Experts in ToxicologyHomeHome
Home PageAbout UsContact UsToxicology SupportProduct SafetyToxicology TopicsOther ServicesDr. Richard A. Parent

Toxicology Notes and Literature

Creosote Notes



Chronic exposures: Increased sensitivity to sunlight, damage to cornea, skin damage(reddening, blistering and peeling), irritation of the respiratory tract, skin cancer and scrotal cancer; pulmonary restrictive and obstructive effects;  (CTX-33170tp)


  1. Two year chronic bioassays conducted using B6C3F1 mice fed several concentrations of two different creosote mixtures from MGP (manufactured gas plant) wastes or BaP in order to estimate cancer potency; dose-reponse relationship for forestomach tumors and lung tumors for both composite creosote mixtures; cancer risks are higher for forestomach cancer if BaP concentration is high but higher for luca if BaP concentration is below 6300ppm; this upper limit of risk of cancer is 2.4x10-2 per ppmBaP in total diet which converts to 1.2x10-3 per ug/kg per day in humans; this is 6x lower than the cancer potency of BaP in humans of 7.3x10-3 per ug/kg bw per day; upper limit of risk for coal tar and lung tumors; upper limit of risk to humans consuming coal tar estimated to be 2.55x10-4 ppm coat tar in total diet per day for continuous lifetime exposure(CTX-33104)
  2. Workers exposed to coal tar creosote, coal tar, coal tar pitch volatiles in various occupational setting have been found to have increase cancer risk involving repiratory tract, skin, lung, pancreas, ,kidney, scrotum, prostae, rectum, bladder and Central Nervous System; leukemia and lymphoma have also been diagnosed; (CTX-33170; tp)
  3. coal tars are byproducts of coal gasification; TEFs for PAHs are described; calculates total TEQs for mixtures; incomplete data but believes that dose-related increase in cancers will be possible also risk calculations(CTX-33040)
  4. TEFs for various PAHs and listing of classifications relative to carcinogenicity by the EPA, NTP and IARC(CTX-33076)
  5. carcinogenicity of two coal tar mixtures compared to BaP after 2 yrs feeding to female B6C3F1 mice; Mixture 1 was composite of coal tar from 7 coal gasification plants; mixture 2 was coal tar mixture from 2 of the 7 sites plus another site high in BaP; coal tar diets induced a dose related increase in hepatocellular adenomas and carcinomas, a/b adenomas and carcinomas, small intestine adenocarcinomas, hitiocytic sarcomas, hemangiosarcomas in multiple organs and sarcomas.  BaP treatment resulted in increased incidence of papillomas and carcinomas of the forestomach, esophagus and tongue; lung and liver tumors from the mixture appeared to be due to other components in the mixture (CTX-33024)
  6. Using infant B6C3F1 mice, BaP and two manufactured gas plant[MPG] residues were used for a single treatment with subsequent observations extending to 52 weeks; persistent DNA adducts were quantified using 32P postlabeling; exposure of males to BaP induced liver tumors in a time and dose dependent manner; BaP could not account totally for the tumorgenicity; MPG was more potent probably due to unidentified components ie: more tumors than expected based on BaP content(CTX-33083)
  1. Female Wistar rats exposed to coal tar/pitch condensation aerosols for 17h/d, 5d/wk for 10-20 months followed by clean air for 20 or 10mo; corresponding lung cancer rates increased with dose of BaP going from 4.2% to 97.2% in aµ with no lung tumors in the control group(CTX-8832)
  2. Female Wistar rats exposed to coal tar pitch condensation aerosols for 17h/d, 5d/wk for 10-20mo followed by clean air for 20 or 10mo; lung tumors were SCCs mostly; concludes that risk of lung cancer is greater when vapors are carried by carbon particles as opposed to being inhaled as pure vapors(CTX-33050)
  3. Early study(1958) of induction of skin tumors by creosote oil in mice; skin painting studies; creosote applied 2x/wk; DMBA as positive control, benzene as solvent control; papillomas developed in mice treated with creosote alone, DMBA then creosote, DMBA then croton oil, creosote for 4 weeks then croton oil(CTX-33010)
  4. Early study(1940): skin painting of BaP and creosote oil fractions 3x/wk for 20 weeks; observations to 52 weeks; skin tumors increased with time in animals treated with creosote fractions; also benzo[a]pyrene; (CTX-33013)
  5. Early study(1957) - creosote used in this study was a #1 oil from a Wilton still; swiss female Jackson mice used; skin application twice weekly with and without DMBA; latency for tumor formation from 39-50 weeks on average; 70 week experiment; malignant skin tumors resulted; mostly carcinomas; (CTX-33063)
  6. Early study(1957): exptl carcinogenesis of coal tar fractions; 2 creosote oils studied here; used blended creosote oil in toluene; benzo[a]pyrene as control; papilloma induction time in high dose group ranged from 19 to 34 weeks; papillomas developed on all animals that received repeated applications of BaP and epidermoid carcinomas developed subsequently at all sites of exposure; all mice exposed to both dilutions of creosote oil also developed papillomas; 7/8 progressed to malignancy; with creosote there was a higher incidence of tumors in a shorter period of time than with BaP; also greater extent of metastasis ; potency of creosote greater than that of BaP control; (CTX-33078)
  7. Early Paper(1958): first experiment skin painted dose sufficient to cause skin tumors and lung tumors; second expt skin painted with smaller dose sufficient to cause lung tumors but not skin tumors; in first expt 139 lung adenomas in 24mice; and 315 in 29mice held in creosoted cages; in second expt 37 lung adenomas in 23 mice; (CTX-33084)
  8. Early Paper(1940); skin painting shows that the basic fraction of creosote enhances the carcinogenicity of BaP in the skin painting assay - a promoting effect; similar effects with dibenzanthracene and basic fraction; here the basic fraction by itself did not produce tumors but when coupled with an initiator produced enhanced responses(CTX-33085)
  9. Early Study(1930): skin painting = tumors(CTX-33097)(1924 epithelioma; CTX-33020)
  10. NHLs produced in mice exposed for 4 months to coal tar pitch smoke and observed for four months(CTX-33062)
  11. Mice exposed by inhalation to coal tar aerosol developed squamous cell tumors one of which was a carcinoma(CTX-33052)
  12. 3-methylcholanthrene induces mammary carcinomas in rats but not during pregnancy suggesting that hormones regulate the promotion process by 3-MC(CTX-33027)
  13. Comment on NTP study using B6C3F1 mice in a two year feeding study found differning tumor site for coal tar mixtures and BaP alone; coal tar treatments resulted in tumors of the lung, liver, forestomach, skin and small intestines; treatment related hemangiosarcomas and histiosarcomas were found at several organ sites; BaP acted more as a point of contact carcinogne with tumors found in tongue, esophagus, forestomach and larynx(CTX-33036)
  • IARC(1982) - Group 1 for soots, tars and oils (evidence for carcinogenicity in humans is sufficient) inadequate for BaP; coal soot, coal-tar and pitch, coal tar fumes cause cancer at several sites including skin, lung, bladder and gut; also sufficient in animals(CTX-31470)
  • IARC(1972) - review of cancer in PAH workers; “Because polycyclic aromatic hydrocarbons are so well established as experimental carcinogens...” Review of human data; cites cases of skin cancer in man(numerous cites); also describes lung cancer, bladder cancer and scrotal cancer(CTX-8835)

