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The natural history of a new disease entity in chronic beer drinkers consisting of pericardial effusion, a low cardiac output, and in about half of the cases of polycythemia is presented. Normalization of the heart volume, the hemoglobin value, and the hemodynamic state was obtained in patients who stopped drinking. Further evidence of the importance of cobalt in the development of the disease is presented. All patients drank beer to which cobalt was added and the disease was not seen in chronic alcoholics drinking wine or other alcoholic beverages. In view of the rather small quantity of cobalt consumed, an hypothesis is formulated which attributes the cobalt toxicity in chronic alcoholics, to a dietary deficiency of sulfhydryl-groups containing amino acids and a dietary deficiency of protein.

Cobalt has been demonstrated to be effective in the treatment of certain anemias.1In combination with iron, it is of value in the treatment of anemia of prematurity and infancy.2Cobalt and iron have been found to be effective in the prevention and treatment of most pregnancy anemias.3In this article, it was stated that no toxic manifestations from cobalt therapy had been observed in pregnant women or their offspring. Because of current interest in cobalt toxicity, specifically, the possibility of cobalt inducing thyroid hyperplasia and hypothyroidism4complete investigations in animals and pregnant women are to be reported. METHOD Observations on 78 pregnant women have been completed; 58 received cobalt and iron, and 20 received cobalt alone. The iron and cobalt preparation given to the first group provided 60 to 90 mg. of cobaltous chloride with iron per day. The second group received 75 to 100 mg.

Background It has been estimated that more than 1 million workers in the United States are exposed to cobalt. Occupational exposure to 59 Co occurs mainly via inhalation and leads to various lung diseases. Cobalt is classified by the IARC as a possible human carcinogen (group 2B). Although there is evidence for in vivo and in vitro toxicity, the mechanisms of cobalt-induced lung toxicity are not fully known. The purpose of this work was to identify potential signatures of acute cobalt exposure using a toxicogenomic approach. Data analysis focused on some cellular processes and protein targets that are thought to be relevant for carcinogenesis, transport and biomarker research. Results A time course transcriptome analysis was performed on A549 human pulmonary cells, leading to the identification of 85 genes which are repressed or induced in response to soluble 59 Co. A group of 29 of these genes, representing the main biological functions, was assessed by quantitative RT-PCR. The expression profiles of six of them were then tested by quantitative RT-PCR in a time-dependent manner and three modulations were confirmed by Western blotting. The 85 modulated genes include potential cobalt carriers (FBXL2, ZNT1, SLC12A5), tumor suppressors or transcription factors (MAZ, DLG1, MYC, AXL) and genes linked to the stress response (UBC, HSPCB, BNIP3L). We also identified nine genes coding for secreted proteins as candidates for biomarker research. Of those, TIMP2 was found to be down-regulated and this modulation was confirmed, in a dose-dependent manner, at protein level in the supernatant of exposed cells. Conclusion Most of these genes have never been described as related to cobalt stress and provide original hypotheses for further study of the effects of this metal ion on human lung epithelial cells. A putative biomarker of cobalt toxicity was identified.