONOGRAPHS VOLUME 65

- Carbon black (channel process) is permitted as a component of polysulfide

polymer-polyepoxy resins that come in contact with dry food (21 CFR 177.1650);
- Carbon black (channel process or furnace combustion process) is permitted as an
optional adjuvant substance: in perfuorocarbon-cured elastomers that come in
contact with non-acid food (pH above 5.0) at concentrations not to exceed 15 parts
per 100 parts of the terpolymer (21 CFR 177.2400) and in phenolic resins in
molded articles that come in contact with non-acid food (pH above 5.0) (21 CFR
177.2410).
Because of the possibility that traces of oil feedstocks can appear in the wastes, the
United States Environmental Protection Agency (1994a) has banned the discharge of
process waste-water polIutants into navigable waters by carbon black manufacturers
utilizing any of the following processes: furnace, thermal, channel, or lamp. The United
States Environmental Protection Agency (1994b) has exempted carbon black from the
requirement of a tolerance when used as a colourant/pigment in animal tags (40 CFR
180.1001).

2. Studies of Cancer in Humans

Industrial exposure to carbon black has occurred in the carbon black production
industry and in a number of user industries, including the rubber, paint and printing
industries. The cancer risks associated with these three exposure circumstances have
been evaluated within the IARC Monographs programme (see IARC, 1982, 1989b; see
also this volume).
The W orking Group felt that epidemiological evidence concerning cancer risk in user
industries, where there has been no attempt to identify which of the workers may have
been exposed to carbon black, carries little weight in the present evaluation. Con
se-
quently, in this monograph, attention was restricted to those studies that explicitly
attempted to identify carbon black-exposed workers. Sorne studies based on carbon black
production workers and some studies of workers in user industries satisfied this criterion.
From the point of view of exposure patterns, the greatest potential for elucidating the
carcinogenicity of carbon black wou
Id seem to be in the carbon black production
industry. Also, it appears that concentration of exposure was substantially higher in the
past in the carbon black production workers than in the user industries. A further
advantage of studies among producers is the fact that, in this industry, carbon black was
the dominant exposure in the industrial environment, whereas workers in user industries
were often exposed to complex mixtures of substances, of which carbon black may have
been a relatively minor component. Potential confounding of results by concomitant
occupational exposures is therefore a significant, potential problem in studies among
users. The potential for such confounding bias is greatest when the study population is
concentrated in an industry in which there is a single, dominant exposure (or a small
number of dominant exposures) other th
an carbon black. To the extent that the study
population includes many different types of carbon black users, each with distinct
 CARBON BLACK 181

profiles of concomitant exposures, the likelihood of a strong confounding effect wou

Id
be diluted. From this point of view, the relative risk estimates due to carbon black
exposure derived from studies that inc1ude a variety of carbon black user industries
an do studies in a user industry in which
provide less opportunity for confounding bias th

most workers have the same profile of concomitant exposures.

2.1 Industry-based studies

Table 18 summarizes cohort studìes and Table 19 case-control studies of workers

exposed to carbon black.

2.1.1 Studies in the carbon black production industry

The cancer occurrence among employees at carbon black production facilities in the
United States has been followed for different periods since 1935 and is described in five
reports (IngalIs, 1950; Ingalls & Risquez-Iribarren, 1961; Robertson & lngalls, 1980,
1989; Robertson & Inman, 1996).
Mortality results from the first two reports were subsumed by Robertson and IngalIs
(1980), which represents the most complete report on the mortality experience of
workers employed by any of four major carbon black manufacturing companies, with
production plants located in Texas, Oklahoma and Louisiana, United States (IngalIs,
1950). Eligible study subjects were male employees aged 15 years and over with 12
months or more service during the years 1935-74 aL any of the carbon black plants.
Between 1950 and 1975, the average number of active workers in aIl participating
companies was about 1250 per year. ln the early years, there were equal numbers of
workers in the two major processes - channel black production and fumace black
production; by 1960, channel black production was dwindling and most workers were
involved in the furnace black plants. The mortality experience of the cohort was traced
via insurance company records. This company provided death benefit insurance to
participating members of the cohort between 1935 and 1974. Over the entire period,
there was a total of 34 739 person-years of observation in the mortality folIow-up. (It is
not stated how man y distinct individuals were in the study.) Only 2% of these person-
years at risk were in the age group 65 and over. Expected numbers of deaths were
ca1culated from state vital statistics (death rates for white men at five-year intervals
starting in 1937 applied to annual employee censuses by age, in five-year groups). There
were 29 observed cancer deaths (standardized mortality ratio (SMR) (0.7 (95%
confidence interval (Ci), 0.5-1.0))) (Table 18). There were six observed deaths due to
cancers of the digestive organs and the peritoneum (SMR (0.6; 95% CI, 0.2-1.4)). There
were 13 observed deaths due to cancers of the respiratory system (SMR (0.9; 95% CI,
0.5-1.5)). For aIl malignancies combined, there was no evidence of increasing mortality
with increasing years of service, no significant excess cancers in any of the eight five-
year periods and no trend in relative risk of cancer over time.
ln a short communication, Robertson and lnman (1996) made a preliminary report of
an extension of the follow-up of this cohort. Cohort members from two of the original
four companies and those from an additional company were traced for an additional
 -
00
N

Table 18. Cohort studies arnong workers exposed to carbon black

Reference Study subjects Period of Occupation/exposure Cancer site/ No. RR 95% CI Comments
location follow-up cause of death obs.

Robertson & Male employees 1935-74 Employees with carbon All causes 190 (0.8) Age- and race-adjusted
Ingalls (1980) of US carbon black exposure All cancers 29 (0.7) (0.5-1.0) comparison with state

?::-
Southern USA black producers (34 729 person-years) Gastrointestinal 6 (0.6) (0.2-1.4 ) populations. No smoking
Respiratory 13 (0.9) (0.5-1.5) information
Subset with ? 20 years All cancers 15 (0.8) Few person-years over age n
service 65 ~
Hodgson & Male employees 1947-80 Employees with carbon All causes 129 0.8 (0.7-1.0) Age-adjusted comparison 0
Z
Jones (1985) of 5 United black exposure All cancers 42 1.0 (0.7-1.3) with local populations. No 0
United Kingdom carbon Lung 25 smoking information. Few c:
(19 266 person-years) 1.5 ( 1.0-2.2) ::
Kingdom black producers Urinary b1adder 3 2.5 (0.5-7.3) person-years over age 65 ?'i
Blair et al. Male employees Not given Subset with carbon Lung 20 1.3 (0.8-2.0) Age-adjusted comparison :i
C/
( 1990) at plants with black exposure with US population. No ~
USA formaldehyde ? 20 years duration Lung 6 2.4 (0.9-5.2) smoking information 0t"
exposure ? 20 years latency Lung Il 1.4 (0.7-2.5) c:
Robertson & Male emp10yees 1935-94 Employees with carbon All causes 377 0.7 0.6-0.8 Age- and race-adjusted com-
~
tT
Inman (1996) of US carbon black exposure (55 784 AlI cancers 79 0.7 0.6-0.9 parison with state popu- 0\
Ui
Southern USA black producers person- years) Gastrointestinal 12 0.5 0.3-0.8 lations. No smoking infor-
Respiratory 34 0.8 0.6-1.1 mation. Short communi-
cation. Incompletely docu-
mented. This cohort largely
overlaps with that of
Robertson & Ingalls (1980).

RR, relative risk estimates - aH SMRs (standardized morta1ity ratios)

Table 19. Case-control studies of workers exposed to carbon black
Reference Study base Cases Controls Exposure Cancer site No. of RR 95% CI Comments
location exposed
cases/
controls

Robertson Male employees Previously diagnosed One matched for Cumulative Skin 24ING 0.9 0.3-3.2 Prevalent cases may weil be
& Ingalls of carbon black with skin cancer age and one exposure index unrepresentative. Not clear
( 1989. producers active (n = 24) matched for age and for carbon black how exposure was
USA in 1980 duration of dichotomized.
employment
(n = 48)
Bourguet Male employees Subsequently Four matched to Intensity of Skin 'Intensity of ex posure'
et al. of rubber diagnosed wIth skin each case on exposure to reflected concentration and
( 1987) manufacturing cancer in local company, year of carbon black: frequency of exposure. The
USA industry active in hospitals birth, year of hire Low 14/47 0.7 NG findings did not indicate any n
1964 or earlier 1. ;:
(n = 65) (n = 254) Medium 14/49 NG exposure-response ::
High 8/48 0.7 NG relationship nor any trend by ti
duration of exposure. 0
Steineck Male general Urothelial cancers Population control Ever exposed to
Z
population of
Urothelial 14/9 2.0 0.8-4.9 Adjusted for year of birth and ti
et aL. 1985-87 frequency matched carbon black smoking l'
( 1990)
Sweden
Stockholm (n = 254) on sex and year of
birth (n = 287)
including
n;:
printing inks
t'
Siemiatycki Male general Incident cases from Cancer controls, not Ever exposed to Adjusted for age, social class,
(199 1 ) population of 1979 to 1985, with any matched carbon black ethnicity and smoking
Canada Montréal of I9 types of cancer (i.e. 'any'
exposure)
Oesophagus (99) 2546 Oesophagus IIING 2.2 (1.1-4.4)
Stomach (251) 2397 Stomach 9ING 0.8 (0.4-1.4)
Colon (497) 2056 Colon 17ING 0.7 (0.5- 1. 1)
Rectum (257) 1299 Rectum ioING 0.7 (0.4-1.)
Pancreas (116) 2454 Pancreas 3ING 0.7 (0.2-2.2)
Lung (857) 1360 Lung 52ING 1.6 (1. 1-2.3)
Prostate (449) 1550 Prostate 25ING 1.2 (0.7-1.9)
Urinary bladder (484) 1879 Urinary bladder 26ING 1.2 (0.7-1.9)
Kidney ( 1 77) 2481 Kidney 14ING 1.9 (1.-3.3)
Skin melanoma (103) 2525 Skin melanoma 2ING 0.4 (0.1-1.8)
Non-Hodgkin's
Iymphoma (215)
2357 Non-Hodgkin's
Iymphoma
9ING 0.9 (0.5-1.8)
-
00
w
 00
.t

Table 19 (contd)

Reference
location
Study base Cases Con trois Exposure Cancer site No. of
exposed
RR 95% CI Comments -~
cases/
controls
nli
~
Parent et al. Male general As in Siemyatycki
0
Cancer control Higher exposure Ali lung cancers 2.2 1.0-4.9 Adjusted for age, social c1ass, Z
( 1 996) populatÎon of (199 1 ) (n = 1360) to carbon black Oat-cell 5.1 1.-14.9 ethnicity, smoking, asbestos 0
Canada Montréal lung (n = 857) Ci
carcinomas and chromium compounds. li
Squamous-cell 0.8 0.2-2.8 'Higher' exposure reflects ~
'i
carcinomas
Adenocarcinomas 0.5-8.2
concentration, frequency, ::
cr
2.1 confidence in attribution and
Population control Ali Jung cancers 1.5 0.6-4.0 duration of exposure. .c
(n = 533) Oat-cell 4.8 1.4-17.0 0l'
carcinomas c:
Squamous-cell
carcinomas
0.4 0.1-1.6 ~
m
Adenocarcinomas 1.8 0.4-7. 0\
Ui

RR, relative risk - ail ORs (odds ratios); NO, not given
 CARBON BLACK 185

20 years to 1994, bringing the total person-years of observation up to 54 784. (Of the
se,
7% were in age groups over 65.) Expected numbers of deaths were based on white male,
age-, calendar year- and state-specific death rates. The overall SMR was 0.7 and the
SMR for aIl cancers was 0.7 (95% CI, 0.6-0.9) (Table 18). The SMR for respiratory
cancer, based on 34 observed cases, was 0.8 (95% CI, 0.6-1.1).
(The W orking Group noted that the system used for ascertainment of vital status,
based on records of the insurance company, may weIl have led to under-ascertainment of
deaths in this cohort of workers. Such under-reporting might not lead to bias in estimates
of risk if departures from the company were unrelated to mortality risk and if the person-
years of observation have been appropriately adjusted for 'loss to view'. The published
reports do not provide sufficient detail to reassure the W orking Group that these
problems have been given adequate consideration. The fairly low overalI SMR of 0.7
lends sorne weight to the hypothesis of a systematic downward bias.)
Information on cancer morbidity was presented in the first, second and fourth reports
from this group. The incidence of cancer for the earlier periods (1944-49 and 1949-57)
was ascertained from an al examinations and insurance claims (IngalIs, 1950; Ingalls &
nu

Risquez-Iribarren, 1961). These cancer incidences were compared with the cancer
incidence reported from New York State in 1950 and with that of workers in the carbon
black industry whose jobs did not involve exposure to carbon black. Among carbon
black workers, only a handful of cases of cancer were ascertained (three in the first report
and six in the second); of these nine cases in the 'exposed' cohort, five were skin cancers
of which two were melanomas. There were three more skin cancers in the presumed
'unexposed' cohort, of which two were melanomas. Based on the absence of an excess of
observed over expected deaths in the entire cohort and the absence of any apparent
difference between the 'exposed' and 'unexposed' subcohorts, the authors concluded that
there was no evidence of excess cancer incidence. (The W orking Group noted that the
data presented in the two early reports are obscure as to case-ascertainment procedures
and the definition of comparison groups, which are based on very small numbers.)
The fourth report from this group described a study examining morbidity among the
same cohort of carbon black industry workers in the United States (Robertson & Ingalls,
1989). The study base consisted of workers aged 15 and over employed in 1980 on site
at any of seven carbon black producers. A nested case-control design was used (see
Table 19). A case was defined as a member of the study population who had filed a
health insurance claim with a physician's diagnosis of either a malignant neoplasm, a
disease of the circulatory system or a disease of the respiratory system. For each case,
two con troIs were selected from the workers in the study base who had none of these
diagnoses, one matched for age alone and one matched for age and duration of
employment. Exposure to carbon black was estimated by attributing to each job the
exposure levels found in a previous hygiene survey of jobs and combining it with
duration of employment to produce a cumulative exposure index. ln total, 36 cases of
malignant neoplasm were ascertained, of which 24 were skin cancers (12 basal-celI and
12 squamous-celI), three were lung cancers and the remainder were spread among other
sites. The odds ratio for aIl cancers was 1.1 (95% CI, 0.4-2.7) and that for skin cancers
was 0.9 (95% CI, 0.3-3.2).
186 IARC MONOGRAPHS VOLUME 65

(The Working Group noted that the use of a study base of workers active at a single
point in time led to smalI numbers. Further, the distribution of cancer sites among
prevalent cases would not reflect the site distribution of incident cases; for examp1e,
cancers with long survival (e.g. skin cancer) wouId be over-represented and cancers with
short survival (e.g. lung cancer) would be under-represented. The exposure contrast used
to compute the odds ratio was unc1ear.)
A historical cohort study was carried out among carbon black production workers in
the United Kingdom (Hodgson & Jones, 1985). Data were collected on 1422 male
manu al workers with at least one year of service between 1947 and 1974 in any of five
major carbon black production factories. For three of the companies, the investigators
believed that they had compiled virtualIy complete rosters of aIl eligible workers; for the
other two, they did not have available those workers who had left the industry before the
late 1960s. The subjects identified were traced via national vital statistics registers. For
the three 'completely enumerated' subcohorts, the folIow-up period began one year after
initial exposure to carbon black (i.e. after beginning employment) and for the two
'incompletely enumerated' subcohorts, the follow-up period began after the late 1960s.
For members of all subcohorts, the follow-up ended on 31 December 1980, unless
truncated by death or emigration. There were a total of 19 266 person-years of obser-
vation in the mortality follow-up, of which only 4% were in the age group over 65 years.
Overall, 9% of the study subjects were known to have died during the period of obser-
vation. Irrespective of whether the comparison was with national mortality rates or with
regionally specific mortality rates, there was a deficit in this cohort of deaths from aIl
causes (of approximately 15%) (this was made up mainly of deficits of circulatory and
non-malignant respiratory deaths). For specific cancer sites, there was a deficit of deaths
from stomach cancer (0 observed, 4.1 expected), parity in deaths from colorectal cancer
(3 observed, 4.0 expected), an excess of deaths from urinary bladder cancer (3 observed,
1.3 expected) and most notably an excess of deaths fram respiratory cancer (SMR, 1.5
(95% CI, 1.0-2.3); 25 observed cases) (Table i 8). (The deficit of deaths from aIl causes
was probably due largely to the 'healthy worker effect but also partI y to a survivor bias
in the two 'incompletely enumerated factories as those inception subcohorts included
workers who had remained (i.e. survived) in the industry for up to 20 years.) The excess
of deaths from lung cancer was most evident in one of the five factories (10 observed,
4.8 expected), although there were slight excesses in the other four factories combined as
weIl (15 observed, 11.7 expected). (The W orking Group noted that this factory was one
that had incomplete early data, but it is unlikely that this could have biased the results in
the observed direction.) Industrial hygiene measurements had been taken in 1976 in the
various factories. About one-half of all personal samples were above the benchmark TL V
for carbon black of 3.5 mg/m'. There was no indication that the factory with the greatest
excess risk had higher exposure levels than the other factories. On the contrary, the
measured levels were somewhat lower on average, although they were based on small
numbers of measurements. A nested case-control study was carried out, comparing the
cases of lung cancer with controls chosen from the unaffected members of the cohort,
matched for factory and date of birth. The duration of employment did not differ between
cases and controls. (The Working Group noted that the report contained too little infor-
 CARBON BLACK 187

mation on this study to evaluate the findings adequately.) While no data were presented
on smoking habits in this population, the authors refer to an early study in this industry
in which smoking habits were not found to have differed greatly from those of the
general population.

A general excess risk of cancer was reported in workers in one carbon black pro-
ducing plant in the former USSR (Troitskaya et al., 1980). (The Working Group noted
that neither absolute figures nor the method of calculating observed to expected ratios
were given.)

2.1.2 Studies in carbon black user industries

A nested case-control study was conducted in the tyre and rubber manufacturing
industry to examine the association of squamous-celI carcinoma of the skin with rubber
manufacturing materials presumed to be contaminated by P AHs (Bourguet et aL. 1987).
Cases of skin cancer were identified from the records of four hospitals located in Akron,
OH, United States, and the se were cross-checked against a list of past and present
employees of two local rubber companies who had been enumerated in 1964 for histo-
rical cohort studies conducted previously in this industry. Sixty-five cases of squamous-
cell skin cancer in white men were thereby ascertained in this cohort. The authors
acknowledge that their case-ascertainment system may not have identified aIl cases in the
cohort. Controls were selected from remaining cohort members and were matched to
cases on company, year of birth and year of hire, and were required to have been
employed in the industry until the corresponding case's date of diagnosis or date of
leaving the industry. A total of 254 matched controls were identified, with approximately
four matched controls selected for each case. Two experienced indus trial hygienists
assessed each study subject s exposure to five substances: carbon black, extender oils,
lubricating oils, rubber sol vents and rubber stocks. Conditional logistic regression
analyses were carried out with aIl five substances included in the models, and each one
categorized into three exposure subgroups reflecting concentration and frequency of
exposure. For carbon black, the odds ratios in these three exposure subgroups were 0.7,
1.2 and 0.7, respectively, indicating the lack of an exposure-response relationship (see
Table 19). There was also no evidence for any trend by duration of exposure.
A historical cohort of 26 561 workers employed in 10 facilities was assembled to
evaluate cancer risks associated with exposure to formaldehyde (see IARC, 1995) (Blair
et aL. 1990). The plants were drawn from a variety of industries in which exposure to
formaldehyde can be substantial and were located across the United States. The project
was characterized by a very extensive assessment of exposure to formaldehyde. About
85% of the workers were thought to have been exposed to formaldehyde at levels above
0.1 ppm (0.123 mg/m'). ln order to assess possible confounding and modification of
effect due to other occupational substances, an assessment was made of each worker' s
exposure to a number of other substances, one of which was carbon black. The exposure
status of subjects was inferred from their recorded work histories, linked to estimates of
exposure in different jobs in these plants. The latter estimates were derived by industrial
hygienists who carried out site visits, discussed exposure conditions with workers and
 188 IARC MONOGRAPHS VOLUME 65

plant managers and consulted available hygiene monitoring data. Although this study
was not designed primarily to assess risk in relation to carbon black exposure, the data
could be used for that purpose, and, in one report focusing primarily on exposure to
formaldehyde and lung cancer risk, results were presented showing the associations
between each of the other substances collected and lung cancer. Expected numbers of
deaths were computed using national rates. For aIl levels and durations of exposure to
carbon black combined, there was a slight excess risk for lung cancer (SMR, 1.3
(95% CI, 0.8-2.0); 20 observed cases) (Table 18). Based on 142 observed cases, the SMR
for formaldehyde was 1.4 (95% CI, 1.2-1.6) for ~ 20 years after first exposure. There
was no c1ear trend by duration of exposure and the pattern of results was similar when
restricted to 20 years or more since first exposure. (The W orking Group noted that the
description of methods of exposure assessment and analysis for carbon black was
limited. It was not c1ear whether aIl workers exposed to carbon black were also exposed
to formaldehyde.)

