Hydrogen

Toxic Gases & Vapors -> Simple Asphyxiants

Flammable agents - 4th degree

0.071 at -423.4 °F (USCG, 1999) - Less dense than water; will float

0.071 at -423.4 °F (USCG, 1999) - Less dense than water; will float

0.082 g/L

Density: 0.069 (gas) (Air= 1); 0.0700 at BP (liq); 0.0763 at 13 K (solid). One liter of gas at 0 °C weighs 0.08987 g

Physical and Thermodynmic Properties Gaseous Hydrogen[Table#5046]

Physical and Thermodynamic Properties of Solid Hydrogen[Table#5048]

Colorless gas

... hydrogen under ordinary conditions consists of two kinds of molecules, known as ortho- and para-hydrogen, which differ from one another by the spins of their electrons and nuclei. Normal hydrogen at room temperature contains 25% of the para form and 75% of the ortho form. The ortho form cannot be prepared in the pure state

In water, 1.62 mg/L at 21 °C

Soluble in about 50 volumes of water at 0 degC

Very low solubility in most liquids

0.00162 mg/mL at 21 °C

Solubility in water, mg/l at 21 °C: 1.62 (very poor)

-423 °F at 760 mmHg (USCG, 1999)

-423 °F at 760 mmHg (USCG, 1999)

-259.16 °C

-253 °C

-252.8 °C @760 [mm Hg]

-434 °F (USCG, 1999)

-434 °F (USCG, 1999)

-252.762 °C

-259.2 °C

-259 °C

-259.18 °C

Danger

H220: Extremely flammable gas [Danger Flammable gases]

P203, P210, P222, P280, P377, P381, and P403 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.1% (2 of 1422) of reports.

Danger

H220 (99.8%): Extremely flammable gas [Danger Flammable gases]

Chemical: Hydrogen

Regulation (EC) No 1935/2004 (amended)

Hydrogen is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Hydrogen are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Hydrogen: HSNO Approval: HSR001002 Approved with controls

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Flammable Gas

Flammable Gas

Excerpt from ERG Guide 115 [Gases - Flammable (Including Refrigerated Liquids)]:

Behavior in Fire: Burns with an almost invisible flame. (USCG, 1999)

· EXTREMELY FLAMMABLE.

· EXTREMELY FLAMMABLE.

Extremely flammable. Many reactions may cause fire or explosion. Gas/air mixtures are explosive.

Highly dangerous fire and severe explosion hazard when exposed to heat, flame, or oxidizers.

... Sudden release of hydrogen into the atmosphere from storage above 79 bars may cause spontaneous ignition. ...

Excerpt from ERG Guide 115 [Gases - Flammable (Including Refrigerated Liquids)]:

If atmosphere does not contain enough oxygen, inhalation can cause dizziness, unconsciousness, or even death. Contact of liquid with eyes or skin causes freezing similar to burn. (USCG, 1999)

· Vapors may cause dizziness or asphyxiation without warning, especially when in closed or confined areas.

· Vapors may cause dizziness or asphyxiation without warning, especially when in closed or confined areas.

1966 115

1049 115

Reducing Agents, Weak

Reducing Agents, Weak

Excerpt from ERG Guide 115 [Gases - Flammable (Including Refrigerated Liquids)]:

Excerpt from ERG Guide 115 [Gases - Flammable (Including Refrigerated Liquids)]:

Shut off supply; if not possible and no risk to surroundings, let the fire burn itself out. In other cases extinguish with water spray, powder, carbon dioxide. In case of fire: keep cylinder cool by spraying with water. Combat fire from a sheltered position.

Fresh air, rest.

ON FROSTBITE: rinse with plenty of water, do NOT remove clothes. Refer immediately for medical attention.

ON FROSTBITE: rinse with plenty of water. Refer immediately for medical attention.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

Excerpt from ERG Guide 115 [Gases - Flammable (Including Refrigerated Liquids)]:

The only effect of exposure to liquid hydrogen is that caused by its unusually low temperature and its action as a simple asphyxiant.

General First Aid:

General First Aid:

· Wear positive pressure self-contained breathing apparatus (SCBA).

· Wear positive pressure self-contained breathing apparatus (SCBA).

To fight fire, stop flow of gas.

Approach fire with caution as high-temperature flame is practically invisible. Stop flow of gas before extinguishing fire. Use water spray to keep fire-exposed containers cool. Use flooding quantities of water as fog or spray. /Hydrogen, refrigerated liquid/

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. Wear self-contained breathing apparatus for firefighting if necessary. Use water spray to cool unopened containers.

