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EC number: 908-296-1 | CAS number: -
- 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
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- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
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- 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
Link to relevant study record(s)
- Endpoint:
- basic toxicokinetics, other
- Remarks:
- in vivo and in vitro study
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- supporting study
- Justification for type of information:
- 1,8-cineole (source substance) is one of the main constituents of the registered substance (target substance).
- Reason / purpose for cross-reference:
- read-across source
- Metabolites identified:
- yes
- Details on metabolites:
- two main metabolites: 2-alpha-hydroxy-1,8-cineole and 3-apha-hydroxy-1,8-cineole.
The formation of 3-apha-hydroxy-1,8-cineole in the presence of human CYP3A4/3A5 with an NADPH-generating system varied depending on incubation time, P450 concentration and substrate concentration. In the absence of human CYP3A4/3A5 no hydroxylation of 1,8-cineole was detected. - Bioaccessibility (or Bioavailability) testing results:
- Not relevant
- Conclusions:
- It was found that 1,8-cineole is metabolized in vitro by human microsome and liver enzymes CYP3A4 and CYP3A5 to 2-alpha-hydroxy-1,8 cineole and 3-alpha-hydroxy-1,8 cineole. This was confirmed in vivo by detection of these metabolites in urine of volunteers exposed orally with cold medication for 5 days.
- Executive summary:
Cytochrome P450-mediated enzymatic assays were used to study the metabolism of 1,8 -cineole by human microsomes and two recombinant enzymes (CYP3A4 and CYP3A5) normally present in human liver. The urine of 3 volunteers was examined after an oral administration of cold medication containing 1,8-cineole for 5 days.
It was found that 1,8-cineole is metabolized in vitro by human liver enzymes CYP3A4 and CYP3A5 to 2-alpha-hydroxy-1,8 cineole and 3-alpha-hydroxy-1,8 cineole. This was confirmed in vivo by detection of these metabolites in the urine of the volunteers.
- Endpoint:
- basic toxicokinetics in vivo
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- supporting study
- Justification for type of information:
- 1,8-cineole (source substance) is one of the main constituents of the registered substance (target substance).
- Reason / purpose for cross-reference:
- read-across source
- Positive control reference chemical:
- not relevant
- Details on excretion:
- In contrast to blood, hydroxy-1,8-cineoles were higher abundant in urine showing highest contents during the first 2 h. In accordance with the plasma levels, 2-hydroxycineole showed highest contents in urine followed by its 9-isomer.
However, in contrast to the plasma contents, 3-hydroxycineole was more abundant in urine than the 7-isomer.
Summing up the urinary excretion over 10 h, 52.5% of the 1,8-cineole dose was identified as metabolites, of which 2-hydroxycineole, the 9- isomer, the 3-isomer and the 7-isomer accounted for 20.9%, 17.2%, 10.6% and 3.8%, respectively. After 10 h, only traces of metabolites could be detected. - Metabolites identified:
- yes
- Details on metabolites:
- After consumption of 1.02 mg 1,8-cineole (19 mg/kg bw), the metabolites 2-hydroxy-1,8-cineole, 3-hydroxy-1,8-cineole, 7-hydroxy-1,8-cineole, and 9-hydroxy-1,8-cineole along with their parent compound were detectable in the blood plasma of the female volunteer under study after liberation from their glucuronides.
All compounds peaked in plasma after 0.75 h with 2-hydroxycineole being the predominant metabolite at a plasma concentration of 86 nmol/L followed by the 9-hydroxy isomer at a plasma concentration of 33nmol/L. The 7- and the 3-isomer were detectable, but their plasma concentrations were below their LOQ. - Conclusions:
- 2-hydroxy-1,8-cineole is the main metabolite of 1,8-cineole in humans.
