Cigarette filter vent blocking: effects on smoking topography and carbon monoxide exposure

Two studies were conducted using smokers of unventilated cigarettes to determine the effects of filter vent blocking on smoke exposure (Experiment 1) and smoking topography (Experiment 2). In both studies, subjects were exposed to ultra low yield cigarettes that had 0%, 50%, and 100% of their filter vents blocked with tape. In Experiment 1, carbon monoxide (CO) exposure from eight 60 ml puffs increased in an orderly fashion as a function of filter vent blocking. By blocking filter vents, smoke was no longer diluted with air as it passed through the filter, and hence, exposure to smoke constituents was increased. In Experiment 2, when puff and inhalation parameters were allowed to vary, subjects took significantly more puffs, and larger puffs from unblocked cigarettes than from completely blocked cigarettes, but CO exposure from the completely blocked cigarette was double that from the unblocked cigarette (8.96 ppm vs. 4.32 ppm). The increased number and volume of puffs taken from ultra low yield cigarettes with unblocked filter vents may be due to changes in physical characteristics of the cigarette, and not to smokers actively compensating for reduced smoke constituent yields.     

Time course of blood volume change with carbon monoxide inhalation and its contribution to the overall cardiovascular response

Adult male Sprague-Dawley rats inhaled 500 ppm CO continuously for 42 days in order to examine the blood volume response in a time course manner. Plasma volume as measured by Evan's blue dye dilution technique did not change significantly from the control value of 3.96% of body weight (BW). Total blood volume estimated using plasma volume and hematocrit increased steadily from 7.34% of BW to 11.69%, almost entirely as the result of a more than 2-fold increase in erythrocyte mass (3.42% increased to 7.55%). Absolute blood volume increased from 28.51 ml to 58.26 ml; normal growth contributed to this increase, i.e. BW increased from 350.0 g to 499.1 g. Real hematocrit determined by dye dilution increased from 46.5% to 64.6%, reaching a near-equilibrium level within 15 days. Hemoglobin concentration increased from 13.68 g/dl to 20.07 g/dl, and erythrocyte count increased from 6150000 per cubic mm to 9140000 per cubic mm. Minor changes in erythrocyte indices (i.e. mean corpuscular hemoglobin concentration and mean corpuscular volume) occurred during the 42 days. Concurrently, the weight of right ventricle increased more than left ventricle + septum, reflecting somewhat greater right-sided cardiomegaly. Increases in both ventricles were correlated with changes in blood volume and hematocrit. Plasma atrial natriuretic peptide activity increased 2.5 fold after 15 and 30 days of CO exposure, possibly reflecting increasing atrial stretch caused by increased blood volume. Like the polycythemic hypervolemic state of chronic hypoxic hypoxia, blood volume in CO hypoxia increases solely through addition of erythrocytes.     

Inhibitory effects of formaldehyde inhalation on the cardiovascular and respiratory systems in unanesthetized rabbits

The mechanisms of the marked inhibitory effects of 10 ppm formaldehyde (HCHO) inhalation on heart rate and respiratory movement were investigated in unanesthetized rabbits. Inhibition of the heart rate and respiratory movement induced by HCHO inhalation was caused by a reflex reaction during sensory irritation of the upper respiratory tract, mainly the nasal mucosa, but not of the lower respiratory tract, mainly the lung. These reflex reactions, particularly decreases in the heart rate, were not blocked by vagotomy, atropine or prazosin, but were blocked by propranolol, phenoxybenzamine, phentolamine, yohimbine and guanethidine. These results suggest that these reflex reactions are derived from sympathetic nervous activity rather than parasympathetic nervous activity, and the reflex bradycardia is caused by inhibiting the transmitter release at the adrenergic nerve endings.     

