These findings reaffirm the leukemogenic effects of benzene exposure and suggest that excess risk diminishes with time.

LTAS.NET incorporates improvements that will facilitate more complex person-years analysis of occupational cohort data.

SummaryThis overview of the epidemiology of chronic lymphocytic leukaemia (CLL) summarizes the evolution of classification and coding systems and describes the intersection of pathogenesis and aetiology. The role of the putative precursor to CLL, monoclonal B-cell lymphocytosis (MBL), is considered, and ideas for future investigations of the MBL-CLL relationship are outlined. We discuss the epidemiology of CLL, focusing on descriptive patterns and methodological considerations. Postulated risk factors are reviewed including the role of ionizing and non-ionizing radiation, occupational and environmental chemical exposures, medical conditions and treatments, and lifestyle and genetic factors. We conclude by raising key questions that need to be addressed to advance our understanding of CLL aetiology. Recommendations for future epidemiological studies are given, including the standardization of reporting of CLL across cancer registries, the clarification of the natural history of MBL, and the circumvention of the methodological shortcomings of prior epidemiological investigations in relation to radiation, chemical exposures and infectious agents.Keywords: chronic lymphocytic leukaemia, aetiology, radiation, chemicals, review. ). In light of these major scientific developments, it seems timely to reconsider key aspects of the epidemiology of CLL together with its similar counterpart, small lymphocytic lymphoma (SLL), which are considered different manifestations of the same lymphoid neoplasm in the WHO classification (Jaffe et al, 2001).This overview of the epidemiology of CLL includes three sections. The first section describes the evolution of classification and coding systems, the intersection of pathogenesis and aetiology, and the putative precursor of CLL, monoclonal B-cell lymphocytosis (MBL). The second section briefly characterizes the epidemiology of CLL, including descriptive patterns; the role of animal models in identifying risk factors, genetic pathways and biological mechanisms; and discusses known risk factors based on our current, albeit limited, understanding of aetiology. Descriptive and analytical epidemiological research on CLL is also considered in more detail in the accompanying reports by Dores et al (2007), SchubauerBerigan et al (2007), Blair et al (2007) and Landgren et al (2007a). The third section poses key questions pertinent to CLL aetiology and provides recommendations for future epidemiological studies.Correspondence: Martha S. Linet, NCI, DCEG, REB; 6120 Executive Blvd. EPS Room 7048,

Objectives-To examine mortality patterns and dose-response relations between ionising radiation and mortality outcomes of a priori interest in 6409 uranium workers employed for at least 30 days , and followed through 2004.Methods-Cohort mortality was evaluated through standardised mortality ratios (SMR). Linear excess relative risk (ERR) regression models examined associations between cause-specific mortality and exposures to internal ionising radiation from uranium deposition, external gamma and x-ray radiation, and radon decay products, while adjusting for non-radiologic covariates.Results-Person-years at risk totalled 236 568 (mean follow-up 37 years), and 43% of the cohort had died. All-cause mortality was below expectation only in salaried workers. Cancer mortality was significantly elevated in hourly males, primarily from excess lung cancer (SMR=1.25, 95% CI 1.09 to 1.42). Cancer mortality in salaried males was near expectation, but lymphohaematopoietic malignancies were significantly elevated (SMR=1.52, 95% CI 1.06 to 2.12). A positive dose-response relation was observed for intestinal cancer, with a significant elevation in the highest internal organ dose category and a significant dose-response with organ dose from internal uranium deposition (ERR=1.5 per 100 µGy, 95% CI 0.12 to 4.1).

Metolachlor, a widely used herbicide, is classified as a Group C carcinogen by the U.S. Environmental Protection Agency based on increased liver neoplasms in female rats. Epidemiologic studies of the health effects of metolachlor have been limited. The Agricultural Health Study (AHS) is a prospective cohort study including licensed private and commercial pesticide applicators in Iowa and North Carolina enrolled 1993–1997. We evaluated cancer incidence through 2010/2011 (NC/IA) for 49,616 applicators, 53% of whom reported ever using metolachlor. We used Poisson regression to evaluate relations between two metrics of metolachlor use (lifetime days, intensity-weighted lifetime days) and cancer incidence. We saw no association between metolachlor use and incidence of all cancers combined (n = 5,701 with a 5-year lag) or most site-specific cancers. For liver cancer, in analyses restricted to exposed workers, elevations observed at higher categories of use were not statistically significant. However, trends for both lifetime and intensity-weighted lifetime days of metolachor use were positive and statistically significant with an unexposed reference group. A similar pattern was observed for follicular cell lymphoma, but no other lymphoma subtypes. An earlier suggestion of increased lung cancer risk at high levels of metolachlor use in this cohort was not confirmed in this update. This suggestion of an association between metolachlor and liver cancer among pesticide applicators is a novel finding and echoes observation of increased liver neoplasms in some animal studies. However, our findings for both liver cancer and follicular cell lymphoma warrant follow-up to better differentiate effects of metolachlor use from other factors.