Wei Jie Seow1, Luoping Zhang2, Roel Vermeulen3, Xiaojiang Tang4, Wei Hu5, Bryan A Bassig5, Zhiying Ji2, Meredith S Shiels5, Troy J Kemp6, Min Shen5, Chuangyi Qiu4, Boris Reiss3, Laura E Beane Freeman5, Aaron Blair5, Christopher Kim5, Weihong Guo2, Cuiju Wen5, Laiyu Li4, Ligia A Pinto6, Hanlin Huang4, Martyn T Smith2, Allan Hildesheim5, Nathaniel Rothman5, Qing Lan5. 1. Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA, Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA, Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands, Guangdong Poison Control Center, Guangzhou, China, and HPV Immunology Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA weijie.seow2@nih.gov. 2. Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA. 3. Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands. 4. Guangdong Poison Control Center, Guangzhou, China, and. 5. Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA, Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA, Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands, Guangdong Poison Control Center, Guangzhou, China, and HPV Immunology Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA. 6. HPV Immunology Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
Abstract
BACKGROUND: Formaldehyde has been classified as a human myeloid leukemogen. However, the mechanistic basis for this association is still debated. OBJECTIVES: We aimed to evaluate whether circulating immune/inflammation markers were altered in workers occupationally exposed to formaldehyde. METHODS: Using a multiplexed bead-based assay, we measured serum levels of 38 immune/inflammation markers in a cross-sectional study of 43 formaldehyde-exposed and 51 unexposed factory workers in Guangdong, China. Linear regression models adjusting for potential confounders were used to compare marker levels in exposed and unexposed workers. RESULTS: We found significantly lower circulating levels of two markers among exposed factory workers compared with unexposed controls that remained significant after adjusting for potential confounders and multiple comparisons using a false discovery rate of 10%, including chemokine (C-X-C motif) ligand 11 (36.2 pg/ml in exposed versus 48.4 pg/ml in controls, P = 0.0008) and thymus and activation regulated chemokine (52.7 pg/ml in exposed versus 75.0 pg/ml in controls, P = 0.0028), suggesting immunosuppression among formaldehyde-exposed workers. CONCLUSIONS: Our findings are consistent with recently emerging understanding that immunosuppression might be associated with myeloid diseases. These findings, if replicated in a larger study, may provide insights into the mechanisms by which formaldehyde promotes leukemogenesis. Published by Oxford University Press 2015.
BACKGROUND:Formaldehyde has been classified as a human myeloid leukemogen. However, the mechanistic basis for this association is still debated. OBJECTIVES: We aimed to evaluate whether circulating immune/inflammation markers were altered in workers occupationally exposed to formaldehyde. METHODS: Using a multiplexed bead-based assay, we measured serum levels of 38 immune/inflammation markers in a cross-sectional study of 43 formaldehyde-exposed and 51 unexposed factory workers in Guangdong, China. Linear regression models adjusting for potential confounders were used to compare marker levels in exposed and unexposed workers. RESULTS: We found significantly lower circulating levels of two markers among exposed factory workers compared with unexposed controls that remained significant after adjusting for potential confounders and multiple comparisons using a false discovery rate of 10%, including chemokine (C-X-C motif) ligand 11 (36.2 pg/ml in exposed versus 48.4 pg/ml in controls, P = 0.0008) and thymus and activation regulated chemokine (52.7 pg/ml in exposed versus 75.0 pg/ml in controls, P = 0.0028), suggesting immunosuppression among formaldehyde-exposed workers. CONCLUSIONS: Our findings are consistent with recently emerging understanding that immunosuppression might be associated with myeloid diseases. These findings, if replicated in a larger study, may provide insights into the mechanisms by which formaldehyde promotes leukemogenesis. Published by Oxford University Press 2015.
Authors: Paul J Hensbergen; Pepijn G J T B Wijnands; Marco W J Schreurs; Rik J Scheper; Rein Willemze; Cornelis P Tensen Journal: J Immunother Date: 2005 Jul-Aug Impact factor: 4.456
Authors: M Nieda; A Nicol; Y Koezuka; A Kikuchi; N Lapteva; Y Tanaka; K Tokunaga; K Suzuki; N Kayagaki; H Yagita; H Hirai; T Juji Journal: Blood Date: 2001-04-01 Impact factor: 22.113