Long-term Effects Of Smoking Research Articles

Effects of ageing and smoking on SP-A and SP-D levels in bronchoalveolar lavage fluid

Surfactant protein (SP)-A and SP-D are collagen-like glycoproteins that are synthesised in the distal pulmonary epithelium. This study examined the effects of ageing and long-term smoking on SP-A and SP-D in the lungs. The possible links to the development of pulmonary emphysema were also investigated. Sequential lavage was performed in young and middle-aged or elderly nonsmokers and asymptomatic current smokers with various smoking histories. Middle-aged or elderly smokers were further categorised according to the presence of emphysema by high-resolution computed tomography. Levels of SP-A and SP-D in bronchial lavage (BL) fluid and in bronchoalveolar lavage (BAL) fluid were quantified by ELISA. Significant decreases in SP-A were seen with age in nonsmokers in BL fluid, but not in BAL fluid. Middle-aged or elderly smokers with emphysema had lower levels of SP-A in both BL and BAL fluids when compared with young subjects, and in BL fluid when compared with middle-aged or elderly smokers without emphysema. SP-D did not change with age alone, however, it was decreased in middle-aged or elderly smokers when compared with similarly aged nonsmokers. In conclusion, surfactant protein-A may decrease with age alone or due to the cumulative effects of long-term smoking and development of emphysema, while surfactant protein-D decreases due to long-term smoking.

Changes in blood pressure and body weight following smoking cessation in women.

Few have studied the long-term effects of smoking and smoking cessation on weight gain and blood pressure increase and compared with the age-related increases experienced by most adults. This study compared the development of weight and blood pressure in female never smokers, continuing smokers and smokers who quit smoking. Weight, systolic (SBP) and diastolic (DBP) blood pressure and smoking habits were assessed at baseline and re-assessed after a mean follow-up of 9.0 +/- 5.8 years. Population-based cohort. A total of 2381 female never smokers and 1550 female smokers. At the re-examination, 388 of the smokers had quit smoking. Mean weight gain was 7.6 +/- 6.1, 3.2 +/- 5.8 and 3.7 +/- 5.2 kg, respectively, in quitters, continuing smokers and never smokers (P < 0.001). In women without blood pressure treatment, mean SBP increase was 20.9 +/- 16.8, 19.1 +/- 15.8 and 16.1 +/- 16.3 mmHg, respectively, in these groups (P < 0.001). Mean DBP increase was 6.2 +/- 8.7, 5.7 +/- 9.3 and 3.1 +/- 8.0 mmHg, respectively (P < 0.001). After adjustments for potential confounders, the increased weight gain in quitters remained highly significant. The differences in SBP and DBP increase were attenuated after adjustments, but remained significant. Incidence of hypertension (> or = 160/95 mmHg or treatment) was significantly higher in quitters [adjusted odds ratio (OR): 1.8; CI: 1.4-2.5] when compared with continuing smokers (OR: 1.3; CI: 1.07-1.6) and never smokers (reference). Over a long follow-up, weight gain was approximately 3-4 kg higher in quitters when compared with continuing smokers or never smokers. Although the differences in blood pressure increase were moderate, smoking cessation was associated with an increased incidence of hypertension.

Importance of smoking habits for longitudinal and age-matched changes in body mass index: a cohort study of Swedish men and women

Background Previous longitudinal studies of smoking and BMI have focused on smoking cessation. The aim of the present study was to disentangle the effects of long-term smoking on longitudinal changes and age-matched BMI differences (time period effects) in a nation-wide Swedish cohort. Methods Men and women ( n = 4349) ages 18–73 years reported height, weight, and smoking status for a baseline survey in 1980–1981. Eight and 16 years after baseline, follow-up surveys were conducted for 3244 (75%) of the 4349 subjects. Long-term smokers and long-term nonsmokers were compared with respect to longitudinal changes and age-matched BMI differences. Results For middle-age adults, the longitudinal increases in BMI were smaller among long-term smokers than long-term nonsmokers regardless of gender. Among the elderly, the longitudinal decrease in BMI was greatest among long-term smokers. Among men, age-matched BMI differences between surveys were smaller for long-term smokers than for nonsmokers. Among women, however, age-matched BMI differences were greater for long-term smokers than for nonsmokers. Conclusions In middle-age subjects, longitudinal BMI increases are smaller among smokers than nonsmokers. During old age, the BMI of smokers decreases more than that of nonsmokers. Unknown factors related to gender contribute to larger time period effects of smoking in women than in men.

