Inverse relation between serum cotinine concentration and blood pressure in cigarette smokers

Blood pressure is, on average, lower in cigarette smokers than in nonsmokers. In a cross-sectional study of 288 normotensive bus drivers, we found a significant inverse correlation between serum cotinine (the major metabolite of nicotine) and systolic and diastolic blood pressure that could not be accounted for by age, body weight, or alcohol consumption. Over the observed range of cotinine values, the average decrease in blood pressure was 10.7 and 7.0 mm Hg for systolic and diastolic blood pressures, respectively. We suggest that cotinine be measured to assess the influence of cigarette smoking in epidemiologic studies of blood pressure.     

Comparative analysis of the effects of hubble-bubble (Sheesha) and cigarette smoking on respiratory and metabolic parameters in hubble-bubble and cigarette smokers

OBJECTIVES AND BACKGROUND: Hazard of smoking tobacco is believed to be minimized by smoking hubble-bubble (HB) instead of cigarettes. Our aims were to (i) develop an assay for estimating nicotine and cotinine; and (ii) evaluate the effect of smoking on respiratory and metabolic parameters in cigarette and HB smokers. METHODS: Urine samples were collected from 152 volunteer smokers (75 cigarette and 77 HB) as well as from 16 healthy controls. We optimized an HPLC method for the determination of nicotine and cotinine. Subjects were asked to complete a chronic respiratory symptoms questionnaire and to undergo spirometry. Fasting blood samples were collected for the determination of their lipid profile. RESULTS: The intra-assay coefficients of variation for nicotine and cotinine were 16.6% and 6.6%, respectively. The mean of cotinine in cigarette smokers (1321.4 ng/mL) was significantly (P = 0.008) higher than the mean cotinine (677.6 ng/mL) in HB smokers. The mean nicotine level in cigarette smokers (1487.3 ng/mL) was significantly (P < 0.0001) higher than the mean nicotine (440.5 ng/mL) in HB smoker. The urinary cotinine and nicotine levels of the control subjects were lower than the detection levels of the assay. The mean high-density lipoprotein cholesterol was lower in cigarette smokers (0.99 mmol/L) compared with HB smoker smokers (1.02 mmol/L) but this was not significant (P = 0.28). Spirometric values were comparable among the three groups but the chronic respiratory symptoms in the smoking groups appeared at an earlier age in the HB smokers compared with the cigarettes smokers (P < 0.05). CONCLUSION: Smoking HB does not reduce the risk of tobacco exposure and it's potentially harmful metabolites on health.     

Relationship of smoking cessation and nicotine gum use to salivary androstenedione and testosterone in middle-aged men

Cross-sectional studies have associated cigarette smoking in men with elevated androstenedione and little net effect on other sex steroids. However, it is not clear if such findings reflect the impact of nicotine exposure or if sex hormone levels change following smoking cessation. The relationship of the reported number of cigarettes smoked per day and salivary continine to salivary testosterone and androstenedione was examined in 221 men aged 35 to 59 years at baseline and 1 year following randomization into a clinical trial including a smoking-cessation intervention. At baseline, salivary cotinine was related to increased salivary androstenedione and testosterone following control for age, body mass, alcohol intake, and time of day of specimen collection (partial r = +.14 and +.30, P < .05 and .01, respectively). The reported number of cigarettes smoked per day was unrelated to either hormone. At the first annual visit, there was a significant decrease in the salivary androstenedione of men who had quite smoking and were currently using nicotine gum (94 v 60 pg/mL, P < .05, n = 34) and of men who had quit smoking and were not exposed to nicotine (86 v 56 pg/mL, P < .05, n = 48), whereas the salivary androstenedione of men who remained smokers at the first annual visit was unchanged (83 v 85 pg/mL, n = 139). Salivary testosterone levels were not significantly affected by a change in smoking status. These findings suggest that cigarette smoking has a primary effect that serves to increase salivary androstenedione, whereas neither cigarette smoking nor nicotine exposure per se has a clear effect on salivary free testosterone levels in men.     

