Hexane, OXFORD, n-Hexane,  110-54-3, 92112-69-1

Hexane, OXFORD, n-Hexane, MARQUIS TEST KIT,  110-54-3, 92112-69-1

Hexane

CAS: 110-54-3;92112-69-1

Molecular Formula: C6H14

Names and Identifiers

Physico-chemical Properties

Risk and Safety

Upstream Downstream Industry

Reference Information

Substance toxicity

Isomer

There are five isomers of hexane.

• n-hexane
• 2-methylpentane
• 3-methylpentane
• 2,2-dimethylbutane
• 2,3-dimethylbutane

Its linear compound Is n-hexane CH3(CH2)4CH3.

Oxidation reaction and substitution reaction

oxidation

hexane is extremely flammable and its vapor forms an explosive mixture with air. It is highly flammable and explosive when exposed to open flame and high heat. A strong reaction occurs in contact with the oxidant and even causes combustion. In a fire scene, a heated container is at risk of explosion. Its vapor is heavier than air, and it can diffuse to a fairly far place at a lower point, and it will lead back to ignition in the event of an open flame. The products of combustion are carbon dioxide, water, and carbon monoxide (carbon monoxide is produced during incomplete combustion).

The chemical equation for complete combustion of hexane is: 2C6H14 19O2=12CO2 14H2O (condition ignition)

substitution reaction

like other alkanes, hexane can also undergo substitution reaction with halogen (F, Cl, Br, I), and there are many kinds of Substituted compounds. Therefore, hexane must be stored away from halogens (e. G., fluorine, chlorine, bromine, iodine).

Quality Index analysis

1. The platinum-Cobalt stock solution for color development (see No.1 of GT-11-1) is 500 to, and this solution (No.10) is used to compare with sample in Nessler's colorimetric tube, the sample should not be deeper than the control solution.

2. Heavy metal a sample of 25ml (about 20g) was evaporated to dryness on a steam bath, cooled, added with 2ml of hydrochloric acid and evaporated to dryness on a steam bath. Add a drop of hydrochloric acid wet, add 10ml of hot water, hydrolysis for 2min, cooling, water volume to 25ml, as a sample solution, according to the GT-16 method.

3. Non-volatile residue a sample of 125ml (about 100g) was taken. In a constant weight evaporation dish, it was evaporated to dryness on a steam bath. The residue was dried at 105 °c for 30min, cooled and weighed.

Limited amount

maximum allowable residue (mg/kg)

The Spice oleoresin was 25, and the hop extract was 2.2. Cocoa butter 5(FAO/WHO,1994).

maximum allowable amount of food additive

generally should be made before the final product out, with the exception of the provisions of the residues in food

Nature

colorless volatile liquid. Insoluble in water, soluble in ethanol, soluble in ether, chloroform, ketones and other organic solvents.

Preparation Method

The raffinate oil (containing 11% to 13% of hexane) of the platinum reformer was separated. The raffinate oil is fractionated and separated to remove light components and recombine to obtain a fraction containing 60%-80% of n-hexane. The double column continuous distillation is adopted, and then the catalyst is hydrogenated to remove benzene and other unsaturated hydrocarbons, and qualified n-hexane is obtained.

Use

It is mainly used as a solvent, such as propylene polymerization solvent, rubber and coating solvent, pigment diluent. For soybean, rice bran, cottonseed and other edible oils and spices in the extraction of oils and fats. High-octane fuel.

Safety

mice inhaled 4H LCsa:48000 x 10-6; Rats oral LD50: 32. N-hexane is low toxic, but its toxicity is greater than that of octyl hexane, and it has high volatility, high fat solubility, and accumulation. The toxic effect is a mild inhibitory effect on the central nervous system and a stimulating effect on the skin and mucosa. Splash into the eye can cause symptoms of conjunctival irritation. Long-term exposure can lead to multiple peripheral neuropathy. Staff should be protected. If the skin and eyes are touched, they should be immediately rinsed with plenty of flowing water.