2.2 Comrnunity-based case-control studies

ln a Swedish case-control study of urothelial cancer during 1985-87 (Steineck et aL.,

1990), described in the monograph on printing trades and printing inks in this volume,
p. 76, the odds ratio for men having been exposed to carbon black was 2.0 (95% CI, 0.8-
4.9; 14 cases), adjusted for year of birth and for smoking (Table 19). However, sorne of
these workers had been exposed to printing inks and other substances.
A population-based case-control study of cancer among male residents of Montréal,
Canada, aged 35-70, inc1uded histologically confirmed cases of cancer at 11 major sites,
newly diagnosed between 1979 and 1985, in 19 major hospitals (Siemiatycki, 1991). With
a response rate of 82%, 3730 cancer patients were successfulIy interviewed. For each site
of cancer analysed, two control groups were used, giving rise to two separate sets of
analyses and results: one control group was selected from among cases of cancer at the
other sites studied (cancer controls; see Table 19) and the other group consisted of 533 age-
stratified population controls from the general population (response rate, 72%). The
interview was designed to obtain detailed lifetime job histories and information on
potential confounders. Each job was reviewed by a trained team of chemists and industrial
hygienists who translated jobs into occupational exposures, using a checklist of 293
common occupation al substances. Cumulative exposure indices were created for each
substance, on the basis of duration, concentration, frequency and the degree of certainty in
the exposure assessment itself, and these were analysed at two levels: 'any' and
'substantial exposure; the latter is a subset of 'any'. Five percent of the entire study
population had been exposed to carbon black at sorne time (i.e. lifetime exposure
prevalence). Among the main occupations in which carbon black was attributed in this
study werepainters (26%), printing industry workers (17%), motor vehic1e rnechanics (8%)
and occupations in rubber and plastics products (6%) (Parent et aL., 1996). The presentation
of published results was based mainly on the cancer control group. For the following
cancer sites, there was no indication of excess risk in relation to any exposure to carbon
black, after adjustment for age, ethnic group, social class and smoking (nurnber of exposed
 CARBON BLACK 189

cases; odds ratio): stomach (9; D.8), colon (17; 0.7), rectum (10; 0.7), pancreas (3; 0.7),
prostate (25; 1.2), urinary bladder (26; 1.2), skin melanoma (2; 0.4) and non-Hodgkin's
lymphoma (9; 0.9). For the following sites there was indication of excess risk (number of
exposed cases; odds ratio (95% CI)): oesophagus (11; 2.2 (1.1-4.4)), kidney (14; 1.9 (1.1-
3.3)) and lung (52; 1.6 (1.1-2.3)).
To investigate further the possible link between carbon black and lung cancer, an
additional analysis of the Montréal data set was carried out. A synthetic exposure index
was created, composed of the indices deduced for each exposed subject (concentration,
frequency, confidence in the attribution of exposure, duration), and this index was used
to designate a lower and a higher cumulative exposure subgroup. Logistic regression
analyses were carried out, adjusting for the same covariates as in the above analyses, as
weIl as for two recognized lung carcinogens, asbestos and chromium compounds. U sing
cancer controls, the odds ratios for lower and higher exposure were 1.1 (95% CI, 0.7-
1.8) and 2.2 (95% CI, 1.0-4.9); using population controls, the odds ratios for lower and
higher exposure were 0.9 (95% CI, 0.5-1.6) and 1.5 (95% CI, 0.6-4.0), respectively. The
excess among highly exposed workers was most pronounced for oat-cell tumours of the
lung: odds ratios, 5.1 (95% CI, 1.7-14.9) using cancer controls and 4.8 (95% CI, lA-
17.0) using population controls (Table 19) (Parent et aL., 1996).

3. Studies of Cancer in Experimental Animais

The studies described in the folIowing sections include those investigating the
potential carcinogenicity of carbon black, solvent-extracted carbon black and the
materials extracted from carbon black (carbon black extracts). However, a detailed
review of individual materials extracted from various carbon blacks is not part of this
monograph. Some of these individuai components (e.g. nitroaromatic compounds) have
been evaluated in previous monographs (IARC, 1989a).
Several early studies compared the carcinogenicity of carbon black or carbon black
extracts when administered orally or by skin or subcutaneous application. More recent
studies have examined the carcinogenicity of inhaled or intratrachealIy administered
carbon black or solvent-extracted carbon black. Many of these studies were part of large
studies carried out to investigate the carcinogenicity of diesel exhaust (see also IARC,
1989c).
The W orking Group also considered sorne issues relating to the interpretation of
several of the inhalation and intratracheal instillation studies of carbon black. A lesion
frequently seen in treated rats has been described variously as 'proliferating squamous
cyst, 'proliferative keratin cyst, 'proliferating squamous epithelioma', 'benign cystic
keratinizing squamous-cell tumour' or 'cystic keratinizing squamous-cell (CKSC)
tumour'. Various authors have inc1uded this lesion in tumour counts, but the neoplastic
nature of this lesion has been debated (Vainio et aL., 1992; Carlton, 1994; Dungworth
et aL., 1994; Mauderly et al., 1994); its relationship to pulmonary neoplasia is uncertain.
Therefore, where possible, the W orking Group has listed incidences of this lesion
separately from those of other pulmonary neoplasms.
 190 lARC MONOGRAPHS VOLUME 65

The Working Group considered reports by von Haam and Mallette (1952), von Haam
et al. (1958), Nau et al. (1958a, 1960, 1962), Shabad et aL. (1972) and Davis et al. (1975)
in their evaluation, but, because of deficiencies in detail of design, performance and/or
reporting, did not use this information in reaching its conclusion.

3.1 Oral adrninistration

3.1.1 Mouse

After two weeks of acclimatization, two groups of 31 and 28 female weanling CFI
mice received a diet for two years that did or did not (controls) include furnace black
(ASTM N-375; 2.05 g/kg diet). At necropsy, aIl tissues were examined for gross patho-
logy. Only tissues with macroscopically diagnosed alterations were examined histolo-
gicalIy. Survival at two years was similar in treated mi
ce (84%) and in controls (71 %).
No increase in tumour incidence was observed (Pence & Buddingh, 1985). (The
W orking Group noted the small numbers of animaIs and the incomplete histopathological
examination.)

3.1.2 Rat

After two weeks of acclimatization, two groups of 29 female weanling Sprague-

Dawley rats received a diet for two years that did or did not (controls) include furnace
black (ASTM N-375; 2.05 g/kg diet). At necropsy, aIl tissues were examined for gross
pathology. Only tissues with macroscopicalIy diagnosed lesìons were examined histolo-
gicalIy. Survival at two years was similar in controls (38%) and treated animaIs (45%).
No increase in tumour incidence was observed (Pence & Buddingh, 1985). (The
Working Group noted the smalI numbers of animaIs and the incomplete histopathological
examination.)

3.2 Inhalation

3.2.1 Mouse

Groups of 80 female Crl: NMRI BR mice, seven weeks old, were exposed to high
purity furnace black (Printex 90; primary particle size, 14 nm; specific surface area,
227:t 18.8 m2/g; MMAD of particles in the exposure chambers, 0.64 !lm). The
extractable organic mass of the carbon black was 0.04%; the content of benzo(a)pyrene
was 0.6 pg/mg and that of I-nitropyrene was -( 0.5 ng/mg'particle mass. For 18 h per day
on five days per week, the animaIs were exposed in whole-body exposure chambers to
7.4 mg/mJ carbon black for four months followed by 12.2 mg/mJ for 9.5 months. After
exposure, the mice were kept in clean air for another 9.5 months. A control group was
exposed to clean air throughout. Histopathology was performed on the nasal and
paranasal cavities, larynx,. trachea and lung. After 11 months and up to 17 months, body
weights were significantly 10wer (5-7%) in the carbon black-exposed group compared
with the control group. During the last months, no difference between the groups was
observed. After 13.5 months, mortality was 20% in the carbon black-exposed group and
 CARBON BLACK 191

10% in the control group; 50% mortality was reached after 19 months in the carbon
black-exposed group and after 20 months in the control group. ln exposed mice, the lung
particle burden was 0.8, 2.3 and 7.4 mg carbon black per lung after three, six and
12 months, respectively; and, at 12 months, this corresponded to a lung partic1e burden of
37 mg/g clean air control lung. Among tissues examined, tumours were only observed in
the lung. However, no statistical difference was observed between experimental and
control animaIs: carbon black-exposed mice, 11.3% (9/80) adenomas and 10% (8/80)
adenocarcinomas; controls, 25% (20/80) adenomas and 15.4% (12/80) adenocarcinomas
(Heinrich et al., 1995).

3.2.2 Rat

Two groups of 72 female Wistar Crl:(WI)BR rats, seven weeks old, were exposed by
inhalation for 17 h per day on five days per week to 6 mg/m3 furnace black (Printex 90;
0.04% extractable mass of organics (content of benzo(a)pyrene, 0.6 pg/mg and that of
I-nitropyrene, .c 0.5 pg/mg carbon black; primary particle size, 15 nm; MM AD of
particles in the exposure chamber, 1.1 i.m; specific surface area, 230 m2/g). One group
was exposed for 43 weeks and kept for an additional 86 weeks in clean air and the other
group was exposed for 86 weeks and housed in c1ean air for an addition al 43 weeks. Two
clean air control groups were kept for 129 weeks. The respiratory tract of aIl animaIs was
examined histopathologically. The 43-week exposure group had a lung tumour rate of
18% (13/72) (2 bronchiolar/alveolar adenomas, 7 benign CKSC tumours, 4 bronchiolar/-
alveolar adenocarcinomas and 1 squamous-cell carcinoma). The 86-week exposure group
had a lung tumour rate of only 8% (6/72) CI bronchiolar/alveolar adenoma, 4 benign
CKSC tumours and 1 squamous-cell carcinoma). ln addition to the six tumours of the
ions in the borderline between non-neoplastic and
latter group, six rats showed lung les

neoplastic (described as marked hyperplasia or marked squamous-celI proliferation).

(The difference in the tumour rates of the two exposure groups was not statisticalIy
significant.) No tumour was observed in the clean air controls (Heinrich et aL., 1994).
A group of 100 female Wistar Crl:(WI)BR rats, seven weeks old, was exposed to high
purity furnace black (Printex 90; partic1e size 14 nm; specific surface area, 227 :!
18.8 m2/g; MMD of partic1es in the exposure chamber, 0.64 i.m). The extractable organic
mass of the furnace black was 0.04%; the content of benzo(a)pyrene was 0.6 pg/mg and
that of I-nitropyrene was .c 0.5 ng/mg particle mass. Rats were exposed for i 8 h per day
on five days per week in who le-body exposure chambers to 7.4 mg/m3 carbon black for
four months followed by 12.2 mg/m3 for 20 months (average 11.6 mg/m\ After
exposure, the rats were kept in clean air for another six months. Controls were exposed to
clean air throughout. Additional groups of 9-20 rats were also exposed to carbon black
and were killed at six, 12, 18 and 24 months. Histopathology was performed on the nasal
and paranasal cavities, larynx, trachea and lung. Mortality in the carbon black-exposed
group was 56% after 24 months of exposure and 92% after 30 months. ln the clean air
group, mortality was 42% after 24 months and 85% after 30 months. Compared to the
controls, the me an lifespan of the treated rats was significantly reduced (Kaplan-Meier
method using the SAS-lifetest programme). Mean body weights were significantly lower
 192 IARC MONOGRAPHS VOLUME 65

from day 300 to the end of exposure (carbon black-exposed, 325 g; control, 417 g). The
lung burden of carbon black at 24 months was 43.9 :t 4.3 mg/lung (equivalent to 31.3
mg/g c1ean air control lungJ and 6.7 mg/animal in the lung-associated lymph nodes
(determined after 22 months of exposure). Benign and malignant lung tumours were
Increased in the treated groups. The numbers of rats with lung tumours are summarized
in Table 20 (Heinrich et aL., 1995).

Table 20. Nurnber of fernale rats with lung

turnours after carbon black exposure
Exposure period Clean air Carbon black-exposed
control (average concentration of
carbon black, -1 1.6 mg/m')

6 months 0/21 0/20

12 months 0/21 0118
18 months 0/18 0116
24 months 0/10 119"
30 months 1121i' 20/100"
1 3/1 OOh
4/100'
13/100,1
No. of animaIs 112 17 39/100
with tumours' (28/100t
From Heinrich et al. (1995)
"Benign CKSC tumours
h Adenocarcinomas
C Squamous-cell carcinomas
,1 Adenomas

'Sorne animaIs had two lung tumours

IExcIuding i 1 animaIs that had only benign cystic kerati-
nizing squamous-cell tumours

Groups of 135--136 female and 138-139 male Fischer 344/N specifie pathogen-free
rats, seven to nine weeks old, were exposed to 0, 2.5 or 6.5 mg/m' furnace black (Elftex-
12) for 16 h per day on five days per week for up to 24 months in whole-body exposure
chambers. The carbon black aerosol was produced by an air jet dust generator and was
diluted with filtered air. The carbon black particle size distribution in the chamber was
bimodal with 67% in the large-size mode (MMAD, 2.0 )lm) and 33% in the small-size
mode (MMAD, 0.1 !lm). The level of extractable organic material was 0.04-0.29%
(mean value during the course of exposure was 0.12%). Observations throughout the
complete lifespan were made for the majority of rats in each group (that is, for approxi-
mately 100 males and 100 females in total). From these data, body weight, survival and
carcinogenicity were evaluated. After exposure for 24 months, surviving rats were kept
in c1ean air until mortality reached 90%. Three female and three male rats selected
randomly from each group were killed after three, six, 12, 18 or 23 months for multiple
evaluations, inc1uding partic1e burden and histopathology. The high-dose exposure to
 CARBON BLACK 193

carbon black reduced the median lifespan of both females and males significantly. The
survival of males was also significantly reduced by the low-dose exposure to carbon
black (Kaplan-Meier method for determining survival curves; statistical method, log-
rank test of HaITington and Flemming). A significant reduction in the body weights of
female and male rats exposed to the high-dose carbon black first occuITed on days 309
and 449, respectively. For the low-dose exposure to carbon black, this effect was seen
only after day 509 of exposure for both males and females. After about 22 months of
exposure to the high-dose carbon black, the mean reduction in body-weight was 16% for
females and 14% for males. For the low-dose exposure to carbon black, these figures
were below 10%. The exposure caused progressive, dose-related accumulation of carbon
black particles in the lungs. After 23 months, the mean lung burden reached 12.4 mg/g of
clean air controllung in low-dose males, 13.9 mg/g of clean air controllung in low-dose
females, 20.2 mg/g of clean air controllung in high-dose males and 30 mg/g of clean air
control lung in high-dose females. FulI necropsies were performed on aIl animaIs and
lungs and suspected lung tumours were examined microscopicalIy. The incidences of the
various types of lung tumours are shown in Table 21. Statistical comparisons were
performed using logistic regression modelIing. The incidences of adenomas and adeno-
carcinomas were significantly increased in females, particularly at the high-dose level.
The percentages of male and female rats with lung tumours are given in Table 22.
Exposure-related squamous cysts in the lung were c1assified as non-neoplastic lesions. ln
animaIs dying later than 18 months after the start of the exposure, squamous cysts (1 or
more per animal) were observed in 0/86 male controls, 1/73 low-dose males and 4/74
high-dose males and in 0/91, 8/90 and 13/87 control, low-dose and high-dose females,
respectively (Mauderly et al., 1994; Nikula et al., 1995).

3.3 Intratracheal adrninistration

Rat
A group of 37 female Wistar rats, 15 weeks old, was instilIed intratracheally under
COz anaesthesia with furnace black (Printex 90) of a high specifie surface area
(270 mZ/g). The carbon black was suspended in 0.9% sodium chloride using
ultrasonication and 3 mg/rat were instilIed once a week for 15 weeks. A control group of
39 female rats was instiled with 0.4 ml 0.9% saline once a week for 15 weeks. The
animaIs died spontaneously or were kiled when moribund or after 131 weeks at the
latest. More than 50% of rats in the treated and control groups survived to 100 weeks.
The respiratory tract was evaluated microscopicalIy. No primary lung tumour was found
in the control group. ln the treated animaIs, 65% (24) of the rats had primary lung
tumours - three rats had adenomas, six rats had adenocarcinomas and one additional rat
had an adenocarcinoma and a CKSC tumour, four rats had CKSC tumours and one
additional rat had a CKSC tumour and an adenoma, three rats had squamous-cell
carcinomas and six rats had squamous-celI carcinomas and additional lung tumours (1
adenoma, 1 adenocarcinoma, 3 adenocarcinomas and CKSC tumours, 1 CKSC tumour)
(Pott & Roller, 1994; Pott et al., 1994).
Table 21. Nurnbers of different types of lung neoplasrns observed and nurnbers of rats with each \0
..
type of neoplasrn a
Type of tumour Control Low-dose carbon b1ack High-dose carbon black
(2.5 mg/m.') (6.5 mg/m.')

Female Male Total Fema1e Male Total Female Male Total

No. of animaIs examinedh 114 118 232 116 iis 231 114 115 229
Adenoma ..
No. of neoplasms 0 1 1 2 3 17 0 17 ;p
n;:
1

No. of rats with neoplasms 0 1 1 2 1 3 13 0 13

AdenocarcInoma ~
No. of neoplasms
0
0 1 1 6 1 7 23 1 24 Z
No. of rats with neop1asms 0
0 1 1 6 1 7 20 1 21 a;:
Squamous-cell carcinoma ;p
No. of neoplasms 0 0 0 0 '"
1 1 1 2 3 ::
(/
No. of rats with neoplasms 0 1 1 0 0 0 1 2 3
-c
Adenosquamous carcinoma 0r
No. of neoplasms 0 0 0 0 0 0 1 1 2 c:
No. of rats with neoplasms 0 0 0 0 0 0 1 1 2 ~
t'
Malignant tumour not otherwise 0\
Ui
specified
No. of neoplasms 0 0 0 1 0 1 0 0 0
No. of rats with neop1asms 0 0 0 1 0 1 0 0 0

From Mauderley et al. (1994)

"Several rats had multiple types of tumours or multiple tumours of a single type or bath; thus, the se rats (or their tumonrs)
are counted more than once in this table
¡, Including aU rats that underwent gross necropsy and microscopic examinations of the lung whether the rats died sponta-
neously, were euthanized or were killed
'This tumour was of a mixed mesenchymal and epithelial type
 CARBON BLACK 195

Table 22. Surnrnary of nurnbers and percentages of rats exarnined for lung
neoplasrns that had one or rnore neoplasrns a
Group Sex No. of rats Rats with malignant Rats with malignant
at risk for neoplasms or benign neoplasms
h
neoplasms
No. Percentage No. Percentage

Control Female 105 0 0 0 0

Male 109 2 1.8 3 2.8
Combined 214 2 0.9 3 1.4
Low-dose carbon black Female 107 7 6.5 8 7.5
(2.5 mg/m') Male 106 1 0.9 2 1.9
Combined 213 8 3.8 10 4.7
High-dose carbon black Female 105 21 20 28 26.7
(6.5 mg/m') Male 106 4 3.8 4 3.8
Combined 211 25 11.8 32 15.2

From Mauderly et al. (1994)

"Each rat with one or more neoplasm was counted only once in each neoplasm category.
h Values include ail rats examIned by gross necropsy and microscopy except rats killed at three, six
and 12 months. The first lung neoplasm was observed between 12 and 18 months of exposure; thus
ail rats that died spontaneously or were euthanized in moribund condition plus those killed at
18 months or later were considered to be at risk for lung neoplasms. The total number of rats
examined, including those killed at three, six and 12 months, is listed in Table 21.

Groups of 48 female Wistar Crl:(WI)BR rats, seven weeks of age, were treated by
intratracheal injection once a week for 16-17 weeks with approximately 1 mg of two
types of extracted carbon black (furnace Black Printex 90 or Lampblack 101). Resultant
total particle doses were 15 mg/animaL. A control group of 47 rats was treated with the
vehicle (0.9% sodium chloride + 0.25% Tween 80 solution). Although the amount of
organic material that could be extracted from the two carbon blacks was small (-: 0.1 %),
the particles were re-extracted with heated toluene for 4 h before they were used in this
experiment. The specific surface areas (extracted) and primary particle sizes of Printex
90 and Lamp Black 101 were 270 m2/g and 14 nm, and 22 m2/g and 95 ntn, respectively.
Satellite groups of two to four animaIs were used to determine the lung particle load one
day after the last treatment. Both groups showed a lung particle load of 11 mg (8.1 mg/g
of clean air control lung). Fifty percent of the animaIs in both groups were alIve at 18
months. After an experimental time of 27 months, the respiratory tract of the 48 treated
animaIs per group was investigated histopathologicalIy. ln the Printex 90 carbon black-
treated rats, i 0 had lung tumours (p -: 0.001, Fisher' s exact test) (9 benign (CK)
squamous-cell tumours, 1 bronchiolar/alveolar adenoma and 4 bronchiolar/-
alveolar carcinomas). ln the lampblack-treated animaIs, four rats had benign (CK)
squamous-cell tumours. No lung tumour was observed in the 47 vehicle-treated controls
(Heinrich, 1994; Dasenbrock et al., 1996).
 196 lARC MONOGRAPHS VOLUME 65
3.4 Skin application

Mouse: ln a series of experiments by Nau et al. (1958b), groups of CFW white and
C3H brown mice (sex unspecified), six to 10 weeks old, received thrice-weekly skin
applications by brush of 10% or 20% carbon black (of several types) suspended in
cottonseed oil or mineraI oil (oil suspension) or in 1 % carboxymethyl celIulose (water
suspension). Tests were also carried out with 20% extracted carbon black or benzene
extracts of various carbon blacks. The types of carbon black were said to be represen-
tative of materials used at that time (see Table 23).
A total of 240 CFW white and C3H brown mice (sex unspecifiedJ, six to ten weeks
old, received thrice-weekly skin applications by brush of 10% or 20% of three carbon
blacks (product No. 5, furnace black; product No. 8, thermal black; and product No. 13,
channel black; see Table 23), which contained 0-1 % benzene-extractable material and
were suspended in cottonseed, mineraI oil or 1 % carboxymethyl cellulose. These were
applied on the shaved back of the mice for 12-18 months (estimated total dose, 3.6-
12.8 g/mouse). No skin tumour was reported, but five tumours occurred in other organs
in channel black-painted mice. Another 130 animaIs received treatment with a benzene-
extracted carbon black (product No. 5, fumace black; see Table 23) (estimated total dose,
6.3-23.4 g/mouse); no skin tumour was observed, but two lymphosarcomas were
reported (Nau et al., 1958b).
Groups of male C3H and CFW mice (numbers and age unspecified) received thrice-
weekly skin applications of carbon black extracts obtained by hot benzene extraction
from eight different carbon blacks for up to 12 months. AIl but one of the ex
tracts was
reported to show moderate to strong carcinogenicity for the skin (see Table 24). Groups
of positive controls (162 mice) received thrice-weekly - skin applications of
3-methylcholanthrene (estimated total dose, 7-24 mg/mouse) or benzo(a)pyrene (26-
27 mg/mou se ) in water, oil or benzene (32 mg/mouse) for six to 18 months. (The
Working Group noted several deficiencies in these experiments, namely inadequacies in
experimental design with the use of 1 % benzene as a vehicle for some extracts, and the
limited reporting.) (Nau et aL., 1958b).

