Moderate ethanol consumption reduces stress and increases feelings of happiness and well-being, and may reduce the risk of coronary heart disease. Heavy consumption of alcohol, however, may cause addiction and increases all types of injury and trauma.
Environmental and genetic factors are involved in susceptibility to alcoholism. Ethanol can lead to malnutrition and can exert a direct toxicological effect due to its interference with hepatic metabolism and immunological functions. A causal effect has been observed between alcohol and various cancers. Cessation of alcohol consumption and balanced nutrition are recommended primary nonspecific therapeutic measures for alcoholics. Drug therapies for alcoholics suffering from liver injury have resulted in mixed results. In end-stage liver disease, liver transplantation may be considered.
The deleterious effects of ethanol on a variety of tissues may result largely from altered ion permeabilities and transport. Clinically relevant ethanol concentrations in blood increase the sodium permeability of the plasma membrane and depress active sodium transport by suppressing Na, K-ATPase activity. As a result, intracellular sodium concentration increases. The total tissue content of calcium increases. Important transport mechanisms deranged by ethanol probably include those regulating calcium-sodium and hydrogen-sodium exchange at the plasma membrane and calcium uptake by the sarcoplasmic reticulum. A modest decline in magnesium content of muscle occurs after chronic exposure to ethanol. This also has been associated with accumulation of calcium.
Unlike gasoline, pure ethanol is non-toxic and biodegradable, and it quickly breaks down into harmless substances if spilled. Chemical denaturants are added to ethanol to make fuel ethanol, and many of the denaturants are toxic. Similar to gasoline, ethanol is a highly flammable liquid and must be transported carefully.
Ethanol and ethanol-gasoline mixtures burn cleaner and have higher octane levels than pure gasoline, but they also have higher evaporative emissions from fuel tanks and dispensing equipment. These evaporative emissions contribute to the formation of harmful, ground-level ozone and smog. Gasoline requires extra processing to reduce evaporative emissions before blending with ethanol.
Producing and burning ethanol results in emissions of carbon dioxide (CO2), a greenhouse gas. However, the combustion of ethanol made from biomass (such as corn and sugarcane) is considered atmospheric carbon-neutral because as the biomass grows, it absorbs CO2, which may offset the CO2 produced when the ethanol is burned. Some ethanol producers burn coal and natural gas for heat sources in the fermentation process to make fuel ethanol, while some burn corn stocks or sugar cane stocks.
" />Moderate ethanol consumption reduces stress and increases feelings of happiness and well-being, and may reduce the risk of coronary heart disease. Heavy consumption of alcohol, however, may cause addiction and increases all types of injury and trauma.
Environmental and genetic factors are involved in susceptibility to alcoholism. Ethanol can lead to malnutrition and can exert a direct toxicological effect due to its interference with hepatic metabolism and immunological functions. A causal effect has been observed between alcohol and various cancers. Cessation of alcohol consumption and balanced nutrition are recommended primary nonspecific therapeutic measures for alcoholics. Drug therapies for alcoholics suffering from liver injury have resulted in mixed results. In end-stage liver disease, liver transplantation may be considered.
The deleterious effects of ethanol on a variety of tissues may result largely from altered ion permeabilities and transport. Clinically relevant ethanol concentrations in blood increase the sodium permeability of the plasma membrane and depress active sodium transport by suppressing Na, K-ATPase activity. As a result, intracellular sodium concentration increases. The total tissue content of calcium increases. Important transport mechanisms deranged by ethanol probably include those regulating calcium-sodium and hydrogen-sodium exchange at the plasma membrane and calcium uptake by the sarcoplasmic reticulum. A modest decline in magnesium content of muscle occurs after chronic exposure to ethanol. This also has been associated with accumulation of calcium.
Unlike gasoline, pure ethanol is non-toxic and biodegradable, and it quickly breaks down into harmless substances if spilled. Chemical denaturants are added to ethanol to make fuel ethanol, and many of the denaturants are toxic. Similar to gasoline, ethanol is a highly flammable liquid and must be transported carefully.
Ethanol and ethanol-gasoline mixtures burn cleaner and have higher octane levels than pure gasoline, but they also have higher evaporative emissions from fuel tanks and dispensing equipment. These evaporative emissions contribute to the formation of harmful, ground-level ozone and smog. Gasoline requires extra processing to reduce evaporative emissions before blending with ethanol.
Producing and burning ethanol results in emissions of carbon dioxide (CO2), a greenhouse gas. However, the combustion of ethanol made from biomass (such as corn and sugarcane) is considered atmospheric carbon-neutral because as the biomass grows, it absorbs CO2, which may offset the CO2 produced when the ethanol is burned. Some ethanol producers burn coal and natural gas for heat sources in the fermentation process to make fuel ethanol, while some burn corn stocks or sugar cane stocks.
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