Months Of Smoking Research Articles

The effects of different types of smoking on recovery from attack in hospitalized multiple sclerosis patients

BackgroundSeveral studies demonstrated the association between tobacco smoking and higher risk and increased progression of multiple sclerosis (MS). Data about the effect of smoking during the recovery from MS attacks is limited. Furthermore, different types of tobacco exposures such as water pipe and passive smoking are not well assessed separately. So this study evaluated the effect of different types of smokes, cigarette and water pipe as well as passive smoking on the function recovery of relapsing-remitting MS (RRMS) attacks MethodsThis cohort study evaluated the adult patients with RRMS and Expanded Disability Status Scale (EDSS) < 5 in the attack phase. Patients were divided into two groups: smokers and non-smokers. The smokers included those who use cigarette, water pipe as well as passive smokers as subgroups for more analyses later. EDSS was monitored after relapse and two months after relapse. Change of EDSS considered as the criteria for functional recovery. The correlation between the amount of consumption and disability level was assessed among smokers by Pearson’s correlation test. While, the difference of EDSS between smoker and non-smoker were assessed by Independent samples T-test. Results142 patients were evaluated. 79 (55.6%) were smokers (43% male) while 63 (44.4%) were non-smokers (36.5% male). There was a statistically significant difference in change of EDSS between smoker and non-smoker groups, which change of EDSS was higher in non-smoker (−2.62 ± 0.90 non-smoker vs. −1.75 ± 0.76 smoker, P < 0.001). Also, only there was a significantly lesser decline in EDSS after two months in the cigarette smokers in subgroups analyses (P < 0.001). A correlation analysis revealed a significant positive correlation between the number per day of cigarette smoking and EDSS after relapse (r = 0.3, P = 0.03) and a significant positive correlation between minutes per month of smoking of water pipe and EDSS two months after relapse (r = ‎0.6‎‎, P > 0.001). ConclusionTobacco smoking especially cigarette smoking is associated with a negative effect on recovery from the attack in patients with RRMS.

Effects of electronic cigarette on platelet and vascular function after one month of use

Abstract Background and aims Smoking is a major factor that contributes to the development of cardiovascular disease. Smoking cessation delays progress of coronary artery disease. Electronic cigarette is proposed as a bridge to smoking cessation. We examined its effects on platelet function after 1 month of use compared to tobacco smoking. Patients and methods 40 current smokers (mean age 48 years±5) without cardiovascular disease were randomized to smoke either a conventional cigarette (conv-cig) or an electronic cigarette (e-cig) (electronic cigarette fluid with nicotine concentration of 12 mg/dL) for one month. All subjects smoked an electronic cigarette with nicotine concentration 12 mg/dL for one month. Measurements were performed at baseline and after one month of smoking the conventional or electronic cigarette. We measured a) perfused boundary region (PBR) of the sublingual arterial micro vessels (range 5–25 micrometers), a marker inversely related with glycocalyx thickness, b) pulse wave velocity (PWV), central systolic blood pressure (cSBP) and augmentation index (AIx), c) platelet function by two different methods, namely the novel Platelet Function Analyzer PFA-100 and the traditional Light Transmission Aggregometry (LTA) d) the exhaled CO level (parts per million-ppm) as a smoking status marker; and e) the plasma malondialdehyde (MDA) levels, as an oxidative stress burden index. Results After 1 month of electronic smoking, we did not observe any significant change in platelet function and arterial stiffness (p&amp;gt;0.05 for all markers) with the exception of a reduction of MDA (1.22±0.1 vs 1.09±0.1 μmol/L, p=0.03) and exhaled CO; 14.9±0.7 vs 5.9±0.7 ppm, p&amp;lt;0.001. Conversely, after continuation of conventional cigarette smoking for a month, platelet function was further impaired as assessed by PFA [125,5±31,1 vs 152,35±51,4 U, p=0.047) and by LTA (epinephrine as stimulator) [59,8%±16,1 vs 35,6%±19.1, p&amp;lt;0.001] and markers of arterial stiffness were deteriorated, as assessed by PWV (9,5±2,8 vs 10,3±2,9, p=0,028) and by Aixc (8,36±35,9 vs 30,4±21,6, p=0,004). Conclusions Electronic Cigarette smoking has a neutral effect on platelet function and arterial stiffness markers compared to conventional tobacco smoking which further deteriorates platelet and vascular function during one moth of use. Funding Acknowledgement Type of funding source: None

PEDF Reduction Induced by Cigarette Smoke: A Potential Role for Breast Tumor Development

