The effect has been studied of sodium cromoglycate (SCG) on the activity of ‘C’ fibre sensory nerve endings in the canine lung. Pretreatment with SCG (100 μg/kg i.v.) reduced the excitation of these endings by capsaicin (10 μg/kg i.v.) for approximately 45 min. This property of SCG may explain its ability to suppress certain types of bronchoconstrictor responses in man.
A review is presented of the scientific literature on the effects of sugars (mono- and disaccharides), when used as tobacco additives, on the formation of acetaldehyde in mainstream (MS) smoke and the potential bioavailablity of MS smoke acetaldehyde derived from sugars to the smoker. The experimental data supports the following conclusions. Sugars, e.g., D-glucose, D-fructose, and sucrose, do not produce greater yields of acetaldehyde in MS smoke than are produced from tobacco itself on a weight-for-weight basis. A variety of studies suggests that natural tobacco polysaccharides, including cellulose, are the primary precursors of acetaldehyde in MS smoke. In a number of different studies using commercial cigarette brands, MS smoke yields of acetaldehyde correlate (r > 0.9) with both MS smoke "tar" and carbon monoxide. MS smoke acetaldehyde yields are affected more by cigarette design characteristics that influence total smoke production, such as filter ventilation, filtration, and paper porosity, than by reducing sugars. MS smoke acetaldehyde deposits primarily in the upper respiratory tract, including the mouth, of the smoker. Acetaldehyde is rapidly metabolized by aldehyde dehydrogenase in the blood and elsewhere in the body, including at the blood-brain barrier. Tobacco sugar-derived MS smoke acetaldehyde from commercial cigarettes is unlikely to result in direct central nervous system effects on the smoker.
The analysis of spent cigarette filters enables the estimation of the nicotine and tar (nicotine-free dry particulate matter) yields obtained by smokers in their everyday environment and has been shown to correlate well with biomarkers of exposure. Leading products across the range of ISO tar yields were selected from Australia, Brazil, Canada, Germany, Japan, New Zealand, South Africa and Switzerland. At least fifty demographically representative smokers were recruited per product. Subjects, ≥ 21 years of age and smoking ≥ 5 cigarettes per day, were asked to collect ≥ 15 filters from cigarettes they had smoked. The collected filters were analysed for nicotine and UV absorbance to enable the smokers' mouth level exposure to nicotine and tar to be estimated and a comparison of countries and tobacco blend styles to be made. Smoking history data were also collected. More than 80,000 filters were collected from 5703 smokers of 106 products from eight countries. Mean ± SD estimated nicotine exposures per cigarette and per day ranged from 0.93 ± 0.34 mg/cigarette (Brazil) to 1.77 ± 0.69 mg/cigarette (South Africa) and from 16.4 ± 11.1mg/day (Germany) to 31.5 ± 14.8 mg/day (South Africa), respectively. Male smokers obtained higher mean estimated tar and nicotine exposures than female smokers. These gender differences were statistically significant for six countries. Significant correlations were found between estimated nicotine exposure and ISO nicotine yield, and between estimated tar exposure and ISO tar yield (p<0.001).
The influence of the tobacco additives diammonium hydrogen phosphate (DAP) and urea on the delivery and respiratory tract retention of nicotine and solanesol and on the uptake of nicotine into venous blood was investigated in 10 smokers under mouth-hold and 75 and 500 mL inhalation conditions. Three cigarettes with identical physical specifications were produced from a common lamina tobacco blend. The control cigarette contained nonammoniated reconstituted tobacco sheet (RTS), whereas DAP and other ammonia compounds were added to the RTS of the second cigarette. Urea was added to the tobacco of the third cigarette. The presence of DAP or urea in the test cigarettes did not significantly influence solanesol retention within the mouth during the mouth-hold condition. Nicotine retention within the mouth during the mouth-hold condition was, however, significantly higher for the DAP cigarette (64.3 +/- 10.5%) than for the urea (53.3 +/- 11.3%) or control cigarette (46.3 +/- 8.6%), but this did not result in an increase in nicotine uptake into venous blood. Solanesol retentions during the 75 and 500 mL inhalation volume conditions and nicotine retentions during the 75 mL inhalation volume condition were not significantly different for the three cigarette types. Although the nicotine retention approached 100% with each cigarette type during the 500 mL inhalation condition, the nicotine retention for the urea-treated cigarette (99.6 +/- 0.2%) was marginally, but statistically, significant, higher than for the control (99.1 +/- 0.5%) and DAP-treated cigarettes (98.8 +/- 0.6%). There were no statistically significant differences between the indices of nicotine uptake into venous blood for the three cigarette types in any of the inhalation conditions.
SUIMMARY1. The ability of histamine, acetylcholine (ACh) and 5-hydroxytryptamine (5-HT) given i.v. and by aerosol to induce reflex bronchoconstriction and to activate lung irritant receptors has been studied in dogs anaesthetized with chloralose. 4. Histamine, 5-HT and ACh given by aerosol and i.v. increased lung irritant receptor discharge. Irrespective of the route of administration, for a given change in RL histamine produced a greater increase in irritant receptor discharge than did ACh or 5-HT, which produced similar increases.5. For a given change in RL, histamine, ACh and 5-HT were more effective in activating lung irritant receptors when given I.v. than by aerosol.6. The mechanisms of irritant receptor activation by histamine, ACh and 5-HT and the relationship between irritant receptor discharge and reflex bronchoconstriction are discussed.
Rationale Nicotine uptake during smoking was estimated by either analyzing the metabolites of nicotine in various body fluids or by analyzing filters from smoked cigarettes. However, no comparison of the filter analysis method with body fluid analysis methods has been published. Objectives Correlate nicotine uptake estimates between filter analysis, salivary cotinine, and urinary excretion of selected nicotine metabolites to determine the suitability of these methods in estimating nicotine absorption in smokers of filtered cigarettes. Materials and methods A 5-day clinical study was conducted with 74 smokers who smoked 1-19 mg Federal Trade Commission tar cigarettes, using their own brands ad libitum. Filters were analyzed to estimate the daily mouth exposure of nicotine. Twenty-four-hour urine samples were collected and analyzed for nicotine, cotinine, and 3′-hydroxycotinine plus their glucuronide conjugates. Saliva samples were collected daily for cotinine analysis.Results Each method correlated significantly (p<0.01) with the other two. The best correlation was between the mouth exposure of nicotine, as estimated by filter analysis, and urinary nicotine plus metabolites. Multiple regression analysis implies that saliva cotinine and urinary output are dependent on nicotine mouth exposure for multiple days. Creatinine normalization of the urinary metabolites degrades the correlation with mouth exposure. Conclusions The filter analysis method was shown to correlate with more traditional methods of estimating nicotine uptake. However, because filter analysis is less complicated and intrusive, subjects can collect samples easily and unsupervised. This should enable improvements in study compliance and future study designs.
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