Neal L Benowitz

University of California, San Francisco, San Francisco, California, United States

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Publications (557)3901.72 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: The reduction of the nicotine content of cigarettes to non-addicting levels is a potential federal regulatory intervention to reduce the prevalence of cigarette smoking and related disease. Many clinical trials on the effects and safety of nicotine reduction are ongoing. An important methodological concern is non-compliance with reduced nicotine content cigarettes in the context of freely available conventional cigarettes. We propose two approaches using biomarkers to estimate non-compliance in smokers of very low nicotine content (VLNC) cigarettes in a clinical trial. Methods: Data from 50 subjects in a study of gradual nicotine reduction were analyzed. Using plasma cotinine concentrations measured at baseline and while smoking VLNC cigarettes, we compared within-subject ratios of plasma cotinine comparing usual brand to VLNC in relation to nicotine content of these cigarettes. In another approach we used nicotine pharmacokinetic data to estimate absolute plasma cotinine/cigarettes per day (CPD) threshold values for compliance based on the nicotine content of VLNC. Results: The two approaches showed concordance indicating at least 60% non-compliance with smoking VLNC. In a sensitivity analysis assuming extreme compensation and extreme values for nicotine metabolic parameters, non-compliance was still at least 40%, much higher than self-reported non-compliance. Conclusion: Biomarker analysis demonstrates a high degree of non-compliance with smoking VLNC cigarettes, indicating that smokers are supplementing these with conventional cigarettes. Impact: We propose a practical approach to assessing compliance with smoking VLNC in clinical trials of nicotine reduction. Copyright © 2014, American Association for Cancer Research.
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    ABSTRACT: Volatile organic compounds (VOC) from tobacco smoke are associated with cancer, cardiovascular, and respiratory diseases. The objective of this study was to characterize the exposure of nonsmokers to VOCs from secondhand smoke (SHS) in vehicles using mercapturic acid metabolites.
  • JAMA Internal Medicine 11/2014; · 13.25 Impact Factor
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    ABSTRACT: Context. 4-Fluoroamphetamine (4-FA) is a para-substituted phenethylamine-type synthetic stimulant that has in recent years gained popularity through internet blogs and market share according to confiscated drug data. No serious toxicity has previously been reported. We report a case of a young man who developed severe toxicity and cardiogenic shock after using 4-FA, with laboratory confirmation. Case details. An 18-year-old man presented to the emergency department with vomiting, shortness of breath, chest tightness, and altered mental status about 5 h after using a new and unfamiliar street drug. Two days prior, he had received naltrexone intramuscular injection as part of an opioid addiction treatment program and was taking fluoxetine and trazodone. Five hours after presentation, he developed cardiogenic shock requiring intraaortic balloon pump, inotropic and ventilatory support. An echocardiogram showed left ventricular (LV) hypokinesia, sparing the apex and ejection fraction (EF) = 10%. Comprehensive toxicology serum testing revealed FA, naproxen, trazodone, and cotinine. The 4-FA urine level was 64,000 ng/ml and serum level was 118 ng/ml. With slow recovery, the patient was discharged after 2 weeks of hospitalization. Discussion. Although no previously reported 4-FA clinical poisoning cases have been published for comparison, by examining 4-FA pharmacology compared with other stimulant drugs, and given this patient's presentation and echocardiogram suggestive of reverse takotsubo cardiomyopathy we suspect the toxic mechanism was an acute cardiomyopathy caused by 4-FA catecholamine-induced myocarditis and/or small vessel myocardial ischemia. Conclusion. Recreational use of 4-FA may present with life threatening toxicity including cardiomyopathy, cardiogenic shock, and pulmonary edema.