Clinical status of ulcerative colitis in patients who smoke

Objectives: Ulcerative colitis (UC) is largely a disease of nonsmokers. There are few patients who are current smokers, but we have identified a group and reviewed their clinical status, disease activity, and nicotine exposure to examine whether they remain well controlled while smoking.
Methods: Fifty-one patients from three centers with verified UC were reviewed.
Results: Thirty of the group were men; mean age 50 yr, with a mean age of onset of 37 yr. Twenty-two patients had proctosigmoid disease, 12 involvement of left colon, and 17 total colitis. All were current smokers; 41 were cigarette smokers averaging 17 daily. At the onset of colitis 30 were nonsmokers, 25 of them were ex-smokers and 19 developed colitis within 2 yr of stopping smoking. Twenty-eight believed smoking improved disease activity and none felt smoking had a detrimental effect on their UC. Eleven were receiving no medication for UC, 40 were receiving 5-ASA (5-aminosalicylic acid) preparations, and only two took oral steroids. All were in clinical remission, with the exception of one patient; mean St. Marks score was 1.5, out of a possible total of 22. Sigmoidoscopic grades were inactive in all patients except three. Histological assessment showed significant activity in only five. Median serum nicotine was 8 ng/ml (range, 0.4–24.4), median serum cotinine 180 ng/ml (range, 20–453), with corresponding salivary cotinine of 255 ng/ml (range, 34–683). Median rise in nicotine 2 min after a cigarette in 35 patients was 12.1 ng/ml (range, 0.4–44).
Conclusions: Because most current smokers with UC have inactive disease, smoking may contribute to the clinical remission in these patients.     

Cardiovascular effects of nasal and transdermal nicotine and cigarette smoking

The purpose of this study was to compare circadian blood pressure and heart rate patterns and other cardiovascular effects of nicotine delivered rapidly (via nasal spray, NNS), slowly (transdermal nicotine, TDN), by cigarette smoking (rapid delivery of nicotine plus other smoke toxins), and placebo NNS. Twelve healthy cigarette smokers were studied on a research ward when they smoked cigarettes (16 per day) or used TDN (15 mg/16 h), NNS (24 1-mg doses per day), or placebo NNS, each for 5 days. There were no significant differences in systolic blood pressure, but diastolic blood pressure was slightly increased during cigarette smoking. Plasma epinephrine, beta-thromboglobulin, and fibrinogen levels were higher during cigarette smoking than with TDN. For most measurements, NNS values were intermediate between and not significantly different from those of cigarette smoking and TDN. We conclude that, at recommended doses, TDN and NNS have fewer effects on biomarkers of cardiovascular risk than does cigarette smoking.     

Ethnic differences in arterial stiffness and wave reflections after cigarette smoking

BACKGROUND: Smoking increases plasma nicotine. Nicotine releases catecholamines and alters arterial distensibility. The nicotine intake per cigarette is greater and serum cotinine levels, the proximate metabolite of nicotine, are higher in Blacks than in Whites. We tested the hypothesis that cigarette smoking increases the pulse wave velocity (PWV), a marker of arterial stiffness, and the augmentation index (AI), a measure of wave reflection, more in Blacks than in Whites. METHODS: We matched Black (n = 30) and White (n = 30) smokers for age, gender, body mass index and height. We determined carotid-femoral PWV (PWVCF) and carotid-radial PWV (PWVCR) (Complior), the AI derived from the aortic pressure waveform (applanation tonometry, Sphygmocor), blood pressure, heart rate (HR) and cotinine levels before and after cigarette smoking. We also performed measurements in 16 participants after sham smoking. RESULTS: Smoking increased the AI, PWVCF and PWVCR in the whole population (all P < 0.05, n = 60). Increases in the AI and PWV were positively related to serum cotinine levels (all P < 0.05). Smoking increased serum cotinine (P = 0.01) and mean blood pressure (P = 0.03) more, but raised the HR to a lesser extent, in Blacks [+8 +/- 4 versus +13 +/- 6 beats/min in Whites (mean +/- SD), P = 0.01]. Blacks disclosed larger increases in AI adjusted for HR (Blacks, +7.2 +/- 8 versus Whites, +4.4 +/- 8%; P = 0.03), PWVCF (Blacks, +1.1 +/- 0.2 versus Whites, +0.6 +/- 0.3 m/s; P < 0.01) and PWVCR (Blacks, +1.4 +/- 0.1 versus Whites, +0.7 +/- 0.4 m/s; P < 0.01) normalized for the mean blood pressure. No changes were observed with sham smoking. CONCLUSIONS: Smoking acutely increases the PWV and AI in Blacks more than in Whites. Differences in nicotine metabolism and beta-adrenergic sensitivity could explain these findings.     