    1. Wood-Preserving Waste Sludge - from surface impoundment at an active wood treatment facility which includes PCP; the study demonstrated mutagenic constituents from land treated wood preservative sludge persisted in surface soil for at least 350 days after sludge application using the Ames test(CTX-32999)
    2. positive mutagenic responses using S typh on bioremediated soil from creosote sites(CTX-33053)
    3. Creosote was assayed for mutagenicity using the ames test; it was positive with TA 1537, 1538, TA98, 100 with S9(CTX-33117, 33118, 33119)
    4. Used chick embryotoxicity screening test and the Ames test for coal tar and its fractionated PAHs and mixtures; dose-dependent increase in embryo mortality observed for all fractions; using TA98 with S9 coal tar and the higher MW fractions induced dose response; compositional information presented on the different fractions(CTX-33069)
    5. Good correlation between DNA adduct levels and mutagenicity by S typh for 19 oils including coal tar(CTX-33080)
    6. Mutagenicity of urine extracts from non-smoking psoriasis patients treated with coal tar and anode plant workers exposed to coal tar pitch volatiles; urine samples which were mutagenic showed elevated levels of PAH metabolites; used S typh TA98 with S9; 1-hydroxypyrene was used as a marker metabolite for coal tar exposure(CTX-33018)
    7. SCEs in peripheral lymphocytes of potroom workers in Al smelter not elevated but is very much elevated in smokers; smokers inhale about 10-40ugPAH per pack whereas potroom workers inhale average of 1mg total PAHs in 8 hr shift (CTX-33144)
    8. Chromosomal aberrations and SCEs in lymphocytes of coke oven workers(ss) 30 steelworker volunteers; (CTX-33011)


    1. 57yo male showed warty plaques on scrotum; gross hyperkeratosis with acanthosis and papillomatosis in the epidermis and a chronic inflammatory infiltrate in the dermis; treated with coal tar and eczema appeared; patch tested: positive for coal tar(CTX-33026)
    2. Irritability and phototoxicity of coal tar on normal skin(CTX-33029)


    1. Human studies of women using crude coal tar skin treatments during pregnancy vs controls; in group using tar(n=56) 19% sp abor, 5% congenital disorder; in group not using tar during pregnancy(n=23), 26% sp abortion and 4% with congenital disorder(CTX-33034)
    2. Animals: Intragastric intubation of heavy distillate to pregnant rats at five dosing levels; treated from 12 to 16 days of gestion = thymic weights decreased, adrenal weights increased; increased intrauterine mortality, fetal abnorms increased in a dose-dependent manner(CTX-33045)
    3. dermally applied coal tar derived complex applied to skin of pregnant mice and rats and shown to produce resorptions and tetratogenic effects in both species(CTX-33102)


