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Description of key information

Key value for chemical safety assessment

Respiratory sensitisation

Endpoint conclusion
Endpoint conclusion:
adverse effect observed (sensitising)
Additional information:

Occupational exposure studies in cobalt facilities:

Swennen et al (1993): Probability of dyspnoea correlated as function of increasing concentration of airborne Co dust during exercise. Reduction of FEV1/ VC ratio correlated with intensity of current cobalt concentration in air and urine. Exposure: 50% of the workers exposed to TWA cobalt air levels above 50µg/m³. 25% exposed to TWA cobalt air levels above 500µg/m³.


Verougstraete et al (2004), follow-up study of Swennen et al.: Strict environmental control implemented between 1988 and 2001 resulted in decreases in airborne and urine cobalt levels. Cobalt exposures (as measured by cobalt in urine) were associated with decreases in FEV1 only in workers who smoked.


Roto (1980): Included case-referent and cross-sectional study. Exposure range of 0.06-0.1 mg cobalt/m³ (cobalt metal powder) were given. A correlation in decrease in FEV1 with increasing exposure to cobalt was analysed. Occupational asthma was defined as more than 15% reduction in FEV1. Overall, it was concluded that the risk for asthma is 5-fold higher in cobalt exposed workers as compared to controls.


Linna et al.2003, follow-up study of Roto: Process changes to hydrometallurgical workplaces now includes exposures to cobalt sulfate, carbonate, sulfide, oxides, hydroxides, as well as cobalt metal powders. Two new cases of occupational or allergic asthma were reported. Workers who smoked had significantly lower lung function parameters than workers who did not smoke.


Sauni et al 2010: Characterised all asthma cases from 1980 until 2003. The incidence of occupational asthma (>15% decrease in FEV1) correlated with an increase on cobalt exposure. Median cobalt air levels ranged from 0.1 mg/m³ in sulfatising and roasting workplaces to 0.03mg/m³ in leaching and solution preparation workplaces. Some work areas had concomitant exposures to sulfur dioxide and hydrochloride gases. The authors concluded that the evidence indicated that irritant gases may enhance the risk of respiratory sensitisation to cobalt. Cobalt air exposure levels below 0.120 mg cobalt/m³ (in the absence of irritant gases) were not associated with occupational asthma.


Pilliere et al (1990), Single-case study on occupational exposure to cobalt resinate: Cobalt resinate and cobalt stearate administration precipitated a positive finding in a bronchio-constriction test. Whereas the administration of cobalt tallate resulted in a negative test result. Cobalt resinate or cobalt stearate exposure decreased FEV1 by 30%. The chemical identity of occupational substance was not verified in the report. Inhalation administration of cobalt stearate, -resinate and -tallate was supervised under clinical conditions.


Cobalt industry-wide questionnaire

A cobalt industry-wide questionnaire exercise for cases of occupational asthma following cobalt exposure was conducted in 2010. A total of 13 facilities producing inorganic cobalt substances or inorganic cobalt substances with an organic anion (“cobalt carboxylates”) responded. The facilities reported in the occupational exposure studies cited above were not included in the questionnaire results. Three facilities reported some experience with cobalt asthma in either cobalt carboxylate production or inorganic cobalt substance production. The questionnaire indicates that there is some cobalt industry experience with occupational asthma in addition to the occupational exposure studies reported in the literature.


Immune vs. non-immune responses

Cobalt exposure has been reported to induce immune responses in some hardmetal workers diagnosed with occupational asthma or reduced lung function (as indicated by measured IgE titres). It is currently accepted that lung function is reduced by inflammatory processes occurring in the lungs. It is not clear (clinically) whether the inflammatory process leads to an immune response or whether the process itself, causes lung function changes in the absence of immune-related mechanisms. The current thinking is that inflammatory mechanisms are associated with reduced lung function by both immune-related and non-immune-related mechanisms. The studies used for the basis if this proposed hazard classification did not evaluate the presence of an immune response. The single-case-study on cobalt resinate and cobalt stearate indicated a late response in the bronchio-provocation test. This finding would favour a non-immune-related response as responses mediated by IgE (immunoglobulin E) are likely to be more-immediate.



Five well-characterised exposure studies in two cobalt facilities producing cobalt substances support observations that occupational exposures to inorganic cobalt substances (in the absence of other metal exposures) is associated with occupational asthma. In these cases occupational asthma was defined by clinically-compliant lung function testing. Neither study was able to discriminate between specific cobalt substances and their individual potential to reduce lung function. Neither study indicated a high frequency of occurrence of occupational asthma among the worker population.


A case report of occupational exposure to cobalt resinate verified respiratory sensitivity of a worker to cobalt resinate and cobalt stearate by bronchio-provocation-testing with each substance. The worker did not respond to bronchio-provocation after the inhalation administration of cobalt tallate. The cobalt industry-wide questionnaire showed that there is industry experience with cobalt resinates and cases of occupational asthma. Based on available information, there is no indication the frequency of occupational asthma in workers is high.


Based on the above argumentation, the following substances will be classified as respiratory sensitiser, category 1B:

Cobalt Powders, Cobalt Sulfate, Cobalt di-Chloride, Cobalt di-Nitrate, Cobalt Carbonate, Cobalt Acetate, Cobalt Monoxide, Tricobalt Tetraoxide, Cobalt Sulfide, Cobalt di-Hydroxide, Cobalt tri-Hydroxide, Cobalt Oxy-Hydroxide and Cobalt Resinate.

Justification for selection of respiratory sensitisation endpoint:
Weight of evidence information

Justification for classification or non-classification

Respiratory sensitisation

Cobalt hydroxide oxide will be classified as respiratory sensitiser according to section 3.4, annex I of regulation (EC) 1272/2008 based on human epidemiological data showing cases of occupational asthma following prolonged exposure towards cobalt salts, -oxides and hydroxides. Cobalt hydroxide oxide will be classified as respiratory sensitiser category 1B (H334). Thus further testing is not required, according to section 1.1.3 and 1.2, annex XI of regulation (EC) 1907/2006.