There are many risk factors for cancer development and subsequent metastasis which include lifestyle choices such as diet, alcohol, and cigarette smoking. Smoking has been linked to several cancers including breast cancer. Many cohort studies have described the link between patients with breast cancer and those with long term smoking history. Despite the claim of correlation, the mechanism by which cigarette smoke alters breast epithelial cells and contributes to tumor cell growth and metastasis remains undefined. Pigment epithelium‐derived factor (PEDF) is a potent anti‐angiogenic factor and is shown to have inhibitory effects in numerous cancers. PEDF is often decreased or absent in tumor tissue when compared to surrounding stroma and its absence has resulted in cellular atypia. Female PEDF knockout mice show histologic changes in the breast at six months of age consistent with atypical ductal hyperplasia. We have shown that cigarette smoke exposure of breast tumor cells resulted in decreased PEDF expression. In order to assess the effects of cigarette smoke on the breast in‐vivo, we exposed six month old female mice to cigarette smoke using the SCIREQ inExpose system for up to six months and harvested mammary tissue for histological and biochemical analysis. Histological analysis revealed changes that include atypical epithelial growth in mammary tissue from mice exposed to six months of cigarette smoke when compared to those exposed to room air only. Immunohistochemistry showed increases in expression of proteins commonly upregulated in breast cancer including Ki‐67, VEGF, and COX‐2 in mammary tissue exposed to six months of smoking when compared to room air controls. Smoke exposure also caused a decrease in PEDF expression when compared to room air tissue. We have shown here for the first time that cigarette smoke alters the histology of the mammary tissue in mice and alters expression of important markers involved in human breast tumor development and progression.Support or Funding InformationPresidents Research Fund Saint Louis University School of Medicine

Electrocardiographic changes in young smokers: a cross-sectional study

This article assesses few electrocardiographic parameters in young adults (students) caused by smoking. The electrocardiogram of young smokers (with a history of at least six months of smoking) and young non-smokers were recorded using 12 leads, three channel ECG machine and the data thus obtained were analyzed statistically. It was found that there is extremely statistically significant difference in the timings of P-R interval and T-P interval when young smokers were compared with young non-smokers.

Effect of reducing the nicotine content of cigarettes on cigarette smoking behavior and tobacco smoke toxicant exposure: 2-year follow up

A broadly mandated reduction of the nicotine content (RNC) of cigarettes has been proposed in the United States to reduce the addictiveness of cigarettes, to prevent new smokers from becoming addicted and to facilitate quitting in established smokers. The primary aim of this study was to determine whether following 7 months of smoking very low nicotine content cigarettes (VLNC), and then returning to their own cigarettes, smokers would demonstrate persistently reduced nicotine intake compared with baseline or quit smoking. In a community-based clinic 135 smokers not interested in quitting were randomized to one of two groups. A research group smoked their usual brand of cigarettes, followed by five types of research cigarettes with progressively lower nicotine content, each for 1 month, followed by 6 months at the lowest nicotine level (0.5 mg/cigarette) (53 subjects) and then 12 months with no intervention (30 subjects completed). A control group smoked their usual brand for the same period of time (50 subjects at 6 months, 38 completed). Smoking behavior, biomarkers of nicotine intake and smoke toxicant exposure were measured. After 7 months smoking VLNC, nicotine intake remained below baseline (plasma cotinine 149 versus 250 ng/ml, P<0.005) with no significant change in cigarettes per day or expired carbon monoxide (CO). During the 12-month follow-up, cotinine levels in RNC smokers rose to baseline levels and to those of control smokers. Quit rates among RNC smokers were very low [7.5 versus 2% in controls, not significant). In smokers not interested in quitting, reducing the nicotine content in cigarettes over 12 months does not appear to result in extinction of nicotine dependence, assessed by persistently reduced nicotine intake or quitting smoking over the subsequent 12 months.

Addiction to lizard: A rare case report.