3-hydroxy-1,8-cineole, 7-hydroxy-1,8-cineole, and 9-hydroxy-1,8-cineole have also been identified as metabolites in plasma and urine. - Executive summary:
The metabolism of 1,8-cineole after ingestion of sage tea was studied. After application of the tea, metabolites 2-hydroxy-1,8-cineole, 3-hydroxy-1,8-cineole, 9-hydroxy-1,8-cineole and, for the first time in humans, 7-hydroxy-1,8-cineole were identified in plasma and urine of one volunteer. For quantitation of these metabolites and the parent compound, stable isotope dilution assays were developed after synthesis of [2H3]-1,8-cineole, [9/10-2H3]-2-hydroxy-1,8-cineole and [13C,2H2]-9-hydroxy-1,8-cineole as internal standards. Using these standards, 1,8-cineole was quantified by solid phase microextraction GC-MS and the hydroxyl-1,8-cineoles by LC-MS/MS after deconjugation in blood and urine of the volunteer. After consumption of 1.02 mg of 1,8-cineole (19 mg/kg bw), the hydroxycineoles along with their parent compound were detectable in the blood plasma of the volunteer under study after liberation from their glucuronides with 2-hydroxycineole being the predominant metabolite at a maximum plasma concentration of 86 nmol/L followed by the 9-hydroxy isomer at a maximum plasma concentration of 33 nmol/L. Parent compound 1,8-cineole showed a low maximum plasma concentration of 19 nmol/L. In urine, 2-hydroxycineole also showed highest contents followed by its 9-isomer. Summing up the urinary excretion over 10 h, 2-hydroxycineole, the 9-isomer, the 3-isomer and the 7-isomer accounted for 20.9, 17.2, 10.6 and 3.8% of the cineole dose, respectively.
- Endpoint:
- basic toxicokinetics in vivo
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- supporting study
- Justification for type of information:
- 1,8-cineole (source substance) is one of the main constituents of the registered substance (target substance).
- Reason / purpose for cross-reference:
- read-across source
- Details on absorption:
- 1,8-Cineole was quickly absorbed from the breathing air and could be detected in the blood 5 min after starting the inhalation procedure.
The half-lives of invasion (t1/2 in) and the time to reach the maximum concentration of 1,8-cineole in blood [t(p)] were in a close range between all individuals (~3-7 min and 14-19 min respectively), whereby the maximum measured concentration [c(tp)] ranged between 459 and 1135 ng/mL. - Details on distribution in tissues:
- The t1/2 alpha representing the distribution half-life of 1,8-cineole into tissue, was between 2 and 4.8 min for the two males, whereas the two females exhibited prolonged values of 6.9-13.1 min.
These differences between males and females-were also observed for the t1/2 beta for which the males had values of 31.1-32.6 min whereas the females had values ~2.5 and 10 times longer. - Details on excretion:
- The elimination from the blood is biphasic, with a mean distribution half-life of 6.7 min and an elimination half-life of 104.6 min.
- Metabolites identified:
- no
- Conclusions:
- 1,8-cineole is well absorbed from breathing air, with a peak plasma concentration after 18 min. The elimination from the blood is biphasic, with a mean distribution half-life of 6.7 min and an elimination half-life of 104.6 min.
- Executive summary:
The present study was undertaken to investigate the pharmacokinetics of 1,8-cineole in human subjects during inhalation for 20 min. The results showed that 1,8-cineole is well absorbed from breathing air, with a peak plasma concentration after 18 min. The elimination from the blood is biphasic, with a mean distribution half-life of 6.7 min and an elimination half-life of 104.6 min.
- Endpoint:
- basic toxicokinetics in vivo
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- supporting study
- Justification for type of information:
- 1,8-cineole (source substance) is one of the main constituents of the registered substance (target substance).
- Reason / purpose for cross-reference:
- read-across source
- Metabolites identified:
- yes
- Details on metabolites:
- Ten metabolites: 2,3-dehydro-, α2,3-epoxy-,α2-hydroxy-, β2-hydroxy-, α3-hydroxy-, 4-hydroxy-, 7-hydroxy-, 9-hydroxy-, 2-oxo- and 3-oxo-1,8-cineole were identified in each human milk sample.
alpha 2-hydroxy-1,8-cineole is the metabolite with the highest concentration in human milk samples (99–233 μg/kg). The concentration ranges of the other metabolites were about 10 to 1000 fold lower than for alpha-2-hydroxy-1,8-cineole.
The ratios of enantiomers were determined: the enantiomer eluting first on the respective GC capillary is named E1, the other E2. E1 of alpha2-, β2-,alpha 3- and 9-hydroxy-1,8-cineole as well as of 3-oxo-1,8-cineole is the (+)-enantiomer. α2-Hydroxy- and 3-oxo-1,8-cineole both consisted of under 10% E1. For 2,3-dehydro-, α2,3-epoxy-, 2-oxo- and β2-hydroxy-1,8-cineole, E1 was in the 20% to 60% range. Also for 9-hydroxy- 1,8-cineole, percentage E1 covered a large range, from about 50 to 80%. Finally, α3-hydroxy-1,8-cineole exhibited a rather narrow data scatter of around 70% to 80% E1. - Conclusions:
- Measured concentrations varied over a range of some tens of μg/kg for most metabolites, both inter and intra-individually, but absolute concentrations were rather low over a range of up to 40 μg/kg milk.
