Hazardous substance assessment: Hydrochloric acid and hydrogen chloride

Identification

Chemical name:

Hydrochloric acid and hydrogen chloride

CAS #:

7647-01-0

Chemical composition:

HCl(aq) [for hydrochloric acid]; HCl [for hydrogen chloride]

Synonyms:

Muriatic acid
Chlorohydric acid

UN #:

UN 1789 [for hydrochloric acid]; UN 1050 [for hydrogen chloride, anhydrous]; UN 2186 [for hydrogen chloride, refrigerated liquid]

Pictogram(s):

Figure 1. - Text Equivalent

The symbol within the pictogram, which applies to hydrochloric acid at a concentration of 5% or greater and to hydrogen chloride, shows a container dripping liquid onto a piece of metal and another container dripping liquid onto a hand. This symbol indicates that hazardous products with this pictogram can:

• damage or destroy metal
• cause irreversible damage to the skin (for example, burns, blisters, scarring)
• produce tissue damage in the eye or vision loss that is irreversible or not fully reversible within 21 days

Figure 2. - Text Equivalent

The symbol within the pictogram, which applies to hydrochloric acid but not to hydrogen chloride, is an exclamation mark. This symbol indicates that hazardous products with this pictogram can cause certain health effects for example:

• skin irritation
• eye irritation
• skin sensitization

Figure 3. - Text Equivalent

The symbol within the pictogram, which applies only to hydrogen chloride, is a human skull with 2 crossed bones behind it. The symbol indicates that hazardous products with this pictogram can cause death or poisoning.

WHMIS classification

Health hazards:

• Acute Toxicity (Oral) – Category 4 (hydrochloric acid)
• Acute Toxicity (Inhalation) – Category 3 (hydrogen chloride)
• Acute Toxicity (Inhalation) – Category 4 (hydrochloric acid)
• Skin Corrosion – Category 1 (hydrochloric acid at a concentration ≥ 17%; hydrogen chloride); Skin Irritation – Category 2 (hydrochloric acid at a concentration of ≥ 3.3% but < 17%)
• Serious Eye Damage – Category 1 (hydrochloric acid at a concentration ≥ 5%; hydrogen chloride); Eye Irritation – Category 2 (hydrochloric acid at a concentration ≥ 3.3% but < 5%)

Physical hazards:

• Corrosive to Metals – Category 1 (hydrochloric acid at a concentration ≥ 15%; hydrogen chloride)

Health hazards

Acute Toxicity (Oral):

Category 4 (hydrochloric acid)

Oral median lethal dose (LD₅₀): 700 milligrams per kilogram of body weight (mg/kg-bw) (rat)^{Footnote 1}.

In an acute oral toxicity study, a 31.45% aqueous hydrochloric acid solution was given to Sprague-Dawley albino rats (5 per dose, with 2 or 3 per sex) in a single administration at a dose of solution of 501, 631, 794, 1 000 or 1 260 mg/kg-bw. At the respective doses, 0, 2, 3, 4 and 5 animals died. The LD₅₀ of the solution was calculated to be 700 mg/kg-bw. Reduced appetite, low activity, increasing weakness and collapse in treated animals were observed. Autopsies revealed lung hyperemia, liver discolouration, and acute gastrointestinal inflammation. Some surviving animals had ulcerated areas of the stomach^{Footnote 1}. The LD₅₀ of a 31.45% aqueous hydrochloric acid solution meets the classification criteria for Category 4.

In a non-guideline oral acute toxicity study in female albino mixed-strain rats, the LD₅₀ for a 3.3% aqueous hydrochloric acid solution was 238 to 277 mg/kg-bw. The solution was administered to 4 different dose groups (10 animals per dose), namely 4.0, 6.3, 10.0 or 16.0 millilitres of solution per kilogram of body weight (mL/kg-bw), with the 3.3% concentration selected to minimize corrosive effects. The number of deaths at each dose were 0, 3, 8 and 10 rats, respectively. No other study details, such as clinical signs or pathology, were reported^{Footnote 2}.

The available data for hydrochloric acid meet the classification criteria for Acute Toxicity (Oral) – Category 4 [subsection 8.1.1(1) of the HPR].

Acute Toxicity (Dermal):

Does not meet criteria

Dermal LD₅₀: >5 000 mg/kg-bw (rabbit)^{Footnote 1}.

A non-guideline study in New Zealand White rabbits (1 male at lower dose and 1 male and 1 female at higher dose) exposed dermally for 24 hours to a 31.45% aqueous hydrochloric acid solution at a dose of solution of 5 010 or 7 940 mg/kg-bw reported only 1 death (female of higher dose) and an LD₅₀ of solution greater than 5 010 mg/kg-bw. Clinical signs included reduced appetite and activity, increasing weakness, collapse and death. Gross autopsy of the decedent revealed lung and liver hyperemia, slightly enlarged gall bladder and darkening of the spleen and kidney, whereas viscera of the 2 survivors appeared normal at 14 days post-exposure^{Footnote 1}.

The available data for hydrochloric acid do not meet the classification criteria for a category of Acute Toxicity (Dermal).

Acute Toxicity (Inhalation – Gases):

Category 3 (hydrogen chloride)

Inhalation median lethal concentration (LC₅₀): 1 562 parts per million (ppm) (4-hour; rat)^{Footnote 3}.

In non-guideline studies, male CFE (Sprague-Dawley-derived) rats and female CF-1 mice (10 per species and concentration) were exposed for 1 hour to hydrogen chloride vapours at an airborne concentration of 1 813, 2 585, 3 274, 3 941 or 4 455 ppm (rats) or of 557, 985, 1 387, 1 902 or 2 476 ppm (mice) and observed for 14 days. Hydrogen chloride vapours were metered via a glass rotameter from a steel cylinder to the exposure chamber. The 1-hour LC₅₀ values were reported as 3 124 and 1 108 ppm for rats and mice, respectively. Clinical signs included eye and nose irritation, laboured breathing, salivation, lacrimation and rhinorrhea. Gross pathological examination of the decedents revealed pulmonary congestion and intestinal and thymic hemorrhages. Among the survivors, such examination revealed no gross lesions in mice but multi-focal areas of red hepatization of the lungs and engorged or pale livers in the rats^{Footnote 3}.

Converted to a 4-hour exposure in accordance with subsection 8.1.1(4) of the HPR, the LC₅₀ values are 1 562 and 554 ppm for rats and mice, respectively.

The available data for hydrogen chloride meet the classification criteria for Acute Toxicity (Inhalation) – Category 3 [subsection 8.1.1(1) of the HPR].

