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age stratification. The power of this study was limited by differences between the case group and the
referent group in the number of smokers and gender composition.
Creosote contains many of the same compounds present in other polycyclic aromatic hydrocarbon
(PAH) mixtures (roofing tar pitch, coke oven emissions) known to be human carcinogens (US EPA,
1986; ATSDR, 1990).
Animal Studies
Female C57BL mice (10 animals/group) were exposed to blended creosote oil (a mixture of creosote,
anthracene oils and naphthalene recovery residue oil) in toluene. One drop (8.7 - 9 µl) of a 20% or
80% solution was applied to the skin three times/week for the animals’ lifetimes or until tumors
developed (21 - 44 weeks and 18 - 35 weeks for the 20% and 80% solution exposure groups,
respectively). All treated mice developed skin papillomas and 7 mice in each group developed
epidermoid carcinomas, some of which metastasized to pulmonary or regional lymph nodes. None of
the vehicle control animals developed skin tumors (Poel and Kammer, 1957).
Female Swiss mice (30/group) were treated twice weekly with one drop of a 2% solution of creosote in
acetone applied dermally for 70 weeks. Skin tumors (including 16 carcinomas) were reported in 23 of
26 surviving mice. The average tumor latency period was 50 weeks. No vehicle control group was
included; however, no animals in a control group of 50 mice receiving a single application of 1% 7,12-
dimethylbenz[a]anthracene in mineral oil developed tumors after 80 weeks (Lijinsky et al., 1957).
Undiluted creosote applied topically twice weekly (25 µl) to 30 random-bred female mice for 28 weeks
induced an average of 5.4 papillomas per animal; 82% of the mice had carcinomas. The average time
to tumor for papillomas and carcinomas was 20 and 26 weeks, respectively. No vehicle control group
was included in the study (Boutwell and Bosch, 1958). In a similar study, a group of 24 albino mice
treated dermally with 25 µl creosote twice weekly for 5 months and housed in stainless steel cages
exhibited 139 lung adenomas (5.8 tumors/mouse) after 8 months. A group of 29 mice born and housed
in creosote-treated wood cages treated dermally with 25 µl creosote for 5 months demonstrated 315
lung adenomas (10.8 tumors/mouse) after 8 months. A control group (19 mice) housed in stainless steel
cages demonstrated 9 lung adenomas (0.5 tumors/mouse) after 8 months (Roe et al., 1958).
V. DERIVATION OF CANCER POTENCY
Basis for Cancer Potency
Creosote has been demonstrated to cause skin and lung tumors in mice after dermal exposure, and is
predominantly composed of PAH; similar PAH-containing coal tar products (roofing tar pitch, coke
oven emissions) have been shown to be human carcinogens (US EPA, 1986; ATSDR, 1990).
Creosote has been given B1 and 2A classifications (probable human carcinogen) by US EPA (1987)
and IARC (1985), respectively. No creosote carcinogenicity bioassay study suitable for quantitative
risk assessment exists. However, a cancer unit risk factor for the PAH benzo[a]pyrene (BaP) derived
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