The only exception was the metabolite alpha 2-hydroxy-1,8-cineole, which showed significantly higher concentrations of about 100–250 μg/kg and, thus, was clearly the main metabolite of 1,8-cineole in human milk. - Executive summary:
The aim of the present study was to characterise the metabolites of 1,8-cineole, identified previously in human milk, after the oral intake of 100 mg of this substance.
Human milk samples were provided voluntarily by breastfeeding mothers after intake of the non-prescription pharmaceutical Soledum® (Klosterfrau Healthcare Group, Cologne, Germany).
Measured concentrations varied over a range of some tens of μg/kg for most metabolites, both inter and intra-individually, but absolute concentrations were rather low over a range of up to 40 μg/kg milk.
The only exception was the metabolite alpha 2-hydroxy-1,8-cineole, which showed significantly higher concentrations of about 100–250 μg/kg and, thus, was clearly the main metabolite of 1,8-cineole in human milk.
The total amount of metabolised 1,8-cineole in the samples increased with the time since the intake of the encapsulated 1,8-cineole, indicating that the metabolite concentrations in human milk were highly dynamic, probably due to transfer from the blood, or even to metabolic activity in the milk itself.
Most of the metabolites were chiral, thus it was also interesting to determine the ratio of enantiomers. Generally, the metabolites alpha 2-hydroxy- and 3-oxo-1,8-cineole were nearly enantiomerically pure in human milk, while all other metabolites of the present study showed enantiomeric ratios of about 30:70 to 80:20.
- Endpoint:
- basic toxicokinetics in vitro / ex vivo
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- supporting study
- Justification for type of information:
- 1,8-cineole (source substance) is one of the main constituents of the registered substance (target substance).
- Reason / purpose for cross-reference:
- read-across source
- Metabolites identified:
- yes
- Details on metabolites:
- See any other information on results incl. tables
- Conclusions:
- The present study showed that 1,8-cineole is highly catalyzed by CYP3A enzymes to form 2-exo-hydroxy-1,8-cineole in rat and human liver microsomes. CYP3A4 is suggested to be a principal enzyme in catalyzing 1,8-cineole 2-hydroxylation by human liver microsomes; the rate catalyzed by liver microsomes of 18 human samples was 26.9 nmol/min/nmol P450.
- Executive summary:
The metabolism of 1,8-cineole by liver microsomes of rats and humans and by recombinant cytochrome P450 (P450 or CYP) enzymes in insect cells in which human P450 and NADPH-P450 reductase cDNAs had been introduced were investigated. 1,8-Cineole was found to be oxidized at high rates to 2-exo-hydroxy-1,8 -cineole by rat and human liver microsomal P450 enzymes. It is suggested that CYP3A4 is a major enzyme involved in the oxidation of 1,8-cineole by human liver microsomes.
Kinetic analysis showed that Km and Vmax values for the oxidation of 1,8-cineole by liver microsomes of human sample HL-104 and rats treated with PCN were 50 mM and 91 nmol/min/nmol P450 and 20 mM and 12 nmol/min/nmol P450, respectively. The rates observed using human liver microsomes and recombinant CYP3A4 were very high among other CYP3A4 substrates reported so far. These results suggest that 1,8-cineole, a monoterpenoid present in nature, is one of the effective substrates for CYP3A enzymes in rat and human liver microsomes.
- Endpoint:
- dermal absorption in vitro / ex vivo
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- supporting study
- Justification for type of information:
- 1,8-cineole (source substance) is one of the main constituents of the registered substance (target substance).
- Reason / purpose for cross-reference:
- read-across source
- Signs and symptoms of toxicity:
- not specified
- Dermal irritation:
- not specified
- Absorption in different matrices:
- The dermal penetration of pure terpenes was studied during 4 h. The terpenes were present on the skin in infinite doses and the system was protected against evaporation. During that time no terpenes were detected in the acceptor fluid but extensive accumulation in the skin tissue occurred (see table 1).