3.5 Subcutaneous and/or intrarnuscular adrninistration

Mouse: Groups of 50 male and female C57Bl mice, 5-5.5 months of age, received
subcutaneous injections of the folIowing: 300 mg of a fumace black (surface area,
15 m2/g; average partic1e diameter of about 80 nm) containing 300 mglkg (ppm) benzo-
(a)pyrene, either suspended in 1 ml tricaprylin or as a pellet; 300 mg of a channel black
(surface area, 380 m2/g; average partic1e diameter of about 17 nm) from which no aro-
matic hydrocarbons were detected after extraction with benzene ('non-benzo( a )pyrene
extractable') either in 1.5 mL tricaprylin or as a pelIet; 300 mg channel black plus
0.09 mg benzo(a)pyrene either in tricaprylin or as a pelIet; benzene extract from 300 mg
furnace black in 1 mL tricaprylin; the extracted carbon black frorn the 300 mg furnace
black after benzene extraction in 1 mL tricaprylin; 300 mg furnace black treated for 3 h
with hot chromic acid and suspended in 1 mL tricaprylin; and 600 mg of a mixture of
Table 23. Types and properties of carbon blacks used in Nau et al. studies
Product Supplier Type Parent material Iodine surface Benzene pH, Volatile, Grade of
"
No. No. area, average extract, average average black
(m2/g) average (%)
(%)

2 1 ail furnace ail residue 52.7 0.374 9.09 3.53 HAF

1 1 ail furnace ail residue 184.5 0.15 8.86 3.17 CF
9 2 Gas furnace Gas 21.5 0.06 9.69 0.70 HMF
10 2 Furnace Gas-oil 28.4 0.07 8.85 1.42 FEF or MAF
IL 2 Furnace Gas-oil 61.7 0.05 9.22 1.29 HAF (J
12 2 Furnace Gas-oil 99.3 0.05
;:
9.02 2.34 ISAF :A
3 3 ails 76.0 0.053 to
ail furnace 9.58 4.5 L HAF 0
4 3 ail furnace ails 35.5 0.125 9.53 2.05 FEF Z
13 4 Channel Gas 108.0 0.00 4.99 5.08 MPC to
r-
14 4 Channel special Gas 126.0 0.02 9.00 2.50 STC ;:
5 5 ail furnace ails 35.5 o. 17 9.08 1.96 FEF (J
;;
8 5 Thermal combustion Gas 11.5 1.04 7.47 1.04 MT
6 5 ail furnace Heavy aromatic tar 67.7 0.246 9.70 2.46 HAF
plus natural gas
7 5 Gas furnace Gas 21.7 0.118 9.83 0.69 SRF
15 5 ail furnace ail 62.4 0.26 6.72 3.01 HAF
16 5 Gas furnace Gas 111.0 0.08 5.81 5.15 Ink b1ack

HAF, high-abrasion furnace; CF, conducting furnace; HMF, high modules furnace; FEF, fast-extruding furnace; MAF, medium-abrasion
furnace; ISAF, intermediate super-abrasion furnace; MPC, medium-processing channel; STC, special thermal channel; MT, medium
thermal; SRF, semi-reinforcing furnace
"Iodine surface area 1eve1s are lower than nitrogen surface are a leve1s.

..
\0
-.
198 IARC MONOGRAPHS VOLUME 65

Table 24. Induction of skin turnours with various carbon

black extracts in rnIce treated for at least 12 rnonths
Type of material used" Total dose of Final tumour
benzene extract indexh (%)
(mg)

High-abrasion furnace black

Product No. 2 12.7 0
45.0 15.0
51.4 16.0
201.7 82.0
Product No. 3 12.6 0
20.0 0
24.3 0
147.4 33.0
Product No. 6 12.6 0
16.5 0
32.5 24.0
36.5 52.0
170.0 85.0
Fast-extruding furnace black
Product No. 4 10.8 0
21.8 7.0
26.6 9.0
135.0 44.0
Product No. 5 27.0 33.0
32.9 25.0
129.0 25.0
201.0 74.0
Semi-reinforcing furnace black
Product No. 7 6.3 0
7.9 14.0
8.9 0
15.4 0
18.0 0
24.0 0
132.6 73.0
Conducting furnace black
Product No. 1 17.9 0
21.5 0
136.6 0
Medium thermal black
Product No. 8 117.1 85.0

From Nau et al. (1 958b)

a See also Table 23
hDefined by the authors as the percentage of animaIs, not dying from
other cases, developing skin tumours during the treatment period
 CARBON BLACK 199

furnace black and channel black in 1.5 mL tricaprylin. Further groups of 50 mice
received injections of 1.0 mL tricaprylin (vehicle controls) or 0.09 mg benzo(a)pyrene
per mouse in 1 mL tricaprylin (positive controls). The experiment was terminated at 20
months after injection of the test materials. AIl questionable tumours found post-mortem
were examined microscopicalIy. Tumour incidence was calculated as a percentage and
was based on the number of animaIs alive five months after the start of the study, which
was the time at which the first deaths from tumours occurred. ln ni ne of the 12 groups
(treated and controls), few or no sarcomas were induced and 70% of the animaIs were
stilI alive 12 months after the start of the experiment; in the other three, 52-66% of the
mice were still alive at this time. ln animaIs treated with the carbon black containing
benzo(a)pyrene (a furnace black), a significantly increased incidence of subcutaneous
sarcomas (a few of which metastasized) was observed when compared with tricaprylin
controls. The incidence of subcutaneous sarcomas induced by the injection of test
materials and the 'average fatal time' (i.e. time to death from subcutaneous sarcoma) are
summarized in Table 25. High incidences of sarcoma (18/46) were observed in mice
receiving furnace black with extractable benzo(a)pyrene administered in tricaprylin, in
those receiving the carbon black extract from furnace black containing benzo(a)pyrene
(22/45) and in positive controls (39/41). It should be noted that administration of furnace
black containing benzo(a)pyrene in pelIet form in the absence of tricaprylin induced an
incidence of sarcomas of only 2/47 and that of non-benzo(a)pyrene-extractable channel
black in pelIet form induced an incidence of only 1/47. Extracted furnace black, that is
furnace black folIowing benzene treatment, induced one sarcoma in 37 animaIs; no
subcutaneous sarcoma developed in any of the other groups. It was found that mixing
non-benzo(a)pyrene-extractable carbon black with benzo(a)pyrene-extractable carbon
black (furnace and channel blacks) resulted in a loss of carcinogenicity of the latter
(Steiner, 1954).

A series of 21 groups of 10-20 male or female C3H brown or CFW white mice (total
number, 344), eight to 10 weeks old, received a total dose of 17-300 mg of different
carbon blacks suspended in cooking oil, tricaprylin or 1 % carboxymethyl cellulose in
water as one or two subcutaneous injections and were observed for 20 months. The
au th ors reported an 8-13% tumour index in three groups receiving subcutaneous
injections of carbon black (product Nos 4, 7 and 8 (two furnace blacks and one thermal
black); see Table 23) in cooking oiL. The tumour index was defined by the author as the
percentage of tumours occurring in 'animaIs excluding those found dead of causes
unknown'. The tumours were described as 'subcutaneous mixed tumours' (Nau et al.,
1960) .

Three groups of 20 C3H, 20 C3H and CFW or 10 C3H male and female mice
received two subcutaneous injections of an extracted furnace black (product No. 5; see
Table 23) (after extraction in hot benzene for 24 h) (total dose, 0.14-150 mg) in cooking
oil or in 1 % carboxymethyl cellulose in water and were observed for 20 months. No
tumour occurred at the injection site among 19 mice killed at the end of the experiment
or in animaIs dying during the course of the experiment (Nau et al., 1960).
 200 IARC MONOGRAPHS VOLUME 65

Table 25. Carcinogenicity of carbon blacks

Materials tested Tumours/ Tumour A verage fatal

survivors at yield (%) time (days)
5 months

Benzo(a)pyrene-containing furnace black", tricaprylin 18/46 39.1 363

Benzo(a)pyrene-containing furnace black", pellets 2/47 4.3 411
Non-benzo(a)pyrene-extractable channel black, tricaprylin 0/48 0.0
Non-benzo(a)pyrene-extractable channel black, pellets l/47 2.1 524
Non-benzo(a)pyrene-extractable channel black plus 0/43 0.0
benzo(a)pyrene, tricaprylin
Non-benzo(a)pyrene-extractable channel black plus 0/48 0.0
benzo( a )pyrene, pellets
Benzene extract of benzo(a)pyrene-containing furnace 22/45 48.9 295
black, tricaprylin
Furnace black" residue, tricaprylin l/37 2.7 405
Benzo(a)pyrene-containing furnace black" treated with 0/47 0.0
chromic acid, tricaprylin
Benzo(a)pyrene-containing furnace black" plus non- 0/41 0.0
benzo(a)pyrene-extractable channel black, tricaprylin
Tricaprylin, 1.0 mL 0/43 0.0
Benzo(a)pyrene (0.09 mg), tricaprylin 39/41 95.1 233

From Steiner (1954)

"Furnace black from which benzo(a)pyrene and six other PAHs can be extracted with benzene

Groups of 10-30 male and female C3H and CFW mice, eight to 10 weeks old,
received one or two subcutaneous injections of benzene extracts of different carbon
blacks in cooking oil (total dose, 0.01-6.5 mg) (product Nos 1-10 and 15-17; see
Table 23). ln 31/36 groups, tumour indices of 15-100% were reported, 22 of which had
an index of;: 50%. No subcutaneous tumour was observed in five groups. Further groups
given subcutaneous injections of 0.2-3.25 mg benzene extracts of carbon black (product
No. 5; see Table 23) in 1 % carboxymethyl cellulose in water or methanol extracts of
carbon blacks (product Nos. 1,5-7; see Table 23) in water were reported to have a nil
tumour index. Similar groups of 9-20 C3H mi
ce received one subcutaneous injection of
0.1 or two subcutaneous injections of 0.2 mg extracted material readsorbed onto carbon
black (product No. 5; see Table 23) in cooking oil or in carboxymethyl cellulose in
water; a nil tumour index was again reported. Further groups of 19-20 C3H mi
ce
received as one or two subcutaneous injections 0.5-1.0 mL of cooking oil, which had
been incubated with carbon black (product No. 5; see Table 23) for one to six months
then centrifuged to remove the carbon black; the subcutaneous tumour index in the
se
animaIs was 17-92% (Nau et al., 1960).
As a positive control, 14 groups of 10-20 CFW and/or C3H mice, eight to 10 weeks
of age, received as one or two subcutaneous injections 0.002-1.0 mg 3-methyl-
cholanthrene (MCA) in cooking oil; the reported tumour indices ranged from 25-100%.
When four groups of 20 C3H mice received as one or two subcutaneous injections 0.05-
 CARBON BLACK 201

0.25 mg MCA in carboxymethyl celIulose in water, reported tumour indices ranged from
12 to 95%, whereas a nil tumour index was reported for five groups of 12 female C3H
mice receiving one subcutaneous injection of 0.002-0.01 mg MCA in carboxymethyl
cellulose io water. Eleven further groups of 15-21 male and female C3H mice received
single subcutaneous injections of 0.01-0.2 mg MCA adsorbed onto different carbon
blacks (product Nos 1,5-7, 13 and 18; see Table 23) in cooking oiL. For three of these
groups (product Nos l, 13 and 7), the reported tumour indices were 5, 5 and 7%,
respectively; for the other products, the tumour index was niL. When four groups of 10-
22 C3H mice received the same amount of MCA adsorbed onto carbon blacks (product
Nos 5 and 14; see Table 23) in carboxymethyl cellulose in water, the reported tumour
index wàs niL. Two groups of 20 C3H mice injected with 0.1 mg benzo(a)pyrene alone or
adsorbed onto carbon black (product No. 5; see Table 23) in carboxymethyl cellulose in
water were reported to have tumour indices of 56 and 0%, respectively. Four groups of
20-31 C3H mice were injected with 0.5-1.0 mL tricaprylin or cooking oil, and the
tumour indices ranged from 0 to 5%. Of a total of 943 untreated CFW and C3H controls,
six were reported to have malignant skin neoplasms, one a malignant neoplasm of the
liver and one a malignant neoplasm of the spleen. (No detail as to the histology of the se
tumours was available.) No animal developed a subcutaneous sarcoma (Nau et al., 1960).
(The W orking Group noted deficiencies in experimental design and reporting in the
above experiments; in particular, difficulty was experienced in interpreting the data
presented in tabular form.)

3.6 Intraperitoneal adrninistration

Rat: A group of 36 female Wistar rats was injected intraperitoneally once per week
for four weeks with 20 mg furnace black 'Corax L' suspended in 2 ml saline (1.2%
volatiles; toluene extract, .: 0.1 %; primary partic1e size, 23 nm; surface area, 150 m2lg).
Fifty percent of the rats lived longer than 119 weeks, and after 132 weeks 20% of the
animaIs were stil al ive. One out of 35 animaIs examined histopathologicalIy at the end
of the experiment had a sarcoma in the abdominal cavity (tumours of the uterus were
excluded). Other groups treated in the same way with total doses of 80 mg diesel soot (no
local tumour in 34 rats), 20 mg titanium dioxide (0/47), 250 mg non-fibrous silicon
carbide (1/22), 250 mg activated carbon (1/25), 160 mg magnetite (2/34) or 160 mg iron
(III) oxide (0/33) did not show an increased tumour incidence either. Fibrous dust
administered in the same way induced significantly increased incidences of meso-
theliomas/sarcomas in the abdominal cavity with total doses sometimes as low as 1-
2 mg; for example, 13/21 rats injected intraperitoneally with 1.25 mg fibrous silicon
carbide developed mesotheliomas/sarcomas (Pott et aL., 1991). (The Working Group
noted the apparent low power of this assay to detect carcinogenesis arising from
exposure to non-fi brous particles.)
202 IARC MONOGRAPHS VOLUME 65
3.7 Cornbined adrninistration with known carcinogens

3.7.1 Mouse

After two weeks of acclimatization, two groups of 30 and 33 female weanling CFI
mice received a diet for 52 weeks that did or did not (controls) include furnace black
(ASTM N-375, 2.05 g/kg diet). Both groups of mice received six weekly intraperitoneal
injections of 20 mg/kg bw 1,2-dimethylhydrazine at the start of the study. At necropsy,
aIl tissues were examined for gross pathology. Only tissues with macroscopically
diagnosed lesions were examined histologicaIly. Survival was similar in treated and
control animaIs. Carbon black did not enhance the incidence of colonic tumours induced
by 1,2-dimethylhydrazine (Pence & Buddingh, 1985).

3.7.2 Rat

After two weeks of acclimatization, two groups of 44 and 45 female weanling

Sprague-Dawley rats received a diet for 52 weeks that did or did not (controls) include
furnace black (ASTM N-375, 2.05 g/kg diet). Both groups of rats received 16 weekly
intraperitoneal injections of 10 mg/kg bw 1,2-dimethylhydrazine at the start of the
experiment. At necropsy, aIl tissues were examined for gross pathology. Only tissues
with macroscopically diagnosed lesions were examined histologically. Carbon black did
not enhance the incidence of colonic tumours induced by 1,2-dimethyl-hydrazine (Pence
& Buddingh, i 985).
Two groups of 72 female Crl:(WI)BR rats, seven weeks old, were exposed by inha-
lation for 17 h per day on five days per week to a P AH-rich hard coal-tar pitch
condensation aerosol (T/P aerosol) that contained no carbon particles. The exposure
concentration of 2.6 mg/m' T/P aerosol contained 50 ¡.g/m' benzo(a)pyrene among other
P AHs. The MMAD of this aerosol was 0.5 ¡.m. Four other groups of 72 female rats each
were exposed to two mixtures of furnace black (Printex 90) and T/P vapour resulting in
benzo(a)pyrene concentrations in these exposure atmospheres of 50 ¡.g/m'. Two of these
four groups were exposed to the T/P aerosol containing 2 mg/m' carbon black and the
other two groups were exposed to the TIP aerosol containing 6 mg/m' carbon black. The
T/P vapour condensed onto the surface of the carbon black particles. One group of each
of the three exposure atmospheres was exposed for 43 weeks and kept in clean air for 86
weeks. The other was exposed for 86 weeks and kept in c1ean air for 43 weeks. The two
control groups of 72 rats each were kept in clean air for 129 weeks. No lung tumour was
observed in clean air groups. Comparing the three 43-week exposure groups, the lung
tumour rates of the groups combining T/P aerosol with carbon black showed an approxi-
mately two-fold higher increase compared to the groups exposed to T/P aerosol only.
There was no difference in the lung tumour rates between the three exposure groups
exposed for 86 weeks (Heinrich et al., 1994).

3.7.3 Hamster

Syrian golden hamsters from the TNO/Holland breeding farm (sex unspecified) were
treated intratracheally with a total dose of 60 mg/animal carbon black (not further
 CARBON BLACK 203

specified) together with 3 and 9 mg benzo(a)pyrene. Benzo(a)pyrene was dissolved in

acetone with the carbon black added to obtain smaller benzo(a)pyrene particles and to
provide condensation of benzo(a)pyrene on carbon black after acetone vaporization. Two
other groups of hamsters were treated with 3 and 9 mg benzo(a)pyrene without carbon
black. The total dose was administered by 40 instilations once per week in 0.1 mL saline
solution containing 0.5% Tween 80. Between 40 and 43 hamsters per group were
examined histopathologicalIy at the end of the experiment. Malignant and benign tumour
incidences in the larynx, trachea and lung were reported. The authors stated that carbon
black did not enhance the carcinogenic effect of benzo(a)pyrene (Pott & Stöber, 1983)
(The Working Group noted the inadequate reporting of many experimental details in
relation to mortality and duration of the study.)