Alterations of plasma antioxidants and mitochondrial DNA mutation in hair follicles of smokers.

The effects of long-term smoking on mitochondrial DNA (mtDNA) deletions in hair follicles were investigated in subjects with different antioxidant capacity. Twenty-two male smokers with a smoking index of greater than 5 pack-years and without any known systemic diseases were recruited for this study. Forty healthy nonsmoking males were included as controls. We found that the concentrations of ascorbate and alpha-tocopherol and the activities of glutathione S-transferase (GST) and glutathione peroxidase in blood plasma were significantly decreased in smokers. The levels of glutathione and protein thiols in whole blood and the incidence of a 4,977 bp deletion of mtDNA (dmtDNA) in hair follicles were significantly increased in smokers. A significantly higher incidence of the 4,977 bp dmtDNA was found in smokers with plasma GST activity less than 5.66 U/l (OR = 7.2, P = 0.020). Using multiple covariate ANOVA and logistic regression, we found that age and low plasma GST activity were the only two risk factors for the 4,977 bp dmtDNA. These results suggest that smoking depletes antioxidants and causes mtDNA deletions and that plasma GST may play an important role in the preservation of the mitochondrial genome in tissue cells of smokers.

Long-term smoking causes nitroglycerin resistance in platelets by depletion of intraplatelet glutathione.

We investigated whether platelet responsiveness to nitroglycerin (NTG) is maintained in long-term smokers and if not, the mechanism. In the absence or presence of NTG, intraplatelet reduced glutathione (GSH) levels and ADP-induced platelet aggregation and intraplatelet cGMP levels were measured in 10 long-term smokers and 10 age-matched nonsmokers. The intraplatelet GSH level was significantly lower in smokers than in nonsmokers (P<0.05). Platelet aggregation was dose-dependently inhibited by NTG in both groups; however, inhibition was significantly weaker in smokers. N-acetylcysteine (1 mmol/L), an exogenous thiol agent, significantly potentiated NTG-induced platelet inhibition in nonsmokers but not in smokers. The ADP-induced intraplatelet cGMP level was significantly greater in the presence of NTG in nonsmokers but not so in smokers. Because the effects of long-term smoking are multifactorial, a rabbit model was made by chronic administration of buthionine sulfoximine (BSO, n=6) to decrease intraplatelet GSH. The intraplatelet GSH level was significantly lower in BSO-treated rabbits than in saline-treated rabbits (P<0.001). The NTG-induced inhibition of platelet aggregation was significantly weaker in BSO rabbits. N-acetylcysteine-induced potentiation was not observed in BSO rabbits, whereas significant potentiation was found in saline rabbits. These findings were similar to those of long-term smokers. In contrast, the intraplatelet GSH-to-oxidized glutathione ratio, which represents the redox state of glutathione, was significantly lower in smokers than in nonsmokers, whereas no difference was found between saline rabbits and BSO rabbits. In conclusion, long-term smoking causes NTG resistance to aggregation in platelets, possibly through the depletion of intraplatelet GSH.

Effects of long-term cigarette smoking on the human locus coeruleus.

It has been hypothesized that cigarette smoking among subjects with major depression is a form of self-medication. To explore a possible biological basis for this hypothesis, noradrenergic proteins in the locus coeruleus (LC) were measured in long-term cigarette smokers and in nonsmokers. The LC was studied because elevated amounts of alpha2-adrenoceptors and tyrosine hydroxylase have been observed postmortem in the LCs of subjects with major depression or who commit suicide, and because long-term administration of antidepressant drugs to rats down-regulates these proteins in the LC. Postmortem LCs were obtained from long-term cigarette smokers (n=7) and from nonsmokers (n = 9), all of whom lacked diagnoses of major depression. Amounts of tyrosine hydroxylase immunoreactivity and radioligand binding to the norepinephrine transporter, monoamine oxidase A, and alpha2-adrenoceptors were measured. Amounts of tyrosine hydroxylase immunoreactivity and radioligand binding to alpha2-adrenoceptors were significantly lower (approximately 60% and 40%, respectively) along the axis of the LCs of long-term smokers compared with nonsmokers. Smoking had no statistically significant effects on binding to monoamine oxidase A or to the norepinephrine transporter. This is the first demonstration that cigarette smoking affects noradrenergic proteins in the LC. The direction of these changes is opposite to that observed when comparing subjects who have major depression with normal controls and the same as that produced by long-term antidepressant treatment in animals. If the present observations reflect long-term effects of smoking on premortem noradrenergic biochemistry, smoking-induced changes in LC biochemistry may strengthen the smoking habit among subjects with major depression.

Patient screening and medical evaluation for implant and preprosthetic surgery.

Implant and preprosthetic surgeries aim to restore normal anatomic contours, function, comfort, aesthetics, and oral health. As such, they are not life-saving procedures. The prime concern must therefore be to not undermine the patient's overall health and safety. It is then that every step must be taken to select the appropriate treatment plan and maximize the longevity of the implanted system, including the overlying prostheses. One important category into which a number of possible complications may fall is the inadequate systemic screening of patients prior to implant and biomaterial insertion. Without wishing to enter into the whole human pathology, it is no longer appropriate to limit the general contraindications of implantology to the traditionally considered malfunctions of the pancreas, liver or hematopoietic system and to ignore the devastating long-term effect of smoking or inadequate dietary habits. There are, in fact, a number of systemic problems that may create major risk factors. On the other hand, modern standards of care should not systematically exclude the use of implant surgery on patients with relative or marginal health conditions without exploring the possibilities of improving and stabilizing those conditions. As newer techniques of general anesthesia and intravenous sedation are more frequently used on an ambulatory basis, allowing implant surgeons to take their patients into various degrees of consciousness or deep sedation, the patient screening should also take into consideration factors related to this form of management. An arbitrary guideline for patient selection may be based on the classification of the American Society of Anesthesiology. This guideline restricts (with very few exceptions) intraosseous implants and implant-related graft surgeries on patients who fall into ASA1 or ASA2 categories of the classification. In the domain of subperiosteal implants for treatment of advanced atrophy of the mandible, the body response seems to be much less dramatic than to endosseous devices or to grafted sites. The cortical histoarchitecture and metabolism are, by far, less affected by organ disorders than are endosseous structures. This article presents a number of absolute contraindications and analyzes a series of relative contraindications for which the doctor's judgment remains the decisive factor. In this latter case, it proposes treatment patterns that could optimize certain marginal health conditions or stabilize unbalanced biological functions prior to or at the time of surgery. As life expectancy in the industrial countries is continuously increasing, a greater number of elderly patients are equipped with implant-supported prosthetics. The effort must therefore be focused on keeping a regular and watchful eye on their general health and screening for possible geriatric conditions responsible for long-term implant failure. Will a minimum knowledge of internal medicine be a prerequisite for future academic implant education?

The effect of long-term smoking on gastroesophageal reflux (GER): A study on 1472 patients

The effect of long-term smoking on gastroesophageal reflux (GER): A study on 1472 patients

The effect of long-term smoking on gastroesophageal reflux (GER): A study on 1472 patients

The effect of long-term smoking on gastroesophageal reflux (GER): A study on 1472 patients

Patient screening and medical evaluation for implant and preprosthetic surgery.

Implant and preprosthetic surgeries aim to restore normal anatomic contours, function, comfort, aesthetics, and oral health. As such, they are not life-saving procedures. The prime concern must therefore be to not undermine the patient's overall health and safety. It is then that every step must be taken to select the appropriate treatment plan and maximize the longevity of the implanted system, including the overlying prostheses. One important category into which a number of possible complications may fall is the inadequate systemic screening of patients prior to implant and biomaterial insertion. Without wishing to enter into the whole human pathology, it is no longer appropriate to limit the general contraindications of implantology to the traditionally considered malfunctions of the pancreas, liver or hematopoietic system and to ignore the devastating long-term effect of smoking or inadequate dietary habits. There are, in fact, a number of systemic problems that may create major risk factors. On the other hand, modern standards of care should not systematically exclude the use of implant surgery on patients with relative or marginal health conditions without exploring the possibilities of improving and stabilizing those conditions. As newer techniques of general anesthesia and intravenous sedation are more frequently used on an ambulatory basis, allowing implant surgeons to take their patients into various degrees of consciousness or deep sedation, the patient screening should also take into consideration factors related to this form of management. An arbitrary guideline for patient selection may be based on the classification of the American Society of Anesthesiology. This guideline restricts (with very few exceptions) intraosseous implants and implant-related graft surgeries on patients who fall into ASA1 or ASA2 categories of the classification. In the domain of subperiosteal implants for treatment of advanced atrophy of the mandible, the body response seems to be much less dramatic than to endosseous devices or to grafted sites. The cortical histoarchitecture and metabolism are, by far, less affected by organ disorders than are endosseous structures. This article presents a number of absolute contraindications and analyzes a series of relative contraindications for which the doctor's judgment remains the decisive factor. In this latter case, it proposes treatment patterns that could optimize certain marginal health conditions or stabilize unbalanced biological functions prior to or at the time of surgery. As life expectancy in the industrial countries is continuously increasing, a greater number of elderly patients are equipped with implant-supported prosthetics. The effort must therefore be focused on keeping a regular and watchful eye on their general health and screening for possible geriatric conditions responsible for long-term implant failure. Will a minimum knowledge of internal medicine be a prerequisite for future academic implant education?

Use of transition probabilities to estimate the effect of smoking on the duration of episodes of respiratory symptoms in diary data: the Swiss Study on Air Pollution and Lung Diseases in Adults (SAPALDIA).

Incompletely documented symptom episodes pose methodological problems in the analysis of diary data. The aim of this study was to develop a method of estimating the average durations of symptomatic and nonsymptomatic episodes, respectively, coping with the problem of bias due to undocumented days and censored episodes that is found in most diary studies. The authors derived their outcome variables from a Markov model using transition probabilities. To evaluate this method, the authors assessed the impact of active smoking on the duration of episodes of bronchitis symptoms and the corresponding nonsymptomatic periods, respectively, using diary data (1992-1993) obtained from 801 participants in the Swiss Study on Air Pollution and Lung Diseases in Adults. Covariate-adjusted distribution curves for the mean durations of individual episodes were estimated by Cox regression. Median values for light smokers (<10 cigarettes/day) were 60.0 symptom-free days (95% confidence interval (CI) 42.0-78.5) and 4.0 symptomatic days (95% CI 3.0-6.0), respectively, compared with medians of only 21.0 days (95% CI 16.2-29.8) for periods without bronchitis symptoms and 6.0 days (95% CI 4.9-9.0) for episodes of bronchitis symptoms in heavy smokers (> or =30 cigarettes/day). The authors suggest that the Markov method is a feasible approach to the assessment of long term effects of smoking and environmental risk factors on the average duration of symptomatic and nonsymptomatic respiratory episodes.

Effects of long-term smoking on myocardial blood flow, coronary vasomotion, and vasodilator capacity.