Acute Toxicity (Inhalation – Vapours):

No data available

No data are available to determine whether hydrochloric acid meets the classification criteria for a category of Acute Toxicity (Inhalation – Vapours).

Acute Toxicity (Inhalation – Dusts and Mists):

Category 4 (hydrochloric acid)

Inhalation LC₅₀: 1.04 milligrams per litre (mg/L) (4-hour; rat)^{Footnote 4}.

In non-guideline acute inhalation toxicity studies, male CFE (Sprague-Dawley-derived) rats and male CF-1 mice (ICR-derived) were exposed for up to 30 minutes to respirable hydrochloric acid aerosols obtained via mixing of hydrogen chloride and a saturated water droplet mist in a Longley exposure chamber. Per airborne concentration tested, 10 rats or 10 mice were exposed. A 30-minute LC₅₀ of 8.3 mg/L was estimated for rats (converted to a 4-hour LC₅₀ of 1.04 mg/L) and of 3.2 mg/L for mice (converted to a 4-hour LC₅₀ of 0.4 mg/L). Exposure to the hydrochloric acid aerosols was extremely irritating to the eyes, mucous membranes and exposed areas of skin. Ulceration of the scrotum was a common finding in both rats and mice. Severe respiratory tract irritation, alterations in the texture and colour of the fur, and erosion and clouding of the cornea were also reported in both species.

Gross pathological examination of the decedents of both species revealed alveolar emphysema, atelectasis, edema and spotted tissue of the lung and damage of the nasal and tracheal epithelia. In surviving animals, particularly those exposed to higher concentrations, bloody nasal discharge was observed along with discolouration and lung damage at the 7-day post-exposure gross pathological examination. Histopathological examination of lung tissue from both species also demonstrated damage, whereas no damage was observed in other tissues^{Footnote 4}.

The available data for hydrochloric acid for the preferred animal species (rat) meet the classification criteria for Acute Toxicity (Inhalation) – Category 4 [subsection 8.1.1(1) of the HPR].

Skin Corrosion / Irritation:

Category 1 (hydrochloric acid at a concentration ≥ 17%; hydrogen chloride); Category 2 (hydrochloric acid at a concentration ≥ 3.3% but < 17%)

Humans: A 10% hydrochloric acid solution was tested on 30 human volunteers in a 4-hour human patch test. The test involved application of 0.2 millilitre (mL) of the test solution to an upper outer arm. Reactions following exposure to the solution occurred in 6 out of the 30 subjects (20%), compared to in 72% of subjects (23 out of 32) exposed to a concurrent positive control, a 20% sodium dodecyl sulfate (SDS) solution. The difference in reaction rate was statistically significant (p < 0.05), though the degree of reactions was not reported. As the reaction rate was lower than that of the 20% SDS solution, which the authors used to define a classification threshold for skin irritation, the authors proposed the 10% hydrochloric acid solution to be non-classified for skin irritation under the European Commission's former Dangerous Substances Directive^{Footnote 5}.

Animals: A 37% hydrochloric acid solution was corrosive when 0.5 mL was applied undiluted to the shaved dorsal skin of 6 New Zealand White rabbits under occlusive or semi-occlusive conditions for 1 or 4 hours. Corrosion was observed in all cases^{Footnote 6Footnote 7}. The results of this study meet the classification criteria for Skin Corrosion – Category 1.

Another animal study demonstrated skin corrosion in 6 female New Zealand White rabbits exposed dorsally to 0.5 mL of a 17% hydrochloric acid solution for 4 hours under occluded conditions. A corrosive response was defined as visible tissue destruction in at least 2 of the test animals. A 15% solution was not corrosive in the same study^{Footnote 8}. The results of this study meet the classification criteria for Skin Corrosion – Category 1.

In an in vitro Organisation for Economic Co-operation and Development Test Guideline (OECD TG) 431-compliant study, application of 40 microlitres (µL) of a 14.4% hydrochloric acid solution to 0.5-square centimetre (cm²) samples of reconstructed human epidermis was corrosive. This determination was made based on a prediction model for inorganic acids applied to the percentages of cell viability, for which the cross-run averages were 76.4, 0.77 and 0.3 following a 3-minute, 1- or 4-hour exposure, respectively^{Footnote 9}.

In another in vitro study performed according to OECD TG 431, 10, 15 (3-minute only), 25 and 30% hydrochloric acid solutions were corrosive when 50 µL of each was applied to 0.38-cm² samples of reconstructed human epidermis for 3 minutes or 1 or 4 hours^{Footnote 7}.

Daily applications of 0.5 mL of a 3.3% hydrochloric acid solution over 5 days to the intact flank skin of 3 rabbits were characterized as moderately irritating to 1 of the rabbits, with slight to marked reddening, isolated small necrosis and slight cracking and bleeding of the skin, whereas similar applications of a 1% solution were not irritating^{Footnote 2}. Grading of the reactions was not provided. As minor necrosis and bleeding were observed in 1 animal, this is considered evidence of severe skin irritation; accordingly, a 3.3% solution is considered to meet the classification criteria for Skin Irritation – Category 2 of subparagraph 8.2.2(3)(b)(iii) of the HPR.

In an acute inhalation toxicity study, male CF-1 mice (15 per concentration and duration) and male CFE rats (10 per concentration and duration) were exposed to hydrogen chloride gas at a concentration ranging from 30 000 to 57 290 ppm (rats; 5-minute exposure), 2 078 to 6 681 ppm (rats; 30-minute exposure), 3 200 to 13 655 ppm (mice; 5-minute exposure) or 410 to 4 045 ppm (mice; 30-minute exposure). Exposure to hydrogen chloride gas was noted to be extremely irritating to exposed areas of the skin, with scrotal ulceration noted in both species^{Footnote 4}.

The available data for hydrochloric acid meet classification criteria for Skin Corrosion – Category 1 at concentrations of 17% or greater and for Skin Irritation – Category 2 for concentrations of 3.3% or greater but less than 17% [subsections 8.2.2(2) and (3) of the HPR].

Hydrogen chloride gas reacts with atmospheric moisture to form aerosolized hydrochloric acid, with the concentration of hydrogen chloride dissolved in aerosol dependent on the air temperature, relative humidity and concentration of hydrogen chloride. The predicted concentration of dissolved hydrogen chloride can exceed 17% at an air temperature of -10 to 40°C and at a relative humidity and concentration of hydrogen chloride as low as around 65% and 10 ppm, respectively^{Footnote 10}. These conditions are relevant to workplaces, with hygroscopic growth of nucleation sites occurring at relative humidities of around 60% or greater^{Footnote 11}. Hydrogen chloride consequently meets the classification criteria for Skin Corrosion – Category 1 based on data on hydrochloric acid [subsection 8.2.2(2) of the HPR]. This classification is supported by an acute inhalation toxicity study on hydrogen chloride gas demonstrating severe dermal effects^{Footnote 4}.

