Cabelleria, J.; "First-pass metabolism of ethanol: its role as a determinant of blood alcohol levels after drinking," HEPATOGASTROENTEROLOGY (1992), 39, Suppl 2: 62-6. (In normal subjects after the intake of a moderate amount of alcohol, ADH is the major enzyme catalyzing the oxidation of ethanol to acetaldehyde, whereas the MEOS play an an important role in the oxidation of ethanol in chronic alcoholics.)

Cahalan, D., et al; "American driving practices: a national study of drinking behavior and attitudes, Monograph #6, Rutgers Center of Alcohol Studies, New Brunswick, New Jersey, 1969, p13. UI (p. 13, "5-6+ high alcohol use" on one occasion.)

Calhoun, Vince, E.; Pekar, James j.; Pearlson, Godfrey Dl, "Alcohol intoxication effects on simulated driving: exploring alcohol-dose effects on brain activation using functional MRI", NEUROPSYCHOPHARMACOLOGY (2004), 29: 2097-2107. "What we found is that wen people were really intoxicated and in a real vehicle. They speeded up, especially on corners, were most people slow down, and crashed more often into other vehicles." When mildly intoxicated, but below the legal alcohol limit, he said the drivers seemed aware of the fact that they were impaired and corrected for the deficit. The researchers also found that alcohol had a profound effect on some, but not all, brain circuits activated in sober driving. Impairment of the cerebellum area of the brain, which related strongly to speeding, was clearly correlated with the alcohol dose. Changes in the frontal and parietal cortex, which govern alertness and attentions, were correlated with weaving while driving."

Campbell, C. H.; Hansen, A. R.; "Blood alcohol concentration in motor vehicle crash victims: a survey of North Carolina Emergency physician attitudes and utilization patterns," NORTH CAROLINA MEDICAL JOURNAL (1992), 53 (9): 461-3. (Here are the facts: 1) motor vehicle crashes are the leading cause of death in Americans aged 6 to 34 years. 2) A driver with a blood alcohol concentration of 0.05 g/dL is twice as likely to be involved in a fatal accident as a non-drinking driver. 3) Driving after drinking is often not a sporadic behavior. Between 20% to 33% of drivers arrested for driving while intoxicated are subsequently arrested again on the same charge. 4. According to Sonderstrom et al, drunken driving signals an underlying alcohol abuse disorder. Indeed, it is reasonable to conclude that any alcohol use leading to injury should be considered a symptom of alcoholism.)

Caplan, Y. H.; "The Determination of alcohol in blood and breath," In; Saferstein, R.; Forensic Science Handbook, Prentice-Hall, Inc., Englewood Cliffs, New Jersey, 1984, 592-653. (Dubowski Method of breath alcohol and chart.)

Carey, K. B., Hustad, J. T.; "Are retrospectively reconstructed blood alcohol concentrations accurate? Preliminary results from a field study", JOURNAL OF STUDIES ON ALCOHOL (2002), 63(6):762-6. (44 persons were studied, 64% male and 34% female.)The purpose of this study was to evaluate the relationship between blood alcohol concentration (BAC) derived from an invivo breath test and retrospective estimates of BAC (eBAC) for the same drinking event. The relationship was expected to be lower at higher levels of BAC as a result of inaccuracies in the recall of self-report data. Conclusions: Although self-report data can be used to approximate the BAC obtained during a naturally occurring drinking event the relationship is moderated by measured level of intoxication. Retrospective calculations are less accurate when estimating higher BACs.

Cassidy, F. H.; "Another nomogram for solving Widmark's equation for blood alcohol levels," JOURNAL OF THE FORENSIC SCIENCES SOCIETY (1984), 24: 557-558.

Chamberlain, E.; Solomon, R.; "The case for 0.05% criminal law blood alcohol concentration limit for driving", INJURY PREVENTION (2002), 8:1-17, suppl3.iii.1. Canada established its current 0.08% "Criminal Code" blood alcohol concentration (BAC) limit for drivers in 1969. At the time, this was a substantial improvement, as it established a per se BAC limit under the criminal law and required impaired driving suspects to provide breath samples. However, in the more than three decades that have followed, breath testing instruments have become more accurate, public attitudes toward impaired driving have hardened, and scientific research as established that impairment begins at levels below 0.08%. In response, the international trend was and continues to be to reduce per se BAC limits to 0.05% or lower. The legal limit is reported to be 0.05% in numerous countries, including Argentina, Australia, Austria, Belgium, Bulgaria, Coatia, Denmark, Finland, France, Germany, Greece, Iceland, Israel, Italy, Macedonia, the Netherlands, Norway, Portugal, Slovenia, and Spain. Russia and Sweden have legal limits of 0.02% and Poland has a limit of 0.03%. Finally, the official limit is reported to be 0.00% in the Czech Republic,Hungary, Malaysia, Romania, Saudi Arabia, and Turkey, while Japan's limit is 0.00% in practice.