The effect of long-term smoking on coronary vasomotion and vasodilator capacity in healthy smokers is unknown. Myocardial blood flow (MBF) was quantified with [13N]ammonia and positron emission tomography (PET) at rest, during cold pressor testing (endothelium-dependent vasomotion), and during dipyridamole-induced hyperemia in 16 long-term smokers and 17 nonsmokers. MBF at rest did not differ between the 2 groups. Cold induced similar increases in rate-pressure product (RPP) in smokers and nonsmokers. However, MBF increased only in nonsmokers and was, during cold, higher than in smokers (0.91+/-0.18 versus 0.78+/-0.14 mL x g(-1) x min(-1), P<0.05). MBF normalized to the RPP (derived from the ratio of MBF ([milliliters per gram per minute] to RPP [beats per minute times millimeters of mercury] times 10000) declined in smokers but remained unchanged in nonsmokers (0.86+/-0.10 versus 0.72+/-0.11, P=0.0006, and 0.99+/-0.25 versus 0.96+/-0.27, P=NS). The hyperemic response to dipyridamole and the myocardial flow reserve did not differ between the 2 groups. In a multiple regression model adjusted for age, sex, serum lipid levels, years of smoking, and pack-years, years of smoking was the strongest predictor of the normalized blood flow response to cold (P<0.001), followed by the HDL/LDL ratio. The normal hyperemic response to dipyridamole in long-term smokers indicates a preserved endothelium-independent coronary vascular smooth muscle relaxation, whereas the abnormal response to cold suggests a defect in coronary vasomotion likely located at the level of the coronary endothelium. Its severity depends on the total exposure time to smoking.

Long-term cigarette smoking is associated with increased myocardial perfusion heterogeneity assessed by positron emission tomography.

The pathophysiology of smoking-related coronary events in patients with normal coronary arteries is incompletely understood. This study was conducted to explore, in subjects without symptoms of cardiovascular disease, the long-term effects of smoking on regional coronary artery vasoactivity, especially during sympathetic stimulation. In ten smoking and ten non-smoking sex- and age-matched healthy volunteers, segmental myocardial perfusion was studied using dynamic parametric nitrogen-13 ammonia positron emission tomography at rest and during sympathetic stimulation evoked by the cold pressor stimulation. Smokers demonstrated a higher myocardial perfusion at rest (116+/-17 ml/min/100 g vs 96+/-20 ml/min/100 g, P <0.01) and an impaired myocardial perfusion increase during cold pressor stimulation (1.02+/-0.15 vs 1.18+/-0.17, P <0.05). The heterogeneity of perfusion, expressed as coefficient of variation, was significantly different between the smoking and the non-smoking group. The coefficient of variation of segmental myocardial perfusion was higher in smokers at rest (17.5%+/-4.2% vs 13.5%+/-1. 9%, P <0.05) and during cold pressor stimulation (17.0%+/-3.2% vs 13. 9%+/-1.8%, P <0.05). We conclude that the long-term effects of smoking in healthy volunteers are associated with (1) increased myocardial perfusion at rest, (2) impaired myocardial perfusion response to cold pressor stimulation, and (3) increased myocardial perfusion heterogeneity both at rest and during cold pressor stimulation. These results may suggest that in healthy subjects the long-term effect of smoking is related to abnormal coronary artery vasoactivity, presumably induced by an interplay of regional endothelial dysfunction and autonomic dysregulation.

Long term effects of smoking on physical fitness and lung function: a longitudinal study of 1393 middle aged Norwegian men for seven years

To study association between smoking habits and long term decline in physical fitness and lung function in middle aged men who remained healthy. Baseline and follow up measurements performed during 1972-5 and 1980-2 respectively. National University Hospital of Oslo, Norway. 1393 men aged 40-59 at baseline who were all healthy at baseline and at follow up. Forced expiratory volume in one second and physical fitness (defined as total work done during a symptom limited bicycle ergometer test divided by body weight. Initial fitness was substantially lower among 347 persistent smokers than among 791 persistent non-smokers (1349 J/kg v 1618 J/kg), as was initial forced expiratory volume (3341 ml v 3638 ml). Mean (95% confidence interval) decline in fitness over 7.2 years was 217 (185 to 249) J/kg among smokers compared with 86 (59 to 113) J/kg among non-smokers (P < 0.001). Corresponding declines in forced expiratory volume were 271 (226 to 316) ml in smokers and 116 (85 to 147) ml in non-smokers (P < 0.001). Differences between smokers and non-smokers remained practically unchanged after adjustment for age and level of physical activity. Changes in fitness and forced expiratory volume among 199 men who had stopped smoking mimicked the findings for persistent non-smokers, and 56 men who started smoking presented findings close to those of persistent smokers. Decline in physical fitness and lung function among healthy middle aged men was considerably greater among smokers than among non-smokers and could not be explained by differences in age and physical activity.