Serious Eye Damage / Eye Irritation:

Category 1 (hydrochloric acid at a concentration ≥ 5%; hydrogen chloride); Category 2 (hydrochloric acid at a concentration ≥ 3.3% but < 5%)

Application of 0.1 mL of a 31.45% hydrochloric acid solution into an eye of each of 3 New Zealand White rabbits resulted in eye corrosion within 15 seconds. The animals immediately exhibited severe discomfort, with pawing, squealing, thrashing about the stocks, and eyes tightly closed^{Footnote 1}. The results meet the classification criteria for Serious Eye Damage – Category 1.

In an OECD TG 405-compliant study, application of 0.1 mL of a 10% hydrochloric acid solution into the lower conjunctival sac of an eye of each of 6 New Zealand White rabbits resulted in group average scores over 24-, 48- and 72-hours post-instillation of 2.9 out of 3 for conjunctivitis, 2.1 out of 4 for chemosis, 1.6 out of 2 for iritis and 2.7 out of 4 for corneal opacity. No observations were made beyond 96 hours post-instillation to permit an assessment of the reversibility of effects nor were individual average scores per animal reported^{Footnote 12}. However, the group average iritis score of 1.6 out of 2 would indicate that the results meet the classification criteria for Serious Eye Damage – Category 1.

In a study conducted similarly to OECD TG 405, 0.1, 0.03, 0.01 or 0.003 mL of a 5% hydrochloric acid solution was administered directly onto the cornea of an eye of each of 3 New Zealand White rabbits without an eye wash. A 0.1- or 0.03-mL application resulted in severe eye damage. Scoring was not possible for the 0.1-mL application due to the extent of injuries, which required sacrifice of the animals on day 2 or 3 of the experiment, while a maximum average Draize score (MAS) of 90 out of 110 was calculated for the 0.03-mL application, with a lack of complete reversal of effects within the 21-day observation period. In contrast, the 0.01- or 0.003-mL applications were only slightly irritating, with MAS scores of 0 and 1 out of 110, respectively, with complete reversal of effects within 1 to 2 days post-application^{Footnote 13}. Based on the results for the 2 larger application volumes, the classification criteria for Serious Eye Damage – Category 1 are met.

In another study, application of 0.1 mL of a 3.3% hydrochloric acid solution to the conjunctival sac of an eye of each of 3 rabbits was only slightly irritating during a 48-hour observation period, with very slight to slight reddening of the eyes, a slight to more marked, somewhat opaque swelling of the conjunctivae and slight corneal opacity, while a similar application of a 0.33% solution was not irritating over the same observation period. Scoring of reactions was not conducted^{Footnote 2}. While the reversibility of the effects was not assessed, based on the mild irritation, the results for the 3.3% solution are considered to meet the classification criteria for Eye Irritation – Category 2.

In an acute inhalation toxicity study, male CF-1 mice (15 per concentration and duration) and male CFE rats (10 per concentration and duration) were exposed to hydrogen chloride gas at a concentration ranging from 30 000 to 57 290 ppm (rats; 5-minute exposure), 2 078 to 6 681 ppm (rats; 30-minute exposure), 3 200 to 13 655 ppm (mice; 5-minute exposure) or 410 to 4 045 ppm (mice; 30-minute exposure). Exposure to hydrogen chloride gas was noted to be extremely irritating to the eyes, with corneal erosion and clouding noted in both species^{Footnote 4}.

In another acute inhalation toxicity study, male English smooth-haired guinea pigs were exposed nose-only to hydrogen chloride gas at a concentration of 0, 320, 680, 1 040 or 1 380 ppm for 30 minutes. For the control and 2 lower exposure groups, 4 animals were used per group whereas for the 2 higher exposure groups, 8 animals were used per group. Corneal opacities were observed in 4 out of 6 survivors at the exposure concentration of 1 040 ppm and in all 5 survivors at 1 380 ppm. At the exposure concentration of 680 ppm, 1 out of 4 animals exhibited corneal opacity while ocular appearance was normal in all animals at 320 ppm^{Footnote 7}.

In another acute inhalation toxicity study, male Swiss Webster mice (4 per exposure concentration) were exposed, presumably whole-body, to hydrogen chloride gas at a concentration of 17, 131, 280, 493, 723, 1 088, 1 973, 3 110 or 7 279 ppm for 10 minutes. Complete destruction of the eyes of the 4 animals exposed at the highest concentration was observed, along with awkward attempts at mouth breathing, an inability to eat or drink, and moribundity at 24 hours following exposure^{Footnote 7}.

In another acute inhalation toxicity study, male Swiss Webster mice (4 per exposure concentration) were exposed head-only to hydrogen chloride gas at a concentration ranging from 0.025 to 29 mg/L for 10 minutes. Ocular damage was noted at an exposure concentration of 0.73 mg/L and above. At 0.73 mg/L, moderate to marked polymorphonuclear leucocyte infiltration of the palpebral and global conjunctiva was noted. At 1.6 mg/L, the exposed cornea exhibited necrosis and marked polymorphonuclear leucocyte infiltration of the eyelids was observed. At 4.57 mg/L, extensive damage and spontaneous rupture of the ocular globes were observed^{Footnote 7}.

The available data for hydrochloric acid meet the classification criteria for Serious Eye Damage – Category 1 at concentrations of 5% or greater and for Eye Irritation – Category 2 at concentrations of 3.3% or greater but less than 5% [subsections 8.3.2(1) and (3) of the HPR].

As hydrogen chloride can react with atmospheric moisture to form aerosols with a dissolved hydrogen chloride content exceeding 5% under relevant workplace conditions, hydrogen chloride meets the classification criteria for Serious Eye Damage – Category 1 based on data on hydrochloric acid [subsection 8.3.2(1) of the HPR]. This classification is also supported by acute inhalation toxicity studies on hydrogen chloride gas demonstrating severe ocular effects^{Footnote 4Footnote 7}.

Respiratory Sensitization:

No data available

No data are available to determine whether hydrochloric acid or hydrogen chloride meets the classification criteria for a category or subcategory of Respiratory Sensitization.

Skin Sensitization:

Does not meet criteria

Humans: In a human repeated-insult patch test study, 50 volunteers were administered 9 applications of 24 hours each of a solution of hydrochloric acid of unspecified induction and challenge concentrations and of vehicle over 3 weeks. None gave positive reactions in a challenge application, which occurred 10 to 14 days after the final induction application^{Footnote 14}.

