Registration Dossier

Administrative data

Description of key information

Not acutely hazardous after ingestion, inhalation or skin contact, based on animal test data.

Key value for chemical safety assessment

Acute toxicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Acute toxicity: via inhalation route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Acute toxicity: via dermal route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Additional information

Information is available on the acute toxicity of the following members of this category:

 

Test substance identity

Route

Oral

Inhalation

Dermal

Hex-1-ene

Alkenes, C6-8-branched, C7-rich

 

Alkenes, C7-9-branched, C8-rich

 

 

Alkenes, C8-10-branched, C9-rich

 

 

Oct-1-ene

Alkenes C10/C11/C12/C13 (aka Alkenes C11-12)

 

 

Alkenes C11-15 (aka tetradecene)

 

Alkenes, C12-14 α-

 

Hexadec-1-ene (MC)

 

 

Hexadecene

 

Octadecene

 

Hydrocarbons, C14-30, olefin-rich

 

Alkenes, C20-24 α-

 

 

Alkenes, C20-24 (aka C20-C22 (even numbered, linear and branched) and C24(branched) alkenes)

 

Alkenes, C24-28 α-

 

 

Alkenes, C24-28 (aka Alkenes, C21-32 linear and branched)

 

 

 

Details of these studies are summarised below.

Acute oral toxicity

In an acute oral toxicity study, groups of fasted Fisher 344 rats (5 male, 5 female) were given a single oral dose via gavage of hex-1-ene (Neodene 6) at doses of 0, 1000, 1800, 3200, or 5600 mg/kg bw and observed for 14 days (Albert et al., 1983). Controls received deionised water. No deaths occurred during this study and body weight was not affected by treatment. Clinical signs of toxicity included mucoid diarrhoea over the first day in treated rats. The only remarkable change observed during necropsy was bilateral luminal dilation with clear fluid in the uterus of some treated females rats. This change, which was not observed in control animals, occurred in 4/5 of 1000 mg/kg treated females, 1/5 of 3200 mg/kg treated females, and 4/5 of 5600 mg/kg treated females. The pathologist noted that this was a common occurrence for the laboratory, and it was not considered treatment-related. The acute oral LD50 for Neodene 6 alpha olefin in male and female rats was reported as >5600 mg/kg. The results of this study indicate that hex-1-ene is not acutely toxic via the oral exposure route.

The acute oral toxicity of octadec-1-ene has been investigated in two studies. In the first investigation, groups of fasted, male and female Fischer 344 rats (5/sex) were given a single oral dose of undiluted Neodene 8 Alpha Olefin (oct-1-ene) at 5.0 mL/kg via oral intubation (Wilborn, 1983). There was no mortality observed in either sex, and no treatment-related clinical signs, necropsy findings or changes in body weight observed through the 14 day observation period. Based on a lack of significant treatment-related findings, the acute oral LD50 was determined to > 5.0 mL/kg (equivalent to 3575 mg/kg bw using a density of 0.7149 mg/cm3 for oct-1 -ene) in male and female rats. In the second key study, 10 fasted, male Sprague-Dawley rats received a single oral dose of undiluted oct-1-ene at 10,000 mg/kg after which the animals were observed for 14 days (Monrose, 1973). There were no treatment-related clinical signs, necropsy findings or changes in body weight reported. The oral LD50 was determined to be > 10,000 mg/kg. These results indicate that oct-1-ene is not acutely toxic by the oral exposure route.

The acute oral toxicity of alkenes, C11 -15 (Internal Olefin 114 LP11) was investigated using two groups of four male and four female Wistar rats, age approximately 12 weeks. The animals were fasted overnight prior to administration of a single oral dose of the test substance (5.0 and 10 mL/kg), followed by a 9 day observation period (Cassidy and Clark, 1977).  No animals died at the 5.0 mL/kg dose level, however two male rats died after receiving 10 mL/kg (females unaffected). There were no treatment related clinical signs, and necropsy data was provided. Animals that did not survive were reported to not eat or drink during the observation period, thus losing weight. The oral LD50 was estimated to be > 10 mL/kg in females (i.e., > 7600 mg/kg) and 10 mL/kg (7600 mg/kg) in males. Based on these results, it can be concluded that alkenes, C11-15 are not acutely toxic by the oral exposure route.

