Surveillance for selected tobacco-use behaviors—United States, 1900-1994

Problem/Condition: Surveillance of tobacco use is an essential component of any tobacco-control program. The information gathered can be used to guide research initiatives, intervention programs, and policy decisions. Reporting Periods: This report covers the period 1900–1994 for per capita cigarette consumption; 1965–1991 for trends in cigarette smoking prevalence and cessation; 1974–1991 for trends in the number of cigarettes smoked daily by current smokers; 1987–1991 for recent patterns of tobacco use; 1970, 1987, and 1991 for trends in cigar/pipe smoking and snuff/chewing tobacco use; 1984–1992 for trends in state-specific prevalences of regular cigarette smoking; 1987–1992 for state-specific estimates of smokeless-tobacco use; and 1976–1993 for trends in cigarette smoking among U.S. high school seniors. Description of Systems: Estimates of cigarette consumption are reported by the U.S. Department of Agriculture, which uses data from the U.S. Department of the Treasury, the U.S. Department of Commerce, the Tobacco Institute, and other sources. The National Health Interview Survey uses household interviews to provide nationally representative estimates (for the civilian, noninstitutionalized population) of cigarette smoking and other behaviors related to tobacco use. The Behavioral Risk Factor Surveillance System uses telephone surveys of civilian, noninstitutionalized adults (³18 years of age) to provide state-specific estimates of current cigarette smoking and use of smokeless tobacco. The University of Michigan’s Institute for Social Research uses school-based, self-administered questionnaires to gather data on cigarette smoking from a representative sample of U.S. high school seniors. Results: During the period 1900–1963, per capita cigarette consumption increased; after 1964, consumption declined. During the years 1965–1991, current cigarette smoking prevalence among persons ages ³18 years declined overall and in every sociodemographic category examined. Decrease in current smoking prevalence was slow in some groups (e.g., among persons with fewer years of formal education). Both the prevalence of never smoking and the prevalence of cessation increased from 1965 through 1991. The prevalence of current cigarette smoking, any tobacco smoking, and any tobacco use was highest among American Indians/Alaska Natives and non-Hispanic blacks and lowest among Asians/Pacific Islanders. The prevalence of cigar smoking and pipe smoking has declined substantially since 1970. The prevalence of smokeless-tobacco use among white males ages 18–34 years was higher in 1987 and 1991 than in 1970; among persons ³45 years of age, the use of smokeless tobacco was more common among blacks than whites in 1970 and 1987. Cigarette smoking prevalence has decreased in most states. The prevalence of smokeless tobacco use was especially high among men in West Virginia, Montana, and several southern states. From 1984–1993, prevalence of cigarette smoking remained constant among U.S. high school seniors. However, prevalence increased slightly for male seniors and white seniors, decreased slightly for female high school seniors, and decreased sharply for black high school seniors. Interpretation: With the exceptions of increases in cigarette smoking among white and male high school seniors and in the use of smokeless tobacco among white males ages 18–34 years, reductions in tobacco use occurred in every subgroup examined. This decrease must continue if the national health objectives for the year 2000 are to be reached. Actions Taken: Surveillance of tobacco use is ongoing. Effective interventions that discourage initiation and encourage cessation are being disseminated throughout the United States

Smoking and Ischemic Heart Disease Disparities Between Studies, Genders, Times, and Socioeconomic Strata

Large, unexplained, but possibly related disparities exist between heart disease risks observed in differing genders, educational levels, times, and studies. Such heart disease disparities might be related to cumulative tobacco smoke damage (smoke load) disparities that are overlooked in standard assessments of point smoking status. So, I reviewed possible relationships between smoke load and heart disease levels across genders, educational strata, years, and leading studies. Smoker heart disease risk assessments in the Nurses Health Study (Nurses), Cancer Prevention Study-II (CPS-II), and British Doctors studies were compared and related to their likely selection and misclassification biases. Relationships between smoke loads and United States (US) education- and gender-related heart disease mortality disparities were qualitatively assessed using lung cancer rates as a smoke load proxy. The high heart disease mortality risks observed in smoking Nurses in 1980–2004 and in less educated US women in 2001 were qualitatively associated with their higher smoke loads and lower selection and exposure misclassification biases than in the CPS-II and Doctors studies. Smoking-attributable heart disease death tolls and disparities extrapolated from mortality ratios from the CPS-II and Doctors studies may be substantial underestimates. Such studies appear to have compared convenience samples of light smokers to lighter smokers instead of comparing representative smokers to the unexposed. Further efforts to minimize smoke exposures and better quantify cumulative smoking-attributable burdens are needed

