Exposure of young infants to environmental tobacco smoke: breast-feeding among smoking mothers

OBJECTIVES: This study examined the degree to which breast-feeding and cigarette smoking by mothers and smoking by other household members contribute to the exposure of infants to the products of tobacco smoke. METHODS: The subjects were 330 mother-infant pairs derived from a cohort of 1000 pairs enrolled in a longitudinal study of the pulmonary effects of prenatal and postnatal smoking. The main outcome measure was corrected urinary cotinine levels. RESULTS: Urinary cotinine levels were 10-fold higher in breast-fed infants of smoking mothers than among bottle-fed infants of smoking mothers. Among infants of nonsmoking mothers, urine cotinine levels were significantly increased in infants living in homes with other smokers; in this group there was no significant difference between bottle-fed and breast-fed infants. Infants whose mothers smoked in the same room as the infant had only nonsignificant increases in cotinine levels compared with infants whose mothers restricted their smoking to other rooms. CONCLUSIONS: Breast-fed infants of smoking mothers have urine cotinine levels 10-fold higher than bottle-fed infants whose mothers smoke, suggesting that breast-feeding, rather than direct inhalation of environmental tobacco smoke, is the primary determinant of cotinine levels in infants whose mothers smoke.     

Conditions for fibronectin fibril formation in the early Xenopus embryo

A longitudinal study on exposure to tobacco smoke among adolescents was carried out in Turin (North-Western Italy) in January-February 1992 and in January-February 1993. In 1992, 394 schoolchildren aged 14-16 years were enrolled in a study protocol which consisted in answering a standardized questionnaire, measurement of urinary cotinine and testing of lung function (flow-volume curve--[FVC] and forced expiratory volume in I sec.--[FEV1]). In 1993, 333 schoolchildren from the same group repeated the survey. By comparison to urinary cotinine, findings obtained showed a reduction of increase, from 1992 to 1993, of -0.57% (p = 0.082) for FVC, and -0.66% (p = 0.05) for FEV1. Assuming that the systematic selection bias did not seem to have occurred, findings, obtained from a multiple regression analysis, showed that active and passive exposure to tobacco smoke, as measured by urinary cotinine, had a significant effect on lung growth (as measured by FEV1) in adolescents; this effect, though small, was dose-related.     

Household and community determinants of exposure to involuntary smoking: a study of urinary cotinine in children and adolescents

The study examines the role of several potential predictors of urinary cotinine levels in a cross-sectional sample of 1,072 nonsmoking children and adolescents in Latium, Italy, during 1990-1991. As expected, there was a strong relation between passive exposure to smoking and the amount of maternal and paternal self-reported smoking. The urinary cotinine level increased with a decreasing level of paternal education and with an increasing index of household crowding; self-report of recent exposure to smoking outside the home was a strong predictor of the biologic marker. The analysis was then restricted to 346 subjects whose parents claimed that they were nonsmokers and that there were no smokers at home. In this group, however, 57 children reported some active smoking at home by their parents. Those with parents suspected to be "deceivers" had higher level of urinary cotinine than did those truly not exposed. In addition, urinary cotinine in this group was clearly associated with duration of exposure to smoking outside home. The study indicates that both factors related to family circumstances and exposure outside the household setting are strong determinants of urinary cotinine levels. The finding may be considered a direct confirmation that passive smoking among children should be viewed as a specific community responsibility.     