Two studies are available which investigated the acute oral toxicity of C12-14 alpha olefin. In the first study (Rinehart, 1967), groups of ten male albino Wistar rats were administered 0, 5000, or 10,000 mg/kg bw C12-16 alpha olefin blend. The animals were observed for 14 days after which they were necropsied and examined for gross histopathological changes. No mortality was observed at 5000 mg/kg bw, however two rats administered 10,000 mg/kg bw C12 -16 blend died during the course of the study. The study authors attributed the deaths to pneumonia since traces of this condition was observed at autopsy in both the treated and control animals. Body weight did not appear to be affected by treatment. Several days after dosing, animals developed very coarse, oily fur over nearly the entire body. The acute oral LD50 for C12 -16 Alpha Olefin blend was reported as > 10,000 mg/kg bw in this study using male rats. In a second acute oral toxicity study, 10 male Sprague Dawley rats were administered a single oral dose of 10,000 mg/kg C12-14 alpha olefin (via intubation) and observed for 14 days (Monrose and Carter, 1973). No mortality, permanent body weight changes or gross pathological changes were observed, however treated animals experienced loss of hair on the inner hind thighs and posterior abdominal surface. The acute oral LD50 for C12-14 blend was reported as >10,000 mg/kg in male rats. These results indicate that C12-14 alpha olefin is not acutely toxic by the oral exposure route.

In an acute oral toxicity study with hexadec-1-ene (Gulftene 16 ), young, fasted Sprague-Dawley albino rats (10/sex/dose), were given a single oral dose of 5,000 or 10,000 mg/kg of the test substance and observed for 14 days (Myers et al., 1992). There was no mortality at 5,000 mg/kg bw dose; however 2/5 males and 2/5 females dosed with 10,000 mg/kg died. Necropsy revealed discoloration in lungs, intestines (with distension), liver (1 animal) and kidneys in rats that died or were sacrificed during the study period. Surviving animals had no remarkable gross lesions. No lesions were found in tissues taken to evaluate neurotoxicity (brains, spinal cords, sciatic nerves and pituitaries). The oral LD50 was reported as > 10,000 mg/kg bw in both male and female rats. The results from this study indicate that hexadec-1-ene is not acutely toxic by the oral exposure route.

In an acute oral toxicity on hexadecene, no treatment-related mortality, body-weight changes or signs of severe toxicity was observed in five male and female young adult Sprague-Dawley rats administered 5050 mg/kg (5.92 mL/kg) of the test substance via oral intubation (Kuhn, 1993). Body weight gain was unaffected as a result of exposure to hexadecane in most animals. One female lost weight between day 0 and day 7, while another female failed to gain weight between day 7 and 14. Notable observations included decreased activity, diarrhoea, piloerection, and polyuria. These effects were no longer present by day 7 of the study period. All treated animals exhibited alopecia from day 7 to day 14. Gross necropsy at study termination revealed no observable abnormalities. None of the treated animals died during the course of the study. Based on these results, the acute oral LD50 for hexadecene in Sprague Dawley rats is > 5050 mg/kg (5.92 mL/kg). The results of this study indicate that hexadecene is not acutely toxic by the oral exposure route.

In an acute oral toxicity study on octadecene, five male and female young adult Sprague-Dawley rats were administered 5050 mg/kg (5.88 mL/kg) of test substance via oral intubation. Body weight gain was unaffected as a result of treatment, however diarrhoea, piloerection, and polyuria were present in treated animals. Gross necropsy at study termination revealed no observable abnormalities. None of the treated animals died during the course of the study. Based on these results, the acute oral LD50 for octadecene in Sprague Dawley rats is > 5050 mg/kg (5.88 mL/kg). The results of this study indicate that octadecene is not acutely toxic by the oral exposure route.

To assess the acute oral toxicity of hydrocarbons, C14 -30, olefin-rich (Ethyl Compound 100-606), five male and five female CFE rats were administered a single oral dose of 10,000 mg test substance/kg body weight via gastric intubation (Springer, 1977). Animals were then observed for mortality, body weight changes, and overt signs of toxicity for 14 days. At study termination all animals were sacrificed and necropsies were performed. None of the 10 treated rats died during the 14 day observation period. Gross autopsy findings revealed blanched and mottled kidneys in almost all animals; however, body weight gain was normal. Based on the lack of mortality, the LD50 was estimated to be >10,000 mg/kg in both sexes. The test material was determined to be non-toxic when administered orally. Based on these results, it is concluded that hydrocarbons C14-30, olefin-rich are not acutely toxic by the oral exposure route.

