Second‐hand smoking and carboxyhemoglobin levels in children: a prospective observational study

Aim: To establish baseline noninvasive carboxyhemoglobin (COHb) levels in children and determine the influence of exposure to environmental sources of carbon monoxide (CO), especially environmental tobacco smoke, on such levels. Background: Second‐hand smoking may be a risk factor for adverse outcomes following anesthesia and surgery in children (1) and may potentially be preventable. Patients and Methods: Parents and their children between the ages of 1–12 were enrolled on the day of elective surgery. The preoperative COHb levels of the children were assessed noninvasively using a CO‐Oximeter (Radical‐7 Rainbow SET Pulse CO‐Oximeter; Masimo, Irvine, CA, USA). The parents were asked to complete an environmental air‐quality questionnaire. The COHb levels were tabulated and correlated with responses to the survey in aggregate analysis. Statistical analyses were performed using the nonparametric Mann–Whitney and Kruskal–Wallis tests. P < 0.05 was statistically significant. Results: Two hundred children with their parents were enrolled. Children exposed to parental smoking had higher COHb levels than the children of nonsmoking controls. Higher COHb values were seen in the youngest children, ages 1–2, exposed to parental cigarette smoke. However, these trends did not reach statistical significance, and confidence intervals were wide. Conclusions: This study revealed interesting trends of COHb levels in children presenting for anesthesia and surgery. However, the COHb levels measured in our patients were close to the error margin of the device used in our study. An expected improvement in measurement technology may allow screening children for potential pulmonary perioperative risk factors in the future.     

Degeneration of intervertebral discs due to smoking: experimental assessment in a rat-smoking model

We have investigated the intervertebral discs of rat-smoking models to demonstrate that smoking is a cause of degenerative intervertebral disc disease. A smoking box was developed for this study. We exposed 8-week-old rats to indirect tobacco smoke inhalation. Each rat was forced to inhale the smoke from one cigarette per hour. The mean blood nicotine level of rodents exposed to cigarette smoke corresponds to about twice that of ordinary human smokers. Histological and immunological studies were then performed to assess the effects of smoking for varying periods of time. After 8 weeks, the chondrocytes in the disordered annulus fibrosus layer tended to grow larger and attain a rounder form than normal chondrocytes. The interleukin-1 level in the 8-week smoking group was significantly higher than that of the control group. Tobacco smoke inhalation increased local production and release of inflammatory cytokines and resultant decomposition of chondrocyte activity.     

Cigarette smoke inhalation and the acute airway response.

The acute airway response to smoking varying numbers (one to four) of identical cigarettes in rapid succession and smoking single cigarettes of differing tar/nicotine yields was assessed repeatedly in 13 healthy smokers. The airway response was variable, indicating airway narrowing consistently in only three subjects. There appeared no difference between forced spirometry and measurement of airway resistance in detecting the airway response. No relationship was observed between the airway response and amount of smoke inhaled into the lungs as measured either by changes in venous blood nicotine or percentage carboxyhaemoglobin. When five smokers inhaled smoke directly from a cigarette acute airway narrowing was consistently observed. A normal smoking pattern consisting of an initial drag of smoke into the mouth, followed after a pause by inhalation of smoke diluted with air, did not consistently cause airway narrowing although similar amounts of smoke as the direct drag were inhaled as assessed by changes in venous blood nicotine. The manner of smoke inhalation affects the relative concentrations of the different constituents of smoke reaching the lungs and also appears to be the main determinant of the acute airway response to smoking, which was unrelated to the number of cigarettes smoked or the tar content of the smoke. This suggests that patterns of smoke inhalation may influence the pathogenesis of bronchial disease associated with smoking.     

