Methylcyclohexane

Endpoint summary

Description of key information

Oral:
Minimum lethal dose (rabbit) = 4000-4500 mg/kg bw
LD50 (mouse) = 2250 mg/kg bw
LD50 (rat) > 3200 mg/kg bw (technical product, 70% pure)
Aspiration toxicity based on kinematic viscosity (0.88 mm²/s at 20°C)
Dermal:
LD50 (rabbit) > 2300 mg/kg bw (similar to OECD 402, read-across from cyclohexane and mass correction)
Inhalation:
Minimum lethal concentration (mouse) = 40-50 mg/L (2 h exposure)
Minimum lethal concentration (rabbit) = 28.75 mg/L (mortality after 2-week exposure, 6 h/day)
LC50 (mouse) = 41 mg/L (2 h exposure)
LC50 (rat/mouse) > 26.3 mg/L (1 h exposure)
LC50 (dog) > 16.3 mg/L (1 h exposure)
LC0 (rat) = 11 mg/L (6 h exposure, technical product, 70% pure )
Minimum narcotic concentration (rat/mouse) = 26.3 mg/L (1 h exposure)
Minimum narcotic concentration (rabbit) = 21.90 mg/L (6 h exposure)
One-hour emergency exposure limit (rat, mouse, dog) = 16 mg/L (1 h exposure)

Key value for chemical safety assessment

Acute toxicity: via oral route

Endpoint conclusion

Endpoint conclusion:

no adverse effect observed

Quality of whole database:

The available information comprises studies which each alone are regarded insufficient for assessment (Klimisch score 2-4). However, the information from these independent sources is consistent and provides sufficient weight of evidence for hazard assessment leading to an endpoint conclusion in accordance with Annex XI, 1.2, of Regulation (EC) No 1907/2006. Therefore, the available information as a whole is sufficient to fulfil the standard information requirements set out in Annex VII, 8.5, of Regulation (EC) No 1907/2006.

Acute toxicity: via inhalation route

Endpoint conclusion

Endpoint conclusion:

adverse effect observed

Dose descriptor:

discriminating conc.

Value:

16 000 mg/m³ air

Quality of whole database:

The available information comprises studies which each alone are regarded insufficient for assessment (Klimisch score 2-4). However, the information from these independent sources is consistent and provides sufficient weight of evidence for hazard assessment leading to an endpoint conclusion in accordance with Annex XI, 1.2, of Regulation (EC) No 1907/2006. Therefore, the available information as a whole is sufficient to fulfil the standard information requirements set out in Annex VII, 8.5, of Regulation (EC) No 1907/2006.

Acute toxicity: via dermal route

Endpoint conclusion

Endpoint conclusion:

no adverse effect observed

Quality of whole database:

The available information comprises an adequate and reliable study (Klimisch score 2) from a structurally similar reference substance. Read-across is justified based on a common functional group, common metabolic pathways and similarities in physico-chemical, ecotoxicological and toxicological properties (refer to endpoint discussion for further details).
The selected study is thus sufficient to fulfil the standard information requirements set out in Annex VII, 8.5, in accordance with Annex XI, 1.5, of Regulation (EC) No 1907/2006.

Additional information

Acute toxicity

The acute toxicity of methylcyclohexane has been investigated in a number of early studies in different animal species with focus on inhalation; this being the most relevant route of human exposure. Due to limitations in study design and/or documentation, no key studies could be identified for any route of exposure. Therefore, assessment of potential toxic effects following acute exposure to methylcyclohexane via the oral and inhalation route was conducted in a weight of evidence approach taking into account all available data from non-standard but well-documented studies along with poorly documented reports of not assignable reliability. For assessment of acute dermal toxicity, a reliable study conducted with cyclohexane was used following the read-across approach described above.

Oral

The minimum lethal dose of methylcyclohexane following oral administration was determined in rabbits (Treon et al., 1943a). The animals (1 per dose) were given the undiluted test substance by gavage at doses ranging from 1000 to 10000 mg/kg bw and observed for up to 14 days. Rabbits given methylcyclohexane at 1000 to 4000 mg/kg bw survived. Rabbits given methylcyclohexane at 4500 to 10000 mg/kg bw died between 5.3 and 84 h post-administration. The minimum lethal dose was therefore considered to be between 4000 and 4500 mg/kg bw.