    Clinical Toxicology. 10/2014;
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    ABSTRACT: Background: Identifying sources of variation in the nicotine and nitrosamine metabolic inactivation pathways is important to understanding the relationship between smoking and cancer risk. Numerous UGT1A and UGT2B enzymes are implicated in nicotine and nitrosamine metabolism in vitro; however, little is known about their roles in vivo. Methods: Within UGT1A1, UGT1A4, UGT1A9, UGT2B7, UGT2B10, and UGT2B17, 47 variants were genotyped, including UGT2B10*2 and UGT2B17*2. The association between variation in these UGTs and glucuronidation activity within European and African American current smokers (n=128), quantified as urinary ratios of the glucuronide over unconjugated compound for nicotine, cotinine, trans-3'-hydroxycotinine, and NNAL, was investigated in regression models assuming a dominant effect of variant alleles. Results: Correcting for multiple testing, three UGT2B10 variants were associated with cotinine glucuronidation, rs2331559 and rs11726322 in European Americans and rs835309 in African Americans (P≤.0002). Additional variants predominantly in UGT2B10 were nominally associated with nicotine (P=.008-.04) and cotinine (P=<.001-.02) glucuronidation in both ethnicities in addition to UGT2B10*2 in European Americans (P=.01, P<.001). UGT2B17*2 (P=.03) in European Americans and UGT2B7 variants (P=.02-.04) in African Americans were nominally associated with 3HC glucuronidation. UGT1A (P=.007-.01), UGT2B10 (P=.02) and UGT2B7 (P=.02-03) variants in African Americans were nominally associated with NNAL glucuronidation. Conclusions: Findings from this initial in vivo study support a role for multiple UGTs in the glucuronidation of tobacco-related compounds in vivo, in particular UGT2B10 and cotinine glucuronidation. Impact: Findings also provide insight into ethnic differences in glucuronidation activity, which could be contributing to ethnic disparities in the risk for smoking-related cancers.
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    ABSTRACT: Bupropion is used clinically to treat depression and to promote smoking cessation. It is metabolized by CYP2B6 to its active metabolite hydroxybupropion, yet alterations in CYP2B6 activity have little impact on bupropion plasma levels. Furthermore, less than 10% of a bupropion dose is excreted as urinary bupropion and its characterized metabolites hydroxybupropion, threohydrobupropion and erythrohydrobupropion, suggesting that alternative metabolic pathways may exist. In vitro data suggested CYP2C19 could metabolize bupropion. The current study investigated the impact of functional CYP2C19 genetic variants on bupropion pharmacokinetics and treatment outcomes. In 42 healthy volunteers, CYP2C19*2 (a reduced activity allele) was associated with higher bupropion AUC, but similar hydroxybupropion AUC. The mean bupropion AUC was 771 versus in individuals with, and without, CYP2C19*2 respectively (P=0.017). CYP2C19*2 was also associated with higher threohydrobupropion and erythrohydrobupropion AUC (P<0.005). Adjusting for CYP2B6 genotype did not alter these associations, and CYP2C19 variants did not alter the utility of the hydroxybupropion/bupropion ratio as a measure of CYP2B6 activity. Finally, in a clinical trial of 540 smokers, CYP2C19 genotype was not associated with smoking cessation outcomes supporting the hypothesis that bupropion response is mediated by hydroxybupropion, which is not altered by CYP2C19. In conclusion, our study reports the first in vivo evidence that reduced CYP2C19 activity significantly increases the steady state exposure to bupropion and its reductive metabolites threohydrobupropion and erythrohydrobupropion. These pharmacokinetic changes were not associated with differences in bupropion's ability to promote smoking cessation in smokers, but may influence the side effects and toxicity associated with bupropion.
    Drug metabolism and disposition: the biological fate of chemicals 09/2014; · 3.74 Impact Factor
  • Circulation 08/2014; · 15.20 Impact Factor
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    ABSTRACT: We evaluated chr6q25.3 organic cation transporter gene (SLC22A1, SLC22A2, SLC22A3) variation and response to smoking cessation therapies. The corresponding proteins are low affinity transporters of choline, acetylcholine and monoamines, and of smoking cessation pharmacotherapies, expressed in multiple tissues.
    Nicotine & Tobacco Research 08/2014; · 2.48 Impact Factor
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    ABSTRACT: Both the Tobacco Control Act in the U.S. and Article 9 of the Framework Convention on Tobacco Control enable governments to directly address the addictiveness of combustible tobacco by reducing nicotine through product standards. Although nicotine may have some harmful effects, the detrimental health effects of smoked tobacco are primarily due to non-nicotine constituents. Hence, the health effects of nicotine reduction would likely be determined by changes in behavior that result in changes in smoke exposure.
