Effects of cigarette smoking on morphological features of platelets in healthy men

Objectives:

To assess the effects of cigarette smoking on thrombocytopoiesis and some platelet morphological parameters in healthy male smokers.

Methods:

In this cross-sectional study, 542 consecutive healthy men (aged 20 to 88 years), referred to the laboratory of Fatemieh Hospital, Semnan, Iran, between November 2011 and November 2012 for checking up were enrolled. The subjects were divided into 2 groups of smokers (n=258 with frequency of 10 or more cigarette per day with more than 12 months duration of smoking) and non-smokers (n=284). The blood samples were extracted to examine values of platelet indices using an ABX Micros 60 cell counter.

Results:

Comparing platelet indices across smokers and non-smokers showed that the mean platelet count was statistically significantly higher in adult smokers than in nonsmokers (264.1 ± 81.2/µl versus 247.7 ± 83.9/µl, p=0.021), while the mean plateletcrit value was contrarily lower in the adult smokers (18.0 ± 12.0% versus 25.0 ± 10.0%, p<0.001). Other platelet indicators were not discrepant between the smokers and non-smokers.

Conclusion:

Cigarette smoking in healthy individuals results in significant and considerable effects on platelet morphological indices. The mean platelet count is significantly increased, and plateletcrit values are reduced, compared with non-smoking status.The International Agency for Research on Cancer (IARC) in its recent reports introduced cigarette smoking as one of the main carcinogenic agents because of thousands of chemical compounds that induce the generation of free radicals, reduce prostacyclin production leading to clot formation, as well as increase the production of fibrinogen and coagulative factor VII.1,2 Smoking has been also identified as a principal underlying etiology for the occurrence and progression of cardiovascular diseases, inflammatory disorders, and oxidative stress stimulation.3 Cigarette smoking’s crucial role in disrupting platelet activation and aggregation, as well as other coagulation processing components leading to thrombotic formations has been recently suggested.4,5 The pathophysiological effects of cigarette smoking on platelet activation have been recently investigated. Cigarette smoking can induce both acute and chronic potential effects on platelet function. Shortly after smoking, acute platelet potentiating can be occurred that may be resulted in chronic desensitization of the cell to activating agents over time.6 A study showed that acute smoking can change the platelet count and induce endothelial damage,7 other study did not lead to platelet aggregation stimulated by adenosine diphosphate (ADP), epinephrine, and collagen such effects.8 Although it was observed that inhalation of cigarette smoke can trigger platelet aggregation mediated by thrombin and ADP.9 Even, reduced platelet agreeability induced by aggregating processes was shown in smokers compared with non-smokers.10 With due attention to this matter which was mentioned above, and because there are few reports on the effect of smoking on thrombocytopoiesis, we assessed the effect of cigarette smoking on thrombocytopoiesis and some platelet morphological parameters in healthy male smokers.     

Detection of reversible platelet aggregates in the blood of smokers and ex-smokers with peripheral vascular disease.

OBJECTIVE: To demonstrate that smoking increases platelet aggregation in vivo, that smoking cessation reverses platelet aggregation and that this explains, in part, why smoking perpetuates the development of peripheral vascular disease. DESIGN: Prospective case-control study involving three groups of patients: smokers with peripheral vascular disease, ex-smokers with peripheral vascular disease and smokers with peripheral vascular disease who quit smoking during the study. SETTING/PARTICIPANTS: Fourteen smokers and seven ex-smokers, new patients with confirmed peripheral vascular disease, attending the vascular clinic at Fremantle Hospital between February and November, 1988. INTERVENTIONS: Blood samples taken weekly from all subjects for five weeks. Week 1 was taken as the baseline before smoking cessation in the six smokers who were assigned to stop smoking during the study. MAIN OUTCOME CRITERIA: Platelet aggregate ratio, an indicator of in-vivo platelet aggregability where an increase in platelet aggregate ratio suggests a decrease in platelet function. RESULTS: Only three of six smokers stopped smoking for the duration of the study. Median platelet aggregate ratios were: smokers = 0.85 (range, 0.79-0.92) v. non-smokers = 0.93 (range, 0.91-1.00). The difference was statistically significant P less than 0.0002. The difference in platelet aggregate ratios between smokers and quitters was not statistically significant. CONCLUSIONS: This study demonstrated an increase in platelet aggregability in smokers compared to ex-smokers but there was no clear evidence that platelet function was fully reversed after only four weeks cessation of smoking. The data suggested that platelet function of the ex-smokers had fully reversed to normal over a longer period. This could explain the decreased incidence of complications of peripheral vascular disease in ex-smokers. The small number of patients able to quit smoking impeded this study.     

