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EC number: 231-595-7 | CAS number: 7647-01-0
- 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
Endpoint summary
Administrative data
Description of key information
Hydrochloric acid is either gas or corrosive aqueous solution, for which the most relevant route of exposure is by inhalation. Testing for acute systemic toxicity of the corrosive substance by oral or dermal route is not appropriate. Available data shows an 30 minute LC50 in rats of 4701 ppm for HCl gas, and 8.3 mg/L for aerosols (MMAD < 5µm).
Key value for chemical safety assessment
Acute toxicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Acute toxicity: via inhalation route
Link to relevant study records
- Endpoint:
- acute toxicity: inhalation
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- Not specified; published in 1974
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Minor reporting deficiencies. (Substance purity, bodyweight data, individual data not reported). Not GLP. However, reporting is in most respects fully adequate for this endpoint, and study design exceeds guideline requirement in many respects.
- Qualifier:
- no guideline followed
- Deviations:
- not applicable
- Principles of method if other than guideline:
- Study conducted according to the "Guide for Laboratory Animal Facilities and Care" (1965), prepared by the Committee on the Guide for Laboratory Animal Resources, Natl. Acad. Sci./Natl. Research Council: and Public Law 89-544, "Laboratory Animal Welfare Act," (1967)
- GLP compliance:
- no
- Remarks:
- not compulsory at the time the study was conducted
- Test type:
- other: Rats were exposed for 5 or 30 minutes in a whole body chamber and observed for 7 days for clinical signs and mortality followed by gross and histopathological examinations
- Limit test:
- no
- Species:
- rat
- Strain:
- other: CFE (Sprague-Dawley derived)
- Sex:
- male
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Source: Carworth Farms Inc.
- Age at study initiation: not specified
- Weight at study initiation: 250 - 300 g
- Fasting period before study: not specified
- Housing: not specified
- Diet (e.g. ad libitum): not specified
- Water (e.g. ad libitum): not specified
- Acclimation period: not specified
ENVIRONMENTAL CONDITIONS
- Temperature (°C): not specified
- Humidity (%): not specified
- Air changes (per hr): not specified
- Photoperiod (hrs dark / hrs light): not specified
IN-LIFE DATES: not specified - Route of administration:
- inhalation
- Type of inhalation exposure:
- whole body
- Vehicle:
- other: unchanged (no vehicle)
- Details on inhalation exposure:
- GENERATION OF TEST ATMOSPHERE / CHAMBER DESCRIPTION
- Exposure apparatus: Modified Rochester chamber (gas) or Longley chamber (aerosol)
- Exposure chamber volume: not specified
- Method of holding animals in test chamber: not specified
- Source and rate of air: predried air at a constant rate of 10 cfm (283.169 L/min)
- Method of conditioning air: sliding cage "drawers" in the wall of the chamber
- System of generating particulates/aerosols:
HCl Gas was metered through a corrosion resistant gas regulator and a flow-meter and introduced into a modified Rochester chamber. The input air to the chamber was pre-dried and supplied at the constant rate of 10 cfm (ca. 283.169 L/min).
HCl Aerosol was produced introducing HCl gas into a Longley chamber which was filled with a saturated water droplet mist. Water was supplied to the DeVilbiss ultrasonic nebulizer at the flow rate of 6.8 mL/min while predried air was maintained at the constant rate of 10 cfm (ca. 283.169 L/min).
- Method of particle size determination: The nebulizer was evaluated to confirm the production of droplets in the range specified by the manufacturer (i.e. 0.5 to 9 microns). Particle size distribution was determined by measuring 456 droplets which were rended visible in the filter by adding a 5% congo red solution.
- Treatment of exhaust air: not specified
- Temperature, humidity, pressure in air chamber: not specified
TEST ATMOSPHERE
- Brief description of analytical method used: Concentrations were measured continuously during exposures using a chloride ion specific electrode with double distilled water as an absorber.