4. Other Data Relevant to an Evaluation of earcinogenicity

and its Mechanisms

4.1 Absorption, distribution, rnetabolisrn and excretion

4.1.1 Humans
Studies of lung tissue from workers in carbon black factories have shown widespread
deposits of large amounts of carbon black (Rosmanith et aL., 1969; Beek et aL., 1985).
(No quantification of data were given.)
Five nonsmoking warehouse packers in a furnace black manufacturing plant were
examined for exposure to dust, the level of which was assessed by air sampling and from
the urinary excretion of I-hydroxypyrene (derived from pyrene) in post-shift urine for
five consecutive days during one work week. The average dust concentrations over the
five days ranged from 1.53 to 13.21 mg/m). The average urinary excretion of I-hydroxy-
pyrene was 0.103-0.475 i.mol/mol creatinine. The urinary excretion was lower on
Mondays than on the other days. The authors concluded that urinary excretion was
affected by dust exposure, and that the pyrene on the dust was bioavailable (Gardiner
992b ). (The Working Group noted the pyrene content of the carbon black was not
et aL., 1

measured. )

4.1.2 ExperImental systems

(a) KInetIcs
Several review articles, mostly focusing on particulate toxicity and carcinogenicity
have also described the retention kinetics of particles (including carbon black) after their
deposition in the lungs of experimental animaIs (Morrow, 1988; Snipes, 1989; Kreyling,
1990; Morrow, 1992; Muhle et al., 1994; Oberdörster, 1995).
Anumber of studies, summarized in Tables 26-33, using intratracheal instillation and
inhalation in mice and rats evaluated the retention kinetics of different carbon black
materials after deposition into the lung. Bowden and Adamson (1984) instilled 4 mg of
 204 lARC MONOGRAPHS VOLUME 65

colIoidal carbon (primary particle size, 30 nm diameter) into the trachea of Swiss mice
and followed its clearance in groups of three mice kilIed at intervals over a six-month
period. They reported that most of the carbon black was cleared via the mucociliary
escalator, but some transepithelial passage via type 1 cells occurred as weIL. Heavily
laden alveolar macrophages stayed in the lung for the whole observation period and there
was sorne, although low, clearance via the lymphatic system. No quantitation of the
results was reported.
Several groups evaluated the retention kinetics of Inhaled carbon black in the lungs of
rats. Lee et al. (1987) and Strom et al. CI 989) used two different furnace blacks
(RCF (regular colour furnace)-7 and Elftex 12), which were inhaled in who
le-body
exposure chambers for 20 h per day on seven days a week for one to 11 weeks (for
details, see Table 26). The MMADs were 0.22 and 0.24 ~m, respectively. Both studies
on half-life with increasing lung burdens. Lee
found a significantly prolonged retenti

et al. (1987) determined the retention kinetics of subsequently administered 14C-diesel

particles and found that pulmonary half-life (ty) increased with increasing lung burden.
Strom et al. (1989) determined carbon black lung burdens and lymph nodal burdens of
carbon black. Lung burdens of 1.1, 3.5 and 5.9 mg carbon black were achieved after one,
three and six weeks' exposure, respectively; the one-year retenti
on fractions were 8, 46
and 61 % of the lung burden at the end of the exposure periods, respectively. Addi-
tionalIy, carbon black was retained in the regional thoracic lymph nodes at 1,21 and27%
of the initial lung burden, respectively. The authors concluded from their results that a
carbon black lung (macrophage compartment) burden in the rat of -0.8 mg results in a
doubling of the normal retenti on half-time of about 50 days.
Muhle et al. (1990) confirmed these results in an inhalation study using Wistar rats.
These inhaled furnace black (Printex 90) of a particle size of 0.64 ~m MMAD. The
inhalation was for 95 h per week at a concentration of 7.4 :: 1.5 mg/m3 for a total of 4.5
months. The retained carbon black at the end of exposure amounted to 13.7 :: 2.0 mg.
The retenti on ty, of subsequently inhaled 85Sr-labelIed polystyrene test particles was 472
days in these rats compared with 61 days in air con
troIs. The carbon black data fitted
weIl into the retention kinetic data obtained with other low-toxicity, low-solubility
particles and the authors concluded that a rat lung burden of -0.5 mg of such particles,
including carbon black, resulted in a prolongation of retention half-time. This
quantitative relationship is similar to that observed with other particulate materials.
Another study by the sa me group (Creutzenberg et aL., 1990; Muhle et aL., 1994) used
the same carbon black material (Printex 90); in a whole-body exposure system, female
Wistar rats inhaled an average exposure concentration of 7.5 mg/m3 for up to four
months, then 12 mg/m3 for 19 h per day on five days a week for up to 24 months. At
three, six, 12, 18 and 24 months of exposure, the retention of carbon black was
determined as weIl as the influence of exposure to carbon black on the alveolar
macrophage-mediated clearance function in the lung. The carbon black lung burden
reached a level of 50.2 :: 10.9 mg at 18 months and the respective retention ty, for carbon
black was determined to be 550 days (95% CI, 322-1868 days) following terrination of
exposure. Test particle clearance of 59FezO, (0.35 ~m diameter) was significantly
prolonged with increasing carbon black exposure duration, with t~ ranging
Table 26. Kinetics of carbon black in experimental animaIs

Particle type Particle Species Route of Duration of study Findings Comments Reference
diameter (age and exposure and
and surface sex) dose/exposure
area concentration

Colloidal 30nm Swiss Intratracheal 6 months Most CB cleared via MC No quantitative Bowden &
carbon mouse instillation, escalator; sorne transepithelial results; findings Adamson
4 mg passage, very low Iymphatic based on qualitative (1984 )
clearance; heavily laden AM histological data
remained for months in lung
7Be-Iabelled 7Be activity was mainly
O.OI-I/lm Swiss Gavage, 7 mg 14 days Very small fraction LeFevre &
carbon (primary mouse confined to the gastrointestinal of CB may penetrate Joel (1986) (J
particles 37 nm) (4 weeks
and 18
tract; retained dose at 14 days: via Peyer' s patches ?~
(Elftex 8; young - 3.3 x 10-'%; old-
CO
fumace months; 8.4 x 10-'%; sorne activity in 0
black) female) non-intestinal tissue Z
CO
RCF-7 0.22 /lm Fischer Inhalation, 1-1 i weeks; followed Linear increase of CB lung Methodology for Lee et al. r'
(fumace MMAD 344 rat 20 h/day, by '4C-diesel exposure burden with exposure duration; determining t,o, is not (1987) ?
(J
black) 7 daysl week, for 45 min + 1 year
(primary
6.6 mg/m'
lung burden -30 mg; increased described adequately ;:
37 nm) observation CB and '4C-diesel pulmonary t'J'
with increasing lung burden
Elftex 12 0.24 /lm Fischer Inhalation, l, 3, 6 weeks exposure, Lung burdens: 1.,3.5,5.9 mg Authors propose AM Strom et al.
(fumace MMAD 344 rat 20 h/day, followed CB; l-year retention: 8,46, sequestration model (1989)
black) 7 daysl week, by up to 1 year 61 %; LN burden: 1,21,27% of to explain retarded
7 mg/m' observation initial lung CB; doubling of CH clearance at
normal t'h of -50 days occurs at higher CH burden
CB lung burden of -0.8 mg
Printex 90 0.64 /lm Wistar rat Inhalation 4.5 months Retained CB: 13.7 mg; t'J' of Quantitati ve Muhle et al.
MMAD 95 h/week, 8'Sr-Iabelled test particles: 472
( fumace relationship observed ( 1 990)
black) (primary 7.4 mg/m' days; prolonged t'h at rat lung is similar to those of
14 nm) burden of -0.5 mg other low-toxicity
low-solubility
paricles
0VIN
 Table 26 (contd) 00\t'
Particle type Particle Species Route of Duration of study Findings Comments Reference
diameter (age and exposure and
and surface sex) dose/exposure
area concentration

Printex 90 0.64¡.m Wistar rat Inhalation 24 months for CB; CB lung burden: 50.2 mg; CB No data are provided Creutzenberg
( furnace MMAD (female) 19 h/day, 3, 12, 18 months for t,,,, 550 days; 59Fe,O, t,,,, 244-591 to demonstrate lower et al. (1990);
59Fe,O, and 85Sr_poly_
black) 5 days/week, days; 85Sr t'M 472 days at 3 alveolar deposition of Muhle et al.
12 mg/mJ styrene particles months then back to normal t'l'
of 50-60 days
85Sr particles at high

lung burdens
(1994 ) -
~
Fischer Inhalation 16 h/day, 7 days/week; Pulmonary retention half-life ;;
Elftex 12

(furnace
2-2.4 ¡.m
MMAD 344 rat 3.5 mg/m3 6 h/day, 5 days/week; t'h not different for different
Henderson n
et aL. (1992)
3:
black) (large mode) 98 mg/mJ 4 h/day, 1 day/week; exposure rates; average t'l' -520 0
0.02-0.1 ¡.m 12 weeks exposure days (95% CI, 350-950) Z
0
DED (small
mode,
+ 24 weeks post-
exposure
a
;;
10-30% ) ~
'i
Elftex 12 20 ¡.m Fischer 2.5 mg/mJ 16 h/day, 5 days/week Double exponential clearance; Mauderly ::
C/
(furnace MMAD 344/N rat 6.5 mg/m' 24 months slow phase, no clearance in CB- et aL. (1994) ..
black) (large mode) exposed group compared to t'l' in 0l'
0.1 ¡.m controls of 1 13- 1 35 days
C
MMDD 3:
(small t'
mode, 33%)
0\
VI
43 m2/g
Printex 90 0.64¡.m Wistar rat 11.6 mg/m3 18 h/day, 5 days/week, CB accumulation kinetics test Heinrich
(furnace MM AD NMRI (average) 24 months (rat) + paricle clearance; CB et al. (1995)
. black) 227 m2/g mouse 6 months post-exposure accumulation in rat and mou se

13.5 months (mouse) + lung similar (at 1 year of

9.5 months post- exposure)
exposure

CB, carbon black; MC, mucociliary; LN, Iymph node; AM, alveolar macrophages; MMAD, mass. median aerodynamic diameter; t,,,, retentIon half-life; DED,
diffusion equivalent diameter
 CARBON BLACK 207

from 244 to 591 days, compared with 61-96 days in air controls. ln contrast, 85Sr-IabelIed
polystyrene microsphere (3.5 llm diameter) clearance showed only a prolonged retention
half-time after three months of exposure to carbon black with a retention t,i, of 472 days,
whereas at the 12- and 18-month exposure time points, the test particle clearance
returned to control values of about 50-60 days. The authors explained this by a change in
the deposition site of the lai'ger 85Sr-Iabelled polystyrene microspheres due to altered lung
architecture (in response to carbon black-induced inflammation and other changes) and
breathing pattern. (The W orking Group noted that this seems to be a reasonable
explanation, especially in view of the increase in lung weight due to inflammatory
responses after the heavy exposure to carbon black particles of 1.7-fold and six-fold at
three and 12 months, respectively. However,no data were provided to ilustrate the lower
alveolar deposition of 85Sr-labelled test particles.)
ln a study of chronic inhalation in Wistar rats and NMRI mice exposed to furnace
black (Printex 90; 11.6 mg/m3), the pulmonary particulate accumulation was measured
(Heinrich et al., 1995). The rats were exposed for 24 months and the mi ce for 13.5
months. Both rats and mice showed similar accumulation kinetics over the exposure
time; at one year of exposure, the normalized lung burden (mg/g of control lung) was
32 mg (rats) and 37 mg (mice). ln addition, rats showed significantly prolonged retention
of tracer particles compared to controls as early as at three months of exposure and which
persisted through 12 and 18 months of exposure and until three months after the
18 months' exposure (see Creutzenberg et al., 1990).
A study by Henderson et al. (1992) evaluated the pulmonary retention of furnace
black (Elftex 12) inhaled at three different dose rates such that the product of
concentration x time was very similar (392 mg x h/m3 per week). Lung burdens ranged
between 3 and 4 mg. The retention ty, determined over a 24-week post-exposure period
was not statistically significant between the different groups and was reported as ~520
days with a 95% CI of 350-950 days.
Mauderley et al. (1994) studied the retention of tracer doses of CBe )-furnace black
(Elftex 12) in rats at three and 18 months of chronic exposure to two concentrations of
unlabelIed carbon black (2.5 mg/m3 and 6.5 mg/m\ Clearance of the labelled carbon
black folIowed a two-exponential model with about 50% of it cleared in control animaIs
with retention tyis of 14 and 19 days and in the exposed rats between 14 and 40% cleared
on tv,s ranging between four and 10 days. The most striking differences were
with retenti

found in the slow-phase clearance components, which showed little or no clearance over
a time period of 126 days for the low- and high-dose groups compared to retention t,lis of
113 and 135 days for control rats.
ln an attempt to determine the translocation of carbon black particles after gastric
administration, LeFevre and Joel (1986) gavaged four-week-old and 18-month-old
female Swiss mice with 7 mg 7Be-labelIed furnace black particles (Elftex 8). They then
determined the isotope distribution at 4 h and one, two, five and 14 days later; they
concluded from their findings that there is uptake and distribution from the gut and that
transit is more rapid in young mice. Peyer' s patches of older mi ce take up more carbon
than those of younger mice.
 208 IARC MONOGRAPHS VOLUME 65

OveralI, these studies demonstrate that exposures to carbon black that'achieve lung
burdens exceeding about 0.5-1 mg/g rat lung result in significant prolongation of the
retention t,i, of carbon black in the lung and, moreover, affect the clearance function of
alveolar macrophages for other particulate material. This is in agreement with the
concept of partic1e lung overload (see review, Morrow 1988), which is defined as a
significant impairment of the alveolar macrophage-mediated partic1e clearance function
due to high loading of alveolar macrophages with low-toxicity, low-solubility particles.
The only study comparing the kinetics of inhaled carbon black in rats and mi
ce found
that the pulmonary accumulation was similar in both species leading to a condition of
particle overload. There are no kinetic data on sex differences in rats or differences in
other species.

(b) Kinetics of carbon black adsorbed material

Con cern had been raised in the past that material, inc1uding carcinogenic compounds,
adsorbed onto carbon black partic1es will be retained longer in the lung upon inhalation
and will subsequently lead to a greater availability of carcinogens to target celIs in the
lung. ln particular, this would be of importance for materials such as diesel exhaust
particles which are known to contain P AHs adsorbed onto a carbon core and which have
been thought to contribute to a carcinogenic response of inhaled diesel exhaust. The
studies considered are summarized in Table 27.
Pylev et al. (l970a,b) used intratracheal instillation of CH)-benzo(a )pyrene adsorbed
onto furnace black partic1es (26-160 nm) and followed retention of radioacti vit
Y for
21 days in Syrian hamsters. Compared to CH)-benzo(a)pyrene suspended in aminosol
vitrum, retention of CH)-benzo(a)pyrene was longer when adsorbed onto carbon black.
Male Fischer 344/Crl rats were exposed by inhalation to Elftex 12 (furnace black;
primary particle size, 37 nm; surface area, 43 m2/g) for 30 days with an adsorbed
(3,4,9,10-'4C)-I-nitropyrene (Wolff et al., 1989) or (7-'4C)benzo(a)pyrene (Sun et al.,
1989). A total concentration of 100 mg/m3 was used with either 2 mg/m3 I-nitropyrene
added or 0.2, 2 or 20% benzo(a)pyrene. The investigators found that the long-term
retention of radioactivity from both I-nitropyrene and benzo(a)pyrene increased when
adsorbed onto carbon black. For both adsorbed compounds, a biphasic clearance was
found with most being cleared from the lungs within one to two days. At aIl time points,
16-60 times more radioactivity was retained after dosing the adsorbed compounds
compared to administration of the p'ure compound. Covalent interaction of these
compounds with lung macromolecules was also higher when they were co-administered
with carbon black partic1es.
These three studies demonstrate that carbon black administered to rat and hamster
lung either by inhalation or instilation can act asa carier of adsorbed material which
subsequently is c1eared much more slowly than thecompound given without carbon
black adsorption.
Table 27. Kinetics and effects of carbon black adsorbed cornpounds

Carbon black
characteristics

Furnace black
26-160 nm
-
Adsorbed
compound

('H)BaP
Test system

Intratracheal instillation,
Syrian hamster
Duration

21 days
End-points

Macrophage
response and
Findings

CB + BaP elicited more macro-

phages; longer BaP retention with
Reference

Pylev et al.
(1970a,b)
BaP retention CB than without
14(QBaP
Elftex 12 Inhalation; Fischer 2 h BaP lung Biphasic lung retention; long-term Sun et al. n
(furnace black) 344/N rat; 100 mg/m' exposure retention retention of BaP increased 16- (1989) ;i
¡:
37 nm; 43 m2/g mass with 0.2, 2 or (nose 60 times when coated onto CB; t;
20% BaP; BaP alone, 2, only) + more pronounced after instilation 0
Z
20 mg/m'; intratracheal 30 days compared to inhalation; covalent t;
instillation of 500 ~g interactions of BaP with lung l'
CB:t 10 or 100 ~g BaP macromolecules increased when n;i
administered as CB coating ~
14(Q_l_ Biphasic nitropyrene retention Wolff et al.
Elftex 12 Inhalation; Fischer 2 h Nitropyrene
(furnace black) Nitropyrene 344/N rat; 98 mg/m' CB exposure lung retention increased when adsorbed to CB; ( 1989)
?
37 nm; 43 m-/g + 2 mg/m3 nitropyrene; (nose nItropyrene covalently bound to
nitropyrene alone only) + macromo1ecules was 10-fold
30 days greater at 30 days when inhaled
adsorbed compared to nitropyrene
alone

BaP, benzo(a)pyrene; CB, carbon black

oIV
\0
210 lARC MONOGRAPHS VOLUME 65

4.1.3 Comparison between animaIs and humans

Although carbon black has been identified in humans, no quantitative data are
available on retention of carbon black in humans. However, based on studies with other
highly insoluble particulate materials, it can be assumed that the normal retention tYi in
humans is longer than that measured in rats by a factor of approximately 10. Thus, Bailey
et al. (1985) found that retention tyis of inhaled monodisperse 1 and 4 !-m diameter fused
aluminosilicate particles in humans ranged from ~ 200-700 days, depending on the time
after exposure, with an average of -500 days for most of the particles to be cleared, in
comparison to rat data (Muhle et al., 1990) which demonstrate a retention tYi of 61-
96 days. This presumes that the retention kinetics of different particles of low solubility
and low toxicity are the same, as has been demonstrated in rats. Normal pulmonary
retention t,/is for low-solubility, low-toxicity particles in mice have been reported as
-55 days (Kreyling, 1990).

Heavy exposure to carbon black in occupational settings may lead to high carbon
black burdens in the human lung. ln anal ogy to the rat, if this lung burden exceeds
-0.5 mg/g lung, it would be expected that the normal retenti
on half-life may be
prolonged. lndeed, there is sorne evidence showing that occupations leading to heavy
particulate loads of the lung (e.g. coal mining) show a prolonged clearance of the dust
from the alveolar space (Stober et al., 1965; Freedman & Robinson, 1988; Freedman
et al., 1988)

4.2 Toxic effects

4.2.1 Humans
Comprehensive reviews of the toxicity of carbon black to humans are available
(United States National lnstitute for Occupational Safety & Health, 1978; Rivin & Smith,
1982; IARC, 1984; Gardiner, 1995a).
Gärtner and Brauss (1951) first described radiological changes analogous to
pneumoconiosis in 31 workers in a carbon black factory. However, the
se individuals had
no functional lung abnormality. Since that time, a series of other reports have been
published on pneumoconiosis in carbon black workers.
ln 56 workers in two German carbon black factories (one produced carbon black from
oil that was burned with lightgas, the other from acetylene), two (both belonging to the
16 workers who had an exposure time exceeding 10 years) had chest X-ray changes,
compared to none among 52 controls (who had had radiographs taken without suspicion
of lung disease) (Mai, 1966). (The selection of workers is not clear, neither are the
criteria for diagnosis.)
ln a study by Valic et aL. (1975), respiratory function was measured in a group of 35
carbon black workers (average age, 38.8 years) and 35 controls matched for age, body
weight and smoking habits examined in 1964 and again in 1971. Measurements of
carbon black concentrations in the work environment showed that the respirable
concentration (mean, .( 1 !-m) was 7.2 mg/m3 in 1964 and 7.9 mg/m3 in 1971. By 1971,
 CARBON BLACK 21l

the average duration of exposure was 12.9 years and was more than 10 years for 26/35
workers. ln 1971, carbon black workers who smoked exhibited a reduced forced vital
capacity and a reduced forced expiratory volume compared with smoking controls. For
carbon black workers who did not smoke, there was no significant difference compared
with nonsmoking controls. However, for both smoking and non
smoking carbon black
workers, the annual declines in these parameters were three- to four fold greater than
expected. Radiological lung changes, characterized by slight interstitial fibrosis, were
found in 17.1 % of the workers. These lung changes progressed between 1964 and 1971.
(The selection of exposed and unexposed populations is unclear.)
ln a study on carbon black (furnace) workers, Cocarla et aL. (1976) found that 29
(20.3%) of 143 workers exposed for a me an of 19 years had pneumoconiosis, often
accompanied by generalized or local emphysema and disturbances of lung perfusion. ln
the same subpopulation, an increase in levels of serum immunoglobulin (Ig)A and a
decrease in IgM were observed. Measurements of air levels of carbon black were not
reported.
ln 125 carbon black-exposed workers in dry-cell battery and tyre manufacture (mean
exposure time of about five years), a reduction in pulmonary function and an increase in
respiratory symptoms were observed in comparison to 145 controls (healthy non-
industrially exposed men with a (sic) history of respiratory disease). The largest
reduction in lung function was observed in the group that had exposure to the highest
mean dust level (31 mg/m3) at the dry-celI battery factory. The most common respiratory
symptoms were cough with phlegm (28 and 22% in the battery and tyre factories,
respectively). Radiographs were reported to show no abnormality (Oleru et aL., 1983).
(Only a fraction of aIl workers was examined; the selection criteria are not clear. No
adjustment was made for smoking; however, only 12.8% of workers in the study group
were smokers.)
ln a Czech factory producing carbon black from anthracene, out of 12 workers
exposed for ? 15 years, one had chest radiographical findings consistent with pneu
mo-
coniosis. One additional worker, who had been exposed for 27 years and who had no
symptoms of respiratory disease or lung function disturbances, had fine, diffuse changes
in the chest radiogram; an open lung biopsy was taken from this worker. There was
heavy pigmentation of the lung surface. Histological examination revealed heavy
deposits of carbon black particles and slight, mainly reticular fibrosis with associated
emphysema (Rosmanith et al., 1969). (No information on exposure levels; selection of
the workers for examination is not clear, neither are the smoking habits.)
Beck et aL. (1985) studied X-radiographs of variolls thicknesses of carbon black
deposits. They concluded that radiographical changes in workers were due to tissue
reaction rather than to simple deposition. Further, the authors examined lung tissue from
two subjects (smoking not defined) with radiographical changes and found fibrous tissue
and emphysema around the carbon deposits. On the other hand, a biopsy from a worker
with generalized nodulation did not reveal fibrosis (Slepicka et aL., 1970).
ln a study of 83 currently exposed carbon black workers (at least two years' exposure)
and 144 controls, the current workers had statisticalIy significantly higher prevalences
 212 IARC MONOGRAPHS VOLUME 65