吸入一氧化碳对大鼠供体肺的保护作用

目的观察一氧化碳对长时间低温保存的供体肺的保护作用。方法建立大鼠肺移植离体肺灌注试验模型，SD大鼠24只，按照有无CO吸入分为空白对照组、CO吸入组，每组均取6对分别作为肺移植的供体鼠和受体鼠。空白对照组大鼠供肺移植全程吸入100％氧气直至再灌注后1h；一氧化碳组移植全程吸入500ppm一氧化碳和氧气的混合气，并且供体肺在冷保存的12h期间肺内仍充盈着一氧化碳和氧气的混合气，余同对照组。于供体肺循环灌注1、20、40、60min测定供肺静脉流出血氧分压、平均肺动脉压、气道峰压：灌注结束后切取供体肺组织，在光镜和电镜下比较肺组织细胞学改变，测定肺组织湿干比、丙二醛含量、髓过氧化物酶活性、白细胞介素8的含量，用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）法比较肺组织细胞凋亡的变化。结果实验选取大鼠24只，作为受体的12只（每组6只）进入结果分析。①与空白对照组比较，一氧化碳组供体肺的PaO2在再灌注20分钟之后明显高于对照组；mPAP、PawP分别在再灌注20分钟和40分钟之后明显低于对照组（P〈0．05）：②与空白对照组比较，一氧化碳组供体肺再灌注后湿干比、丙二醛含量、髓过氧化物酶活性、白细胞介素8含量均明显降低（P〈0．05）。③CO组肺组织细胞损伤较对照组明显减轻，凋亡细胞数量明显减少。结论吸入低剂量CO可以减轻供肺的缺血再灌注损伤，保护供体肺功能。     

Contingent reinforcement for reduced breath carbon monoxide levels: Target-specific effects on cigarette smoking

This study determined the effects on smoking behavior of providing contingent reinforcement for nonsmoking versus reduced smoking afternoon breath carbon monoxide (CO) target levels. Twenty-eight hired chronic smoker volunteers were randomly assigned to one of three experimental conditions during a 10-day intervention: (a) 8 ppm target CO, $5 per day incentive (n = 11); (b) 16 ppm target CO, $4 per day incentive (n = 8); or (c) 8 ppm target CO, no incentive (n = 9). Both payment groups showed significantly lower CO levels and greater amounts of daytime smoking reduction than the no-pay group. A specific effect of CO target was also seen; 45% of subjects in the 8 ppm group compared with 0% of subjects in the 16 ppm target and no-pay groups produced average afternoon CO levels of 8.5 ppm or lower during the intervention. Average levels of CO and smoking reduction did not differ for the two paid groups, however, because some subjects in the 8 ppm group failed to reduce CO sufficiently to contact the reinforcer. Contingent reinforcement based on expired air CO levels can exercise powerful and precise (target-specific) control over smoking behavior, but there may be individual differences in ability to meet reinforcement contingencies if difficult targets are introduced abruptly.     

Recent marijuana blunt smoking impacts carbon monoxide as a measure of adolescent tobacco abstinence

Adolescent tobacco smokers have a higher prevalence of marijuana (MJ) smoking than adolescents who do not smoke tobacco. As part of an adolescent smoking cessation trial, we examined whether MJ smoking, and specifically "blunt" (gutted cigars filled with MJ) smoking, elevated participants' likelihood of a false indication of cigarette smoking on the basis of breath carbon monoxide (CO) testing. Using clinical data from 37 adolescents (mean age 15.1+/-1.4 years, 78% female) who participated in a smoking-cessation trial in Baltimore between 1999 and 2002, and who on at least one occasion, reported abstinence from tobacco smoking for at least 7 days, we analyzed 146 cigarette-abstinent-visit exhaled CO concentrations classified into blunt occasions (12 participants, 33 visits), nonblunt MJ occasions (seven participants, 20 visits), and non-MJ occasions (27 paricipants, 93 visits). Repeated-measures logistic regression revealed that blunt occasions were associated with CO > or = 8 ppm, compared to nonblunt occasions (p = 0.013). Blunt occasions also tended to be associated with the more youth-appropriate cutoff CO > or = 6 ppm, compared to non-MJ occasions (p =0.054). Blunt smoking impacted the interpretation of measures of exhaled CO for tobacco cessation.     

