A historical mortality study among bus drivers and bus maintenance workers exposed to urban air pollutants in the city of Genoa, Italy.

OBJECTIVE: A historical mortality cohort study was conducted in Genoa, Italy among public transport workers ever employed between 1949 and 1980, to estimate overall and cause-specific mortality from January 1970 to December 2005 and to examine associations between exposure to urban air pollutants and overall and cause-specific mortality. METHODS: Causes of death for 9267 males (6510 bus drivers, 2073 maintenance workers and 601 white collar workers) were coded according to ICD-9. Standardised mortality ratios (SMRs) and 95% CIs were computed by applying Italian and regional male death rates to person-years of observation for the entire cohort and following stratification by longest held job title and length of and time since first employment using the Poisson regression model. RESULTS: There were 2916 deaths and 230,009 person-years of observation; 17 subjects were lost to follow-up. SMRs for all causes, diseases of the circulatory, respiratory, digestive and genitourinary systems, and for accidents were lower than expected. SMRs (95% CI) were increased for lung cancer (1.16, 1.05 to 1.28), non-Hodgkin's lymphoma (1.23, 0.85 to 1.78), Hodgkin's lymphoma (2.14, 1.19 to 3.87) and diabetes mellitus (1.16, 1.05 to 1.28). The SMR for leukaemia was 0.77 (0.51 to 1.16). Hodgkin's lymphoma mortality was significantly increased among bus drivers (1.62, 1.37 to 5.04). Lung cancer risk was significantly increased among all workers after 30 years' employment and among maintenance workers. CONCLUSIONS: The study failed to show any increased risk for leukaemias. The increased mortality from Hodgkin's lymphoma and lung cancer may be associated with long-term exposure to urban air pollution.

Early effects of low benzene exposure on blood cell counts in Bulgarian petrochemical workers.

OBJECTIVES: Only few studies have examined early hematological effects in human populations exposed to low benzene levels and their findings are controversial. We evaluated hematological outcomes (WBC, neutrophils, lymphocytes, monocytes, eosinophils, basophils, RBC, Hb, HCT MCV, platelets and MPV) in a population of 153 Bulgarian petrochemical workers exposed to benzene (range 0.01-23.9 ppm) and 50 unexposed subjects. METHODS: Written informed consent was obtained and a self-administered questionnaire used to collect information on current smoking habits, lifestyle, and occupational activities. Exposure assessment was based on personal monitoring sampling the day before phlebotomy. Urinary trans-trans-muconic acid (t,t-MA) was determined at the beginning and end of the work shift. Based on individual airborne benzene measurements, study subjects were categorized in three exposure categories (referents, <1 and > or =1 ppm). Mean values of each hematologic outcomes in each exposure category were compared with the referent group using a multiple linear regression model adjusted for age, gender, current smoking habits and environmental toluene level. The influence of the CYP2E1 (RsaI and DraI) and NQO1 609C>T genetic polymorphisms on differential hematological parameters was also investigated. RESULTS: No dose-response effect was observed for most of the examined hematological outcomes (WBC, lymphocytes, neutrophils, monocytes, RBC, Hb, HCT, MCV, platelets and MPV). The eosinophil count was inversely related to benzene exposure only among smokers. Conversely, basophils increased with increasing exposure. No effect on benzene hematotoxicity was found for any of the investigated polymorphisms. CONCLUSION: In our study we did not find a decline in WBC and lymphocytes related to benzene exposure. A myeloproliferative effect of benzene is highly unlikely to explain the observed reduction in eosinophils and increase in basophils as it would lead to a concordant depression in all granulocyte subpopulations. Whether benzene effects at low doses are present in Caucasian populations remains uncertain, thus warranting further investigations.

Baseline chromosome aberrations in children.

Field studies conducted in children exposed to ionizing radiation and industrial chemicals have consistently reported increased frequencies of chromosome aberrations in those environmentally exposed than in referent subjects. Exposure(s) occurring during childhood--as well as in utero--may continue for several years, become chronic, and eventually play a relevant role in the etiology of childhood as well as adulthood cancers. Indeed the statistical association between CA frequency in peripheral blood lymphocytes and cancer risk detected in occupationally exposed adults supports the hypothesis that CA is a predictor of cancer. These facts suggest the usefulness of including CA as biomarkers of genetic damage in epidemiologic studies of children exposed to environmental pollutants. As reported for other cytogenetic biomarkers, CA frequency may vary with gender and age in children as well as in adults. Estimates of the baseline frequency of CA in a pediatric population is a prerequisite in planning epidemiologic investigations of children exposed to low level of environmental genotoxic agents. The CA baseline levels were estimated from 16 published epidemiologic studies and from a large sample of Czech children aged 7-16 years (n=1214) and 206 newborns, all serving as referents (not exposed individuals). For the whole referent population (age range 0-19 years) the mean CA frequency estimated from the published findings was 1.24% (95%CI=1.05-1.47). Similar baseline levels were found for chromosome breaks frequency in boys and girls: 1.22% (95%CI=1.12-1.32) and 1.21% (95%CI=1.10-1.31), respectively. Among newborns CA baseline frequency was 1.14% (95%CI=0.96-1.32). Based on the reviewed studies and the reanalysed data, CA baseline levels were similar in boys and girls and failed to show any increase with age.