    1. Cohort of 15,818 coke oven workers with over 30yrs of work history showing increased risks of respiratory cancer and prostate cancer; RR lung,bronchus, trachea = 1.95ss; RR prostate 1.57ss overall; with employment over 20 years: RR resp ca = 2.71ss; 20yrs at top side jobs(increased exposures)RRresp=4.34ss; for weighted exposure index of >=650mg/m3-mo RR = 3.13 for resp cancer; for weighted exposure index of 200-399, RR for prostate cancer = 1.93ss; strong exposure-response relationship(CTX-33021)
    2. Case-referent study of incidence of glioma in wood workers; found ss increased OR in teachers (4.1) and increased incidence among wood worker(OR=1.6) who had frequent exposure to organochlorine wood preservatives and solvents; no referents had gliomas; 9 cases of gliomas(astrocytoma, glioblastoma) in woodworkers many of whom were exposed to creosote and organochlorine compounds(CTX-32980)
    3. City of St Louis Park, a suburb of Minneapolis water supply contaminated with PAHs; found pyrene, flouanthene, anthracene and naphthalene in water; looked as SIRs for breast cancer compared to three reference areas and found SIRs of 3.38ss, 10.85ss and 13.64ss; and all female cancers at 19.9ss, 21.18ss and 24.31ss; age adjusted incidence rates; for males no ss increase in rates; for female breast cancer, GI cancer were higher and were statistically significant(CTX-33030)
    4. Case-control study of 183 histologically confirmed cases of neuroblastoma in 0-14yo children; risk factors including paternal exposure to creosote(OR=2.1ss), dioxin(OR=6.9ss); petroleum(OR=1.8ss)(CTX-32950)
    5. Case-referent study of 131 cases of multiple myeloma and 431 randomized referents; crude OR for creosote = 6.0(p=0.001)(CTX-32984)
    6. Disease prevalence study based on household interviews of 214 residents around a hazardous waste site and 212 comparison residents in a neighborhood away from the site; prevalence of skin rashes 27.9% vs 4.9%(RR=5.7ss); dose response related to anthracene concentration in soil (p=0.02); difficulty becoming pregnant ave 1.3 vs 3.4 pregnancies(p<0.04); among residents reported digging in their yard 30.3% reported difficulty while those who denied digging reported 10.0% with difficulty(RR = 2.8ss); during flup in second year: 34 site people reported skin rashes while only 4 control (std morbidity ratio = 8.5ss and among site residents, RR for digging vs not digging = 2.95ss (CTX-33012)
    7. Cancer in a community exposed to low levels of creosote components in municipal water when compared to two other communities without contamination; no male cancer was any different but female age adjusted rates for all cancer sites combined, for breast cancer and for cancers of the gastrointestinal tract were higher in the contaminated area; excess gastrointestinal cancer was slight sign(p<0.05) but all cancer sites combined had a high degree of statistical significance(p<0.0005)(CTX-33030)
    8. Cancer suvey of coke oven workers; resp cancer O/E=14/10; basically negative study(CTX-33082)
    9. Case-referent study of 85 cases of bladder cancer among aluminum smelter workers previously reported; each case with three matched controls; here estimates of past exposure to total tar(benzene soluble) and BaP; assuming a minimum latency period of 10 years, the data were compatible with a linear relationship between cumulative exposure and relative risk(DOSE-RESPONSE); RR for bladder cancer increases to 5.75ss for 30+ years in potroom(D/R); RR= 6.3ss for 30mg/m3-years exposure to benzene soluble material(D/R) and RR= 5.89ss for exposure to BaP at 300ug/m3-years (D/R) (CTX-33123)
    10. EEH(Equitable Environ Health for Al Assn) cohort of 22,010 workers in 15 Aluminum reduction plants is examined here in more detail; more than 1000 records were added to the cohort; 5 or more years of exposure bet Jan 1 1946 and Dec 31, 1977; increased risk of pancreatic cancer in potroom; SMR=168.2ss; one plant showed SMR = 365.9ss for luca in men with 25yrs or more experience in the carbon shop; SMR emphysema for potroom workers = 194ss and for carbon workrs =267ss; (CTX-33126)
    11. Update of study of respiratory cancer in coke oven workers; for respiratory cancer:

    work area                                                                                                                                5+yrs                           10+yrs                         15+yrs
    coke ovens                                                                                                                                          n          RR                        n          RR                        n          RR

    coke oven overall                                                                                                                    54        3.02ss              16        3.42ss              33        4.14ss
    oven topside full time                                                                                                             25        9.19ss              16        11.79ss            8          15.72s
    oven topside part time                                                                                                12        2.29ss              16            3.07ss              18            4.72ss

    overall pancreas ca                                                                                                                  8          3.67ss              7          3.75ss              6          4.29ss
    overal respiratory disease                                                                                            34        1.47ss              31            1.82ss              25            2.01ss
    authors claim that the 150ug/m3 BSFTPM (benzene soluble fraction of total particulate matter) PEL may not be a safe level(CTX-33141)

    1. Retrospective mortality study of 610 coke oven workers studied over a period of 11 years; during this period 82 deaths; ( British Steel Paper): health worker effects; no sign elevations of any disease is obvious from this study(CTX-33028)
    2. Cohort of 534 male coke oven workers who had retired from 1963 to 1982; SMR luca = 2.51ss relative to overall French population(CTX-33002)
    3. Historical cohort study of 4213 men who worked 5 or more years at a Soderberg aluminum reduction plant in British Columbia; SMRs compared to BC population: found increased incidence of bladder cancer (SIR=1.69ss) with risk of bladder cancer strongly [p<0.05] related to cumulative exposure to coal tar pitch volatiles(D/R); also brain cancer mortality was increased (SMR=2.17ss); based on 193 diagnosed cancer cases; for those exposed for 10+ years to benzene soluble material(BSM-yrs) SIR = 5.0ss for bladder cancer; (CTX-33125)


    1. Based on case-referent study, suggestion: “...there is some evidence , though falling short of concentional statistical significance, for the multiplicative model” - combined BSM and smoking/bladder cancer(CTX-33123)
    2. Urinary excretion of PAH metabolites show a sign higher level in smokers than in controls(CTX-33143)
    3. urinary excretion of 1-hydroxypyrene based on 45 smokers compared to non smokers reported 0.12umol/mol creat for smokers and 0.07umol/mol creat - no difference(CTX-32966)
    4. Urinary excretion of 1-hydroxypyrene does not increase in smokers but does increase significantly in those undergoing coal tar treatment and in rats painted with coal tar solutions(CTX-33056)


    1. ACGIH TLV for BSM(benzene soluble material from creosote,coal tar) is 0.2mg/m3; if inhaled at this level for 40 years risk of contracting bladder cancer is about 2.5 times that of unexposed individual(CTX-33123)
    2. Criteria for Recommended Standard: Occupational Exposure to Coal Tar Products; 1977: NIOSH/CDC: effects on humans: phototoxicity of skin resulting in erythema and burning and itching of skin; photophobia, conjunctivitis, skin and lung cancer in humans; workers complained about tingling sensation, papular dermatitis, hyperpigmentation; skin carcinomas; lots of studies cited(CTX-33120)


    1. 67yo male with 25y hx of generalized psoriasis presented with a 2 yr history of slowly enlarging scrotal lesion - invasive SCC ; he had been applying 10% crude coal tar ointment(CTX-33070)
    2. Multiple cutaneous carcinomas after creosote exposure; mixed basal cell and epidermoid carcinomas from painting creosote by 64yo male(CTX-33060)
    3. Epithelioma of skin in a worker exposed many years to creosote; metastatic lesions also(CTX-33020)
    4. 64yo male with mixed basal cell and epidermoid carcinomas with marked inflammation - shipyard painter of creosote(CTX-33060)