Exposure to smoking cues: cardiovascular and autonomic effects

Laboratory exposures to smoking cues have been shown to reliably induce self-reported cigarette cravings among smokers, a model of environmentally triggered urges to smoke that can contribute to poorer cessation success. Several studies have also demonstrated that cue exposures give rise to changes in heart rate and blood pressure. Few studies, however, have investigated possible cue effects on heart rate and blood pressure variability (HRV and BPV). Particularly intriguing in this regard are cardiac oscillations in the low (i.e., 0.04-0.15 Hz), and high (i.e., 0.15-0.50 Hz) frequency range, which are thought to reflect components of autonomic control and response to environmental challenges. A closer examination of cardiovascular reactivity may thus help characterize the autonomic response to smoking cue exposure. To that end, an experimental study was conducted in which nicotine dependent daily smokers (n=98) were exposed to guided imagery of neutral and smoking situations, while continuous, noninvasive, beat-to-beat cardiovascular data were collected. Consistent with previous research, the findings revealed significant increases in both systolic and diastolic blood pressure during smoking imagery, relative to neutral imagery. In addition, power spectral density analyses of heart rate and blood pressure variability revealed elevated HRV and BPV in both the low- and high-frequency ranges during the smoking imagery. The results suggest the presence of an autonomic component to smoking cue reactivity, and also raise the possibility of long-term negative cardiac consequences for smokers who ubiquitously encounter cues in their daily environments.     

Toxic effects of selenium inhalation: acute damage of the respiratory system of mice

Accidental inhalation of selenium by humans has been associated with damage of respiratory tissues that is lacking a detailed histological definition. We have investigated the natural history of injury to the tracheal epithelium and lungs induced by a single intratracheal instillation of CD-1 mice with two different doses of dimethyl selenide (0.05 and 0.1 mg Se/kg of body weight). The animals were sacrificed 1, 7, 14, and 28 days after the single selenium treatment. Samples of the trachea and lungs were studied by light microscopy. The tracheal epithelium showed loss of cilia and acute necrosis that was followed by metaplastic transformation. Edema and diffuse alveolar damage was observed in the lungs. Our data suggest that: i) severity of respiratory lesions caused by selenium is dose dependent; ii) selenium causes transient metaplastic transformation of the tracheal epithelium; iii) chronic inflammation and increased thickness of alveolar septa occur in the lungs; iv) 4 weeks after selenium treatment, mice recover from the tracheal injury, whereas no amelioration of pulmonary lesions was observed.     

CO inhalation at dose corresponding to tobacco smoke worsens cardiac remodeling after experimental myocardial infarction in rats.

