학술논문

Comparison of hematological alterations and markers of B-cell activation in workers exposed to benzene, formaldehyde and trichloroethylene
Document Type
article
Source
Carcinogenesis. 37(7)
Subject
Biomedical and Clinical Sciences
Oncology and Carcinogenesis
Stem Cell Research
Rare Diseases
Cancer
Prevention
Lymphoma
Hematology
Adult
B-Lymphocytes
Benzene
Biomarkers
Tumor
China
Female
Formaldehyde
Hemolytic Agents
Humans
Leukemia
Lymphocyte Activation
Lymphoma
Non-Hodgkin
Male
Myeloid Progenitor Cells
Occupational Exposure
Trichloroethylene
Oncology & Carcinogenesis
Oncology and carcinogenesis
Language
Abstract
Benzene, formaldehyde (FA) and trichloroethylene (TCE) are ubiquitous chemicals in workplaces and the general environment. Benzene is an established myeloid leukemogen and probable lymphomagen. FA is classified as a myeloid leukemogen but has not been associated with non-Hodgkin lymphoma (NHL), whereas TCE has been associated with NHL but not myeloid leukemia. Epidemiologic associations between FA and myeloid leukemia, and between benzene, TCE and NHL are, however, still debated. Previously, we showed that these chemicals are associated with hematotoxicity in cross-sectional studies of factory workers in China, which included extensive personal monitoring and biological sample collection. Here, we compare and contrast patterns of hematotoxicity, monosomy 7 in myeloid progenitor cells (MPCs), and B-cell activation biomarkers across these studies to further evaluate possible mechanisms of action and consistency of effects with observed hematologic cancer risks. Workers exposed to benzene or FA, but not TCE, showed declines in cell types derived from MPCs, including granulocytes and platelets. Alterations in lymphoid cell types, including B cells and CD4+ T cells, and B-cell activation markers were apparent in workers exposed to benzene or TCE. Given that alterations in myeloid and lymphoid cell types are associated with hematological malignancies, our data provide biologic insight into the epidemiological evidence linking benzene and FA exposure with myeloid leukemia risk, and TCE and benzene exposure with NHL risk.