    1. Cohort of coke oven workers showing strong dose-reponse relationships based on years of employment, exposure parameters using weighted exposures, for both lung cancer and prostate cancer(CTX-33021)


    1. Both estrogen receptor(ER) and aryl hydrocarbon receptor(AhR) mediated activities studied; coal tar creosote bindings to mouse ER in vitro and human sex hormone-binding globulin; the results demonstrate that coal-tar creosote exhibits AhR and ER mediated activity in vitro but its dioxin like activity may suppress estrogenic responses in vivo; the dioxin like activity in creosote is likely due to the presence of dioxin-like PAHs within creosote such as benzo[k]fluoranthene, dibenzo[ah]anthracene, chrysene, anthracene, benzo[a]pyrene and benzo[a]anthracene; concludes that coal-tar creosote can elicit ER-mediated and AhR mediated activity in vitro despite low concentrations; thus creosote can act as an endocrine disruptor via these receptors(CTX-33033)


    1. assessment of levels of cytochrome CYP1A1 gene experssion in human peripheral lymphocytes as a molecular biomarker assay for PAH exposure; basal and 3-methylcholanthrene induced levels of gene expresion measured in mitogen-stimulated cultures of peripheral blood lymphocytes from creosote-exposed railroad workers and unexposed controls; seasonal study found induced basal CYP1A1 mRNA ratios from workers sampled in the summertime when the exposures were the greatest were sign higher than controls (P<0.01); these studies demonstrate the utility of specific gene expression assays in human periph lymphocytes for the assessement of carcinogen exposure in humans(CTX-32976)
    2. PAH-DNA adducts in humans has become more reliable allowing for detn of background lelvels of adducts in exposed persons; immunoassays and immunocytochemistry using polyclonal or monoclonal antisera specific for DNA adducts or modifed DNA and 32P postlabeling assay and adduct identification using physiochemical instrumentation; here PAH-DNA have been identified in a variety of human tissues including target organs in smokers; here look at WBCs of exposed foundry workers by various techniques with references; this is a review(CTX-33136)
    3. Use of PAH-DNA adducts in leukocytes and plasma cotinine measured in umbiical cord blood as dosimeters of transplacental PAH and cigarette smoke respectively; studied 70 newborns from industrial area and 90 from rural area; describes median PAH-DNA adducts at 3.85/108 nucleotides; babies above that value showed decrease birth length, weight and head circumference; cotinine was inversely associated with birth weight and length; these results provide a molecular link between PAH exposure and developmental effects - prelim data; (CTX-33140)
    4. In Poland where PAHs in air are similar to those in coke oven workers showed increased DNA- adducts by 32P post-labeling techniques; these were correlated with SCEs and showed adducts at as much as 10 times those of controls sampled in uncontaminated rural areas(CTX-33135)
    5. DNA binding in B6C3F1 mouse lung is dose-related to coal tar in feed; DNA adducts detected in lung, liver spleen in all treated animals; 1-pyrenol was the major PAH detected in urine; BaP alone cannot account for the levels of DNA adducts observed(CTX-33100)
    6. DNA adducts measured in peripheral lymphocytes of 90 coke-oven workers and compared to postal workers; DNA adducts in WBCs ranged from <1 to >5adducts/108 nucleotides using 32P postlabeling techniques(CTX-33061)
    7. Rats exposed to coke oven topside emissions in short term exposures and to coal tar pitch aerosol in long term studies by inhalation; DNA adduct levels in the lung and heart tissue were over four times higher than levels measured in the WBCs(CTX-33061)
    8. Chromosomal aberrations and SCEs in lymphocytes of coke oven workers(ss) 30 steelworker volunteers; (CTX-33011)
    9. Urinary 1-naphthol excretion in assessment of exposure at creosote site; coal tar creosote in yard coating RR ties; sensitive to low concentrations of naphthalene; mean urinary level of 1-naphthol was 20.5umol/l(3.5-62.1) where as referent population was <dl of 0.07umol/l; non-smokers; (CTX-32961)
    10. Urinary excretion of 1-hydroxypyrene over 24 hrs; a good biomarker for 3-6 ring PAHs but not airborne naphthalene; naphthalene present in air at 1000x conc of the particulate PAHs; no correlation between pyrene and naphthalene in air; dermal absorption was high because the urinary 1-hydroxypyrene output was much higher then that you could have expected by inhalation alone(CTX-32965)
    11. Urinary excretion of 1-hydroxypyrene does not increase in smokers but does increase significantly in those undergoing coal tar treatment and in rats painted with coal tar solutions(CTX-33056)
    12. Urinary excretion profile following exposure to pyrene in a psoriasic patient under treatment with coal tar; also treated dermally volunteers with pyrene and creosote; first order apparent half lives of 11.5-15hrs; 1-OH pyrene should reflect average weekly exposure of workers with constant exposure to pyrene(CTX-32967)
    13. Urinary 1-naphthol and 1-pyrenol as indicators of exposure to coal tar products; at this facility the airborne concentrations were high; sum of PAHs 440ug/m3 and 4-6 aromatic ring PAHs was 290ug/m3; naphthalene concentrations were 1000ug/m3 and 160ug/m3 for the assemblers and chislers respectively; urinary 1-naphol concs were 15-20x higher in assemblers versus chislers; workers were smokers; concludes that urinary sampling of naphthol and pyrenol provides better estimate of exposure than airborne concentrations since dermal absorption sometimes may be the most important route of exposure(CTX-32968)
    14. 1-hydroxypyrene in urine used to assess dermal exposure to coal tar sludge in coke oven workers(CTX-33068)
    15. 1-hydroxypyrene in urine after therapeutic coal tar treatment(CTX-32986)
    16. Suggestion for using 1- and 2-hydroxynaphthalene in urine as a biomarker for PAH exposures; correlates to total PAH exposure and to 1-hydroxypyrene in urine(CTX-32941)
    17. 1-hydroxypyrene as a biomarker in urine for creosote exposure(CTX-32962)
    18. Based on 140 individuals with no occupational exposure to PAHs; geometric mean excretion of 1-hydroxypyrene was 0.02, 0.09, 0.32umol/mol creat for 5th, 50th and 95th percentile; creosote workers showed mean level of 1.63(0.18-10.47)umol/mol creatine during their workweek(CTX-32966)
    19. 1-hydroxypyrene as a biomarker in urine for exposure to topical coal tar corresponds well with muctagenicity of urine using S typh with S9(CTX-33019)
    20. 1-hydroxypyrene as biomarker for occupational exposure to coal tar pitch; HPLC with fluorescence detector; net mean before and after shift was 17-fold greater than found in controls; strong correlation between 1-pyrenol and 17 environmental PAHs measured(CTX-33092)
    21. 1-hydroxypyrene found in urine of creosote worker; noted a fast excreting component with a half live of 1-2 days and a slow component with a half live of 16 days; also increased 1-hydroxypyrene in road workers dealing with asphalt; no sign increase in 1-hydroxypyrene in diesel workers or in smokers(CTX-32981)
    22. 1-hydroxypyrene measured in 38 smokers and 52 nonsmokers and found no difference in urine of smokers vs controls(smokers: 1.3umol/mol creatinine); workers in creosote impregnation plant, in coal tar distillation plant(levels up to 11.8umol/mol creatinine); coke oven workers (levels up to 3.3umol/mol creatinine with control at about 0.3)(CTX-33009)                  
    23. Look at PAH metabolites in urine by reduction to the original PAHs and then HPLC with fluorescence detection(CTX-33143)
    24. Detection of acridine(a nitrogen heterocycle) in urine of 28 pts who were treated dermally with coal tar(CTX-33016)
    25. Full shift personal air samples wre obtained on 36 creosote-exposed workers along with post shift and next day urine measurements of 1-hydroxypyrene; there was little or no correlation between airborne measures(benzene soluble fraction)  and urinary 1-hydroxypyrene; more than 90% of 1-hydroxypyrene in urine could be attributed to dermal exposure(CTX-32945)                                                                                                                                                                                               


