Fatal Myocardial Disease Associated With Industrial Exposure to Cobalt

Kennedy, Amanda G.; Dornan, James; King, Roni

doi:10.1016/s0140-6736(81)91793-1

Cited by 71 publications

(20 citation statements)

References 5 publications

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“…With regard to mortality from circulatory and respiratory diseases, no excess was observed among cobalt production workers, so that this study does not agree with previous publications suggesting such risks [Brooks, 1981;Horowitz et al , 1988;Kennedy et al, 1981;Meyer-Bisch et al, 1986;Sprince et al, 19881. The relationship between lung cancer and cobalt exposure has received scant attention [Hogstedt and Alexandersson, 1990;Leonard and Lauwerys, 19901. These studies were reviewed recently by the International Agency for Research of Cancer (IARC) [IARC, 19911. According to these authors, the evidence for the carcinogenicity of cobalt in experimental animals is sufficient or limited depending on which compound is considered.…”

Section: Discussioncontrasting

confidence: 90%

“…The aims of this study were: i) a new assessment of the lung cancer risk among cobalt production workers; and ii) an appraisal of possible risks of heart and respiratory diseases which might be related to cobalt exposure according to previous studies [Brooks, 1981;Horowitz et al, 1988;Kennedy et al, 1981;Meyer-Bisch et al, 1986;Payne, 1977;Sprince et al, 19881.…”

Section: Introductionmentioning

confidence: 99%

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A mortality study of cobalt production workers: An extension of the follow‐up

Moulin

Wild

Mur

et al. 1993

American J Industrial Med

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The follow-up of a cohort of workers employed in an electrochemical plant producing cobalt and sodium, previously studied from 1950-1980, has been extended from 1981-1988. The standardized mortality ratio (SMR) for all causes of death was 0.85 (95% confidence interval [CI] = 0.76-0.95, 309 observed) for the whole cohort, and 0.95 (95% CI = 0.83-1.08, 247 observed) for the subcohort of workers born in France. With regard to lung cancer mortality among cobalt production workers, which is the main objective of the study, the SMRs were, respectively, 0.85 (95% CI = 0.18-2.50, 3 observed) and 1.16 (95% CI = 0.24-3.40, 3 observed). Neither did any excess of mortality from diseases of the circulatory and of the respiratory systems appear among cobalt production workers. Maintenance workers, however, exhibited high SMRs for lung cancer, reaching statistical significance for duration of exposure and time since first exposure > or 30 years. This study does not support the hypothesis of a relationship between lung cancer and cobalt exposure.

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Section: Discussioncontrasting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

A mortality study of cobalt production workers: An extension of the follow‐up

Moulin

Wild

Mur

et al. 1993

American J Industrial Med

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“…Cobalt also accumulates in the heart and hair of humans employed in the mineral assay industry [40] or in some way exposed to industrial cobalt [41,42,43,44]. Cobalt is thought to produce the fatal disease by causing extensive lipid peroxidation and by arresting oxidative phosphorylation in heart muscle, thus impeding the regeneration of intracellular macroergic phosphates [45], but the detailed mechanism of its action still remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Calcium-dependent changes in potassium currents in guinea-pig coronary artery smooth muscle cells after acute cobalt loading in vivo

Hristov

Altankova²,

Gagov

et al. 2004

Pflugers Arch - Eur J Physiol

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The aim of the present study was to determine whether cobalt poisoning induces haem oxidase isoenzyme-1 (HO-1) in coronary artery smooth muscle, or accounts for any changes in coronary smooth muscle cell (SMCs) membrane ionic currents that could result from this type of heavy metal poisoning. In SMCs isolated from cobalt-treated guinea-pig coronaries, K+ channel currents (IK) were much smaller than those in cells isolated from non-treated animals. Haemin (HO substrate) increased IK concentration dependently. This effect was mimicked by 1% CO and was abolished by pretreatment of cells with a competitive HO inhibitor, by inhibitors of guanylyl cyclase, protein kinase G or phospholipase C, as well as by blocking inositol trisphosphate-dependent Ca release, or sarcoplasmic reticulum Ca-ATPase, or by bathing cells in Ca-free external solution. Expression of the Na/Ca exchanger-1 (NCX-1) protein was reduced substantially in SMCs from coronary arteries of cobalt-treated animals. No expression of HO-1 was detected. It is concluded that acute cobalt poisoning in vivo depresses Ca-sensitive K currents via CO-dependent modulation of intracellular calcium availability, most probably by suppressing the expression of NCX-1 protein.

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“…Similarly, a study of Finnish cobalt workers revealed that cumulative cobalt exposure was associated with subclinical echocardiographic changes [20]. Cobaltinduced myocardial injury has also been implicated in hard metal workers [21][22][23].…”

Section: Thyroid Dysfunctionmentioning

confidence: 99%

Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases

et al. 2013

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Safety concerns regarding cobalt-containing metal alloy hip prosthetics (Co-HP) have resulted in product recalls, a medical device alert, and issuance of guidance for clinicians. Recently, cases of suspected prosthetic hip-associated cobalt toxicity (PHACT) from Co-HP have been reported. Although little is known about suspected PHACT, these patients may be referred to medical toxicologists for evaluation and management recommendations. We searched MEDLINE, EMBASE, and unpublished abstracts from toxicology scientific meetings for references relevant to PHACT. Authors independently screened publications for inclusion criteria: publication in English, human study population, subject(s) are symptomatic (except for isolated hip pain), and cobalt values in any matrix (blood, serum, urine, CSF, synovial fluid) available for review. Data from 10 cases are reviewed. Patients with suspected PHACT had findings consistent with cobalt toxicity, including thyroid, cardiac, and neurologic dysfunction.Signs and symptoms appeared between 3 and 72 months after arthroplasty (median 19 months). Neurologic symptoms were most common. Ancillary testing varied considerably. All patients had elevated cobalt levels in one or more matrices. Enhanced elimination was attempted in 27 % of patients. At this time, the information currently available regarding patients with suspected PHACT is inadequate to guide clinical decision making. No consensus has been reached regarding the management of Co-HP patients with systemic symptoms. Indications for chelation have not been established and require further study. Improved case definitions, improved surveillance, and controlled studies are needed to elucidate the scope of this problem and guide future investigations.

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Fatal Myocardial Disease Associated With Industrial Exposure to Cobalt

Cited by 71 publications

References 5 publications

A mortality study of cobalt production workers: An extension of the follow‐up

A mortality study of cobalt production workers: An extension of the follow‐up

Calcium-dependent changes in potassium currents in guinea-pig coronary artery smooth muscle cells after acute cobalt loading in vivo

Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases

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