Effects Of Chronic Smoking Research Articles

Effect of Chronic Smoking on Cardiovascular

Effect of Chronic Smoking on Cardiovascular

Acute effect of cigarette smoking on frontal planar QRS-T angle in apparently healthy subjects with habitual smoking

Aim: It has been well recognized that smoking exerts various detrimental cardiovascular effects. Although the effect of chronic smoking on cardiac electrophysiology is well known, little is known about the effect of acute smoking on surface ECG. Previous reports suggested that frontal planar QRS-T angle (fpQRS-Ta), measured by surface ECG, may be associated with ventricular arrhythmias and cardiac death. Hence, we primarily aimed to assess the effect of acute smoking on fpQRS-Ta. Methods: A total of 92 apparently healthy subjects [44 female, 48 male, mean age 38.7(8.02) years] with smoking habit were enrolled in this prospective cohort study between May-July 2019. Demographic and clinical characteristics were recorded, and fpQRS-Ta together with some ECG parameters were noted before and 10 minutes after smoking for comparison. Spearman’s analysis was implemented to seek the probable correlation of the difference between pre- and post-smoking ECG parameters. Results: Ten minutes after smoking, median heart rate, QRS duration and fpQRS-Ta increased significantly (72.6 beats/min vs 81.5 beats/min, P<0.001; 84 ms vs 86 ms, P=0.012; 14.5° vs 25°, P<0.001; respectively), while PR and QTc duration did not significantly change (150.0 ms vs 150.0 ms, P=0.774; and, 423.5 ms vs 429.5 ms, P=0.372). In Spearman’s correlation analysis, the difference between pre- and post-smoking fpQRS-Ta significantly and negatively correlated with C-reactive protein (CRP) levels (r: -0.272, P=0.027). Conclusion: Acute smoking may widen fpQRS-Ta in healthy habitual smokers, and serum CRP negatively correlates with the degree of fpQRS-Ta widening. Our observation may further enlighten the pathophysiological mechanism of smoking in cardiac arrhythmias and sudden death.

Irreversible effects of long-term chronic smoking on arterial stiffness: An analysis focusing on ex-smokers among otherwise healthy middle-aged men

ABSTRACTObjective: Smoking is a modifiable cardiovascular risk factor closely related to arterial stiffness (AS). However, data are lacking regarding the chronic effects of smoking on AS, especially in ex-smoker (ES) who faces remnant cardiovascular risk when compared to never-smokers (NS).Methods: Among 1722 health screening participants, we retrospectively evaluated 652 healthy men with different smoking history [240 current smoker (CS) vs. 228 ES vs. 184 NS]. To assess AS, augmentation index (AIx), pulse pressure amplification (PPamp), and carotid-femoral pulse wave velocity (cfPWV) were measured and compared.Results: Baseline characteristics were similar except age and triglyceride level. AIx was lowest in NS, followed by ES, and was highest in CS. PPamp was highest in NS, lowest in CS, and ES was of intermediate level. The differences were more robust after adjustment for baseline covariates (AIx, p = 0.005; PPamp: p = 0.001). On the other hand, no significant intergroup difference was observed for cfPWV in our middle-aged population. With the regression analyses revealing an independent association between smoking duration and AS in ES, subgroup analysis demonstrated that long-term ES (smoking duration ≥20 years) had significantly higher AS than short-term ES (<20 years) and NS, approaching levels comparable to CS (AIx and PPamp: p < 0.0001).Conclusions: Our study demonstrated impaired arterial elastic properties in long-term ES, suggesting that AS caused by chronic smoking might be irreversible even after smoking cessation. Further longitudinal studies are warranted to determine the impacts of past smoking on AS and its clinical relevance.

The effects of chronic smoking on lung tissue and the role of alpha lipoic acid

We investigated the effects of alpha lipoic acid (ALA) on blood and lung tissue exposed chronically to cigarette smoke (CS). Female Sprague-Dawley rats were divided into three groups. Group 1 was the control group (CON): fresh air was supplied twice daily and 0.1 ml physiological saline was given orally for 8 weeks. Group 2 was exposed to CS: 12 cigarettes were smoked daily at two sessions for 1 h and 0.1 ml saline was given orally for 8 weeks. Group 3 (CS + ALA) was exposed to 12 cigarettes daily in two sessions for 1 h and 100 mg/kg/day ALA was given orally for 8 weeks. DNA damage was assessed using comet analysis; oxidative damage was assessed using ischemia-modified albumin (IMA) from blood; and total oxidant status (TOS), total antioxidant status (TAS) and oxidative stress index (OSI) were measured in blood and lung tissue. Histopathological and immunohistochemical evaluation of hypoxia-inducible factor (HIF)-1α, and −2α, caspase-3, vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF2) were conducted using lung tissue. The oxidative markers, TOS, OSI and IMA, and the comet analysis score were increased and the TAS level was decreased in the blood of the CS group compared to the CON group. IMA levels in blood, and TOS and OSI levels in the lung were decreased significantly in the CS + ALA group compared to the CS group. We observed increased septal wall thickness, marked and diffuse inflammatory reaction, emphysema, and necrotic cell debris in bronchial and bronchiolar lumens in the CS group. HIF-1α, HIF-2α, caspase-3 and FGF2 expressions were increased, while VEGF expression decreased in the lung tissues of the CS group compared to the CON group. ALA slightly ameliorated the damage caused by chronic exposure to CS in the lungs, but further investigation is needed to determine its possible protective effects at different dosages.

Linking Cigarette Smoking/Tobacco Exposure and Cluster Headache: A Pathogenesis Theory.

To propose a hypothesis theory to establish a linkage between cigarette smoking and cluster headache pathogenesis. Cluster headache is a primary headache syndrome grouped under the trigeminal autonomic cephalalgias. What distinguishes cluster headache from all other primary headache conditions is its inherent connection to cigarette smoking. It is undeniable that tobacco exposure is in some manner related to cluster headache. The connection to tobacco exposure for cluster headache is so strong that even if an individual sufferer never smoked, then that individual typically had significant secondary smoke exposure as a child from parental smoking behavior and in many instances both scenarios exist. The manner by which cigarette smoking is connected to cluster headache pathogenesis is unknown at present. If this could be determined this may contribute to advancing our understanding of cluster headache pathophysiology. Hypothesis statement. The hypothesis theory will include several principles: (1) the need of double lifetime tobacco exposure, (2) that cadmium is possibly the primary agent in cigarette smoke that leads to hypothalamic-pituitary-gonadal axis toxicity promoting cluster headache, (3) that the estrogenization of the brain and its specific sexually dimorphic nuclei is necessary to develop cluster headache with tobacco exposure, and (4) that the chronic effects of smoking and its toxic metabolites including cadmium and nicotine on the cortex are contributing to the morphometric and orexin alterations that have been previously attributed to the primary headache disorder itself.

The effects of chronic smoking on total cerebral blood volume measured by carotid and vertebral artery doppler ultrasonography.

To evaluate the effects of chronic cigarette smoking on total cerebral blood flow in healthy adults by Doppler ultrasonography (US). We evaluated 50 smoker (median age 29) and 50 nonsmoker (median age 28) healthy, 20- to 40-year-old subjects without any cardiovascular and cerebrovascular disease. Peak systolic maximal blood flow velocity (PSV), end-diastolic maximal blood flow velocity (EDV), time-averaged mean blood flow velocity (TAMV), resistance index (RI), and pulsatility index (PI) were measured in the left and right carotid and vertebral arteries, and total cerebral blood flow volume was calculated. There was no significant difference of smoking rate between genders. Blood pressure and PSV values were similar in both groups. EDV values of internal carotid artery (ICA) and vertebral artery (VA) were lower and RI and PI values were higher in smokers. TAMV, total ICA (-10.8%) and VA (-6%) flow volume, and tCBF (-9.2%) were lower in smokers. Doppler US is an effective tool to detect tCBF volume decrease in chronic cigarette smokers. Although minimal, this decrease, as demonstrated here in asymptomatic, healthy people, might be critical in patients with subclinical cerebral arterial insufficiency. © 2017 Wiley Periodicals, Inc. J Clin Ultrasound 45:561-565, 2017.

Acute and Chronic Effect of Cigarette Smoking on Pupil Size, Accommodation and Tear film

Purpose: To evaluate the acute and chronic effects of cigarette smoking on pupil size, accommodation and tear film. Methods: Thirty non-smokers and twenty-five cigarette smokers were recruited. For acute effect of smoking all smoking subjects were asked to smoke an identical single cigarette containing 0.5 mg nicotine. Photopic and mesopic pupil sizes, contrast visual acuities, contrast sensitivities, higher-order aberrations (HOAs), accommodations and tear-film stability were measured before smoking and immediately after smoking. The pupil sizes and HOA were measured with Pupilometer (VIP, NeurOptics) and Wavefront Analyzer (KR-1W) as 4 mm area of pupil size respectively. 100% and 10% contrast visual acuity, and contrast sensitivities were measured and amplitude of accommodations were assessed by push-up method and the tear film stability was assessed by TBUT (tear break-up time). For the chronic effect of smoking, all measurements of the cigarette smokers without smoking were compared with those of non-smokers. Results: For acute effect of smoking, pupil size decreased significantly after smoking regardless of illuminance and luminance level (p 0.05), the amplitudes of accommodation and tear film stability were decreased significantly after smoking (p<0.05). Conclusions: Acute effect of smoking resulted in decreased pupil size, accommodation, and tear film stability, and improved in low contrast visual acuity. However, chronic effect of smoking has no influence on pupil size, visual acuity, accommodation, tear film stability that it is thought that smoking has temporary effect on visual function.

Oxidative stress in cigarette smokers and patients with chronic obstructive pulmonary disease

Cigarette smoking is the most important exogenous risk factor for chronic obstructive pulmonary disease (COPD). Oxidative stress induced by smoking is considered to play major roles in the pathogenesis of COPD. In this review, we describe the theory of oxidant/antioxidant imbalance and the cellular and molecular reactions induced by oxidative stress. In addition, we discuss the effects of cigarette smoking on oxidative stress in smokers and patients with COPD. Smoking leads to increased acute pulmonary and systemic oxidative stress in cigarette smokers. As chronic effects of smoking, both pulmonary and systemic oxidative stress are increased in cigarette smokers and patients with COPD compared to non-smokers, the level of oxidative stress increases in association with duration of smoking history. Furthermore, pulmonary and systemic oxidative stress has been reported to be increased in response to exercise in cigarette smokers with a short smoking history, compared to non-smokers, although no difference was seen in baseline oxidative stress levels. Cigarette smoking affects the pulmonary and systemic oxidative stress response even in cigarette smokers with a short smoking history as well as smokers with a long smoking history and COPD patients.

The effects of chronic smoking on the pathology of alcohol-related brain damage

Both pathological and neuroimaging studies demonstrate that chronic alcohol abuse causes brain atrophy with widespread white matter loss limited gray matter loss. Recent neuroimaging studies suggest that tobacco smoking also causes brain atrophy in both alcoholics and neurologically normal individuals; however, this has not been confirmed pathologically. In this study, the effects of smoking and the potential additive effects of concomitant alcohol and tobacco consumption were investigated in autopsied human brains. A total of 44 cases and controls were divided into four groups: 16 non-smoking controls, nine smoking controls, eight non-smoking alcoholics, and 11 smoking alcoholics. The volumes of 26 gray and white matter regions were measured using an established point-counting technique. The results showed trends for widespread white matter loss in alcoholics (p<0.007) but no effect on gray matter regions. In contrast, smoking alone had no effect on brain atrophy and the combination of smoking and alcohol showed no additional effect. Neuronal density was analyzed as a more sensitive assay of gray matter integrity. Similar to the volumetric analysis, there was a reduction in neurons (29%) in the prefrontal cortex of alcoholics, albeit this was only a trend when adjusted for potential confounders (p<0.06). There were no smoking or combinatorial effects on neuronal density in any of the three regions examined. These results do not support the hypothesis that smoking exacerbates alcohol-related brain damage. The trends here support previous studies that alcohol-related brain damage is characterized by focal neuronal loss and generalized white matter atrophy. These disparate effects suggest that two different pathogenic mechanisms may be operating in the alcoholic brain. Future studies using ultrastructural or molecular techniques will be required to determine if smoking has more subtle effects on the brain and how chronic alcohol consumption leads to widespread white matter loss.

The effects of smoking on dry eye parameters in healthy women

Aim: To investigate the effects of chronic smoking on dry eye parameters.Methods: Ocular surface disease index (OSDI) and tear function tests such as Schirmer’s test, tear break-up-time (TBUT) test and impression cytology of 63 female chronic smokers and 40 age-matched female non-smokers were analyzed statistically.Results: The mean OSDI scores, Schirmer test results and TBUT levels were 35.85 ± 24.01 point, 14.25 ± 5.94 mm and 5.17 ± 2.85 s in chronic smokers and 15.20 ± 12.93 point, 15.48 ± 7.01 mm and 10.03 ± 3.44 s in non-smokers, respectively. Differences in OSDI scores, TBUT levels and impression cytology grades among the chronic smokers and non-smokers were statistically significant.Conclusion: Smoking behavior seems to affect the dry eye parameters negatively.

Relationship between hair nicotine levels with blood pressure, body composition, lipid profile and leptin among healthy male smokers in Kelantan

Abstract Objectives Cigarette smoking has been reported to cause acute blood pressure elevation. Therefore, it is important to assess the relationships between chronic smoking and blood pressure, body composition, and the metabolic profile to gain an understanding of the long-term effects of smoking on an individual's body weight and health. This study examined the relationships between the hair nicotine level, blood pressure, body composition, lipid profile, and leptin in healthy male smokers. Methods For this cross-sectional study, 107 male smokers aged between 20 and 50 years old were recruited as volunteers. The nicotine levels in the volunteers' hair were measured using gas chromatography-mass spectrometry. Moreover, the subjects' blood pressure, body composition (weight, height, body mass index, body fat percentage, visceral fat, waist and hip circumferences, and basal metabolic rate), lipid profile, and leptin concentration were also measured. Results The means for age and BMI among the subjects were 37.00 (9.42) years and 24.59 (4.33) kg/m2, respectively. The average length of time as a smoker was 16.91 years. The hair nicotine level was found to be positively correlated with the total cholesterol (r = 0.314, r2 = 0.099, p = 0.028) and triglyceride (r = 0.351, r2 = 0.0.123, p = 0.013) levels. However, no significant correlations were found between the hair nicotine level and blood pressure, body composition, or leptin concentration. Conclusion The positive correlations between the hair nicotine level and total cholesterol and triglyceride levels highlighted the harmful effects of chronic smoking, even among healthy male subjects.

Impact of chronic smoking on P3 components in a three-stimulus oddball paradigm

Background: The P3 is related to cognitive functions, psychopathology and effects of cognition-improving and -impairing drugs. Studies assessing the chronic effects of smoking on P3 mostly reported a reduction of P3 amplitude for chronic and former smokers. To date, only a few studies have analyzed this impact by using a three-stimulus oddball paradigm. This study tries to replicate previous smoking associations applying an eyes-closed active three-stimulus oddball paradigm in a well-diagnosed population based sample of healthy elderly subjects who were allowed to smoke ad libitum. The study also tries to estimate whether smoking is a relevant confounder in P3 assessment within the analyzed sample. Methods: From the Leipzig Health Care Study (LIFE) current, former and non-smokers without mental or neurological disorders were matched by age, sex and qualification. Risky alcohol consumption was further exclusion criterion given the strong association between alcoholism and P3 amplitude reduction. Results: Smoking status was not associated with any P3 parameter, with exception of prolonged P3a latency at Fz in former smokers compared to never smokers. Also, there were no significant effects of smoking status on any of the behavioral measures or a correlation with smoking-related data. Discussion: This study indicates that smoking does not seem to relevantly impact the P3 components in non-abstaining healthy elderly subjects when confounders are controlled for. This publication is supported by LIFE – Leipzig Research Center for Civilization Diseases, Universitat Leipzig. LIFE is funded by means of the European Union, by the European Regional Development Fund (ERDF) and by means of the Free State of Saxony within the framework of the excellence initiative.

Clinical and Radiologic Disease in Smokers With Normal Spirometry.