- Samples taken from breathing zone: not specified
TEST ATMOSPHERE (if not tabulated)
- Particle size distribution: reported in "Any other information on materials and methods incl. tables"
- MMAD (Mass median aerodynamic diameter) / GSD (Geometric st. dev.): not specified - Analytical verification of test atmosphere concentrations:
- yes
- Remarks:
- Concentrations were measured continuously during exposures using a chloride ion specific electrode with double distilled water as an absorber.
- Duration of exposure:
- >= 5 - <= 30 min
- Remarks on duration:
- 5 minutes or 30 minutes
- Concentrations:
- Gas concentrations (5 min exposure): 30000, 32255, 39850, 45200 and 57290 ppm
Gas concentrations (30 min exposure): 2078, 2678, 3071, 5180, 6068 and 6681 ppm
Aerosol concentrations (5 min exposure): 9.7, 28.4, 37.3, 43.6, 57.0, 60.1 and 91.3 mg/litre (equivalent to 6571, 19312, 25324, 29648, 38746, 40810 and 62042 ppm)
Aerosol concentrations (30 min exposure): 4.3, 6.6, 9.0 and 9.8 mg/litre (equivalent to 2910, 4481, 6078 and 6640 ppm) - No. of animals per sex per dose:
- 10 rats per group
- Control animals:
- no
- Details on study design:
- - Duration of observation period following administration: 7 days
- Frequency of observations and weighing: Daily observations
- Necropsy of survivors performed: yes
- Other examinations performed: clinical signs, body weight, histopathology, other: food consumption - Statistics:
- Not specified.
- Preliminary study:
- Not applicable; not a fixed dose study.
- Sex:
- male
- Dose descriptor:
- LC50
- Effect level:
- 40 989 ppm
- Exp. duration:
- 5 min
- Remarks on result:
- other: HCl gas, range: 34803 - 48272 ppm
- Sex:
- male
- Dose descriptor:
- LC50
- Effect level:
- 4 701 ppm
- Exp. duration:
- 30 min
- Remarks on result:
- other: HCl gas, range: 4129-5352 ppm
- Sex:
- male
- Dose descriptor:
- LC50
- Effect level:
- 45.6 mg/L air
- Exp. duration:
- 5 min
- Remarks on result:
- other: HCl aerosol, range: 39.5-52.8 mg/L. Equivalent to 31008 ppm, range: 26824-35845 ppm
- Sex:
- male
- Dose descriptor:
- LC50
- Effect level:
- 8.3 mg/L air
- Exp. duration:
- 30 min
- Remarks on result:
- other: HCl aerosol, range: 7.2-9.7 mg/L. Equivalent to 5666 ppm, range: 4855-6614 ppm
- Mortality:
- Mortalities were observed at all the doses, with the exception of the lowest ones. Mortality tables are described in an attached document (PDF).
- Clinical signs:
- other: Toxic signs during exposure to HCl gas or aerosol were essentially identical. HCl was severely irritating to the eyes, mucous membranes and exposed areas of skin. Animals usually exhibited a rapid and shallow breathing pattern by the end of the exposure p
- Body weight:
- Weight loss following exposure was noted.
- Gross pathology:
- Gross examination of the animals which died during or at some time following exposure showed that the respiratory tract was the main target for the HCl damage. Moderate to severe alveolar emphysema, atelectasis and oedema of the lungs were observed, and occasional ‘spotting’ of the lung tissue was also noted. The upper respiratory tract was severely irritated with severe damage of the epithelia tissue of nose and trachea. Animals surviving up to terminal sacrifice (7 days after exposure) showed that recovery was not complete with abnormally coloured grey lungs failing to collapse upon opening the chest cavity. There was also evidence of consolidation of lung tissue.
- Other findings:
- - Histopathology: Histopathological examination confirmed the damage of respiratory tract while no abnormality was detected in other tissues.