th an the controls of the following: chronic bronchitis (60% versus 19%), 'obstructive
disturbance of ventilation' at spirometric examination (24% vers
us 6%) and nonspecific
bronchial hyper-reactivity on histamine test (28% versus 3%). ln a total of 83 currently
and 46 formerly exposed workers, 2.3% (average exposure time, 23.3 years) displayed
findings in chest radiograms suggesting pneumoconiosis and an additional 6.9% had
slighter changes. Data on dust exposure were not given (Kandt, 1985). (The type of
carbon black factory and the selection of workers and controls are not weIl described.)
ln 3027 carbon black workers (92.3% men, 7.7% women) employed in 19 plants
(mean employment time, 10.9 years), slight associations were found between prevalences
of chronic cough and sputum production and dust exposure, as assessed from job titles in
nonsmokers (39-49% in different exposure intensity categories). ln smokers, there was
no association. There were no data on dust levels. Further, spirometry indicated minor
exposure-associated reductions in the forced vital capacity and forced expiratory volume.
Moreover, routine chest radiographs, taken during the previous two years, of 935 of the
workers from 11 of the 19 plants where they could be obtained revealed six cases of a
simple type of pneumoconiosis (smoking status not stated), aIl belonging to the group of
396 workers who had been employed for more than 10 years (Crosbie, 1986). (A large
proportion of the radiographs was taken by the mass miniature technique, which is not
optimal for detection of minor changes.)
ln a multicentre European study, a population of 1742 employees (92% men, 8%
women in the original study base) in 15 carbon black factories were examined (mean
duration of employment 14.2 years). (Most of them were identical to those studied earlier
by Crosbie (1986).) ln a total of 1317 samples of total inhalable dust, the geometric me
an
level was 0.57 (geometric standard deviation, 4.0) mg/m3 and in 1298 respirable dust
samples the geometric mean level was 0.21 (2.7) mg/mJ. Associations were found
between frequencies of cough, sputum and symptoms of chronic bronchitis (mean pre-
valence, 10%) and current exposure. Forced vital capacity and forced expiratory volume
showed slight decreases with increasing dust exposure in both smokers and nonsmokers.
Chest radiographs could only be taken in 10 of the 15 plants, and they were taken for
1096 workers. Of the se, 24.4% showed smalI opacities (International Labour Organi-
zation category 0/1 or greater), with a strong association with rising cumulated exposure
(five categories). Preliminary analyses indicated associations between radiographical
findings and lung function (Gardiner et aL., 1993).
ln 913 employees of six carbon black producers, there was no consistent association
between forced vital capacity or forced expiratory volume (fractions of predicted values)
and cumulative dust exposure (range -( 50-2200 mg/m3 x months), when age and
smoking habits were taken into consideration. Information on exposure was obtained
from measurements made one year earlier in 24 plants (relation to the population studied
for health effects unc1ear). Some 1500 total dust samples obtained by personal moni-
toring showed geometric me an time-weighted average levels ranging from 0 to
2.0 mg/mJ, with 76% below 1.0 mg/m3 (Robertson et aL., 1988). (Because of the lack of
occupational histories from several of the factories, there was a major loss of workers
(804) from the original study base (1717), and this might have affected the outcome. The
Working Group noted that the spirometry values had already been standardized by
 CARBON BLACK 213

comparison with referents to calculate their predicted percentage before being used again
in the age-specific two-way analysis of variance.)
Three years later, 697 (76%) of these workers were retested. The total group showed
smalI, statisticalIy nonsignificant increases in forced vital capacity and forced expiratory
volume. The author states that the most likely explanation for those findings is the varia-
bility of lung function testing (Robertson, 1996).
ln a cross-sectional study, chest radiograms were taken for 507 predominantly male
workers in a German carbon black factory. The average duration of employment was
given as approximately 25 years. Of the radiograms, 75.5% were cIassified as Interna-
tional Labour Organization (ILO) category 0/0, i 3.0% as 0/1, 8.9% as 1/0, 2.4% as 1/1
and 0.2% as 2/1. The authors ascribed the findings in the latter two categories to two
cases of silicosis unrelated to exposure to carbon black and to prevalent smoking (70%
smokers or ex-smokers) (Küpper et al., 1994a,b).
ln the same factory, lung function (body plethysmography, including measurements
after inhalation of a single concentration of methacholine) was investigated in 578
carbon black-exposed and 99 unexposed workers. The fine dust concentration was 0.01-
9.14 mg/m" (total dust, 1.08-19.95 mg/m"' The duration of exposure was not stated, but
the average 'dust-years' (dust exposure times duration of exposure) were 11.3 in non-
smokers, 21.5 in ex-smokers and 16.3 in smokers. ln multiple linear regression analysis
(alIowing for age), exposure to carbon black had a significant effect on deterioration of
lung function in the nonsmoking group only. Thus, there was a significant decrease in
airway resistance(which, however, was dependent on two extreme values) and expi-
ratory flow. However, in the smokers' group, pathological findings (as compared to
expected values in reference populations) in airway resistance were more frequent among
the carbon black-exposed workers th
an in the unexposed controls. There was no signi-
ficant association between bronchial hyper-reactivity and exposure to carbon black
(Küpper et al., 1996).
ln a case-control study of employees of seven carbon black producers in the United
States, workers who had submitted medical insurance cIaims with diagnoses of selected
diseases of the respiratory and circulatory systems were individually matched for age and
year of service with undiseased co-workers. Individual cumulative total dust exposures
for cases and controls were estimated. Cases with a disease of the respiratory system (27
pairs) had a nonsignificantly higher cumulative total dust exposure than did the controls;
cases with diseases of the circulatory system (48 pairs) had significantly lower
cumulative total dust exposure than the controls (Robertson & Ingalls, 1989).
Among other effects of exposure to carbon black (lampblack), dermatologicallesions,
such as the presence of carbon black 'tattoos' on hands and forearms, as weIl as follicular
blackheads containing carbon black on uncovered skin surfaces, have been reported
(Capusan & Mauksch, 1969). A brownish discoloration of the conjunctiva has occurred
after long-term use of eye-liner containing carbon black, with accumulation of pigment
in the tissues (Sugar & Kobernick, 1966; Haddad & Zehetbauer, 1980).
ln a study of 58 current and 35 former male workers (at least two years of exposure)
1
in a carbon black factory (channel black) and 60 controls, the currently exposed workers
214 IARC MONOGRAPHS VOLUME 65

had a significantly higher prevalence of nasal complaints (including hyposmia) th an

either former workers or controls. Moreover, rhinoscopy revealed mucosal findings in
27% of the currently exposed workers versus only 9% of the controls. However, X-rays
of the paranasal sinuses and cytology of nasal secretions did not reveal differences. The
total dust concentration ranged from 9.0 to 13.35 mg/m' in the machine room and from
4.4 to 8.2 mg/m' in the operators' room (Kandt & Biendara, 1985).

4.2.2 Experimental systems

(a) Inhalation studies

A number of inhalation studies discussed in the following paragraphs are summarized
in Table 28.
An early study by Snow (1970) showed that inhalation of thermal black with a
particle diameter of -0.15-0.2 llm and a surface area ofbetween 10 and 15 m2/g resulted
in oedema of the laryngeal folds in Syrian hamsters exposed for 6 h per day on five days
per week for a total of 53 and 172 days to a concentration of 105 mg/m'and for 236 days
to a concentration of 56 mg/m' (see Table 28). Evaluation was limited to the larynx and
trachea and consequendy no effects on the lower respiratory tract were reported.
ln another early study by Rhoades (1972), Long-Evans rats were exposed to gas
channel black with a mass median diameter of 2.2 llm at a concentration of 4 mg/m'
continuously for 16 days. The focus here was on the surfactant system, and findings of
alveolar thickening and atelectasis were reported but no further effect related to
surfactant. (The Working Group noted the lack of detail in the reporting of lung damage.)
Nau et aL. (1976) exposed rhesus monkeys, Syrian hamsters and guinea-pigs to
thermal black at a concentration of 53 mg/m' for 6 h per day on six days per week; the
rodents were exposed for a total of 236 days and the monkeys for three years. No
significant change in the lung was found in guinea-pigs despite the high concentration
and long duration of exposure and no finding was given for the hamster lung. ln
monkeys, particles were adsorbed in regional lymph nodes and a moderate to severe
emphysematous response with massive particle accumulation was observed in the lung.
The investigators also reported right hypertrophy of the ventricular septum and, to a
degree, of the left ventric1e in the exposed monkeys. (The reporting of the findings was
inadequate and no determination of the lung dose was made.)
Fenters et al. (1979) exposed CD-l mice to a concentration of 1.5 mg/m' (0.3 llm
MMAD) Sterling MT CT-6729 medium thermal black by inhalation for 3 h per day on
five days per week for a total of four, 12 and 20 weeks. A chalIenge with virus and
bacteria was included and it was found that there was decreased resistance to these
infections, as seen by a reduced bactericidal capacity in the lung. They also observed
morphological changes in the conducting airways and alveoli by scanning electron
microscopy. (Alterations in immune responses using a plaque-forming assay were
inconsistent, and no lung dose was reported.)
Wright (1986) found no increased type II celI proliferation after exposure of Fischer
344 rats to a concentration of 6.1 mg/m'of an unspecified carbon black (MMAD,
0.22 llm) for 20 h per day on seven days a week for 14 days (no lung burden data given).
Table 28. Non-neoplastic effects of carbon black in inhalation studies in experimental animaIs
Parti cIe Particle Species Exposure Duration of study End-points Findings Comments Reference
type diameter (age and concentration
and surface sex)
area

Thermal 0.15-0.2 Syrian -56 mg/m' 6 h/day, Histology of Oedema of laryngeal folds; Study limited to Snow
,
black Ilm, hamster - lOS mg/m 5 days/week, 53 larynx and retention of tracheal and larynx and trachea (1970)
10-15 m'/g and 172 days trachea subglottic glands of amorphous
(high), 236 days eosinophilic material; no
(low) morphological changes
Gas 2.2 Ilm Long- 4 mg/m
.'
16 days Surfactant Alveolar thickening, atelectasis; No lung dose; poor Rhoades n
channel MMD Evans properties no surfactant effects ;J
black rats
(continuous) reporting of lung (1972) ~
damage CO

Thermal Rhesus 53 mg/m' Monkey: particles in the Iymph;

0
6 h/day, Histology of Inadequate Nau et al. Z
black monkey, 6 days/week, lung and heart; moderate to severe reporting of (1976) CO
C3H 236 days pulmonary emphysematous lesions; massive findings; high l'
;J
mou se, (rodents), function particle accumulation; ventricular concentration n
hamster, 3 years (monkey) (monkey) hypertrophy; guinea-pig: no ;;
guinea- significant lung changes
pig
,
Sterling 0.3 Ilm CD-I 1.5 mg/m 3 h/day, Immune Decreased resistance to infection; Changes in immune Fenters
MT MMAD mouse 5 days/week, response; bactericidal capacity in lung response were et al. (1979)
CT-6729 4, 12, 20 weeks infectivity reduced; SEM changes in inconsistent
(medium challenge conducting airways and alveoli (plaque-forming
thermal (virus and assay); no lung dose
bJack) bacteria) reported
,
Carbon 0.22 Ilm Fischer 6.1 mg/m 20 h/day, Cell Type II cell proliferation Lung burden not Wright
black MMAD 344 rat 7 days/week up to proliferation increased after diesel exhaust or determined (1986)
(unspeci- 14 days NO, but not after CB
fied)

N
..
VI
Table 28 (contd)

ParticIe ParticIe Species Exposure Duration of study End-points Findings Comments Reference
type diameter (age and concentration
and surface sex)
area

Printex 90 0.64 /lm Wistar rat 6 mg/rn

)
18h/day, Histopatho- Hyperplastic bronchiolar Focus is on cellular Nolte et al.
(fumace MM AD 5 days/week, logy; focus on
black) 227 m2/g 10 months + hyperplasia
epithelium, metaplasia,
inflammation, alveolar
changes rather than (1994 ) \.
CB specifie effects; ;¡
(i: pyro- 20 months post- and metaplasia histiocytosis, alveolar no cIear distinction ¡c
lyzed CO

pitch)
exposure Iipoproteinosis was made between 0Z
effects of CB and
pitch to
Regal GR 2.4 /lm Swiss 10 mg/m , 4 h/day, 4 days +
l'
Infecti vit No effect of CB alone on integrity Short exposure Jakab ;¡
(fumace MMAD, mouse 7 days model,
y

of lung defences against bacterial duration; no lung

\.
black) 88 m2/g (5 weeks; observation bacterial and and viral challenge; no pulmonary
(1993 ) ~
burden data
(96.9% female) viral challange inflammation by BAL; co-
carbon) the day exposure to 2.5 ppm acrolein
following impaired aIl defences
exposure
Regal GR 2.4 /lm Swiss 10 mg/m' 4 h, 24 h post- BAL analysis No change from controls; co- Exposure duration Jakab &
(fumace MMAD, mouse exposure and AM exposure to 1.5 ppm 0, showed short Hemenway
black) 88 m2/g (5 weeks; phagocytosis significant inflammation and (1994 )
female) suppression of phagocytosis

N
..
-.
Table 28 (contd)

Particle Paricle Species Exposure Duration of study End-points Findings Comments Reference
type diameter (age and concentration
and surface sex)
area

Monarch 0.88 ¡.m Fischer 1.1,7.1,52.8 6 h/day, BAL Lung burdens, 0.35, 1.8 and Driscoll
880 MMAD 344 rat mg/m' 5 days/week, for parameters; 7.8 mg; no change in any et al. (1996)
( furnace (16 nm 13 weeks cell prolifera- parameter at lowest concentration;
black) primary exposure; tion; histo- dose-related increase at middle
particle) 3 months and pathology; and high dose in cellular and
220 m2/g 8 months post- dosimetry biochemicallavage parameters;
exposure dose-related increase in alveolar n
cell proliferation ;i
;:
Printex 90 0.64 ¡.m Wistar rat 1 1.6 mg/m' Rats: Histopatho- Rats: body weights decreased, Responses were Heinrich t:
( furnace MMAD (female) (average) 18 h/day, logy; lung lung weight increased; lung very similar in both et al. (1995)
o
black) NMRI 5 days/week,
Z
227 m2/g clearance; burden, 44 mg; LN, 6.7 mg; species compared to t:
mou se 24 months + dosimetry impaired lung clearance; BAL: concurrently run l'
(female) 6 months post- cellular and biochemical diesel exhaust and n;i
exposure parameters increased; moderate to ultrafine titanium ;;
high-grade bronchiolar/alveolar dioxide
hyperplasia; slight to moderate
interstitial fibrosis
Mice: Mice: body weights decreased,
18 h/day, lung weights increased; lung
5 days/week burden, 7.4 mg (37 mg/g control
13.5 months lung, similar to rat)
+ 9.5 months
post -exposure

MMD, mass median diameter; MMAD, mass median aerodynamic diameter; SEM, scanning electron microscopie; CB, carbon black; MMDD, mass median diffusion
diameter; PMN, polymorphonuclear neutrophils; BAL, bronchoalveolar; c x t, concentration x time; LDH, lactate dehydrogenase; BaP, benzo(a)pyrene; AM, alveolar
macrophages; LN, Iymph no de

..N
\0
220 IARC MONOGRAPHS VOLUME 65

More detailed characterizations of pulmonary responses to carbon black were

reported by Wolff et aL. (1990) and Henderson et al. (1992). Elftex 12 (ftlrnace black)
was aerosolized to give a large and small mode particle size distribution with a MMAD
of 2 /-m and mass median diffusive diameter (MMDD) of 0.02-0.12 /-m. ln the study by
Wolff et aL. (1990) an exposure concentration of 10 mg/m3 was delivered to 14-15-week-
old male Fischer 344/N rats for 7 h per day on five days per week for a total of 12 weeks.
At a carbon black lung burden of 2.2 mg, it was found that 12% of the lavageable cells
consisted of polymorphonucIear neutrophils. Aggregates of macrophages engorged with
carbon black were found in the terminal bronchioles and alveolar ducts, and type II cell
hyperplasia was also observed. Concurrently tested diesel exhaust particIes showed very
similar effects.
ln the study by Henderson et al. (1992), the aim was to expose the rats to a different
dose rate such that the product of concentration x time was very similar. Thus, 11-15-
week-old female Fischer 344/N rats were exposed to concentrations of 3.5 mg/m3 for
16 h per day on seven days a week, 13 mg/m3 for 6 h per day on five days a week and
98 mg/m3 for 4 h on one day per week. Each exposure lasted for a total period of 12
weeks, followed by a 24-week post-exposure period. Resulting lung burdens ranged
between 3 and 4 mg. ln spite of the different exposure rates, the cellular and biochemical
parameters of bronchoalveolar lavage fluid increased to the same degree. ln aIl exposure
groups, a slight thickening of alveolar septa with hypertrophic epithelial cells was found
and lung weights were significantly increased. The authors concluded that the exposure
rate over this range does not influence resulting toxic effects of inhaled carbon black in
the lungso

Histological and morphological end-points were evaluated in a study by Nolte et aL.

(1993, 1994) following inhalation of Printex 90 (furnace black) by Wistar rats with or
without the addition of pyrolyzed pitch and irritant gases such as nitrogen dioxide. The
exposure concentration was 6 mg/m3 for 18 h per day on five days per week for a total of
10 months with a 20-month post-exposure observation period. Findings were squamous
metaplasia and squamous differentiation of type II cells, which was considered to be a
precursor stage of the squamous metaplasia in this rat model of particle inhalation.
However, it was difficult to differentiate the results due to exposure to carbon black only
from those of chanOges induced by the combination of carbon black and pitch. (The
Working Group noted the poor reporting of exposure concentration, exposure details and
results specific to carbon black.)
Jakab (1993) determined the ii;fluence of carbon black inhalation on the resistance of
mice to a bacterial and viral challenge one day after exposure. Five-week-old female
Swiss mi ce were exposed to 10 mg/m3 Regal GR (furnace black) (particle size, 2.4 :t
2.75/-m MMAD) for 4 h per day for a total of four days followed by a seven-day
observation period. Carbon black alone had no effect on the integrity of lung defences
against the bacterial and viral challenges and no pulmonary inflammatory response was
detected in parameters of bronchoalveolar lavage fluid. ln contras
t, co-exposure to
2.5 ppm (5.7 mg/m3) acrolein resulted in an impairment of the measured lung defence
parameters (total and differential cell counts and albumin levels)o This change in biolo-
gical effect was not observed with acrolein alone. (The W orking Group noted the rela-
 CARBON BLACK 221

tively short duration of exposure to carbon black by inhalation. No lung burden data were
reported. )
ln an effort to determine the effect of exposure to carbon black in combination with
ozone on alveolar macrophage phagocytosis, Jakab and Hemenway (1994) exposed five-
week-old female Swiss mice to 10 mg/m-i Regal GR (furnace black) (MMAD, 2.4 =t
2.75 ¡.m) for 4 h. Analysis of bronchoalveolar lavage fluid 24 h later showed that there
was no change in comparison to contraIs in animaIs exposed to carbon black only, and
alveolar macrophage phagocytosis was not affected. Exposure to ozone alone caused
significant changes in these parameters. (The W orking Group noted that the exposure
duration was rather short to see a significant effect of carbon black on the end-points
studied.)
A detailed study comparing exposures to carbon black and diesel exhaust particles
was reported by Mauderly et aL. (1994) and Nikula et al. (1995). Male and female
Fischer 344 rats were exposed to 2.5 mg/m-i and 6.5 mg/m3 Elftex 12 (furnace black) for
16 h per day on five days per week for a total of 24 months. Three males and three
females each were sacrificed at three, six, 12, 18 and 23 months of exposure for
evaluation of lung burden and lymph node burdens, histopathology, bronchoalveolar
parameters and clearance of test particles. Particle size measurements resulted in a
bimodal distribution with 2.0 ¡.m MMAD for the large fraction, measured by a cascade
impactor, and 0.1 ¡.m MMDD for the smalI fraction, measured by parallel-flow diffusion
battery (33%). Results showed a reduction in body weight at a finallung burden of 21.0
and 38.5 mg carbon black in the two exposure groups. Significant accumulation of
carbon black with time occurred in the lymph nodes, and there was a dose-related
increase in lung weight. Polymorphonuclear neutrophils and biochemical (protein, lactate
dehydrogenase, ß-glucuronidase) parameters of bronchoalveolar lavage fluid showed
significant dose-dependent increases. Table 29 lists the occurrence of these and other
non-neoplastic lung lesions found in the carbon black-exposed rats before and after
18 months of exposure. For most of the end-points examined, no significant difference in
severity or incidence was observed between female and male rats. However, chronic
active inflammation, alveolar proteinosis and bronchiolar/alveolar metaplasia occurred
consistently with greater incidences and somewhat greater severity in females compared
to males. Alveolar hyperplasia and squamous cysts were also found. Even at the low-
exposure level, alveolar epithelial hyperplasia was observed in 4/6 rats after three months
and 6/6 rats after six months of exposure. Bronchiolar/alveolar metaplasia was first
observed in the high-dose group after 12 months of exposure (2/6 rats) and was present
in 18/18 rats of this group and 22/24 rats of the low-dose group killed after either
23 months of exposure or after an additional six weeks without exposure. A total of
12 rats with squamous cysts were observed, 10 of which were in the group kept the
additional six weeks without exposure. None of 19 squamous cysts increased in size after
implantation into athymic mice, compared with 1/2 squamous-cell carcinomas and
2/8 lung adenocarcinomas. When 7Be carbon black partic1es were administered at three
and 18 months of exposure, significant retardation of theit respective lung clearance was
observed which increased with duration of exposure. Moreover, inhalation of fluo-
rescent-labelIed microspheres at three and 18 months of exposure caused significant
 N
N
N

Table 29. Percentages (and severity scores) of rats dying, euthanized or sacrifced that had non-neoplastic lung lesions during a two-year exposure to carbon black (CB)"b

Lesion Female rats

Control Low CB (2.5 mg/m') High CB (6 mg/m')

Male rats

Control Low CB (2.5 mg/m') High CB (6 mg/m')

-;p
::
.e 18 ;: 18 .e 18 ;: 18 .e 18 ;: 18 .e 18 ;: 18 .e 18 ;: 18 .e 18 ;: 18 (J
months months months months months months months months months months months months ~
0
o (0-0) i 00 (1-3) 100 (2-4) Z
Alveolar macrophage o (0-0) 4 (0-1) 100 (1-3) 100 (2-4) 96 (0-4) 100 (3-4) 30 (0-2) 100 (1-3) 100 (2-4)
0
hyperplasia Ci
Alveolar epithelial o (0-0) 9 (0-2) 90 (0-3) 100 (1-4) 93 (0-4) 100 (2-4) 9 (0-0) 2 (0-2) 98 (0-4) 100 (1-3) 100 (1-4) 100 (1-4) ::
;p
hyperplasia 'i
Chronic active inflammation o (0-0) 5 (0-1) 24 (0-2) 34 (0-2) 37(0-3) 63 (0-2) o (0-0) i (0-3) 9 (0-2) 14 (0-2) 20 (0-2) 34(0-3) ::
C/
78(0-3) 3 (0-1) 1 (0-1) 61 (0-3) 92 (0-3) 75 (0-4) 99 (0-4)
Septal fibrosis o (0-0) 2 (0-1) 52 (0-3) 96 (0-3) 100 (1-4)
~
Alveolar proteinosis o (0-0) 1 (0-2) 29 (0-2) 66 (0-3) 52 (0-3) 97 (0-4) o (0-0) o (0-0) 2 (0- 1) 15 (0-1) 25 (0-2)
2 (0-2)
66 (0-4)
0r'
o (0-0) o (0-0) a (0-0) 17(0-4) 7 (0-2) 31 (0-3) a (0-0) a (0-0) 0(0-0) 6 (0-2) 25 (0-3)
Focal fibrosis with epithelial C
hyperplasia
o (0-0) o (0-0) 2,(0-1) i (0-1) 2 (0-3) 3 (0-2) ~
Squamous metaplasia o (0-'0) o (0-0) 0(0-0) 6 (0-2) o (0-0) 24 (0-3) m
23 91 21 95 27 87 32 86 44 71 44 71 0'
Number of rats Ui

From Nikula et al. (1995)

U Animais dying, euthanized or sacrificed before and after 18 months of exposure were pooled
"Severity scores range from 1 to 4, with 4 being the most severe effect/lesion
 CARBON BLACK 223

sequestration of the se particles in aggregated alveolar macrophages in the alveolar space

as weIl as in the pulmonary interstitium, and this increased wIth exposure time and
exposure concentration. Thus, at 18 months of exposure, both the low-dose and high-
dose carbon black-exposed groups exhibited -50% of the fluorescent microspheres in
aggregated macrophages in the alveolar parenchyma. AIl of these results were nearly
identical to those of comparison groups exposed concurrently to the same concentration
of diesel exhaust.

