of 1 /1
95 but earlier than palytoxin, and the increase in the level of c-myc mRNA was accompanied by a drop in DNA synthesis. These results suggestthat palytoxin does not act by growth stimulation, differential cytotoxicity or terminal differentiation of normal versus neoplastic cells which are proposed mechanisms of tumor promotion. Contribution of polycyclic aromatic compounds to the carcinogen- icity of sidestream smoke of cigarettes evaluated by implantation into the lungs of rata. Grimmer G, Brune H, Dettbam G, Naujack K-W, Mohr U, Wenzel- Hartung R. Biological Institute for Environmental Carcinogens, D- 2070 Grosshansdorf. Cancer Lett 1988;43: 173-7. Particles and semivolatiles from sidestream smoke of cigarettes smoked on a smoking machine were collected by a filter combination consisting of a glass Ebre filter and silanized polystyrene b&s. The extract of the glass Iibre filter was separated by a Sephadex LH-20 column chromatography into a fraction containing non-aromatic mate- rial plus polycyclic aromatic compounds (PAC) with 2 and 3 rings and a fraction consisting of PAC with 4 and more rings. To evaluate the carcinogenicity, both fractions as well as the semivolatiles were im- planted into the lungs of Osborne-Mendel rats at a dose level of one cigarette per animal and compared with three dose levels of benzo[a]pyrene (BaP). The most pronounced carcinogenic effect of the sidestream smoke (100 ng BaP per cigarette) was caused by the fraction containing polycyclic aromatic hydrocarbons (PAH) with 4 and more rings (5 carcinomas of the lungsn5 rats). This fraction represents only 3.5% by weight of the total sidestream smoke condensate. By contrast, the semivolatile material did not provoke any tumors. Only a small contribution to the total carcinogenicity (1 carcinoma of the lungs/35 rata) was observed for the fraction containing non-aromatic material and 2- and 3-ring PAHs. Proportion of lung cancers in males, due to occupation, in different areas of the USA. Vineis P, Thomas T, Hayes RI3 et al. f/nit of Cancer Epidemiology. DipartimentodiScienzeBiomedichee Oncologia Vmana, Universitadi Torino. Torino. Int J Cancer 1988;42:851-6. Occupational dam from 5 case-control studies in the United States involving2,973malecasesand3,2lOcontrolswereanalyzedtoestimate the percentage of lung cancer attributable to well-known and suspected lung carcinogens. The studies were conducted in areas heterogeneous in termsofindustrialactivities. Thepercentageoflungcancersattributable to occupations entailing potential exposure to well-recognized carcmo- gens ranged, by study area, from 3 to 17%. The further inclusion of occupational groups with suspect carcinogenic exposures changes these estimates very little. Exclusion of data derived from next-of-kin inter- views influenced the estimates of attributable risks, but not in a systematicfashion.Theestimatesalsovariedaccordingtoethnicgmup, smoking status and bii cohort, with higher values in non-whites, non- smokers and among members of more recent birth cohorts. Possible errors in exposure classification, which may make these estimates conservative, are discussed. Personal and family history of lung disease as risk factors for adeuocarcinoma of the lung. WuAH,YuMC,ThomasDC,PikeMC,HendersonBE. Depmtmentof Preventive Medicine, University of Southern California, Los Angeles. CA 90033. Cancer Res 1988;48:7279-84. To identify risk factors for adenocarcinoma of the lung, a population- based case-control study of 336 female cancers of this cell type and an equal number of neighborhood controls was conducted between 1983 and 1986. After adjusting for personal smoking, personal and family histories of lung disease emerged as additional risk factors. A personal history of any lung disease was associated with a 40% increase in risk [smoking adjusted relative risk (SARR) = 1.4,95% confidence interval (Cl) = 1.O, 2.01 with a more marked increase in risk for lung diseases occurring during childhood (SARR = 1.9,95% Cl = 1.2, 3.2) and for tuberculosis (SARR = 10.0,95% Cl = 1.1, 90.1). Family histories of tuberculosis (SARR= 2.0,95% Cl= 1,1,3,6)andoflungcancer(SARR = 