ISSN:0271-3586    

DOI:10.1002/ajim.4700070502

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractMeasurements for benzene exposure were performed for different work places. In addition, breath benzene concentrations were measured in different occupations in order to establish toxico‐kinetics of benzene in man; chromosomal aberrations in lymphocytes of exposed workers were also examined. Smoking appears to result in a large increase in benzene concentration in exhaled breath. The smoke from one cigarette contains 60‐80 μg of benzene. It was found that exposure levels of 10 ppm are rather uncommon among workers handling gasoline or gasoline equipment. It was concluded that the gasoline load of road tankers cannot be responsible for chromosome changes of the driver, as milk truck drivers showed the same changes. These results did not prove that benzene was the cause of the observed changes. Smoking is the confounding factor, with a potency of at least the same order of magnitude as benzene. In addition, our present knowledge about mechanisms of benzene is not sufficiently developed to permit quantitative conclusions as to the human health r

ISSN:0271-3586    

DOI:10.1002/ajim.4700070503

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractThe national occupational standard values for benzene are 10 ppm for Australia, 10 ppm for Denmark, 10 ppm for Finland, 10 ppm for Japan, 10 ppm for The Netherlands, 10 ppm for the United States, and 5 ppm for Sweden; in the Federal Republic of Germany the technical guideline value is 8 ppm. Crude mineral oil contains benzene as a natural constituent of approximately 0.1%. Gasoline in Sweden may contain 4–5% benzene by volume. The 8‐hour time‐weighted average (TWA) exposure levels of Swedish petroleum refinery workers vary between 0.1 to 1 mg benzene/m3in air. The exposures of benzene in various other occupations were measured and described. Other environmental exposures to benzene may have their origin in pyrolysis, such as tobacco smoking and burning of substances such as polyvinylchl

ISSN:0271-3586    

DOI:10.1002/ajim.4700070504

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractDue to the interest in reducing the benzene exposure limit from 10 to 1 ppm, the benzene exposure data collected since 1977 were compiled and evaluated. Some 38,000 data points representing either time‐weighted air samples or persons exposed were collected from five industries which produce and/or use benzene and two government organizations. Of the reported data, 87% represented exposure levels of 1.0 ppm or less. Petroleum and chemical operations where elevated exposure levels were reported included petrochemical and bulk loading operations. Benzol and by‐product plants in the iron and steel industry showed similar elevated resu

ISSN:0271-3586    

DOI:10.1002/ajim.4700070505

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractThere is no doubt about the leukemogenic effect of benzene in man. The evidence is as follows: (1) The incidence of leukemia in shoeworkers exposed to benzene in a period of 8 years in Istanbul was 13.6/100,000, which is significantly higher than that for leukemia in the general population. (2) Following the phase‐out of benzene in Istanbul, the number of leukemic workers decreased and none were reported in the subsequent 3 years. (3) The development of leukemia in pancytopenic patients with benzene exposure was observed in 13 out of 51 patients. (4) The differences in the distribution of the types of leukemia in individuals exposed and in nonexposed groups were as follows: acute leukemia 96.1% in the former group, and 46% in the latter group. The high percentages of acute erythroleukemia and preleukemia were other interesting findings in the exposed group. (5) Two cases of leukemia were observed in a 6‐year period at a tire cord manufacturing plant with 550 workers. At one location in the plant the concentration of benzene measured by gas chromatography was nearly 110 ppm. Additionally, we have studied 12 cases of malignant lymphoma, four cases of multiple myeloma, and six cases of lung cancer, all of whom were chronically exposed to benzene. The possible role of benzene in the etiology of these malignancies is discus

ISSN:0271-3586    

DOI:10.1002/ajim.4700070506

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractIn 1982, White et al published an assessment of quantitative leukemia risk associated with lifetime occupational exposure to benzene. At about the same time, IARC (1982) published estimates of quantitative cancer risk associated with industrial chemicals. Benzene was one of the two chemicals selected by IARC for its risk estimation. This paper presents a summary of these assessments along with new study results demonstrating adverse effects on bone marrow and peripheral blood cells as a result of low‐level benzene exposure.Mathematical extrapolations based on epidemiologic studies are consistent with a finding of significant risk of dying from leukemia under the current occupational permissible exposure limit of 10 ppm. Although a significant reduction of risk could be expected to be achieved by reducing exposure to 1 ppm, a significant risk may still remain. The uncertainty of the dose‐response projections rests on the underlying estimates of relative risk of death from leukemia, the estimates of benzene exposure (dose), and the appropriateness of the mathematical model.Recent findings in experimental animals demonstrate chromosomal damage to bone marrow cells, significant depression of the bone marrow, and disturbances of immune system function as a result of less than 1 week of exposure to the current permissible benzene exposure limit of 10 ppm. This was the lowest dose tested. These experimental findings provide further evidence of a potentially significant risk of bone marrow proliferative cancer (leukemia) as a result of low‐dose benzene exp