- Other observations: Decrease in food consumption was noted - Interpretation of results:
- not classified
- Remarks:
- Migrated information Criteria used for interpretation of results: not specified
- Conclusions:
- Toxic signs during exposure to HCl gas or aerosol were essentially identical. HCl was severely irritating to the eyes, mucous membranes and exposed areas of skin. The calculated LC50 values were the following:
HCl gas (5 min exposure): 40989 ppm (34803-48272)
HCl gas (30 min exposure): 4701 ppm (4129-5352)
HCl aerosol (5 min exposure): 45.6 mg/L (39.5-52.8) equivalent to 31008 ppm (26824-35845)
HCl aerosol (30 min exposure): 8.3 mg/L (7.2-9.7) equivalent to 5666 ppm (4855-6614)
Reference
Mortalities were observed at all the doses, with the exception of the lowest ones. HCl was severely irritating to the eyes, mucous membranes and exposed areas of skin. Animals usually exhibited a rapid and shallow breathing pattern by the end of the exposure period. Corneal erosion and clouding were noted, as well as excessive grooming and ulceration of the scrotum. Animals which survived the exposure, especially at the higher concentrations of either HCl gas or aerosol, had bloody discharges from their nostrils and exhibited audible difficulty in breathing (producing a laboured ‘clicking’. The fur had a ‘singed’ appearance and was discoloured to a greenish hue. Decrease in food consumption and weight loss following exposure was also noted.
Gross examination of the animals which died during or at some time following exposure showed that the respiratory tract was the main target for the HCl damage. Moderate to severe alveolar emphysema, atelectasis and oedema of the lungs were observed, and occasional ‘spotting’ of the lung tissue was also noted. The upper respiratory tract was severely irritated with severe damage of the epithelia tissue of nose and trachea. Animals surviving up to terminal sacrifice (7 days after exposure) showed that recovery was not complete with abnormally coloured grey lungs failing to collapse upon opening the chest cavity. There was also evidence of consolidation of lung tissue.
Histopathological examination confirmed the damage of respiratory tract while no abnormality was detected in other tissies.
Table A6.1.3/01-1: HCl gas (5 min exposure) Acute Inhalation Toxicity in Rats
Concentration (ppm) | Mortality ratio | Time of deaths (No./day) | |||||||
0(during exposure) | 1 | 2 | 3 | 4 | 5 | 6 | 7 | ||
30000 | 0/10 | ||||||||
32255 | 1/10 | 1 | |||||||
39850 | 6/10 | 2 | 3 | 1 | |||||
45200 | 7/10 | 5 | 2 | ||||||
57290 | 9/10 | 5 | 4 |
LC50 value: 40989 ppm (34803-48272)
Table A6.1.3/01-2: HCl gas (30 min exposure) Acute Inhalation Toxicity in Rats
Concentration (ppm) | Mortality ratio | Time of deaths (No./day) | |||||||
0(during exposure) | 1 | 2 | 3 | 4 | 5 | 6 | 7 | ||
2078 | 0/10 | ||||||||
2678 | 1/10 | 1 | |||||||
3071 | 0/10 | ||||||||
5180 | 5/10 | 2 | 1 | 1 | 1 | ||||
6068 | 8/10 | 7 | 1 | ||||||
6681 | 10/10 | 7 | 1 | 2 |
LC50 value: 4701 ppm (4129-5352)
Table A6.1.3/01-3: HCl aerosol (5 min exposure) Acute Inhalation Toxicity in Rats
Concentration | Mortality ratio | Time of deaths (No./day) | ||||||||
mg/L | ppm | 0(during exposure) | 1 | 2 | 3 | 4 | 5 | 6 | 7 | |
9,7 | 6571 | 0/10 | ||||||||
28,4 | 19312 | 1/10 | 1 | |||||||
37,3 | 25324 | 3/10 | 2 | 1 | ||||||
43,6 | 29648 | 6/10 | 1 | 4 | 1 | |||||
57 | 38746 | 6/10 | 2 | 1 | 3 | |||||
60,1 | 40810 | 7/10 | 2 | 4 | 1 | |||||
91,3 | 62042 | 10/10 | 8 | 1 | 1 |
LC50 value: 45.6 mg/L (39.5-52.8) equivalent to 31008 ppm (26824-35845)
Table A6.1.3/01-4: HCl aerosol (30 min exposure) Acute Inhalation Toxicity in Rats
Concentration | Mortality ratio | Time of deaths (No./day) | ||||||||
mg/L | ppm | 0(during exposure) | 1 | 2 | 3 | 4 | 5 | 6 | 7 | |
4,3 | 2910 | 1/10 | 1 | |||||||
6,6 | 4481 | 0/10 | ||||||||
9 | 6078 | 6/10 | 1 | 3 | 1 | 1 | ||||
9,8 | 6640 | 8/10 | 3 | 1 | 2 | 2 |
LC50 value: 8.3 mg/L (7.2-9.7) equivalent to 5666 ppm (4855-6614)
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LC50
- Value:
- 7 051 mg/m³ air
- Quality of whole database:
- Based on 30 minute HCl inhalation LC50 (gas) values of 4701 ppm (equivalent to 7051 mg/m3) in rats.