In healthy habitual smokers acetylsalicylic acid abolishes the effects of tobacco smoke on the platelet aggregate ratio.

After abstinence for at least 8 hours, 20 healthy habitual smokers smoked two unfiltered cigarettes during each of two 20-minute periods separated by 48 hours. They had taken one 0.32-g tablet of acetylsalicylic acid (ASA) the night before the second period. The mean platelet aggregate ratios in venous blood taken immediately before and after each period of smoking were 0.79 and 0.70 respectively when ASA had not been taken beforehand and 0.89 and 0.91 when it had. The mean after smoking was significantly higher when ASA had been taken beforehand. In conjunction with the previous finding that in nonsmokers ASA prevented a lowering of the platelet aggregate ratio by experimental smoking without affecting the ratio before smoking, the data from the present study suggest that ASA abolishes both acute and longer-lasting effects of tobacco smoke on the platelet aggregate ratio in healthy habitual smokers.     

Respiratory effects of non-tobacco cigarettes

Data from the Tucson epidemiological study of airways obstructive disease on smoking of non-tobacco cigarettes such as marijuana were analysed to determine the effect of such smoking on respiratory symptoms and pulmonary function. Among adults aged under 40, 14% had smoked non-tobacco cigarettes at some time and 9% were current users. The prevalence of respiratory symptoms was increased in smokers of non-tobacco cigarettes. After tobacco smoking had been controlled for men who smoked non-tobacco cigarettes showed significant decreases in expiratory flow rates at low lung volumes and in the ratio of the forced expiratory volume in one second to the vital capacity. This effect on pulmonary function in male non-tobacco cigarette smokers was greater than the effect of tobacco cigarette smoking. These data suggest that non-tobacco cigarette smoking may be an important risk factor in young adults with respiratory symptoms or evidence of airways obstruction.     

吸烟对健康人血液流变学影响的观察

本文报道对59例健康吸烟者血液流变学9项指标的观察,并与非吸烟组进行比较。吸烟组的血小板粘附率、红细胞压积和全血粘度均较非吸烟组升高,差异非常显著(P<0.001)血浆比粘度在大量吸烟组升高,差异有显著性(P<0.05)说明吸烟使部份血粘滞因素升高,给血液的流变性带来不利影响。不同吸烟量的两组之间各项指标变化无显著差异。本文对发生机制及临床意义略加讨论。     

低剂量γ射线与香烟对胎鼠脑蛋白质及热休克蛋白的影响

目的　探讨低剂量γ射线、香烟及其联合作用对脑蛋白质及热休克蛋白 (HSP70 )合成的影响。方法　利用Westerndotblot和Lowrey方法对经低剂量γ射线 (6 0 Co,0～ 1.0Gy)和香烟烟雾 (0～ 2支 /只 )处理的孕鼠的胎脑蛋白质和HSP70进行定量研究。结果　 0 .2 5Gy以上的照射和高浓度的香烟烟雾(2支 /只 )与对照组比较胎脑蛋白质明显减少 ,并且低剂量γ射线与香烟具有联合作用 ;低剂量γ射线、香烟烟雾及其联合作用下 ,胎脑HSP70明显升高 (P <0 .0 1) ,其中高照射组和高浓度香烟组脑HSP70升高明显低于低照射组和低浓度香烟组 (P <0 .0 1) ,照射与高浓度的香烟组联合明显较单独照射组低 ,有剂量依存关系。结论　低剂量γ射线、香烟及其联合可引起脑蛋白质的含量减少 ,并诱导胎脑HSP70的合成 ,提示胎脑发育损伤与脑蛋白和HSP70的合成有一定关系。     

