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.

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.

Background & Aims: It is not known why some people with Helicobacter pylori infection develop gastric cancer whereas others do not. Whether the CagA phenotype of H pylori infection affected risk for cancer independently of other posited risk factors was evaluated.

Subjects: 242 persons who participated in a previous nested case-control study of gastric cancer. 179 (90 cases and 89 controls) were infected with H pylori as determined by enzyme linked immunosorbent assay (ELISA) in serum and 63 (13 cases and 50 controls) were uninfected.

Methods: Serum samples from cases and controls, obtained a mean of 14.2 years before diagnosis of cancer in the cases, were tested by ELISA for IgG antibodies against the CagA gene product of H pylori. They had previously been tested for pepsinogen I. Using logistic regression analysis, risk for cancer was compared among infected persons with CagA antibodies, infected persons without CagA antibodies, and uninfected persons.

Results: Subjects infected with H pylori who had CagA antibodies were 5.8-fold more likely than uninfected subjects to develop gastric cancer (95% confidence interval (95% CI) = 2.6-13.0). This was true for both intestinal (odds ratio (OR) 5.1, 95% CI = 2.1-12.2) and diffuse type (OR 10.1, 95% CI = 2.2-47.4) cancers. By contrast, H pylori infected subjects without CagA antibodies were only slightly, and not significantly, at increased risk for cancer (OR 2.2, 95% CI = 0.9-5.4) and any possible association was restricted to diffuse type carcinoma (OR 9.0, 95% CI = 1.2-65.8). Pepsinogen 1 50 ng/ml significantly increased risk for both cancer types in H pylori infected persons and lessened the magnitude of association between CagA and cancer. Educational attainment, cigarette smoking, and ABO blood group were not associated with malignancy.

Conclusions: When compared with uninfected subjects, persons infected with CagA positive H pylori are at considerably increased risk of gastric cancer. CagA negative H pylori are less strongly linked to malignancy and may only be associated with diffuse type disease.