Two acute oral toxicity studies are available for C24-28 alpha olefin. In the first investigation (Rinehart, 1967), C22-28 alpha olefin blend (prepared as a 25% w/v solution in corn oil) was administered to ten male Wistar rats at 0 or 5000 mg/kg bw and the animals observed for 14 days. An additional group of 10 rats received 20 ml/kg of corn oil and served as an internal control. No mortalities were reported; however several days after dosing, animals developed very coarse, oily fur over nearly the entire body with occurrence being particularly severe around the hindquarters. Based on these results, the LD50 for Alpha Olefin C22-28 blend was reported as > 5000 mg/kg. In the second study (Rausina, 1982), two male Fischer 344 rats were given a single oral dose of alpha olefin C30+ at 5000 mg/kg bw via oral intubation Both animals died immediately post administration so another study was undertaken using 5 rats/sex dosed at 2000 mg/kg. The animals were observed for 14 days. Mortality, observed in one animal, was attributed to trauma resulting from the dosing procedure and was not considered treatment-related. There were no changes in body weight. Yellow staining of the inguinal area and mouth were observed in some test animals in addition to excessive salivation and laboured breathing that was exhibited by a few test animals. These effects however, were diminished 2 days post-exposure. The acute oral LD50 for alpha olefin C30+ was considered to be >2000 mg/kg bw and <5000 mg/kg bw in male rats. These results indicate that C24-28 alpha olefin is not acutely toxic by the oral exposure route.

To assess acute oral toxicity of alkenes, C20-24, groups of 5 fasted female Sprague-Dawley CD strain rats were given a single oral dose (2000 mg/kg bw ) of ENORDET O241 and observed for 14 days (Sanders, 2008). There were no treatment related clinical signs, necropsy findings or changes in body weight. The oral LD50 was determined to be greater than 2000 mg/kg in this single sex study. Based on these results, it is concluded that alkenes, C20-24 are not acutely toxic by the oral exposure route.

The acute oral toxicity of C20-24 alpha olefin (Gulftene 24) was investigated in young, fasted male and female Fischer 344 rats (5/sex) (Rausina, 1982) after administration of a single oral treatment of 5000 mg/kg bw given in corn oil. No treatment-related adverse effects were noted during the 14-day observation period in body weight or necropsy findings, and the only clinical signs noted (yellow staining of the inguinal region, oil around mouth, and brown staining on lower jaw) all disappeared by day 5 of the study period. The oral LD50 for Gulftene 20-24 was determined to be > 5000 mg/kg in male and female rats. These results indicate that C20-24 alpha olefin is not acutely toxic by the oral exposure route.

The acute oral toxicity of alkenes, C24-28 was studied in five male and five female rats administered 5000 mg/kg of the test substance via gavage in arachis oil BP (Driscoll, 1998). The animals were observed for mortality or overt signs of toxicity 1, 2.5, and 4 hours after dosing and once daily thereafter for 14 days until study termination. At study termination, the animals were sacrificed and subject to gross necropsy. None of the animals died during the course of the study. Clinical observations included hunched posture and pilo-erection in males. All animals exhibited normal body weight gain during the course of the study and no abnormalities were noted at necropsy. Based on these results, the authors concluded that the acute oral LD50 for C24-C30 alkenes, branched and linear, in Sprague- Dawley rats is >5000 mg/kg. Based on these results, it is concluded that alkenes, C24-28 are not acutely toxic by the oral exposure route.

Acute inhalation toxicity

In a study reported by Rinehart (1967), rats were exposed to hex-1-ene vapour for 4 hours. The study was well conducted and reported, although high exposure concentrations were used (above the 20 mg/L limit for vapours required for classification and labelling; EU CLP). No mortality was reported in the lowest dose group (95 mg/L) although mild signs of anaesthesia were noted among treated animals.

