Abstract
ObjectiveIt has been suspected that cobalt is toxic to the heart. It can cause cardiotoxicity in heavily exposed humans and in experimental systems. The issue of interest for this study is whether cobalt also affects the myocardium at occupational exposure levels.MethodsTo study the effect of occupational cobalt exposure on the heart, we conducted a follow-up of workers at a cobalt production plant. The workers’ hearts had been examined by echocardiography in 1999–2000. Altogether 93 exposed and 49 non-exposed workers examined in 1999–2000 were re-examined in 2006. Occupational history and health data were collected with a questionnaire. Blood pressure was measured, and electrocardiography (ECG), laboratory tests, Holter registration, and echocardiography were conducted for all participants. Analysis of covariance (ANCOVA) was used to analyse the data.ResultsNo differences were found between the exposed and unexposed groups for any of the echocardiographic parameters in 2006. There were no differences in the laboratory values, the ECG parameters, or the results of the Holter registration of the exposed and unexposed workers.ConclusionsAlthough the previous results in 2000 suggested an association between cumulative exposure to cobalt and echocardiographic findings, the results of this new cross-sectional study with a tissue Doppler 6 years later did not confirm the association in the present cohort. If cobalt exposure affects heart muscle functions at this exposure level, the effects are smaller than those caused by physiological changes due to ageing, medication, and traditional cardiovascular risk factors, such as elevated blood pressure.
Highlights
The toxic potential of cobalt and related health risks have been investigated thoroughly in animal and human toxicity studies
There was no significant difference in reported stress between the exposed and unexposed groups
In our cross-sectional study in 2000, we found that higher cobalt exposure was associated with altered left ventricular diastolic function as measured by echocardiography (Linna et al 2004) The isovolumic relaxation time (IVRT) was prolonged in the highly exposed group when compared with that of the less exposed and reference groups, and a prolonged deceleration time (DT) was observed among the exposed persons
Summary
The toxic potential of cobalt and related health risks have been investigated thoroughly in animal and human toxicity studies. Systemic toxic reactions may arise when Co ions enter the blood and lymphatic circulation and subsequently disseminate to different organs. In vitro experiments have demonstrated that ionized cobalt (Co2 +) is the primary toxic form for systemic toxicity (Leyssens et al 2017). Various pathogenetic mechanisms related to possible cardiac effects have been suspected in hard-metal workers. The most likely effect is the inhibition of cellular respiration due to the inhibition of mitochondrial dehydrogenase (Seghizzi et al 1994). Systemic Co toxicity manifests as a clinical syndrome with a variable presentation of neurological, cardiovascular, sensitizing, and endocrine symptoms, depending on the systemic Co levels (blood/ urine)
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