Induction-intubation response--smokers vs non-smokers--

BACKGROUND AND OBJECTIVES: Tobacco smoking has been established to be a hazardous activity. Changing social attitude is bringing a decline in tobacco consumption but a significant proportion of patients presenting for surgery still continues to smoke, putting themselves at risk of perioperative complications. We evaluated induction-intubation response in 40 male patients (ASA-I) divided into two groups of 20, each consisting of smokers and non-smokers. METHODS: All patients received standard premedication and general anesthesia. Heart rate, blood pressure and rate-pressure product were measured prior to induction, just before intubation and at 1, 3, 5 and 10 minutes after intubation. Continuous electrocardiography (EKG lead II) monitoring was done. Carboxyhemoglobin and total hemoglobin were estimated at the time of securing venous access. Arterial blood gases were analysed 5 minutes before and after the tracheal intubation. RESULTS: Incidence of arrhythymias (30%) was higher in smokers compared to non-smokers (10%). Mean carboxyhemoglobin (COHb) level in smokers was 3.81 +/- 2.17 gdL(-1) as compared to 2.95 +/- 1.33 gdL(-1) in non-smokers. Four patients who continued to smoke till the day of surgery had higher COHb levels (8.2, 5.9, 6, 8.8 gdL(-1)). PaO2 and PaCO2 levels were comparable in both groups. CONCLUSIONS: During induction-intubation period, heart rate; systolic, diastolic and mean arterial pressure and rate-pressure product showed more pronounced fluctuations in smokers than in non-smokers (p < 0.05).     

Relation of urinary cotinine concentrations to cigarette smoking and to exposure to other people''s smoke.

The relation of urinary cotinine measurements to tobacco consumption in smokers and to exposure to other people's smoke in non-smokers was studied in 49 smokers and 184 reported non-smokers attending a health screening centre. The median urinary cotinine concentration was 1623 ng/ml in the smokers and 6.1 ng/ml in the non-smokers. In smokers the average urinary cotinine concentration increased with reported habitual cigarette consumption; in non-smokers it increased with the reported total seven day duration of exposure to other people's tobacco smoke. Cotinine concentrations were approximately three times higher in non-smokers living with a spouse or partner who was a smoker than in those living with a non-smoker; their reported duration of exposure to tobacco smoke was also three times higher. Non-smoking subjects who were exposed to any tobacco smoke and who lived with a smoker reported 70% of their exposure to be at home (56% for men and 86% for women); the men reported more exposure at work than non-smoking men who lived with a non-smoker. This study confirms the relation of urinary cotinine to stated tobacco smoke exposure in both smokers and non-smokers and further validates the use of information on the smoking habits of the spouse or partner as a measure of tobacco smoke exposure in epidemiological studies of non-smokers.     

Differential effects of nicotine and smoke condensate on bone cell metabolic activity

OBJECTIVE: Delayed or impaired healing of skeletal trauma in patients who smoke has been attributed to vascular responses of nicotine absorption and/or a direct effect of nicotine or other smoke components on bone cells. In vivo studies indicate variability in osteosynthetic response to nicotine versus smoke inhalation. We tested the hypothesis that components of cigarette smoke other than nicotine may be responsible for the adverse skeletal effects of smoking. DESIGN: In vitro cultures of MC3T3-E1 osteoblastlike cells were exposed to varying doses of nicotine or condensates of cigarette smoke. Metabolic assays included alkaline phosphatase activity, collagen synthesis, and total protein synthesis as well as cell proliferation. RESULTS: Variations in the degree of response were noted between bone cell preparations. Nicotine elicited a significant dose-dependent stimulation of bone cell metabolism in all studies. This was detected as increases in alkaline phosphatase activity and increases in total protein and collagen synthesis. Responses were noted with nicotine doses as low as 12.5 ng/mL (half the nicotine level circulating in smokers). In one study, maximum stimulation occurred at 250 ng/mL with levels reaching 74% (total protein) and 104% (collagen) greater than control cultures. In a second study, 222% and 627% stimulation of protein and collagen synthesis over controls was noted using 100 ng/mL. Addition of the nicotine receptor antagonist mecamylamine reduced the nicotine stimulation. Preparations of smoke condensate with equivalent nicotine concentrations reduced all indices of metabolic activity. Cell proliferation was stimulated by both nicotine (20-25%) and smoke condensate (38-46%). CONCLUSION: The data suggest that nicotine acts as a direct stimulant of bone cell metabolic activity. Smoke condensate containing equivalent levels of nicotine elicits an inhibitory effect. A probable speculation is that the delay in clinical healing of skeletal trauma in smoking patients may in part be a result of absorption of components of smoke other than nicotine.     