    Preventive medicine. 06/2014;
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    ABSTRACT: Cigarette smoke exposure has recently been found to be associated with increased susceptibility to trauma- and transfusion-associated acute respiratory distress syndrome. We sought to determine 1) the incidence of cigarette smoke exposure in a diverse multicenter sample of acute respiratory distress syndrome patients and 2) whether cigarette smoke exposure is associated with severity of lung injury and mortality in acute respiratory distress syndrome.
    Critical Care Medicine 06/2014; · 6.12 Impact Factor
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    ABSTRACT: Water pipe tobacco smoking is spreading globally and is increasingly becoming popular in the United States, particularly among young people. Although many perceive water pipe smoking to be relatively safe, clinical experimental studies indicate significant exposures to tobacco smoke carcinogens following water pipe use. We investigated biomarkers of nicotine intake and carcinogen exposure from water pipe smoking in the naturalistic setting of hookah bars.
  • Source
    Rachel Grana, Neal Benowitz, Stanton A Glantz
    Circulation 05/2014; 129(19):1972-86. · 15.20 Impact Factor
  • Circulation 05/2014; 129(19):e490-2. · 15.20 Impact Factor
  • Saul Shiffman, Michael S Dunbar, Neal L Benowitz
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    ABSTRACT: Background: Non-daily or intermittent smokers (ITS) are increasingly common, but how much nicotine, if any, ITS take in and how quickly they metabolize it has not yet been studied. Methods: We compared carbon monoxide (CO), urinary cotinine, and nicotine metabolism (nicotine metabolite ratio [NMR]: 3-hydroxycotinine:cotinine) in 224 ITS and 222 daily smokers (DS). Effects of gender and ethnicity were examined. Results: DS had higher cotinine concentrations than ITS (1396 ± 69 vs. 478 ± 44 ng/ml), attributable to higher CPD. In both groups, cotinine rose more slowly as CPD increased. There were no differences in cotinine between White (WH) and African American (AA) DS; among ITS, AA cotinine was over twice that of WH. Among DS, CO was significantly higher among WH than AA smokers, but significantly lower among WH ITS than AA ITS. Although AA ITS smoked more than WH ITS (CPD: 4.13 ± 0.55 vs. 3.31 ± 0.41), this did not account for the observed cotinine nor CO differences. There were no differences in NMR by group or race, nor any gender effects. Conclusions: At comparable CPD, DS' and ITS' intake of nicotine per cigarette was similar, as were their rates of nicotine metabolism. Among ITS, AA smokers smoke more and take in more nicotine per cigarette than WH ITS, consistent with the view of ITS as a heterogeneous group. Impact: Differences in nicotine intake per cigarette and metabolism likely cannot account for differences in DS and ITS smoking. Future studies should explore ethnic differences in ITS smoking.
    Cancer Epidemiology Biomarkers &amp Prevention 04/2014; · 4.56 Impact Factor
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    ABSTRACT: Associations between CHRNA5-A3-B4 variants and smoking behaviors exist, however the association with smoking abstinence is less understood, particularly among African Americans. In 1295 African Americans enrolled in two clinical trials, we investigated the association between CHRNA5-A3-B4 and smoking abstinence. Rs2056527[A] was associated with lower abstinence with active pharmacotherapy (during-treatment: OR=0.42&P<0.001; end of treatment (EOT): OR=0.55&P=0.004), or with nicotine gum alone (during-treatment: OR=0.31&P<0.001; EOT: OR=0.51&P=0.02), but not significantly with bupropion, although similar directions and magnitudes were observed (during-treatment: OR=0.54&P=0.05; EOT: OR=0.59&P=0.08). Additionally, rs588765[T] was associated with abstinence with gum during treatment (OR=2.31&P<0.01). Rs16969968 occurred at a low frequency and was not consistently associated with abstinence. CHRNA5-A3-B4 variants were not associated with tobacco consumption and adjustments for smoking behaviors did not alter the associations with smoking abstinence. Together, our data suggest that in African Americans CHRNA5-A3-B4 variants are not associated with baseline smoking, but can influence smoking abstinence during active pharmacotherapy.Clinical Pharmacology & Therapeutics (2014); Accepted article preview online 14 April 2014; doi:10.1038/clpt.2014.88.
