|dc.contributor.author||National Institute on Alcohol Abuse and Alcoholism|
|dc.publisher||Rockville, MD: U.S. Department of Health, Education and Welfare||en_US|
|dc.relation.ispartofseries||DHEW Publication No. (HSM) 73-9060;|
|dc.subject||occupational alcoholism programs||en_US|
|dc.subject||alcoholism in the workplace||en_US|
|dc.title||Occupational alcoholism: some problems and some solutions||en_US|
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Binge alcohol exposure transiently changes the endocannabinoid system: A potential target to prevent alcohol-induced neurodegenerationLiput, D.J.; Pauly, J.R.; Stinchcomb, A.L. (MDPI AG, 2017)Excessive alcohol consumption leads to neurodegeneration, which contributes to cognitive decline that is associated with alcohol use disorders (AUDs). The endocannabinoid system has been implicated in the development of AUDs, but little is known about how the neurotoxic effects of alcohol impact the endocannabinoid system. Therefore, the current study investigated the effects of neurotoxic, binge-like alcohol exposure on components of the endocannabinoid system and related N-acylethanolamines (NAEs), and then evaluated the efficacy of fatty acid amide hydrolase (FAAH) inhibition on attenuating alcohol-induced neurodegeneration. Male rats were administered alcohol according to a binge model, which resulted in a transient decrease in [3H]-CP-55,940 binding in the entorhinal cortex and hippocampus following two days, but not four days, of treatment. Furthermore, binge alcohol treatment did not change the tissue content of the three NAEs quantified, including the endocannabinoid and anandamide. In a separate study, the FAAH inhibitor, URB597 was administered to rats during alcohol treatment and neuroprotection was assessed by FluoroJade B (FJB) staining. The administration of URB597 during binge treatment did not significantly reduce FJB+ cells in the entorhinal cortex or hippocampus, however, a follow up "target engagement" study found that NAE augmentation by URB597 was impaired in alcohol intoxicated rats. Thus, potential alcohol induced alterations in URB597 pharmacodynamics may have contributed to the lack of neuroprotection by FAAH inhibition. Copyright 2017 by the authors. Licensee MDPI, Basel, Switzerland.
The Effects of the 2011 Maryland Alcohol Sales Tax Increase on Alcohol-Impaired Drivers Involved in Fatal and Non-Fatal Crashes.Lavoie, Marie-Claude; Smith, Gordon S., M.B., Ch.B., M.P.H. (2016)Background: Increasing alcohol excise taxes has been shown to reduce alcohol-impaired driving. However, no study has examined the effects of increasing alcohol sales tax on motor vehicle injuries. Objectives: The aims of this study were to evaluate the effects of the 2011 Maryland alcohol sales tax increase on the rates of (a) alcohol-related motor vehicle fatalities, (b) alcohol-involved drivers in fatal crashes, (c) alcohol-involved drivers in all-injury crashes (nonfatal and fatal), and (d) different age groups of alcohol-involved drivers in all-injury crashes. Methods: We used a time series study to analyze data from the Fatality Analysis Reporting System and the Maryland Automated Accident Reporting System from 2001 to 2013 using a generalized estimating equations model with a negative binomial distribution and log link. Results: For fatal motor vehicle crashes there was no immediate significant change in the rates of alcohol-related motor vehicle fatalities (rate ratio [RR]: 1.13, 95% confidence interval (CI): 0.98-1.13) and alcohol-involved drivers (RR: 1.06, 95% CI: 0.96-1.11) with BAC>0.08 g/dL after the 2011 alcohol sales tax increase. However, there was a significantly larger gradual decline in the rates of alcohol-impaired drivers involved in fatal crashes, and alcohol-related fatalities with BAC>0.08 g/dL following the 2011 alcohol sales tax increase (p-value for trend change=0.03). For all-injury crashes among younger drivers ages 15 to 20, and 21 to 34, we observed a significantly larger gradual decline in the rate of alcohol-involved drivers after the 2011 alcohol sales tax increase (p-value for trend change<0.01); however, there was still no significant immediate reduction in rates. Conclusion: There was no immediate reduction in the rate of alcohol-impaired driving or alcohol-related fatalities following the 2011 alcohol sales tax but we did observe a larger gradual decline in rates for alcohol-impaired drivers and alcohol-related fatalities with BAC>0.08 g/dL. Drivers aged 15 to 34 appear to be more sensitive to a 3% tax increase in comparison to drivers aged 35 and over. Increasing the alcohol sales tax can be an effective means to save lives and prevent injuries from alcohol-impaired driving.
The role of mother/infant alcohol dehydrogenase 2, cytochrome P450 2E1 and aldehyde dehydrogenase 2 genotype in the development of fetal alcohol spectrum disordersWeeks, Nicole M.; Squibb, Katherine S. (2008)Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Spectrum Disorders (FASD) are the most common forms of preventable mental retardation affecting children today resulting from prenatal ethanol exposure. It is not currently known if ADH2, Cyp2E1 and/or ALDH2 genotypes or some combination of the three, in mothers and infants, in addition to maternal ethanol intake, increase the likelihood of developing FAS/FASD. A better understanding of the influence of genetic factors on the development of FAS/FASD should allow identification of high risk mothers to target for intervention and improved quality of life for potentially affected infants. To more clearly determine the role of ADH2, Cyp2E1, and ALDH2 in the development of FAS, this research examined the collective effects of polymorphisms in these enzymes. ADH2, Cyp2E1 and ALDH2 genotypes were analyzed in a cohort of 69 mother/infant pairs well characterized with respect to maternal alcohol consumption. The influence of genotype combinations on correlations between maternal ethanol intake and infant outcomes including birth weight, birth length, head circumference Six and twelve month developmental indices were also examined. Mothers possessing the ADH2*3 allele were shown to drink borderline significantly less than mothers lacking the allele (p=0.08). Mothers possessing the Cyp2E1 insertion also showed a borderline significant trend toward lighter drinking (p=0.07). Overall, maternal possession of the ADH2*3 allele after prenatal alcohol exposure was associated with better infant outcomes, as was maternal possession of the Cyp2E1 insertion. A trend emerged in the twelve month MDI/PDI scores where infants born to high-drinking mothers had higher MDI and PDI scores than those born to low-drinking mothers also lacking the insertion (p=0.09 and p=0.11, respectively). There were significant associations between the possession of the ALDH2*2 polymorphism and smaller birth length and head circumference. Analysis did not show any correlation between the ADH2/Cyp2E1 combined genotypes and infant outcome. Overall, this study indicated that polymorphisms in the three major genes responsible for alcohol catabolism can play a role in the development of FAS/FASD after prenatal alcohol exposure. Though this study lacks the statistical power to make strong conclusions, trends towards significance were apparent and indicate a need for future studies.