Experience in employing pulse CO-Oximetry

BACKGROUND: In U.S.A., Pulse CO-Oximetry has emerged as a quick, simple, and non-invasive diagnostic modality to measure the concentration of COHb in arterial blood. To investigate its efficiency, we measured COHb levels by employing Pulse CO-Oximetry and by CO-Oximeter in arterial blood. METHODS: Normal healthy volunteers with a habit of smoking, smoked three cigarettes consecutively for nine minutes. RESULTS: Through this experiment, it was confirmed that the COHb level by Pulse CO-Oximetry rose after smoking (6.9 +/- 2.7%: mean +/- SD) and fell after oxygen inhalation (2.5 +/- 2.2%). The correlation coefficient of COHb levels between Pulse CO-Oximetry and blood sample was 0.34. CONCLUSIONS: The correlation coefficient between the COHb level by Pulse CO-Oximetry and that in the blood sample was not so high, but Pulse CO-Oximetry has the potential of changing the way victims of CO exposure are diagnosed and treated, because of its easiness.     

Relationship between type of tobacco used and localization of tumour in patients with gastric cancer.

The relationship between the type of tobacco used and the localization of the tumour was studied in 493 patients with gastric cancer. The relative frequency of tumour site was found to vary significantly with the type of tobacco. In men who used all kinds of tobacco, a pipe was the most common form of smoking. Women smoked only cheroots or cigarettes or both. Male smokers showed a significantly higher percentage of tumours at the cardia than did female smokers. Female smokers had a significantly higher percentage of tumours involving the entire stomach than male smokers. Male smokers with tumours at the cardia were significantly more often pipe smokers and cigarette smokers than cheroot smokers. Male smokers with tumours involving the entire stomach were significantly more often cheroot smokers than cigarette smokers. The localization of tumours in cigarette smokers differed in men and women, indicating that cigarette smoking per se possibly plays a subordinate causal role. On the other hand, the distribution pattern of the localization among cheroot smokers was practically the same in both sexes, which might indicate that this type of smoking plays an important role. The same probably applies to pipe smoking, especially when combined with snuff or chewing tobacco, but these types of tobacco had not been used by the women. It is mentioned that not only the nature of tobacco used, but also concurrent factors may influence the localization of the tumours.     

Tobacco control for anesthesiologists

Anesthesiologists daily witness the consequences of tobacco use, the most common preventable cause of death. Smoking-related diseases such as atherosclerosis and chronic obstructive pulmonary disease increase anesthetic risk, and even smokers without overt disease are at increased risk for morbidity such as pulmonary and wound-related complications. Evidence suggests that stopping smoking will reduce the frequency of these complications. Nicotine and the other constituents of cigarette smoke, such as carbon monoxide, have important physiologic effects that may affect perioperative management. In addition, it is now apparent that the scheduling of elective surgery represents an excellent opportunity for smokers to quit in the long term. This review serves as an introduction to tobacco control for anesthesiologists, first examining issues of importance to perioperative management. It then discusses how anesthesiologists and other perioperative physicians can help address tobacco use, both at an individual level with their patients, and by contributing to the implementation of effective public health strategies in their countries. Anesthesiologists can play a key role in helping their patients quit smoking. Effective tobacco control measures applied to surgical patients will not only improve immediate perioperative outcomes but also long-term health.     

The tar reduction study: randomised trial of the effect of cigarette tar yield reduction on compensatory smoking.