A novel thermostable nitrile hydratase

Adverse effects of maternal smoking have been mostly identified through epidemiologic investigations that have used questionnaires to assess active and passive smoking. However, unvalidated self-reports of cigarette smoking may bias true estimates of relative risk of smoking-related health outcomes. This report is based on two separate investigations. First, within a molecular epidemiologic study of the relationship between environmental exposures (smoking, air pollution, diet) and developmental impairment, we have compared self-reported tobacco smoke exposure during pregnancy to plasma cotinine measurements in mothers. One hundred and fifty-eight patients from obstetrical wards in Cracow and in Limanowa, Poland were included in the parent study. Biochemically-identified smokers were defined as persons with plasma cotinine levels greater than 25 ng/mL. The data showed that exposure classification based on self-reported smoking status compared with cotinine values was of low sensitivity (52%) but of high specificity (98%). We assessed the effect of this exposure classification error on the association between low birth weight (LBW) and smoking in pregnancy using data from a related epidemiologic study of children's health in Cracow involving 1115 subjects. The odds ratio (OR) estimates for smoking and LBW after adjustment for exposure misclassification error were significantly higher than before adjustment (crude OR = 2.9, corrected OR = 5.1). The estimated attributable fraction (AF(pop)) based on the crude OR amounted to 22%; however, after adjustment it reached 50%. The corresponding values for the attributable fraction in the exposed group (AF(exp)) were 66% and 80%. These results illustrate the value of validating questionnaire responses on smoking during pregnancy against reliable biologic markers.     

Human ecology and tropical medicine]

Previous work with the autoradiographic mutant lymphocyte assay has provided information about the time-course of development of hprt mutations and the persistence of detectable mutant cells in human subjects following therapeutic exposures to genotoxic agents. These early studies also revealed elevations in frequencies of mutant cells in pretreatment blood samples from patients who were current tobacco smokers, but no information was available on former smokers. In the present study, blood samples were obtained from 21 healthy former tobacco smokers who had quit smoking at least 1 year before sampling, 42 subjects who had never smoked, and 23 tobacco smokers. Plasma from all samples was tested for cotinine, a metabolite of nicotine. Current smokers were categorized as heavy smokers (> or = 10 cigarettes per day, cotinine > or = 90 ng/ml plasma) and light smokers (< 10/day, cotinine < 90 ng/ml). Lymphocytes from the blood samples were isolated, cryopreserved, and later thawed and assayed with the autoradiographic hprt assay. The 21 former tobacco smokers had a mean variant (mutant) frequency (Vf +/- standard error) of 1.97 (+/-0.13) per million evaluatable cells. The Vf of 42 subjects who had never smoked was 1.74 (+/-0.13) x 10(-6), not significantly different from the former smokers. The smokers had Vfs of 8.09 (+/-0.78) x 10(-6) for 18 heavy smokers and 5.22 (+/-1.02) x 10(-6) for five light smokers. The two categories of smokers had frequencies of mutant cells significantly different from each other, and each was significantly higher than non-smokers and former smokers (P < 0.05). Vfs were significantly correlated with both cotinine concentrations and the number of cigarettes smoked per day, P < 0.001. This study demonstrates the sensitivity of the autoradiographic hprt assay for detecting mutagenic effects related to chronic low-level exposures to genotoxins, and indicates that this assay is more likely to detect the effects of recent rather than past exposures.     

Clinical status of ulcerative colitis in patients who smoke

OBJECTIVES: Ulcerative colitis (UC) is largely a disease of nonsmokers. There are few patients who are current smokers, but we have identified a group and reviewed their clinical status, disease activity, and nicotine exposure to examine whether they remain well controlled while smoking. METHODS: Fifty-one patients from three centers with verified UC were reviewed. RESULTS: Thirty of the group were men; mean age 50 yr, with a mean age of onset of 37 yr. Twenty-two patients had proctosigmoid disease, 12 involvement of left colon, and 17 total colitis. All were current smokers; 41 were cigarette smokers averaging 17 daily. At the onset of colitis 30 were nonsmokers, 25 of them were ex-smokers and 19 developed colitis within 2 yr of stopping smoking. Twenty-eight believed smoking improved disease activity and none felt smoking had a detrimental effect on their UC. Eleven were receiving no medication for UC, 40 were receiving 5-ASA (5-aminosalicylic acid) preparations, and only two took oral steroids. All were in clinical remission, with the exception of one patient; mean St. Marks score was 1.5, out of a possible total of 22. Sigmoidoscopic grades were inactive in all patients except three. Histological assessment showed significant activity in only five. Median serum nicotine was 8 ng/ml (range, 0.4-24.4), median serum cotinine 180 ng/ml (range, 20-453), with corresponding salivary cotinine of 255 ng/ml (range, 34-683). Median rise in nicotine 2 min after a cigarette in 35 patients was 12.1 ng/ml (range, 0.4-44). CONCLUSIONS: Because most current smokers with UC have inactive disease, smoking may contribute to the clinical remission in these patients.     

Damage from passive tobacco smoking

The author presents data on the biological casualties and consequences of tobacco-smoking. Smoking is the most dangerous addiction in the scale of the world and in Poland. It causes numerous premature decrease and tobacco-dependent sickness. The author characterises the spread of this addiction in Poland concentrating on the problem of the passive smoking harmfulness. Non-smokers, children and youth, embryo and foetus during the pregnancy are exposed to the passive smoking. The experimental examinations of animals and the analysis of the lateral stream of the tobacco smoke confirm not the least, but rather the greater damage of the passive smoking than the active one. The mechanisms of acting of the tobacco smoke on the passive smokers' body and the health consequences are discussed. The manners, means and activities that are useful for the health protection of non-smokers against the tobacco smoke and the ways of the smoking prevention are described.     

Orthotopic neobladder in management of tubercular thimble bladders: initial experience and long-term results

We describe a technique for endobronchial surgery with the neodynium:yttium-aluminum-garnet laser, in which an insufflation catheter with side holes placed into the contralateral mainstem bronchus is used for high-frequency positive pressure ventilation. Thirty-five patients (45 procedures) were treated during general anesthesia using a rigid bronchoscope in combination with a fiberoptic bronchoscope. Perioperatively, oxygen saturation (SaO2), mean arterial pressure, and heart rate were recorded. SaO2 during the recovery period was comparable to that during the intraoperative period but was significantly (P < 0.05) higher than that before the induction of anesthesia. There was a considerable (> or = 5%) increase in SaO2 at the end of the treatment in six patients, which indicates that the recanalization of the treated airway was successful. Our data support the assumption that, during endobronchial resection, selective ventilation of the nonaffected lung was adequate; in addition, subcarinal placement of the insufflation catheter with side holes was advantageous. We conclude that this technique contributes to the prevention of lung complications during endobronchial laser surgery. Implications: We describe a technique in which an insufflation catheter with side holes placed into the contralateral mainstem bronchus largely prevented inhalation of laser smoke and aspiration of blood and debris.     

Estimated gains in birth weight associated with reductions in smoking during pregnancy

OBJECTIVE: To compare the estimated effect on birth weight of reductions in maternal cigarette consumption and urinary cotinine during pregnancy. STUDY DESIGN: An observational study of 641 women with complete data on cigarette consumption, urinary cotinine and infant birth weight. Correlation and regression analyses were used to examine relationships between birth weight, cigarette consumption and urinary cotinine at first and last prenatal visits. RESULTS: Correlations of cigarette consumption and urinary cotinine with infant birth weight were -.23 and -.30 (first visit) and -.26 and -.31 (last visit); all P values were < .001. The regression equation relating urinary cotinine concentrations at first and last visits to infant birth weight explained a significantly larger proportion of the variability in birth weight than the equation relating cigarette consumption at these visits to infant birth weight, 11% vs. 7%, P = .04. Among continuing smokers, both equations predicted gains in birth weight in association with reductions in cigarette consumption, but quitting smoking before the first visit was associated with the most weight gain. As compared to the average infant birth weight of a woman who smoked 20 cigarettes per day throughout pregnancy, the estimated gain in birth weight would be 105 g if she cut down by 10 cigarettes per day after the first visit, 210 g if she quit after this visit and 310 g if she quit before the first visit. CONCLUSION: For women still smoking at their first prenatal visit, infant birth weight is already compromised, but subsequent reductions in cigarette consumption are associated with gains in birth weight. For women who cannot quit smoking, these reductions need to be substantial if increases in birth weight of > 100 g are to be achieved.     

