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Background: The age-adjusted incidence rate of breast cancer has increased for Israeli women. Our aim was to explore the hypothesis that occupational exposures are important risk factors, taking into consideration main known risk factors., Methods: The study population included 326 breast cancer cases from one hospital in the center of the country and 413 women without known diagnosis of cancer. Every participant was interviewed using a structured questionnaire., Results: We found that working in textile and clothing and in various industries, OR (95% confidence interval), 1.8 (1.1-3.0), 4.3 (2.0-9.3) respectively, and exposure to ionizing radiation OR 5.3 (2.4-14.1) as well as age and having a family history of breast cancer significantly increased the risk of developing breast cancer. Administrative work, adherence to high fiber diet and low salt diet significantly lowered the risk of breast cancer., Conclusions: Our study supported the assumption that occupational exposure may contribute to the etiology of breast cancer.

Background: Laboratory work is associated with exposure to a mixture of carcinogens., Methods: The cohort is comprised of 4,300 laboratory workers. Cancer incidence was followed from 1960 to 1997., Results: A total of 230 cases were included in the cohort. The overall cancer standardized incidence ratio (SIR) was 1.04 (0.91-1.18). When a 20-year latency was introduced, SIR was increased significantly: 1.35 (1.13-1.61). Among routine workers and researchers, SIR was elevated significantly for the total population and for women, when a 20-year latency was introduced. SIR was also elevated significantly in research, routine, bacteriology and virology, and isotope laboratories. With respect to specific sites, significantly increased SIR was observed in breast, ovary, and thyroid cancer among women; and prostate cancer, leukemia, and melanoma among men., Conclusions: We suggest that work in research and biomedical laboratories might involve an increased risk of certain types of cancer. Am. J. Ind. Med. 44:600-610, 2003., (Copyright 2003 Wiley-Liss, Inc.)

Background: A case-control study nested within a cohort study of biomedical laboratory workers was conducted to examine whether the excess cancer morbidity that we found can be explained by exposure to a particular group of substances, taking into consideration potential confounders., Methods: The study population included 163 cases and two matched control groups: laboratory workers (311) and general population (448) workers., Results: Multiple conditional regression analysis showed that working in research laboratories involved an increased risk of cancer generally among women [risk ratio 2.2 (1.2-4.3)], and of breast cancer particularly [risk ratio 2.3 (1.1-4.7). Seventy-six percent (76%) of breast, 87% of thyroid, 60% of ovary and prostate, 94% of melanoma, and 50% of leukemia cases were ever exposed to at least one known human carcinogen., Conclusion: Our results exclude the possibility that the excess cancer morbidity was related to personal risk factors but they may be explained by exposure factors. Am. J. Ind. Med. 44:611-626, 2003., (Copyright 2003 Wiley-Liss, Inc.)

Background: Formaldehyde (FA) is classified as a probable human carcinogen., Aims: To examine DNA protein crosslinks (DPC) and p53, which are generally known to be involved in carcinogenesis, in peripheral blood lymphocytes of workers exposed to FA., Methods: DPC and p53 ("wild type" and mutant) were examined in peripheral blood lymphocytes of 186 workers exposed to FA (mean years of exposure = 16) and 213 unexposed workers. Every worker completed a questionnaire on demographic data, occupational and medical history, smoking, and hygiene., Results: The adjusted mean level of DPC in the exposed and the unexposed workers differed significantly. Adjustment was made for age, sex, years of education, smoking, and origin. Exposure to FA increased the risk of having a higher level of pantropic p53 above 150 pg/ml (OR 1.6, 95% CI 0.8 to 3.1). A significant positive correlation was found between the increase of pantropic p53 protein and mutant p53 protein, as well as between pantropic p53 >150 pg/ml and mutant p53 protein. In the exposed group a significantly higher proportion of p53 >150 pg/ml was found among workers with DPC >0.187 (55.7%) (0.187 = median level of DPC) than among workers with DPC < or =0.187 (33.3%). The risk of having pantropic p53 protein >150 pg/ml was determined mainly by levels of DPC. Workers with DPC above the median level had a significantly higher risk of having pantropic p53 >150 pg/ml (adjusted OR 2.5, 95% CI 1.2 to 5.4)., Conclusions: Results suggest that DPC and mutation in p53 may represent steps in FA carcinogenesis and a possible causal relation between DPC and mutation in p53. These biomarkers can be applied in the assessment of the development of cancer due to FA exposure.