Sir, Drug use and abuse is as old as mankind itself. Human beings have always had a desire to eat or drink substances that make them feel relaxed, stimulated, or euphoric. As time went by, “home remedies” were discovered and used to alleviate aches, pains and other ailments. Most of these were naturally occurring substances. No refinement had occurred and isolation of specific compounds (drugs) had not taken place. The use of various insects as substances of abuse is interesting and has not been reported in detail in medical literature. The Indian spiny tailed lizard (Uromastyx hardwickii) is found patchily distributed in the Thar desert, Kutch and surrounding arid zones in India and Pakistan. Since ancient times, these are hunted by the locals in the belief that the oil extracted from the fat of the lizard's body is an aphrodisiac and is used as an embrocation and as a cure for impotence.[1] We would like to illustrate a case report on lizard being used as a substance of abuse in a cannabis addict. A 25-year-old male prisoner, with a 15-year history of cannabis abuse, shifted his drug of abuse to lizards due to non-availability of cannabis in prison. He would burn lizards and take the charred remains and fill them in a bidi and inhale deeply. He claimed “instant high” on this substance equating it as pleasurable as cannabis. He was introduced to this practice of smoking lizard powder by other jail inmates who were drug addicts and due to non-availability of drugs, started abusing lizard powder. On his release from prison, he started using cannabis again and also continued the use of lizard powder by mixing it with cannabis (sulfa) and smoked it in a bidi. After a month of smoking this combination, he presented with an acute psychotic episode with grossly disorganized behavior and was admitted for the same. He was diagnosed with cannabis induced psychosis. His initial Brief Psychiatric Rating Scale score (BPRS) was 59 and he was treated with tablet risperidone 6 mg/day and benzodiazepines for sedation. His condition improved in a week, BPRS score was 30; but he continued to be apathetic, anergic and slothful. His attention and concentration were also impaired. There was also history of apathy, anergia and amotivation for the past few years. Past history and family history of any psychiatric disorder was negative. The diagnosis of comorbid amotivational syndrome was considered and patient was started on tablet dothiepin 75 mg/day. His symptoms improved and he was followed-up for 1 year during which he did not abuse any substance and his mental condition was normal. During adverse conditions due to non-availability of drugs or other substances of abuse, the man has found alternatives in the form of lizard powder, snake and scorpion venom and wasp sting.[2345] The psychoactive properties of lizard, which cause addiction are not known. Thus, future research should be directed at finding the root cause of this addiction and long term affects of such addictions.

Cotinine and Tobacco-Specific Carcinogen Exposure Among Nondaily Smokers in a Multiethnic Sample

Nondaily smoking has increased among current U.S. smokers during the past decade and is practiced by a significant percentage of smokers. Although research in nondaily smoking has grown, little is known about levels of exposure to tobacco toxicants among nondaily smokers and their variation across ethnic groups. We examined urinary levels of cotinine and a tobacco-specific nitrosamine (NNAL) in community participants. Associations between the biomarker data and smoking characteristics were evaluated with Spearman's correlation analysis. Participants included 28 Blacks, 4 Latinos, and 25 Whites who smoked at least 1 cigarette on 4-24 days in the past 30 days. Participants averaged 3.3 (SD = 2.1) cigarettes per day (cpd) on days smoked, they smoked an average of 13.0 (SD = 5.4) days in the past month, and they smoked nondaily for 10.5 (SD = 10.5) years. Median levels of creatinine-normalized cotinine and NNAL were 490.9 ng/mg and 140.7 pg/mg, respectively. NNAL and cotinine were highly correlated (r = .84); NNAL and cotinine were modestly correlated with cpd (r = .39 and r = .34; all p values <.05). The number of days smoked per month was not associated with any biomarker levels. Our findings demonstrate that nondaily smokers are, on average, exposed to significant levels of nicotine and carcinogenic nitrosamines, with exposures of 40%-50% of those seen in daily smokers. This level of exposure suggests a significant health risk. Nicotine and carcinogen exposure is most closely related to number of cigarettes smoked per day but not to number of days per month of smoking.

Smoking Behavior and Exposure to Tobacco Toxicants during 6 Months of Smoking Progressively Reduced Nicotine Content Cigarettes

Recent federal legislation gives the U.S. Food and Drug Administration authority to regulate the nicotine content of cigarettes. A nationwide strategy for progressive reduction of the nicotine content of cigarettes is a potential way to reduce the addictiveness of cigarettes, to prevent new smokers from becoming addicted, and to facilitate quitting in established smokers. We conducted a trial of progressive nicotine content tapering over 6 months to determine the effects on smoking behaviors and biomarkers of tobacco smoke exposure and cardiovascular effects. One hundred and thirty-five healthy smokers were randomly assigned to one of two groups. A research group smoked their usual brand of cigarettes followed by five types of research cigarettes with progressively lower nicotine content, each smoked for one month. A control group smoked their own brand of cigarettes for the same period of time. Nicotine intake, as indicated by plasma cotinine concentration, declined progressively as the nicotine content of cigarettes was reduced. Cigarette consumption and markers of exposure to carbon monoxide and polycyclic aromatic hydrocarbons, as well as cardiovascular biomarkers remained stable, whereas urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) excretion decreased. No significant changes in biomarkers of exposure or cardiovascular effects were observed in controls. Our data support the proposition that the intake of nicotine from cigarettes of smokers can be substantially lowered without increasing exposure to other tobacco smoke toxins. These findings support the feasibility and safety of gradual reduction of the nicotine content in cigarettes.

