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EC number: 200-848-3 | CAS number: 75-20-7
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data

Toxicological Summary
- Administrative data
- Workers - Hazard via inhalation route
- Workers - Hazard via dermal route
- Workers - Hazard for the eyes
- Additional information - workers
- General Population - Hazard via inhalation route
- General Population - Hazard via dermal route
- General Population - Hazard via oral route
- General Population - Hazard for the eyes
- Additional information - General Population
Administrative data
Workers - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 2 mg/m³
- Most sensitive endpoint:
- irritation (respiratory tract)
Acute/short term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 4 mg/m³
- Most sensitive endpoint:
- irritation (respiratory tract)
DNEL related information
Workers - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- skin irritation/corrosion
Acute/short term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- skin irritation/corrosion
Workers - Hazard for the eyes
Local effects
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
Additional information - workers
In aqueous solution, calcium carbide rapidly decomposes into calcium hydroxide and acetylene. Calcium hydroxide dissociates into calcium and hydroxyl ions. As hydroxyl ions are readily buffered in biological tissue, only calcium ions and gaseous acetylene need to be assessed for systemic adverse effects. Calcium is the most abundant mineral in the human body and part of the normal diet (approx 700 mg/day; SCF 2003). The second decomposition product, acetylene, has been used for over 100 years as an anaesthetic and as an industrial chemical, and few complications of using this gas have surfaced (US EPA, HPV review 2006).
Thus, the risk assessment of calcium carbide is driven by local effects in the lung related to calcium hydroxide. Potential respiratory irritation of calcium hydroxide and calcium oxide has been assessed in several epidemiological studies and studies in volunteers. Key studies for the assessment of respiratory irritation are summarized on IUCLID section 7.9.3, 7.10.2 and 7.10.3.
No relevant respiratory effect was found at an exposure level at 1.2 (0.4–5.8) mg/m³ (lime, total dust, Torén et al. 1996), or 2.9 (0.01–79) mg/m³ (Portland cement, total dust, Abrons 1988). Fell (2003) concluded that cement dust exposure has no negative impact on lung function respiratory symptoms at total dust levels of 7.9 mg/m³ (SD = 12.9) and for respirable dust 0.91 mg/m³ (SD = 0.55). Yang (1996) concluded that occupational exposure to 3.6 (1.3-8.1) mg/m³ Portland cement dust may lead to higher prevalence of chronic respiratory symptoms and the reduction of ventilatory capacity. Mwaiselange (2004) concluded an association between reduced lung function and current total dust exposures in excess of 3 mg/m³ cement. SCOEL (2008) concluded that no consistent effect of cement factory dust appeared in the range from 0.57 to 1.5 mg/m³ respirable dust and from 3.3 mg/m³ and lower levels of total dust. Decrease in lung function occurred somewhere in the range from 1.6 to 3.9 mg/m³ respirable dust and from > 5.7 mg/m³ total dust. However, it is a limitation for the extrapolation of this range to effects of CaO and Ca(OH)2 that the reported dust concentrations often were mixed levels from production of raw materials (e.g. clay, limestone and quartz) and cement dust. Only Mwaiselange (2004) allows the comparison of lung function in relation to the specific production processes and their dust levels. From the effect in the kiln and cement milling workers, it appears that the NOAEL may be about 3 mg/m³ total dust. It is, however, noted that the groups are small and an abrupt change in effect from 2.9 to 3.2 mg/m³ is not biologically plausible taking the modest effect even at much higher concentrations into account. However, overall the NOAEL of 3 mg/m³ total dust from this study is bracketed by the NOAEL of the total dust range, which is up to 3.3 mg/m³ from the other epidemiological studies.
The results form occupational exposure are complemented by a well conducted acute study in human volunteers with defined exposure to calcium oxide (Cain 2004). Here, sensory irritation is expected to be prevented by 1–2 mg/m³ respirable CaO dust (no relation to inhalable dust could be derived).
Cain et al. (2004) exposed 12 lightly exercising volunteers (breathing through the nose) for 20 min to 1 to 5 mg/m³ CaO. Nasal resistance, nasal secretion, mucociliary transport time, and chemesthetic magnitude were assessed. The mass median aerodynamic diameter was 6.53 ± 0.76 µm. In the nose, 1 and 2 mg/m³ gave rise to an equivalent effect at the end of the exposure. The 5 mg/m³ level had an effect equivalent to 20 % CO2. The values were significantly above the background, but no significant effect occurred in nasal secretion and mucociliary clearance, determined by the saccharin test. The study interpreted the effects as “very few people used the term irritation to describe the nasal sensation evoked by 10 % CO2. Some would use that term at 15 % CO2 and the majority would use it at 20 % CO2”, and also the authors conclude “that the psychophysical judgements produced results consistent with the known effect that calcium oxide would evoke irritating chemesthesis at exposures in the range of 2 to 5 mg/m³”. It was concluded that the effects of CaO, which were not dose dependent in the range from 1 to 2 mg/m³, were of no adverse health significance. The effect had not reached the maximum within the 20 min of exposure although the effect was levelling off. Taking these two facts into account, an exposure limit of 1 mg/m³ was proposed by the authors to protect against adverse sensory irritation.
In a second study, Cain et al. (2008) investigated the airway effects of 2.5 mg/m³ CaO in 6 male and 6 female volunteers, who were exposed for 45 min. The maximum effect was reached about 30 min after initiation of exposure, followed by adaptation. The authors interpreted their results as “the highest levels studied here lay at the edge of where people would agree that feel in the nose becomes irritating about 17–18 % carbon dioxide”. Thus, the 2.5 mg/m³ level can be considered at the LOAEL. Due to the fact that 1 and 2 mg/m³ calcium oxide gave rise to an equivalent effect in Cain (2004) and for calcium oxide, irritating chemesthesis is considered to start at concentrations below physiologically adverse responses. Thus, 2 mg/m³ is considered to be a protective value when used as occupational exposure limit.
Due to the fact that irritating chemesthesis reaches a peak after approximately 30 min, it is considered justified to set a short term exposure limit STEL of 4 mg/m³, in agreement with Cain (2004) and SCOEL (2008).
General Population - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- irritation (respiratory tract)
Acute/short term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- irritation (respiratory tract)
DNEL related information
General Population - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- skin irritation/corrosion
Acute/short term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
General Population - Hazard via oral route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- skin irritation/corrosion
Acute/short term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- skin irritation/corrosion
DNEL related information
General Population - Hazard for the eyes
Local effects
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
Additional information - General Population
Exposure of the general population to calcium carbide is restricted to the use of carbide lamps or carbide welding. In these settings, exposure is limited to very short periods of loading of technical equipment (carbide lamp or welding equipment). Thus, prolonged exposure to calcium carbide is not expected and risk management measures related to local effects (chemical burns of the skin and eyes) are considered to be sufficient.
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