    1. 7H-benzo[c]fluorene has been determined to be a major DNA adduct former in the lungs of mice and may be responsible in part for the increased lung lesions resulting from treatment with coal tar since there is little correlation with BaP(CTX-33059)
    2. undertaken study to look at DNA adducts formed by incubation of coal tar with liver microsomes in several strains of mice; found AhR less important for coal tar; cP450 CYP1A and its isoforms are involved in the formation of genotoxic materials and the reactive metabolites formed are substrates for epoxide hydrolase; also CYP1A and its isoforms are not the only enzymes responsible for the genotoxicity of the coal tar fragments(CTX-33037)
    3. Human DNA adducts in WBCs and skin after dermal application of coal tar; urinary 1-hydroxypyrene and 3-hydroxybenzo[a]pyrene were monitored as measures that PAHs were absorbed through the skin; DNA adducts increased in skin, in monocytes, in lymphocytes and in granulocytes; 3-hydroxybenzo[a]pyrene correlated well with skin DNA adducts but not 1-hydroxypyrene(CTX-33038)



    1. Study of population living near a hazardous waste site; divided area into zones, creosote site; describes expsoure scenarios; matched symptoms with those expected from creosote such as redening, blistering and peeling of skin, increased photosensitivity; not much here(CTX-32959)
    2. Risk Analysis of creosote site where PAHs and metal risks were negligible so focused on PCDDs and PCDF’s specifically the octachloro dioxins and dibenzofurans; using TEFs; focuses on dioxins suggesting slight increased risk of cancer, immune system effects are diverse and limited, lots of animal but limited human data on repro effects; TCDD thought to be a promotor rather than an initiator; very complicated risk assessment resulting in conclusion of no additional risk(Chem-Risk Publ)(CTX-32971)
    3. Azaarenes are more soluble and migrate more readily than other PAHs; here a method is developed using HPLC to analyze for these; here oxygen containing metabolites of quinoline, isoquinoline, and acridine are detected in groundwater emanating from creosote site in Pensacola Florida(CTX-32979)
    4. Exposure to creosote in the impregnation and handling of impregnanted wood: monitored both vapors and particulate matter; vapors including main components of naphthalene, methyl naphthalenes, indene, phenol, methy phenols, benzothiophene, diphenyl, acenaphthene and fluorene; used XAD-2 resin to sample air and GC analysis; 30 vaporous constituents identified(CTX-32982)
    5. Potential for bioremediation of creosote sites; employs PCB, creosote and CCA(copper, chrome and arsenate); creosote may be lost from the cite by volatilization, leaching and photodegredation as well as biotic processes; phenols can be biodegraded as well as PAH and heterocyclics(CTX-33071)
    6. Abandoned creosote site in Conroe Texas: studied with 14 monitoring wells and 35 boreholes; groundwater contaminated >800ug/L for naphthalene; 400ug/L methyl naphthalene; 150ug/L for dibenzofuran; organic contaminants have been degraded in the course of migration(CTX-33000)
    7. Migration and fate of coal tar creosote plume below water table; naphthalene and 1-methyl naphthalene migrated and increased over two years; phenols disappeared; dibenzofuran attained steady state; —xyleen migrated outward to a max distance in about 2 years and then receded back(CTX-33058)