In another human repeated-insult patch test study, 119 subjects were exposed under occlusive conditions to 9 induction applications of 24 hours each of 0.5 mL of an aqueous hydrogen chloride solution of unspecified concentration over 3 weeks. After a 2-week rest period, subjects were exposed to a challenge patch containing 0.5 mL of the same solution for 24 hours, with the patch site subsequently graded at 48 and 96 hours after application. While 8 of the subjects exhibited mild skin irritation as a result of challenge, none exhibited a response indicative of skin sensitization^{Footnote 7}.

Animals: In a mouse ear swelling test, female CF-1 mice were prepared by shaving and tape stripping of the abdominal skin and abdominal application of 2 intradermal injections totalling 0.05 mL of Freund's complete adjuvant (FCA) emulsion. Groups of 10 (or 15) test and 5 (or 10) control mice were topically dosed with 0.1 mL of a 1% solution of hydrochloric acid in a 70% aqueous ethanol solvent and solvent alone, respectively, to the shaved regions. Tape stripping and topical applications were repeated for 3 additional days consecutively. A week after the final topical application, 20 µL of a 5% solution of hydrochloric acid in a 70% aqueous ethanol solvent was applied to the left ear of each test and control animal, and 20 µL of the solvent alone applied to the contralateral ear. The thicknesses of both ears of each animal were measured at 24 and 48 hours after challenge. No skin sensitization was reported in any test animal nor a difference in the sum of ear thicknesses between test and control ears^{Footnote 14}.

In a guinea pig maximization test involving groups of 15 test and 6 control Hartley guinea pigs, 2 intradermal injections of a 1% hydrochloric acid solution in ethanol, of FCA emulsion or of a 1% hydrogen chloride acid solution in FCA were administered to each test group animal. A week later, a 1% hydrochloric acid solution in ethanol was applied via a closed patch to the intradermal injection site for 48 hours. After a 2-week rest period, a 1% hydrochloric acid solution in ethanol was applied via a closed patch to naïve skin for 24 hours, with rechallenge 1 week later when necessary. None of the test animals exhibited skin sensitization^{Footnote 14}.

The available data do not meet the classification criteria for a category or subcategory of Skin Sensitization.

Germ Cell Mutagenicity:

Does not meet criteria

In vivo: No human or animal studies are available.

In vitro: Microbial assays on hydrochloric acid of unspecified concentration did not demonstrate a positive response for gene mutations in Salmonella typhimurium TA 1535, TA 1537, TA 1538, TA 98 and TA 100, for mitotic recombination in Saccharomyces cerevisiae D4 or for DNA repair in Escherichia coli W3110, with or without S-9 Aroclor 1254-induced rat-liver metabolic activation^{Footnote 15}. Mammalian cell assays for gene mutation, chromosomal aberrations, sister-chromatid exchanges and DNA damage on Fischer L5178Y mouse-lymphoma cells similarly did not demonstrate a positive response to exposure to hydrochloric acid for any endpoint, with or without S-9 uninduced CD-1 mouse-liver metabolic activation^{Footnote 15}.

In a chromosomal aberration assay similar in design to OECD TG 473 in Chinese hamster ovary-K1 cells, a significant increase in clastogenic activity, primarily in the frequency of chromatid breaks, was observed in response to exposure to hydrochloric acid at concentrations resulting in pH values below 5.5 or 6.0, in the respective absence or presence of S-9 phenobarbital- and 5,6-benzoflavone-induced rat-liver metabolic activation^{Footnote 16}.

In a mammalian cell assays in mouse lymphoma L5178Y^TK+/- cells, hydrochloric acid exposure resulted in only a small increase in the frequency of TK^-/- mutants at a concentration resulting in a pH of 6.3 in the absence of S-9 Aroclor 1254-induced Fischer 344 rat-liver metabolic activation. However, a large increase in the frequency of mutants was observed in the presence of such activation at hydrochloric acid concentrations resulting in pH values of 6.0 to 6.5. These results demonstrate that even weakly acidic conditions, particularly in the presence of activation, can result in mutagenic activity. The induced mutations were primarily of the clastogenic variety, as confirmed by an increase in the proportion of small colonies and by a statistically significant increase (p ≤ 0.01) in the frequency of cells with chromosomal aberrations. Aberrant cells primarily contained multiple chromatid breaks and complex rearrangements^{Footnote 17}.

The positive results from both of the mammalian cell in vitro tests are considered artifacts of low pH^{Footnote 2}.

The available data do not meet the classification criteria for a category or subcategory of Germ Cell Mutagenicity.

Carcinogenicity:

Does not meet criteria

Hydrochloric acid and hydrogen chloride have been classified as Group 3 ("Not classifiable as to its carcinogenicity to humans") by the International Agency for Research on Cancer (IARC) and as A4 ("Not classifiable as a human carcinogen") by the American Conference of Governmental Industrial Hygienists (ACGIH), while neither have been reviewed by the National Toxicology Program^{Footnote 18Footnote 19}. IARC has also classified mists from strong inorganic acids, such as those of hydrochloric acid, as Group 1 ("Carcinogenic to humans")^{Footnote 20}.

Humans: A mortality cohort study of 8 854 men who worked at any of 4 acrylamide plants in the U.S. or the Netherlands identified a statistically significant excess of deaths resulting from cancers of the respiratory system in workers not exposed to acrylamide (i.e., cumulative acrylamide exposure of less than 0.001 milligrams per cubic metre (mg/m³) per year). The standardized mortality ratio (SMR) of such deaths, indirectly standardized for race and plant, was 1.31, largely due to an excess of deaths resulting from lung cancer (SMR of 1.32). The excess of deaths was found to be limited to 2 groups of men, 1 of which was men (n = 11 deaths) who had worked in a former hydrochloric acid department. The detailed analysis supporting this conclusion was not provided^{Footnote 21}.

A mortality cohort study was conducted of 1 165 workers in 3 steel-manufacturing facilities in the U.S. who had been employed in a steel-pickling job for at least 6 months starting from 1920 to 1964, of which 189 had been exposed by inhalation primarily only to hydrochloric acid aerosolized during its use as a pickling agent at 1 of the facilities. Of these 189 workers, 68 (36%) were deceased as of October 27, 1981, the end of vital status follow-up. Of these 68 deaths, 9 were attributed to lung cancer when only 4 had been expected based on U.S. general population rates from 1940 to 1978 (SMR of 2.24; p < 0.05). To control for differences between the study cohort and the U.S. general population in respect of variables such as smoking habits and socioeconomic status, a comparison of 813 of the 1 165 workers, who were white males employed from 1950 to 1954, was also conducted with a comparison group of 51 472 white male steel workers employed in 1953 in 7 other mills in the U.S. Mortality from lung cancer was still statistically significantly elevated in the subset of the 813 workers who were primarily only exposed to hydrochloric acid (SMR of 2.00), but was reduced compared to that based on the U.S. general population^{Footnote 22}. Although an excess lung cancer risk was observed in workers exposed primarily only to hydrochloric acid, these workers may have also been exposed to nitric, hydrofluoric or hydrocyanic acid noted in the study.