Severe diarrhoea occurred within 1-1.5 h after treatment. Other symptoms were reported to be similar to those described for cyclohexane: these included increased respiratory rate remaining elevated for a few hours, within few minutes after administration, the ears became reddened and slightly cyanotic, ear veins were distended and conjunctival congestion was observed at higher doses. Animals were generally lethargic without exhibiting true narcosis. Convulsions were not observed.

Rabbits given methylcyclohexane at 1000 to 4000 mg/kg bw lost weight (226-550 g) within 8-10 days after administration. Body weight was regained in the ensuing 10-14 days. 3/4 rabbits given methylcyclohexane at 4500 to 10000 mg/kg bw lost weight (221-579 g) before they died. The weight loss among the rabbits that died correlated with the length of survival irrespective of the dose level. Survival time was, however, not always determined by the dose level.

According to the authors, when administered orally in sufficient dosage (not further specified), the test material produced severe widespread vascular damage, with fibrinocellular thrombi in the capillaries and venules, and toxic coagulation necrosis in the heart muscle, liver spleen and kindneys. The results of blood examinations obtained during two months prior to and two months following administration showed no treatment-related abnormalities in the cellular elements of the blood (no details reported) (Treon et al., 1943a).

In other studies, the oral LD50 values of methylcyclohexane and technical grade methylcyclohexane (70% pure, containing 10% cyclohexane and 20% dimethylcyclohexane) were reported to be 2250 and > 3200 mg/kg bw in mice and rats, respectively (Izmerow et al., 1982; Sutton, 1969). No further details were available.

In conclusion, the available data suggest that methylcyclohexane is of low acute toxicity via the oral route, the lowest LD50 reported being 2250 mg/kg bw in mice (Izmerow et al., 1982).

However, based on the available data on dynamic viscosity and density (see Sections Viscosity and Density), the kinematic viscosity of methylcyclohexane (0.88 mm²/s at 20°C) indicate that the substance is likely to cause aspiration toxicity, as expected for certain hydrocarbons according to Regulation (EC) No 1272/2008. Therefore, a human health hazard related to physico-chemical properties and exposure by the oral route is identified, leading to classification for Aspiration toxicity Category 1.

Inhalation

The minimum lethal concentration of methylcyclohexane after repeated inhalation exposure was determined in rabbits (Treon et al., 1943b; see also Repeated dose toxicity). 4 animals per concentration level were whole body-exposed to methylcyclohexane vapours at 0.948, 4.57, 11.35, 21.90, 28.75, 39.55 and 59.9 mg/L, 6 h/day, 5 days/week for up to 10 weeks. Different groups of animals each exposed to clean air for different periods of time (6-8 h/day, 5 days/week for 10-26 weeks) served as control.

No mortality occurred in animals exposed to 0.948-21.90 mg/L. At 28.75 and 39.55 mg/L: mortality occurred in 1/4 and 4/4 animals, respectively, after 2 weeks of exposure. All 4 animals died within 70 min after exposure initiation at 59.9 mg/L. Therefore, 59.9 mg/L was the LC100 following single inhalation exposure to methylcyclohexane. An LC50 was not determined in the study. However, since no animals died after the first (and up to the ninth) exposure to 39.55 mg/L, the LC50 value is likely to be higher.

During the course of the study, no clinical signs of toxicity were observed in animals exposed to 0.948-11.35 mg/L. At higher concentrations, narcotic effects were noted and included lethargy, impaired leg coordination, convulsions, narcosis, laboured breathing, salivation and conjunctival congestion. The number and severity of observed effects increased with concentration and indicated that the central nervous system is a potential target at high concentrations. The minimum narcotic concentration was 21.90 mg/L based on the reported slight lethargy.

Body weight gain was not affected in animals exposed to non-lethal concentrations (0.948-21.90 mg/L), while animals exposed to lethal concentrations lost weight: 39 and 390 g after a 2 week exposure to 28.75 and 39.55 mg/L, respectively.

After a 3-week exposure to 11.35 mg/L barely demonstrable evidence of cellular liver and kidney injury (not further specified) was reported (Treon et al., 1943b).

In another study, the one-hour emergency exposure limit for methylcyclohexane (MCH), i.e. the "concentration of MCH that will not cause chronic or irreversible tissue damage nor produce CNS effects which could impair coordination or prevent a man from self rescue", was sequentially determined in rats, mice and dogs (MacEwen and Vernot, 1979).