ISSN:0271-3586    

DOI:10.1002/ajim.4700070507

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractIn 1977 Maltoni and Scarnato were the first to demonstrate that benzene is an experimental carcinogen in rats. With that and other experiments, Maltoni et al have shown that benzene administered by ingestion (stomach tube) or inhalation is a multipotential carcinogen in rats (of two different strains) and mice and produces a variety of tumors, namely: Zymbal gland carcinomas, oral and nasal cavity carcinomas, skin carcinomas, acanthomas, dysplasias and carcinomas of forestomach, mammary malignant tumors, hepatomas, liver angiosarcomas, hemolymphoreticular neoplasias, and pulmonary tumors. The incidence of Zymbal gland carcinomas and carcinomas of the oral and nasal cavitities is affected by the length of treatment by inhalation and by the age of animals. However, the available epidemiological and experimental data at present do not provide precise information on the risk of doses around or below 10 ppm. Long‐term carcinogenicity bioassays at 50, 25, 10, 5 and 1 ppm may be helpful for scientific risk assessment. In addition, these experiments have shown that toluene, xylene, and ethylbenzene, at high concentrations, cause an increase in the number of total malignant tumor

ISSN:0271-3586    

DOI:10.1002/ajim.4700070508

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractEight‐to‐twelve‐week‐old male and female C57B1/6 BNL mice were exposed to air or benzene vapor in air at a concentration of 10, 25, 100, 300, or 400 ppm. Benzene at concentrations of 100 ppm or higher for 10 exposures of 6 hours per day 5 days a week produced a reduction in bone marrow cellularity and the number of pluripotent stem cells in the bone marrow. The fraction of stem cells in DNA synthesis was also increased. Exposure to 300 ppm 6 hours a day 5 days a week for 2, 4, 8, and 16 weeks produced a diminution in the stem cell levels in bone marrow which returned to those of controls 2 weeks after benzene exposure for 2 and 4 weeks, 16 weeks after exposure for 8 weeks, and to 92% of controls 25 weeks after 16 weeks of exposure. There was a more rapid return of blood lymphocytes to the control level. Mice exposed to 300 ppm for 6 hours/day, 5 days per week for 16 weeks began dying at 330 days of age, whereas no deaths were observed in sham‐exposed mice until 440 days of age. The benzeneexposed mice died in two waves: the first was from 330‐390 days of age, with a second wave commencing at 570 days of age. The first wave of mortality was due primarily to thymic lymphomata. The second wave was due to a mixture of nonthymic lymphomata and s

ISSN:0271-3586    

DOI:10.1002/ajim.4700070509

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractA subchronic inhalation toxicity study of benzene was conducted in CD‐1 mice and Sprague‐Dawley rats. Four groups of animals consisting of 150 mice and 50 rats/sex each were exposed to concentrations of 1, 10, 30, and 300 ppm benzene vapor, 6 hours/day, 5 days/week, for 13 weeks. Additional groups of mice and rats, of equal size, were exposed under similar conditions to filtered air and served as control groups. Thirty mice and 10 rats/sex in each group were sacrificed after 7, 14, 28, 56, and 91 days of treatment. Criteria used to evaluate exposure‐related effects included behavior, body weights, organ weights, clinical pathology, gross pathology, and histopathology. Fifty animals per sex of each species were exposed concurrently for cytogenetic studies. In addition, blood serum was obtained for immunological assays. The results of these two studies will be reported separately.No consistent exposure‐related trends were seen in the clinical observations and body weight data. Exposure‐related clinical pathology changes were seen in the high‐level (300 ppm) animals of both species. In the mice, these changes included decreases in hematocrit, total hemoglobin, erythrocyte count, leukocyte count, platelet count, myeloid/erythroid ratios, and percentage of lymphocytes. Mean cell volume, mean cell homoglobin, glycerol lysis time, and the incidence and severity of red cell morphologic changes were increased in the mice. In the rats, decreased lymphocyte counts and a relative increase in neutrophil percentages were the only exposure‐related clinical pathology alterations. Histophathologic changes were present in the thymus, bone marrow, lymph nodes, spleen, ovaries, and testes of mice exposed to 300 ppm and in most cases the incidence and severity of the lesions were greater in the males. These changes in the testes and ovaries at 300 ppm were also seen at lower concentrations, but they were of doubtful biological significance. In rats, the only exposure‐related lesion consisted of slightly decreased femoral marrow cellularity in the animals exp

ISSN:0271-3586    

DOI:10.1002/ajim.4700070510

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractUsing the micronucleus test we have found no significant difference between germ‐free and conventional (non‐germ‐free) male CD‐1 mice gavaged twice with 440 or 880 mg benzene/kg. Hence, the higher myeloclastogenicity observed previously with the p.o. (4‐6 times) than with the i.p. route of benzene administration was ruled out as being due to the involvement of gut flora in benzene biotransformation. Pretreatment of males with 3‐methylcholanthrene or β‐naphthoflavone, inducers of P‐448 monooxygenase, but not phenobarbital, an inducer of P‐450, significantly enhanced the myeloclastogenic effect of a single oral dose of benzene (440 mg/kg). Single oral doses of phenol, catechol, or hydroquinone (250, 150, and 200 mg/kg, respectively) failed to reproduce the potent myeloclastogenic effect of benzene. In fact, only hydroquinone was mildly clastogenic. The relation between benzene's myeloclastogenicity and metab

ISSN:0271-3586    

DOI:10.1002/ajim.4700070511

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY