Stanford Health Policy is a joint effort of the Freeman Spogli Institute for International Studies and the Stanford School of Medicine
This issue of CHP/PCOR's quarterly newsletter covers news and developments from the summer 2004 quarter. It features articles about:
PURPOSE
Smoking is the leading controllable risk factor for heart disease. Only about 69% of U.S. indoor workers are currently covered by a smoke-free workplace policy. This analysis projects the cardiovascular health and economic effects of making all U.S. workplaces smoke free after 1 year and at steady state.
METHODS
We estimated the number of U.S. indoor workers not covered by smoke-free workplace policies, and the effects of making all workplaces smoke free on smoking behavior and on the relative risks of acute myocardial infarctions and strokes. One-year and steady-state results were calculated using an exponential decline model. A Monte Carlo simulation was performed for a sensitivity analysis.
RESULTS
The first-year effect of making all workplaces smoke free would produce about 1.3 million new quitters and prevent over 950 million cigarette packs from being smoked annually, worth about $2.3 billion in pretax sales to the tobacco industry. In 1 year, making all workplaces smoke free would prevent about 1500 myocardial infarctions and 350 strokes, and result in nearly $49 million in savings in direct medical costs. At steady state, 6250 myocardial infarctions and 1270 strokes would be prevented, and $224 million would be saved in direct medical costs annually. Reductions in passive smoking would account for 60% of effects among acute myocardial infarctions.
CONCLUSION
Making all U.S. workplaces smoke free would result in considerable health and economic benefits within 1 year. Reductions in passive smoking would account for a majority of these savings. Similar effects would occur with enactment of state or local smoke-free policies.
This is the first controlled prospective study of the effects of nicotine deprivation in adolescent smokers. Heart rate and subjective withdrawal symptoms were measured over an 8-hr period while participants smoked normally. Seven days later, participants were randomized to wear a 15-mg (16-hr) nicotine patch or a placebo patch for 8 hr, and they refrained from smoking during the session. Those wearing the placebo experienced a decrease in heart rate across sessions and an increase in subjective measures of nicotine withdrawal. Those wearing the active patch also reported significant increases for some subjective symptoms. Expectancy effects were also observed. The findings indicate that adolescent smokers experience subjective and objective changes when deprived of nicotine. As in previous research with adults, expectancies concerning the effects of nicotine replacement also influenced perceptions of withdrawal.
The association of nutrient intake with the risk of amyotrophic lateral sclerosis (ALS) was investigated in a population-based case-control study conducted in three counties of western Washington State from 1990 to 1994. Incident ALS cases (n = 161) were identified and individually matched on age and gender to population controls (n = 321). A self-administered food frequency questionnaire was used to assess nutrient intake. Conditional logistic regression analysis was used to compute odds ratios adjusted for education, smoking, and total energy intake. The authors found that dietary fat intake was associated with an increased risk of ALS (highest vs. lowest quartile, fiber-adjusted odds ratio (OR) = 2.7, 95% confidence interval (CI): 0.9, 8.0; p for trend = 0.06), while dietary fiber intake was associated with a decreased risk of ALS (highest vs. lowest quartile, fat-adjusted OR = 0.3, 95% CI: 0.1, 0.7; p for trend = 0.02). Glutamate intake was associated with an increased risk of ALS (adjusted OR for highest vs. lowest quartile = 3.2, 95% CI: 1.2, 8.0; p for trend < 0.02). Consumption of antioxidant vitamins from diet or supplement sources did not alter the risk. The positive association with glutamate intake is consistent with the etiologic theory that implicates glutamate excitotoxicity in the pathogenesis of ALS, whereas the associations with fat and fiber intake warrant further study and biologic explanation.
The associations of cigarette smoking and alcohol consumption with the risk of amyotrophic lateral sclerosis (ALS) were investigated in a population-based case-control study conducted in three counties of western Washington State from 1990 to 1994. Incident ALS cases (n = 161) were identified and were matched to population controls (n = 321) identified through random digit dialing and Medicare enrollment files. Conditional logistic regression analysis was used to compute odds ratios adjusted for age, gender, respondent type, and education. The authors found that alcohol consumption was not associated with the risk of ALS. Ever having smoked cigarettes was associated with a twofold increase in risk (alcohol-adjusted odds ratio (OR) = 2.0, 95% confidence interval (CI): 1.3, 3.2). A greater than threefold increased risk was observed for current smokers (alcohol-adjusted OR = 3.5, 95% CI: 1.9, 6.4), with only a modestly increased risk for former smokers (alcohol-adjusted OR = 1.5, 95% CI: 0.9, 2.4). Significant trends in the risk of ALS were observed with duration of smoking (p for trend = 0.001) and number of cigarette pack-years (p for trend = 0.001). The finding that cigarette smoking is a risk factor for ALS is consistent with current etiologic theories that implicate environmental chemicals and oxidative stress in the pathogenesis of ALS.
BACKGROUND: Cigarette smoking is a major risk factor for several chronic oxidative diseases that can be ameliorated by antioxidants.
OBJECTIVES: This study identified the typical dietary intakes and the major food group contributors of the antioxidants beta-carotene, vitamin C, and vitamin E by smoking status.
DESIGN: The 1994-1996 Continuing Survey of Food Intakes by Individuals (CSFII) provided the current sample (n = 6749), who were categorized as non- (n = 3231), former (n = 1684), and current (n = 1834) smokers. In the CSFII, individuals' food intakes were estimated with two 24-h dietary recalls. Data were analyzed by using a chi-square test with a simultaneous Fisher's z test, analysis of variance with Scheffe's test, multivariate analysis of covariance, and analysis of covariance with Bonferroni adjustment for multiple comparisons.
RESULTS: The sample consisted of 3707 men and 3042 women. Current smokers tended to be younger with less education and lower incomes than nonsmokers and former smokers. The average body mass index (in kg/m(2)) of current smokers was 25.8, the lowest of the 3 groups. Current smokers had the lowest dietary antioxidant intake. Fatty foods such as luncheon meats, condiments and salad dressings, and ground beef contributed more to the antioxidant intakes of current smokers than to those of the other 2 groups, whereas fruit and vegetables contributed less. Current smokers consumed the fewest numbers of servings of all nutrient-bearing groups in the food guide pyramid, except the meat group.
CONCLUSION: Future interventions should target the clustering of cigarette smoking and other unhealthy lifestyle habits, eg, an imprudent diet.
Thomas N. Robinson, MD, MPH is the Irving Schulman, MD Endowed Professor in Child Health, Professor of Pediatrics and of Medicine, in the Division of General Pediatrics and the Stanford Prevention Research Center at Stanford University School of Medicine, and Director of the Center for Healthy Weight at Stanford University and Lucile Packard Children's Hospital at Stanford. Dr. Robinson focuses on "solution-oriented" research, developing and evaluating health promotion and disease prevention interventions for children, adolescents and their families to directly inform medical and public health practice and policy.
His research is largely experimental in design, conducting school-, family- and community-based randomized controlled trials to test the efficacy and/or effectiveness of theory-driven behavioral, social and environmental interventions to prevent and reduce obesity, improve nutrition, increase physical activity and decrease inactivity, reduce smoking, reduce children's television and media use, and demonstrate causal relationships between hypothesized risk factors and health outcomes. Robinson's research is grounded in social cognitive models of human behavior, uses rigorous methods, and is performed in generalizable settings with diverse populations, making the results of his research more relevant for clinical and public health practice and policy.
His research is published widely in the peer-reviewed scientific literature. Robinson received both his B.S. and M.D. from Stanford University and his M.P.H. in Maternal and Child Health from the University of California, Berkeley. He completed his internship and residency in Pediatrics at Children's Hospital, Boston and Harvard Medical School, and then returned to Stanford for post-doctoral training as a Robert Wood Johnson Clinical Scholar. Robinson joined the faculty at Stanford in 1993, was appointed Assistant Professor in 1996, and promoted to Associate Professor with tenure in 2003. He was a Robert Wood Johnson Foundation Generalist Physician Faculty Scholar, was a member of the Institute of Medicine's Committees on Prevention of Obesity in Children and Adolescents and Progress in Preventing Childhood Obesity, and is Principal Investigator on numerous prevention studies funded by the National Institutes of Health. Dr. Robinson also is Board Certified in Pediatrics, a fellow of the American Academy of Pediatrics, and practices General Pediatrics at Lucile Packard Children's Hospital at Stanford.