    1. skin/vapor contact = skin irriation, phototoxicity; inhalation of PAHs which are known to be carcinogenic; PPOM(polycyclic organic material) measured and PEL for this is 0.2mg/m3 ; describes studies that have shown concentrations of creosote in ari from 19 to 195mg/m3 in summer; creosote may escape plant through water, and air; use of creosote for wood preservation involves environmental and occupational health risks(CTX-33051)
    2. 1999 review of tox: PAHs are ubiquitous; coal tars are complex combinations of hydrocarbons, phenols and heterocyclic oxygen, sulfur and nitrogen compounds; over 400 cmpds have been identified but there may be as many as 10,000cmpds in these tars; coke oven workers have 7.5fold risk of dying of kidney cancer than non coke workers; another study lung cancer was 2.5 x expected; discusses metabolism, dermal uptake, skin cancer in animals and humans; DNA interactions; (CTX-33077)
    3. Epi evidence of cancer in aluminum plant workers; 19 studies reviewed; bladder cancer risk related to duration of employment and cumulative exposure; also risk of luca(ss), risk of NHL(ss) from various studies; also leukemia(ss); this cumulative review of 47000men from 35 Al reduction plants and 4700 men from nine carbon plants: indicates work in Soderberg pot rooms associated with increased risk of bladder cancer in a dose-response manner; lung cancer risk assessments are limited by the limited amount of data on smoking; questions are raised about possible NHL and HD assns(CTX-33122)


    1. Creosote from posts after 26 years: (industry paper); major components of residual creosote: acenaphthene, dibenzofuran, fluorene, anthracene, carbazole, methylphenanthrenes, methylanthracenes, fluoranthene, pyrene, benzofluorenes, chrysene, benz[a]anthracene(CTX-32997)
    2. Leaching behavior of wood treated with creosote; leached with deionized water, in a pH 4.7 solution and a solution of humic substances; concludes PAHs as well as nitrogen heterocyclics are leacheable(CTX-32949)
    3. Plume Development - a controlled study -  followed representative group of seven compounds including phenol, —xylene, naphthalene, phenanthrene, 1-methylnaphthalene, dibenzofuran and carbazol; concludes: plume development can differ dependent on chemical nature of the components relative to physical properties and susceptibility to biological degredation(CTX-33057)
    4. PAH composition of coal tar that had undergone varying degrees of environmental degradation; solubility and volatility appear to be the main processes that control the changing composition; (CTX-33054)
    5. Contaminated Finnish lake finds PAHs in lake sediment; highest concentration in 0-10cm layer of lake(CTX-32954)
    6. PCB and phenanthrene biodegredation in creosote contaminated aquifer; this site also includes pentachlorophenol; mineralization of phenanthrene and soil binding resulted in decreased phenanthrene concentrations(CTX-32956)
    7. Leaching from pilings(CTX-33033)
    8. Non-Aqueous Phase Liquids(NAPL) such as coal tar or creosote can vary with time based on the dynamics of the site and on the solubilities of the individual components. Some lower MW components are more apt to migrate but the higher MW components are more likely to be carcinogenic(CTX-33076)
    9. groundwater pollution from disposal of creosote wastes; creosote contaminated groundwater contains a complex mixture of phenols, aromatic hydrocarbons, nitrogen-, sulfur-, and oxygen-containing heterocyclic compounds and aromatic compounds; subsurface microorganisms play an important part in degrading this compounds; this paper discusses microbial biodegredation; important classes of compounds in leachate from 10 creosote sites include phenols, N,S,O compounds such as indole, quinoline, pyrroles, BTEX compounds, naphthalenes, PAHs, ammonia and cyanides(CTX-32995)
    10. four creosote sites selected; shows groundwater contamination profiles showing dowgradient direction of flow; each case contamination moved downward from the source to the water table and continued to the first most permeable strata; vertical movement ranged from 20 to 60 feet below the surface; in two cases contam moved horizontally 500 feet from the source(CTX-32998)
    11. Groundwater from creosote sites contain a complex mixture of phenols, aromatic hydrocarbons, heterocyclics; here: overview of biological degredation of creosote contaminants under aerobic and anerobic conditions; in general, creosote contains about 85% PAH, 10% phenolics, 5% heterocyclic NS&O compounds; also small amounts of BTEX solvents(CTX-32991)
    12. When creosote comes into contact with water, the low MW aromatics are enriched in the water and the fraction of phenols increases to 45%, the NSO fraction to 38% and the PAHs decrease to 17%(CTX-32991)
    13. Based on 10 creosite sites; leachate contains 10-800mg/l of phenols, 1-25ppm NSO compounds; 1-10ppm BTEX compounds; 1-15ppm naphthalenes, 1-25ppm PAH, 1-10ppm cyanide(CTX-32991)


    1. Ingestion of soil by children; various factors that relate to bioavailability: concentration,m volatility, lipophilicity, soil particle size, percent organic content, percent clay content, and physiological factor such as body temperature, hydration, site of application and surface area and skin condition(CTX-33089)
    2. PAH contaminated soils fed to Lewis rats and metabolites measured in blood, feces and urine; used both industrially contaminated soil and pure model compounds such as anthracene, pyrene and BaP - metabolites 1-pyrenol and 3-hydroxybenzo[a]pyrene measured in blood, feces and urine(HPLC + fluorescence detector); because of rapid biotransformation, only minimal unmetabolized model PAHs could be found in the blood; very little excreted unchanged in feces; metabolites were considerably higher in both feces and urine; thus PAHs are rapidly absorbed and excreted; difference between pure mixture of PAHs and those absorbed on soil; more unmetabolized PAHs in feces from contaminated soil samples combined with lower excretion of 1-pyrenol in urine and species; concludes soil matrix capable of reducing absorption of pyrene(CTX-33095)
    3. Using radiolabled phenanthrene and naphthalene, different soils and SD rats; applied to skin and mixed with soil and applied to skin; also applied orally; concludes that there are gender differences for phenanthrene absorption; oral phenanthrene was more bioavailable than dermal; both phenanthrene and naphthalene have more tendency to absorb to sandy soil than to clay(CTX-33089)
    4. presence of PAHs in human placenta, umbilical cord blood, maternal blood and breast milk of normal healthy non-smoking Indian women; exposure is mainly through diet; here detected BaP, dibenzo[a,c]anthracene, and chrysene; therefore developing fetus exposed to PAHs(CTX-33067)
    5. F344 rats fed (17d feeding study) soil, soil with coal tar, soil with coal tar aged for 9mo and control diet; observed for liver enzymes, DNA adducts; study suggests that soil but not aging decreases the bioavailability of genotoxic components in coal tar as evidenced by DNA adduct analysis(adducts 3x higher in lung than liver)(CTX-33008)


