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Respiratory Health and Inflammatory Markers-Exposure to Cobalt in the Swedish Hard Metal Industry
Lena Andersson1, Alexander Hedbrant, Ing-Liss Bryngelsson
1Department of Occupational and Environmental Medicine, Faculty of Medicine and Health, Örebro University, SE 701 82 Örebro, Sweden (Dr Lena Andersson, Ing-Liss Bryngelsson, Anders Johansson, Annette Ericsson, Per Vihlborg, Håkan Westberg); School of Medical Sciences, Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden (Dr Lena Andersson, Dr Alexander Hedbrant, Dr Alexander Persson, Eva Särndahl, Håkan Westberg); Inflammatory Response and Infection Susceptibility Centre (iRiSC), Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden (Dr Lena Andersson, Dr Alexander Hedbrant, Dr Alexander Persson, Eva Särndahl, Håkan Westberg); Integrative Toxicology, Institute of Environmental Medicine, Karolinska Institute, SE-171 77 Stockholm, Sweden (Bengt Sjögren); Unit of Occupational and Environmental Medicine, School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg and Sahlgrenska University Hospital, PB 414, SE-405 30 Gothenburg, Sweden (Dr Leo Stockfelt).
Objective:
To study the relationship between inhalable dust and cobalt, and respiratory symptoms, lung function, exhaled nitric oxide in expired air, and CC16 in the Swedish hard metal industry.
Methods:
Personal sampling of inhalable dust and cobalt, and medical examination including blood sampling was performed for 72 workers. Exposure-response relationships were determined using logistic, linear, and mixed-model analysis.
Results:
The average inhalable dust and cobalt concentrations were 0.079 and 0.0017 mg/m, respectively. Statistically significant increased serum levels of CC16 were determined when the high and low cumulative exposures for cobalt were compared. Nonsignificant exposure-response relationships were observed between cross-shift inhalable dust or cobalt exposures and asthma, nose dripping, and bronchitis.
Conclusions:
Our findings suggest an exposure-response relationship between inhalable cumulative cobalt exposure and CC16 levels in blood, which may reflect an injury or a reparation process in the lungs.
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