Ethanol mortality

A number of investigators have found a consistent relationship between mortality from esophageal cancer and ethanol consumption (3-5). These observations have been supported by case-control studies (6-8) which have shown strong correlations between alcohol consumption and esophageal cancer but without consistent association with any specific type of beverage (9,10). ... 

Jacobson MZ (2007) Effects of ethanol (E85) versus gasoline vehicles on cancer and mortality in the United States. Environ Sci Technol. doi 10.1021/es062085v Jacobson MZ, Lu R, Turco RP, Toon OB (1996) Development and application of a new air pollution modelling system. Part I Gas-phase simulations. Atmos Environ 30B 1939-1963 Jacobson MZ, Seinfeld JH (2004) Evolution of nanoparticle size and mixing state near the point of emission. Atmos Environ 38 1839-1850... 

Bioactivity-guided fractionation of the ethanolic extract of the Patagonian starfish Anasterias minuta using the brine shrimp (Artemia salina L.) larvae mortality assay led us to the isolation of three sulfated... 

Phenformin is the only biguanide to have been marketed in the United States and removed from the market by the US Food and Drug Administration (FDA) in 1977 because of its association with the development of lactic acidosis, a metabolic aberration that results in mortality in 50-75% of cases. Ethanol intake before the administration of phenformin therapeutic doses or excessive dose appears to predispose the patient to the development of lactic acidosis with a serious outcome. Phenformin and its other relative biguanides are still sold in European and other countries worldwide. 

Lactic acidosis occurs in two clinical settings (1) type A (hypoxic), associated with decreased tissue oxygenation, such as shock, hypovolemia, and left ventricular failure and (2) type B (metabolic), associated with disease (e.g., diabetes melUtus, neoplasia, liver disease), drugs and/or toxins (e.g., ethanol, methanol, and salicylates), or inborn errors of metabolism (e.g., methylmalonic aciduria, propionic acidemia, and fatty acid oxidation defects). Lactic acidosis is not uncommon and occurs in approximately 1% of hospital admissions. It has a mortality rate greater than 60%, which approaches 100% if hypotension is also present. Type A is much more common. 

Alcoholism affects about 10% of the drinking population and alcohol (ethanol) abuse has been implicated in at least 20% of admissions to general hospitals. This chronic disease exhibits high mortality due to a wide variety of factors. Ethanol produces effects in virtually every organ system. The biochemical effects of ethanol are due to increased production of NADH that decreases the [NAD ]/[NADH] ratio in the cytoplasm of liver cells at least tenfold from the normal value of about 1000. Increased production of lactate and inhibition of gluconeo-genesis (Chapter 15) result. The hyperuricemia associated with ethanol consumption has been attributed to accelerated turnover of adenine nucleotides and their catabolism to uric acid (Chapter 27). Alcohol increases hepatic fatty acid and triacylglycerol synthesis and mobilization of fat from adipose tissue, which can lead to fatty liver, hepatitis, and cirrhosis. These effects are complicated by a deficiency of B vitamins and protein. 

Patients with alcoholic CP usually present with an initial acute attack followed by successive attacks that are slower to resolve. Continued alcohol use leads to chronic abdominal pain and progressive exocrine and endocrine insufficiency. In about 50% of patients, the pain diminishes 5 to 10 years after the onset of symptoms. Steatorrhea, calcification, and diabetes usually develop after 10 to 20 years of heavy ethanol ingestion. Most patients present with varying degrees of pain, malnutrition, and glucose intolerance. The mortality rate of CP is approximately 50% within 20 to 25 years of the diagnosis. About 15% to 20% actually die of complications associated with acute attacks. Most deaths occur as a consequence of malnutrition, infection, or ethanol, narcotic, and tobacco nse. The clinical course of idiopathic CP is more favorable than that of alcoholic pancreatitis. ... 

Certain substances have been reported to potentiate the toxicity of paraquat. These include transition metal ions such as copper (Kohen and Chevion 1985) and ethanol (Kuo and Nanikawa 1990). Blood paraquat levels showed significant elevation in rabbits, and the mortality rates increased when the animals were orally administered paraquat combined with ethanol in amounts of 2.0 and 3.8 g/kg. Continuous breathing of high oxygen concentrations 12-24 hours after administration of paraquat caused severe and extensive pulmonary lesions and interstitial fibrosis (Selman et al. 1985). On the other hand, a reverse sequence of treatment— inhalation of high oxygen concentrations followed by paraquat administration—caused no mortality and pulmonary lesions. 

No significant mortality was observed in mice orally administered single doses of up to 3 g/kg of an ethanol extract of greater galangal (Qureshi et al. 1992). 

In mice orally administered 100 mg/kg of an ethanol extract of cinnamon daily for 90 days, no signs of mortality were observed. Hematological studies indicated a reduction in hemoglobin levels. Increases in reproductive organ weights, sperm motility, and sperm count were observed with no spermatotoxic effects (Shah et al. 1998). 

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