Parkinson＇s Disease and Smoking： An Integral Part of PD＇s Etiological Study

OBJECTIVE: To explore the association of Parkinson's disease (PD) with cigarette smoking. METHODS: One hundred of fourteen PD patients were compared with 205 control subjects who were matched by gender, race and residency. A previously validated questionnaire including smoking, alcohol/tea consumption as well as some other environmental exposure data was administered. RESULTS: With never-smokers as the reference category, we observed reduced risk for PD among ever smokers (OR=0.49, 95% CI: 0.30 to 0.79) current smokers (OR=0.44, 95% CI: 0.23 to 0.86) and ex-smokers (OR=0.54, 95% CI: 0.30 to 0.96). When ever smokers were stratified by years of smoking, there was an inverse correlation between those whose smoking history was longer than 20 years (OR=0.40 95% CI: 0.21 to 0.81) and an even mild protective correlation between those who smoked less than 20 years (OR=0.57, 95% CI: 0.33 to 0.99). Those who had quitted smoking for more than 20 years were less likely to have the disease than never smokers, and those who had quitted for less than 20 years were least likely to have PD, while those who were current smokers were still least likely to have the disease. We found significant inverse gradient with pack-day smoking (trend P<0.05), and the inverse correlation between cigarette smoking and PD was not confounded by alcohol/tea consumption and other confounding bias. CONCLUSIONS: The inverse correlation between Parkinson's disease risk and smoking as well as the trend of gradient dose response is again observed in our study. More future researches are needed to confirm these correlations and to explore further biochemical evidence.     

吸烟与CYP2C19功能缺失性等位基因的交互作用对急性冠脉综合征患者氯吡格雷抗血小板反应性的影响

目的 探讨吸烟和CYP2C19功能缺失性等位基因交互作用对氯吡格雷抗血小板反应性的影响。方法 该研究连续募集2011年9月—2013年9月解放军总医院住院并接受阿司匹林和氯吡格雷双联抗血小板治疗的急性冠脉综合征（ACS）患者。采用光密度比浊法（LTA）测定氯吡格雷治疗前后的血小板聚集率,SnaPshot法检测CYP2C19功能缺失性等位基因变异型。利用单因素和多因素统计方法,分析吸烟和CYP2C19基因型交互作用对氯吡格雷治疗前后的血小板聚集率和治疗期间高血小板反应性（HPR）的影响。结果 该研究共纳入500例患者,吸烟组203例（40.6%）,非吸烟组297例（59.4%）。在非吸烟组,氯吡格雷治疗后的稳定血小板聚集率在CYP2C19＊2携带者（＊1/＊2：43.24±19.39;＊2/＊2：53.52±19.88）和非携带者（＊1/＊1：37.91±19.12）之间差异均有统计学意义（校对后P值分别为P=0.029,P〈0.001）;而在吸烟组中未见上述差异。非吸烟组中至少一个CYP2C19＊2等位基因携带者与非携带者之间的HPR的发生率差异有统计学意义（校正后OR：2.13,95%CI：1.23-3.72,P=0.008）,而在吸烟组中未见上述差异（校正后OR：1.41;95%CI：0.65-3.04,P=0.387）。结论 吸烟和CYP2C19功能缺失性等位基因的交互作用能够影响ACS患者中氯吡格雷的抗血小板反应性。     

Abstention from cigarette smoking improves cerebral perfusion among elderly chronic smokers

A cross-sectional study of cerebral blood flow (CBF) levels in 268 neurologically normal volunteers contrasting nonsmokers, smokers who quit, and current cigarette smokers indicated that subjects who quit smoking had significantly higher cerebral perfusion levels than subjects who had continued to smoke but remained lower than subjects without a history of cigarette smoking. All subjects were matched for age and sex, and smoking groups were matched for duration and amount of smoking. A prospective study of 11 subjects who were able to stop smoking in which CBF levels were available both antecedent to and following cessation of the habit indicated that significant gains occurred in cerebral perfusion levels within one year following cessation of smoking. A control group of 22 subjects who continued to smoke (matched for age, sex, duration of smoking, and duration of time between baseline and follow-up) showed no change in CBF values. A correlation between magnitude of CBF change and duration of cessation of cigarette smoking demonstrated a significant linear increase in CBF during the one-year period. These results suggest that elderly individuals who have smoked for three to four decades can benefit substantially by abstaining from cigarette smoking and that significant improvement in cerebral circulation occurs within a relatively short period.     