We hypothesized that inhalation of carbon monoxide (CO) (500 ppm), similar to that in tobacco smoke, disturbs the cardiovascular adaptation after myocardial infarction by increasing remodeling. Four groups of rats were assessed. Two groups had myocardial infarction induced by the ligation of the left coronary artery: the first group was exposed to air (infarcted air group, n = 12), and the second was exposed to CO (infarcted CO group, n = 11). They were compared to two sham-operated groups, a control air group (n = 10), and a control CO group (n = 7) exposed (3 weeks) to CO. Aerobic endurance capacity was assessed in both the infarct CO and infarct air group (endurance capacity = 0.043 +/- 0.006 m.min(-1).g(-1) vs. 0.042 +/- 0.005 m.min(-1).g(-1), not significant). In the infarcted CO group compared to the infarcted air group, the dilatation of the left ventricle observed 3 weeks after infarction was increased, (left ventricular diastolic (LVD) diameter (D) = 9 +/- 0.4 vs. 7 +/- 0.4 mm, p < 0.05; left ventricular systolic (LVS) diameter (D) = 6 +/- 0.6 vs. 4.1 +/- 0.4, p < 0.05), and the diastolic posterior wall thickness was augmented (posterior wall diastolic thickness = 1.7 +/- 0.1 vs. 1.3 +/- 0.1 mm, p < 0.05). Hemodynamic pressure measurements in both ventricles and pulmonary artery showed elevated diastolic pressure after CO exposure compared to air exposure (LVD pressure = 32 +/- 1.6 vs. 19 +/- 2.3 mm Hg, p < 0.05; right ventricular diastolic pressure = 16 +/- 1.6 vs. 8.6 +/- 1.6 mm Hg, p < 0.05; pulmonary arterial pressure in diastole (PAD) = 27 +/- 1.6 vs. 20 +/- 2.3 mm Hg, p < 0.05). In the infarcted CO group, the infarct size increased. Echocardiography and histology showed hypertrophy of the contralateral wall similar to that observed in the noninfarcted control CO group. In conclusion, chronic CO inhalation worsens heart failure in rats with myocardial infarction by an increase in the infarct size and hypertrophy remodeling.     

Adverse respiratory effects in rats following inhalation exposure to ammonia: respiratory dynamics and histopathology

Acute respiratory dynamics and histopathology of the lungs and trachea following inhaled exposure to ammonia were investigated. Respiratory dynamic parameters were collected from male Sprague–Dawley rats (300–350?g) during (20?min) and 24?h (10?min) after inhalation exposure for 20?min to 9000, 20,000, and 23,000?ppm of ammonia in a head-only exposure system. Body weight loss, analysis of blood cells, and lungs and trachea histopathology were assessed 1, 3, and 24?h following inhalation exposure to 20,000?ppm of ammonia. Prominent decreases in minute volume (MV) and tidal volume (TV) were observed during and 24?h post-exposure in all ammonia-exposed animals. Inspiratory time (IT) and expiratory time (ET) followed similar patterns and decreased significantly during the exposure and then increased at 24?h post-exposure in all ammonia-exposed animals in comparison to air-exposed controls. Peak inspiratory (PIF) and expiratory flow (PEF) significantly decreased during the exposure to all ammonia doses, while at 24?h post-exposure they remained significantly decreased following exposure to 20,000 and 23,000?ppm. Exposure to 20,000?ppm of ammonia resulted in body weight loss at 1 and 3?h post-exposure; weight loss was significant at 24?h compared to controls. Exposure to 20,000?ppm of ammonia for 20?min resulted in increases in the total blood cell counts of white blood cells, neutrophils, and platelets at 1, 3, and 24?h post-exposure. Histopathologic evaluation of the lungs and trachea tissue of animals exposed to 20,000?ppm of ammonia at 1, 3, and 24?h post-exposure revealed various morphological changes, including alveolar, bronchial, and tracheal edema, epithelial necrosis, and exudate consisting of fibrin, hemorrhage, and inflammatory cells. The various alterations in respiratory dynamics and damage to the respiratory system observed in this study further emphasize ammonia-induced respiratory toxicity and the relevance of efficacious medical countermeasure strategies.     

Expired air carbon monoxide and saliva thiocyanate: Relationships to self-reports of marijuana and cigarette smoking

This study examined the relationship between self-reports of marijuana and cigarette smoking, and the psysiological measures of expired air carbon monoxide (CO) and saliva thiocyanate (SCN) in a sample of 1,130 seventh, ninth, tenth, eleventh, and twelfth graders. Subjects who reported marijuana smoking were likely to also report cigarette smoking. The correlation between self-reported marijuana smoking and SCN was negligible. The correlation between CO and self-reported marijuana smoking was statistically significant, but when the variance due to cigarette smoking was removed, this relationship also became negligible. The existence of a sizeable number of marijuana smokers in this sample of adolescents did not alter the correlation between CO and self-reports of cigarette smoking. However, in adult samples, where marijuana and cigarette smoking are less highly correlated, marijuana smoking could affect the relationship between CO and self-reported cigarette smoking. Carbon monoxide predicted self-reported cigarette smoking better than did saliva thiocyanate. There was an interaction between grade and the CO/cigarette smoking correlation. The correlations were generally higher in upper grades.     