Effects of 4 months of smoking in mice with ovalbumin‐induced airway inflammation

The effects of smoking on asthma pathogenesis are complex and not well studied. We have shown recently that 3 weeks of smoking attenuates ovalbumin (OVA)-induced airway inflammation in mice and that 4-6 months of smoking induces emphysema in mice without airway inflammation. Effects of combined long-term smoking and OVA exposure have not been investigated so far. To study whether long-term smoking affects progression of allergic airway inflammation and/or enhances the development of emphysema in mice. Mice were sensitized to OVA and challenged with saline or OVA aerosols for 6 months. From 2 months onwards, mice were also exposed to air or smoke. Lung tissue was analysed for extent of inflammation, emphysema, remodelling and for cytokine levels, and serum for OVA-specific IgE levels. Chronic OVA exposure of 6 months resulted in a T helper type 2 (Th2)-type inflammation with increased levels of IL-4, IL-5, IL-6 and infiltration of eosinophils, CD4(+) T cells, macrophages and plasma cells. Smoking induced a Th17-type of airway inflammation, characterized by neutrophils, macrophages, B cells and increased levels of IL-17, IL-6, granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor and monocyte chemoattractant protein-1. Concomittant smoking and OVA exposure resulted in inflammation similar to OVA exposure alone. OVA exposure increased IgE levels compared with saline exposure, and smoking did not further increase these levels. We did not find evidence for increased inflammation, IgE levels or emphysema in mice with allergic airway inflammation after 4 months of smoking compared with non-smoking. However, a 4-month exposure to smoke alone did enhance neutrophilic airway inflammation characterized by high pulmonary IL-17 levels. A Th2 inflammatory environment due to OVA exposure may be one explanation as to why no further detrimental effects of smoking on allergic airway inflammation were found.

Alpha1-antitrypsin determines the pattern of emphysema and function in tobacco smoke-exposed mice: parallels with human disease.

Cigarette smoking in humans is associated with various patterns of emphysema and functional consequences. We tested the hypothesis that variations in alpha1-antitrypsin expression modulate the pattern of emphysema and functional consequences in cigarette smoke-exposed mice. We compared the effects of up to 6 months of cigarette smoke exposure in C57BL/6J (C57) mice and in low-alpha1-antitrypsin, C57BL/6J pa+/pa+ (pallid) mice. At the end of the experiment, we determined lung mechanical properties, the extent (mean linear intercept) and type of emphysema, and the cellular inflammatory response. After 4 months of cigarette smoking, pallid smoking mice, but not C57 smoking mice, had a significant increase in mean linear intercept. After 6 months of smoke exposure, C57 smoking mice and pallid smoking mice had similar degrees of emphysema. The pattern of emphysema in pallid smoking mice was more diffuse than in C57 smoking mice, affecting all airspaces. Pallid mice, but not C57 mice, developed a T cell inflammation in the alveolar wall after 6 months of smoking (p < 0.01). Although lung compliance was not changed in C57 smoking mice after smoke exposure, it increased significantly in pallid smoking mice over the 6 months of exposure (p < 0.0082). In summary, cigarette smoking induces emphysema in C57 and pallid mice, but the emphysema, inflammatory infiltrate, and resulting physiologic abnormalities were substantially different in the two strains, with the C57 and pallid mice exhibiting features similar to centrilobular and panlobular emphysema, respectively.

Mucus hypersecretion and viscoelasticity changes in cigarette-smoking dogs.

Chronic cigarette smoke exposure is well known to cause mucus hypersecretion in experimental animals, but the alterations in mucus rheology have not been described. We studied mucus hypersecretion and viscoelasticity changes in nine tracheostomized beagle dogs exposed to cigarette smoke. The dogs were trained to stand quietly in a harness, and smoke was delivered via a cuffed tracheostomy tube. A 35-cm3 bolus was introduced to the inspiratory line each 20 s, using unfiltered 70-mm cigarettes (20 mg tar, 1.2 mg nicotine). Each dog smoked 10 cigarettes per day over 2.5 h, 5 days per week. Two dogs were exposed for 6 months; 7 dogs were exposed for 10 months. Five dogs served as sham-smoking controls. Mucus was collected twice weekly without drugs by resting a cytology brush on the lower trachea for 2-5 min. The rheological properties of the mucus samples were determined by magnetic rheometry, which yields elasticity and viscosity as a function of frequency. The mucus was also weighed, and the galactose content was determined by phenolsulfuric acid assay. The mucus collection rate served as an index of tracheal mucus flux, and the galactose assay as a marker of mucous glycoprotein content. The tracheal mucus linear velocity (TMV) was determined periodically under xylazine analgesia by observing charcoal particle transport bronchoscopically. Eight of 9 smoking dogs developed mucus hypersecretion (flux greater than 2 X control) versus 1 of 5 controls (p less than .01). TMV did not change significantly in 10 months of exposure. In the first 2-4 months of smoking, the elasticity and viscosity of the mucus both decreased (mean at 4 months = 42% control, p less than .001), as did the galactose content (mean at 4 months = 48% control, p less than .01). At this stage, according to model studies, the mucus should have been more easily clearable by ciliary action. After 6 months, the viscoelasticity returned toward the initial control level, while the galactose content remained low, suggesting an alteration in the nature of the mucous glycoprotein.