In an acute inhalation toxicity study on alkenes, C6-8-branched, C7-rich (MRD-ECH-78-32), groups of 5 male and female Swiss Albino mice, ARS/Sprague-Dawley rats, and Hartley guinea pigs were exposed whole body to vapour concentrations of 42.3 mg/L for six hours (Duckworth, 1979). All animals were observed for overt signs of toxicity during the exposure period and for 14 days thereafter. Individual body weights were recorded prior to exposure and on days 1, 2, 4, 7 and 14. All animals (survivors and decedents) were subjected to gross necropsy. At study termination, surviving animals were sacrificed and all animals, including animals that died prior to study termination, were necropsied. Lungs, trachea, liver and kidneys were preserved for possible histopathological examination. Exposure to MRD-ECH-78-32 led to the death of one mouse at the one hour observation period. One guinea pig died 20 minutes after exposure began, while another died after 45 minutes. No mortality was observed in rats. Body weights were reported to be comparable to the control animals. Clinical signs in all species during exposure included ataxia, laboured breathing, tremors, reduced activity and prostration. Clinical signs in all species during the 14-d post-exposure period included nasal discharge, chromodacryorrhea, rales and excessive lacrimation. Necropsy examinations revealed lung and liver discolouration in both decedents and survivors. Based on these results, it may be inferred that the LC50 for the test chemical in mice, rats and guinea pigs is > 42.3 mg/L.

In an acute inhalation study on alkenes, C7-9-branched, C8-rich (MRD 76-51), groups of ten male Swiss Albino mice, Albino Sprague-Dawley rats, and Albino Hartley guinea pigs were exposed to vapour concentrations of 0, 5.39, 18.50 and 47.37 mg/L for six hours (Kapp, 1977). Animals surviving the exposure were monitored for an additional 14 days once exposure has ceased.   At study termination, live animals were sacrificed and all animals, including animals that died prior to study termination, were necropsied. Exposure of the 47.37 mg/L groups was terminated at 76 minutes due to the death of all animals except for one mouse. Two mice, six rats, and five guinea pigs were found dead in the group receiving 18.5 mg/L MRD 76-51. No mortality was observed in the group exposed to 5.39 mg/L test chemical or in the controls. Clinical signs recorded during exposure included agitation, inactivity tremors and convulsions. Necropsy results indicated discolouration in the lungs of three guinea pigs and one mouse and the right kidney of one rat was discoloured in the group receiving 5.39 mg/L test chemical. Guinea pigs in the group receiving 18.5 mg/L test chemical exhibited pale liver and kidneys and dark areas in the lung. Rats that died during exposure had spots on the thymus, darkened areas in the lung and adrenals, discolouration in the heart, pale kidneys, reddened medulla, discoloured liver, and dark spotted cervical lymph nodes and/or salivary glands. Mice exhibited lung discolouration, clot formation on top of the heart, spotted liver and necrotic tissue. Necropsy was not performed on animals exposed to 47.37 mg/L test chemical per sponsor’s request. Based on these results, the inhalation LC50 of alkenes, C7-9-branched, C8-rich in mice is > 18.5 mg/L while in rats it is < 18.5 mg/L and is equal to 18.5 mg/L in guinea pigs.

The acute inhalation toxicity of alkenes, C8-10 branched, C9-rich was investigated by Dorato (1976) using ten male Swiss Webster mice, Sprague-Dawley rats, and Hartley guinea pigs exposed to 28 mg/L vapour for six hours. Six mice, 10 rats, and 10 guinea pigs died during the 6 hour exposure period. Based on the mortality data, it may be inferred that the test material is lethal to mice, rats, and guinea pigs at a concentration of 28 mg/L.

In an acute inhalation study on oct-1-ene, 9 out of 10 young male adult Sprague-Dawley rats died during exposure to 87.5 mg/L test substance for 1 hour (Monrose, 1973). Subsequently, 6 groups of male Sprague-Dawley rats (10/group) were exposed (whole body) to vapour concentrations of 6113, 6833, 7860, 8842, 10,567, and 11,702 parts per million (equivalent to 28.0, 31.1, 36.0, 40.5, 48.4, and 53.6 mg/L) for 4-hours. The LC50 was reported as 8050 parts per million (37 mg/L), with a 95% confidence interval of 6600-9800 parts per million.

In an acute inhalation study on alkenes, C10/C11/C12/C13, rats (number not reported) were exposed 2.1 mg/L vapour (equivalent to 2.2 mg/L) for 4 hours (Blair and Sedgwick, 1980). Lachrymation and salivation were observed during exposure. No other toxic signs were reported during exposure or during the 14 day observation period. No gross pathology or histopathology was conducted and although body weights were taken, the results were not presented. The results indicate that the LC50 was >2.1 mg/L.