3.9,95% Cl = 2.0.7.6) were also risk factors for adenocarcinoma of the lung. Increasing risk was observed with decreasing intake of dietary O-carotene. After adjustingfor personal smoking, women in the lowest quartile of intake showed a two-fold increased risk relative to those in the highest quartile of intake (P = 0.003). There were also some suggestive differences between cases and controls in their reproductive history and hormone use. Promotion of pulmonary carcinogenesis by plutonium particle aggregation following inhalation of “‘PuO,. Sanders CL, McDonald KE, LauhaIa KE. Biology and Chemistv Department, Pacific Northwest Laboratory, Richland, WA 99352. Radiat Res 1988;116:393405. Promotion of lung tumor formation fmm inhaled ,,Pu02 in rats may be associated with aggregation of plutonium particles near bronchioles. The relationship of plutonium particle aggregation in the lung and me development of lung tumors after inhalation of u9Pu0, was studied in 664 life span rats with mean lung doses ranging from 0.35 to 20 Gy. Plutonium particle concentration and aggregation were determined from autoradiographic sections of the left lung lobe. The increase in particles/cm2 and mean number of particles per aggregate up to 20 Gy were directly proportional to lung dose. Aggregates with > 25 particles increased linearly with dose from 0.2% at 1.4 Gy to 8.2% at 20 Gy, in a pattern similar to increasing severity of pulmonary fibrosis and incidence of lung tumors. Lung tumor incidence increased from about 6% at 1.4 Gy to 83% at 8 Gy: no further increase in lung tumors was seen at doses > 8 Gy. Maximum lung tumor incidence at 8 Gy corresponded to a particle concentration of 130/cm* and four particles/aggregate with 4% of aggregates having > 25 particles. Aggregation of inhaled pluto- nium particles in clusters of > 25 particles resulted in daily doses of only a few centigray to focal tissue regions containing clustered particles, yet these doses appeared sufficient to cause pulmonary fibrosis and pmmo- tion of pulmonary carcinogenesis. The risk of lung cancer from polycyclic aromatic hydrocarbons in Sydney air. Freeman DJ, CattellFCR. CentreforEnvironmentaland UrbanStudies, Macquarie University, North Ryde, NSW 2109. Med J Aust 1988:149:612-5. Air pollution often is suggested as being partly responsible for an increased incidence of lung cancer in cities. A problem with epidemi- ological studies is that the comparatively-small effect of air pollution is difficult to identify in the presence of larger and variable effects of cigarette smoking and other factors. This articledescribes an alternative approach to the estimation of cases of lung cancer that may be a result of airpollution. Theconcentration of anumber of carcinogenicpolycy- clic aromatic hydrocarbons has been measured at two sites in Sydney and the relative contributions from various pollutant sources have been deduced. By means of a source inventory and an atmospheric dispersion model, concenuations have been derived for the whole Sydney region. Lung-cancer induction is calculated from the population that is exposed and the concentration of benzo(a)pyrene, which is used as a surrogate forthecarcinogenicproductsofincompletecombustion.FortheSydney region, it is estimated that about 30 lung cancers a year could arise from polycyclic aromatic hydrocarbons in the ambient air. Effects of serum, transforming growth factor type 0, or 12-0- tetradecanoylphorbol-13-acetate on ionized cytosolic calcium con- centration in normal and transformed human bronchial epithelial cells. MiyashitaM.SmithMW,WilleyJC,LechnerJF,TmmpBF,HarrisCC. Laboratory of Human Carcinogenesis. Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Cancer Res 1989;49:63-7. Fluctuations in ionized cytosolic calcium ([Ca**](i))are considered important signals for induction of growth or differentiation in mammal- ian cells. The resting concentrations of [Caz*](i) in normal and aden- ovirus 12-SV40 hybrid virus-transformed (BEAS2B) human bronchial epithelial cells were 63 ?? 15 nM (SD) and 44 ?? 15 nM, respectively. Eight % calcium-free fetal bovine serum rapidly caused a significant

