1 and 2. No associations between any of the pneumoprotein selleck products concentrations and exposure to endotoxins or dust were observed. The spirometric lung function variables, reported previously (Heldal et al. 2010), were not significantly associated to any of the serum concentrations of the determined pneumoproteins. Table 4
Results from multiple linear regression analysis assessing relation between pneumoproteins, (log) bacteria, and cigarette smoking (yes/no) Pneumoproteins α β Bacteria 95%CI β smoke 95%CI CC-16 (ng/ml) 3.6 0.8** 0.1–1.6 −1.6A −2.5 to 0.3 SP-D (ng/ml) 8.6 18.8** 3.5–34.1 −1.4ns HKI272 −31.5 to 28.7 Intercepts (α), regression coefficients (β), and confidence intervals (CI) are given A p = 0.11; ** p < 0.05; ns not significant Fig. 1 The univariate relationship between serum CC16 concentrations in 14 smoking (filled square) and 27 non-smoking (filled diamond) sewage workers and exposure to bacteria (CC16 = 3.6 + 0.8* log Bacteria cells, R 2 = 0.11, p < 0.05) Fig. 2 The univariate relationship between serum SP-D concentrations in 14 smoking (filled square) and 23 non-smoking (filled diamond) sewage workers and exposure to bacteria (SP-D = 8.6 + 18.8* log Bacteria cells, R 2 = 0.15, p < 0.05) Discussion The results show that the mean serum concentration
of CC16 was significantly lower with a tendency for SP-D in workers exposed to sewage dust as compared to the referents. However, the serum concentrations of CC16 and SP-D increased find more by higher personal exposure to bacterial cells sampled on the same day shortly before the collection of the blood samples. Exposure to endotoxin and dust was not associated with the pneumoproteins. No
effect of exposure on the serum concentrations of SP-A was observed. To our knowledge, pneumoprotein concentrations have only been reported in one earlier study among sewage workers. A cohort of 247 wastewater workers and 52 garbage collectors was followed up for 5 years to study respiratory health (Tchopp et al. 2011). The exposure characterization included only 11 personal exposure measurements, and only Parvulin exposure to endotoxins was determined. The reported concentrations seemed to be lower than in the present study (mean 52.5 EU/m3, range 7.1–158 EU/m3) (Oppliger et al. 2005). In contrast to the present study where exposure measurements and blood sampling were performed on the same day, the exposure measurements were carried out at the beginning of that study. The authors concluded that exposure to organic dust containing endotoxins did not affect the lung-specific proteins, although earlier reports from the same cohort found increased serum concentrations of CC16 and lower SP-A concentrations in asthmatics (Steiner et al. 2005; Widmeier et al. 2007). This is contradictory to the findings in the present study where lower concentrations of CC16 were observed in exposed workers and no group differences were found in the SP-A concentrations.
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