Acute dermal toxicity

The acute dermal toxicity of hex-1-ene (Neodene 6) was investigated in groups of New Zealand White rabbits (4 males, 4 females) exposed to undiluted test substance at a dose of 2000 mg/kg bw (Albert et al., 1983). The test substance was applied to abraded skin under occlusion. All animals survived until the end of the study (14-days post treatment). There were no clinical signs of toxicity or effects on body weight. The skin was the only area affected, with minimal irritation noted after the 24 -hour exposure period. This had resolved by day 14, however white crusty material on the skin and fur, alopecia, and abrasions and focal reddened areas were noted at necropsy in treated animals. The acute dermal LD50 for undiluted Neodene 6 alpha olefin was reported as >2000 mg/kg in rabbits. The results of this study indicate that hex-1-ene is not acutely toxic by the dermal exposure route.

The acute dermal toxicity of alkenes, C6-8-branched, C7-rich (MRD-ECH-78-36) was examined by Moreno (1978) using eight New Zealand White rabbits. The test substance was applied at 200 or 3160 mg/kg to abraded skin for 24-hours under occlusion. The animals were observed for 14-days, and dermal responses at the test site recorded using the Draize (1959) method. None of the treated animals died during the course of the study. Clinical signs included lethargy (all animals), respiratory noise in one animal, ataxia in 4 animals, tachypnea in one animal and, yellow nasal discharge in two animals and diarrhea. Body weights gain appeared to be normal. Necropsy findings included white nodules in the liver and mottled kidneys in four animals, red areas in the intestine in two animals, and the nodular adhesions on the left half of the liver, adhered to the abdominal wall and stomach, in one animal. Based on these results, the acute dermal LD50in rabbits is > 3160 mg/kg. Based on these results, it is concluded that alkenes, C6-8-branched, C7-rich are not acutely toxic by the dermal exposure route.

In an acute dermal toxicity study on oct-1-ene (Neodene 8 alpha olefin), groups of New Zealand rabbits (8/sex) were exposed to 2 mL/kg of undiluted test substance for 24 hours under occlusion (Jud et al., 1983). The test site was abraded in four animals per sex and treatment, and intact in the others. The animals were then observed for 14 days. There was no treatment-related lethality, clinical signs of toxicity, changes in body weight, or necropsy findings. The only notable finding was mild to moderate skin irritation following the removal of the wrappings at 24 hours. Mild skin irritation was still present on day 14. Skin irritation was not effected by abrading the skin. The dermal LD50 was determined to be greater than 2.0 mL/kg (equivalent to > 1430 mg/kg using a density of 0.7149 g/cm3 for oct-1 -ene) in male and female rabbits.

The acute dermal toxicity of undiluted alkenes, C11 -15 (Internal Olefin 114 LP11) was investigated in groups of young Wistar rats, 4 male and 4 female, exposed to doses of 1, 2, and 4 mL/kg bw for 24-hours under occlusion (Cassidy and Clark, 1977). Animals then were observed for 9 days. Three males died at the 4.0 mL/kg dose level. The rats that died were noted to not eat or drink thus losing a considerable amount of body weight. No other deaths were reported. The acute percutaneous LD50 of Internal Olefin 114 LP11 in rats was greater than 4 mL/kg (i.e., 3040 mg/kg) in females and between 2 and 4 mL/kg (i.e., 1520 to 3040 mg/kg) in males. Based on these results, it can be concluded that alkenes, C11 -15 are not acutely toxic by the dermal exposure route.

The acute dermal toxicity of C12 -14 alpha olefin has been examined in two studies. In the first investigation (Rinehart, 1967), 0 or 10,000 mg/kg bw test substance was applied for 24-hours to intact and abraded skin from groups of 4 male albino rabbits. No mortality or gross histopathological changes were observed. Signs of pneumonia were observed in both treated and control groups while treated animals exhibited taut, dry and scaly skin with no re-growth of hair in the clipped areas. The acute dermal LD50 for C12-14 Alpha Olefin blend was reported as >10,000 mg/kg bw in male rabbits. In the second study (Monrose and Carter,1973), C12-14 alpha olefin was applied at 10,000 mg/kg bw to intact and abraded skin from four white rabbits (sex not specified) for 24 hours under occlusion. Animals were observed for 14 days post treatment for mortality, body weight changes and clinical signs. Following the 14 day observation period, the animals were sacrificed and subject to gross necropsy. Treated animals showed an average weight loss of 17 grams during the 24 hour exposure period. Average initial weight was regained at the 14 day observation period. One of the treated animals died on the 4thday of the observation period following a weight loss of 64 grams. The authors did not provide an explanation for this death. The reported dermal LD50 for C12-14 alpha olefins was >10,000 mg/kg in rabbits which indicates that it is not acutely toxic by the dermal exposure route.