BACKGROUND--Observational and short term intervention studies have reported that smokers of low tar cigarettes inhale more deeply (that is, compensate) than those who smoke high tar cigarettes. To quantify this effect a long term randomised trial was conducted on the effects of switching to low tar cigarettes. METHODS--The trial was carried out between April 1985 and March 1988 among cigarette smokers in the British Civil Service, measuring blood carboxyhaemoglobin (COHb) levels and serum cotinine levels as markers of tobacco smoke intake. Volunteers first switched to a cigarette brand yielding around 10% less tar than their usual brand to identify smokers able to change brand. The 434 subjects who successfully switched were then randomly allocated to one of three groups: (a) "fast reduction" group which changed to a brand of cigarettes with a tar yield of about half that of their usual brand; (b) "slow reduction" group which reduced to the same level in steps over several months; and (c) a control group which continued smoking cigarettes with a tar yield 10% lower than their usual brand. RESULTS--Over the course of the trial cigarette consumption declined slightly in all three groups. In both the "fast reduction" and the "slow reduction" groups, intake of COHb and cotinine was reduced, though not to the same extent as the yield reduction. Comparison of the results before randomisation with those at the end of the trial showed that a reduction in carbon monoxide yield of 45% was associated with a decrease in carbon monoxide intake of 19% (95% confidence interval 14% to 24%) and that a reduction in nicotine yield of 40% was associated with an 11% (6% to 16%) reduction in nicotine intake, reflecting relative intakes of about 1.5 for both carbon monoxide and nicotine in the "fast reduction" group. Results were similar in the "slow reduction" group with a 42% reduction in carbon monoxide yield, a 16% (11% to 22%) reduction in carbon monoxide intake, a 37% reduction in nicotine yield, and a 6% (0% to 13%) reduction in nicotine intake. Estimates of compensation derived from these results were 65% for carbon monoxide, 79% for nicotine, and 62% for tar. CONCLUSIONS--Compensation, demonstrated when switching from a high tar cigarette to a low tar one, was incomplete. Advising people who have failed to give up smoking to switch to low tar cigarettes will reduce the intake of smoke constituents to a small extent. This would be expected to decrease their risk of smoking-related diseases, although by a smaller amount than would be achieved by giving up smoking altogether.     

Carboxyhaemoglobin levels and inhaling habits in cigarette smokers.

In 520 men who currently smoked only cigarettes, carboxyhaemoglobin (COHb) levels were measured as a method of estimating the extent to which cigarette smoke was inhaled and the results were compared with the smokers' own assessment of their inhaling habits. The mean COHb level after standardising for the number of cigarettes smoked before the blood test on the day of the test was 4.0% in self-described non-inhalers. This was much higher than the mean level of 0.7% in 1891 similar non-smokers, but not very different from the standardised mean levels of 5.2%, 5.3%, and 5.6% in men who said they inhaled slightly, moderately, or deeply, respectively. The increasing trend in the COHb levels of men in the four self-described inhaling categories (nil to deep) was small but statistically highly significant. The data from this study may help to explain some of the anomalous epidemiological results regarding the relationship between self-described inhaling habits and the development of diseases associated with smoking, such as coronary heart disease and lung cancer.     

Recent smoking behavior and postoperative nausea and vomiting

The risk of postoperative nausea and vomiting (PONV) is reduced in cigarette smokers by unknown mechanisms. If protection is related to an acute effect of smoke constituents, smokers with the most recent exposure to cigarette smoke would be most protected. We tested the hypothesis that in cigarette smokers, postoperative nausea is correlated with recent exposure to cigarette smoke as quantified by exhaled carbon monoxide (CO) concentrations. In this observational study, exhaled CO levels were measured in 140 female smokers preoperatively. PONV was assessed over the first 24 h after surgery. There was no correlation (assessed with Spearman rank correlation) between preoperative CO and nausea scores at recovery room discharge. Significant correlations were found between nausea assessed over the first 24 h postoperatively and a history of PONV or motion sickness, the use of intraoperative antiemetic prophylaxis, duration of anesthesia, and use of opioids in the postanesthesia care unit. However, there was no correlation between preoperative CO and nausea over the first 24 h. These preliminary data suggest that the effect of smoking in reduced PONV is not directly related to preoperative exhaled CO levels.     