Effect of intermittent carbon monoxide inhalation on erythropoiesis and organ weights in rats

Sprague-Dawley rats were exposed to 450 ppm carbon monoxide (CO) for 6 h per day, 5 days per week for 33 days. The effect of CO on reticulocyte count, hematocrit, hemoglobin concentration, body weight and selected organ weights was measured. Exposure to CO caused a three-fold increase in the youngest reticulocyte population, concomitant with an increase in the total reticulocyte count. Despite continued CO exposure, reticulocyte number and distribution returned to normal by day 9, suggesting that reticulocyte response of the organism to CO had changed. Both hematocrit and hemoglobin concentrations began to increase 16 days after CO exposure and remained at the increased level for the duration of the exposure period. There were no changes in kidney, liver and adrenal weights throughout the course of study. However, spleen weight was increased after 5 days of CO exposure. Left and right ventricular organ weight ratios increased equally at the same time during the study. These results indicate that the increase in the young reticulocyte population and the subsequent increase in total reticulocyte count are the earliest erythropoietic responses to intermittent CO exposure and that CO-induced polycythemia is associated with cardiac hypertrophy in rats.     

The acute effects of nicotine, tobacco smoke and carbon monoxide on myocardial oxygen tension in the anaesthetized cat

1 The acute effects of nicotine, tobacco smoke, and carbon monoxide on myocardial oxygen tension (MPo₂) were estimated amperometrically in 33 anaesthetized open-chest cats with a glass-insulated 25 μm platinum cathode within a 22-gauge needle implanted in the left ventricular wall.     

Effect of tobacco smoking and smoking cessation on plasma lipoproteins and associated major cardiovascular risk factors: a narrative review

Abstract

Cigarette smoking, active or passive, kills about 6 million people each year worldwide. Cardiovascular disease (CVD) is responsible for 40% of all smoking-related deaths, lung cancer accounts for 20% of all smoking-related deaths, and chronic obstructive pulmonary disease is related to another 20% of deaths. In this narrative review we consider the relationship between cigarette smoking and CVD. We discuss disease states and/or CVD risk factors related to smoking, such as dyslipidaemia, vascular inflammation, endothelial dysfunction, arterial stiffness, insulin resistance, type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), and non-alcoholic fatty liver disease (NAFLD) as well as their complex interrelations. Smoking cessation can correct abnormalities related to smoking; however, success rates are relatively low. In cases of inability to quit, measures to minimize the adverse effects of smoking specifically related to CVD should be taken. Smokers should receive best practice treatment, according to guidelines, as for non-smokers.     

Effects of carbon monoxide inhalation on erythropoiesis and cardiac hypertrophy in fetal rats.

Pregnant rats were exposed to four CO concentrations over 21 days, and the effects of CO on fetal hemoglobin, hematocrit, heart weight, and body weight were measured. The exposure to 250 and 500 ppm of CO caused a sharp depression in fetal hemoglobin and hematocrit, coincident with a marked reduction of the weight of the fetuses, indicating a high vulnerability to CO of both fetal erythropoiesis and growth. The concentration of 125 ppm of CO did not affect fetal red blood cells, while 60 ppm of CO caused a slight increase in hematocrit. This low dose is below the threshold of an adaptive response in adult animals. The hearts of the fetuses exhibited a large increase in weight, which was even present in the 60-ppm group in contrast to reported data for adult animals. Since a severe anemia rather than polycythemia occurred, an increased blood viscosity cannot be responsible for the hypertrophic heart of the fetuses and consequently also of the adult animals, if the principal mechanisms for heart growth are identical in fetuses and adult animals. It is further unlikely that pulmonary hypertension causes the cardiac hypertrophy because the fetal lung circulation is only slightly developed. The reason of the heart weight increase therefore remains unknown.     