B-mode-guided vector-A-mode versus A-mode biometry to determine axial length and intraocular lens power

Studies of nicotine replacement by 2 mg nicotine polacrilex gum (NG) have typically found that one half to one third of plasma nicotine in recent smokers is replaced. This 5-year study sought to find the extent of nicotine replacement among ex-smokers in the longer term and to identify a mechanism for this relationship. The sample was the special intervention group (N = 3923) in the Lung Health Study, a controlled clinical trial involving smoking cessation. The extent of nicotine replacement was assessed by levels of salivary cotinine. Cotinine levels of ex-smokers using NG after 1 year (219 +/- 149 ng/ml) were similar to those in continuing smokers (290 +/- 159 ng/ml). After 5 years, cotinine levels were the same for NG-using ex-smokers (316 +/- 276 ng/ml), NG-using smokers (309 +/- 240 ng/ml), and NG-non-using smokers (311 +/- 198 ng/ml). Salivary cotinine among NG users at 1 year was only weakly correlated with baseline cotinine levels prior to smoking cessation. Although NG users appear to re-establish cotinine levels characteristic of their smoking, the mechanism by which this occurs remains unclear.     

Human immunodeficiency virus and resistance]

CONTEXT: Racial differences in tobacco-related diseases are not fully explained by cigarette-smoking behavior. Despite smoking fewer cigarettes per day, blacks have higher levels of serum cotinine, the proximate metabolite of nicotine. OBJECTIVE: To compare the rates of metabolism and the daily intake of nicotine in black smokers and white smokers. DESIGN: Participants received simultaneous infusions of deuterium-labeled nicotine and cotinine. Urine was collected for determination of total clearance of nicotine and cotinine, fractional conversion of nicotine to cotinine, and cotinine elimination rate. Using cotinine levels during ad libitum smoking and clearance data, the daily intake of nicotine from smoking was estimated. SETTING: Metabolic ward of a university-affiliated public hospital. PARTICIPANTS: A total of 40 black and 39 white smokers, average consumption of 14 and 14.7 cigarettes per day, respectively, of similar age (mean, 32.5 and 32.3 years, respectively) and body weight (mean, 73.3 and 68.8 kg, respectively). MAIN OUTCOME MEASURES: Clearance (renal and nonrenal), half-life, and volume of distribution of nicotine and cotinine and the calculated daily intake of nicotine. RESULTS: The total and nonrenal clearances of nicotine were not significantly different, respectively, in blacks (17.7 and 17.2 mL x min(-1) x kg(-1)) compared with whites (19.6 and 18.9 mL x min(-1) x kg(-1)) (P=.11 and .20). However, the total and nonrenal clearances of cotinine were significantly lower, respectively, in blacks (0.56 and 0.47 mL x min(-1) x kg(-1)) than in whites (0.68 vs 0.61 mL x min(-1) x kg(-1); P=.009 for each comparison). The nicotine intake per cigarette was 30% greater in blacks compared with whites (1.41 vs 1.09 mg per cigarette, respectively; P=.02). Volume of distribution did not differ for the 2 groups, but cotinine half-life was higher in blacks than in whites (1064 vs 950 minutes, respectively; P = .07). CONCLUSIONS: Higher levels of cotinine per cigarette smoked by blacks compared with whites can be explained by both slower clearance of cotinine and higher intake of nicotine per cigarette in blacks. Greater nicotine and therefore greater tobacco smoke intake per cigarette could, in part, explain some of the ethnic differences in smoking-related disease risks.     