Effectiveness of bupropion as an aid to stopping smoking before elective surgery: a randomised controlled trial

Smoking is a risk factor for complications during and after surgery, but most smokers are unable to quit before elective surgery. We tested the efficacy of bupropion in improving smoking cessation rates in this setting by enrolling 47 patients from the elective surgery waiting list in a double-blind randomised controlled trial. Patients receiving bupropion had a lower daily cigarette consumption at the time of hospital admission, median (IQR) cigarettes per day: 6 (2-7) vs. 15 (9-20), p = 0.046. They also had a reduction in end-expired carbon monoxide (p = 0.004), a known contaminant of cigarette smoke, and increased arterial oxygen saturation on pulse oximetry (p = 0.011). They were more likely to have stopped smoking at the 3-week visit (p = 0.036), but not at the 6-week visit (p = 0.25) or at the time of hospital admission for surgery (p > 0.99). This study found that smokers waiting for elective surgery are more likely to reduce or stop smoking when treated with bupropion.     

Response and acclimatisation of symptomless smokers on changing to a low tar, low nicotine cigarette.

Ten symptomless smokers were switched from their usual cigarette to a low tar, low nicotine test cigarette for two weeks to investigate their immediate response and subsequent acclimatisation to the test cigarette. The tar (T) and nicotine (N) yields of the test cigarettes were T = 3.8 mg, N = 0.6 mg; the median yields of the usual cigarettes were T = 16.4 mg, N = 1.4 mg. The subjects were monitored over a six week period comprising a control period (usual cigarette), a test period (test cigarette), and a return period (usual cigarette), each lasting two weeks. The inhaled smoke volume (smoke from the burning tip of the cigarette which is subsequently inhaled) was measured with a non-invasive radiotracer technique. Puffing indices were recorded using an electronic smoking analyser and flowhead cigarette holder. Measurements were made at the beginning of the control period, at the beginning and end of the test period, and at the end of the return period. Subjects kept records of their cigarette consumption during each of the three periods. Apart from a small change in puff duration, cigarettes were smoked in the same way during the control and return periods. Mean and total puff volumes increased with the low tar, low nicotine cigarette but did not change from the beginning to the end of the test period. There was no significant change between the control, test, and return periods for mean inhaled smoke volume, total inhaled smoke volume, or cigarette consumption. It is concluded that when smokers are switched to a low tar, low nicotine cigarette the puff volume increases but there is no change in the inhaled smoke volume or daily consumption.     

Effects of ibuprofen on pulmonary oedema in an animal smoke inhalation model

The ability of ibuprofen to lower extravascular lung water significantly was examined in an animal smoke inhalation model. Adult New Zealand White rabbits weighing 3–5 kg were anaesthetized and intubated. They were then allowed to breathe cooled cotton smoke until the carboxyhaemoglobin (COHb) reached a level of 60 per cent or higher. Each ibuprofentreated animal received a dose of 50 mg/kg either intraperitoneally or intravenously. Ibuprofen was administered to animals that received smoke inhalation alone and those that received smoke inhalation combined with a 10 per cent BSA partial skin thickness thermal injury. Control groups were established for both of the above-mentioned groups. Peak carboxyhaemoglobin levels as well as CO half-lives were not significantly different between ibuprofen-treated groups and the controls. Ibuprofen treatment resulted in significantly (P < 0.05) decreased lung water in both smoke, and smoke plus thermal injury groups as compared to controls. These results suggest that ibuprofen promotes the reduction of early-onset lung water resulting from smoke inhalation injury alone or from smoke inhalation injury plus a thermal injury.     

Absorption of nicotine and carbon monoxide from passive smoking under natural conditions of exposure.

Seven non-smokers were exposed to tobacco smoke under natural conditions for two hours in a public house. Measures of nicotine and cotinine in plasma, saliva, and urine and expired air carbon monoxide all showed reliable increases. The concentrations of carbon monoxide and nicotine after exposure averaged 15.7% and 7.5% respectively of the values found in heavy smokers. Although the increase in expired air carbon monoxide of 5.9 ppm was similar to increases in smokers after a single cigarette, the amount of nicotine absorbed was between a tenth and a third of the amount taken in from one cigarette. Since this represented a relatively extreme acute natural exposure, any health risks of passive smoking probably depend less on quantitative factors than on qualitative differences between sidestream and mainstream smoke.     