Store in a cool, dry, well-ventilated location. Outside or detached storage is preferred. Isolate from oxygen, halogens, other oxidizing materials. /Hydrogen, refrigerated liquid/

A safe storage method for hydrogen for possible use as automotive fuel involves the use of metal hydrides from which the hydrogen is released at specified temperatures. Iron titanium hydride has been found the most satisfactory.

Keep container tightly closed in a dry and well-ventilated place. Contents under pressure. Storage class (TRGS 510): Gases

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Remove all sources of ignition. Evacuate personnel to safe areas. Beware of vapors accumulating to form explosive concentrations. Vapors can accumulate in low areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Clean up promptly by sweeping or vacuum.

Eliminate all ignition sources. Approach release from upwind. Stop or control the leak, if this can be done without undue risk. Use water spray to disperse vapors and protect personnel. /Hydrogen, refrigerated liquid/

Excerpt from ERG Guide 115 [Gases - Flammable (Including Refrigerated Liquids)]:

Excerpt from ERG Guide 115 [Gases - Flammable (Including Refrigerated Liquids)]:

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Contact a licensed professional waste disposal service to dispose of this material. Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product

Substantial evidence indicates that molecular hydrogen (H2) has beneficial vascular effects because of its antioxidant and/or anti-inflammatory effects. Thus, hydrogen-rich water may prove to be an effective anti-aging drink. This study examined the effects of H2 on endothelial senescence and clarified the mechanisms involved. Hydrogen-rich medium was produced by a high-purity hydrogen gas generator. Human umbilical vein endothelial cells (HUVECs) were incubated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for various time periods in normal or hydrogen-rich medium. The baseline H2concentration in hydrogen-rich medium was 0.55 +/- 0.07 mmol/L. This concentration gradually decreased, and H2 was almost undetectable in medium after 12 hr. At 24 hr after TCDD exposure, HUVECs treated with TCDD exhibited increased 8OHdG and acetyl-p53 expression, decreased nicotinamide adenine dinucleotide (NAD(+))/NADH ratio, impaired Sirt1 activity, and enhanced senescence-associated beta-galactosidase. However, HUVECs incubated in hydrogen-rich medium did not exhibit these TCDD-induced changes accompanying Nrf2 activation, which was observed even after H2 was undetectable in the medium. Chrysin, an inhibitor of Nrf2, abolished the protective effects of H2 on HUVECs. H2 has long-lasting antioxidant and anti-aging effects on vascular endothelial cells through the Nrf2 pathway, even after transient exposure to H2. Hydrogen-rich water may thus be a functional drink that increases longevity. /Hydrogen-rich water/

We observed the effect of hydrogen-rich medium on lipopolysaccharide (LPS)-induced human umbilical vein endothelial cells (HUVECs), hyaline leukocyte conglutination, and permeability of the endothelium. Endotheliocytes were inoculated on 6-well plates and randomly divided into 4 groups: control, H2, LPS, LPS+H2, H2, and LPS+H2 in saturated hydrogen-rich medium. We applied Wright's staining to observe conglutination of hyaline leukocytes and HUVECs, flow cytometry to determine the content of vascular cell adhesion protein 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1), enzyme-linked immunosorbent assay to measure the E-selectin concentration in the cell liquor, the transendothelial electrical resistance (TEER) to test the permeability of endothelial cells, and Western blot and immunofluorescence to test the expression and distribution of vascular endothelial (VE)-cadherin. Compared with control cells, there was an increase in endothelium-hyaline leukocyte conglutination, a reduction in VCAM-1, ICAM-1, and E-selectin, and the TEER value increased obviously. Compared with LPS, there was an obvious reduction in the conglutination of LPS+H2 cells, a reduction in VCAM-1, ICAM-1, and E-selectin levels, and a reduction in the TEER-resistance value, while the expression of VE-cadherin increased. Fluorescence results showed that, compared with control cells, the VE-cadherin in LPS cells was in-complete at the cell joints. Compared with LPS cells, the VE-cadherin in LPS+H2 cells was even and complete at the cell joints. Liquid rich in hydrogen could reduce LPS-induced production of adhesion molecules and endothelium-hyaline leukocyte conglutination, and influence the expression and distribution of VE-cadherin to regulate the permeability of the endothelium. /Hydrogen-rich medium/