高温和香烟对鼠早期胚胎脑HSP70及蛋白质的影响

目的　探讨高温、香烟及其联合对鼠胎脑热休克蛋白 70 (HSP 70 )及蛋白质合成的影响。方法　孕d 10的大鼠给予高温 (4 0～ 42℃ )和香烟烟雾水溶物 (0～ 2支 /只鼠 )处理 ,取胎鼠全脑 ,用Westerndotblot和Lowrey方法测量HSP 70和蛋白质含量。结果　高温 (4 0～ 41℃ )、高浓度的香烟烟雾 (1.5支 /只鼠和 2 .0支 /只鼠 )及其联合与对照组比较胎脑蛋白质明显减少 ,与温度、温度持续时间及香烟浓度明显相关 ,并且高温与香烟具有联合作用 ;结果还显示高温和高浓度香烟均使胎脑HSP 70明显升高 ,高温与香烟联合其胎脑HSP70合成量与单独高温组相比HSP 70变化不明显。结论　高温、香烟烟雾及其联合可引起胎脑蛋白质含量减少 ,并诱导胎脑HSP 70合成 ,但香烟的诱导作用较高温弱 ,与高温联合胎脑HSP70的合成表现出交叉适应性反应。     

长期吸烟对健康成人血脂和血糖的影响

为探讨长期吸烟对空腹血脂、血糖、胰岛素及胰岛素敏感性指标的影响及其变化规律,在８２例健康成人通过多元逐步回归分析,探讨长期吸烟对血脂、血糖、胰岛素及胰岛素敏感性指标影响的显著性及影响程度;并以协方差分析校正其它影响因素后,对比分析长期吸烟者与不吸烟者血脂、血糖、胰岛素及胰岛素敏感性指标的差异程度。结果：长期吸烟者伴随有糖代谢及脂代谢指标异常变化。并与吸烟程度有显著性相关关系。校正其它可能影响的因素     

Cigarette smoking increases the risk of albuminuria among subjects with type I diabetes

The effect of cigarette smoking on diabetic renal and retinal complications was evaluated in 359 young subjects with insulin-dependent diabetes mellitus. The prevalence of increased albumin excretion rates was 2.8 times higher in smokers than nonsmokers. Mean glycohemoglobin levels and duration of diabetes were also significant factors in the development of diabetic nephropathy and retinopathy in a logistic regression model. Smoking remained a significant factor in the logistic regression model for albuminuria (but not retinopathy) when controlled for glycohemoglobin level, duration of diabetes, age, gender, and blood pressure. The progression of albuminuria and of retinopathy was also greater in smokers. Albuminuria improved significantly when subjects ceased smoking. It is concluded that cigarette smoking is an independent risk factor and is associated with the development and progression of early diabetic renal damage (albuminuria) and with the worsening of retinal disease in young subjects with diabetes.     

吸烟对血浆尿酸水平的影响

目的 测定吸烟对血浆尿酸的影响及其与烟草代谢物的关系.方法 选取健康体检者300例,其中吸烟者162例（男性145例,女性17例）,不吸烟者138例（男性62例,女性76例）,测定血浆尿酸、肌酐以及尿可替宁水平.结果 吸烟者血浆尿酸水平较不吸烟者明显降低,差异有统计学意义.血浆尿酸水平与吸烟量、吸烟时间呈负相关.结论 在排除影响血浆尿酸的因素以后,吸烟者尿酸水平较不吸烟者明显降低,且这种降低与尿酸内源性生成减少有关,是吸烟促发人体应激反应作用的结果.由于血浆尿酸测定方法简单,而且能反映人体的抗氧化物水平,因此它有可能作为了解吸烟应激状态的常规测定指标.     

Cigarette smoking as a risk factor for stroke. The Framingham Study

The impact of cigarette smoking on stroke incidence was assessed in the Framingham Heart Study cohort of 4255 men and women who were aged 36 to 68 years and free of stroke and transient ischemic attacks. During 26 years of follow-up, 459 strokes occurred. Regardless of smoking status and in each sex, hypertensive subjects had twice the incidence of stroke. Using the Cox proportional hazard regression method, smoking was significantly related to stroke after age and hypertension were taken into account. Even after pertinent cardiovascular disease risk factors were added to the Cox model, cigarette smoking continued to make a significant independent contribution to the risk of stroke generally and brain infarction specifically. The risk of stroke increased as the number of cigarettes smoked increased. The relative risk of stroke in heavy smokers (greater than 40 cigarettes per day) was twice that of light smokers (fewer than ten cigarettes per day). Lapsed smokers developed stroke at the same level as nonsmokers soon after stopping. Stroke risk decreased significantly by two years and was at the level of nonsmokers by five years after cessation of cigarette smoking.     

