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EC number: 215-157-2
CAS number: 1308-06-1
exposure studies in cobalt facilities:
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.
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
(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.
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.
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.
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 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.
vs. non-immune responses
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.
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
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.
on the above argumentation, the following substances will be classified
as respiratory sensitiser, category 1B:
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
Weight of evidence information
Tricobalt tetraoxide 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. Tricobalt tetraoxide 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
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