Introduction

hexane, chemical formula C6H14, is the sixth member of alkanes.

hexane is a commonly used non-polar organic solvent with a gasoline odor, and is widely used in chromatography.

n-hexane as a good organic solvent, is widely used in chemical organic synthesis, mechanical equipment surface cleaning decontamination and other links. But it has a certain degree of toxicity, through the respiratory tract, skin and other ways to enter the human body, long-term contact can lead to the human body Head Pain, dizziness, Fatigue, limb numbness and other symptoms of chronic poisoning, severe can lead to fainting, loss of consciousness, and even death.

Relevant academic research

chronic peripheral neurotoxicity

to study the time course change characteristics of n-hexane peripheral neurotoxicity, to verify the feasibility of exposure markers through occupation Epidemiologic Study, and to find and explore the biomarkers of early neurotoxicity.

① nine patients with n-hexane poisoning in an electronic enterprise in 2009 were investigated, the occupational history of the patients was collected, and the exposure to poison was identified, the patients were examined by nerve specialist examination and regular nerve electromyography, and the characteristics of nerve electromyography in patients with poisoning were analyzed. (7) taking all workers exposed to n-hexane in a furniture factory in Minhang district as the subjects of the survey, conducting a questionnaire survey and collecting the workers' urine samples, sampling the air in the workshop, the concentration of n-hexane in air and 2, 5-hexanedione (2,5-HD) in urine were measured by gas chromatography to evaluate the exposure level, and the effects of occupational exposure to n-hexane on health were analyzed. ③ rats were given subchronic oral n-hexane at doses of (0, 104mg/kg/d, 417mg/kg/d, 1667mg/kg/d, peripheral nerve injury was verified by specific symptoms and pathological examination, and the amplitude, latency and latency of caudal nerve sensory and motor potential of rats were measured dynamically at multiple time points during exposure by nerve electrophysiology method, several electrophysiological indexes, such as nerve conduction velocity, were compared with the time course change sequence and trend of each index. At the same time, the serum levels of myelin basic protein (MBP), neuron specific alkylase (NSE), nerve growth factor (NGF) and neurofilament protein (NF) were detected. Levels of these several possible early effector biomarkers.

Results: ① the investigation of 9 patients with n-hexane poisoning showed that the Achilles tendon reflex, knee reflex, radial membrane reflex and biceps brachii reflex were weakened or disappeared in the neurological examination, nerve electrophysiological examination showed that the muscle spontaneous generation increased, the phase of contraction was abnormal, the amplitude decreased, the motor unit time was prolonged, the nerve conduction velocity decreased p0.01), the distal latency was prolonged p0.01), the amplitude decreased p0.05. After the nutritional nerve symptomatic treatment supplemented by exercise treatment, 9 patients were improved (p0.05). ② the air concentration range of N-hexane TWA in this furniture factory in Minhang district of Shanghai is 1.8-9.9mg/m3. 206 workers were investigated, and 95.15% of the respondents provided urine samples, the arithmetic mean of urinary HD concentration in workers was 0.50 μg/ml, and the geometric mean was 0.33 μg/ml, there was a certain correlation between HD concentration in urine and air hexane TWA concentration (correlation coefficient 0.174 P = 0.015); there was a certain degree of correlation between the concentration of HD in urine and the total exposure to n-hexane (correlation coefficient 0.280, P = 0.000). There was a correlation between the subjective symptoms of workers and the total exposure to n-hexane (correlation coefficient 0.159,P = 0.045). ③ 18 weeks after the rats were exposed to n-hexane, the hind limbs of the rats in the 1667mg/kg · d dose group were paralyzed, the paralysis rate was 81.2%, the body weight was significantly reduced, and the typical symptoms of peripheral nerve poisoning occurred, pathological changes showed thinning of nerve atrophy, thinning of axons, enlargement of gaps, demyelination and demyelination. Nerve conduction velocity examination showed that the latency of the distal end of the sensory nerve was prolonged by 78.78%,P0.05, the conduction velocity decreased by 64.26%,P0.05, the amplitude decreased, and the indexes changed significantly at 4 weeks. The latency of motor nerve was prolonged by 264.02%, p0.05, conduction velocity decreased by 51.95%,P0.05, amplitude decreased by 62.86%, and the indicators changed significantly after 2 weeks. Several possible early effect biomarkers in serum showed that the content of NSE and NF in rat serum increased, P0.05, the maximum increase was 122.94% and 193.35% respectively. The level of MBP in rat serum was unknown. Significant change, P0.05, serum NGF level decreased at individual time points, p0.05.

