Thyroid enlargement probably induced by cobalt

Chamberlain, John L.

doi:10.1016/s0022-3476(61)80213-8

Cited by 12 publications

(9 citation statements)

References 16 publications

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“…Paley et al (1958) reported decreased iodine uptake by the thyroid in two of four patients exposed to 0.54 mg Co/kg-day for 14 days (Paley et al, 1958). Gross et al (1955), Kriss et al (1955), Little and Sunico (1958), Chamberlain (1961), Robey et al (1956) and Jaimet and Thode (1955) all describe the development of endocrine effects in children experiencing long-term (up to seven months) Co exposures of approximately 0.5-10 mg/kg-day. The effects were typically reported as being reversible when treatment was ceased .…”

Section: Endocrine Toxicitymentioning

confidence: 99%

“…High oral doses of Co have resulted in adverse effects in humans and animals; numerous case reports and studies of anemic children, for example, have described thyroid effects (including the development of goiters) following oral Co doses of approximately 1.4-10 mg Co/kg-day Kriss et al, 1955;Little and Sunico, 1958;Paley et al, 1958;Chamberlain, 1961;Robey et al, 1956). Co-induced cardiomyopathy was reported in individuals who consumed large quantities of beer that contained Co sulfate (CoSO 4 ) or CoCl 2 as a foam stabilizer (Alexander, 1969;Morin and Daniel, 1967;Bonenfant et al, 1969).…”

Section: Introductionmentioning

confidence: 99%

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Derivation of a chronic oral reference dose for cobalt

Finley¹,

Monnot²,

Paustenbach³

et al. 2012

Regulatory Toxicology and Pharmacology

110

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Section: Endocrine Toxicitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Derivation of a chronic oral reference dose for cobalt

Finley¹,

Monnot²,

Paustenbach³

et al. 2012

Regulatory Toxicology and Pharmacology

110

View full text Add to dashboard Cite

“…Furthermore, numerous human studies have reported endocrine effects (e.g. goiter development and reduced iodide uptake) in orally Cotreated subjects, with daily Co doses ranging between 0.5 and 10 mg/kg bw/day and the treatment duration between 2 weeks and 10 months [275][276][277][278][279][280][281][282] . These effects mostly disappeared after cessation of the exposure 275,279 .…”

Section: Endocrine Systemmentioning

confidence: 99%

Cobalt toxicity in humans—A review of the potential sources and systemic health effects

et al. 2017

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Cobalt (Co) and its compounds are widely distributed in nature and are part of numerous anthropogenic activities. Although cobalt has a biologically necessary role as metal constituent of vitamin B, excessive exposure has been shown to induce various adverse health effects. This review provides an extended overview of the possible Co sources and related intake routes, the detection and quantification methods for Co intake and the interpretation thereof, and the reported health effects. The Co sources were allocated to four exposure settings: occupational, environmental, dietary and medical exposure. Oral intake of Co supplements and internal exposure through metal-on-metal (MoM) hip implants deliver the highest systemic Co concentrations. The systemic health effects are characterized by a complex clinical syndrome, mainly including neurological (e.g. hearing and visual impairment), cardiovascular and endocrine deficits. Recently, a biokinetic model has been proposed to characterize the dose-response relationship and effects of chronic exposure. According to the model, health effects are unlikely to occur at blood Co concentrations under 300μg/l (100μg/l respecting a safety factor of 3) in healthy individuals, hematological and endocrine dysfunctions are the primary health endpoints, and chronic exposure to acceptable doses is not expected to pose considerable health hazards. However, toxic reactions at lower doses have been described in several cases of malfunctioning MoM hip implants, which may be explained by certain underlying pathologies that increase the individual susceptibility for Co-induced systemic toxicity. This may be associated with a decrease in Co bound to serum proteins and an increase in free ionic Co. As the latter is believed to be the primary toxic form, monitoring of the free fraction of Co might be advisable for future risk assessment. Furthermore, future research should focus on longitudinal studies in the clinical setting of MoM hip implant patients to further elucidate the dose-response discrepancies.

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“…National reports in 2002 and 2008 declared that Iran's control program for iodine deficiency is ongoing [ 3 , 4 ], but nonetheless, goiters remain an endemic condition in most parts of Iran, especially among school-aged children [ 3 , 4 , 5 , 6 , 7 ]. Thus, it is feasible that factors other than iodine deficiency either directly or indirectly contribute to the etiology of endemic goiter [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ]. One possible contributing factor is cobalt, which is a rare trace element that has been shown to have goitrogenic effects [ 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

The Association between Cobalt Deficiency and Endemic Goiter in School-Aged Children

Sanjari

Gholamhoseinian

Nakhaee³

2014

Endocrinol Metab

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BackgroundIn Iran, an iodine deficiency control program was initiated in 1989 by iodizing salt. Despite this program, goiters have remained an endemic condition in most parts of Iran. Thus, it is possible that other factors aside from iodine deficiency may contribute to endemic goiter. The aim of this study was to investigate the association between cobalt deficiency and endemic goiter in a region of Iran with a high prevalence of goiter.MethodsA cross-sectional study was conducted among school children aged 9 to 11 years in the city of Kerman, Iran. In the first phase of the study, a multistage, proportional-to-size, cluster sampling method was used to screen 5,380 out of 29,787 students. After the screening phase, 170 students (130 goitrous and 40 nongoitrous) were randomly selected, and serum and urine specimens were obtained. We measured thyroid function, serum cobalt level, and urinary iodine excretion. Univariate and multiple logistic regression analyses were performed.ResultsThe prevalence of grade 2 goiters was 34.8% (95% confidence interval [CI], 31.5 to 42.5), with both sexes being equally affected. The weight and body mass index of goitrous subjects was significantly lower (P<0.001) than those of nongoitrous subjects. The serum cobalt levels were lower in goitrous subjects than in nongoitrous subjects (4.4±2.9 µg/L vs. 6.4±2.7 µg/L). The urinary iodine levels were also lower in goitrous subjects than in nongoitrous subjects (198.3±108.3 µg/L vs. 270.2±91.1 µg/L). Multiple regression analysis showed that only cobalt deficiency, not iodine deficiency, significantly contributed to the presence of goiter (odds ratio, 0.78; 95% CI, 0.61 to 0.99; P=0.042).ConclusionCobalt deficiency may be an important independent predicator for goiter in endemic regions, especially areas in which goiters persist despite salt iodization programs.

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Thyroid enlargement probably induced by cobalt

Cited by 12 publications

References 16 publications

Derivation of a chronic oral reference dose for cobalt

Derivation of a chronic oral reference dose for cobalt

Cobalt toxicity in humans—A review of the potential sources and systemic health effects

The Association between Cobalt Deficiency and Endemic Goiter in School-Aged Children

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