    Clinical Pharmacology &#38 Therapeutics 04/2014; · 6.85 Impact Factor
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    ABSTRACT: We examined homes of hookah-only smokers and nonsmokers for levels of: indoor air nicotine, a marker of secondhand smoke, and indoor surface nicotine, a marker of thirdhand smoke; and child uptake of nicotine, the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and the toxicant acrolein, by analyzing their corresponding metabolites cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and NNAL-glucuronides (total NNAL) and 3-hydroxypropylmercapturic acid. Data were collected during 3 home visits during a 7-day study period from a convenience sample of 24 households with a child, 5 years or younger. Three child urine samples, and 2 air and surface samples from the living room and the child bedroom, were taken in homes of nonsmokers (n = 5), and hookah-only smokers (n = 19) comprised of daily hookah smokers (n = 8) and weekly/monthly hookah smokers (n = 11). Nicotine levels in indoor air and on surfaces in the child bedrooms in homes of daily hookah smokers were significantly higher than in homes of nonsmokers. Uptake of nicotine, NNK, and acrolein in children living in daily hookah smoker homes was significantly higher than in children living in nonsmoker homes. Uptake of nicotine and NNK in children living in weekly/monthly hookah smoker homes was significantly higher than in children living in nonsmoker homes. Our data provide the first evidence for uptake of nicotine, the tobacco-specific lung carcinogen NNK, and the ciliatoxic and cardiotoxic agent acrolein in children living in homes of hookah smokers. Our findings suggest that daily and occasional hookah use in homes present a serious, emerging threat to children's long-term health.
    Nicotine & Tobacco Research 03/2014; · 2.48 Impact Factor
  • Neal L Benowitz
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    ABSTRACT: The idea of clean nicotine delivery systems that would satisfy nicotine craving and promote smoking cessation has been considered as a possible public health tool for many years. Nicotine medications have been useful for smoking cessation but have not found widespread popularity among smokers, perhaps because of slow nicotine delivery and other sensory characteristics that differ from cigarettes. Traditional smokeless tobacco delivers as much nicotine as cigarettes and has been advocated for harm reduction but contains carcinogenic nitrosamines and has not been proven to promote cessation. Furthermore, there is concern that dual use of smokeless tobacco and cigarettes may inhibit quitting smoking. Newer oral dissolvable tobacco products contain lower levels of toxicants than other smokeless tobacco but also deliver much less nicotine and have not been popular with consumers. Electronic cigarettes that aerosolize nicotine without generating toxic tobacco combustion products have become quite popular and hold promise as a way to attract smokers away from cigarettes, although efficacy in promoting smoking cessation has not yet been demonstrated. There are concerns about safety of long-term use, and there is evidence that youth, including nonsmokers, are taking up e-cigarette use. E-cigarettes are marketed for use when one cannot smoke conventional cigarettes, and such use might result in more persistent cigarette smoking. Although their benefits and risks are being vigorously debated, e-cigarettes or other clean nicotine delivery devices could play an important role as an adjunct to a U.S. Food and Drug Administration regulatory intervention to make cigarettes less addictive and in this context could contribute to the end of cigarette smoking and smoking-induced disease.
    Annals of the American Thoracic Society. 02/2014; 11(2):231-5.