A number of studies performed at the Fraunhofer InstItute (Hannover, Germany)

focused on histopathological events after exposure to carbon black, as weIl as inflam-
matory responses and parameters of lung clearance. The carbon black material used was
Printex 90 (furnace black) with a surface area of 227 m"/g; the aerosolized particles had
an MMAD of 0.64 llm. Heinrich et al. (1995) reported results in female Wistar rats and
female NMRI mice exposed to an average concentration of 11.6 :: 1.9 mg/m3 Printex 90
for 18 h per day on five days per week for a total of 24 months (in rats) with an
addition sure period, or 13.5 months (in mice) with an additional
al six-month post-ex po

9.5-month post-exposure time. Findings included decreased body weight and pro-
gressively increasing lung weight in rats, first measured at three months, with a lung
burden (not contributing to lung weight) of 44 mg carbon black per lung at the 24-month
time point. Carbon black (6.7 mg) was found in the lung-associated lymph nodes, and
impaired lung clearance of test particles 'was found during this study (see Muhle et aL.,
1994). Significant increases in cellular and biochemical parameters of lung lavage were
also observed. Histologically, moderate to high-grade bronchiolar/alveolar hyperplasia
and slight to moderate interstitial fibrosis were observed in addition to significant
findings of lung tumours which are reported in the previous section.

ln mice, there was also a decrease in body weight and an increase in lung weight at a
lung burden of 7.4 mg at 12 months of exposure. This lung burden, when normalized to a
controllung, corresponded to 37 mg carbon black/g controllung which was similar to the
normalized rat lung burden of carbon black of 32 mg/g control lung. No detailed des-
cription of nonneoplastic histological changes in the lungs of mice was provided,
although there was elevated mortality during exposure in this and, more so, in other
groups so that the planned 18-month exposure duration had to be shortened to
13.5 months. Overall, responses found in rats and mice exposed to carbon black were
very similar to the responses in the respective groups of animaIs concurrently exposed to
diesel exhaust or ultrafine titanium dioxide particles (Heinrich et aL., 1995).

Dungworth et aL. (1994) gave a more detailed description of effects induced in female
Wistar rats by inhalation of 6 mg/m3 carbon black for 17 h per day on five days a week
for 10 months with a subsequent 20-month post-exposure period (72 rats) or inhalation
for 20 months with a subsequent 10-month post-exposure period (72 rats). Another group
(100 rats) was exposed to 11.3 mg/m3 for 18 h per day on five days a week for a total of
24 months with up to a six-month post-exposure period. Findings were chronic active
inflammation, including bronchiolar/alveolar hyperplasia, alveolar histiocytosis, lipo-
proteinosis and squamous metaplasia (probably originating from type II celIs).
224 IARC MONOGRAPHS VOLUME 65

Nolte et al. (1994) also reported results after exposure of Wistar rats to 6 mg/m3 of
this same material for 18 h per day on five days a week for a total of 10 months with an
additional 20-month post-exposure period. As in the study described previously (Nolte
et al., 1993), a clear distinction in their reporting was not drawn between those effects
found in animaIs exposed to carbon black only and those found in animaIs that were co-
exposed to carbon black and pyrolyzed pitch - the focus of this study was on celIular
changes and cell dynamics. Thus, the y reported hyperplastic bronchiolar epithelium and
metaplasia as weIl as inflammatory responses including alveolar histiocytosis and
alveolar lipoproteinosis.
A subchronic inhalation study with Monarch 880 (furnace black) was performed in
Fischer 344 rats exposed to 1.1, 7.1 and 52.8 mg/m' for 6 h per day on five days a week
for a total of 13 weeks with an eight-month post-exposure period (DriscolI et al., 1996).
The MMAD of the carbon black aerosol was 0.88 ¡.m and the primary particle size was
16 nm with a specific surface area of 220 m2/g. Lung burdens at the end of exposure were
0.35, 1.8 and 7.8 mg, respectively; there was continued accumulation of carbon black in
the tracheobronchial lymph nodes during the post-exposure period in the mid- and high-
dose groups only. Inflammatory cellular and biochemical parameters of lung lavage
(total and differential cell counts; protein and lysosomal and cytoplasmic enzymes) and
cell proliferative responses as weIl as histopathological evaluation showed no change in
the low-exposure group as compared to controls at any time point. The groups exposed to
the higher concentrations had dose-related increases in cellular and biochemical broncho-
alveolar parameters as weIl as in alveolar cell proliferative responses at the end of
exposure which remained elevated throughout the post-exposure period in the highest
exposure group. Cellular inflammatory parameters also remained elevated during post-
exposure in the mid-exposure group whereas lavage protein and enzyme levels returned
ter-
to control values. Table 30 summarizes the findings of non-neoplastic end-points de

mined in this study at the end of the subchronic exposure and up to eight months post-
exposure.
ln summary, these studies show that once a certain lung burden has been achieved,
inhalation of carbon black in rats results in significant inflammatory responses in the
lung. The reported inflammatory pulmonary responses may be mechanisticalIy related to
subsequent fibrotic as weIl as neoplastic effects observed in long-term chronic inhalation
studies at high-exposure concentrations. The effects of carbon black appear to be more
severe in rats th an in mice, based on the single mouse study. ln addition, female rats
seemed to respond with higher incidence and greater severity than males with respect to
chronic, active inflammation, alveolar proteinosis and bronchiolar/alveolar metaplasia.

(b) Instillation studies

A number of studies evaluating non-neoplastic effects of carbon black were
performed by intratracheal instillation (see Table 31). Bowden and Adamson in a number
of studies from 1978 through 1982 evaluated celIular responses in mice, specificalIy
focusing on the kinetics of macrophages and polymorphonuclear neutrophils. They used
India ink (Pelikan Co.) in most of their studies which has a primary partic1e diameter of
 CARBON BLACK 225

Table 30. Three-rnonth rnulti-exposure inhala-

tion study of carbon black in rats

End-point Exposure concentration

,
(mg/m )

l. 1 7.1 52.8

Continued post -exposure + +

accumulation in Iymph nodes
No. of AM increased:
End of exposure + +
Post-exposure +
No. of PMN increased:
End of exposure + +
Post -exposure + +
Cell proliferation:
End of exposure + +
Post-exposure (+)
Fibrotic response (+) +

Compiled from Driscoll et al. (1996)

-, no response; +, marked response; (+), mild response;
AM, alveolar macrophages; PMN, polymorphonuclear
macrophages

30-40 nm and was instilled mostly at doses of 4 mg into Swiss mi ce (sex not always
specified). Subsequent evaluation showed that there was generally a biphasic
macrophage response in which the first phase occurred without mitotic activity whereas
the second phase showed mitosis of primarily interstitial macrophages. There was also a
high initial response in terms of elicitation of polymorphonuclear neutrophils, which
reached twice the number of alveolar macrophages (Adamson & Bowden, 1978; Bowden
& Adamson, 1978). They also observed that this very high dose and extremely high dose
rate (4 mg instilled) resulted in rapid migration of blood monocytes to pulmonary alveolI
and rapid production of monocytes in the bone marrow (Adamson & Bowden, 1980). ln
a study with male Swiss mice using doses as low as 0.1 mg and as high as 8 mg (dose-
response study), these authors observed (Adamson & Bowden, 1981) that the number of
alveolar macrophages elicited was correlated to the dose delivered and that this response
was very similar to that to other different types of particles administered. ln further
studies (Adamson & Bowden, 1982a), they confirmed that the responses are not unique
to carbon black but also occur after different particles, including latex, are instilled into
the mouse. Further, they showed that chemotactic factors are elicited in the alveolar
space and detectable in bronchoalveolar lavage fluid. They further determined the
le-body irradiated
importance of the macrophage to elicit the initial response; when who

mice were instilled with carbon black, a limited macrophage response occurred which
was folIowed by proliferation of interstitial macrophages stilI present in the lungs of
these irradiated mice (Adamson & Bowden, 1982b; Bowden & Adamson, 1982).
 N
N
0\
Table 31. Non-neoplastic effects of carbon black by instilation studies in experimentai animaIs
Partic1e Paric1e Species Dose Observation End-points Findings Comments Reference
type diameter (age and period
and surface sex)
area

India ink 30-40 nm Swiss 4 mg Up to 28 Macrophage Biphasic macrophage response; first Very high dose Adamson &
(Pelikan mouse days proliferation phase without mitotic activity; second- and dose rate Bowden
Co.) and CB phase mitosis of interstitial (1978);
transport in macrophages; initial large PMN Bowden & ..
lung increase in BAL (twice AM numbers); Adamson
?
~
some CB partic1es crossed epithelium (1978) n
to reach peribronchial and perivascular ~
sites 0
Z
India ink 30-40 nm Swiss 4mg U p to 7 Macrophage Rapid migration of blood monocytes to Very high dose Adamson & 0
el
(Pelikan mouse weeks and blood pulmonary alveoli and rapid and dose rate Bowden ~
Co.) monocyte production of monocytes in bone ( 1 980) ?'i
response marrow after CB dos'¡ng ::
C/
India ink 30 nm Swiss 0.1, 1,2,4,8 Up to 14 Macrophage Confirming findings (Adamson & Focus of study Adamson &
-i
mouse mg days response Bowden (1978); number of AM was on macro- Bowden 0l'
(male) elicited is related to dose delivered; phage kinetics (1981 )
lowest dose showed very liule response after different
C
particle types
~
tT
Colloidal 30nm Swiss 4mg 2 days PMN and Chemotactic factors in BAL after CB Similar response Adamson &
0\
Ui
carbon mou se (donor)" Up to 14 macrophage cause PMN and AM influx also after latex Bowden
BAL days response partic1es, not ( 1982a)
supernatant unique to CB
(recipient)"
Colloidal 30 nm Swiss 4mg, Up to 20 Macrophage Limited initial macrophage response Response not Adamson &
carbon mouse who le-body weeks response after monocyte depletion, followed by specifie to CB; Bowden.
irradiated after interstitial macrophage proliferation; importance of AM (1982b);
and controls monocyte increased translocation of CB to for containment of Bowden &
depletion interstitium in depleted mice with partic1es in Adamson
decreased AM output alveolar space (I982)
Table 31 (contd)

Particle Particle Species Dose Observation End-points Findings Comments Reference

type diameter (age and period
and surface sex) n
;p
area :;
tJ
Furnace Fischer BAL Inflammatory response (PMN and Oberdörster
0
- 20 nm 0.5 mg 24 h Surface area Z
black 344 rat response, protein in BAL) is correlated with correlation apphes et al. (1992) tJ
Regal 660 interstitial particle surface area; CB passage to ta both ultrafine L'
(male) ;p
passage interstitium is less th an for ultrafine and larger-sized n
TiO,; Înterstitial access can influence Ti01 particles ~
alveolar inflammation

CB, carbon black; PMN, polymorphonuc1ear macrophages; BAL, bronchoalveolar lavage; AM, alveolar macrophages; TiO" titanium dioxide
a 4 mg carbon black instiled into donor mice, from which supernatant of BAL was obtained and administered to recipient mice

N
..N
228 IARC MONOGRAPHS VOLUME 65

Macrophage depletion also resulted in an increased translocation of administered carbon

black to interstitial sites. Overall, the studies of these investigators confirmed the
importance of the alveolar macrophage in pulmonary defences to partic1es including
carbon black. Both the alveolar macrophage and the interstitial macrophage systems are
of importance in this response as part of the pulmonary defence system against partic1es.
Oberdörster et aL. (1992) administered 0.5 mg furnace black (Regal 660) with a
primary particle size of ~20 nm to male Fischer 344 rats by intratracheal instillation. ln
addition, other particle types (ultrafine and larger-sized titanium dioxide) were admi-
nistered at different dose levels, and the bronchoalveolar lavage response and interstitial
access of partic1es was determined 24 h later. They found that the inflammatory response
as measured by lavaged polymorphonuc1ear macrophages and lavage protein was corre-
lated best with the particle surface area of different particle types of titanium dioxide; the
inflammatory response induced by carbon black also fitted the same regression.
Interstitial access of ultrafine titanium dioxide partic1es was greater than that for carbon
black, with higher doses resulting in a diminished inflammatory response in the alveolar
space (larger polymorphonuclear macrophage) and a shift of the inflammation towards
the interstitium.

ln a study of the effects of benzo(a)pyrene on rat lung, Davis et aL. (1975) dosed
intratracheally groups of 18 female Wistar rats, 12-16 weeks of age at the beginning of
the experiment, with 0.5, 1.0 or 2.0 mg benzo(a)pyrene with or without 0.5 mg carbon
black on 18 occasions at biweekly intervals. One group received carbon black alone and
one recei ved no treatment. Group mean survi val times ranged from 73 to 109 weeks. At
autopsy, aIl rats given carbon black had black deposits in their lungs, mainly in alveolar
macrophages. These animaIs also showed significantly mor~ severe columnar and
cuboidal metaplasia of the alveolar epithelium, whereas rats receiving benzo(a)pyrene
alone showed no increased severity of metaplasia. However, squamous metaplasia of the
alveolar epithelium was increased in rats receiving carbon black alone as weIl as carbon
black with benzo(a)pyrene.
OveraIl, the se results from intratracheal instilIation studies with carbon black show
that high acute doses of carbon black elicit a significant pulmonary inflammatory
response which is possibly related to the large specific surface area of the partic1es.

(c) Ex-vivo and in-vitro studies

A number of studies have been performed with carbon black using either in-vivo
exposure to the particulate compound with subsequent isolation of cells and specific in-
vitro investigations or primary in-vitro exposure of cell systems to evaluate effects.
These studies are summarized in Table 32.
MilIer and Zarkower (1974) exposed Balb/c mice by inhalation to 5.4 mg/m' carbon
black (unspecified) with a mass median diameter of 1.8 !lm continuously for seven to 28
days. The aim was to investigate effects on the immune system. After exposure, spleen
and lung lymph node T and B celllymphocytes were isolated and an in-vitro lymphocyte
as say , inc1uding a transformation test, was performed. They reported significant changes
in the responsiveness to mitogens of both Band T lymphocytes as weIl as changes in
 Table 32. ln-vitro toxicity studies of carbon black
PartIcle Particle Test system Dose/exposure Findings Comments Reference
type diameter concentration
and surface
area

Not 1.8/lm Balb/c mouse: inhalation 5.4 mg/ml, Significant changes in responsi veness Lung dose not Miller &
specified exposure; isolation of spleen 7-28 days to both B- and T-lymphocyte-specific determined; altered Zarkower
and lung Iymph node T and B continuously mitogens; changes in lymphocyte immune response, (1974)
cells; in-vitro transformation of populations possibly due to high CB
lymphocyte and migration of lung burden and
macrophage inflammation
Fisher 25 /lm Effect of adsorption of BaP; 16.7 mg CB + BaP was not released from CB and Relevancy of test system Lakowicz &
carbon 31 m'/g uptake into 1 ml of rat liver 5 /lg BaP; 30 there was no uptake into microsomes,
black microsomes
(high doses) is Bevan (1979, n
min incubation in contrast to other partic1es (Fe,O" questionable 1980) ::
(thermal SiO" asbestos) ~
black) I:
0
Fisher 25 /lm Effect of adsorption of BaP on 16.7 mg CB + BaP was not released from CB, no Relevancy of test system Lakowicz
Z
carbon 31 m'/g particles for uptake rate into 5 /lg BaP; 30 uptake into membranes in contrast to CO
(high doses) is et al. (1980) l'
n::
black model membranes min incubation BaP adsorbed on other partic1es questionable
(thermal
black) ~
30il 96, 168, 220 ln-vitro elution of BaP from CB ln-vitro: 5-20 g Less th an 0.005% of adsorbed BaP Results are in contrast to Buddingh
furnace nm using plasma, serum, lung CB with can be eluted by biological media; in- other in-vivo et al. (1981)
blacks 128, 101,70 lavage fluid; in-vivo feeding biological vivo feeding at high dose does not bioavailability studies of
m'/g study with CB in mice to study medium, 24 h induce AHH in mouse lung or liver BaP; test system may not
AHH induction ln-vivo: 0.08, be relevant
2 and 20 g/kg
diet, 30- 1 80

days
40il 96, 168, Elution of adsorbed BaP from 100 /lg CB Elution of BaP from CB depends on Study aims at Bevan &
furnace 175,220 nm CB into phospholipid vesicles amount of BaP present; rate and bIoavaIlabIlity of PAH W orrell
blacks 128, LOI, extent of elutIon Is lowered wIth less adsorbed onto CB (1985)
90, 70 m'/g adsorbed BaP partic1es; high-dose

l'l'
study not relevant for ¡n
vivo \0
 N
ow

Table 32 (contd)

Particle Particle Test system Dose/exposure Findings Comments Reference

type diameter concentration
and surface
area -
;p
:;
40il 96, 168, Elution of adsorbed BaP from Up to 200 mg 0.2-0.6% of BaP can be eluted; more Very low elution in vitro Bevan & n
fumace 175,220 nm CB into phospholipid vesicles CB a CB and using biological systems Y onda ~
elution from low surface are
o
blacks 128, 101,
90, 70 m2/g
from rat lung homogenate and
simulated lung fluid
high BaP content (1985) z
o
Regal 660 10 m2/g ln-vitro activation of rat serum 5-25 mg CB/ml CB has highest activity for different High doses Oberdörster
a:;
(fumace with particles to determine serum; 10% particles (SiG" asbestos, PVC, TiO,) et al. (1989) ;p
'"
black) chemotactic activity for AM serum for AM to activate serum chemotactic factors ::
C/
chemotaxis
~
20il Not given. Phagocytosis assay with AM 1.5 ml of 0.04 AM phagocytosis of CB + adsorbate Surface properties are Jakab et al. or
fumace Surface area from Wistar rats; CB adsorbed mg/ml suppressed only for low surface CB; important for fate of (1990) c:
carbon of N 339 is with polar and semi-po1ar suspension for Fc-receptor mediated phagocytosis of particle-pollutant ~
blacks 15-fold less compounds 2x 105 AM, sheep red blood cells was impaired complexes tT
(N339 & than that of 45 min after previous uptake only of low 0\
Ui
Black Black Pearl surface area CB + adsorbate
Pearl 2000
2000)

CB, carbon black; BaP, benzo(a)pyrene; AHH, arylhydrocarbon hydroxylase; PAH, polycyclic aromatic hydrocarbons; AM, alveolar macrophage
 CARBON BLACK 231

lymphocyte populations. Spleen lymphocytes of carbon black-exposed mice also

exhibited significantly enhanced ratios of transformation after sensitization of the mice
with tuberculosis antigen.