Two groups of 20 male rats were whole body-exposed to vapours of methylcyclohexane at 4172 and 6564 ppm (ca. 16.7 and 26.3 mg/L) for 1 h. Control animals were included in the study, but no further details were reported. 10 animals of each control and test group were sacrificed at the end of the 1 h exposure period; the remaining animals were necropsied at the end of a 28-day post-exposure observation period.

No mortality occurred during the study period. Exposure to 16.7 mg/L caused increased activity in the animals for the duration of the experiment (1 h). The activity demonstrated in this exposure was less than that seen during the 26.3 mg/L exposure, and the rats maintained normal coordination throughout with no observable CNS effects. At 26.3 mg/L, immediate hyperactivity was observed. A slight loss of coordination was seen at 29 min. Prostration was noted at 54 min. No signs of stress were noted during the subsequent 28-day observation period.

No relevant effects were observed in body weight development. Gross pathology examination failed to show any treatment-related lesions.

During histopathological examination, two test rats that had been held 28 days post-exposure had convoluted tubule adenomas of the kidneys. The authors stated that it is unusual to find lesions of this kind in rats of this age (73 days), and that it is unlikely that this lesion would develop in this short time span after a single exposure to the compound. However, this lesion was not seen in the rats sacrificed immediately after exposure or in either of the two control rat groups.

To determine whether this lesion was real or an anomaly, the kidneys from the 26.3 mg/L group were examined. Three sections were examined from the kidneys of each of the ten test rats. No adenomas or abnormal lesions were found in the kidneys of these rats. Therefore, it appears that the two adenomas seen in the low level rats were anomalies and had nothing to do with exposure effects.

Based on the reported results, the one-hour emergency exposure limit was set at 4172 ppm (16.7 mg/L), while the LC50 (rat, male) after a 1 h exposure to methylcyclohexane was considered to be greater than 6564 ppm (26.3 mg/L). At the same time, 26.3 mg/L is considered the minimum narcotic concentration in male rats for a 1 h exposure period (MacEwen and Vernot, 1979).

In the same series of studies, two groups of 20 female mice were treated in the same way as described above for rats. Instead of 4172 and 6564 ppm, animals were exposed to 4758 and 6564 ppm (ca. 19.1 and 26.3 mg/L).

No mortality occurred during the study period. At 19.1 mg/L, the only observable sign of toxicity noted was hyperactivity which lasted during the extent of the exposure period. Following exposure, the mice returned to their normal activity pattern. No loss of coordination or CNS effects were noted during or after the one-hour exposure. At 26.3 mg/L, immediate hyperactivity was observed. A slight loss of coordination was seen in mice at 12 min. Prostration was noted at 42 and 54 minutes. At 55 minutes, one mouse experienced tonoclonic spasms which lasted for 15 to 20 seconds. No signs of stress were noted during the subsequent 28-day observation period.

No relevant effects on body gain were observed. Gross pathology examinations of the animals that were sacrificed immediately following exposure and those sacrificed after a 28-day observation period revealed no lesions which could be attributed to the exposure.

The only histopathological change noted in mice exposed to the lowest level of methylcyclohexane was a minimal to mild reversible cytoplasmic change in the liver. This lesion was seen in five of the test mice and in one control mouse.

The one-hour emergency exposure limit was 4758 ppm (19.1 mg/L) and the LC50 (mouse, female) after a 1 h exposure to methylcyclohexane was considered to be greater than 6564 ppm (26.3 mg/L). At the same time, 26.3 mg/L is considered the minimum narcotic concentration in female mice for a 1 h exposure period (MacEwen and Vernot, 1979).

Based on the data from the two rodent studies, a concentration of approximately 4200 ppm (ca. 17 mg/L) was considered a safe one-hour exposure limit in those species. This nominal concentration was thus selected by MacEwen and Vernot (1979) to conduct a further study in dogs.

A group of 4 purebred beagle dogs (sex not reported) was exposed to methylcyclohexane at a mean analytical concentration of 4071 ppm (ca. 16.3 mg/L) for 1 h. A group of 4 additional dogs was also maintained for comparative purposes. During the 28 -day post-exposure period, animals were observed for mortality, clinical signs and body weight gain. In addition, field trial evaluations, neurological, haematological and clinical chemistry examinations were performed. At the end of the post-exposure period, animals were sacrificed for gross necropsy and histopathological examinations.

