Evaluation of serum type III procollagen peptide as an exposure marker in retired coal workers

Abstract

Serum type III procollagen peptide (PIIIP), a degradation product of the type III collagen precursor, has been put forward as an exposure marker for mineral dust. We evaluated PIIIP levels as a marker of exposure to and effects of coal dust in retired coal miners (n = 104). To this end: (a) the individual cumulative dust exposure was calculated from job-exposure matrices, and (b) in addition to routine chest radiography (CR) of all miners according to the criteria of the International Labour Organisation (ILO), a subgroup (n = 46) was screened by high-resolution computed tomography (HRCT). Profusion score (CR and HRCT) tended to increase with cumulative dust exposure, even in the absence of CR evidence for pneumoconiosis (i.e. CR < or = 0/1, n = 35). In contrast to our previous findings in active miners, PIIIP levels were not increased in miners as compared with non-dust-exposed controls (n = 29), and no differences were observed between miners without (ILO = 0/0) and miners with coal workers' pneumoconiosis (CWP; ILO > or = 0/1). No trend in PIIIP versus pneumoconiosis stage was present, either by CR or by the more sensitive HRCT score. PIIIP was also unrelated to any lung function parameter (FEV1, FVC, impedance, diffusion capacity). Age, medication, medical history and smoking habits had no significant effect on PIIIP levels. In the miners with CWP (i.e. ILO > 0/0, n = 28) a significant negative correlation was present between PIIIP values and (log) cumulative dust exposure. This decrease in serum PIIIP levels with increasing cumulative exposure may be due to chronic adaptive changes in type III collagen deposition and/or breakdown. Other relations between exposure and PIIIP were not observed. In conclusion, the present findings do not support the use of serum type III procollagen peptide as a marker of exposure to and (early) interstitial or respiratory effects of coal dust.

Biological responses of workplace particles and their association with adverse health effects on miners

“…3,4 Studies carried out by Borm et al and Vanhee et al indicated individual susceptibility of cytokine responses in pneumoconiosis cases. [23][24][25] In this study, excluding individual susceptibility, hazard of particle and cumulative exposure seemed to play more important roles in the elevated risk of pneumoconiosis. In the Limu tin mine, high hazard such as fibrogenic potential of particles was observed in tests for highest TNF-a release of AM.…”

“…Other studies have confirmed that TNF-a is a biomarker to indicate pulmonary fibrosis and was observed to be elevated in humans with pneumoconiosis. [23][24][25] Moreover, dust cumulative exposure level for miners in the Limu tin mine was higher than the other mines. Both were attributed to elevated risk of pneumoconiosis in the Limu tin mine.…”

A method for routine quantitation of urinary 8‐hydroxy‐2′‐deoxyguanosine based on solid‐phase extraction and micro‐high‐performance liquid chromatography/electrospray ionization tandem mass spectrometry

“…Direct analysis of urinary 8OHdG excretion is preferred to DNA analysis, where oxidation of 2′‐deoxyguanosine during DNA isolation leads to artifactual 8OHdG levels 16. Therefore, urinary 8OHdG is considered a good biomarker of oxidative DNA insults which can be used for investigation of different forms of exposure to DNA‐damaging factors, such as body irradiation,17 cigarette smoking,18, 19 environmental agents such as benzene,20, 21 benzo[ a ]pyrene,22 or mineral dusts 23…”

Carboxyterminal propeptide of type I procollagen in ELF: elevation in asbestosis, but not in pleural plaque disease

“…Silica‐exposed workers had elevated PIIINP in BALF, but this change was only seen in progressive disease [29]. In coal workers′ pneumoconiosis, SPIIINP was not a marker of interstitial or respiratory effects of coal dust [30]. Furthermore, SPIIINP did not predict the development of pneumoconiosis in coal workers during 5 yrs follow‐up [31].…”