Analysis of stratum corneum (SC) collected with an adhesive tape and merged into three groups demonstrates cumulation of terpenes in the outer (SC I), middle (SC II) and inner (SC III) layers. The results demonstrate rapid penetration of terpenes not only to the SC I layers but also to viable epidermis and dermis. The distance-dependent decreasing gradient of concentration for all terpenes is observed, although the concentrations were not normalized in respect of the collected SC mass. A steady-state concentration of terpenes in the SC can be assumed as soon as after 1 h. Maximum concentration in the SC was achieved as soon as after 1 h and did not further increase in the course of the study.
All studied terpenes are absorbed in high amounts in the viable epidermis with dermis (ED), however penetration into this layers is time-dependent process, constantly increasing during 4 h. - Total recovery:
- No data
- Conversion factor human vs. animal skin:
- None
- Conclusions:
- Eucalyptol absorption into the different skin layers is rapid (steady-state concentrations in the skin obtained after 1-h exposure) but do not permeate through the skin to the acceptor medium due to large accumulation into the skin tissue.
- Executive summary:
Skin absorption and elimination kinetics were studied using human skin from the region of thorax of 40-50 years old Caucasian women, mounted on flow-through Teflon diffusion cells. Eucalyptol (500 mg) was applied onto the human skin (0.65 cm²), and after 1 to 4-h exposure, the content in the stratum corneum layers (separated by a tape-stripping method) and in the epidermis/dermis was determined using GC. Similarly, the elimination kinetics in the skin were analysed during 4 h following 1 h absorption. Quadruplicates were used for each time point.
The results demonstrate rapid penetration of terpenes not only to the first stratum corneum layers but also to viable epidermis and dermis (steady-state concentrations assumed to be obtained at 1-h exposure). However, eucalyptol did not permeate across the skin to the acceptor medium due to large cumulation in the skin tissue. Two mechanisms of elimination process of terpenes from the SC are suggested: evaporation and slightly progressive penetration from inner layer into dermis.
Referenceopen allclose all
Kinetic analysis of 1,8-cineole 3a-hydroxylation by Human CYP3A4/3A5:
The Michaelis-Menten Km values for this reaction were: 10µM for human CYP3A4 and 141 µM for human CYP3A5. The Vmax values were 64.5 nmol/min/nmol P450 for human CYP3A4 and 10.9 nmol/min/nmol P450 for human CYP3A5. Finally, the efficiencies of catalysis (Vmax/Km value) were 3.4 nM-1.min-1 for CYP3A4 and 0.08 nM-1.min-1 P450 for CYP3A5.
The metabolism was found to occur very fast within the first hour after consumption and gave rise to four hydroxycineols, of which the 7-isomer was identified for the first time in humans.
Identification of 2-Hydroxylated Metabolite of 1,8-Cineole on Incubation with Human Liver Microsomes: only one metabolite was detected by GC-MS equipped with EI-MS: 2-exo-hydroxy-1,8-cineole. 1,8-cineole is actually oxidized at the 2-position forming 2-hydroxy-1,8-cineole by CYP3A4 in human liver microsomes.
Metabolism of 1,8-Cineole to 2-exo-Hydroxy-1,8-Cineole by Human and Rat Liver Microsomes:
The formation of 2-exo-hydroxy-1,8-cineole metabolite was increased with increasing incubation time, P450 levels in liver microsomes, and substrate concentrations.
Ketoconazole, an inhibitor of CYP3A-dependent activities, significantly inhibited the 1,8-cineole 2-hydroxylation catalyzed by rat and human liver microsomes.
Anti-CYP3A4 IgG was found to inhibit very significantly the 1,8-cineole 2-hydroxylation activities catalyzed by liver microsomes of HL-11 and HL-104.