Chamberlain, E; Solomon, R.; "The tooth fairy, Santa Claus, and the hard cord drinking driver," INJURY PREVENTION (2001), 7: 272-75. "The recent focus on 'hard core' drinking drivers marginalizes the impaired driving problem and inhibits substantive legislative reform. A sizable percentage of so-called 'social drinkers' engage in binge drinking behavior that is sufficient to produce BACs in the typical 'hard core' range. Nearly 20% of licensed drivers in Canada continue to drink and drive. Infrequent drinkers have a much higher relative risk of crash than heavy drinkers with the same BACs. It would be prudent to discard the value laden labels of 'social drinkers' and 'hard cord' drinking drivers and focus instead on high risk drinking behaviors."

Chambers, R . Andrew; Taylor, Jane R.; Potenza, Marc N., "Developmental neurocircuitry of motivation in adolescence: a critical period of addiction vulnerability, AMERICAN JOURNAL OF PSYCHIATRY (2003), 160: 1041-1052. Epidemiological studies indicate that experiments with addictive drugs and onset of addictive disorders is primarily concentrated in adolescence and young adulthood. The authors describe basic and clinical data supporting adolescent neurodevelopment as a biologically critical period of greater for experimentation with substances and acquisition of substance use disorders. Results: Adolescent neurodevelopment occurs in brain regions associated with motivation, impulsivity, and addiction. Adolescent impulsivity and/or novelty seeking as a transitional trait behavior can be explained in part by maturational changes in frontal cortical and subsoritcal monoaminergic systems. These developmental processes may advantageously promote learning drives for adaptation to adult roles but may also confer greater vulnerability to the addictive actions of drugs. Conclusions: An exploration of developmental stages in neurocircuitry involved in impulse control has significant implications for understanding adolescent behavior, addiction vulnerability, and the prevention of addiction in adolescence and adulthood.

Chan, A.W.K.; "Factors affecting the drinking driver," DRUG AND ALCOHOL DEPENDENCE (1987), 19 : 99-119.

Chang, Grace; McNamara, Tay K.; Orav, E. John; Wilkins-Haug, Louise; "Alcohol use by pregnant women: partners, knowledge, and other predictors", JOURNAL OF STUDIES ON ALCOHOL (2006), 67 : 245-251. Because previous alcohol consumption sue by the pregnant woman was the strongest predictor of prenatal alcohol use, the importance of its accurate identification is emphasized. Although pending further investigation, knowledge about healthy pregnancy behaviors may exert greater impact if it is shared by the pregnant woman and her partner.

Chang, I., Lapham, S. C.; Barton, K. J.; "Drinking environment and sociodemographic factors among DWI offenders," JOURNAL OF STUDIES ON ALCOHOL (1996), 57: 659-69.

Chang, R. B.; Smith, W. A.; Walkin, E., Reynolds, P. C.; "The Stability of ethyl alcohol in forensic blood specimens," JOURNAL OF ANALYTICAL TOXICOLOGY (1984), 8: 66-67. (Blood samples stored at room temperature for 3.0 and 6.75 years which showed a loss in ethanol concentration.)

Charlebois, R. C.; Corbett, M. R.; Wigmore, J. G.; "Comparison of ethanol concentrations in blood, serum, and blood cells for forensic application," JOURNAL OF ANALYTICAL TOXICOLOGY (1996), 20: 171-177. (SAC:BAC ratios ranged between 1.04 and 1.26. The mean was 1.14 and the normal distribution had a standard deviation of 0.041.)

Charness, M. E.; "Alcohol and the brain," ALCOHOL HEALTH AND RESEARCH WORLD (1990), 14 (2): 85-89. Alcohol alters the properties of nerve cell membranes and interferes with many of the chemical systems that transmit and process information.