An association between smoking habits and blood pressure in normotensive Japanese men

We conducted a cross-sectional study to clarify the dose-effect relationship of smoking habits with blood pressure in Japanese men. The subjects were 2781 normotensive male steelworkers ranging in age from 40 to 54 years. They were classified into five categories according to their smoking habits: non-smokers, ex-smokers, light smokers, moderate smokers and heavy smokers. Age, body mass index, salt intake, physical activity, drinking habits, and levels of gamma-glutamyl transpeptidase, total serum cholesterol, uric acid, creatinine and plasma glucose were analysed as covariates. The association between smoking habits and blood pressure was evaluated using analysis of covariance. Our results showed that there was no significant difference in the adjusted systolic and diastolic blood pressure between non-smokers and ex-smokers. The adjusted systolic and diastolic blood pressures in light, moderate and heavy smokers were significantly lower than in non- and ex-smokers. However, among smokers, no significant difference was observed in correlation with smoking amount. In conclusion, blood pressure of smokers was lower than that of non- and ex-smokers. However, there were no significant dose-effect relationships between smoking amount and blood pressure when lifestyle and other confounding factors were considered.     

Acute effects of cigarette smoking on platelet-dependent thrombin generation.

AIMS: Thrombin is an important factor in the pathogenesis of thrombotic diseases. To clarify whether smoking has an effect in platelet-dependent thrombogenesis, we studied the acute effects of smoking on platelet-dependent thrombin level in smokers. METHODS AND RESULTS: Subjects consisted of ten smokers and nine non-smokers. Platelet-dependent thrombin level measured after overnight fasting was greater in smokers than in non-smokers (smokers vs non-smokers, 121 +/- 47 vs 56 +/- 5 mIU. ml(-1), P < 0.01). When subjects in the smokers group smoked two cigarettes containing 0.9 mg of nicotine per cigarette, platelet-dependent thrombin levels showed a transient three-fold increase in blood samples obtained immediately after smoking (365+/-76 mIU. ml(-1), P < 0.001). Thrombin levels in the blood samples obtained 10 min and 30 min after smoking were less than that in the samples obtained immediately after smoking ceased, but were not significantly different from those in the samples obtained before smoking. Blood nicotine level increased significantly immediately after smoking (P < 0.001), and plasma protein C activity decreased significantly 30 min after smoking (P < 0.05). When nicotine or cotinine was added to the platelet-rich plasma of non-smokers ex vivo, the platelet-dependent thrombin level increased significantly (P < 0.002). CONCLUSION: Platelet-dependent thrombin level is enhanced in smokers, even when not smoking, when compared with non-smokers and increases immediately after smoking. Increases in nicotine and cotinine levels caused by smoking induced a prothrombotic state in smokers via increased platelet-dependent thrombogenesis.     

Relation between blood pressure and smoking in a population of Quebec workers

Relations between blood pressure and cigarette smoking were investigated on the basis of a health survey conducted in a population of 3034 mine workers from Quebec Province. Blood pressure was found to be lower among smokers than among non-smokers, the difference between these two groups being: systolic pressure 2.3 mmHg, diastolic pressure 3.0 mmHg. After adjustment for age and bodyweight this relation persisted but only as far as diastolic pressure was concerned. The prevalence of hypertension was 1.5 times higher in non-smokers than in smokers. On the other hand, the number of cigarette-smoking years and the number of cigarettes smoked per day seemed to have little effect on mean arterial pressure.     