The risk of lung cancer from polycyclic aromatic hydrocarbons in Sydney air

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95

but earlier than palytoxin, and the increase in the level of c-myc mRNA was accompanied by a drop in DNA synthesis. These results suggestthat palytoxin does not act by growth stimulation, differential cytotoxicity or terminal differentiation of normal versus neoplastic cells which are proposed mechanisms of tumor promotion.

Contribution of polycyclic aromatic compounds to the carcinogen- icity of sidestream smoke of cigarettes evaluated by implantation into the lungs of rata. Grimmer G, Brune H, Dettbam G, Naujack K-W, Mohr U, Wenzel- Hartung R. Biological Institute for Environmental Carcinogens, D- 2070 Grosshansdorf. Cancer Lett 1988;43: 173-7.

Particles and semivolatiles from sidestream smoke of cigarettes smoked on a smoking machine were collected by a filter combination consisting of a glass Ebre filter and silanized polystyrene b&s. The extract of the glass Iibre filter was separated by a Sephadex LH-20 column chromatography into a fraction containing non-aromatic mate- rial plus polycyclic aromatic compounds (PAC) with 2 and 3 rings and a fraction consisting of PAC with 4 and more rings. To evaluate the carcinogenicity, both fractions as well as the semivolatiles were im- planted into the lungs of Osborne-Mendel rats at a dose level of one cigarette per animal and compared with three dose levels of benzo[a]pyrene (BaP). The most pronounced carcinogenic effect of the sidestream smoke (100 ng BaP per cigarette) was caused by the fraction containing polycyclic aromatic hydrocarbons (PAH) with 4 and more rings (5 carcinomas of the lungsn5 rats). This fraction represents only 3.5% by weight of the total sidestream smoke condensate. By contrast, the semivolatile material did not provoke any tumors. Only a small contribution to the total carcinogenicity (1 carcinoma of the lungs/35 rata) was observed for the fraction containing non-aromatic material and 2- and 3-ring PAHs.

Proportion of lung cancers in males, due to occupation, in different areas of the USA. Vineis P, Thomas T, Hayes RI3 et al. f/nit of Cancer Epidemiology. DipartimentodiScienzeBiomedichee Oncologia Vmana, Universitadi Torino. Torino. Int J Cancer 1988;42:851-6.

Occupational dam from 5 case-control studies in the United States involving2,973malecasesand3,2lOcontrolswereanalyzedtoestimate the percentage of lung cancer attributable to well-known and suspected lung carcinogens. The studies were conducted in areas heterogeneous in termsofindustrialactivities. Thepercentageoflungcancersattributable to occupations entailing potential exposure to well-recognized carcmo- gens ranged, by study area, from 3 to 17%. The further inclusion of occupational groups with suspect carcinogenic exposures changes these estimates very little. Exclusion of data derived from next-of-kin inter- views influenced the estimates of attributable risks, but not in a systematicfashion.Theestimatesalsovariedaccordingtoethnicgmup, smoking status and bii cohort, with higher values in non-whites, non- smokers and among members of more recent birth cohorts. Possible errors in exposure classification, which may make these estimates conservative, are discussed.

Personal and family history of lung disease as risk factors for adeuocarcinoma of the lung. WuAH,YuMC,ThomasDC,PikeMC,HendersonBE. Depmtmentof Preventive Medicine, University of Southern California, Los Angeles. CA 90033. Cancer Res 1988;48:7279-84.

To identify risk factors for adenocarcinoma of the lung, a population- based case-control study of 336 female cancers of this cell type and an equal number of neighborhood controls was conducted between 1983 and 1986. After adjusting for personal smoking, personal and family histories of lung disease emerged as additional risk factors. A personal history of any lung disease was associated with a 40% increase in risk [smoking adjusted relative risk (SARR) = 1.4,95% confidence interval (Cl) = 1 .O, 2.01 with a more marked increase in risk for lung diseases occurring during childhood (SARR = 1.9,95% Cl = 1.2, 3.2) and for tuberculosis (SARR = 10.0,95% Cl = 1.1, 90.1). Family histories of tuberculosis (SARR= 2.0,95% Cl= 1,1,3,6)andoflungcancer(SARR

= 3.9,95% Cl = 2.0.7.6) were also risk factors for adenocarcinoma of the lung. Increasing risk was observed with decreasing intake of dietary O-carotene. After adjusting for personal smoking, women in the lowest quartile of intake showed a two-fold increased risk relative to those in the highest quartile of intake (P = 0.003). There were also some suggestive differences between cases and controls in their reproductive history and hormone use.