    1. Levels in human fat for various PAHs on a wet weight basis with no smoking histories ; a 1981 paper(CTX-33073)


    1. In SD rats using labeled phenanthrene and naphthalene(CTX-33089)
    2. Metabolites of PAHs measured in psoriasis patients treated with coal tar prepns; metabolites of BaP and pyrene were detected in urine(CTX-33099)
    3. dermal absorption by creosote workers was high because the urinary 1-hydroxypyrene output was much higher then that you could have expected by inhalation alone based on airborne measurements during the period of sampling(CTX-32965)
    4. Urinary excretion of 1-hydroxypyrene does not increase in smokers but does increase significantly in those undergoing coal tar treatment and in rats painted with coal tar solutions(CTX-33056)
    5. Urinary excretion of 1-hyroxypyrene after use of coal tar shampoo was 10x conc before shampooing(CTX-33096)
    6. Urinary excretion profile following exposure to pyrene in a psoriasic patient under treatment with coal tar; also treated dermally volunteers with pyrene and creosote; first order apparent half lives of 11.5-15hrs; 1-OH pyrene should reflect average weekly exposure of workers with constant exposure to pyrene(CTX-32967)
    7. Using 1-hydroxypyrene as urinary biomarker, demonstrated that main route of exposure in creosote workers is via dermal absorption(CTX-32972); also in coke-oven workers(CTX-33068)
    8. here looked at 43 hospitalized psoriasis patients with coal tar medication and 39 untreated controls; looked at 1-hydroxypyrene glucuronidide(49.96+-72.62pmol/umol creatinine in treated vs 0.38+-0.32pmol/umol creatine in controls(p<-0.0001); also looked at BaP 7,10/8,9 tetrol and found difference also(p=0.0006)(CTX-33011)
    9. Coal tar ointment applied to skin of volunteers on various sites and excretion of 1-pyrenol measured; disappearance from skin surface measured by measuring fluorescence on skin; surface disappearance was shoulder>forhead, forearm, groin>ankle,palmar hand; data indicates that from 20-56% disappears after 6h; urinary excretion of 1-pyrenol did not show differences between sites(CTX-33093)
    10. Dermal absorption of PAHs on blood perfused pig ear; compare dermal absorption flux of pyrene with other PAHs to determine if 1-pyrenol is a good marker for total PAH absorption; concludes that using 1-pyrenol as a marker, the cumulative absorption of PAHs with lower molecular weight will be underestimated(fluorene 10x, phenanthrene 12x, anthracene and fluoanthene 2x); for higher MW PAHs will be overestimated (BaP 7x, indeno[123cd]pyrene about 100x); it is likely that these relationships will hold for dermal absorption in man(CTX-33094)
    11. Detection of acridine(a nitrogen heterocycle) in urine of 28 pts who were treated dermally with coal tar(CTX-33016)
    12. dermally applied coal tar derived complex applied to skin of pregnant mice and rats and shown to produce resorptions and tetratogenic effects in both species(CTX-33102)
    13. dermal absorption of 7,10 14C benzo[a]pyrene and 1,12 14C dimethylbenz[A]anthracene in mice; both penetrated skin rapidly and were excreted more in feces than in urine; absorption site became saturated and % absorption decreased beyond that point; (CTX-33086)


    1. Keratitis - case reports - both from creosote vapors; eye irritation after working with creosote(CTX-33005)


    1. use of MDHS 68 Sampler, a 7 hole sampler and a cyclone respirable dust sampler; recommended that the MDHS 68 sampler be replaced by a 7 hole head containing a sliver or PTFE filter with a graphitized carbon back up if efficient collection of 2-4ring PAHs is required; (CTX-33088)
    2. Azaarenes are more soluble and migrate more readily than other PAHs; here a method is developed using HPLC to analyze for these; here oxygen containing metabolites of quinoline, isoquinoline, and acridine are detected in groundwater emanating from creosote site in Pensacola Florida(CTX-32979)


    1. DNA adducts are thought to be an essential aspect of PAH-induced tumorgenicity and could be a biomarker for estimating risk; here we compare tumor induction by BaP and coal tars in several assays; conclude that risk assessment based on BaP content may not accurately predict risk to human health posed by environmental PAHs(an EPRI paper); they question the use of TEF in cancer risk assessments for coal tar and other mixtures of PAH(CTX-33041)
    2. Estimates risk based on large aluminum smelter for workmans compensation; “Allowing for all the uncertainties, we think that a causal association between exposure to coal tar pitch volatiles and lung cancer in the smelter studied is beyond reasonable doubt.”; simple estimate of global attributable risk in all exposed workers (>10ug/m3-years BaP exposure” relative to unexposed workers RR = 1.75(1.41-2.19); they also consider contribution of risk of lung cancer from smoking(CTX-32992)
    3. Estimate of lifetime unit lung cancer risk for BaP based on tumor rates in rats exposed to coal tar/pitch condensation aerosol; Female Wistar rats exposed to coal tar pitch condensate containing 20 or 46ug/m3 BaP for 10-20mo followed by clean for 10-20mo; lung tumor rate was dose related; using EPA linearized multistage model, the lifetime risk for rats exposed to 1ug/m3 BaP as a consituent of a complex PAH mixture may be 2% or correspondingly 2 per 100,000 with a BaP concentration of 1ng/m3  - note: this does not account for the contribution of other PAHs in the mixture which may contribute even more to the carcinogenic risk(CTX-8832)