The relation of anger expression with blood pressure levels and hypertension in rural and urban Japanese communities.

OBJECTIVE: To examine the relation of anger expression with blood pressure and hypertension among Japanese. DESIGN: A cross-sectional study. METHODS: Subjects were 4374 men and women aged 30-74 years from rural and urban communities. Anger expression was estimated using the anger-out and anger-in scores of the Spielberger Anger Expression Scale. Multiple linear regression analyses were performed to estimate the associations of anger expression scores with blood pressure. Proportions of hypertensives among the tertiles of anger expression scores and the relative odds of hypertension for low versus high tertiles of anger expression scales were calculated using logistic regression models. RESULTS: The anger-out score was inversely associated with systolic and diastolic blood pressure levels for men; a four-point (one standard deviation) lower anger-out score was associated with 1.6 mmHg [95% confidence interval (CI), 0.6-2.6] greater systolic blood pressure and 0.6 mmHg (95% CI, -0.03 to 1.2) greater diastolic pressure after adjustment for age, body mass index, alcohol intake, smoking category, and parental history of hypertension. The adjusted relative odds of hypertension for low versus high tertiles of anger-out was 1.60 (95% CI, 1.19-2.15). These inverse associations were more evident among men with low coping behavior than among those with high coping behavior. For women, the anger-out score was not associated with blood pressure. There was no relation between the anger-in score and either blood pressure or hypertension in either men or women. CONCLUSIONS: This study suggests that Japanese men who do not express their anger, especially when they have low coping behavior, may have an increased risk of high blood pressure.     

Heightened acute circulatory responses to smoking in women

Objective. Smoking, a major risk factor for cardiovascular morbidity and mortality, may be particularly harmful to women. Sympathetic and hemodynamic responses to cigarette smoking may be implicated in the link between smoking and acute cardiovascular events. We tested the hypothesis that acute effects of smoking on cardiovascular function are potentiated in women compared with men. Methods. We examined the effects of cigarette smoking and sham smoking on muscle sympathetic nerve activity, blood pressure and heart rate in 20 female and 20 male middle-aged healthy habitual smokers. Results. Sham smoking had no effect on muscle sympathetic nerve activity, blood pressure, or heart rate. Although cigarette smoking increased average systolic blood pressure and heart rate in both females and males, systolic blood pressure increased more in women (12+/-2 mmHg) than in men (6+/-2 mmHg; p = 0.02), as did heart rate (16+/-2 beats/min in women vs 9+/-2 beats/min in men; p = 0.002). Female smokers also had greater smoking-related increases in systolic blood pressure variability compared with males (2.2+/-0.6 vs 0.4+/-0.4 mmHg, respectively; p = 0.01) and greater decreases in RR variability (-28+/-5 vs -7+/-4 ms; p = 0.002). Despite the potentiated blood pressure increase in females, which would be expected to inhibit sympathetic activity to a greater extent in females than in males, changes in muscle sympathetic nerve activity during smoking were similar in both sexes. Conclusions. Acute pressor and tachycardic effects of smoking are potentiated in women compared with men. These findings may have important implications for understanding increased vulnerability to acute cardiovascular events in women who smoke.     

Association between cigarette smoking and hypoxanthine guanine phosphoribosyltransferase activity

The aim of this study was to investigate the association between smoking behavior and hypoxanthine guanine phosphoribosyltransferase (HGPRT) activity. A cross-sectional study was performed of 82 men, including 38 non-smokers and 44 smokers. Inosine monophosphate (IMP), the product of HGPRT (used as the index of activity), was measured in peripheral blood mononuclear cells using high-performance liquid chromatography. The factors potentially associated with HGPRT activity included age, glutamyl oxaloacetic transaminase, glutamyl pyruvic transaminase, cholesterol, uric acid, triglycerides, creatinine, body mass index, gout, systolic blood pressure, diastolic blood pressure, alcohol consumption, and cigarette smoking. Mean HGPRT activity was 7.05 +/- 3.44 nmol/10(6) viable cells/hour for all participants, and was significantly lower for smokers than for non-smokers (6.24 +/- 3.40 vs 7.98 +/- 3.28 nmol/10(6) viable cells/hour; p = 0.02). In addition, as the number of smoked cigarettes increased, the HGPRT activity decreased (p < 0.05). The age at onset of cigarette smoking showed a positive correlation with HGPRT activity after adjusting for smoking duration, serum uric acid, and cigarettes smoked per year using a multiple regression model (p < 0.001). We concluded that the greater the number of cigarettes smoked, the lower the HGPRT activity, and that HGPRT activity was higher in smokers who had started smoking later.     

Modification of the association of alcohol drinking with blood pressure by cigarette smoking

The purpose of this study was to investigate whether the association of alcohol drinking with blood pressure was modified by cigarette smoking. The subjects were healthy male workers aged 40-59 years and were divided into three different groups by average daily consumption of alcohol (non-drinkers; light drinkers, less than 30 g ethanol per day; heavy drinkers, 30 g or more ethanol per day) and cigarettes (non-smokers; light smokers, less than 20 cigarettes per day; heavy smokers, 20 cigarettes or more per day). The mean levels of both systolic and diastolic blood pressures were significantly lower in the light and heavy smoker groups than in the non-smoker group. In the light and heavy smoker groups, systolic blood pressure was higher in the light drinker subgroup than in the non-drinker subgroup, while there was no significant difference between systolic blood pressures in the non- and light drinker subgroups of non-smokers. In the non-, light and heavy smoker groups, systolic and diastolic blood pressures were significantly higher in the heavy drinker subgroup than in the non-drinker subgroup, and these differences tended to be greater in light and heavy smokers than in non-smokers. The above differences in the relationships of alcohol drinking with blood pressure in non-, light and heavy smokers were also observed when age and body mass index were adjusted and when alcohol intake-matched groups were used. These results suggest that the association of alcohol drinking with blood pressure is stronger in smokers than in non-smokers, independently of age, body mass index and alcohol intake.     

Cardiovascular effects immediate to the inhalation of tobacco smoke with different concentrations of nicotine

Fifteen healthy and non smoking men, age range 20 to 27 years (23.6 +/- 2.5 (SD) were subject of a double blind study designed to compare the immediate cardiovascular effects of smoking "regular" and "light" cigarettes (nicotine content: 1.1 mg and 0.6 mg, respectively). The measured cardiovascular parameters were: heart rate, blood pressure, echographic calculations of the left ventricle fractional shortening, amplitude of the posterior wall systolic movement and posterior wall contraction velocity, as well as QTc interval and T wave amplitude. All those measurements were obtained before and after smoking one or two other kind of cigarette. When the changes evoked by the regular cigarette were compared to the changes evoked by the light cigarette, no significant difference was detected. When analyzing the modifications that each kind of cigarette produced to its respective basal-control measurement the following observations were detected: heart rate increased after smoking both types of cigarette (p less than 0.001), blood pressure was raised only with regular cigarette (systolic, p less than 0.002; diastolic, p less than 0.005). QTc interval was prolonged (p less than 0.05) and T wave amplitude decreased (p less than 0.02) after regular and light cigarette. It is concluded that tobacco of regular and light cigarettes significantly and immediately affects diverse cardiovascular parameters, but there is no a clear or definite difference when the changes produced by the two types of cigarette are compared to each other, at least at the level of nicotine here utilized.     