Background: We describe the results of a cancer mortality study among asphalt workers in Israel., Methods: Personal identifiers and employment histories of 2,176 workers were extracted from company records., Results: Mortality from all malignant neoplasms was significantly reduced in the whole cohort (SMR 0.68, 95% confidence interval (CI) 0.56-0.83). SMR for lung cancer was elevated in workers exposed to bitumen (SMR 1.05, 95% CI 0.62-1.66). No significant elevation or reduction in mortality was observed in relation to a specific site. SMRs for lung cancer was higher among ever exposed to bitumen than among unexposed. There was no association between lung cancer risk and estimated exposure to bitumen fume, and no dose-response was apparent., Conclusions: While the results of this cohort study indicate a slightly increased SMR for lung cancer, it did not produce evidence of a causal link between lung cancer and exposure to bitumen fume., (Copyright 2003 Wiley-Liss, Inc.)

Sister chromatid exchange (SCE) was measured in peripheral lymphocytes of 90 workers from 14 hospital pathology departments in Israel who were occupationally exposed to formaldehyde (FA) and of 52 unexposed workers from the administrative section of the same hospitals. The mean exposure period to FA was 15.4 years (range 1-39). The results of SCEs are expressed in two variables: (a) mean number of SCEs per chromosome and (b) proportion of high frequency cells (cells with more than eight SCEs). A high correlation was found between these two variables. The adjusted means of both SCEs variables were significantly higher among the exposed compared with that of the unexposed group (P<0.01). Adjustment was made for age, sex, smoking habits, education workers and origin. Evaluation of the influence of years of exposure on the frequency of SCEs showed that the two variables of SCEs were higher among those who were exposed to FA for 15 or more than among those with less than 15 years of exposure. Concerning levels of exposure, both variables of SCEs were the same in the low and in the high levels of exposure sub-groups. However, among the smokers, both variables of SCEs were higher in the high exposure sub-group than in the low exposure sub-group. Our finding of a significant increase of SCEs frequency in peripheral lymphocytes in pathology staff indicates a potential cytogenetic hazard due to FA exposure. We conclude that our data indicate that FA is mutagenic to humans.

Sister-chromatid exchange (SCE) was measured in peripheral lymphocytes of 104 greenhouse farmers exposed to pesticides and 44 unexposed workers. The results of SCEs are expressed in two variables: (a) mean number of SCEs per chromosome and, (b) proportion of high frequency cells (cells with more than eight SCEs). A high correlation was found between these two variables. The adjusted means of both SCEs variables were significantly higher among the farmers compared with the unexposed group (P < 0.01). Adjustment was made for smoking, age, education, and origin. The adjusted means of both SCE variables, were significantly elevated (P < 0.05) among the farmers who prepared and applied more than 70% of the pesticides by themselves compared with those who prepared and applied less than 70% of the pesticides by themselves. Both SCEs variables were also significantly elevated (P < 0.05) among farmers who were involved in more than 7.4 sprays per year compared with those with 7.4 or less sprays per year (P < 0.05). We found a tendency towards elevation of the two variables of SCEs among those who did not use protective measures while preparing the pesticides. Evaluation of the influence of years of exposure on the frequency of SCEs showed that the two variables of SCEs were higher among those farmers who were exposed to pesticides for more than 21 years than among those with less than 21 years of exposure. The variables that had the most influence on the elevation of SCEs were self-preparation of the pesticide mixtures and the number of sprayings per year. Because the farmers used a mixture of almost 24 different chemical classes it was impossible to attribute exposure to a specific pesticide or group of pesticides to single farmers. Our finding of a significant increase of SCEs frequency in peripheral lymphocytes in greenhouse farmers indicates a potential cytogenetic hazard due to pesticides exposure.

We conducted a cross-sectional study to determine whether occupational exposure to low levels of ethylene oxide can cause hematological abnormalities. Blood samples were collected from a group of 47 hospital workers who were exposed to ethylene oxide during a mean period of 6.6 years (standard error, 1.1). Ethylene oxide range levels measured were < 0.01 to 0.06 ppm. The control group, individually matched by age, sex, and smoking habits, consisted of 88 workers from the administrative sector. We found significant differences between the exposed and the control group in the frequency of workers with white blood cells lower than the normal range. Although there was no significant difference in the absolute mean number of the total white blood cells, we found an elevation in the absolute mean number of monocytes and eosinophils (P < 0.01) and a decrease (P < 0.01) in the absolute mean number of lymphocytes in the exposed group compared with the control group. We also found an elevation (P < 0.01) in the percentage of hematocrit and the mean absolute number of the red blood cells, and a decrease (P < 0.01) in the mean absolute number of platelets, in the exposed group compared with the control group. The mean absolute number of eosinophils, red blood cells, and percentage of hematocrit was significantly higher, and the mean absolute number of lymphocytes and platelets was significantly lower, in the subgroups with a higher cumulative dose of exposure. A positive dose-response was found between cumulative dose exposure and the absolute mean number of eosinophils. In view of our findings, we suggest that the use of complete blood cells with differential in routine medical surveillance and for early detection of hygiene problems should be reexamined with special attention to the eosinophils count.