Maternal inflammation is associated with spontaneous preterm birth and respiratory impairment among premature infants. Recently, molecular hydrogen (H2) has been reported to have a suppressive effect on oxidative stress and inflammation. The aim of this study was to evaluate the effects of H2 on fetal lung injury caused by maternal inflammation. Cell viability and the production of interleukin-6 (IL-6) and reactive oxygen species (ROS) were examined by treatment with lipopolysaccharide (LPS) contained in ordinal or H2-rich medium (HM) using a human lung epithelial cell line, A549. Pregnant Sprague Dawley rats were divided into three groups: Control, LPS, and HW + LPS groups. Rats were injected with phosphate-buffered saline (Control) or LPS intraperitoneally (LPS) on gestational day 19 and provided H2 water (HW) ad libitum for 24 hr before LPS injection (HW + LPS). Fetal lung samples were collected on day 20, and the levels of apoptosis, oxidative damage, IL-6, and vascular endothelial growth factor (VEGF) were evaluated using immunohistochemistry. The number of apoptotic cells, and levels of ROS and IL-6 were significantly increased by LPS treatment, and repressed following cultured with HM in A549 cells. In the rat models, the population positive for cleaved caspase-3, 8-hydroxy-2'-deoxyguanosine, IL-6, and VEGF was significantly increased in the LPS group compared with that observed in the Control group and significantly decreased in the HW + LPS group. In this study, LPS administration induced apoptosis and oxidative damage in fetal lung cells that was ameliorated by maternal H2 intake. Antenatal H2 administration may decrease the pulmonary mobility associated with inflammation in premature infants. /Hydrogen-rich medium/

An anesthetized rat preparation was used for breathing studies in hyperbaric H2/CO2 atmospheres in which total gaseous pressure was varied in the safe pressure range 8.3-19.1 atm. PCO2 (partial pressure of CO2) was studied at levels of 0.05 and 0.10 atm. The response variables measured were respiration rate, blood pH and an isotonic index of diaphragm twitch amplitude, in the presence of He/O2 gas mixtures used for compression and H2/O2/Co2 saturation gases. The rat preparation can be well maintained in H2/O2 environments at pressures in excess of 8 atm. Elevated PCO2 in these environments can evoke rapid increases in respiration rate and twitch amplitude, without any marked changes in blood pH. Graded increases in PH2 (partial pressure of H2) are able to lower and ultimately abolish the effects of either 0.05 or 0.10 atm levels of CO2 in breathing parameters. The intrinsic ability of hyperbaric H2 to effect a CO2-sparing action on this preparation is greater than that previously seen with hyperbaric Ar or He. The potency sequence for the sparing action by the inert component of the hyperbaric breathing gas is H2 > Ar > He.

For more Interactions (Complete) data for Hydrogen (30 total), please visit the HSDB record page.

IDENTIFICATION AND USE: Hydrogen is a colorless gas. Its many uses include the following: production of ammonia, ethanol, and aniline; hydrocracking, hydroforming, and hydrofining of petroleum; hydrogenation of vegetable oils; hydrogenolysis of coal; reducing agent for organic synthesis and metallic ores; reducing atmosphere to prevent oxidation; as oxyhydrogen flame for high temperatures; atomic-hydrogen welding; instrument-carrying balloons; making hydrogen chloride and hydrogen bromide; production of high-purity metals; fuel for nuclear rocket engines for hypersonic transport; missile fuel; cryogenic research. In addition, hydrogen is a versatile energy carrier that can be used to power nearly every end-use energy need (Fuel cells). Molecular hydrogen (H2) emerged as a novel therapeutic agent, with antioxidant, anti-inflammatory and anti-apoptotic effects demonstrated in plethora of animal disease models and human studies. HUMAN STUDIES: Hydrogen is a simple asphyxiant. Contact with liquid hydrogen will cause frostbite or severe burns of the skin. Hydrogen-rich water has been tested for treating oxidative stress-induced disorders because of its reactive oxygen species scavenging abilities. Hydrogen therapy may be an effective and specific innovative treatment for exercise-induced oxidative stress and sports injury, with potential for the improvement of exercise performance. ANIMAL STUDIES: A large bubble of the gas injected into anterior chamber of rabbit eyes was absorbed within three days and caused no injury. H2 was believed to be inert and nonfunctional in mammalian cells. More recently it was demonstrated that H2 reacts with highly reactive oxidants such as hydroxyl radical and peroxynitrite inside cells. Beneficial effects of molecular hydrogen in animal models were observed especially in oxidative stress-mediated diseases, such as diabetes mellitus, brain stem infarction, rheumatoid arthritis, or neurodegenerative diseases. H2 affects cell signal transduction.

Dizziness. Headache. Lethargy. Suffocation.

ON CONTACT WITH GAS: FROSTBITE.

ON CONTACT WITH GAS: FROSTBITE.