Airflow obstruction on spirometry is universally used to define chronic obstructive pulmonary disease (COPD), and current or former smokers without airflow obstruction may assume that they are disease free. To identify clinical and radiologic evidence of smoking-related disease in a cohort of current and former smokers who did not meet spirometric criteria for COPD, for whom we adopted the discarded label of Global Initiative for Obstructive Lung Disease (GOLD) 0. Individuals from the Genetic Epidemiology of COPD (COPDGene) cross-sectional observational study completed spirometry, chest computed tomography (CT) scans, a 6-minute walk, and questionnaires. Participants were recruited from local communities at 21 sites across the United States. The GOLD 0 group (n = 4388) (ratio of forced expiratory volume in the first second of expiration [FEV1] to forced vital capacity >0.7 and FEV1 ≥80% predicted) from the COPDGene study was compared with a GOLD 1 group (n = 794), COPD groups (n = 3690), and a group of never smokers (n = 108). Recruitment began in January 2008 and ended in July 2011. Physical function impairments, respiratory symptoms, CT abnormalities, use of respiratory medications, and reduced respiratory-specific quality of life. One or more respiratory-related impairments were found in 54.1% (2375 of 4388) of the GOLD 0 group. The GOLD 0 group had worse quality of life (mean [SD] St George's Respiratory Questionnaire total score, 17.0 [18.0] vs 3.8 [6.8] for the never smokers; P < .001) and a lower 6-minute walk distance, and 42.3% (127 of 300) of the GOLD 0 group had CT evidence of emphysema or airway thickening. The FEV1 percent predicted distribution and mean for the GOLD 0 group were lower but still within the normal range for the population. Current smoking was associated with more respiratory symptoms, but former smokers had greater emphysema and gas trapping. Advancing age was associated with smoking cessation and with more CT findings of disease. Individuals with respiratory impairments were more likely to use respiratory medications, and the use of these medications was associated with worse disease. Lung disease and impairments were common in smokers without spirometric COPD. Based on these results, we project that there are 35 million current and former smokers older than 55 years in the United States who may have unrecognized disease or impairment. The effect of chronic smoking on the lungs and the individual is substantially underestimated when using spirometry alone.

From rest to stressed: endothelin-1 levels in young healthy smokers and non-smokers

IntroductionEndothelin-1 (ET-1) is a potent vasoconstrictor produced by vascular endothelial cells, and a known marker of endothelial dysfunction. However, the acute and chronic effects of smoking and nicotine gum on the ET-1 response to acute physical stress in young healthy smokers have not been investigated. MethodsHealthy smokers (n=35) and non-smokers (n=35) underwent an exercise test to exhaustion (maximal oxygen consumption) on a treadmill. Smokers were assessed a) after 12h smoking abstinence (termed chronic smoking), b) immediately after smoking one cigarette (termed acute smoking), and c) immediately after chewing nicotine gum. Blood was drawn immediately pre-exercise, and 3minutes post-exercise. During exercise, cardiorespiratory parameters were obtained breath-by-breath using an automated metabolic cart. Plasma ET-1 levels were quantified using enzyme-linked immunosorbent-assay. The above protocol was designed to incorporate exercise as a vascular stressor to reveal changes that would not be detected at rest. ResultsMean age was 28.6±7.2years and body mass index (BMI) was 23.6±3.2kg/m2. Post-exercise ET-1 levels were significantly lower than pre-exercise levels in non-smokers (P<0.001) and smokers under all three conditions (P=0.005, P<0.001, P=0.001, respectively). There were no differences in post-exercise ET-1 levels between non-smokers and smokers under all three conditions, however the absolute and relative decrease in ET-1 levels was significantly smaller in chronic smokers compared with non-smokers (P=0.007 and P=0.004). Chronic smokers had a significantly lower exercise-induced change in tidal volume (P=0.050), fraction of expired CO2 (P=0.021), oxygen consumption (P=0.005), carbon dioxide elimination (P=0.004) and peak expiratory flow (P=0.003) compared with non-smokers. Furthermore, the decrease in ET-1 observed in non-smokers in response to exercise was significantly associated with exercise induced-changes in inspiratory time, time for a tidal volume cycle, respiratory frequency, inspired minute ventilation and peak inspiratory flow. ConclusionsAn acute decrease of circulating ET-1 in response to acute maximal exercise in young healthy individuals was noted. Chronic smokers had a significantly diminished decrease in ET-1 compared with non-smokers, however there were no significant differences in the ET-1 response between smokers under the three smoking conditions. Smokers were not able to achieve the same exercise-induced changes in cardiorespiratory parameters as non-smokers. By incorporating exercise as a vascular stressor in our study, we have taken a novel approach to provide evidence of an altered ET-1 and cardiorespiratory response that would not otherwise be observed at rest in young active healthy smokers.