Effect of acute and long-term smoking on myocardial blood flow and flow reserve.

Cigarette smoking is a major preventable risk factor for coronary artery disease and sudden cardiac death. However, the effect of acute and long-term cigarette smoking on coronary vasodilatory capacity and myocardial flow reserve has not been quantified in humans. To examine the effect of short-term and long-term smoking, myocardial blood flow was quantified at rest and during dipyridamole-induced hyperemia (0.56 mg/kg) in 12 smokers (10 males and 2 females; mean age, 27 +/- 4 years) under baseline conditions (reflecting the effect of long-term smoking) and during short-term cigarette smoking with 13N ammonia, positron emission tomography, and a two-compartment model. Twelve sex- and age-matched nonsmokers served as control subjects. Smoking significantly increased the rate-pressure product at rest from 7525 +/- 1290 to 9160 +/- 1125 (P < .001 versus baseline), which was paralleled by a proportional increase in myocardial blood flow at rest (0.70 +/- 0.17 versus 0.88 +/- 0.17 mL.g-1.min-1; P < .05 versus baseline). In contrast, hyperemic blood flow declined from 2.23 +/- 0.35 at baseline (P = NS versus control) to 1.98 +/- 0.32 mL.g-1.min-1 during smoking (P < .01 versus baseline). Accordingly, the myocardial flow reserve declined from 3.36 +/- 0.83 in smokers at baseline to only 2.28 +/- 0.28 during smoking (P < .0001 versus baseline). Thus, myocardial blood flow and flow reserve were similar in young, long-term smokers and young, healthy nonsmokers. Short-term smoking increases the coronary vasomotor tone during dipyridamole-induced hyperemia and markedly reduces the myocardial flow reserve. In contrast, long-term smoking does not attenuate the coronary vasodilatory capacity in young individuals with a relatively short smoking history. It might be speculated that the short-term reduction in the coronary vasodilatory capacity during smoking could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for sudden cardiac death.

Short and long-term effects of smoking on arterial wall properties in habitual smokers

Objectives. This study investigated the short-term effects of smoking on hemodynamic function and distensibility function and compliance of large arteries in habitual smokers. In addition, the effect of smoking was not measured in nonsmokers, but vessel wall properties were compared between smokers and nonsmokers(basal state).Background. Smoking is a well known risk factor for atherosclerosis. Loss of distensibility and compliance of large arteries may play a role in the onset of atherosclerosis.Methods. The distensibility and compliance coefficients of the common cartoid and brachial arteries were determined from the arterial wall displacement during systole and the end-diastolic diameter by using a vessel wall defector and from the pulse pressure as assessed in the upper arm. Cardiac function (cardiac output, stroke volume) was measured with Doppler echocardiography. Systemic vascular resistance was calculated as mean arterial pressure divided by cardiac output.Results. In habitual smokers, smoking one cigarette caused a sharp increase in blood pressure (6%) and heart rate (14%). Cardiac index increased (16%), mainly because of the marked increase in heart rate. Stroke and systemic vascular resistance indexes did not change significantly. Smoking enhanced forearm blood flow after wrist occlusion (17%), but total forearm blood low was unchanged, suggesting an increase in muscle blood flow and a decrease in skin flow. Because of higher blood pressure, the diameter of the elastic common carotid artery increased by 3% (passive phenomenon). Distensibility of the carotid artery decreased (7%), and as a result, carotid compliance was preserved. In contrast, despite blood pressure, the diameter of the muscular brachial artery did not change, suggesting an increased vascular tone. Brachial distensibility and compliance decreased (18% and 19%, respetively). Habitual smokers were comparable to nonsmokers with regard to blood pressure, cardiac function, vascular resistance and vessel wall properties of large arteries. Heart rate was higher in habitual smokers (14%).Conclusions. These data indicate that in habitual smokers, smoking one cigarette causes short-term increases in arterial wall stiffness that might be harmful to the artery and increase the risk for plaque rupture. Except for a higher heart rate, no obvious long-term effect of smoking was observed on hemodynamic variables and arterial stiffness. Because acute cardiovascular events are mainly due to plaque rupture, the short-term of smoking might be a more important risk than long-term for these acute ischemic events.