... Hydrogen is the most abundant of all elements in the universe, and it is thought that the heavier elements were, and still are, being built from hydrogen and helium. It has been estimated that hydrogen makes up more than 90% of all the atoms or three quarters of the mass of the universe. It is found in the sun and most stars, and plays an important part in the proton-proton reaction and carbon-nitrogen cycle, which accounts for the energy of the sun and stars. It is thought that hydrogen is a major component of the planet Jupiter and that at some depth in the planet's interior the pressure is so great that solid hydrogen is converted into solid metallic hydrogen.

Occurrence in earth's atmosphere 0.00005% H2.

Hydrogen from natural sources consists of more than 99.8% protium. ...

/SIGNS AND SYMPTOMS/ No specific toxic action. In high concn can act as a simple asphyxiant.

/SIGNS AND SYMPTOMS/ Contact with cryogenic liquid hydrogen will cause frostbite or severe burns of the skin. Simple asphyxiant.

/SIGNS AND SYMPTOMS/ The relation between the /CNS depressant/ effect of nitrogen and that of hydrogen is 1:0.26.

/SIGNS AND SYMPTOMS/ Hydrogen has no known toxic effect on the eye.

For more Human Toxicity Excerpts (Complete) data for Hydrogen (11 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Acute Exposure/ The nuclear protein high-mobility group box 1 (HMGB1) is a key trigger for the inflammatory reaction during liver ischemia reperfusion injury (IRI). Hydrogen treatment was recently associated with down-regulation of the expression of HMGB1 and pro-inflammatory cytokines during sepsis and myocardial IRI, but it is not known whether hydrogen has an effect on HMGB1 in liver IRI. A rat model of 60 minutes 70% partial liver ischemia reperfusion injury was used. Hydrogen enriched saline (2.5, 5 or 10 mL/kg) was injected intraperitoneally 10 minutes before hepatic reperfusion. Liver injury was assessed by serum alanine aminotransferase (ALT) enzyme levels and histological changes. We also measured malondialdehyde (MDA), hydroxynonenal (HNE) and 8-hydroxy-guanosine (8-OH-G) levels as markers of the peroxidation injury induced by reactive oxygen species (ROS). In addition, pro-inflammatory cytokines including TNF-a and IL-6, and high mobility group box B1 protein (HMGB1) were measured as markers of post ischemia-reperfusion inflammation. Hydrogen enriched saline treatment significantly attenuated the severity of liver injury induced by ischemia-reperfusion. The treatment group showed reduced serum ALT activity and markers of lipid peroxidation and post ischemia reperfusion histological changes were reduced. Hydrogen enriched saline treatment inhibited HMGB1 expression and release, reflecting a reduced local and systemic inflammatory response to hepatic ischemia reperfusion. These results suggest that, in our model, hydrogen enriched saline treatment is protective against liver ischemia-reperfusion injury. This effect may be mediated by both the anti-oxidative and anti-inflammatory effects of the solution. /Hydrogen enriched saline/

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Hydrogen has been reported to relieve damage in many disease models, and is a potential additive in drinking water to provide protective effects for patients as several clinical studies revealed. However, the absence of a dose-response relationship in the application of hydrogen is puzzling. We attempted to identify the dose-response relationship of hydrogen in alkaline electrolyzed drinking water through the aspirin induced gastric injury model. In this study, hydrogen-rich alkaline water was obtained by adding H2 to electrolyzed water at one atmosphere pressure. After 2 weeks of drinking, we detected the gastric mucosal damage together with MPO, MDA and 8-OHdG in rat aspirin induced gastric injury model. Hydrogen-dose dependent inhibition was observed in stomach mucosal. Under pH 8.5, 0.07, 0.22 and 0.84 ppm hydrogen exhibited a high correlation with inhibitory effects showed by erosion area, MPO activity and MDA content in the stomach. Gastric histology also demonstrated the inhibition of damage by hydrogen-rich alkaline water. However, 8-OHdG level in serum did not have significant hydrogen-dose dependent effect. pH 9.5 showed higher but not significant inhibitory response compared with pH 8.5. Hydrogen is effective in relieving the gastric injury induced by aspirin-HCl, and the inhibitory effect is dose-dependent. The reason behind this may be that hydrogen-rich water directly interacted with the target tissue, while the hydrogen concentration in blood was buffered by liver glycogen, evoking a suppressed dose-response effect. Drinking hydrogen-rich water may protect healthy individuals from gastric damage caused by oxidative stress. /Hydrogen water/