A follow-up morbidity study of a subset of 879 of the 1 165 steel workers (77%) was conducted to investigate laryngeal cancer incidence compared to U.S. referent rates from 1940 to 1985. The average exposure duration of this "incidence" cohort to a steel-pickling acid was 9.5 years, compared to 8.8 years for the original mortality cohort, and 17% of the incidence cohort was exposed primarily only to hydrochloric acid. The standardized incidence ratio (SIR) for the entire incidence cohort for laryngeal cancer was 2.30, with the expected number of such cancers in the referent group adjusted to account for excess risk related to smoking and alcohol consumption. This excess laryngeal cancer risk was statistically significant^{Footnote 23}. While the study identified 2 cases of laryngeal cancer in those exposed primarily only to hydrochloric acid, the excess risk analysis was only performed on the whole incidence cohort.

A case-control study was conducted on a case population of 28 decedents who had died of a primary intracranial neoplasm and had worked at a chemical plant in Texas, U.S., matched with 110 or 111 decedents in 2 control groups. Among the case population, 13 had presumptively been exposed to hydrogen chloride compared to 42 or 51 in the 2 control groups. The matched odds ratios (OR) for brain tumour mortality for this subset of the case population compared to the corresponding subsets of the control populations of 1.02 and 1.40 were not considered to be significantly elevated. Further restricting the analysis to those decedents presumptively exposed to hydrogen chloride who had only been employed for 1 to 4 years or had a glioblastoma resulted in respective ORs of 2.02 and 0.97^{Footnote 24}. Despite the OR of 2.02, the study did not report an elevated risk of brain tumour mortality in decedents presumptively exposed to hydrogen chloride who had been employed for longer than 20 years.

A case-control study of a case population of 26 former employees of a chemical plant in Texas, U.S., who had died between 1958 and 1980 of a primary renal cancer, was conducted against 2 comparison groups of a 5% random sample of present and former employees at the plant. The first comparison group was all white male decedents in the random sample who did not have cancer, with matching of control subjects to cases based on year of birth and duration of employment (n = 92). The second comparison group was also selected from among the white males of the random sample but without regard to their vital status or cause of death (n = 98). These control subjects were matched to cases based on year of birth and dates of hire and termination. Based on information on work area assignment and job function, 12 subjects in the case population were presumed to have been exposed to hydrochloric acid in comparison to 44 or 50 in the comparison populations. The ORs for renal cancer mortality were 0.90 and 0.86 compared to the 2 comparison populations, indicating exposure to hydrochloric acid does not increase risk^{Footnote 25}.

A case-control study was conducted of a case population nested in a cohort of 19 608 males employed at a chemical plant in Texas, U.S. for at least 1 year between 1940 and 1980. The case population was 308 former male employees who had died of primary lung cancer prior to December 31, 1980. For comparison purposes, 2 control groups of 308 male subjects each, a deceased group and a "living" group, were selected from among cohort members without lung cancer. Each control subject was individually matched to a case subject, with 28 subjects common to both control groups. Subjects were presumptively exposed to an average of 7.5 different chemical and physical agents during their career with the plant employer. The ORs for lung cancer incidence without and with regard to a 15-year latency were 1.02 and 0.92, respectively, for presumptive exposure to hydrogen chloride compared to pooled control subjects, indicating a lack of an elevated risk in the case population^{Footnote 26}.

A subsequent case-control study on the same case population of 308 former male employees of a chemical plant in Texas, U.S. who had died of lung cancer was conducted. The 2 control groups were likewise the same. While the previous study evaluated presumptive hydrogen chloride exposure as a dichotomous variable, this study estimated an 8-hour time-weighted average (TWA) exposure for each job using 4 TWA categories. Hydrogen chloride exposures to subjects were measured through duration of exposure, a cumulative exposures score and the highest TWA category achieved in a career. A crude relative risk (RR) for lung cancer of 1.0 was calculated against pooled controls, with no evidence of confounding by smoking assessed through pack-years. Accounting for a 15-year latency only slightly lowered the RR to 0.9. The smoking-adjusted RRs were at or near unity for each category of each measure of exposure (duration, cumulative exposure, and highest TWA), with none achieving statistical significance, nor was an exposure-response trend observed^{Footnote 27}.

Animals: In a repeated-dose toxicity study, 100 male Sprague-Dawley rats were exposed to hydrogen chloride gas at a single concentration of 10 ppm for 6 hours per day, 5 days per week for up to 128 weeks. No statistically significant difference was noted in the mortality of the treated group and an air sham-exposed control group, nor was a significant difference noted in the mean body weight. While hyperplasia of the larynx and trachea was observed, no tumours of the nasal mucosa were found in any treated animal. Furthermore, there was no statistically significant difference in the total incidence of tumours in other organs between treated and air sham-exposed or colony control groups^{Footnote 28}.

The human studies did not find an elevated cancer risk, did not provide sufficient supporting information, did not account for exposures to other acids or did not demonstrate a dose-response relationship. The animal study did not find an elevated cancer risk. Although IARC has classified strong inorganic acid mists as human carcinogens, the cohort and case-control studies considered involved exposures to various acids, including sulphuric, nitric, hydrochloric or other unenumerated acids.

The available data on hydrochloric acid and hydrogen chloride do not meet the classification criteria for a category or subcategory of Carcinogenicity.

Reproductive Toxicity:

Does not meet criteria

A non-guideline study was conducted in sexually mature nulliparous female Wistar rats (8 to 15 per exposure group) exposed once by inhalation to gaseous hydrogen chloride at a concentration of 0.45 mg/L for 1 hour either before pregnancy, with mating starting 12 days thereafter, or on gestational day (GD) 9. The study reported severe fetal effects, including increased mortality of the progeny of dams exposed on GD 9, reduced body weight by 4 weeks post-parturition of the progeny of dams exposed pre-conception, disturbed kidney function in the progeny of both groups at 2 and 3 months post-parturition, and disturbed liver function and an increased relative weight of kidneys in the male progeny of dams exposed pre-conception. A third of the parental animals of both exposure groups died, with congestion, edema and hemorrhage of the lungs in the decedents along with severe dyspnea and cyanosis. Disturbed lung function was observed in the survivors of both groups. Kidney function was disturbed in both groups while liver function was disturbed only in pregnant animals. An increase in relative liver weight was found only in non-pregnant animals^{Footnote 29}. The effects in progeny are found to be a secondary non-specific consequence of the severe concurrent maternal toxicity.