No mortality occurred during the study period. The dogs all acted normally throughout the exposure showing no signs of eye or nose irritation or effects upon coordination. During the 28-day post-exposure observation period all dogs appeared normal and gained weight normally. Gross pathology at necropsy revealed no exposure related lesions. Histopathological examination of the test and control dogs showed no significant lesions. Immediately following the exposure, each of the dogs performed trained tasks with its assigned trainer. All dogs performed this exercise adequately to the standard established during the training program. The subsequent neurological testing of each dog revealed no exposure-related effect. Blood samples examined at 14 and 28 days post-exposure showed all normal values.

The results indicate that the LC50 (dog) of methylcyclohexane after a 1-hour exposure is expected to be greater than 4071 ppm (16.3 mg/L). Furthermore, no signs of CNS effects were observed at this concentration (McEwen and Vernot, 1979).

On the basis of the studies in rats, mice and dogs, McEwen and Vernot (1979) concluded that a concentration of 4000 ppm (16 mg/L) of methylcyclohexane would not prevent a person from self-rescue or cause irreversible damage within an exposure period of 1 h.

In an early study in mice, a 2-hour exposure to methylcyclohexane (and other linear and cyclic hydrocarbons) caused lethargy, narcosis, prostration, clonic convulsions and laboured breathing before death occurred. In some cases, animals died within 1-2 min after begin of exposure (Lazarew, 1929). Sudden death was preceded by extensor spasms. The minimal narcotic concentration was reported to be at 30-40 mg/mL, while the minimal lethal concentration after 2 h exposure was at 40-50 mg/L.

In rats exposed to vapours of technical grade methylcyclohexane (70% pure) at 82-260 mg/L, mortality occurred within 13-70 min. Prior to death, animals showed lethargy, ataxia and terminal convulsions (Sutton, 1969). The author reported that a 6 h exposure to 11 mg/L induced minor symptoms (lethargy in 3 h).

Without providing further details, another study reported the LC50 (mouse) of methylcyclohexane after 2 h exposure to be 41 mg/L (Izmerow et al., 1982).

In conclusion, based on mortality data, the available studies suggest that methylcyclohexane is of low of acute toxicity via inhalation; the lowest values for minimal lethal concentration/LC50 reported being 40-41 mg/L in mice exposed to vapours for 2 h (Izmerow et al., 1982; Lazarew, 1929). However, the weight of evidence from all available studies indicates that short-term inhalation exposure to methylcyclohexane is likely to induce narcotic effects at high concentrations. The lowest concentration reported to cause slight narcotic effects was 11 mg/L in rats exposed for 6 h (Sutton, 1969). The one-hour emergency exposure limit as determined in rats, mice and dogs was about 16 mg/L (McEwen and Vernot, 1979).

The available data provides sufficient weight of evidence to support classification of methylcyclohexane for Specific target organ toxicity-single exposure (STOT-SE) Category 3, narcotic effects. The one-hour emergency exposure limit of 16 mg/L (16000 mg/m³) determined by MacEwen and Vernot (1979) is selected as dose descriptor for human health hazard and risk assessment of specific, non-lethal target organ toxicity arising from a single exposure.

Dermal

There are no studies available in which the acute dermal toxicity of methylcyclohexane was investigated. There are limitedly reliable indications for local and systemic effects after repeated dermal exposure at very high doses.

In an early study, methylcyclohexane was applied to the clipped skin of one rabbit in twelve 5 mL portions at 5 min intervals within 1 h, after which the material was removed by washing with soap and water (Treon et al., 1943a). This uncovered skin procedure was done on 6 consecutive days. Based on the reported total amount of test substance applied daily (60 mL) and the animal body weight (3.185 kg), the applied dose was roughly equivalent to 14450 mg/kg bw/day.

Slight hypothermia and a slight loss in body weight (no further details given) were observed in the treated animal during the 6-day study period. The loss in body weight was regained within 2 days. Repeated application of methylcyclohexane to the skin of a rabbit induced local irritation and thickening. The irritation appeared on the second day and increased with successive treatments. Hardening of the skin, thickening and ulceration appeared later and the experiment was terminated after the 6th day.

The results of this study suggest that a dermal lethal dose (rabbit) of methylcyclohexane after a single application is likely to be greater than 14450 mg/kg bw (Treon et al, 1943a).

In order to fulfil the standard information requirements set out in Annex VII, 8.5, read-across from the reference substance cyclohexane (CAS No. 110-82-7) is conducted in accordance with Annex XI, 1.5, of Regulation (EC) No 1907/2006.