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The prevalence of sleep apnea is very high in patients with heart failure (HF). The aims of this study were to investigate the influence of intermittent hypoxia (IH) on the failing heart and to evaluate the antioxidant effect of hydrogen gas. Normal male Syrian hamsters (n = 22) and cardiomyopathic (CM) hamsters (n = 33) were exposed to IH (repeated cycles of 1.5 min of 5% oxygen and 5 min of 21% oxygen for 8 hr during the daytime) or normoxia for 14 days. Hydrogen gas (3.05 vol/100 vol) was inhaled by some CM hamsters during hypoxia. IH increased the ratio of early diastolic mitral inflow velocity to mitral annulus velocity (E/e', 21.8 vs. 16.9) but did not affect the LV ejection fraction (EF) in normal Syrian hamsters. However, IH increased E/e' (29.4 vs. 21.5) and significantly decreased the EF (37.2 vs. 47.2%) in CM hamsters. IH also increased the cardiomyocyte cross-sectional area (672 vs. 443 sq um) and interstitial fibrosis (29.9 vs. 9.6%), along with elevation of oxidative stress and superoxide production in the left ventricular (LV) myocardium. Furthermore, IH significantly increased the expression of brain natriuretic peptide, beta-myosin heavy chain, c-fos, and c-jun mRNA in CM hamsters. Hydrogen gas inhalation significantly decreased both oxidative stress and embryonic gene expression, thus preserving cardiac function in CM hamsters. In conclusion, IH accelerated LV remodeling in CM hamsters, at least partly by increasing oxidative stress in the failing heart. These findings might explain the poor prognosis of patients with HF and sleep apnea.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Maternal inflammation is associated with spontaneous preterm birth and respiratory impairment among premature infants. Recently, molecular hydrogen (H2) has been reported to have a suppressive effect on oxidative stress and inflammation. The aim of this study was to evaluate the effects of H2 on fetal lung injury caused by maternal inflammation. Cell viability and the production of interleukin-6 (IL-6) and reactive oxygen species (ROS) were examined by treatment with lipopolysaccharide (LPS) contained in ordinal or H2-rich medium (HM) using a human lung epithelial cell line, A549. Pregnant Sprague Dawley rats were divided into three groups: Control, LPS, and HW + LPS groups. Rats were injected with phosphate-buffered saline (Control) or LPS intraperitoneally (LPS) on gestational day 19 and provided H2 water (HW) ad libitum for 24 hr before LPS injection (HW + LPS). Fetal lung samples were collected on day 20, and the levels of apoptosis, oxidative damage, IL-6, and vascular endothelial growth factor (VEGF) were evaluated using immunohistochemistry. The number of apoptotic cells, and levels of ROS and IL-6 were significantly increased by LPS treatment, and repressed following cultured with HM in A549 cells. In the rat models, the population positive for cleaved caspase-3, 8-hydroxy-2'-deoxyguanosine, IL-6, and VEGF was significantly increased in the LPS group compared with that observed in the Control group and significantly decreased in the HW + LPS group. In this study, LPS administration induced apoptosis and oxidative damage in fetal lung cells that was ameliorated by maternal H2 intake. Antenatal H2 administration may decrease the pulmonary mobility associated with inflammation in premature infants. /Hydrogen-rich medium/

For more Non-Human Toxicity Excerpts (Complete) data for Hydrogen (16 total), please visit the HSDB record page.

According to the 2016 TSCA Inventory Update Reporting data, nn reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of hydrogen in the United States may be as low as <10 workers and as high as <10,000 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Flammable gases/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations as necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Treat frostbite with rapid rewarming ... . /Flammable gases/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Flammable gases/

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Simple asphyxiants and related compounds/

For more Antidote and Emergency Treatment (Complete) data for Hydrogen (6 total), please visit the HSDB record page.

Hydrogen

1

10000

Flammable chemical that can be released at a facility.

Substantial evidence indicates that molecular hydrogen (H2) has beneficial vascular effects because of its antioxidant and/or anti-inflammatory effects. Thus, hydrogen-rich water may prove to be an effective anti-aging drink. This study examined the effects of H2 on endothelial senescence and clarified the mechanisms involved. Hydrogen-rich medium was produced by a high-purity hydrogen gas generator. Human umbilical vein endothelial cells (HUVECs) were incubated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for various time periods in normal or hydrogen-rich medium. The baseline H2concentration in hydrogen-rich medium was 0.55 +/- 0.07 mmol/L. This concentration gradually decreased, and H2 was almost undetectable in medium after 12 hr. At 24 hr after TCDD exposure, HUVECs treated with TCDD exhibited increased 8OHdG and acetyl-p53 expression, decreased nicotinamide adenine dinucleotide (NAD(+))/NADH ratio, impaired Sirt1 activity, and enhanced senescence-associated beta-galactosidase. However, HUVECs incubated in hydrogen-rich medium did not exhibit these TCDD-induced changes accompanying Nrf2 activation, which was observed even after H2 was undetectable in the medium. Chrysin, an inhibitor of Nrf2, abolished the protective effects of H2 on HUVECs. H2 has long-lasting antioxidant and anti-aging effects on vascular endothelial cells through the Nrf2 pathway, even after transient exposure to H2. Hydrogen-rich water may thus be a functional drink that increases longevity. /Hydrogen-rich water/

