Abstract

Objective: To assess the association between circulating C-reactive protein (CRP), and CRP polymorphisms in the diesel engine exhaust (DEE)-exposed workers. Methods: In 137 DEE-exposed workers and 127 unexposed comparable control workers, six urinary mono-hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) and serum CRP levels were assayed. Genotyping of four CRP single-nucleotide polymorphisms (SNPs) was measured. Results: Serum CRP levels increased in exposed versus control workers (all p < 0.001). In the DEE-exposed workers, two CRP polymorphisms were associated with serum CRP levels, the subjects of rs1205 TT genotype had lower serum CRP levels (p < 0.05 compared to TC or CC). Conclusions: Our findings suggest that polymorphisms in CRP and circulating CRP involved in the inflammatory process may play significant roles in human sensitivity to lung function injury caused by DEE exposure. This study will help investigate the underlying mechanisms of adverse respiratory effects induced by DEE.

Highlights

  • Diesel engines that produce diesel engine exhaust (DEE) are used for road and off-highway transportation and equipment in various industries

  • Our findings suggest that polymorphisms in C-reactive protein (CRP) and circulating CRP involved in the inflammatory process may play significant roles in human sensitivity to lung function injury caused by DEE exposure

  • This study will help investigate the underlying mechanisms of adverse respiratory effects induced by DEE

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Summary

Introduction

Diesel engines that produce diesel engine exhaust (DEE) are used for road and off-highway transportation and (heavy) equipment in various industries. Considering the significant number of urban residents and workers exposed to DEE, there is an increased concern about DEE exposure-related adverse health effects. Because of their small size, diesel particles can be inhaled and a portion will eventually become trapped within the small airways and the alveolar regions of the lung. Workers exposed to DEE report decreases in lung function [2], and showed an increased mortality from chronic obstructive pulmonary disease (COPD) [3]. The International Agency for Research on Cancer classified DEE as a group I carcinogen in 2012 [5]

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