In a subchronic inhalation toxicity study, Sprague-Dawley and Fischer 344 rats (10 per sex, dose and strain) and B6C3F₁ mice (10 per sex and dose) were exposed to gaseous hydrogen chloride at a concentration of 0, 10, 20 or 50 ppm for 6 hours per day, 5 days per week for 90 days. No exposure-related effects were observed upon histopathological examination of the testis, epididymis, prostate and seminal vesicles of the males and of the ovaries, uterus, oviducts and mammary glands of the females^{Footnote 2}.

The available data do not meet the classification criteria for a category or subcategory of Reproductive Toxicity.

Specific Target Organ Toxicity – Single Exposure:

Does not meet criteria

Oral Route of Exposure:

Humans: A study of 25 cases of human consumption of hydrochloric acid reported serious necrosis of the gastrointestinal (GI) tract followed by high morbidity and mortality^{Footnote 30}. A case report of a 57-year-old male reported extensive hemorrhagic gastric necrosis after ingestion of 20 cubic centimetres (cm³) of a solution containing hydrochloric acid at an unspecified concentration^{Footnote 31}.

Animals: In an acute oral toxicity study, the LD₅₀ in rats of a 31.45% aqueous hydrochloric acid solution was 700 mg/kg-bw. Reduced appetite, low activity, increasing weakness and collapse in treated animals were observed. Autopsies revealed lung hyperemia, liver discolouration, and acute gastrointestinal inflammation. Some surviving animals had ulcerated areas of the stomach^{Footnote 1}. Although the gastrointestinal effects were not invariably lethal, the deaths observed may be attributable to acidic corrosion of the GI tract. As hydrochloric acid meets the classification criteria of Acute Toxicity (Oral) - Category 4, further classification of these acute effects is considered superfluous.

In a non-guideline oral acute toxicity study in female rats, the LD₅₀ for a 3.3% aqueous hydrochloric acid solution was 238 to 277 mg/kg-bw. However, no other study details, such as clinical signs or pathology, were reported that would permit an evaluation of specific target organ toxicity. In another study, the oral LD₅₀ of hydrochloric acid in rabbits was 900 mg/kg-bw but neither the concentration nor other study details were provided^{Footnote 2}.

Dermal Route of Exposure:

A non-guideline dermal acute toxicity study in rabbits reported an LD₅₀ of a 31.45% hydrochloric acid solution as being greater than 5 010 mg/kg-bw. Clinical signs included reduced appetite and activity, increasing weakness, collapse and death. Gross autopsy of the decedent revealed lung and liver hyperemia, slightly enlarged gall bladder and darkening of the spleen and kidney, whereas viscera of the survivors appeared normal at 14 days post-exposure^{Footnote 1}. Given the normal autopsy findings in the survivors, the results of the study are not adequate to support a non-lethal specific target organ toxicity.

Inhalation Route of Exposure:

Humans: A human case study examined the health effects that followed an 800-litre hydrochloric acid leak from a truck near a mobile home park. The case population consisted of 45 adult and 24 child residents in this mobile home park who had been putatively exposed to hydrochloric acid fumes. Statistically significant increases in symptom-frequency scores from self-administered questionnaires of subjects were found in 33 of 35 symptoms of respiratory, neurobehavioural, general and vegetative functions, such as of chest tightness, shortness of breath, headache and nausea. Neurobehavioural, neurophysiological and spirometry testing was administered 20 months later to the putatively exposed adults and children and results were compared to unexposed age-matched controls in a different mobile home park that was distant to the spill (56 adults; 39 children).

Statistically significant differences in some of the measures of neuropsychological function and of affective scores were found between putatively exposed and unexposed adults. For neuropsychological function, simple and choice reactions times were significantly delayed, balance, as measured by sway speed with eyes open and closed, was significantly more rapid, and significant differences were noted in the cognitive function score of the digital symbol test and of the perceptual motor speed score of the Trail Making Test B. The total mood disturbance score was significantly elevated in the putatively exposed adults compared to the unexposed adults, with the scores for the tension, depression, anger, fatigue and confusion subscales likewise being significantly elevated. In children of 8 to 17 years of age (14 putatively exposed; 29 unexposed), significant impairment of neuropsychological function was similarly found.

Statistically significant reductions in some measures of lung function were observed in the putatively exposed children compared to unexposed children, but not in the putatively exposed adults. No measurements of the airborne concentration of hydrochloric acid were made, however the 50% of putatively exposed subjects who lived in the visual drift-profile of the fume cloud showed greater impairment of some measures of neuropsychological and pulmonary function compared to those living farther away or in other directions^{Footnote 32}. The study identified hydrochloric acid in a nearby pond and ditches, confirming the release.

Uncertainty exists as to the causality of the assumed hydrochloric acid exposure and the neurobehavioural effects observed. This study was the only human study identified that examined for these effects. The study authors noted that a dose-response analysis could not be undertaken due to the lack of air measurements. Furthermore, as a retrospective study, comparative pre-spill tests of neurobehavioural function had not been conducted. Although the study supports the potential role of inhalation exposure to hydrochloric acid in the development of neurobehavioural effects, it alone is not considered adequate for a classification determination.

Animals: In an acute inhalation toxicity study, male Fischer 344 rats were exposed for 30 minutes to gaseous hydrogen chloride at an airborne concentration of around 1 300 ppm either unmanipulated (nasal exposure) or through an endotracheal tube attached to a mouthpiece (mouth exposure). At 24 hours post-exposure, compared to filtered air-exposed controls, a statistically significant increase in body weight loss was observed in exposed nose breathers while statistically significant increases in lung wet and right cranial lobe dry weights were found in exposed pseudo-mouth breathers. Histopathological examination found significant damage to the nasal cavity in exposed nose breathers and to the trachea and lungs in exposed pseudo-mouth breathers. Lung plethysmography found reductions in minute ventilation and tidal volume and an increase in breathing frequency in exposed nose breathers. In pseudo-mouth breathers, increases in minute ventilation and tidal volume were found. Within 24 hours of exposure, 6 and 46% of the nose and pseudo-mouth breathers, respectively, had died^{Footnote 33}.