Smoking acutely impaired endothelial function in healthy college students

Objective Cigarette smoking has been clearly pointed out as a risk factor for cardiovascular disease. Endothelial dysfunction contributes to the development of cardiovascular disease. Flow-mediated dilation (FMD) has been known as one of the endothelial function markers. We investigated the acute and chronic eff ects of smoking on endothelial function in college-aged smokers.Methods Eighteen smokers (mean age: 21 ± 1 y) and 14 non-smokers (mean age: 20 ± 1 y) were enrolled in this study. Brachial-ankle pulsed wave velocity (baPWV), systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were measured using a plethysmograph. Endotheliumdependent FMD was induced by reactive hyperaemia. High-resolution ultrasound with a 7.5-MHz linear array transducer was used to measure the diameter of the right brachial artery. Measurement of baPWV, SBP, DBP, HR, artery diameter, and %FMD was performed in smokers and non-smokers after 10 min bed rest, and after smoking one cigarette in the smokers. The interval between the two measurements was more than 15 minutes.Results There were no signifi cant diff erences on baPWV, SBP, DBP, HR, baseline brachial artery diameter between smokers and non-smokers. Percent FMD after smoking was signifi cantly lower than that at rest values in smokers (8.7 ± 4.0 vs 5.3 ± 2.4, P< 0.005), although %FMD at rest was not signifi cantly diff erent between smokers and non-smokers. No other markers showed any signifi cant diff erences between smokers at rest and after smoking.Conclusion Even the smoking of one cigarette dramatically impaired endothelial function, although habitual cigarette smoking did not decrease FMD in young healthy smokers.

Resting-state EEG, impulsiveness, and personality in daily and nondaily smokers

ObjectivesResting EEG is sensitive to transient, acute effects of nicotine administration and abstinence, but the chronic effects of smoking on EEG are poorly characterized. This study measures the resting EEG profile of chronic smokers in a non-deprived, non-peak state to test whether differences in smoking behavior and personality traits affect pharmaco-EEG response. MethodsResting EEG, impulsiveness, and personality measures were collected from daily smokers (n=22), nondaily smokers (n=31), and non-smokers (n=30). ResultsDaily smokers had reduced resting delta and alpha EEG power and higher impulsiveness (Barratt Impulsiveness Scale) compared to nondaily smokers and non-smokers. Both daily and nondaily smokers discounted delayed rewards more steeply, reported lower conscientiousness (NEO-FFI), and reported greater disinhibition and experience seeking (Sensation Seeking Scale) than non-smokers. Nondaily smokers reported greater sensory hedonia than nonsmokers. ConclusionsAltered resting EEG power in daily smokers demonstrates differences in neural signaling that correlated with greater smoking behavior and dependence. Although nondaily smokers share some characteristics with daily smokers that may predict smoking initiation and maintenance, they differ on measures of impulsiveness and resting EEG power. SignificanceResting EEG in non-deprived chronic smokers provides a standard for comparison to peak and trough nicotine states and may serve as a biomarker for nicotine dependence, relapse risk, and recovery.

Kronik Sigara Kullanımının Koroid Kalınlığı Üzerine Olan Etkilerinin Spektral Optik Koherens Tomografi ile Değerlendirilmesi