Lakowicz and Bevan (1979, 1980) and Lakowicz et al. (1980) investigated the effect
of adsorption of benzo(a)pyrene onto Fisher carbon black (thermal black) (25 !-m
particle size) on uptake into either rat liver microsomes or into model membranes. 5 !-g
benzo(a )pyrene had been adsorbed onto 16.7 mg carbon black which was incubated with
model systems for 30 min. Release of benzo(a)pyrene from the carbon black was not
detected, and no uptake into liver microsomes or model membranes occurred. This is in
contrast to the enhanced uptake of benzo(a)pyrene absorbed onto certain other particles
(haematite, silica and asbestos) that were also tested by these authors.
Additional studies were performed to evaluate the in-vitro elution of benzo(a)pyrene
from carbon black using either plasma, serum or lung lavage fluid from rats, phospho-
lipid vesicles, or phospholipid vesicles, rat lung homogenates and simulated lung fluids
(Buddingh et al., 1981; Bevan & Worrell, 1985; Bevan & Y onda, 1985). These studies
are listed in Table 32 and show that very little of the benzo(a)pyrene adsorbed onto
carbon black particles can be eluted by biological media. The eluted amount depends on
the total amount of benzo(a)pyrene present on the carbon black. Together with their in-
vitro studies, Buddingh et al. (1981) also reported results of a feeding study with carbon
black in mice designed to examine the induction of arylhydrocarbon hydroxylase in the
lung and liver; they did not find induction of this enzyme even at the highest dose level
of 20 g/kg of diet carbon black for up to 180 days.
Oberdörster et aL. (1989) investigated activation of chemotactic serum factor in vitro
by furnace black (Regal 660) and compared it to other particle types such as titanium
dioxide, polyvinyl chloride (PVC), asbestos and silicon dioxide. They found that, on a
mass basis, carbon black showed the greatest ability to induce chemotactic factors for
alveolar macrophages in rat serum. The authors suggested that surface area may play an
important role in the inducibility of such factors, since titanium dioxide, with a very low
surface area, showed the lowest response.
Jakab et al. (1990) studied alveolar macrophage phagocytosis of two different oil
furnace carbon blacks with high and low surface areas and with adsorbed polar and semi-
polar compounds. The carbon blacks (1.5 ml of a 0.04 mg/ml suspension) were incubated
with 2 x 105 alveolar macrophages from Wistar rats for 45 min. For the 10w surface area
carbon black particles only, they observed depressed alveolar macrophage phagocytosis
of the carbon black and the adsorbates as well as for sheep red blood celIs that had
previously been incubated with the carbon black-adsorbate complex. The authors sug-
gested that surface properties are important parameters to determine the fate of particle-
pollutant complexes in the lung.
No firm conclusions about the in-vitro toxicity or effects on cell systems can be
drawn from these limited in-vitro studies reported in the literature. With respect to
elution of adsorbed benzo(a)pyrene, it appears that desorption from carbon black
particles occurs at a very low rate and to a very low degree. However, in-vivo studies
232 IARC MONOGRAPHS VOLUME 65

(see section 4. L.2(b)) have demonstrated clearly that adsorbed material can be eluted
readily.

(d) Other studies

A number of studies have been performed with carbon black that may not be directly
relevant for an evaluation of carcinogenicity - the route of exposure was in most cases
rather unusuaL. These studies consist of experiments of intracardiac, intravenous,
intrabladder-wall and intraventricular (central nervous system) injections of carbon black
into experimental animaIs. The material used was mostly India ink (Pelikan Co.) and the
major conclusion from these studies is that systemicalIy administered carbon black
particles can be trapped in the pulmonary circulation and be transported to pulmonary
interstitial sites and alveolar macrophages. This is a suggested route of elimination of
foreign bodies from the systemic circulation according to the authors (Blau & Veall,
1967; Vales et aL., 1967; Bertheussen & Nissen, 1976; Bertheussen et al., 1978 (see
Table 33)).

4.3 Reproductive and developrnental effects

No data were available to the Working Group.

4.4 Genetic and related effects

4.4.1 Humans

No data were available to the Working Group.

4.4.2 Experimental systems (see also Table 34 and Appendices 1 and 2)

The activity of carbon black partic1es and of their corresponding solvent extracts in
short-term assays must be considered separately. When carbon black particles are tested,
results may be influenced by such experimental conditions as the presence of serum, the
concentration of dimethyl sulfoxide or other solvents, or the duration of exposure. ln
addition, these assays may underestimate in-vivo exposure owing to the short duration of
the experiments. Conversely, the amount of chemicals eluted by solvent ex
tracts of
carbon blacks may be greater than that which wou Id be eluted by biological fluids
(Buddingh et al., 1981). Additionally, the nature of the solvent and the temperature and
duration of the Soxhlet extraction influence the final biological response (Sanders, 1981;
Giammarise et al., 1982; Butler et al., 1983).
Several different carbon blacks have been assayed in short-term tests. These inc1ude a
rubber-grade furnace black (N339), a nitric acid after-treated black (Black Pearls), a third
carbon black of unspecified type, and several unspecified carbon black pastes. ln
addition, extracts of three of the above and 20 other carbon black sarnples have been
tested. The data are summarized in Table 34.
Table 33. Other studies of carbon black related to non-neoplastic end-points

Partic1e Particle Test system Dose Findings Comments Reference

type diameter
and surface
area

India ink 20-50 nm Guinea-pig: intracardiac 0.1-0.15 ml/100 g CB found in macrophages Not relevant for Blau &
(Pelikan) injection (animaIs turned bw of 10% throughout thymus. Foreign CB toxicity Veall
(+ 4.3% slaty grey for a few min); suspension bodies can reach thymus (1967) n
fish glue, study of thymus uptake ~
¡o
1 % phenol) t:
0
Not given 16 and 70 Intravenous injection into 5 mg, up ta 13 Formation of emboli in Not relevant for Va1es et al. Z
nm rabbits; reaction of weeks follow-up pulmonary vessels; CB toxicity (1967)
t:
pulmonary vessels
l'
endothelial hyperplasia; ~
passage of CB to alveolar n
;ï
space and elimination
India ink Not given Injection into Ulinary 0.1-0.2 ml of CB found in AM at 24 h, Not relevant for Bertheussen
(Pelikan) bladder wall of rat; 25% suspension suggesting pulmonary CB toxicity & Nissen
sacrifice after 1-24 h excretion of foreign bodies (1976)
India ink Not given Injection into ventricular 3 : 1 mixture of CB found in macrophages in Not relevant for Bertheussen
(Pelikan) system of Wistar rat saline: CB alveolar septae of lung as CB toxicity et al.
elimination pathway (1978)
CB, carbon black; AM, alveolar macrophages

N
W
W
 N
w
.t
Table 34. GenetIc and related effects of carbon blacks or their forrnulations
Test system Resu1t" Dose
h
Reference
(LED/HID)
Without With
exogenous exogenous
metabo1ic metabolic
system system

SAO, Salmonella typhimurium TAI 00, reverse mutation - e

- 3750 Kirwin et aL. (1981) ..
+d +d ~
SAO, Salmonella typhimurium TAI 00, reverse mutation NR Agurell & Löfroth ;;
("
(1983 )
SAO, Salmonella typhimurium TAI 00, reverse mutation - e
- e ~
SA5, Salmonella typhimurium TA 1535, reverse mutation - -
50 Venier et al. (1987) 0
e
3750 Kirwin et aL. (1981) Z
SA 7, Salmonella typhimurium TA 1537, reverse mutation - e
- e 0
SA8, Salmonella typhimurium TA1538, reverse mutation - ('
- e
3750 KIrwin et al. (1981) a;;
3750 Kirwin et aL. (1981)
SA9, Salmonella typhimurium T A98, reverse mutation l'
0 250 Rosenkranz et aL.
~
'"
( 1980)
:i
C/
SA9, Salmonella typhimurium T A98, reverse mutation (+Y 0 500 Rosenkranz et aL. ~
(1980) 0l'
SA9, Salmonella typhimurium TA98, reverse mutation +
Ii
0 5.0 Rosenkranz et al. e
(1980) ~
- - m
SA9, Salmonella typhimurium T A98, reverse mutation e e
3750 KirwIn et aL. (1981) 0\
SA9, Salmonella typhimurium T A98, reverse mutation +d +d lJ
NR Agurell & Löfroth
(1983)
SA9, Salmonella typhimurium T A98, reverse mutation (+)' +' 2.5 VenIer et aL. (1987)
d
SAS, Salmonella typhimurium T A98NR, reverse mutation + 0 NR Agurell & Löfroth
(1983 )
d
SAS, Salmonella typhimurium T A98/ 1 ,8DNP, reverse mutation + 0 NR Agureli & Löfroth
(1983 )
DMM, Drosophila melanogaster, somatic mutation (mosaics) -('
10 000 larva1 KirwIn et aL. (1981)
feeding
Table 34 (contd)
b
Test system Resulta Dose Reference
(LED/HID)
Without With
exogenous exogenous
metabolic metabolic
system system

DMX, Drosophila melanogaster, sex-linked recessive mutation - c

10 000 1arva1 Kirwin et al. (1981)
feeding
DML, Drosophila melanogaster, dominant 1etha1 test - c
Kirwin et al. (1981) n
10 000 larva1
feeding
?
¡o
- c tt
DMN, Drosophila melanogaster, aneuploidy (sex-chromosome 10ss) 10 000 larval Kirwin et aL. (1981) 0
feeding Z
G5T, Gene mutation, mouse 1ymphoma L5 178Y cells, tk locus in vitro - c
- c
40 000 Kirwin et al. (1981) tt
l'
sic, Sister chromatid exchange, Chinese hamster ovary CHO cells - c
- c
1000 Kirwin et aL. (1981) ?n
in vitro t;
+i
MIA, Micronucleus induction, M3E3/C3 hamster epithelia1 cells 0 1 Riebe- Imre et al.
in vitro (1995)
TCM, Cell transformation, C3HIl OTYi mouse fibroblasts in vitro - c
0 16 000 Kirwin et al. (1981)
TCL, Anchorage independent growth, M3E3/C3 hamster epithelial cells ~ 0 100 Riebe-Imre et aL.
in vitro (undifferentiated and small mucus granule cell stage) (1995)
GV A, p53, K-ras in pu1monary carcinomas in F344/N rats - k
3.5 inh 16 hld x Swafford et aL. (1995)
5 d/wk x 24 mo
+1
GV A, hprt Mutation analysis in type II alveolar cells isolated from rats 1.5 inh. 6 h/d x Driscoll et aL. (1995)
after exposure 5 d/wk x 13 wk
BVD, Binding to DNA C2p-post1abellng) in F344/N rat aIveo1ar type II +k 3.5 inh 16 hld x Bond et al. (1990)
cens in vivo 5 d/wk x 12 wk

IV
w
VI
 N
W
0\
Table 34 (contd)

Test system Resulta Dose" Reference

(LED/HID)
Without With
exogenous exogenous
metabolic metabolic
system system

BVD, Binding to DNA C"P-postlabellng) in Wistar rat lung in vivo 7.3 inh 18 h/d x Gallagher et aL. (1994) ..
5 d/wk x 2 yr ;i
::
n
Il +, positive; (+), weak positive; -, negative; 0 not tested; ?, inconc1usive 3:
o
¡, LED, lowest effective dose; HID, highest ineffective dose. ln-vitro tests, ¡.g/mL; in-vivo tests, mg/kg bw; NR, dose not reported; MMAD, mass z
o
median aerodynamic diameter; MMDD, mass median diffusion diameter a::
C Rubber-grade furnace black N339, sudace are
a 100 m2/g, 48-h toluene extractables 0.15%; particles suspended in DMSO (Ames test + SCE
assay), acetone (cell transformation test) or culture media (mou se lymphoma test). ~
'i
dCarbon blacks from various manufacturers (20 samples). Soxhlet extraction of l-g samples with 200 mL benzene for 16 h and solvent exchange ::
CI
into DMSO ~
t Carbon black used for refining tanned skins (7 samples). (a) Sonication of 2 g samples in 40 mL benzene for 0.5 h; (b) Soxhlet extraction of 4-g ol'
samples with 50 mL toluene for 48 h. Solvent exchange into DMSO (1 g extract/ml). C
f Black Pearls L (furnace black, manufacture of which involves a nitration-oxidation step). Suspension in DMSO at 5 mg/mL for 5 h before 3:
testing.
t'
0\
VI
g Raven 5750 (furnace black, oxidative aftertreated). Soxhlet extraction of 1O-g samples with toluene for 48 h. Low-temperature concentration
and solvent exchange into 1 mL DMSO.
ii Black Pearls L (furnace black, manufacture of which involves a nitration-oxidation step). Soxhlet extraction of 10 g samples with toluene for
48 h. Low-temperature concentration and solvent exchange into 1 mL DMSO.
¡Carbon black (not otherwise characterised); carbon black suspended in the culture medium containing undifferentiated cells for 72 h.
j Carbon black (not otherwise characterisedJ; carbon black suspended in the culture medium containing undifferentiated or differentiated cells for
72 h.
kElftex-12 (furnace b1ack); 2 ¡.m MMAD (large mode); 0.1 ¡.m MMDD (small mode); surface area, 43 m2/g. Whole-body exposure
/ Monarch 880 (furnace black); 0.8 ¡.m MMAD (16 nm primary partic1e); sudace area, 220 m"/g. Who1e-body exposure
~"Printex 90 (furnace black); MMAD, 0.65 m; surface area, 270 m"/g. Carbon black in air at 2 yr mean of 11.3 mg/m3. Whole-body exposure
 CARBON BLACK 237

ln an extensive study, Kirwin et al. (1981) tested a rubber-grade furnace black (N339;
surface area, 100 m2/g; toluene extractables (48-h), 0.15 wt%) in the folIowing five short-
term assays:
(1) Mutagenicity in Salmonella typhimurium: no mutagenic activity was observed in
S. typhimurium strains TA1535, TA1537, TA1538, TA98 or TAI00 at concen-
trations of carbon black of up to 7.5 mg/plate in the presence or absence of an
Aroclor-induced rat-liver homogenate supernatant fraction (S9); cellular toxicity
(TA nt was reduced by 27% at 7497 /lg/plate of
100) was assessed and viable cou

carbon black. (It was not reported whether, or for how long, the carbon black
particles were suspended in dimethyl sulfoxide (DMSO) prior to testing.)
(2) Sister chromatid exchange in Chinese hamster ovary cells: the carbon black was
suspended in DMSO at 100 mg/mL (time and temperature unspecified) and then
diluted in culture medium to give a final concentration range of 0.00032-
1 mg/mL; cells were exposed for 2 h both in the presence and absence of S9;
very small increases in the frequency of sister chromatid exchange as compared
to the control value with and without S9 were observed for several concen-
trations, but these were not dose related.
(3) L5178Y tk+l- mouse lymphoma mutagenicity assay: celIs were exposed for 4 h
(time extended for an unspecified time owing to difficulty in separating carbon
black from cells) to concentrations of carbon black of 10-40 mg/mL in the
absence of S9 and of 5-15 mg/mL in the presence of S9; cell survival was ~ 1 %
at the highest concentration; no mutagenicity was observed.
(4) C3HIlOTYi CL8 mouse embryo morphological celI transformation assay: carbon
black suspended in acetone was tested at four concentrations ranging from 2-
16 mg/mL; no transformed focus was observed.
(5) Genetic activity in Drosophila melanogaster: larvae were fed diets containing
1 % carbon black until pupation; flies were scored for mosaics, Y -chromosome
loss, chromosomal aberrations and dominant lethal and sex-linked lethal
mutations; no genetic effect was observed.
A nitric acid-treated fumace black (Black Pearls; surface area, 115 m2/g; toluene
extractables (48-h), 0.3 wt%) (Sanders, 1981) was tested for mutagenicity in S. typhi-
murium. Particles were first suspended in DMSO for 5 h and an aliquot containing
500/lg carbon black was then tested in strain T A98. No mutagenic activity was observed
(Rosenkranz et al., 1980).
An aliquot of a 48-h Soxhlet toluene extract (solvent exchanged into DMSO) equi-
valent to 10 l.g of the above carbon black was, however, mutagenic in the same strain.
This carbon black contained nitrated pyrenes at a level of 67 mg/kg (Sanders, 1981).
More recent production lots of this grade of carbon black had a 200-fold reduction in
nitrated pyrene content; extracts had a mutagenicity that was reduced by the same order
of magnitude (Rosenkranz et al., 1980; AgurelI & Löfroth, 1983; Butler et al., 1983).
Benzene or acetone extracts of 20 commercial carbon blacks were tested in the
Salmonella mutagenicity assay. Of the 20 extracts (sorne of which required activation
238 IARC MONOGRAPHS VOLUME 65

with rat-liver S9), 15 were mutagenic to strains T A98 and/or T A 100 and five were
inactive (AgurelI & Löfroth, 1983).
Venier et al. (1987) tested the mutagenicity in S. typhimurium strains T A98 and
TA 1 00 of seven carbon black pas tes that are used as commercial leather dyes. Samples
were assayed for mutagenicily either directly or after extraction with benzene. The
compounds that were tested were in the form of thick pas tes and the carbon black content
ranged from 5 to 8%. ln aIl compounds but one, carbon black was dispersed in 10-15%
casein solution in water containing smalI amounts of sulfonated castor oil and cresols.
Different extraction procedures were used for the pastes. No mutagenicity was observed
either directly or after sonication with benzene in any of the carbon black samples tested.
After a 48-h extraction of carbon blacks with boiling toluene, four carbon black samples
were mutagenic in strain TA98 in the presence of S9. The activity ranged from 1.3 to 9.7
induced revertants/mg equivalent of extract. A weak direct mutagenic activity in strain
T A98 was shown by one extract. The presence of P AHs in the toluene extracts was
reported by the authors to explain the mutagenicity of only one carbon black sample.
Low or undetectable levels of P AHs were found in other mutagenic extracts.
Two studies analysed the extent to which exposure of rats to carbon black induced
DNA adducts in lung tissue (Bond et aL., 1990; GalIagher et al., 1994). Both studies
employed the 32P-postlabelIing assay to measure DNA adducts.
Gallagher et al. (1994) exposed female Wistar rats (Crl:(WI)BR) to furnace black
(Prin tex 90) partic1es. The carbon black exposure was 7.5 mg/m 3 for the first four months
and 12 mg/mJ for the last 20 months. Exposures were for 18 h per day on five days a
week for two years using who le-body exposure chambers. The carbon black surface area
was 270 m2/g. The MMAD of the carbon black partic1es for the exposures was 0.65 llm.
The extractable organic matter, as determined by solvent extraction with di oro- chI

methane, was 0.039%. After two years of exposure, animaIs were kiled and the distal tip
of the peripheral left lung lobe was removed for analysis of DNA adducts using the
nuc1ease PI or butanol extraction versions of the 32P-postlabelIing assay. J2P-PostlabelIing
analysis detected one major radiolabelled spot that was referred to as adduct 1. DNA
adduct levels for adduct 1 after two years of exposure to carbon black were about 9
adducts/l 09 bases and about 17 for the filtered-air contraIs. Adduct 1 was found to
increase in an age-related fashion and was presumed by the au th ors to be a 32P-labelIed
I-compound. Adduct levels were determined for the diagonal radioactive zone; however,
no significant elevation in adduct levels in this zone was observed in lung DNA isolated
from the carbon black-exposed animaIs.,
Bond et al. (1990) exposed male and female Fischer 344/N rats to filtered air or
carbon black (6.2 mg/m3) for 12 weeks. The carbon black was Elftex-12 (furnace black)
of which 59% of the mass had a 1.9 llm MMAD and 41 % of the mass had a 0.10 llm
geometric mean diameter and surface area characteristics similar to those of eluted diesel
soot but negligible amounts of extractable organic chemicals and no measurable muta-
genic activity. Rats were exposed for 16 h per day on five days a week for 12 weeks.
DNA adducts in alveolar type II celIs were assessed at the end of the exposure. The
authors report the presence of several adducts as assessed by the nuc1ease PI version of
 CARBON BLACK 239

the l2p-postlabelIing assay. The level of carbon black-induced adducts was significantly
elevated above that seen in controls. Totallevels of DNA adducts in type II celIs from
control and carbon black-exposed rats were approximately 5 and 25 adducts/l09 bases,
respectively. The authors could not determine whether exposure to carbon black induced
an increase in the level of adducts already present in cells from sham-exposed rats or if
carbon black induced the formation of new adducts with chromatographic characteristics
of I-spots.