Smoking and the risk of incident hypertension in middle-aged and older men

BACKGROUND: Cigarette smoking is a known risk factor for cardiovascular disease (CVD), but its relationship to the development of hypertension is unclear. Previous epidemiological studies have shown inconsistent results, having demonstrated inverse and positive associations between cigarette smoking and the development of hypertension. METHODS: We analyzed 13,529 male participants from the Physicians' Health Study free of baseline hypertension and CVD who provided information about smoking status. Smoking status was categorized as never, past, or current <20 cigarettes/day, or current > or =20 cigarettes/day. Incident hypertension was defined as either the initiation of antihypertensive treatment, self-reported systolic blood pressure (BP) > or =140 mm Hg, or diastolic BP > or =90 mm Hg. RESULTS: Over a median follow-up of 14.5 years, 4,904 men developed hypertension. We modeled the risk of developing hypertension by baseline smoking status adjusting for known risk factors for hypertension or CVD. In a fully adjusted Cox proportional hazards model, we found that compared with never smokers, past smokers and current smokers had corresponding relative risks (RRs) of 1.08 and 1.15 of developing hypertension. The risk for smokers did not appear to differ based on number of cigarettes smoked daily. Further, the RR of hypertension was higher for men with normal vs. prehypertensive levels of systolic (SBP) or diastolic BP (DBP). CONCLUSIONS: This prospective cohort data suggests that cigarette smoking may be a modest but important risk factor for the development of hypertension.     

Effect of smoking on arterial stiffness and pulse pressure amplification

The brachial artery pressure waveform is abnormal in smokers, but the effect of smoking on the aortic pressure waveform in both smokers and nonsmokers, particularly in the younger population, is unknown. We compared the acute and chronic effects of smoking on large-artery properties in 185 healthy young smokers and nonsmokers (mean+/-SD, 22+/-5 years). We matched 41 chronic smokers for age, height, weight, and gender with 116 nonsmokers. The augmentation index, a measure of arterial wave reflection in the aorta, was measured by applanation tonometry (Sphygmocor). We also compared augmentation index, aortic pulse wave velocity (Complior), and blood pressure in 28 subjects (11 chronic smokers) before and for 15 minutes after smoking 1 cigarette (nicotine content, 1.2 mg). Although brachial blood pressure was not different, the aortic systolic blood pressure (101+/-8 versus 97+/-9 mm Hg) and augmentation index (0.7+/-13 versus -5.7+/-14) were higher (P<0.01) in chronic smokers than in nonsmokers, whereas aortic-brachial pulse pressure amplification was reduced (13.7+/-8 versus 17.7+/-5 mm Hg, P<0.01). These effects were seen in both male and female subjects. Acutely in both groups, smoking significantly increased (P<0.01) both brachial and aortic blood pressure, augmentation index, and pulse wave velocity. No changes were seen after sham smoking. This study shows an acute increase in arterial stiffness after smoking 1 cigarette in chronic smokers and nonsmokers. Higher aortic systolic blood pressure and greater arterial stiffness, in part due to reduced pulse pressure amplification and increased arterial wave reflection, suggest that the adverse hemodynamic effects have hitherto been underestimated in young chronic smokers.     

Acute hemodynamic effect of cigarette smoking and its relationship with nicotine content

We studied the acute effects of cigarette smoking on the cardiovascular system, especially regarding nicotine-related hemodynamic effects using cigarettes with low and high nicotine contents. 40 healthy men who were habitual smokers were divided into two groups: 20 subjects smoked cigarettes of low nicotine content [0.4 mg/cigarette; group 1 (G1)] and another 20 tested cigarettes containing high nicotine [2 mg/cigarette; group 2 (G2)]. All of the subjects were requested to abstain from cigarette smoking for at least 12 hours prior to study, and to rest in the supine position for 30 minutes just prior to the test. They smoked two consecutive cigarettes for 10 minutes, inhaling every 30 seconds by drawing on the cigarette for two seconds, and holding the smoke for three seconds before exhaling. Blood pressure (BP), heart rate (HR) and cardiac output (CO) were measured and blood samples were taken before, and 5, 10 and 30 minutes after the start of smoking. Smoking with a high nicotine content (G2) produced a significant increase in both systolic and diastolic BP (124 +/- 14/78 +/- 8----138 +/- 21/90 +/- 10 mm Hg), but no significant changes in BP were observed in the low nicotine group. HR and CO increased predominantly in both groups (HR: G1; 62 +/- 7----66 +/- 7, G2; 64 +/- 7----76 +/- 9/min, CO: G1; 4.85 +/- 1.36----5.31 +/- 1.37, G2; 4.95 +/- 1.58----5.63 +/- 2.01 l/min), but the present increases were significantly less in G1 than in G2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute subjective and physiological responses to smoking in adolescents