Basic and Clinical Psychopharmacology of Nicotine

Nicotine acts on nearly every physiological system of the human body. While the actions of nicotine on the autonomic nervous system may be of interest in understanding possible deleterious long-term effects of smoking on the cardiovascular system, the actions of nicotine on the central nervous system are of the most interest in understanding why people smoke. Many studies of the effects of nicotine on human cognitive function have been performed. Improvement in attention, learning, reaction time, and problem solving have been reported. However, most of the results are inconclusive owing to methodologic problems. Whether the enhanced performance observed after smoking is attributable to relief of symptoms of abstinence or to a primary effect of nicotine on the brain is not clear. The pharmacodynamic effects of nicotine must be considered in the design of studies of the effects of nicotine on human performance. It is not known if the effects of nicotine on performance are subject to tolerance. The facilitation of performance, perceived as a reinforcement, may tend to lessen throughout the day, as do other effects of nicotine. Studies of chronic tolerance to the behavioral effects of nicotine are needed; comparisons between regular smokers and occasional smokers may be helpful. At present, the facilitatory actions of nicotine on human performance have been explained in terms of arousal. However, nicotine actions cannot be explained in terms of this single concept. Different processes, including attention, stimulus evaluation, and response selection, appear to be involved in the effect of nicotine on human information processing. Finally, one must consider that the predominant effects of nicotine may differ among individuals, as different people smoke for different reasons, and the motives for (rewards of) smoking may vary in different situations.

A comparison of active and passive smoking during pregnancy: Long-term effects

Previous research has determined that maternal smoking during pregnancy is associated with negative effects for the child at birth and throughout childhood. Much less is known about the consequences of exposure to secondary smoke during fetal development. The present study investigates and compares the long-term consequences of active and passive smoking during pregnancy. Ninety-one children between the ages of six and nine years were tested using a comprehensive neuropsychological test battery. After considering potential confounds, children of nonsmoking mothers generally were found to perform better than the two smoking groups on tests of speech and language skills, intelligence, visual/spatial abilities and on the mother's rating of behavior. The performance of children of passive smokers was found, in most areas, to be between that of the active smoking and nonsmoking groups. It was concluded that there is a continuum of long-term smoking effects and that, although active maternal smoking is associated with effects of greater breadth and magnitude than passive maternal smoking, children of passive smokers are also at risk for a pattern of negative developmental outcomes.

SMOKING DURING PREGNANCY IMPAIRS OFFSPRING'S INTELLECTUAL ACHIEVEMENTS.

To assess the long-term effects of smoking during pregnancy on the physical and intellectual development of the offspring, Fogelman and Manor analyzed …

Some long term effects of smoking on the haemostatic system: a report from the Caerphilly and Speedwell Collaborative Surveys.

Data from two community studies on men from South Wales and the west of England suggest that the effects of smoking on the haemostatic system remain for many years after giving up. Long term correlations between several variables, including plasma fibrinogen and white cell count, and the length of time after giving up were seen in ex-smokers. Dose response relations were apparent in current smokers in terms of the white cell count and two haematological variables, the packed and mean cell volumes. These long term correlations probably reflect the toxicity of other agents in tobacco smoke besides nicotine and carbon monoxide, which act only in the short term. Identification of these agents may further our understanding of the mechanism by which cigarette smoking is associated with atherosclerotic disease.