The acute dermal toxicity of hexadecane was investigated by Kuhne (1993). In this study, five male and female New Zealand White rabbits were clipped free of hair on the dorsal surface of the trunk and treated with 2020 mg/kg (2.37 mL/kg) undiluted test substance under occlusion 24 hours. Body weight gain was not affected by treatment, however, one male that died on day 14 lost weight during the study. There were no signs of dermal irritation during the 14 day observation period, while gross necropsy at study termination revealed no observable abnormalities in most animals. However, the male that died on day 14 of the study revealed mottled lungs with white nodules. None of the other treated animals died during the course of the study. Based on these results, the LD50 for hexadecene in albino rabbits is > 2020 mg/kg (2.37 mL/kg). The results from this study indicate that hexadecene does not cause acute systemic toxicity following a single dermal application to the skin.

In an acute dermal toxicity study on octadecene, five male and female New Zealand White rabbits were clipped free of hair on the dorsal surface of the trunk and the test substance applied at mg/kg bw for 24 hours under occlusion (Kuhn, 1993). Body weight gain was affected by octadecene treatment. Four males and females either lost weight or failed to gain weight between days 7 and 14, however all animals survive to the end of the test. There were no signs of dermal irritation during the 14 day observation period and with the exception of one female with slight diarrhoea on days 9 and 10 clinical observations were unremarkable. Gross necropsy at study termination revealed no observable abnormalities. Based on these results, the LD50 for octadecene in albino rabbits is > 2020 mg/kg (2.35 mL/kg). The results from this study suggest that octadecene does not cause systemic toxicity following a single application to the skin.

The acute dermal toxicity of hydrocarbons C14-30 (Ethyl Compound 100-606) was assessed in three male and three female albino rabbits treated dermally with a single application of 10,000 mg/kg (Springer, 1977). The test chemical was held in contact with the skin under occlusion for 24 hours. Post treatment, the animals were observed for mortality and overt signs of toxicity for 14 days. On day 14, all surviving animals were sacrificed and necropsies were performed. None of the six treated rabbits died during the 14 day observation period. Gross autopsy findings revealed no gross pathological changes in any rabbit and all animals gained weight normally. Based on the lack of mortality, the LD50 was estimated to be > 10,000 mg/kg in both sexes. Based on these results, it is concluded that hydrocarbons C14-30, olefin-rich is not acutely toxic by the dermal exposure route.

Information is available from two acute dermal toxicity studies conducted on alkenes, C20-24. In the first study, groups of young adult Sprague-Dawley rats (5/sex) were dermally exposed to undiluted test substance for 24 hours under semi-occlusion at a limit dose of 2000 mg/kg bw (Driscoll, 1998). There were no treatment related clinical signs, necropsy findings or changes in body weight. The dermal LD50 was determined to be > 2000 mg/kg in males and females. In the second acute dermal toxicity study, groups of 10 (5 male and 5 female) Sprague-Dawley CD strain rats were dermally exposed to ENORDET O241 for 24 hours under semi-occlusion (Sanders, 2008). There were no deaths, signs of systemic toxicity or dermal irritation noted during a 14 day follow-up period, and no gross abnormalities found at necropsy. An increase in body weight was shown over the study period. The dermal LD50 was determined to be > 2000 mg/kg/bw in male and female rats. Based on these results, it can be inferred that alkenes, C20-24 are not acutely toxic by the dermal exposure route.


Justification for selection of acute toxicity – oral endpoint
Acute oral toxicity testing has been conducted on 12 members of this category ranging from C6 to C24-28. The results of these studies demonstrate that higher olefins are not acutely hazardous after ingestion.

Justification for selection of acute toxicity – inhalation endpoint
Acute inhalation toxicity testing has been conducted on 6 members of this category ranging from C6 to C10/C11/c12/C13. The results of these studies demonstrate that higher olefins are not acutely hazardous after inhalation.

Justification for selection of acute toxicity – dermal endpoint
Acute dermal toxicity testing has been conducted on 9 members of this category ranging from C6 to C20-24. The results of these studies demonstrate that higher olefins are not acutely hazardous after skin contact.

Justification for classification or non-classification

Acute toxicity testing has been conducted on 16 members of this category, including 12 acute oral studies (covering C6 – C24-28), 6 acute inhalation studies (covering C6 – C10/C11/C12/C13) and 9 acute dermal studies (covering C6-C20-24). Based on the results obtained, no classification is necessary according to the CLP regulation.