Probing the Production of Amidated Peptides following Genetic and Dietary Copper Manipulations

Amidated neuropeptides play essential roles throughout the nervous and endocrine systems. Mice lacking peptidylglycine α-amidating monooxygenase (PAM), the only enzyme capable of producing amidated peptides, are not viable. In the amidation reaction, the reactant (glycine-extended peptide) is converted into a reaction intermediate (hydroxyglycine-extended peptide) by the copper-dependent peptidylglycine-α-hydroxylating monooxygenase (PHM) domain of PAM. The hydroxyglycine-extended peptide is then converted into amidated product by the peptidyl-α-hydroxyglycine α-amidating lyase (PAL) domain of PAM. PHM and PAL are stitched together in vertebrates, but separated in some invertebrates such as Drosophila and Hydra. In addition to its luminal catalytic domains, PAM includes a cytosolic domain that can enter the nucleus following release from the membrane by γ-secretase. In this work, several glycine- and hydroxyglycine-extended peptides as well as amidated peptides were qualitatively and quantitatively assessed from pituitaries of wild-type mice and mice with a single copy of the Pam gene (PAM+/−) via liquid chromatography-mass spectrometry-based methods. We provide the first evidence for the presence of a peptidyl-α-hydroxyglycine in vivo, indicating that the reaction intermediate becomes free and is not handed directly from PHM to PAL in vertebrates. Wild-type mice fed a copper deficient diet and PAM+/− mice exhibit similar behavioral deficits. While glycine-extended reaction intermediates accumulated in the PAM+/− mice and reflected dietary copper availability, amidated products were far more prevalent under the conditions examined, suggesting that the behavioral deficits observed do not simply reflect a lack of amidated peptides

Rank-Order of Potencies for Inhibition of the Secretion of Aβ40 and Aβ42 Suggests that Both Are Generated by a Single Γ-Secretase

The Alzheimer\u27s disease amyloid peptide Aβ has a heterogeneous COOH terminus, as variants 40 and 42 residues long are found in neuritic plaques and are secreted constitutively by cultured cells. The proteolytic activity that liberates the Aβ COOH terminus from the β-amyloid precursor protein is called γ-secretase. It could be one protease with dual specificity or two distinct enzymes. By using enzyme-linked immunosorbent assays selective for Aβ40 or Aβ42, we have measured Aβ secretion by a HeLa cell line, and we have examined the dose responses for a panel of five structurally diverse γ- secretase inhibitors. The inhibitors lowered Aβ and p3 secretion and increased levels of the COOH-terminal 99-residue β-amyloid precursor protein derivative that is the precursor for Aβ but did not alter secretion of β- amyloid precursor protein derivatives generated by other secretases, indicating that the inhibitors blocked the γ-secretase processing step. The dose-dependent inhibition of Aβ42 was unusual, as the compounds elevated Aβ42 secretion at sub-inhibitory doses and then inhibited secretion at higher doses. A compound was identified that elevated Aβ42 secretion at a low concentration without inhibiting Aβ42 or Aβ40 at high concentrations, demonstrating that these phenomena are separable pharmacologically. Using either of two methods, IC50 values for inhibition of Aβ42 and Aβ40 were found to have the same rank-order and fall on a trend line with near-unit slope. These results favor the hypothesis that Aβ variants ending at residue 40 or 42 are generated by a single γ-secretase