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Biomedical subjects

W Barkley

Publications and source records attributed to W Barkley.

14 recordsLinked to original sources
PubMed1994

Carcinogenicity of 7H-dibenzo[c,g]carbazole, dibenz[a,j]acridine and benzo[a]pyrene in mouse skin and liver following topical application.

N-Heterocyclic aromatics are by-products of incomplete combustion of organic material. The overall objective of this study was to determine the relative carcinogenic potencies of 7H-dibenzo[c,g]carbazole (DBC) and dibenz[a,j]acridine (DBA) in a bioassay of complete carcinogenicity on mouse skin in a sensitive strain (Hsd:ICR(Br)) which has been used in metabolism and DNA binding studies of N-heterocyclic aromatics. No-treatment, acetone and benzo[a]pyrene (BaP)-treated animals were used as negative and positive control groups. DBC (50 nmol), DBA (50 nmol), BaP (50 nmol) or DBC plus BaP (25 nmol + 25 nmol) were applied twice weekly in 50 microliters acetone to the backs of 50 female mice/group for 99 weeks or until the appearance of a tumor. DBC, DBA, BaP and DBC plus BaP produced skin tumors in 43, 32, 49 and 42 of 50 mice each based on weekly visual observations with latent periods of 55.1, 62.2, 33.4 and 33.8 weeks, respectively. The histopathology data indicated primary skin lesions in 42, 27, 48 and 47 mice for DBC, DBA, BaP and DBC plus BaP, respectively. In addition, primary liver lesions in 37 mice were present in the DBC group. The morphological and morphometric data indicated a significant increase (P < or = 0.05) in mononuclear cells in the dermis for the BaP and DBC plus BaP groups relative to the control group. Significant increases (P < or = 0.05) were observed in the nuclear area, nucleoli per nucleus and cellular area of hepatocytes in the DBC treatment group relative to the control group. These data indicate that DBC is a potent liver carcinogen as well as a skin carcinogen following topical application.

Acridines↗
PubMed1993

Factors affecting carcinogenic potential of mixtures.

Historically, exposure to complex mixtures such as soot, coal tar, mineral oils, and cigarette smoke has been associated with increased cancer mortality. Benzo[a]pyrene (BaP) has been used to predict the carcinogenic potency of mixtures. Two complete carcinogenicity C3H/HEJ mouse skin bioassays were undertaken to determine the effect of low doses of BaP on the carcinogenic potential of mixtures. A toluene solution containing 0.1% each of five noncarcinogenic polycyclic aromatic hydrocarbons (PAHs), anthracene, chrysene, pyrene, fluoroanthene, and phenanthrene, produced tumors in 23% of the mice with a latent period of 73 weeks. With the addition of a 0.001% BaP to the above solution, 47% of the mice produced tumors with a latent period of 66 weeks. In the second study, coal tar in toluene, which was determined to contain 0.0006% BaP, produced tumors in 51% of mice with a latent period of 73 weeks. In both studies the BaP solutions by themselves did not produce tumors. In a third study, the 9-, 2-, and 3-methylbenz[a]-anthracene compounds were noncarcinogenic using toluene as the solvent. With the substitution of n-dodecane for toluene all three compounds produced significant numbers of tumors. The results indicate that (1) low dose levels of BaP can have an impact on the carcinogenic potential of mixtures, (2) the presence or absence of BaP is not always sufficient to account for the observed potency and the synergistic effects of other substances which might be present, and (3) that certain noncarcinogenic methylbenz[a]anthracenes can have their carcinogenic potential altered by a change in the solvent used.

Alkanes↗
PubMed1992

Comparative tumor-initiating ability of 7H-dibenzo(c,g)carbazole and dibenz(a,j)acridine in mouse skin.

N-heterocyclic aromatics are environmentally important carcinogenic pollutants produced by incomplete combustion of organic material. 7H-Dibenzo-(c,g)carbazole (DBC), is a potent skin and systemic carcinogen, whereas dibenz(a,j)acridine (DBA), is a carcinogen with local effects. Therefore, the overall objective of these studies was to determine the initiating ability of DBC and DBA in mouse skin using an initiation-promotion protocol. Acetone-, TPA- or BaP-treated animals were used as negative and positive controls, respectively. DBC, DBA or BaP (200 nmol) dissolved in acetone was applied once to the backs of thirty shaved Hsd:(ICR)Br female mice, followed 2 weeks later with 2 micrograms of TPA in 50 microliters of acetone applied twice a week for up to 24 weeks. Skin tumors developed in 26, 17 and 27 animals, respectively. DBC plus TPA produced a significant influx of dermal macrophages similar to that seen for BaP. Initiation with BaP, DBC or DBA moderated the effect of TPA on most other dermal parameters, particularly neutrophils. These data indicate that, DBC, with apparently different activation pathways than BaP shows similar tumor initiating ability and morphological changes as BaP.