Cyclohexane was tested for acute dermal toxicity in rabbits (3 males and 3 females) in a study conducted following a protocol equivalent to OECD 402 (Pence, 1982a). The test substance was applied at 2000 mg/kg bw to an area of shaved dry skin covering approx. 10% of the total body surface, and held in contact with the skin for 24 h. Animals were observed for mortality and clinical signs for a period of 14 days following application. Body weights were determined weekly and skin reactions were evaluated according to the Draize scoring system 24 and 72 h and 7, 10 and 14 days post-application. No mortality occurred and the only clinical sign reported was phonation upon application. Animals showed normal body weight development and necropsy revealed no treatment-related changes. In 5/6 animals, very slight to slight erythema was observed at the 24 and 72 h reading time points, and very slight to slight edema was seen only at 24 h. Skin redness was fully reversible within 7 days post-application. One animal showed epidermal scaling on Day 10. Based on the study results, the dermal LD50 in male and female rabbits is greater than 2000 mg/kg bw (Pence, 1982a).

After correction for differences in molar mass (cyclohexane: 84.16 g/mol; methylcyclohexane: 98.19 g/mol), the dermal LD50 of methylcyclohexane is estimated to be greater than 2300 mg/kg bw.

In conclusion, the available data indicates that methylcyclohexane is of low acute toxicity via the dermal route in regard to systemic effects, as these have been reported only after repeated exposure to very high dose levels. In contrast, local skin effects are likely to occur (see Irritation/Corrosion). The notion of a low acute dermal toxicity is supported by the available information on the structurally similar reference substance cyclohexane.

Justification for read-across approach

In accordance with Article 13 (1) of Regulation (EC) No 1907/2006, "information on intrinsic properties of substances may be generated by means other than tests, provided that the conditions set out in Annex XI are met. In particular for human toxicity, information shall be generated whenever possible by means other than vertebrate animal tests", which includes the use of information from structurally related substances (grouping or read-across).

Having regard to the general rules for grouping of substances and read-across approach laid down in Annex XI, 1.5, of Regulation (EC) No 1907/2006, whereby physicochemical, toxicological and ecotoxicological properties may be predicted from data for reference substance(s) by interpolation to other substances on the basis of structural similarity, cyclohexane (CAS No. 110-82-7) is selected as reference substance for assessment of ecotoxicological and toxicological endpoints, for which no methylcyclohexane data are available.

Similarity is based on:

(1) common functional group: Methylcyclohexane and cyclohexane share a 6-membered saturated alicyclic ring as a common molecular structure and are therefore allocated to the group of monocyclic hydrocarbons (cycloalkanes);

(2) common precursors and likelihood of common breakdown products via physical and biological processes, which result in structurally similar chemicals: Methylcyclohexane and cyclohexane do not share a common precursor; however, both substances are produced by hydrogenation of the corresponding aromatic compounds toluene (see Section Manufacture and Use) and benzene (EC-ECB, 2004), respectively, which are in turn structurally similar substances. In general, methylcyclohexane and cyclohexane are likely to undergo the same chemical reactions characteristic of cycloalkanes, e.g. combustion to CO₂ and H₂O and halogenation (Breitmeier and Jung, 2005). The assessment of toxicokinetic behaviour indicates that both substances share a common main metabolic pathway, namely mono- and dihydroxylation of the alicyclic ring resulting in the respective isomers of methylcyclohexanol/-diol and cyclohexanol/-diol, followed by conjugation to the corresponding glucuronides (see Toxicokinetics); and

(3) constant pattern in the changing of the potency of the properties between substances: For methylcyclohexane and cyclohexane, the constant pattern is characterized by similarities in the potency of properties.

- Physicochemical properties:

Both substances show overall similar physico-chemical properties, being liquids, moderately volatile, lipophilic and slightly soluble in water. (see Section 4, Physical and chemical properties and EC-ECB, 2004).

- Environmental fate and ecotoxicological profile:

Methylcyclohexane and cyclohexane show similar properties in environmental fate and ecotoxicological profile: both substances are volatile, not bioaccumulative and show corresponding adsorption values (see section 5, Environmental fate and pathways and EC-ECB, 2004). Furthermore the available experimental data demonstrate that both substances exhibit a similar ecotoxicity profile. Both are acute very toxic to aquatic organisms (see Section 6, Aquatic toxicity and EC-ECB, 2004) with invertebrates and/or algae being the most sensitive organism groups. The available data on algae indicate a chronic toxicity potential with NOErC being 0.067 mg/L for methylcyclohexane and 0.94 mg/L for cyclohexane, resulting in chronic classification for both substances.

