Seow Wei Jie, Zhang Luoping, Vermeulen Roel, Tang Xiaojiang, Hu Wei, Bassig Bryan A, Ji Zhiying, Shiels Meredith S, Kemp Troy J, Shen Min, Qiu Chuangyi, Reiss Boris, Beane Freeman Laura E, Blair Aaron, Kim Christopher, Guo Weihong, Wen Cuiju, Li Laiyu, Pinto Ligia A, Huang Hanlin, Smith Martyn T, Hildesheim Allan, Rothman Nathaniel, Lan Qing
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
Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA.
Carcinogenesis. 2015 Aug;36(8):852-7. doi: 10.1093/carcin/bgv055. Epub 2015 Apr 23.
Formaldehyde has been classified as a human myeloid leukemogen. However, the mechanistic basis for this association is still debated.
We aimed to evaluate whether circulating immune/inflammation markers were altered in workers occupationally exposed to formaldehyde.
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.
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.
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.
甲醛已被归类为人类髓系白血病致癌物。然而，这种关联的机制基础仍存在争议。
我们旨在评估职业接触甲醛的工人循环免疫/炎症标志物是否发生改变。
在中国广东的一项横断面研究中，我们对43名接触甲醛的工厂工人和51名未接触甲醛的工厂工人进行了研究，使用基于多重微珠的检测方法测量了38种免疫/炎症标志物的血清水平。采用调整潜在混杂因素的线性回归模型比较接触组和未接触组工人的标志物水平。
我们发现，与未接触组相比，接触甲醛的工厂工人中两种标志物的循环水平显著降低，在调整潜在混杂因素并使用10%的错误发现率进行多重比较后，这一差异仍然显著，包括趋化因子（C-X-C基序）配体11（接触组为36.2 pg/ml，对照组为48.4 pg/ml，P = 0.0008）和胸腺与活化调节趋化因子（接触组为52.7 pg/ml，对照组为75.0 pg/ml，P = 0.0028），这表明接触甲醛的工人存在免疫抑制。
我们的研究结果与最近出现的免疫抑制可能与髓系疾病有关的认识一致。如果在更大规模的研究中得到验证，这些发现可能会为甲醛促进白血病发生的机制提供见解。
