Raymond B. Bridges

Puffing topography as a determinant of smoke exposure

Puffing topography variables were measured in a well-characterized, male population smoking their own brand of cigarette. Of the puffing topography variables, interpuff interval appeared to be the primary determinant of blood concentrations of smoke constituents: however, preliminary data in a homogeneous population according to the nicotine yield of their cigarette suggest that total puff volume per cigarette may also be a significant determinant of blood levels of smoke constituents. Smokers of low nicotine yield cigarettes partially compensated for these lower yields by increasing the total volume puffed per cigarette. Observed differences in puffing topography associated with increased daily cigarette consumption and cumulative smoking history were consistent with a higher smoke exposure per cigarette. Further, although both alcohol and coffee consumption are associated with present and cumulative smoking history, coffee consumption is uniquely associated with differences in puffing topography consistent with a higher smoke exposure per cigarette. However, by multiple regression analyses, neither coffee nor alcohol consumption histories added significantly to the prediction of blood concentrations of smoke constituents over that obtained by smoking history and puffing topography.

Population characteristics and cigarette yield as determinants of smoke exposure

Relationships of population characteristics, smoking history, and cigarette yield with smoke exposure as measured by peripheral blood concentrations of thiocyanate, carboxyhemoglobin, nicotine and cotinine were sought in 170 male smokers. This population of smokers had significant elevations of serum thiocyanate, blood carboxyhemoglobin and plasma nicotine and cotinine concentrations as compared with an equal number of age- and sex-matched nonsmokers and these concentrations correlated significantly with past 24-hour cigarette consumption. Although the nicotine yield of the cigarette correlated significantly with plasma cotinine and marginally with plasma nicotine, the reduction in plasma nicotine and cotinine was not proportionate to the reduced yield of the cigarettes, suggesting that smokers partially compensate for the lower yields of their cigarettes. Blood levels of carboxyhemoglobin, nicotine and cotinine were also significantly associated with the weight of the subjects, presumably due to the relationship between weight and the volume of distribution. Univariate and multiple regression analyses provided evidence that coffee and alcohol consumption and years smoked also may be important determinants of smoke exposure.

Increased plasma concentrations of C9, C1-inhibitor and α1-protease inhibitor associated with cigarette smoking

The association between various parameters of acute and chronic smoking status and plasma levels of three proteins, C9, C1-inhibitor (C1-INH) and alpha 1-protease inhibitor (alpha 1-PI) were determined for 49 male cigarette smokers and 49 age-matched nonsmokers (mean age = 32.2 years). The mean number of cigarettes smoked was 28.7 per day while the cumulative consumption was only 18.1 pack-years. Plasma levels of all three proteins were significantly higher in the smokers than nonsmokers. Plasma C9 and alpha 1-PI concentrations correlated with cumulative cigarette consumption and plasma nicotine concentrations. While C1-INH concentration did not correlate with either cumulative cigarette consumption or plasma nicotine concentration, it correlated significantly with serum thiocyanate concentration. No consistent correlation was found between plasma concentration of these proteins and parameters of pulmonary function.

The Ca2+ and Mg2+ activated ATPase and ADPase in subcellular fractions of beaver (Castor canadensis) enamel organ

Abstract 1. 1. Ca 2+ and Mg 2+ stimulated ATPase activities were indistinguishable according to their subcellular distribution. 2. 2. Ca 2+ and Mg 2+ ATPase activities were chiefly associated with the microsomal and mitochondrial fractions. 3. 3. Ouabain did not inhibit Ca 2+ ATPase activity. 4. 4. The Ca 2+ and M 2+ activated ADPase associated with the supernatant fraction may be largely attributed to myokinase and non-specific phosphatase activities. 5. 5. Ca 2+ and Mg 2+ activated ADPases, separate from the action of myokinase and non-specific phosphatases, were associated chiefly with the microsomal and mitochondrial fractions.

Serum Antioxidant Activity as a Determinant of Pulmonary Dysfunction in Cigarette Smokers

Cigarette smoking is a significant risk factor for the development of chronic obstructive pulmonary disease (COPD), and the primary etiology of COPD in smokers is presumably a pulmonary protease-antiprotease imbalance.1 Oxidants in cigarette smoke2,3 and those generated by activated phagocytes4 have both been shown to inactivate the pulmonary antiproteases. This cross-sectional study examined the effects of smoking on total serum antioxidant activity (AOA), the components of peripheral blood which contributed to this AOA, and the relationships between AOA and smoking history or pulmonary dysfunction.