In non-guideline acute inhalation toxicity studies, male CFE rats and male CF-1 mice were exposed for 5 or 30 minutes to various concentrations of gaseous hydrogen chloride (10 rats and 15 mice per exposure duration and concentration) or to a respirable hydrochloric acid aerosol (10 per species, exposure duration and concentration). Clinical signs from exposure to either the gas or aerosol in both species included severe irritation to the eyes, mucous membranes and skin, scrotal ulceration, increased grooming and preening activity, rapid and shallow breathing, altered fur appearance and texture, and corneal erosion and clouding. Gross pathological examination revealed the respiratory tract as the primary target organ, with moderate to severe alveolar emphysema, atelectasis, pulmonary edema, spotted lung tissue, and severe epithelial damage of the nasal and tracheal passages. In survivors, residual damage was noted even at 14 days post-exposure, with lung discolouration and impaired collapsibility, alveolar damage and consolidated lung tissue reported. Mortality was observed of at least 1 animal at most exposure concentrations and was attributed primarily to respiratory effects^{Footnote 34}.

Although the respiratory effects were not invariably lethal in the 3 studies, the deaths of animals were attributed primarily to respiratory effects in 1 of the studies. As hydrochloric acid and hydrogen chloride meet the classification criteria of Acute Toxicity (Inhalation) – Category 4 and 3, respectively, further classification of these acute effects is considered superfluous.

The available data do not meet the classification criteria for a category of Specific Target Organ Toxicity – Single Exposure.

Specific Target Organ Toxicity – Repeated Exposure:

Does not meet criteria

Oral Route of Exposure:

A repeated-dose toxicity study involving 3 experiments was conducted in albino Wistar rats to examine the effect of dietary supplementation with hydrochloric acid on food intake and metabolism. In the first experiment, weanling rats (4 per sex and exposure concentration) were administered for 7 weeks a commercial rat diet containing hydrochloric acid at a dietary concentration of 0, 280, 420 or 560 millimoles per kilogram of dry matter (mmol/kg DM). In the second experiment, adult rats (4 per sex and exposure concentration) were administered for 9 weeks the same rat diet containing hydrochloric acid at a dietary concentration of 0, 312, 625, 937 or 1 250 mmol/kg DM. In the third experiment, weanling rats (6 males and 4 females per exposure concentration) were administered for 12 weeks the same rat diet containing hydrochloric acid at a dietary concentration of 0, 300, 600 or 900 mmol/kg DM. An inverse relationship between dietary hydrochloric acid concentration and pH was observed, with the pH of the highest doses being 3.50, 1.82 and 2.54 for the first, second, and third experiments, respectively, compared to the control diet pH of 5.8 to 5.9.

In the first experiment, no significant treatment-related changes in food intake, liveweight gain, hematological or bone-related parameters were noted. In the second experiment, statistically significant reductions in food intake and liveweight gain were noted at the highest 2 doses tested, with 100% mortality of rats at both of these doses within the 9-week exposure period. A statistically significant reduction in blood pH was observed at the lowest 2 doses tested. No other changes in hematological or bone-related parameters were identified at those doses, which were the only 2 doses with such measurements in this experiment. In the third experiment, a 30% mortality rate and statistically significant reductions in food intake and liveweight gain were found at the high dose. Plasma carbon dioxide content was significantly reduced at the intermediate and high doses and plasma base excess was statistically significantly reduced at the high dose. Statistically significant reductions in femur length, weight of fat free solids (FFS) in femurs and ash content in the FFS were found at the high dose^{Footnote 35}. The doses at which effects occurred exceed the guidance values of this hazard class adjusted by exposure duration.

Dermal Route of Exposure: No data available

Inhalation Route of Exposure:

A repeated-exposure inhalation toxicity study of 10 sensory irritants was conducted in 16 to 24 male Swiss-Webster mice per irritant to examine pathological changes of the respiratory tract at target concentrations causing a 50% decrease in respiratory rate (RD₅₀). For gaseous hydrogen chloride, mice were exposed 6 hours per day for 3 days at a mean analytical time-weighted average (TWA) concentration of 304 ppm. Exposures to hydrogen chloride resulted in decreased body weight, presence of exudate in nasal passages, abdominal distension and fur discolouration. Within the 3 days of exposure, all exposed mice were found either dead or moribund. Histopathological examination revealed severe exfoliation, erosion, ulceration and necrosis and mild inflammation of the respiratory epithelium, mild ulceration and necrosis of the olfactory epithelium, minimal presence of serous exudate, slight exfoliation and inflammation of doubtful significance of the squamous epithelium, and no lesions of the lower respiratory tract. A distinct anterior-to-posterior gradient of declining severity of histological changes of the nasal passages was noted^{Footnote 36}. The results of the study reflect an acute corrosive effect and do not inform an understanding of the repeated-exposure toxicity at non-corrosive concentrations.

A subchronic inhalation toxicity study was conducted in B6C3F₁ mice and Sprague-Dawley and Fischer-344 rats exposed to gaseous hydrogen chloride at a target concentration of 0, 10, 20 or 50 ppm for 6 hours per day, 5 days per week for 90 days. For each exposure concentration and species or strain, 31 males and 21 females were exposed. Several deaths of exposed mice and 1 death of an exposed Sprague-Dawley rat were reported but were not considered treatment-related. After 90 days of exposure at the high concentration, mice of both sexes and male Fischer-344 rats demonstrated decreased body weights relative to controls. No biologically significant differences in any exposure group for hematologic, serum chemistry and urinalysis parameters were found relative to controls. A reduction in liver weight relative to controls was noted in mice of both sexes and female Fischer-344 rats exposed at the high concentration; however, this reduction may have been related to reduced growth.

Minimal to mild rhinitis was found in the anterior portion of the nasal cavity of both strains of rat at 5 days (interim sacrifice) and at 90 days of exposure; the severity was concentration- and time-dependent. After 90 days of exposure at the high concentration, mice had developed cheilitis and an accumulation of hemosiderin-laden macrophages at the perioral tissues. Furthermore, after 90 days of exposure at the low, intermediate and high concentrations, mice had developed eosinophilic globules in the epithelium of the nasal turbinates^{Footnote 37}. Although the concentrations tested are within the guidance value of a category of this hazard class, the effects are considered to reflect mild irritation or to be an adaptive response to the inhaled substance.

The available data do not meet the classification criteria for a category of Specific Target Organ Toxicity – Repeated Exposure.

Aspiration Hazard:

No data available

No human data are available and neither hydrochloric acid nor hydrogen chloride is a liquid hydrocarbon.