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    ABSTRACT: Objective: Individuals with serious mental illness (SMI) are dying on average 25 years prematurely. The leading causes are chronic preventable diseases. In the context of a tobacco-treatment trial, this exploratory study examined the behavioral risk profiles of adults with SMI to identify broader interventional needs. Method: Recruited from five acute inpatient psychiatry units, participants were 693 adult smokers (recruitment rate = 76%, 50% male, 45% Caucasian, age M = 39, 49% had income < $10,000) diagnosed with mood disorders (71%), substance-use disorders (63%), posttraumatic stress disorder (39%), psychotic disorders (25%), and attention deficit-hyperactivity disorder (25%). The Staging Health Risk Assessment, the primary measure used in this study, screened for risk status and readiness to change 11 health behaviors, referencing the period prior to acute hospitalization. Results: Participants averaged 5.2 (SD = 2.1) risk behaviors, including smoking (100%), high-fat diet (68%), inadequate fruits/vegetables (67%), poor sleep (53%), physical inactivity (52%), and marijuana use (46%). The percent prepared to change ranged from 23% for tobacco and marijuana to 76% for depression management. Latent class analysis differentiated three risk groups: the global higher risk group included patients elevated on all risk behaviors; the global lower risk group was low on all risks; and a mood and metabolic risk group, characterized by inactivity, unhealthy diet, sleep problems, and poor stress and depression management. The global higher risk group (11% of sample) was younger, largely male, and had the greatest number of risk behaviors and mental health diagnoses; had the most severe psychopathologies, addiction-treatment histories, and nicotine dependence; and the lowest confidence for quitting smoking and commitment to abstinence. Conclusion: Most smokers with SMI engaged in multiple risks. Expanding targets to treat co-occurring risks and personalizing treatment to individuals' multibehavioral profiles may increase intervention relevance, interest, and impact on health. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
    Health Psychology 01/2014; · 3.95 Impact Factor
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    ABSTRACT: The rates of nicotine metabolism differ widely, even after controlling for genetic variation in the major nicotine-metabolizing enzyme, CYP2A6. Genetic variants in an additional nicotine-metabolizing enzyme, flavin-containing monooxygenase (FMO)-3, and an obligate microsomal CYP-supportive enzyme, cytochrome P450 oxidoreductase (POR), were investigated. We examined the impact of FMO3 E158K and POR A503V before and after stratifying by CYP2A6 metabolism group. In 130 nonsmokers of African descent who received 4 mg oral nicotine, FMO3 158K trended toward slower nicotine metabolism in reduced CYP2A6 metabolizers (P=0.07) only, whereas POR 503V was associated with faster CYP2A6 activity (nicotine metabolite ratio) in normal (P=0.03), but not reduced, CYP2A6 metabolizers. Neither FMO3 158K nor POR 503V significantly altered the nicotine metabolic ratio (N=659), cigarette consumption (N=667), or urine total nicotine equivalents (N=418) in smokers of African descent. Thus, FMO3 E158K and POR A503V are minor sources of nicotine metabolism variation, insufficient to appreciably alter smoking.
    Pharmacogenetics and Genomics 01/2014; · 3.61 Impact Factor
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    ABSTRACT: Cigarette smoking remains a significant health threat for smokers and nonsmokers alike. Secondhand smoke (SHS) is intrinsically more toxic than directly inhaled smoke. Recently, a new threat has been discovered - Thirdhand smoke (THS) - the accumulation of SHS on surfaces that ages with time, becoming progressively more toxic. THS is a potential health threat to children, spouses of smokers and workers in environments where smoking is or has been allowed. The goal of this study is to investigate the effects of THS on liver, lung, skin healing, and behavior, using an animal model exposed to THS under conditions that mimic exposure of humans. THS-exposed mice show alterations in multiple organ systems and excrete levels of NNAL (a tobacco-specific carcinogen biomarker) similar to those found in children exposed to SHS (and consequently to THS). In liver, THS leads to increased lipid levels and non-alcoholic fatty liver disease, a precursor to cirrhosis and cancer and a potential contributor to cardiovascular disease. In lung, THS stimulates excess collagen production and high levels of inflammatory cytokines, suggesting propensity for fibrosis with implications for inflammation-induced diseases such as chronic obstructive pulmonary disease and asthma. In wounded skin, healing in THS-exposed mice has many characteristics of the poor healing of surgical incisions observed in human smokers. Lastly, behavioral tests show that THS-exposed mice become hyperactive. The latter data, combined with emerging associated behavioral problems in children exposed to SHS/THS, suggest that, with prolonged exposure, they may be at significant risk for developing more severe neurological disorders. These results provide a basis for studies on the toxic effects of THS in humans and inform potential regulatory policies to prevent involuntary exposure to THS.