Objective: To estimate excess direct medical costs of low birth weight from maternal smoking and short-term cost savings from smoking cessation programs before or during the first trimester of pregnancy.
Methods: Simulations using data on neonatal costs per live birth. Outcome measures are mean US excess direct medical cost per live birth, total excess direct medical cost, reductions in low birth weight, and savings in medical costs from an annual 1 percentage point drop in smoking prevalence among pregnant women.
Results: Mean average excess direct medical cost per live birth for each pregnant smoker (in 1995 dollars) was $511; total cost was $263 million. An annual drop of 1 percentage point in smoking prevalence would prevent 1300 low birth weight live births and save $21 million in direct medical costs in the first year of the program; it would prevent 57,200 low birth weight infants and save $572 million in direct medical costs in 7 years.
Conclusions: Smoking cessation before the end of the first trimester produces significant cost savings from the prevention of low birth weight.
To assess whether Helicobacter pylori-related inflammation increases oxidative DNA damage, we evaluated the association between H. pylori infection and urinary excretion of an adduct of oxidative DNA damage, 8-hydroxy-2-deoxyguanosine (8ohdG). Subjects included 555 healthy persons, ages 20-39, within the Kaiser Permanente Medical Care Program in Northern California. We tested sera for antibodies to H. pylori by ELISA; collected demographic, dietary, smoking, and alcohol data by questionnaire; and assayed 24-h urine samples for 8ohdG with a newly developed ELISA kit. Two hundred eighty-one subjects provided adequate 24-h urine samples for 8ohdG and creatinine assays and had detectable levels of 8ohdG. After adjusting for 24-h urinary creatinine (Ucr) and demographic factors, persons without H. pylori infection had significantly higher amounts of 24-h urinary 8ohdG than infected persons (geometric mean, 18.04 microg 8ohdG/Ucr g versus 14.36 microg 8ohdG/Ucr g, respectively; P = 0.008). Excretion of 8ohdG was higher in whites and Hispanics (17.44 and 18.09 microl/Ucr g) than in blacks (13.21 microg/Ucr g; P 0.001). Gender was not significantly associated with 8ohdG excretion (16.18 microg/Ucr g for males versus 16.01 microg/Ucr g for females; P = 0.883). Of the dietary factors evaluated, vitamin C negatively correlated (P 0.001) and carbohydrate intake positively correlated with 8ohdG excretion (P = 0.003). Infection with H. pylori was strongly associated with decreased 8ohdG excretion in the urine. This unexpected finding suggests either that DNA repair is deficient in infected subjects, that inflammation destroys the adduct, or that urinary 8ohdG is not an accurate measure of gastric damage.
OBJECTIVE: To compare the probability of cancer in a solitary pulmonary nodule using standard criteria with Bayesian analysis and result of 2- [F-18] fluoro-2-deoxy-D-glucose-positron emission tomographic (FDG-PET) scan.
SETTING: A university hospital and a teaching Veteran Affairs Medical Center.
METHODS: Retrospective analysis of 52 patients who had undergone both CT scan of the chest and a FDG-PET scan for evaluation of a solitary pulmonary nodule. FDG-PET scan was classified as abnormal or normal. Utilizing Bayesian analysis, the probability of cancer using "standard criteria" available in the literature, based on patient's age, history of previous malignancy, smoking history, size and edge of nodule, and presence or absence of calcification were calculated and compared to the probability of cancer based on an abnormal or normal FDG-PET scan. Histologic study of the nodules was the gold standard.
RESULTS: The likelihood ratios for malignancy in a solitary pulmonary nodule with an abnormal FDG-PET scan was 7.11 (95% confidence interval [CI], 6.36 to 7.96), suggesting a high probability for malignancy, and 0.06 (95% CI, 0.05 to 0.07) when the PET scan was normal, suggesting a high probability for benign nodule. FDG-PET scan as a single test alone was more accurate than the standard criteria and standard criteria plus PET scan in correctly classifying nodules as malignant or benign.
CONCLUSION: FDG-PET scan as a single test was a better predictor of malignancy in solitary pulmonary nodules than the standard criteria using Bayesian analysis. FDG-PET scan can be a useful adjunct test in the evaluation of solitary pulmonary nodules.