Chen L H, Baler SP and Li G. Drinking history and risk of fatal injury: comparison among specific injury causes", ACCIDENT ANALYSIS PREVENTION, (2005). 37(2):245-51. People who regularly drink alcohol are three times as likely to die from injury as are nondrinkers and former drinkers of alcohol. The researchers found that drinkers, anyone who had at least 12 drinks in the survey year, had a higher risk of dying from each cause of injury when compared to nondrinkers and former drinkers. The greatest increase in risk was drowning: drinkers were 3.6 times as likely to drown as nondrinkers. Female drinkers had a greater increase in risk of committing suicide or homicide than male drinkers. The study authors said these gender differences might be due to psychological factors. Past studies have shown that for the same alcohol intake, blood alcohol concentrations rise more quickly, reach a higher peak and stay elevated for a longer time in women.

Cherpitel, Cheryl J.; Ye, Yu; Bond, Jason; Borges, Guilherme; "The causal attribution of injury to alcohol consumption: a cross-national meta-analysis from the emergency room collaborative alcohol analysis project." ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH (2003), 27 (11): 1805-1812. " Pooled odds rations for both log-transfromed blood alcohol concentrations at the time of the emergency room visit and the amount of alcohol consumed in the 6 hr. before injury were positively predictive (1.19 and 1.80, respectively) and heterogeneous across studies. Effect size changed little when age and gender were controlled. When stratifying on reporting five or more drinks on an occasion during the last year (5+ yearly drinkers. The effect size of feeling drunk at the time of injury, controlling for the amount of alcohol consumed, was positively predictive (2.04) but heterogeneous across studies. Meta-analysis regression found the level to which alcohol is consumed in a detrimental pattern to be a significant predictor of blood alcohol concentration, and of the amount consumed and feeling drunk at the time of injury, on causal attribution, with a lower detrimental pattern level with a larger effect size. The association of acute use of alcohol on causal attribution may be affected by chronic use to some extent, but this association is negatively affected by the degree to which society exhibits harmful drinking patterns.

Chesher, G.; Greeley, J.; "Tolerance to the effects of alcohol," ALCOHOL, DRUGS, AND DRIVING (1992), 8 (2): 93-106. (Clinical data reveal that a considerable number of people fail to show obvious signs of drunkenness even though they have very high BACs.)

Chesson, Harrell W.; Harrison, Paul; Stall, Ron; "Changes in alcohol consumption and in sexually transmitted disease incidence rates in the United States: 1983-1998", JOURNAL OF STUDIES ON ALCOHOL (2003), 64: 623-630. "Results: From 1983 to 1998, changes in alcohol consumption were significantly associated with changes in gonorrhea and syphilis rates. Each 1? increase in per capita alcohol consumption was associated with increase of about ).4% to ).7% in reported gonorrhea incidence rates and 1.8% to 3.6% in reported syphilis incidence rates. Conclusions: The association between alcohol and risky sex, well document at the level of the individual, might hold at the population level as well."

Chou, S. Patricia; Grant, Bridget F.; Dawson, Deborah A.; Stinson, Frederick S.; Saha, Tulshi; Pickering, Roger P.; "Twelve-Month prevalence and changes in driving after drinking: United States, 1991-1992 and 2001-2002", DRUG AND ALCOHOL DEPENDENCE (2005), 80 (2): 223-230. "Drinking and driving has been identified as one of the most important contributors of motor vehicle fatalities. This paper addressed the existing gap in our public health knowledge regarding the current prevalence of driving after drinking and how this has changed over the past decade. Prevalence rates of drinking and driving in 2001-2002, and changes in those prevalence rates between 1991-1992 and 100102002, were examined in two large nationally representative surveys of the U. S. population. Overall, the prevalence of driving after drinking as 2.9 percent in 2001-2002, representing approximately six million U. S. adults. This rate was about three-quarters of the rate observed in 1991-1992 (3.7 percent), reflecting a 22-percent reduction. Generally, the male-female differentials in the rate of driving after drinking decreased over the past decade. However, the sex rations increased substantially for underaged youth over the past decade, reflecting the sharp decrease in prevalence of driving after drinking among 18- to 20-year -old women. Constant and emerging subgroups at high risk for drinking and driving included Whites, Native Americans, males, underaged young adults, and 21-to-25-year-olds. The results of this study highlighted the need to continue to monitor prevalence and changes in driving after drinking."