Comparative effects of tobacco smoking and nasal nicotine

OBJECTIVE: Compare the electroencephalographic (EEG) and cardiovascular effects of tobacco smoking and nasal nicotine in the same subjects. METHODS: Eleven volunteer smokers were studied after >10 h of overnight tobacco deprivation. Quantitative EEG was used to measure brain electrical changes produced by four different treatments. Each subject smoked a low (0.08 mg) and average nicotine (1 mg) yield cigarette on one test day and received placebo and nicotine nasal spray (0.5 mg/spray) on a second day in a counterbalanced design. EEG activity was measured from 16 scalp electrodes and analyzed as delta, theta, alpha (1), alpha (2), beta (1), and beta (2) frequency bands. Heart rate (HR), blood pressure (BP), and plasma venous nicotine concentrations (VNC) were monitored during both sessions. EEG data from all 16 channels at each of six frequencies were compared over 10 min using repeated measures ANOVA analysis. Changes in HR, BP, and VNC from baseline were compared using ANOVA followed by post hoc Scheffe's test. RESULTS: Smoking an average nicotine delivery cigarette resulted in highly significant decreases in alpha (1) activity, significant increases in alpha (2) activity, and significant increases in both HR and VNC compared to all other conditions. CONCLUSION: When smokers are allowed to pace themselves, cigarette smoking is far more effective than nasal nicotine in activating the EEG and increasing HR and VNC. This lack of equivalent physiological effects may explain the low success rate when nicotine nasal spray is used by those trying to quit smoking.     

Differential inhibition of mitochondrial respiratory complexes by inhalation of combustion smoke and carbon monoxide,in vivo,in the rat brain

Combustion smoke contains gases and particulates, which act via hypoxia and cytotoxicity producing mechanisms to injure cells and tissues. While carbon monoxide (CO) is the major toxicant in smoke, its toxicity is exacerbated in the presence of other compounds. Here, we examined modulations of mitochondrial and cytosolic energy metabolism by inhalation of combustion smoke versus CO, in vivo, in the rat brain. Measurements revealed reduced activities of respiratory chain (RC) complexes, with greater inhibition by smoke than equivalent CO in ambient air. In the case of RC complex IV, inhibition by CO and smoke was similar—suggesting that complex IV inhibition is primarily by the action of CO. In contrast, inhibition of complexes I and III was greater by smoke. Increases in cytosolic lactate dehydrogenase and pyruvate kinase activities accompanied inhibition of RC complexes, likely reflecting compensatory increases in cytosolic energy production. Together, the data provide new insights into the mechanisms of smoke inhalation-induced perturbations of brain energetics, which impact neuronal function and contribute to the development of neuropathologies in survivors of exposures to CO and combustion smoke.     

Effect of carbon monoxide inhalation exposure in mice on drug metabolism in vivo

Experiments were undertaken to evaluate the action of carbon monoxide (CO) on the mixed-function oxidase (MFO) system in vivo. Mice were exposed to 500 ppm CO for 8 h per day in an inhalation chamber under dynamic airflow conditions. Hexobarbital (150 mg/kg, i.p.), zoxazolamine (150 mg/kg, i.p.) or ethanol (2 mg/g, i.p.) was given to each group of mice during CO exposure and disappearance of the drug from blood or brain was determined while CO exposure continued. The experiments were repeated with different groups of animals which were exposed to CO for 3 or 5 days. Hexobarbital and ethanol metabolism were not affected by CO following either one day exposure or repeated exposure. There was no statistically significant difference in the brain level of zoxazolamine in animals exposed to CO when compared to control. These studies indicate that in vivo metabolism of hexobarbital, zoxazolamine and ethanol in mice is not affected by exposure to 500 ppm CO under the conditions employed in the present study.