Amyloid beta (Abeta) peptides are identified /as a/ cause of neurodegenerative diseases such as Alzheimer's disease (AD). Previous evidence suggests Abeta-induced neurotoxicity is linked to the stimulation of reactive oxygen species (ROS) production. The accumulation of Abeta-induced ROS leads to increased mitochondrial dysfunction and triggers apoptotic cell death. This suggests antioxidant therapies may be beneficial for preventing ROS-related diseases such as AD. Recently, hydrogen-rich water (HRW) has been proven effective in treating oxidative stress-induced disorders because of its ROS-scavenging abilities. However, the precise molecular mechanisms whereby HRW prevents neuronal death are still unclear. In the present study, we evaluated the putative pathways by which HRW protects against Abeta-induced cytotoxicity /in SK-N-MC cells/. Our results indicated that HRW directly counteracts oxidative damage by neutralizing excessive ROS, leading to the alleviation of Abeta-induced cell death. In addition, HRW also stimulated AMP-activated protein kinase (AMPK) in a sirtuin 1 (Sirt1)-dependent pathway, which upregulates forkhead box protein O3a (FoxO3a) downstream antioxidant response and diminishes Abeta-induced mitochondrial potential loss and oxidative stress. Taken together, our findings suggest that HRW may have potential therapeutic value to inhibit Abeta-induced neurotoxicity. /Hydrogen-rich water/

The NLRP3 inflammasome, an intracellular multi-protein complex controlling the maturation of cytokine interleukin-1beta, plays an important role in lipopolysaccharide (LPS)-induced inflammatory cascades. Recently, the production of mitochondrial reactive oxygen species (mtROS) in macrophages stimulated with LPS has been suggested to act as a trigger during the process of NLRP3 inflammasome activation that can be blocked by some mitochondria-targeted antioxidants. Known as a ROS scavenger, molecular hydrogen (H2) has been shown to possess therapeutic benefit on LPS-induced inflammatory damage in many animal experiments. Due to the unique molecular structure, H2 can easily target the mitochondria, suggesting that H2 is a potential antagonist of mtROS-dependent NLRP3 inflammasome activation. Here we have showed that, in mouse macrophages, H2 exhibited substantial inhibitory activity against LPS-initiated NLRP3 inflammasome activation by scavenging mtROS. Moreover, the elimination of mtROS by H2 resultantly inhibited mtROS-mediated NLRP3 deubiquitination, a non-transcriptional priming signal of NLRP3 in response to the stimulation of LPS. Additionally, the removal of mtROS by H2 reduced the generation of oxidized mitochondrial DNA and consequently decreased its binding to NLRP3, thereby inhibiting the NLRP3 inflammasome activation. Our findings have, for the first time, revealed the novel mechanism underlying the inhibitory effect of molecular hydrogen on LPS-caused NLRP3 inflammasome activation, highlighting the promising application of this new antioxidant in the treatment of LPS-associated inflammatory pathological damage.

... H2 decreased the tyrosine nitration level and suppressed oxidative stress damage in retinal cells. S-nitroso-N-acetylpenicillamine treatment decreased the cell numbers in the ganglion cell layer and inner nuclear layer, but the presence of H2 inhibited this reduction. These findings suggest that H2 has a neuroprotective effect against retinal cell oxidative damage, presumably by scavenging peroxynitrite. H2 reduces cellular peroxynitrite, a highly toxic reactive nitrogen species. Thus, H2 may be an effective and novel clinical tool for treating glaucoma and other oxidative stress-related diseases.