Clayton, Mark; "Websites use waistline factor to cut down on student drinking", THE CHRISTIAN SCIENCE MONITOR (2002), October 15. Scott Walters and William Miller surveyed students at the University of New Mexico about their drinking habits. Dr. Walters and colleagues responded with personalized data. Students found out how much alcohol is in their blood when they drink, how much money they spend on drinking, and how many calories their drinks contain. They were also given information about genetic risk factors and how their drinking habits compared with the average student on campus. The authors came up with the idea of a website on alcohol use called e-CHUG. Most materials is written from a student's point of view, to crate the feeling that peers are giving the information about drinking's impact on grades, its, secondhand effects, and ways to manage money and control anger. The website's core is a multilevel questionnaire soliciting information about student's beliefs about drinking, the risks they typically run, and lifestyle concerns, and so on.

Clifasefi, Seema, L.; Kakarangi, Melanie K. T.; Bergman, Jonah S.; "Blind drunk : the effects of alcohol on attentional blindness", APPLIED COGNITIVE PSYCHOLOGY (2006), 20: 697-704. (47 subjects aged 21 to 35) Alcohol consumption is a major contributor to road accidents. The authors know that even sober drivers can fail to detect unexpected salient objects that appear in their visual fields, a phenomenon know as inattentional blindness. The authors were interested in whether these visual errors become more or less likely when subjects are under the influence of alcohol or just think that they are drunk. Subjects were told half of our subjects that they had received alcohol, and half that they had received a placebo. This information was either true or false. The experiment involved giving subjects 10 minutes to consume beverages which either contained alcohol or did not to achieve .04 BAL. The subjects then watched 25 seconds of a video clip showing two teems of three people playing with a ball and were instructed to count the ball passes. Part way through the video clip, an individual dressed in a gorilla suit appeared on the screen, walked directly through the players, beat its chest and then walked away. Subjects who were mildly intoxicated were twice as likely to miss seeing the gorilla, even though it had screen time of over a third of the video. Intoxicated subjects (regardless of what they were told) were more likely to show 'blindness' to an unexpected object in their visual field. This finding has practical implications for human performance issues such as driving and eyewitness memory, and theoretical implications for visual cognition.

"Cognitive impairment and recovery from alcoholism," ALCOHOL ALERT (July 2001), 53. "Alcohol use over a period of time, even at low levels of drinking, can produce varying degrees of cognitive damage, a problem that is of particular concern because alcohol is so widespread. Thus, the brain's self-repairing ability may help defer or reduce alcohol-induced cognitive problems among a large portion of the population. Second, the brain's ability to rewire itself may have implications in terms of adolescent drinking. Recent evidence suggests that the adolescent brain, which is still forming important cellular connections, is more vulnerable than the adult brain to alcohol-induced damage. The brain's ability to rewire important neurological systems might help mitigate a lifetime of cognitive difficulties resulting from chronic drinking during adolescence, but we do no yet know if this is true.")
Address: http://pubs.niaaa.nih.gov/publications/aa53.htm

**Cohen, Deborah A.; Mason, Karen; Farley, Thomas A.; "Beer consumption and premature mortality in Louisiana: an ecologic analysis." JOURNAL OF STUDIES ON ALCOHOL (2004), 65: 398-403. The population association between beer consumption and mortality may reflect population-level determinants of beer consumption as well as indirect health effects of alcohol consumption on persons who are not heavy drinkers. "Per capita alcohol consumption consistently has been found to be associated with several types of alcohol-related mortality at national levels, and in Louisiana we found that beer consumption is independently associated with premature mortality at the local level. Since beer is currently the most popular alcoholic beverage, it seems likely that population-level approaches targeting beer consumption could complement traditional individual-level approaches to controlling the negative consequences of alcohol use.

Cohen, H. M.; "Blood alcohol concentration and time factors," DWI JOURNAL, : 12-16. (A reasonable doubt that the BAC at the time of the incident was less than at the time of the offense. Only in his mind.)

Cohen, H. M.; "Calculation of blood alcohol concentration: use and limitations," DWI JOURNAL (1986), 1 (5): 7-13. (Author has too many mistakes in his formulas on Total Body Water!!!)

Cole, T. B.; Patetta, M. J.; "Why does the injured drunk driver escape arrest and conviction? A case presentation and discussion by health care and law enforcement professionals," NORTH CAROLINA MEDICAL JOURNAL (1992), 53 (9): 453-58.

