Cause of Death Men Women

Cancer 102,812 54,664

Cardiovascular disease 90,906 57,699

Respiratory disease 53,713 44,429

Residential fires 589 377

Perinatal deaths 598 407

Lung cancer and heart disease attributable to passive smoking 15,517 22,536

Total 264,135 80,112

Data from CDC. Annual smoking-attributable mortality, years of potential life lost, and economic costs—United States, 1995–1999. MMWR 51:300, 2002.

exposure to silica, coal dust, grain dust, cotton dust, and welding fumes.

Tobacco use also increases the prevalence of peptic ulcers; smoking impairs healing of ulcers and increases the likelihood of recurrence. Smoking may also increase pyloric reflux and

decrease bicarbonate secretion from the pancreas.

In addition to the health hazards of mainstream tobacco smoke, there are risks associated with exposure to sidestream smoke, also called passive smoking or environmental tobacco smoke

(ETS). In 1986, two reports issued by the National Research Council and the Surgeon General concluded that ETS increases the risk of lung cancer, ischemic heart disease, and acute

myocardial infarction.[14] The Environmental Protection Agency classified ETS as a known human carcinogen in 1992. ETS is especially hazardous for infants and young children.

Maternal smoking increases the incidence of sudden infant death syndrome. Young children in households of cigarette smokers suffer from an increased incidence of respiratory and ear

infections and exacerbation of asthma.

Alcohol Abuse

Ethanol is the most widely used and abused agent throughout the world. There are 15 to 20 million alcoholics in the United States; approximately 100,000 deaths in the United States are

attributed to alcohol abuse per year, with an economic cost of $100 to $130 billion.[15] Ethanol is ingested in alcoholic beverages such as beer, wine, and distilled spirits. A blood alcohol

concentration of 80 to 100 mg/dL is the legal

definition for driving under the influence of alcohol in many states. Approximately 3 ounces (44 ml) of ethanol are required to produce this blood alcohol level in a 70-kg person. This is

equivalent to 12 ounces of fortified wine, 8 bottles of beer (12 ounces each), or 6 ounces of 100-proof whiskey. In occasional drinkers, a blood alcohol level of 200 mg/dL produces

inebriation, with coma, death, and respiratory arrest at 300 to 400 mg/dL. Habitual drinkers can tolerate blood alcohol levels up to 700 mg/dL. This metabolic tolerance is partially

explained by a fivefold to tenfold induction of the cytochrome P-450 xenobiotic-metabolizing enzyme CYP2E1. Such induction increases the metabolism of ethanol as well as that of other

drugs and chemicals, including cocaine and acetaminophen. Although no specific receptor for ethanol has been identified, chronic use results in psychologic and physical dependence. The

biologic basis for ethanol addiction is unknown, although genetic factors may be involved.

Ethanol is metabolized to acetaldehyde by alcohol dehydrogenase in the gastric mucosa and liver, and by cytochrome P-450 (CYP2E1) and catalase in the liver ( Fig. 9-5 ). Acetaldehyde is

converted to acetic acid by aldehyde dehydrogenase. There are genetic polymorphisms in aldehyde dehydrogenase that affect ethanol metabolism; approximately 50% of Chinese,

Vietnamese, and Japanese people have reduced activity of this enzyme due to a point mutation that converts glutamine to lysine at amino acid 487. These ethnic groups also rapidly convert

ethanol to acetaldehyde, which builds up and triggers a facial flushing syndrome. Women have lower levels of gastric alcohol dehydrogenase activity than men do; therefore, they may

develop higher blood alcohol levels than men after drinking the same quantity of ethanol.[15]

The metabolism of ethanol is directly responsible for most of its toxic effects. In addition to its acute action as a

Figure 9-5Metabolism of ethanol. ADH, alcohol dehydrogenase; ALDH, aldehyde dehydrogenase. (From Parkinson A: Biotransformation of xenobiotics. In Klassen CD [ed]: Casarett

and Doull's Toxicology: The Basic Science of Poisons, 5th ed. New York, McGraw-Hill, 1996, p. 128.)

TABLE 9-5-- Mechanisms of Disease Caused by Ethanol Abuse

Date: 2016-04-22; view: 839