    1. Environmental coal tar mixture (CTX-33041)
    2. Composition of volatiles from coal tar/pitch condensation aerosol(CTX-8832)
    3. Commercial Grade PCP contains about 85-90% PCP, 40-8% 2,3,4,6-tetrachlorophenol, 2-6% other chlorophenols, and trace quantities(around 0.1%) chlorinated dibenzodioxins and dibenzofurans(CTX-32999)
    4. Flame ionization detection of components of commercially available PAHs(CTX-33007)
    5. Acridines(azaarenes)by GC and LC; creosote found to contain 547ug/g benzo(c)acridine(CTX-33035)
    6. Characterization of wood-preserving coal-tar creosote by GLC: six whole coal-tar creosotes examined; (CTX-33072)
    7. Organic bases in coal tar waste: listing of chemicals include methyl pyridines, methyl aniline, aniline, dimethyl aniline, quinoline, trimethyl aniline, methyl quinoline, tetrahydro quinoline, dimethyl quinolines, pheny pyridine, 1-naphthylamine, 2-naphthylamine, 2-aminobiphenyl, tetrahydro-methylquinoline, aminoacenaphthene, 4-azafluorene, quinolinone, benzo[h]quinoline; acridine, benzo[f]quinoline, methyl isomer of quinolinone, benzoquinoline methyl isomer, anthracene nitrile, azapyrene in aquaeus phase; another set of compounds identified in oily phase of groundwater(CTX-33075)
    8. PAHs, phenols and heterocyclics listed as predominant components of creosote sites - see listing of individual compounds(CTX-33071)
    9. Some components of coal tar creosote including PAHs, and N,S,O-heterocyclics(CTX-33047)
    10. Determination of multiple PAH metabolites by treating urine with glucuronidase and arylsulfatase then treat toluene extract with diazomethane forming the methyl ether of the phenol and then GC/MS: method quantifies phenols and dihydrodiols of phenanthrene, fluoanthene, pyrene, chrysene and BaP - a total of about 25 metabolites; three coke workers excreted about 22% 1-hydroxypyrene as well as metabolites of phenanthrene, fluoanthene, chrysene, and benzo[a]pyrene(CTX-33044)
    11. exposure to creosote during impregnation of wood: vapors included naphthalene, methyl naphthalenes, indene, phenol and methylated phenols, benzothiophene, diphenyl, acenaphthene and fluorene; particulates included fluorene, phenathrene, anthracene, pyrene, benzo[a]fluorene, crysene, benzo[e]pyrene, benzo[k]fluoanthene, benzo[a]pyrene, dibenzo[ah]anthrancene, benzo[ghi]perylene(CTX-32982)


    1. “Coal tar is a complex mixture that exhibits high carcinogenic potency in lungs of animals when administered in the diet”(CTX-33059)
    2. “Ingestion of PAH contaminated soil is considered to be a major exposure route, specifically for small children living on these soils” (CTX-33095)
    3. The EU Scientific Advisory committed concluded “...the German study provided evidence to support the opinion that there is a cancer risk to consumers from creosote containing less than 50ppm BaP and/or from wood treated with creosote”(CTX-32947)


    1. “The concern about potential cancer hazard in the aluminum industry has primarily arisen because of exposures to polynuclear aromatic hydrocarbons and coal tar pitch volatiles(“tars”). These substances evaporate from carbon electrode materials used to produce aluminum by electrolysis of aluminum oxide dissoved in molten cryolite” “Anodes and pot lining materials are usually manufactured from coal tar pitch and coke in the plant’s carbon area.”(CTX-33122)


    1. F344 rats exposed for 13 weeks to high boiling coal liquid resulted in dose related effects including increases in liver weights, decreases in thymus and ovary weights, dose related decreases in erythrocytes, hemoglobin, vol of packed red cells, lymphocytes, eosinophils, and total WBC. Mixture did contain 0.16% benzene, 42% phenanthrene, 19% pyrene, etc (CTX-33090)
    2. Liver damage in pigs fed pitch and showed disturbances of appetite, progressive los of weight and death; post mortem exam showed marked necrosis of the lobules of the liver(CTX-33066)
    3. Outbreaks of creosote poisoning in pigs; symptoms were short due to rapid death; at autopsy - gross degenerative changes in liver; anemia noted; central necrosis of hepatic lobule; sinusoids engorged with red corpuscles; (CTX-33042)
    4. Intratracheal instillation of coal tar pitch in rat respiratory tract; ten weekly it injections at different dosing levels and control animals received charcoal; lesions in bronchioalveolar area including hyperplastic, metaplastic and dysplastic changes to extensive cancers; lesions were usually multiple; lung cancers were found in 12.5% and 25% of the rats treated in the higher doses and the cancer incidence was directly related to dose(D/R) ; histo types included SCCs, and one adenocarcinoma and some combined adeno/squamous cell carcinomas; confirm carcinogenic effects of coal tar pitch(CTX-33139)
    5. carcinogenicity of creosote oil when painted on the skin of mice; creosote alone caused rapid papilloma development; initiation with DMBA followed by creosote shortened the time for tumor development; carcinomas developed in both groups at around 23-26 weeks(CTX-33010)
    6. skin painting of mice with a single drop of creosote oil produced almost ten times the lung adenomas as the control group of mice and when mice were housed in creosote impregnated wooden cages, the rate of increase was about 20 times; both skin and lung tumors were increased in treated mice(CTX-33084)
    7. skin painting of mice with creosote oils resulting in skin tumors including benign papillomas, localized malignant papillomas, invasive epitheliomas(CTX-33078)
    8. skin painting resulting in skin tumors in mice(CTX-33063)
    In This Section

    Causation Reports

    Toxicology Notes and Literature

    Toxicology Litigation Support