Endothelial injury is a primary cause of sepsis and sepsis-induced organ damage. Heme oxygenase-1 (HO-1) plays an essential role in endothelial cellular defenses against inflammation by activating nuclear factor E2-related factor-2 (Nrf2). We found that molecular hydrogen (H2) exerts an anti-inflammatory effect. Here, we hypothesized that H2 attenuates endothelial injury and inflammation via an Nrf2-mediated HO-1 pathway during sepsis. First, we detected the effects of H2 on cell viability and cell apoptosis in human umbilical vein endothelial cells (HUVECs) stimulated by LPS. Then, we measured cell adhesion molecules and inflammatory factors in HUVECs stimulated by LPS and in a cecal ligation and puncture (CLP)-induced sepsis mouse model. Next, the role of Nrf2/HO-1 was investigated in activated HUVECs, as well as in wild-type and Nrf(-/-) mice with sepsis. We found that both 0.3 mmol/L and 0.6 mmol/L (i.e., saturated) H2-rich media improved cell viability and cell apoptosis in LPS-activated HUVECs and that 0.6 mmol/L (i.e., saturated) H2-rich medium exerted an optimal effect. H2 could suppress the release of cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1), and pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-a, interleukin (IL)-1beta and high-mobility group box 1 protein (HMGB1). Furthermore, H2 could elevate anti-inflammatory cytokine IL-10 levels in LPS-stimulated HUVECs and in lung tissue from CLP mice. H2 enhanced HO-1 expression and activity in vitro and in vivo. HO-1 inhibition reversed the regulatory effects of H2 on cell adhesion molecules and inflammatory factors. H2 regulated endothelial injury and the inflammatory response via Nrf2-mediated HO-1 levels. These results suggest that H2 could suppress excessive inflammatory responses and endothelial injury via an Nrf2/HO-1 pathway. /Hydrogen-rich media/

The ability of mammalian tissues to oxidize hydrogen under conditions similar to those encountered by deep divers breathing mixtures containing hydrogen was investigated. The kidneys, livers, spleen, heart, lungs, and quadriceps muscle were removed from guinea-pigs and rats. After mincing or homogenization, the tissues, along with myocytes prepared from rat hearts and porcine cerebral cortex capillary endothelial cells were placed in petri dishes and exposed to tritium tagged hydrogen at a pressure of 1 or 5 megapascals (MPa) for 1 hour in a specially designed exposure system. Helium at a pressure of 1 MPa was used as a carrier. Petri dishes filled with distilled water or saline served as negative controls. After decompression, the extent of hydrogen oxidized by the mammalian tissues and cells was determined by measuring the amounts of incorporated tritium by liquid scintillation counting. The tissues and cells incorporated tritium only at the rate of 10 to 50 nanomoles per gram per minute (nmol/g/min), rates that were similar to those of the negative controls. The authors conclude that mammalian tissues do not oxidize hydrogen under hyperbaric conditions. The small amounts of tritium label incorporation observed in the tissues is probably due to radioisotope phenomena, which sets the detection limit for determining hydrogen oxidation at 100 nmol/g/min.

Molecular hydrogen (H2) is an agent with potential applications in oxidative stress-related and/or inflammatory disorders. H2 is usually administered by inhaling H2-containing air (HCA) or by oral intake of H2-rich water (HRW). Despite mounting evidence, the molecular mechanism underlying the therapeutic effects and the optimal method of H2 administration remain unclear. Here, we investigated whether H2 affects signaling pathways and gene expression in a dosage- or dose regimen-dependent manner. We first examined the H2 concentrations in blood and organs after its administration and found that oral intake of HRW rapidly but transiently increased H2 concentrations in the liver and atrial blood, while H2 concentrations in arterial blood and the kidney were one-tenth of those in the liver and atrial blood. In contrast, inhalation of HCA increased H2 equally in both atrial and arterial blood ...

Hydrogen exerts beneficial effects in disease animal models of ischemia-reperfusion injury as well as inflammatory and neurological disease. Additionally, molecular hydrogen is useful for various novel medical and therapeutic applications in the clinical setting. In the present study, the hydrogen concentration in rat blood and tissue was estimated. Wistar rats were orally administered hydrogen super-rich water (HSRW), intraperitoneal and intravenous administration of hydrogen super-rich saline (HSRS), and inhalation of hydrogen gas. A new method for determining the hydrogen concentration was then applied using ... sensor gas chromatography, after which the specimen was prepared via tissue homogenization in airtight tubes. This method allowed for the sensitive and stable determination of the hydrogen concentration. The hydrogen concentration reached a peak at 5 minutes after oral and intraperitoneal administration, compared to 1 minute after intravenous administration. Following inhalation of hydrogen gas, the hydrogen concentration was found to be significantly increased at 30 minutes and maintained the same level thereafter. These results demonstrate that accurately determining the hydrogen concentration in rat blood and organ tissue is very useful and important for the application of various novel medical and therapeutic therapies using molecular hydrogen. /Hydrogen super-rich water or saline/

Used in welding (oxy-hydrogen and autogenous), petroleum refining, and as a coolant; Used to hydrogenate oils and other organic compounds and to reduce metal oxides; [Merck Index]

Petroleum Production and Refining [Category: Industry]

In oxy-hydrogen blowpipe (welding) and limelight; autogenous welding of steel and other metals; manufacturing ammonia, synthetic methanol, HCl, NH3; hydrogenation of oils, fats, naphthalene, phenol; in balloons and airships; in metallurgy to reduce oxides to metals; in petroleum refining; in thermonuclear reactions (ionizes to form protons, deuterons (D) or tritons (T).