Amaç: Kronik sigara kullanımının spektral optik koherens tomografi (OKT) ile ölçülen koroid kalınlığı (KK) üzerine olan etkilerini incelemektir. Gereç ve Yöntemler: Bu ileriye dönük çalışmaya, uzun süredir (>5 yıl) sigara kullanan 40 gönüllü (çalışma grubu) ve hiç sigara kullanmamış 40 sağlıklı birey (kontrol grubu) dâhil edildi. Oküler hastalık veya cerrahi hikâyesi olanlar ve sistemik hastalığı olanlar çalışma dışı bırakıldı. Tüm ölçümler sabah saatlerinde yapıldı. Tüm hastalara göz içi basıncı ölçümü ve optik biyometri (Lenstar) ile aksiyel uzunluk ölçümünü de kapsayan detaylı oftalmolojik muayene yapıldı. KK dikey olarak fovea merkezi ile foveadan 1,5 mm ve 3,0 mm temporal ve nazal mesafelerden OKT (RTVue-100, Optovue) kullanılarak ölçüldü. Bulgular: Çalışma grubundaki 32 erkek, sekiz kadın hastanın ortalama yaşı 43,60±11,65 yıl iken, kontrol grubundaki 30 erkek 10 kadın bireyin ortalama yaşı 45,02±11,69 yıl idi. Gruplar yaş ve cinsiyet açısından homojen dağılım göstermekte idi (p>0,05). Çalışma grubundaki hastalar 22,50±18,37 paket/yıl sigara kullanmakta idiler. Çalışma grubundaki hastaların ortalama KK ölçümleri tüm bölgelerde kontrol grubuna göre istatistiksel olarak anlamlı azalmış bulundu (hepsi, p<0,05). Sigara içim miktarı ve süresi ile fovea altındaki KK arasında anlamlı negatif korelasyon mevcuttu (p<0,05, r=-0,556). Sonuç: Uzun süredir sigara kullanan bireylerde KK'da azalma görülmektedir. Bu azalma özellikle sigara ile ilişkili kuru tip yaşa bağlı makula dejenerasyonu gibi hastalıkların patofizyolojisinde önemli olabilir.

The Effect of Chronic Smoking on Lens Density in Young Adults

To investigate the effect of chronic cigarette smoking on lens density by Pentacam HR lens densitometry in young adults. Sixty chronic smokers who smoked at least 10 cigarettes per day for at least 2 years and 60 age- and sex-matched healthy control subjects were included in this prospective cross-sectional, comparative study. Presence of an ocular or systemic disease that might affect lens were determined as exclusion criteria. All individuals underwent complete ocular examination. Lens densitometry (LD) measurements were performed with Pentacam HR (Oculus, Wetzlar, Germany), dividing the lens into 3 areas: anterior area (anterior subcapsular and anterior cortical), nuclear area, and posterior area (posterior subcapsular and posterior cortical). Three-dimensional scan modes were used for measurements. The mean ages of group 1 and 2 were 25.85 ± 4.32 and 25.60 ± 5.14 years, respectively. The mean LD values in the 3 areas were higher in group 1 than group 2. However, only the mean LD value at the anterior area of group 1 was found to be statistically significantly higher (p = 0.047). There was no statistically significant difference in the mean LD measurements at the nuclear and posterior areas between the groups. Our study demonstrated that the mean LD value of the anterior area was significantly higher in group 1, suggesting that chronic smoking may contribute to anterior cortical and subcapsular cataract development in young adults.

PW175 Effects of Chronic Smoking on Arterial Stiffness in Healthy People

PW175 Effects of Chronic Smoking on Arterial Stiffness in Healthy People

Effect of smoking on selected blood parameters

Background: Smoking is not only a physical recidivism, but also a psychological inveteracy. Chronic effects of cigarette smoking on haematological parameters, with a good control side by side, were studied by very few. Evectics (including deaddiction) should be based on harm profile. Aims & Objectives: To find out age-wise Hb, BP, leucocyte (total/ differential) count, monocyte count, and eosinophil count in smokers. Materials and Methods: Study was carried out on a group of 108 otherwise healthy subjects from medical college campus –including 36 each in non-smoker, light-smoker and heavy smoker group – further subdivided into 9 each in 4 age ranges of 21-30years, 31-40 years, 41-50 years and 51-60 years. Data regarding age, sex, height, weight and various blood parameters were noted as per standard methods. Results: Chronic effects of smoking on cardiovascular system were found. SBP of both light and heavy smokers were significantly less than control group. DBP of light smokers and non-smokers did not differed very much. TLC and eosinophil count was higher while monocyte count was lower in smokers (insignificantly low in light smokers). Conclusion: The TLC and eosinophil count rise, while BP and monocyte counts fall in smokers. Smoking may lead to isolated systolic hypertension. In Evectics, the improvement/ outcome can be measured by assessing the rate/ extent of normalization of these parameters.