- Toxicological profile:

Methylcyclohexane and cyclohexane show similar toxicokinetic behaviour (see Section 7.1, Toxicokinetics). For those toxicological endpoints, for which both substances have been tested, similar levels of toxicity have been observed. Thus, both substances are of low acute toxicity via the oral and inhalation route, but fulfil the classification criteria for Aspiration toxicity (Category 1) and Narcotic effects (STOT-SE 3) according to Regulation (EC) No 1272/2008. Both substances were not skin and eye irritating in experimental studies, but are classified for Skin irritation (Category 2), mainly based on their defatting properties. Methylcyclohexane and cyclohexane have been extensively studied for repeated dose toxicity mainly via inhalation. For methylcyclohexane, the lowest chronic NOAEC for systemic effects is 400 ppm (1600 mg/m³) in rats, while for cyclohexane the most reliable subchronic systemic NOAEC in rats and mice is 2000 ppm (6880 mg/m³). Applying a time-extrapolation factor of 3 (ECHA, 2010), the chronic NOAEC for cyclohexane would be 667 ppm (2293 g/m³), which would be in the same order of magnitude as for methylcyclohexane. Both substances have been tested negative for mutagenicity in vitro.

Conclusion:

In order to avoid the need to test methylcyclohexane for every endpoint for which information gaps are identified, the read-across approach is applied for the assessment of environmental and human health hazards. Thus, environmental and human health effects are predicted where applicable from adequate and reliable data for cyclohexane by interpolation to methylcyclohexane in accordance with Annex XI, Item 1.5 of Regulation (EC) No 1907/2006.

A detailed justification for the read-across approach is provided in the technical dossier (see IUCLID Section 13).

References

Breitmaier, E. and Jung, G. (2005). Organische Chemie. Grundlagen , Stoffklassen, Reaktionen, Konzepte, Molekülstruktur. 5th ed. Georg Thieme Verlag, Stuttgart.

ECHA (2010). Guidance on information requirements and chemical safety assessment Chapter R.8: Characterisation of dose [concentration]-response for human health. Source: European Chemicals Agency, http://echa.europa.eu/

EUROPEAN COMMISSION - European Chemicals Bureau (EC-ECB) (2004). European Union Risk Assessment Report: Cyclohexane; CAS No: 110-82-7; EINECS No: 203-806-2. European Chemical Bureau - Institute for Health and Consumer Protection.

Justification for selection of acute toxicity – oral endpoint
Hazard assessment is based on the weight of evidence from all available studies.
Aspiration hazard is based on physico-chemical properties (kinematic viscosity) and thus not linked to a dose descriptor. Therefore, no effect level is given.

Justification for selection of acute toxicity – inhalation endpoint
No study was selected, since the identified hazard is based on the weight of evidence from all available studies. In particular, three of these studies taken together provide the lowest dose descriptor for human health hazard and risk assessment of specific, non-lethal target organ toxicity arising from a single exposure (STOT-SE, Category 3, narcotic effects).

Justification for selection of acute toxicity – dermal endpoint
Hazard assessment is conducted by means of read-across from a structural analogue. The selected study is the most adequate and reliable study based on the identified similarities in structure and intrinsic properties between source and target substance and overall quality assessment (refer to the endpoint discussion for further details).

Justification for classification or non-classification

The available data on the acute oral toxicity of methylcyclohexane do not meet the criteria for classification according to Regulation (EC) No 1272/2008 and Directive 67/548/EEC, and are therefore conclusive but not sufficient for classification. However, based on kinematic viscosity, methylcyclohexane meets the classification criteria for Aspiration Toxicity Category 1 (H304: May be fatal if swallowed and enters airways) according to Regulation (EC) No 1272/2008 and Harmful (Xn; R65 Harmful; Harmful: may cause lung damage if swallowed) according to Directive 67/548/EEC.

The available data on the acute toxicity of methylcyclohexane by inhalation meet the classification criteria for STOT Single Exposure Category 3 (narcotic effects) (H336: May cause drowsiness or dizziness) according to Regulation (EC) No 1272/2008 and R67 (Vapours may cause drowsiness and dizziness) according to Directive 67/548/EEC.

Based on read-across from the structurally similar reference substance cyclohexane, the available data on acute dermal toxicity do not meet the criteria for classification according to Regulation (EC) No 1272/2008 or Directive 67/548/EC, and are therefore conclusive but not sufficient for classification.

CLP: Asp. Tox. 1, STOT Single Exp. 3

DSD: R65-67