Biohazardous Infectious Materials:

Not applicable

Neither hydrochloric acid nor hydrogen chloride is a microorganism, protein or nucleic acid.

Physical hazards

Explosives:

Not evaluated*

* Explosives are excluded from the Hazardous Products Act and its regulations. Explosives are regulated under the Explosives Act. For more information, visit Natural Resources Canada.

Flammable Gases:

Does not meet criteria

Samples weighing 10 to 20 milligrams of polyvinyl chloride polymer or of polyvinyl chloride formulated with plasticizers, stabilizers and fillers were heated to a temperature of up to 800°C at a heating rate of 10°C per minute and at a carrier gas flow rate of 500 cm³ per minute. The samples decomposed and released 9.6 to 100% of the theoretical hydrogen chloride content as determined by a modified micro thermogravimetric technique with an ion selective electrode^{Footnote 38}. Hydrogen chloride was identified as a product of complete combustion of the chlorinated hydrocarbon polymer.

The available data do not meet the classification criteria for a category or subcategory of Flammable Gases.

Aerosols:

Not evaluated

Classification of a hazardous product in the Aerosols hazard class is product dependent.

Oxidizing Gases:

No data available

No data are available to determine whether hydrogen chloride meets the classification criteria for a category of Oxidizing Gases.

Gases Under Pressure:

Not evaluated

Classification of a hazardous product in the Gases Under Pressure hazard class is product dependent.

Flammable Liquids:

No data available

A study summary reported a 37% hydrochloric acid solution as being non-flammable based on a flash point measured by an open-cup method^{Footnote 2}. As the classification criteria of subsection 7.6.1(2) of the HPR require flash points measured by a closed-cup method, and as open-cup methods tend to result in higher flash points, the result of the study is not suitable for the classification evaluation.

No suitable data were identified to determine whether hydrochloric acid meets the classification criteria for a category of Flammable Liquids. Furthermore, this hazard class does not apply to gases, such as hydrogen chloride.

Flammable Solids:

Not applicable

Neither hydrochloric acid nor hydrogen chloride is a solid. The classification criteria for Flammable Solids do not apply to either.

Self-reactive Substances and Mixtures:

No data available

No data are available to determine whether hydrochloric acid meets the classification criteria for a category of Self-reactive Substances and Mixtures. Furthermore, this hazard class does not apply to gases, such as hydrogen chloride.

Pyrophoric Liquids:

No data available

No data are available to determine whether hydrochloric acid meets the classification criteria for a category of Pyrophoric Liquids. Furthermore, this hazard class does not apply to gases, such as hydrogen chloride.

Pyrophoric Solids:

Not applicable

Neither hydrochloric acid nor hydrogen chloride is a solid. The classification criteria for Pyrophoric Solids do not apply to either.

Self-heating Substances and Mixtures:

No data available

No data are available to determine whether hydrochloric acid meets the classification criteria for a category of Self-heating Substances and Mixtures. Furthermore, this hazard class does not apply to gases, such as hydrogen chloride.

Substances and Mixtures which, in Contact with Water, Emit Flammable Gases:

Does not meet criteria

Hydrochloric acid is a stable aqueous solution that does not contain metals or metalloids. It is consequently excluded from evaluation under this hazard class in accordance with paragraphs 7.12.1(1)(a) and (c) of the HPR. Furthermore, this hazard class does not apply to gases, such as hydrogen chloride.

Oxidizing Liquids:

No data available

No data are available to determine whether hydrochloric acid meets the classification criteria for a category of Oxidizing Liquids. Furthermore, this hazard class does not apply to gases, such as hydrogen chloride.

Oxidizing Solids:

Not applicable

Neither hydrochloric acid nor hydrogen chloride is a solid. The classification criteria for Oxidizing Solids do not apply to either.

Organic Peroxides:

Not applicable

Neither hydrochloric acid nor hydrogen chloride is an organic peroxide. Furthermore, this hazard class does not apply to gases, such as hydrogen chloride. The classification criteria for Organic Peroxides consequently do not apply to hydrochloric acid or hydrogen chloride.

Corrosive to Metals:

Category 1 (hydrochloric acid at a concentration ≥15%; hydrogen chloride)

In an investigation of the performance of corrosion inhibitors, weight loss measurements of mild steel immersed in a 15% hydrochloric acid solution were taken at a temperature of 303, 313, 323 or 333 Kelvin (K) in the absence of inhibitors. The respective corrosion rates were 37.7, 66.4, 115.2 and 169.8 millimetre penetration per year (mmpy). In another investigation of the performance of corrosion inhibitors, weight loss measurements of N80 carbon steel immersed in a 15% hydrochloric acid solution were taken at a temperature of 298, 303, 313 or 323 K in the absence of inhibitors. The respective corrosion rates were 9.54, 12.09, 19.27 and 30.42 mmpy^{Footnote 39Footnote 40}.

Given the positive relationship between corrosion rate and temperature observed in both experiments, and as the corrosion rates at temperatures below 55°C exceeded 6.25 mmpy, the available data for hydrochloric acid meet the classification criteria of Corrosive to Metals – Category 1 [section 7.16.1 of the HPR].

As hydrogen chloride can react with atmospheric moisture to form aerosols with a dissolved hydrogen chloride content exceeding 15% under relevant workplace conditions, hydrogen chloride likewise meets the classification criteria for Corrosive to Metals – Category 1 based on data on hydrochloric acid [section 7.16.1 of the HPR].

Combustible Dusts:

Not applicable

Neither hydrochloric acid nor hydrogen chloride is a solid. The classification criteria for Combustible Dusts do not apply to either.

Simple Asphyxiants:

No data available

No data are available to determine whether hydrogen chloride meets the classification criteria for a category of Simply Asphyxiants. Furthermore, this hazard class does not apply to liquids, such as hydrochloric acid.

Chemicals Under Pressure:

Not evaluated

Classification of a hazardous product in the Chemicals Under Pressure hazard class is product dependent.

Regulatory and other information

Regulatory information:

Hazardous substance assessments are prepared by Health Canada as educational and information resources. Under the HPA, suppliers of hazardous products must, upon the sale or importation of a hazardous product, provide a safety data sheet and label that meet the requirements set out in the HPR.

Other information:

The information and classifications contained in these hazardous substance assessments are based on publicly available sources, such as peer-reviewed literature or reports by international bodies. New information, including proprietary information, could have an impact on the classification of substances or hazardous products containing them. It is the responsibility of the supplier to ensure the accuracy, sufficiency and reliability of their hazardous product classifications.

Last updated:

2025

Prepared by:

Workplace Hazardous Materials Bureau, Health Canada