    PLoS ONE 01/2014; 9(1):e86391. · 3.53 Impact Factor

Publication Stats

19k Citations
3,901.72 Total Impact Points


  • 1976–2014
    • University of California, San Francisco
      • • Division of Clinical Pharmacology & Experimental Therapeutics
      • • Division of Cardiology
      • • Division of Hospital Medicine
      • • Department of Physiological Nursing
      • • Department of Pediatrics
      • • Department of Psychiatry
      San Francisco, California, United States
  • 2013
    • Stanford University
      • Stanford Prevention Research Center
      Palo Alto, CA, United States
    • Roswell Park Cancer Institute
      • Department of Health Behavior
      Buffalo, NY, United States
  • 2006–2013
    • University of Toronto
      • Department of Pharmacology and Toxicology
      Toronto, Ontario, Canada
    • IWK Health Centre
      Halifax, Nova Scotia, Canada
    • Environmental Science & Research
      Окленд, Auckland, New Zealand
    • Johns Hopkins University
      • Department of Biostatistics
      Baltimore, MD, United States
    • University of Texas MD Anderson Cancer Center
      • Department of Epidemiology
      Houston, TX, United States
  • 2000–2013
    • University of California, Los Angeles
      • • Division of Adult Psychiatry
      • • Department of Medicine
      Los Angeles, CA, United States
  • 1998–2013
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
  • 1995–2013
    • CSU Mentor
      Long Beach, California, United States
  • 1979–2013
    • San Francisco VA Medical Center
      San Francisco, California, United States
    • Clinical pharmacology of Miami
      Miami, Florida, United States
  • 2012
    • University of Minnesota Twin Cities
      • Department of Family Medicine and Community Health
      Minneapolis, MN, United States
    • Emory University
      • Department of Behavioral Sciences and Health Education
      Atlanta, Georgia, United States
  • 2007–2012
    • Robert Wood Johnson University Hospital
      New Brunswick, New Jersey, United States
    • SRI International
      • Centre for Health Sciences
      Menlo Park, CA, United States
    • Queen's University
      Kingston, Ontario, Canada
  • 2003–2012
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States
  • 2011
    • University of California, Berkeley
      • School of Public Health
      Berkeley, CA, United States
    • Azienda Ospedaliero - Universitaria Policlinico - Vittorio Emanuele
      Catania, Sicily, Italy
  • 2010–2011
    • University of Oulu
      • Department of Internal Medicine
      Oulu, Oulu, Finland
    • Oulu University Hospital
      Uleoborg, Oulu, Finland
    • University of Birmingham
      • School of Geography, Earth and Environmental Sciences
      Birmingham, ENG, United Kingdom
  • 2005–2010
    • Rutgers New Jersey Medical School
      • Department of Psychiatry (RWJ Medical School)
      Newark, NJ, United States
    • Instituto Nacional de Salud Pública
      Cuernavaca, Morelos, Mexico
    • South Dakota State University
      Brookings, South Dakota, United States
  • 2009
    • Washington University in St. Louis
      • Department of Psychiatry
      Saint Louis, MO, United States
  • 2006–2009
    • San Diego State University
      • • Graduate School of Public Health
      • • Department of Psychology
      San Diego, CA, United States
  • 2008
    • University of Southern California
      • Department of Preventive Medicine
      Los Angeles, CA, United States
    • Yale-New Haven Hospital
      • Department of Pathology
      New Haven, Connecticut, United States
  • 2006–2008
    • Yale University
      New Haven, Connecticut, United States
  • 1990–2008
    • University of Pittsburgh
      • • Department of Psychiatry
      • • Psychology
      Pittsburgh, PA, United States
  • 2006–2007
    • Columbia University
      • • Department of Sociomedical Sciences
      • • Department of Psychiatry
      New York City, NY, United States
  • 1991–2007
    • National Cancer Institute (USA)
      • • Division of Cancer Control and Population Sciences
      • • Occupational and Environmental Epidemiology
      Bethesda, MD, United States
  • 2003–2005
    • Dokuz Eylul University
      Ismir, İzmir, Turkey
  • 2004
    • Brigham and Women's Hospital
      • Center for Brain Mind Medicine
      Boston, MA, United States
    • Boston College, USA
      Boston, Massachusetts, United States
  • 2002
    • University of North Carolina at Chapel Hill
      North Carolina, United States
  • 1998–2001
    • Shaare Zedek Medical Center
      • Department of Internal Medicine
      Yerushalayim, Jerusalem District, Israel
  • 1989
    • The University of Arizona
      • College of Pharmacy
      Tucson, AZ, United States
  • 1988
    • Oregon Health and Science University
      • Department of Pediatrics
      Portland, OR, United States