Table 1: Absorption of eucalyptol (mg/cm2) into human skin layers (mean ± S.D., n = 4)
Skin layer |
1-h exposure |
2-h exposure |
4-h exposure |
SC I |
42.7 ± 11.3 |
41.7 ± 5.9 |
40.0 ± 12.9 |
SC II |
8.3 ± 1.0 |
19.6 ± 5.4 |
21.2 ± 7.8 |
SC III |
9.7 ± 3.8 |
10.8 ± 2.7 |
17.5 ± 6.6 |
SC total |
60.7 ± 9.0 |
72.1 ± 8.9 |
78.7 ± 20.1 |
ED |
290.1 ± 75.0 |
384.6 ± 94.7 |
410.7 ± 76.0 |
Skin total |
350.8 ± 68.7 |
456.7 ± 95.5 |
489.4 ± 80.6 |
Table 2: Elimination of eucalyptol (mg/cm2) from human skin layers following 1 h absorption (t = 0) (mean ± S.D., n = 4)
|
Time after 1-h exposure |
||||
Skin layer |
0 |
1 |
2 |
3 |
4 |
SC I |
42.7 ± 11.3 |
42.5 ± 4.1 |
26.6 ± 4.6 |
25.6 ± 6.7 |
25.1 ± 14.5 |
SC II |
8.3 ± 1.0 |
7.2 ± 4.6 |
6.5 ± 1.7 |
6.3 ± 2.3 |
4.8± 1.1 |
SC III |
9.7 ± 3.8 |
7.9 ± 4.1 |
5.5± 1.7 |
5.2 ± 0.9 |
1.8± 1.8 |
SC total |
60.7 ± 9.0 |
57.6 ± 11.5 |
38.6 ± 3.5 |
37.1 ± 9.1 |
31.7 ± 17.2 |
ED |
290.1 ± 75.0 |
262.7 ± 44.5 |
260.3 ± 75.7 |
259.9 ± 69.3 |
143.6 ± 20.5 |
Skin total |
350.8 ± 68.7 |
320.3 ± 37.7 |
298.9 ± 72.3 |
297.0 ± 78.4 |
175.3 ± 37.5 |
Description of key information
Data were available from scientific litterature about the toxicokinetics of 1,8-cineole, one of the main contituents of the registered substance.
1,8-cineole is well absorbed from breathing air, with a peak plasma concentration after 18 min. Rapid skin penetration occurs not only to the first stratum corneum layers but also to viable epidermis and dermis (steady-state concentrations assumed to be obtained at 1-h exposure). However, 1,8-cineole did not permeate across the skin to the acceptor medium due to large cumulation in the skin tissue.
1,8-cineole is metabolized in vitro by human microsome and liver enzymes CYP3A4 and CYP3A5 to 2-alpha-hydroxy-1,8-cineole and 3-alpha-hydroxy-1,8-cineole. This was confirmed in vivo by detection of these metabolites in urine of volunteers exposed orally with cold medication for 5 days.
Metabolite alpha 2-hydroxy-1,8-cineole is the main metabolite of 1,8-cineole in human milk. Therefore, 2-hydroxy-1,8-cineole is the main metabolite of 1,8-cineole in humans. 3-hydroxy-1,8-cineole, 7-hydroxy-1,8-cineole, and 9-hydroxy-1,8-cineole have also been identified as metabolites in plasma and urine.
The elimination from the blood after inhalation is biphasic, with a mean distribution half-life of 6.7 min and an elimination half-life of 104.6 min.
Key value for chemical safety assessment
- Bioaccumulation potential:
- low bioaccumulation potential
- Absorption rate - oral (%):
- 100
- Absorption rate - dermal (%):
- 100
- Absorption rate - inhalation (%):
- 100
Additional information
Data were available from scientific litterature about the toxicokinetics of 1,8-cineole, one of the main contituents of the registered substance.
1,8-cineole is well absorbed from breathing air, with a peak plasma concentration after 18 min. Rapid skin penetration occurs not only to the first stratum corneum layers but also to viable epidermis and dermis (steady-state concentrations assumed to be obtained at 1-h exposure). However, 1,8-cineole did not permeate across the skin to the acceptor medium due to large cumulation in the skin tissue.
1,8-cineole is metabolized in vitro by human microsome and liver enzymes CYP3A4 and CYP3A5 to 2-alpha-hydroxy-1,8-cineole and 3-alpha-hydroxy-1,8-cineole. This was confirmed in vivo by detection of these metabolites in urine of volunteers exposed orally with cold medication for 5 days.
Metabolite alpha 2-hydroxy-1,8-cineole is the main metabolite of 1,8-cineole in human milk. Therefore, 2-hydroxy-1,8-cineole is the main metabolite of 1,8-cineole in humans. 3-hydroxy-1,8-cineole, 7-hydroxy-1,8-cineole, and 9-hydroxy-1,8-cineole have also been identified as metabolites in plasma and urine.
The elimination from the blood after inhalation is biphasic, with a mean distribution half-life of 6.7 min and an elimination half-life of 104.6 min.
These data on 1,8-cineole are confirmed for the whole registered substance in the available repeated dose toxicity data: liver centrilobular hypertrophy, associated with increased liver weights was observed in rats exposed up to 6 weeks to the registered substance, showing adaptative changes in the liver due to the metabolisation of the substance. Also, the sex and species-specific alpha-2 -microglobulin nephropathy was observed in male rats, showing potential excretion in urine.
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