Long-term exposure to diesel engine exhaust induced lung function decline in a cross sectional study

• Published in: Industrial Health Vol. 55; no. 1; pp. 13 - 26
• Main Authors: NIU, Yong, YU, Shan Fa, DUAN, Hua Wei, MENG, Tao, HUANG, Chuan Feng, GAO, Wei Min, ZHENG, Yu Xin, ZHANG, Li Ping, ZHANG, Xiao
• Format: Journal Article
• Language: English
• Published: Japan National Institute of Occupational Safety and Health 01.01.2017; National Institute of Occupational Safety and Health, Japan
• Subjects: Adult; Cross-Sectional Studies; Cytokinesis; Diesel engine exhaust; Gasoline - adverse effects; Humans; Long-term exposure; Lung - physiopathology; Lung function; Male; Micronucleus Tests; Occupational Exposure - adverse effects; Original; Polycyclic Aromatic Hydrocarbons - urine; Respiratory Function Tests; The cytokinesis-block micronucleus cytome index; Urinary mono-hydroxylated polycyclic aromatic hydrocarbons; Vehicle Emissions - poisoning; Vital Capacity; Young Adult
• ISSN: 0019-8366; 1880-8026
• DOI: 10.2486/indhealth.2016-0031

To clarify the effects of lung function following exposure to diesel engine exhaust (DEE), we recruited 137 diesel engine testing workers exposed to DEE and 127 non-DEE-exposed workers as study subjects. We performed lung function tests and measured cytokinesis-block micronucleus (CBMN) cytome index and levels of urinary polycyclic aromatic hydrocarbons (PAHs) metabolites. There was a significant decrease of forced expiratory volume in 1 second (FEV1), ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1/ FVC), maximal mid expiratory flow curve (MMF), forced expiratory flow at 50% of FVC (FEF50%), and forced expiratory flow at 75% of FVC (FEF75%) in the DEE-exposed workers than non-DEE-exposed workers (all p<0.05). Among all study subjects, the decreases of FEF75% were associated with the increasing levels of PAHs meta­bolites (p<0.05), and there were negative correlations between FEV1, FEV1/FVC, MMF, FEF50%, and FEF75% with CBMN cytome index (all p<0.05). Our results show that long-term exposure to DEE can induce lung function decline which shows mainly obstructive changes and influence of small airways function. The decreased lung function is associated with internal dosage of DEE exposure, and accompany with the increasing CBMN cytome index.