In bubble chambers to study subatomic particles; as a coolant. /Liquid hydrogen/

In cryogenics; in study of superconductivity /Liquid hydrogen/

Production of ammonia, ethanol, and aniline; hydrocracking, hydroforming, and hydrofining of petroleum; hydrogenation of vegetable oils; hydrogenolysis of coal; reducing agent for organic synthesis and metallic ores; reducing atmosphere to prevent oxidation; as oxyhdrogen flame for high temperatures; atomic-hydrogen welding; instrument-carrying balloons; making hydrogen chloride and hydrogen bromide; production of high-purity metals; fuel for nuclear rocket engines for hypersonic transport; missile fuel; cryogenic research.

(1977) 5.91X10+8 CU FT

(1979) 1.27X10+8 CU FT

2023: 20,000,000,000 - <25,000,000,000 lb

(1977) 8.48X10+10 CU FT

(1979) 9.93X10+10 CU FT

Daily Capacity: 4,197,260 thousands of cu ft

U.S. ... about 3 billion cu ft/yr

For more U.S. Production (Complete) data for Hydrogen (6 total), please visit the HSDB record page.

CHEMICAL INTERMEDIATE FOR AMMONIA, 56%; PETROLEUM REFINING, 25%; CHEMICAL INTERMEDIATE FOR METHANOL, 7%; OTHER, 12% (1980)

U.S. consumption of hydrogen in 1988: 49% as chemical intermediate for ammonia; 37% in petroleum refining; 8% as chemical intermediate for methanol; 6% as other uses

The main commercial processes for the on-purpose production of hydrogen are steam reforming, partial oxidation (coal, coke, resid), or electrolysis of water. Hydrogen is also commercially produced as a by-product of chemical processes (ethylene crackers, styrene, MTBE etc) or gasoline manufacturing (catalytic reforming).

Obtained by passing water vapors over heated iron; by electrolysis of water or by action of hydrochloric acid or sulfuric acid on iron or zinc; by hydrolysis of metal hydrides.

(1) Reaction of steam with natural gas (steam reforming) and susequent purification; (2) partial oxidation of hydrocarbons to carbon monoxide and interaction of carbon monoxide and steam; (3) gasification of coal; (4) dissociation of ammonia; (5) thermal or catalytic decomposition of hydrocarbons gases; (6) catalytic reforming of naphtha; (7) reaction of iron and steam; (8) catalytic reaction of methanol and steam; (9) electrolysis of water.

Hydrogen can be produced using diverse, domestic resources including fossil fuels, such as natural gas and coal (preferentially with carbon capture, utilization, and storage); biomass grown from renewable, non-food crops; or using nuclear energy and renewable energy sources, such as wind, solar, geothermal, and hydroelectric power to split water. This diversity of potential supply sources is an important reason why hydrogen is such a promising energy carrier.

Hydrogen is produced on a laboratory scale from the action of an aqueous acid on a metal or from the reaction of an alkali metal in water ... These reactions can be carried out at room temperature. Hydrogen gas can also be produced on a laboratory scale by the electrolysis of an aqueous solution. Production of hydrogen through electrolysis is also used industrially. ... Hydrogen atoms can be produced in significant quantities in the gas phase by the action of radiation on or by extreme heating of H2 (3000 K).

All Other Basic Inorganic Chemical Manufacturing

Hydrogen: ACTIVE

Production of hydrogen in usa alone now amounts to about 3 billion cu ft/yr.

Method of purification: by scrubbing with various solutions (especially the Girbitol absorption process). For very pure hydrogen, by diffusion through palladium.

More efficient methods than electrolysis for obtaining hydrogen from water are under investigation. One of these is thermochemical decomposition. Another is photochemical decomposition by solar radiation, either directly or via a solar power generator. Photolytic decomposition of water with platinum catalyst has been achieved. Hydrogen can also be obtained by photolytic decomposition of hydrogen sulfide with cadmium sulfide catalyst.

Most U.S. hydrogen production ... is used captively.