Acute toxicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
Substance is either gas or corrosive aqueous solution. The most relevant route of exposure for acute toxicity of hydrogen chloride is by inhalation. Further testing for acute systemic toxicity of the corrosive substance by oral or dermal route is not appropriate.
Due to its high solubility and immediate dissociation properties, an aqueous solution of hydrochloric acid is not expected to be systematically available in living organisms.The absorption, distribution, metabolism and excretion of acids and chloride are well known from human and mammalian physiology. Both ions are regulated within a narrow range to maintain homeostasis. As consequence, effects following acute exposures will be localized following its corrosive/irritant nature. Acute systemic toxicity is not expected.
After acute inhalation exposure to concentrations below the limit of classification for acute inhalation (20,000 mg/m3) adverse effects were observed in human case and human experimental studies.
Toxic signs in rats during exposure to HCl gas or aerosol were essentially identical. HCl was severely irritating to the eyes, mucous membranes and exposed areas of skin. The calculated LC50 values were the following:
HCl gas (5 min exposure): 40989 ppm (34803-48272)
HCl gas (30 min exposure): 4701 ppm (4129-5352) = 7521 mg/m3
HCl aerosol (5 min exposure): 45.6 mg/L (39.5-52.8) equivalent to 31008 ppm (26824-35845)
HCl aerosol (30 min exposure): 8.3 mg/L (7.2-9.7) equivalent to 5666 ppm (4855-6614)
Based on possible short-term effects, the SCOEL recommends a STEL (15 min) of 10 ppm (15 mg/m3). This value will be used as DNEL for acute inhalation exposure.
Justification for selection of acute toxicity – oral endpoint
Substance is either gas or corrosive aqueous solution.
Justification for selection of acute toxicity – inhalation endpoint
Most appropriate data for classification purposes.
Justification for selection of acute toxicity – dermal endpoint
Substance is either gas or corrosive aqueous solution.
Justification for classification or non-classification
Hydrogen chloride is available commercially as an anhydrous gas or as aqueous solutions (hydrochloric acid), at the concentrations of 33 to 36%. Acute systemic toxicity is not expected. Effects following exposures are characterised by local effects.
For classification based on available data via inhalation, use can be made of Haber rule (C.t = k) to extrapolate from LC50 values based on 30 minutes to 4h-LC50 values to derive appropriate classification:
HCl gas:
Extrapolation for 30 minutes LC50 of4701 ppmresults to 4h-LC50 of 588 ppm. This leads to Cat.3, H331 (Toxic if inhaled) which the current harmonised classification for HCl gas.
There is no need for classification for systemic toxicity by dermal and oral route for HCl gas.
Aqueous HCl solutions:
Exposure by inhalation to aerosol from aqueous solutions will be limited. Effects are localaised in nature and depend on the aqueous concentration of HCl in the aerosol. Being a corrosive substance classification the current harmonised classification to STOT SE 3, H335 (May cause respiratory irritation), is appropriate.
Acute toxicity by dermal and oral route: not classified (data lacking)
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