Riebe- Imre et al. (1994) assessed the ability of carbon black partic1es (the W orking
Group was aware that this was Printex 90 (fumace black)) to induce cytotoxicity, cell
transformation and micronuc1ei formation in a fetal Syrian hamster lung epithelial cell
line. The cytotoxicity of the carbon black particles was negligible. Carbon black partic1es
induced in-vitro transformation in smalI mucus granule cell-differentiated M3E3/C3 cells
and in undifferentiated M3E3/C3 celIs. Carbon black partic1es showed a much weaker
activity in undifferentiated cells compared to differentiated cells. They also reported
cytoskeletal changes. Concentrations of carbon black used in the transformation studies
ranged from 100 to 300 ¡.g/mL. Peak responses in the differentiated celIs occurred at
200 ¡.g/mL and were approximately four-fold over those of controls. ln the undifferen-
tiated cells, peak concentrations were observed at 300 ¡.g/mL and were approximately
eight-fold over those of controls. A dose-related increase was observed in the frequency
of micronuc1ei over the dose range 0.1-2.0 ¡.g/mL. However, maximal responses were
only approximately 50% greater than the control frequency of about 4.5%; there was no
indication of variation, and the possibility of different responses at higher doses (that
were tolerated in the cell transformation test) were not reported.
Swafford et al. (1995) analysed pulmonary carcinomas from rats exposed to diesel
exhaust, furnace black (Elftex 12) and air for alterations in K-ras and p53 to determine if
mutations were similar. Details of the exposure conditions are described in Nikula et al.
(1995). Briefly, male and female Fischer 344/N rats (seven to nine weeks of age) were
exposed for 16 h per day on five days per week for 24 months to diesel exhaust or carbon
black at concentrations of 2.44 and 6.33 mg/ml for diesel exhaust and 2.46 and
6.55 mg/ml for carbon black. Controls were exposed ,to air only. The number of
carcinomas analysed were 28 for diesel exhaust, 18 for carbon black and five for air only.
K-ras exon 1 mutations were found in two neoplasms, one each from diesel exhaust and
carbon black exposure groups. No mutations in the K-ras gene were observed in lung
neoplasms from control rats. Immunohistochemical staining revealed evidence of p53
inactivation in 2/4 squamous-cell carcinomas and adenocarcinomas from carbon black-
exposed rats. p53 Mutational analyses revealed the presence of one mutation in a diesel
exhaust-induced squamous-cell carcinoma. This mutation was reported by the authors to
be a silent mutation. (The W orking Group noted that it is not c1ear whether the only
(silent) mutation was in a diesel exhaust or carbon black-exposed rat.)
A subchronIc inhalation study with Monarch 880 (furnace black) was performed in
Fischer 344 rats exposed to 1.1, 7.1 and 52.8 mg/m 3 for 6 h per day on fi ve days a week
for a total of 13 weeks with an eight-month post-exposure period (DriscolI et aL., 1996).
The MMAD of the carbon black aerosol was 0.88 ¡.m and the primary particle size was
16 nm with a specific surface area of 220 m2/g. The rat alveolar type II celI isolation and
240 IARC MONOGRAPHS VOLUME 65

the hprt clonaI selection assay were used. Mutant frequencies ranged froID 8.2 to 5.2
mutants/l06 epithelial cells in the air control animaIs. Exposure to 52.8 mg/m3 carbon
black resulted in hprt mutant frequencies which were 4.3-, 3.2- and 2.7-fold greater than
the air control group, immediately, three and eight months after exposure, respectively. A
significant increase in the frequency of hprt mutants was detected immediately after
13 weeks of exposure to 7.1 mg/m3 carbon black but not after three or eight months of
recovery. No significant changes in the hprt mutant frequency were observed for alveolar
epithelial cells from rats exposed to 1.1 mg/m' carbon black. This mutagenic response
occurred at exposures that also resulted in significant pulmonary inflammation, epithelial
hyperplasia and fibrosis.

4.5 Mechanistic considerations related to carcinogenicity

Figure 1 describes a hypothesized mechanistic modei for effects of particle exposure
in the lung. More specifically, the model, derived from inhalation studies in rats, pertains
to exposure to low-toxicity low-solubility particles. This topic has also been discussed at
a recent symposium (Mauderly & McCunney, 1996). Phagocytosis of such particles by
alveolar macrophages leads to activation by alveolar macrophage and the subsequent
release of inflammatory cytokines, growth factors, chemokines, enzymes and reactive
oxygen species. This in turn recruits polymorphonucleocytes from the circulatory system
into the alveolar space, thus amplifying the inflammatory response including the release
of additional reactive oxygen species. This inflammatory response is dependent on the
dose of deposited and phagocytized particles. Particularly, impairment of alveolar macro-
phage-mediated particle clearance due to Iung particle overload results in further particle
accumulation and amplifies this process, leading to chronic inflammation, including
fibrotic changes. The continuous release of reactive oxygen species can result in
increased mutation frequencies in specific target cells, which become manifest during
increased cell proliferative responses. Subsequent responses include metaplastic changes,
which finally result in tumour formation.
This specific mechanism involving reactive oxygen species is based on studies by
DriscolI et al. (1996), which showed that carbon black in rats led in a dose-dependent
manner to increased mutation frequency of the type II cells in those cases where signi-
ficantly increased numbers of inflammatory celIs were present. Earlier studies by
DriscolI (1996) have shown that co-incubation of rat lung epithelial celIs with inflam-
matory polymorphonucleocytes also resulted in increased mutation frequencies and that
this response could be significantly decreased in the presence of antioxidants. Thus, oxi-
dative damage to DNA due to released reactive oxygen species from inflammatory cells
appears to be a plausible mechanism underlying the particle-induced rat tumour
response. ln further support of this hypothesis are the studies of Bond et al. (1990) who
reported elevated levels of DNA damage in alveolar type II celIs of rats exposed to
concentrations of carbon black known to induce an inflammatory response.
An alternative mechanism relates to physical phenomena due to particles taken up by
target cells. As pointed out in Figure 1, high pulmonary particle burdens result in
 CARBON BLACK 241

Figure 1. Mechanistic chain of events for pulrnonary effects of low-toxicity, low-

solubilty particles assurned to be operative in rats

Particle exposure

j
Alveolar macrophage
Acute inflammation
activation Impaired clearance

j
Particle accumulation Chronic ~ Fibrosis
Epithelial and interstitial inflammation
uptake .
.

j
Mutations

j .. ..
Epithelial cell
proliferation ~ Metaplasia
(Hyperplasia)

j
Tumours

Adapted from Oberdörster (1995)

increased uptake by epithelial cells and access of particles into the pulmonary inters-
titium. A study by Riebe-Imre et al. (1994) reported that a fetal Syrian hamster lung
epithelial celI line, when incubated with different doses of carbon black, showed
increased transformation, particularly when these celIs were already differentiated.
Carbon black also induced a dose-dependent enhancement of micronucleus formation in
these celIs, mostly due to clastogenic effects. Since these effects were observed in an
epithelial cellline derived from hamsters after in-vitro exposures, the relevance to the in-
vivo situation needs to be addressed. Particle-induced lung tumours have not been
observed in hamsters, and target celIs in the only species that shows particle-induced
tumours (the rat) are most likely of alveolar origin, including the type II cells. This
mechanistic hypothesis, based on physically induced DNA alterations, may be less
plausible and relevant than the one of particle-induced oxidative damage.
The particle-associated rat lung tumours (e.g. diesel exhaust) cannot be extrapolated
to mi ce or hamsters; these species do not, at comparable lung burdens of particles,
develop lung tumours. For carbon black specifically, this species difference has been
demonstrated between rats and mice. Several inhalation studies with low-solubility, low-
toxicity particles, one of thern with carbon black, have shown that no lung tumour was
242 IARC MONOGRAPHS VOLUME 65

induced in mice at exposure concentrations and lung burden that exceeded the capacity
of the lung to clear the particles and induced significant toxicity.
A central question is whether the toxic and defensive mechanisms suggested to
operate in rats also operate in humans. Very little is known about the relationship
between overload and lung cancer risk in humans, although it may be assumed that this
overload-related mechanism could occur in humans exposed to sufficient levels (or
doses). Limited indirect inferences regarding this issue may be derived from the available
epidemiological studies of workers exposed to carbonaceous particles. The epidemio-
logical studies of carbon black workers are not very informative in this regard. It is
interesting to note that studies of coal miners have generally failed to detect an increased
risk for lung cancer (Merchant et al., 1986; Harrington & Levy, 1994). This evidence has
been interpreted by sorne scientists as suggesting that a lung overload-related mechanism
does not induce cancer in humans. However, there are other plausible interpretations for
these observations that should be considered. lt is difficult, as with nearly aU
epidemiological studies, to mIe out that limitations in sample size, bias and other study
design issues might explain these negative findings. The Working Group considered that
the fact that coal miners are not permitted to smoke while working may have introduced
a negative confounding bias for lung cancer in these studies. This bias is consistent with
the observation of a deficit in lung cancer risk in these studies. Furthermore, it is
important to consider the surface area characteristics of the inhaled low-toxicity,low-
solubility particle (including coal dust) and its impact on dose.
Lung particle burden in the lungs of these workers by mass were on average ~ 15 mg/g
lung. However, although pulmonary particle accumulation by mass is very high 'in coal
miners, particle mass may not be the most relevant dose parameter for a correlation with
specific long-term effects. It has been suggested, based on results of a number of studies,
that surface area of retained particles may be a better parameter for correlation with
pulmonary inflammation and neoplastic events. Thus, it may weIl be that coal miners, in
spite of the high mass loading of particles in the lungs, did not reach a sufficient surface
area of the retained particles. Also in rats, it has been found in sorne studies that lung
particle mass burdens in this range, and even higher, did not result in increased tumour
incidences. For example, chronic studies in rats with toner particles and pigment-grade
titanium dioxide at exposure concentrations of 16 mg/mJ and 50 mg/mJ, respectively,
resulted in typical findings of particle overload (e.g. impaired particle clearance at lung
burdens of ~ 12 and 60 mg/g lung, respectively) but with less inflammatory response and
without induction of lung tumours. When these pulmonary mass particle burdens are
expressed in terms of their surface area, the retained dose (by particle surface area) is
lower than the dose (by surface area) observed to induce lung tumours in rats in other
studies.
Epidemiological studies of diesel-exposed workers may also contribute something to
this issue. A recent review of the epidemiological literature in this area concluded that
these studies suggest a small-to-moderate increase in lung cancer risk, and that these
findings do not appear to be fully explicable by confounding or other sources of bias
(Cohen & Higgins, 1995). These studies an~ pertinent because it has been suggested,
based on the recent experimental studies of rats exposed to high concentrations of diesel
 CARBON BLACK 243

exhaust and carbon black (Nikula et aL., 1994; Heinrich et aL., 1995), that the increased
risk for lung cancer associated with diesel exhaust in rats might be explained by the
carbonaceous core rather than the organic fraction of diesel soot. W orkers in these
studies were generally exposed to diesel exhaust levels below 200 llg/m3, which is below
the level at which overload of the lung in humans is believed to occur (Cohen & Higgins,
1995). These findings might be interpreted as suggesting either that lung overload occurs
at lower levels than expected among humans, or that an overload-related mechanism may
play the dominant role only at the high-exposure levels used in experimental studies.
ln addition to these dose considerations, it is also of importance to consider
differences in specific defence mechanisms between rats, mice and humans. The
Working Group is not aware of studies which have evaluated specific pulmonary
defences, including antioxidant levels, in humans under partic1e load conditions; such
data, in contrast, are available for rats and mice. Thus, whether humans respond to
chronic inhalation of particles, inc1uding carbon black, more like a rat or more like a
mouse cannot be decided at present. lt should be emphasized that the dose plays a most
important role in the chain of mechanistic events outlined in Figure 1.

5. Summary of Data Reported and Evaluation

5.1 Exposure data

Carbon black is a powdered form of elemental carbon manufactured by the vapour-

phase pyrolysis of hydrocarbon mixtures, such as heavy petroleum distillates and
residual oils, coal-tar products, natural gas and acetylene. W orldwide production of
carbon black in 1993 was approximately 6 million tonnes.
Carbon blacks are categorized as acetylene black, channel black, furnace black,
lampblack or thermal black, according to the process by which they are manufactured.
Lampblack is the oldest type of carbon black, having been used as a pigment for
centuries. Channel black, produced from natural gas, was introduced in the late
nineteenth century and was the major carbon black used worldwide in the early twentieth
century for rubber and pigment applications; with the exception of a special product
made in Germany, it is no longer produced. Acetylene, furnace and thermal blacks have
been produced since the early twentieth century. Over 90% of aIl carbon black produced
today is furnace black.
The primary use of carbon black is in rubber prqducts, mainly tyres and other
automotive products, but also in many other rubber products such as hoses, gaskets and
coated fabrics. Much smaller amounts of carbon black are used in inks and paints, in
plastics and in the manufacture of dry-cell batteries.
Types of carbon black are characterized by the size distribution of the primary
partic1es, the degree of their aggregation and agglomeration and the various chemicals
adsorbed onto the surfaces. Average primary partic1e diameters in several cOllmercially
produced carbon blacks range from lOto 400 nm, while average aggregate diameters
244 lARC MONOGRAPHS VOLUME 65

range from 100 to 800 nm. Typical classes of chemicals adsorbed onto the carbon black
surface are polycyc1ic aromatic hydrocarbons (PAHs), nitro derivatives of PAHs and
sulfur-containing P AHs. Examples of P AHs extracted most frequently from carbon black
using a variety of extraction methods (e.g. prolonged Soxhlet extraction with benzene or
toluene) inc1ude benzopyrenes, benzo(ghi)perylene, coronene, fluoranthene and pyrene.
Exposures to carbon black vary markedly within any production facility. The highest
levels of exposure are experienced by those who interact with the process the most,
including fitters/welders, warehouse packers and site cleaners. Exposures can vary
greatly among factories and regionally.
Several studies in the 1960s found very high levels of exposure, even up to
1000 mg/m' in furnace, lamp- and channel black plants. Later studies in sorne countries
have found lower levels, although many of these were in excess of the existant occupa-
tional exposure limits. ln the late 1980s and early 1990s, more extensive studies in
western Europe and the United States have found (geometric mean) personal exposure to
total inhalable carbon black to be on average less than 1 mg/m'. Even lower exposures
may occur among sorne workers in industries using carbon black, such as rubber,
printing ink and paint manufacture, and exposures to carbon black in the use of rubber,
printing ink or paint are negligible.

5.2 Hurnan carcinogenicity data

The greatest potential for elucidating the carcinogenicity of carbon black is in the
carbon black production industry where carbon black has been the prime industrial
exposure and where exposure levels have been high. Cohort studies of carbon black
production workers have been conducted in the United States and in the United
Kingdom. Interpretation of the study in the United States is hampered by problems of
uncertainty in the completeness of the cohort and in the definition and completeness of
follow-up. The study in the United Kingdom also had some problems in completeness of
the cohort, but the follow-up was probably complete. ln both cohorts, fewer observed
than expected deaths due to aIl causes occurred and, in the study in the United States, this
may in part have been attributable to under-ascertainment of deaths or to inflation of
person-years of follow-up. The study in the United States found no excess mortality due
to any type of cancer when compared to state vital statistics rates; in fact there were
deficits for sorne types of cancer. The study in the United Kingdom found an excess of
respiratory cancer deaths (standardized mortality ratio, 1.5; 95% confidence interval,
1.0-2.2).
A nested case-control study within the United States cohort was hampered by very
small numbers and problems of interpretation. Most cases were of non-melanoma skin
cancer. Neither for aIl cancers combined nor for skin cancers alone was there evidence
that cases had higher cumulative exposure to carbon black than contraIs.
A cohort study was carried out among workers in the United States to assess cancer
risks due to exposure to formaldehyde. Ten participating plants were spread across
several industries in which workers may have experienced exposure to formaldehyde. To
control for confounding and modification of effect by other exposures, workers'
 CARBON BLACK 245

ex sures to various other chemicals, including carbon black, were assessed by industrial
po

hygienists. For aIl assessed levels and durations of exposure to carbon black combined,
there was a slight nonsignificant excess of lung cancer. There was no clear trend by
duration of exposure. Carbon black-exposed workers in this cohort may also have been
exposed to formaldehyde and other substances.
Another industry-based study was a nested case-control study conducted in the tyre
and rubber manufacturing industry to examine the association of squamous-cell
carcinoma of the skin with rubber manufacturing materials. For each study subject,
industrial hygienists assessed exposure to five substances, including carbon black, based
on evaluations of each subject s job history. The results of this study indicated no effect
of carbon black on skin cancer.
ln a community-based case-control study in Canada, interviews were designed to
obtain detailed lifetime job histories and information on potential confounders. Potential
occupational exposures were identified for each job description, and among the
exposures assessed was carbon black. ln this study population, potential exposure to
carbon black occurred in some individuals in user industries, notably among painters and
in the printing and rubber industries. For the folIowing cancer sites, there was no
indication of excess risk in relation to carbon black: stomach, colon, rectum, pancreas,
prostate, urinary bladder, skin melanoma and non-Hodgkin's lymphoma. For the
following sites there was indication of excess risk: oesophagus, kidney and lung. The
lung cancer excess was particularly concentrated among oat-celI cancers.
A Swedish case-control study reported a nonstatistically significantly increased risk
for urothelial cancer for men exposed to carbon black.
ln assessing aIl the available data, there is no evidence of an effect of carbon black for
most cancer sites. For cancers of the urinary bladder, kidney and oesophagus, isolated
results indicate excess risks, but these are not sufficient to support an evaluation of
human carcinogenicity.
Two studies were informative for non-melanoma skin cancer (a nested case-control
study among the United States carbon black production cohort and a nested case-control
study among rubber workers); neither demonstrated any excess risk for skin cancer due
to carbon black.
Of the studies listed above, four were considered informative for lung cancer. Of
those, two indicated excess risk among carbon black-exposed workers at borderline
statistical significance (the carbon black production cohort in the United Kingdom and
the Canadian community-based study), one indicated excess risk but was not significant
(the United States formaldehyde cohort) and the other indicated no excess (the United
States carbon black production cohort).
Each of the available studies has limitations for the specific purpose of assessing the
carcinogenicity of carbon black. The W orking Group considered the study of carbon
black producers in the United Kingdom to be the most informative for this purpose. That
study indicated an excess risk of borderline significance. Confounding by smoking could
not be excluded, although some information was presented indicating that it was
unlikely. The formald¿hyde cohort study indicated a slight excess of lung cancer among
246 IARC MONOGRAPHS VOLUME 65

the subgroup exposed to carbon black, but this could easily have been due to chance or
confounding by formaldehyde or other occupational substances. The community-based
study in Montréal of exposure in a variety of user industries showed an elevated risk in
the subgroup categorized as having high exposure to carbon black; the result was of
borderline statistical significance using a cancer series control group and not significant
using a population control group. It is not clear which control group provides the most
valid estimates. Even the high-exposure subgroup of this study was unlikely to have
experienced exposure levels of the same order of magnitude as did workers in the carbon
black production industry. Although the United States carbon black worker study, which
was negative, was large, its methodological limitations detracted from its value. The
Working Group therefore considered the whole body of evidence rather weak and the
results conflicting.

5.3 Anirnal carcinogenicity data

No adequate study of the carcinogenicity of carbon black admInistered by the oral

route was available.
ln one study in female mice by inhalation exposure, carbon black did not increase the
incidence of respiratory tract tumours.
Two different carbon black products were tested in two inhalation studies in female
rats and in one study using rats of each sex. Significant increases in the incidence of
malignant lung tumours and the incidence of benign and malignant lung tumours
combined were observed in female rats in aIl three studies. ln addition, increased
incidences of lesions described as benign cystic keratinizing squamous-cell tumours or
squamous cysts were observed.
ln two studies in female rats by intratracheal administration, using one type of carbon
black, both extracted and non-extracted material increased the incidence of benign and
malignant lung tumours. ln one of the studies, a different type of extracted carbon black
with a larger primary particle size increased the incidence of les ions described as benign
cystic keratinizing squamous-celI tumours.
ln several skin-painting studies in mice using various carbon blacks, no carcinogenic
effect on the skin was observed; the painting of several carbon black extracts (benzene
extracts) resulted in skin tumours.
ln a series of studies in male and female mice by subcutaneous injection, a carbon
black containing demonstrable quantities of carcinogenic P AHs produced local sarco-
mas, whereas a carbon black from which no P AH was detected did not produce such
sarcomas. ln several studies in mice, solvent extracts of carbon black produced sarcomas
folIowing subcutaneous injection.

5.4 Other relevant data

Upon inhalation exposure of humans to carbon black, these particles are deposited in
the lung. The exposure may cause slight radiological changes. The prevalence of
radiological findings has varied considerably among different studies, probably because
 CARBON BLACK 247

of varying radiological techniques and possibly also due to different exposure

circumstances and possible concomitant exposures to other compounds. Further, workers
may develop chronic bronchitis and a slight reduction in lung function. These findings
may be interpreted mainly as a slight nonspecific irritant effect of heavy dust exposure.
On the other hand, sorne data indicate a fibrous tissue reaction in the area surrounding
the carbon deposits in the lung parenchyma.
Studies on the pulmonary retention of inhaled carbon blacks in rats and mice have
shown that the se particles behave very similarly to other low-solubility, low-toxicity
particles. Carbon black displayed normal retention characteristics in rats at lung burdens
not exceeding a certain level which is approximately in the range of 0.5-1 mg/g of lung.
At higher lung burdens, a prolonged clearance is found. Impaired particle clearance due
to high loading of carbon black in experiments with rats results in increased accumu-
lation of particles. Subsequent inflammatory responses occur which develop into chronic
active inflammation. Increased colIagen deposition from proliferating fibroblasts,
increased epithelial celI proliferation and metaplasia have been found at high lung
burdens of carbon black. it appears that the high specific surface area of most carbon
blacks may be an important parameter in the induction of inflammatory and subsequent
other responses in the lung. One study with carbon black in rats confirmed findings with
other particles that females are more sensitive th
an males.
Most assays for mutagenicity are negative for carbon black. ln rats exposed to carbon
black by inhalation, hprt mutant frequency was elevated in type II celIs folIowing a 12-
week exposure. Carbon black did not indu
ce a significant increase in DNA adducts in
peripheral lung tissue of rats after two years of inhalation exposure. ln another study,
exposure of rats by inhalation to carbon black increased DNA adduct levels in type II
celIs. K-ras mutations were found in one out of 18 neoplasms analysed from a carbon
black-exposed rat. No exposure-related p53 mutation was found.
Sorne mechanistic considerations on particle-induced lung neoplasms are presented.

5.5 Evaluation 1

There is inadequate evidence in humans for the carcinogenicity of carbon black.

There is suffcient evidence in experimental animaIs for the carcinogenicity of carbon
black.
There is suffcient evidence in experimental animaIs for the carcinogenicity of carbon
black extracts.

OveraU evaluation
Carbon black ispossibly carcinogenic to humans (Croup 2B).

i
'For definition of the italicized terms, see Preamble, pp. 24-27.
248 lARC MONOGRAPHS VOLUME 65

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