Cigarette smoking inhibits the anti-platelet activity of aspirin in patients with coronary heart disease

Objective  Tobacco smoking results in increased platelet aggregability, which suggests that low-dose aspirin used in common clinical practice may not effectively inhibit platelet activity in smokers with coronary heart disease (CHD). This review was performed to assess the effect of aspirin on platelet aggregation in patients with CHD.

Data sources  We performed an electronic literature search of MEDLINE (starting from the beginning to March 15, 2009) using the term “smoking” or “tobacco” paired with the following: “platelet”, “aspirin” or “coronary heart disease”.

Study selection  We looked for review articles regarding the effect of tobacco smoking on platelet activity and on the anti-platelet efficacy of aspirin in healthy people and patients with CHD. The search was limited in “core clinical journal”. In total, 1321 relevant articles were retrieved, and 36 articles were ultimately cited.

Results  Tobacco smoking results in increased platelet aggregability, which can be inhibited by low-dose aspirin in the healthy population. However, in patients with CHD, the increased platelet aggregability can not be effectively inhibited by the same low-dose of aspirin. A recent study indicated that clopidogrel or an increased dose of aspirin can effectively inhibit the increased platelet aggregability induced by tobacco smoking in patients with CHD.

Conclusions  It is important for patients with CHD to quit smoking. For the current smoker, it may be necessary to take larger doses of aspirin than normal or take an adenosine diphosphate receptor inhibitor along with aspirin to effectively inhibit the increased platelet activity.

     

中国大学生吸烟行为和吸烟态度研究

目的:对我国大学生的吸烟现状进行调查;并检验“吸烟态度与吸烟行为具有一致性”的假设。方法:用问卷法对805名中国大学生进行了研究。结果:大学生中有19.1％的人为当前吸烟者;男生吸烟普遍性显著高于女生;吸烟的普遍性随着年级的增高而增高;大学生对尼古丁没有依赖性;不吸烟者抗烟态度强,吸烟者抗烟态度弱。结论:吸烟态度与吸烟行为具有一致性。     

The effect of anosmia on smoking habits.

Sixteen cigarette smokers who had developed complete anosmia were questioned about their smoking habits. Four subjects increased their cigarette consumption, 8 were unchanged and 4 decreased. The development of anosmia has no consistent effect on cigarette smoking.     

基于社会认知理论的小组戒烟研究

目的探索社会认知理论指导下的“我能戒烟”小组式戒烟方法，并对干预效果进行评价。方法在基线调查的基础上，采用随机对照分组，将225名吸烟者随机分为干预组和对照组，干预组接受社会认知理论为基础的小组式戒烟干预，并在6个月后再次对两组进行问卷调查，评价干预效果。结果6个月后干预组的戒烟率达到40．5％，远高于对照组（5．2％）。干预组每日吸烟量平均减少了11．5支，而对照组在这段时间内减少了1．7支，差别有显著性。根据阶段变化理论，干预组所处的戒烟阶段普遍向前推进；并且情感效能、社会效能得分有明显提高。学员对干预形式也较满意。年龄、是否参加干预和基线时对自己戒烟成功的预测成为是否戒烟的影响因素。结论“我能戒烟”小组式戒烟法能够有效地提高戒烟率，并为广大烟民接受，值得推广。     

吸烟对慢性阻塞性肺疾病患者血清D二聚体的影响

目的了解慢性阻塞性肺疾病(COPD)患者的吸烟量和其血清D二聚体水平的动态变化,探讨吸烟对COPD患者凝血功能的影响。方法 142例COPD急性加重期(AECOPD)患者依据吸烟量分为3组:不吸烟组、轻度吸烟组和中重度吸烟组,检测AECOPD患者治疗前后血清D二聚体水平。结果 COPD急性加重后,D二聚体水平明显升高(P<0.01),且无论是COPD还是AECOPD,D二聚体水平都随着吸烟量的递增而升高(P<0.01)。结论 COPD患者急性加重后凝血功能可进一步受损,而吸烟则是加速这一不良过程的重要因素。