Acetone↗
PubMed1987

Comparative carcinogenic potencies of 7H-dibenzo[c,g]carbazole, dibenz[a,j]acridine and benzo[a]pyrene in mouse skin.

The relative carcinogenic potencies of three combustion products of fossil fuels, 7H-dibenzo[c,g]carbazole (7H-DB[c,g]C), dibenz[a,j]acridine (DB[a,j]A) and benzo[a] pyrene (B[a]P) were compared using complete carcinogenicity C3H mouse skin bioassays. Both 7H-DB[c,g]C and B[a]P produced tumors in 48 of 50 mice with latency periods of 36.6 and 32.4 weeks, respectively. DB[a,j]A produced tumors in 25 of 50 mice with a latency period of 80 weeks. 7H-DB[c,g]C was found to be as potent a carcinogen as B[a]P when applied to mouse skin. These results have important implications in the determination of relative carcinogenic potencies of complex mixtures.

Acridines↗
PubMed1981

A carcinogenic bioassay of certain roofing materials.

The carcinogenic potentials of certain present day roofing materials and dust produced during the removal of an old coal tar pitch roof were evaluated using a mouse skin bioassay. Traditional coal tar pitch and dust from removal of an old roof were significantly more carcinogenic than coal derived roofing bitumen, but all were strongly carcinogenic. The benzo(a)pyrene concentration of these materials ranged from 0.064 to 0.08%, but each was significantly more carcinogenic than 0.1% benzo(a)pyrene alone. No tumors were produced by the application of petroleum derived roofing asphalt.

Animals↗
PubMed1979

Cyanide toxicity from the thermal degradation of rigid polyurethane foam.

Thermal degradation products (tdp) from a model, rigid polyurethane foam were collected in such a manner as to eliminate carbon monoxide and other gases with low boiling points. The effects in rats resulting from intratracheal intubation (I.T.) of the tdp are discussed. Cyanide was found to be a major factor associated with severe toxic responses of the experimental rats.

Animals↗
PubMed1979

Bioassay of complex mixtures derived from fossil fuels.

The conversion or processing of shale, coal, or petroleum involves elevated temperatures and altered pressures, and under these conditions polynuclear aromatic hydrocarbons are likely to form. Certain compounds of this type exhibit carcinogenic activity for a variety of organ sites in experimental animals and epidemiological evidence strongly implicates their role as carcinogens in man. It is then not unexpected that many liquid fractions derived from shale and coal are carcinogenic when subjected to bioassay. Benzo(a)pyrene, [B(a)P], is frequently considered to be an indicator substance. It is clear that when a small quantity of B(a)P is present in a fraction, the fraction will exhibit carcinogenic activity in a bioassay (mouse skin). However, it does not follow that the lack of detectable B(a)P insures that the fraction will be noncarcinogenic. Several fractions have been analyzed for their content of B(a)P and then subjected to bioassay. A method for testing complex mixtures for their carcinogenic potential is described. The carcinogenic potency of these fractions are compared to petroleum fractions.

Animals↗
PubMed1975

Pulmonary response to polyurethane dust.

Weanling and 9 months or older rats were exposed to particles of an aged (PUF I) or freshly prepared (PUF II) rigid polyurethane foam by intratracheal intubation. The dose was 5 mg of particles. The response of the lung tissue was examined morphologically by serial sacrifices. Inflammation and macrophage activity were the initial responses. Fibrosis developed after 6 months. Nodular scars and perifocal emphysema were seen after 12 months. Four rats had a papillary adenoma in a major bronchus after 18 months exposure to PUF II.

Age Factors↗
PubMed1975

Investigation of alveolar macrophages from rats exposed to coal dust.

Rats were exposed to the inhalation of coal dust from either Utah (low prevalence coalworkers' pneumoconiosis (CWP)) or Pennsylvania (high prevalence CWP). Rats were sacrificed, the lungs removed and lavaged to obtain free cells. The number of alveolar macrophages recovered from rats inhaling these two coal dusts (exposures up to 4 months) was not remarkably different from the number recovered from rats inhaling filtered room air. This is in contrast to results obtained after intratracheal intubation of the dust. The capacity of the lavaged cells to phagocytize and kill bacteria decreased after exposure to either dust. The activity of certain enzymes also decreased.

Acid Phosphatase↗
PubMed1968

Alveolar macrophages: reduced number in rats after prolonged inhalation of lead sesquioxide.

A decreased number of alveolar macrophages was found in washings from lungs of rats inhaling small particles of lead sesquioxide for 3 to 12 months, as compared with control animals exposed to filtered air. This result contrasts with that reported by others for animals given massive exposures to various dusts for short periods of time. Because the concentrations of lead were comparable to those observed in some industrial(150 microg/m(3)) or urban (10 microg/m(3)) environmental conditions, the results may be significant in terms of human lung clearance processes after such exposures.

Aerosols↗