Conclusion:

(1) in the case of chronic hexane poisoning, the nerve myoelectricity [electrogram shows that the peripheral nerve of the extremities is damaged, the lower limbs are more serious than the upper limbs, and the motor nerves are more likely to be damaged than the sensory nerves, but the recovery after treatment was better. The condition will continue to worsen within a few months after loss of contact. The changes of nerve electromyography are not completely parallel with the clinical evolution of the disease. The improvement of clinical symptoms precedes the changes of nerve electromyography, in the assessment of the degree of recovery of patients with n-hexane poisoning, even if the clinical manifestations are improved, the performance of nerve electromyography should be paid attention. The treatment of n-hexane poisoning is based on neurotrophic drug therapy, and the prognosis is good.

② workers in furniture factories surveyed in Minhang district of Shanghai were exposed to lower concentrations of n-hexane, among which workers in the glue spraying workshop had the highest exposure concentration, resulting in a corresponding increase in urinary 2,5-HD levels, at this point to Strengthen occupational protection is expected to have a better effect. Under the current exposure limits, the health of workers can be protected.

③ n-hexane on rat peripheral nerve injury caused by obvious toxicity, motor nerve injury earlier than the sensory nerve is more obvious, the nerve electrophysiological indicators of abnormal changes earlier than the actual symptoms, and it has a good correlation with neurobehavioral symptoms, in which peripheral nerve conduction velocity and distal latency are more sensitive. The sensitivity of serum NSE and NF was the highest, the concentration increased earlier than the animal symptoms, and the change range was large, which could be used as the sign of n-hexane toxic effect, the significance of serum MBP as a sign of n-hexane toxicity still needs to be further confirmed.

induced Peripheral nerve injury

to investigate the effect of increased CYP2E1 activity on n-hexane-induced peripheral nerve injury. Methods adult male SD rats were randomly divided into control group, ethanol group, n-hexane group and ethanol + n-hexane group. Rats in the control group were orally given corn oil; Rats in the ethanol control group were first fed with 30% ethanol for 7 days, and the drinking water contained 4% ethanol; Rats in the N-hexane group were fed with n-hexane, the dose was 1500 mg/kg; Ethanol + n-hexane rats combined with ethanol group and N-hexane group treatment, a total of 16 weeks. After the experiment, liver CYP2E1 enzyme activity detection; Sensory and motor function test; Gait score; Motor nerve conduction velocity measurement; Determination of mitochondrial complex enzyme activity in the spinal cord and sciatic nerve, electron microscopic observation of sciatic nerve. Results after oral administration of human ethanol, the activity of CYP2E1 in liver increased by 42.3%, and the activity of CYP2E1 in n-hexane group and ethanol + n-hexane group also increased by 58.2% and 100.9%, respectively.

The residence time of n-hexane group and ethanol + n-hexane group was longer than that of the control group, but there was no difference between the two groups. The distance between the hind toes of ethanol + n-hexane rats was higher than that of N-hexane group and control group. Compared with the control group and N-hexane group, the conduction velocity and amplitude of tibial nerve in ethanol + n-hexane group decreased. Electron microscopy showed partial release of myelin lamina of sciatic nerve in n-hexane group, vacuolization and balloon change of myelin lamina of nerve in n-hexane + ethanol group. The activity of compound enzyme Ⅰ, Ⅲ and Ⅳ increased after N-hexane exposure in the spinal cord tissue of experimental rats, while the compound enzyme Ⅰ, Ⅲ and Ⅳ of ethanol + n-hexane group decreased to the control level, compared with n-hexane group, the activity of compound enzyme II in n-hexane group was significantly decreased, and the activity of compound enzyme II in ethanol + n-hexane group was lower than that in n-hexane group. The activities of mitochondrial complex enzyme Ⅰ and complex enzyme Ⅱ in n-hexane group increased, but the activities of these two complex enzymes decreased after ethanol induction, and the difference was statistically significant compared with n-hexane group. Conclusion the activity of CYP2E1 in the liver is increased after ethanol induction. Ethanol-induced injection of n-hexane can aggravate the peripheral nerve injury caused by n-hexane, accompanied by changes in the activity of mitochondrial ATPase and mitochondrial complex enzyme.