Effect of carbon monoxide on hemodynamics and oxygen metabolism in inhalation lung injury

Chemical pneumonitis and carbon monoxide (CO) poisoning may be the etiologic factors in inhalation injury. Since the CO poisoning related with smoke inhalation has a much high mortality we tested the hypothesis that superimposed CO poisoning deteriorates hemodynamics and oxygen metabolism in acid inhalation injury. Ten anesthetized dogs were ventilated in room air to maintain normal PaCO2. Lung injury was produced with 2 ml/kg 0.1 N HCL intratracheally. Five dogs (ACID) were then ventilated with room air, while the others were exposed to 1% CO in air for 10 minutes to produce CO poisoning simultaneously with acid instillation (CO-ACID). Hemodynamic changes, oxygen metabolism and carboxyhemoglobin (COHb) were monitored for 4 hours. Thirty minutes following the challenge PaO2 in ACID and CO-ACID groups fell to 65 +/- 10 and 43 +/- 4 (p less than 0.05), respectively. Acid caused significantly decreased cardiac output and increased pulmonary vascular resistance. CO did not accentuate hemodynamic changes following acid inhalation. However, a significant increase of COHb in CO-ACID group resulted in deterioration of oxygen transportation. Though oxygen extraction increased markedly in both groups the oxygen consumption decreased significantly in CO-ACID group. A constantly depressed mixed venous oxygen tension in CO-ACID group suggests the deterioration of tissue oxygen metabolism.     

Effect of cigarette smoking on nasal mucociliary clearance and ciliary beat frequency.

Despite the in vitro ciliotoxicity of tobacco smoke and the abnormal mucociliary clearance found in smoking related chronic bronchitis, studies of mucociliary clearance in healthy smokers have produced variable results. The nasal mucociliary clearance of saccharin and the in vitro nasal ciliary beat frequency were studied in healthy smokers and non-smokers. One of 29 smokers had a nasal mucociliary clearance time of over 60 minutes; in the remaining 28 the mean (SD) clearance time was 20.8 (9.3) minutes, which was significantly longer (p less than 0.001) than the mean time of 11.1 (3.8) minutes in 27 lifelong non-smokers. There was no significant difference between the mean nasal ciliary beat frequency of 10 smokers and 10 non-smokers. There were no significant differences in mean ciliary beat frequency or mean nasal mucociliary clearance time after 10 healthy non-smoking volunteers had smoked two cigarettes each, exhaling the smoke through their nostrils. Unless there is a prompt reversal of any ciliotoxic effect of tobacco smoke when cilia are removed for in vitro examination, the defective clearance seen in chronic cigarette smokers seems unlikely to be due to slowed ciliary beat frequency. It may be due to reduction in number of cilia or to change in the viscoelastic properties of mucus. The failure to detect any acute effect of tobacco smoke is in keeping with this hypothesis.     

Adherence to Long-Term Oxygen Therapy. Influence of Tobacco Use

IntroductionDomiciliary oxygen therapy (DOT) is a treatment that requires a high level of cooperation from patients due to the time it takes every day. A high level of non-compliance has been determined among patients receiving DOT. The aim of our study was to assess the level of non-compliance and the influence of active tobacco consumption on compliance.Material and methodsPatients were monitored in the home using direct and indirect methods, to assess both compliance and tobacco consumption.ResultsThe level of non-compliance detected by indirect methods was 22.6%, and 66.3% by direct methods. Tobacco consumption determined by indirect methods was 5.8%–8%, depending on the method used, and 16.2% when CO in exhaled air ≥10 ppm was established as an indicator of tobacco use. The group of smokers complied with oxygen therapy for a significantly fewer number of hours per day (P<.001) than non-smokers.ConclusionsThere is a high level of therapeutic non-compliance and a significant percentage of patients receiving DOT continue to smoke. Compliance must be monitored, and the correct use of DOT must be emphasized. Additional efforts should also be made to help smokers with DOT to stop smoking, since continued smoking impacts negatively on therapeutic non-compliance.