Promotion of pulmonary carcinogenesis by plutonium particle aggregation following inhalation of “‘PuO,. Sanders CL, McDonald KE, LauhaIa KE. Biology and Chemistv Department, Pacific Northwest Laboratory, Richland, WA 99352. Radiat Res 1988;116:393405.

Promotion of lung tumor formation fmm inhaled ,,Pu02 in rats may be associated with aggregation of plutonium particles near bronchioles. The relationship of plutonium particle aggregation in the lung and me development of lung tumors after inhalation of u9Pu0, was studied in 664 life span rats with mean lung doses ranging from 0.35 to 20 Gy. Plutonium particle concentration and aggregation were determined from autoradiographic sections of the left lung lobe. The increase in particles/cm2 and mean number of particles per aggregate up to 20 Gy were directly proportional to lung dose. Aggregates with > 25 particles increased linearly with dose from 0.2% at 1.4 Gy to 8.2% at 20 Gy, in a pattern similar to increasing severity of pulmonary fibrosis and incidence of lung tumors. Lung tumor incidence increased from about 6% at 1.4 Gy to 83% at 8 Gy: no further increase in lung tumors was seen at doses > 8 Gy. Maximum lung tumor incidence at 8 Gy corresponded to a particle concentration of 130/cm* and four particles/aggregate with 4% of aggregates having > 25 particles. Aggregation of inhaled pluto- nium particles in clusters of > 25 particles resulted in daily doses of only a few centigray to focal tissue regions containing clustered particles, yet these doses appeared sufficient to cause pulmonary fibrosis and pmmo- tion of pulmonary carcinogenesis.

The risk of lung cancer from polycyclic aromatic hydrocarbons in Sydney air. Freeman DJ, CattellFCR. CentreforEnvironmentaland UrbanStudies, Macquarie University, North Ryde, NSW 2109. Med J Aust 1988:149:612-5.

Air pollution often is suggested as being partly responsible for an increased incidence of lung cancer in cities. A problem with epidemi- ological studies is that the comparatively-small effect of air pollution is difficult to identify in the presence of larger and variable effects of cigarette smoking and other factors. This articledescribes an alternative approach to the estimation of cases of lung cancer that may be a result of airpollution. Theconcentration of anumber of carcinogenicpolycy- clic aromatic hydrocarbons has been measured at two sites in Sydney and the relative contributions from various pollutant sources have been deduced. By means of a source inventory and an atmospheric dispersion model, concenuations have been derived for the whole Sydney region. Lung-cancer induction is calculated from the population that is exposed and the concentration of benzo(a)pyrene, which is used as a surrogate forthecarcinogenicproductsofincompletecombustion.FortheSydney region, it is estimated that about 30 lung cancers a year could arise from polycyclic aromatic hydrocarbons in the ambient air.

Effects of serum, transforming growth factor type 0, or 12-0- tetradecanoylphorbol-13-acetate on ionized cytosolic calcium con- centration in normal and transformed human bronchial epithelial cells. MiyashitaM.SmithMW,WilleyJC,LechnerJF,TmmpBF,HarrisCC. Laboratory of Human Carcinogenesis. Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Cancer Res 1989;49:63-7.

Fluctuations in ionized cytosolic calcium ([Ca**](i)) are considered important signals for induction of growth or differentiation in mammal- ian cells. The resting concentrations of [Caz*](i) in normal and aden- ovirus 12-SV40 hybrid virus-transformed (BEAS2B) human bronchial epithelial cells were 63 ?? 15 nM (SD) and 44 ?? 15 nM, respectively. Eight % calcium-free fetal bovine serum rapidly caused a significant