Aims . To determine the topography of cigarette smoking and the subjective and physiological effects of abstinence and nicotine in adolescents who smoke on a daily versus a non-daily basis.
Design . Repeated measures experiment, non-blinded, involving a single test session.
Setting . Human psychopharmacology laboratory.
Participants . Twenty-one daily and 21 non-daily adolescent cigarette smokers (21 females; 21 males; age 13-18 years) with life-time use greater than 10 cigarettes, responding to radio and print advertisements.
Intervention . Overnight abstinence from cigarettes followed by smoking of a single cigarette furnished by the participant at test.
Measurements . The Fagerstrom Test for Nicotine Dependence, saliva nicotine and cotinine, expired air carbon monoxide (CO), heart rate (HR), self-report scales and smoking topography. Most measurements were performed before and after smoking.
Findings . Saliva nicotine, CO and HR increased, and self-reported intention and desire to smoke decreased, after smoking ( p < 0.001). Fagerstrom scores indicated greater dependence and desire to smoke in daily than in non-daily smokers. HR increased substantially over pre-smoking levels in both groups. Puff topography did not differ between the groups, although collectively these participants appeared to take smaller and more puffs than adult smokers tested under similar conditions.
Conclusion . This study provides initial evidence that adolescent cigarette smokers self-administer physiologically active doses of nicotine very early in their smoking careers. Nicotine dependence in adolescents appears to be a function of the current frequency of cigarette use, and subjective-behavioral consequences of abstinence and smoking are evident even in non-daily smokers.     

Cigarette smoking augments sympathetic nerve activity in patients with coronary heart disease

It has been shown that cigarette smoking increases blood pressure (BP) and heart rate (HR), and decreases muscle sympathetic nerve activity (MSNA) in healthy young smokers. The decrease in MSNA might be secondary to baroreflex responses to the pressor effect. We tested the hypothesis that cigarette smoking increases MSNA in smokers with impaired baroreflex function. The effects of cigarette smoking on BP, HR, forearm blood flow (FBF), forearm vascular resistance (FVR), and MSNA were examined in 14 patients with stable effort angina (59+/-3 years, group CAD) and 10 healthy smokers (23+/-1 years, group C). In group CAD, the arterial baroreflex sensitivity (BRS) was significantly lower than in group C (4.7+/-0.8 versus 15.1+/-2.2 msec/mmHg, P<0.01). In both groups, cigarette smoking increased the plasma concentration of nicotine, systolic and diastolic BP, HR, and FVR significantly (P<0.01), but decreased FBF significantly (P<0.01). After smoking, MSNA was decreased significantly in group C (from 35.2+/-3.5 to 23.5+/-3.2 bursts/100 beats, P<0.01), but increased significantly in group CAD (from 48.8+/-5.4 to 57.3+/-5.5 bursts/100 beats, P<0.01). There was significant correlation between BRS and changes in MSNA (r= -0.62, P<0.01). Cigarette smoking increased MSNA in smokers with impaired baroreflex function. This demonstrates that cigarette smoking stimulates sympathetic nerve activity by both a direct peripheral effect and a centrally mediated effect.     

Saliva Cotinine as an Indicator of Cigarette Smoking in Adolescents

Saliva cotinine and expired-air carbon monoxide (CO) concentrations were measured in 508 girls aged 11–16 years attending an inner London comprehensive school. A saliva cotinine cut-point of 14.7 ng/ml detected 99% of regular daily smokers and performed better than expired-air CO (cut-point 7 ppm) in identifying smoking (69% versus 54%). The mean saliva cotinine among the regular daily smokers was 200.8 ng/ml, and comparisons with adult smokers suggested that these adolescents were inhaling a similar dose of nicotine per cigarette. Within our sample no evidence was found for an increase in smoke inhalation per cigarette with increasing age suggesting that inhalation develops early in the smoking career.