Cole-Hardin, S.; Wilson, J. R.; "Ethanol metabolism in men and women," JOURNAL OF STUDIES ON ALCOHOL (1987), 48 (4): 380-387. (Twins and breath alcohol reproducibility.)

*Colquitt, M.; Fielding, L. P.; Cronan, J. F.; "Drunk drivers and medical and social injury," NEW ENGLAND JOURNAL OF MEDICINE (1987), 317 (20): 1262-6. ("Society has the right to demand that innocent people not be endangered by intoxicated people who drive motor vehicles.")

Compton, Wilson M.; Conway, Kevin P.; Stinson, Frederick S.; Colliver, James D.; Grant, Bridget F., "Prevalence, correlates, and comorbidity of DSM-IV antisocial personality syndromes and alcohol and specific drug use disorders in the United States: results from the National Epidemiologic Survey On Alcohol and Related Conditions", JOURNAL OF CLINICAL PSYCHOLOGY (2005), 66 (6):677-685. Data from a survey of 43,000 U. S. adults show that antisocial syndromes--marked by little concern for the rights or others and violations of age-appropriate societal rules--are more common among people with substance abuse disorders than those without these disorders. The analysis showed lifetime prevalence of 3.6 percent of adults diagnosed with antisocial personality disorder, 1.1 percent with conduct disorder only and more than 12 percent with adult antisocial behavior only while the lifetime prevalence for any drug abuse Results of other investigations have pointed to impairments in executive decision-making as fundamental characteristic in substance abuse disorders that may be associated with impaired development of certain brain structures and functions. It is speculated that substance abuse disorders and antisocial personality syndromes share common underlying physiological features that may be related to the same neural systems involved in decision-making.

**"Computing a BAC estimate," ALCOHOL ALERT, U. S. Department of Transportation, National Highway Traffic Safety Administration, October, 1994, 3 pages. http://ntl.bts.gov/card_view.cfm?docid=5188 (Interestingly the U. S. Department of Transportation espouses BAC estimates using Widmarks.)

**Cooper, W. E.; Schwar, T. G.; Smith, L. S.; Alcohol, drugs and road traffic; Juta & Company Limited, c1979, 402p. (Schwar quotes a person absorbing from the gastrointestinal tract in fasting conditions of about 1.5 to 2 hours in humans subjects and prolongation of the process to 6 hours or more in the presence of food. These figures are based on work published by Tuovenin in 1930 (!) performed with the same individual (!) after the ingestion of 60 ml of alcohol (5%, 20% and 40% concentrations) in fasting condition and immediately after eating 1,1 kg potatoes", (Cooper,Schwar, Smith, 1979, p. 91.).

Cortot, A.; Gilles, J.; DuCrot, F.; Aymes, C.; Giraudeaux, V.; Modigliani, R.; "Gastric emptying and gastrointestinal absorption of alcohol ingested with a meal," DIGESTIVE DISEASES AND SCIENCES (1986), 31 (4): 343-348. (Food and alcohol.)

Cummings, P.; Rivara, F. P.; Olson, C. M.; Smith, K. M.; "Changes in traffic crash mortality rates attributed to use of alcohol, or lack of a seat belt, air bag, motorcycle helmet, or bicycle helmet, United States, 1982-2001.", INJURY PREVENTION (2006), 12: 148-154. There were 858,741 traffic deaths during the 20 year period. Estimated deaths attributed to each factor were: (1) alcohol use 366,606; (2) not wearing a seat belt, 259,239; (3) lack of an air bag 31, 377; (4) no motorcycle helmet 12,095; (5) no bicycle helmet 10,552. Over the 20 years mortality rates attributed to each risk factor declined: alcohol by 53%, not wearing a seat belt 49%; lack of an air bag 17%; no motorcycle helmet by 74%; no bicycle helmet by 39%. There were 153,168 lives saved by decreased drinking and driving, 129,297 by increased use of seat belts, 4305 by increased air bag prevalence, 6475 by increased use of motorcycle helmets, and 239 by increased use of bicycle helmets. Decreased alcohol use and increased use of seat belts were associated with substantial reductions in crash mortality from 1982 through 2001. Increased presence of air bags, motorcycle helmets, and bicycle helmets were associated with smaller reductions.

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updated 07/19/10