Yanhua Wang1, Huawei Duan2, Tao Meng1, Meili Shen1, Qianpeng Ji3, Jie Xing4, Qingrong Wang3, Ting Wang1, Yong Niu1, Tao Yu1, Zhong Liu5, Hongbing Jia6, Yuliang Zhan6, Wen Chen7, Zhihu Zhang8, Wenge Su9, Yufei Dai1, Xuchun Zhang9, Yuxin Zheng10. 1. Key Laboratory of Chemical Safety and Health, National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China. 2. Key Laboratory of Chemical Safety and Health, National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China. Electronic address: duanhw@niohp.chinacdc.cn. 3. Key Laboratory of Chemical Safety and Health, National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China; Faculty of Public Health, Weifang Medical University, Weifang, China. 4. Faculty of Public Health, Weifang Medical University, Weifang, China. 5. Jinan Municipal Center for Disease Control and Prevention, Jinan, China. 6. China-Japan Friendship Hospital, Beijing, China. 7. Faculty of Preventive Medicine, School of Public Health, Sun Yat-sen University, Guangzhou, China. 8. Shandong Academy of Occupational Health and Occupational Medicine, Jinan, China. 9. Laigang Hospital attached to Taishan Medical University, Laiwu, China. 10. School of Public Health, Qingdao University, Qingdao, China. Electronic address: yxzheng@qdu.edu.cn.
Abstract
BACKGROUND: Exposure to fine particulate matter (PM2.5) pollution is associated with increased morbidity and mortality from respiratory diseases. However, few population-based studies have been conducted to assess the alterations in circulating pulmonary proteins due to long-term PM2.5 exposure. METHODS: We designed a two-stage study. In the first stage (training set), we assessed the associations between PM2.5 exposure and levels of pulmonary damage markers (CC16, SP-A and SP-D) and lung function in a coke oven emission (COE) cohort with 558 coke plant workers and 210 controls. In the second stage (validation set), significant initial findings were validated by an independent diesel engine exhaust (DEE) cohort with 50 DEE exposed workers and 50 controls. RESULTS: Serum CC16 levels decreased in a dose response manner in association with both external and internal PM2.5 exposures in the two cohorts. In the training set, serum CC16 levels decreased with increasing duration of occupational PM2.5 exposure history. An interquartile range (IQR) (122.0μg/m3) increase in PM2.5 was associated with a 5.76% decrease in serum CC16 levels, whereas an IQR (1.06μmol/mol creatinine) increase in urinary 1-hydroxypyrene (1-OHP) concentration was associated with a 5.36% decrease in serum CC16 levels in the COE cohort. In the validation set, the concentration of serum CC16 in the PM2.5 exposed group was 22.42% lower than that of the controls and an IQR (1.24μmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 12.24% decrease in serum CC16 levels in the DEE cohort. CONCLUSIONS: Serum CC16 levels may be a sensitive marker for pulmonary damage in populations with high PM2.5 exposure.
BACKGROUND: Exposure to fine particulate matter (PM2.5) pollution is associated with increased morbidity and mortality from respiratory diseases. However, few population-based studies have been conducted to assess the alterations in circulating pulmonary proteins due to long-term PM2.5 exposure. METHODS: We designed a two-stage study. In the first stage (training set), we assessed the associations between PM2.5 exposure and levels of pulmonary damage markers (CC16, SP-A and SP-D) and lung function in a coke oven emission (COE) cohort with 558 coke plant workers and 210 controls. In the second stage (validation set), significant initial findings were validated by an independent diesel engine exhaust (DEE) cohort with 50 DEE exposed workers and 50 controls. RESULTS: Serum CC16 levels decreased in a dose response manner in association with both external and internal PM2.5 exposures in the two cohorts. In the training set, serum CC16 levels decreased with increasing duration of occupational PM2.5 exposure history. An interquartile range (IQR) (122.0μg/m3) increase in PM2.5 was associated with a 5.76% decrease in serum CC16 levels, whereas an IQR (1.06μmol/mol creatinine) increase in urinary 1-hydroxypyrene (1-OHP) concentration was associated with a 5.36% decrease in serum CC16 levels in the COE cohort. In the validation set, the concentration of serum CC16 in the PM2.5 exposed group was 22.42% lower than that of the controls and an IQR (1.24μmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 12.24% decrease in serum CC16 levels in the DEE cohort. CONCLUSIONS: Serum CC16 levels may be a sensitive marker for pulmonary damage in populations with high PM2.5 exposure.
Authors: Seagal Teitz-Tennenbaum; Steven P Viglianti; Ahmad Jomma; Quentin Palone; Halia Andrews; Kayla N Selbmann; Shayanki Lahiri; Natalia Subbotina; Natalie Walker; Anne-Karina T Perl; Vibha N Lama; Thomas H Sisson; John J Osterholzer Journal: Am J Pathol Date: 2021-12-23 Impact factor: 4.307