Passive cigarette smoking and reduced HDL cholesterol levels in children with high-risk lipid profiles

BACKGROUND: HDL cholesterol levels are known to be lower in smokers than in nonsmokers. Previous studies have demonstrated an association of decreased HDL cholesterol with passive smoking in children but have not adjusted for potential confounding factors. METHODS AND RESULTS: In a cross-sectional, pilot-scale study, we examined the relationship of HDL cholesterol levels to passive smoking in children and adolescents referred to a tertiary hyperlipidemia clinic. Eligibility criteria included (1) first visit to a lipid clinic, (2) LDL cholesterol >95th percentile for age or HDL cholesterol <5th percentile, (3) age between 2 and 18 years, and (4) absence of secondary causes of hyperlipidemia. Sociodemographic information, diet record, medical history, and fasting lipid profiles were obtained. Of 109 eligible patients, 103 (94%) were studied. Twenty-seven percent came from households with cigarette smokers. HDL cholesterol levels were 38.7+/-1.2 mg/dL (mean+/-SEM) in passive smokers versus 43.6+/-1.2 mg/dL in children without smoke exposure (P=.005). Smoking exposure was not significantly associated with other lipid values. The effect of smoking on HDL cholesterol was minimally affected by potential confounders. In multivariate regression adjusting for body mass index, age, sex, exercise, and dietary fat intake, passive smoking remained a significant risk factor for decreased HDL cholesterol (P=.012). CONCLUSIONS: Mean HDL cholesterol levels are lower in dyslipidemic children from households with smokers than in those without household smoke exposure. Passive smoking may worsen the risk profile for later atherosclerosis among high-risk young persons.     

Procalcitonin--a sepsis parameter in severe burn injuries

Procalcitonin (PCT) levels increase in patients with systemic infections; the highest levels have been found in sepsis. This study tested whether plasma procalcitonin level was related to sepsis, CRP, burn size, inhalation injury or mortality in severely burned patients over the entire clinical course. In 27 patients with 51 (20-91)% TBSA, PCT was measured three times weekly from admission over the entire course of stay in a single ICU. Daily scoring by the "Baltimore Sepsis Scale" was performed. The patients were assigned to three groups depending on the clinical course and outcome: A = no septic complications, B = septic complications-survivors, C = septic complications non-survivors. PCT levels were elevated slightly at admission (mean 2.1 ng/ml) except in three patients who suffered electrical burns (mean 15.7 ng/ml). PCT peak levels correlated well with the Scoring values (r = 0.84) while CRP did not (r = 0.64). Peak PCT levels were significantly higher (p < 0.005) in septic patients (B and C) who averaged 49.8+/-76.9 ng/ml, than in non-septic patients (A) who averaged peak levels of 2.3+/-3.7 ng/ml. The highest PCT levels were found immediately before death (86.8+/-97 ng/ml). Seven patients had an inhalation injury 3rd degree. In these patients at 24 h postburn, there was no relationship between PCT levels and inhalation injury but during the later days postburn there were significant differences in PCT levels in patients with versus without inhalation injury. All patients with inhalation injury 3rd degree developed septic complications. There was no positive correlation between the PCT-admission-levels and the TBSA, but there was a positive correlation between the TBSA and the mean peak PCT levels during the later days postburn (r = 0.73; p < 0.05). The cut-off value of 3 ng/ ml we found reliable to indicate severe bacterial or fungal infection. PCT values over 10 ng/ml increasing over the following days were found only in life-threatening situations due to systemic infections. The individual course of PCT in one patient is more important than absolute values. PCT presented in this study as a useful diagnostic parameter in severely burned patients.     

Joint influence of alcohol, tobacco, and coffee on biological markers of heavy drinking in alcoholics

BACKGROUND: Recent reports suggest that gamma-glutamyl transferase (GGT) decreases with coffee intake. The aim of this study was to examine the joint influence of alcohol, tobacco, cotinine, coffee, and caffeine on biological markers of heavy drinking in an alcoholic population. METHODS: Subjects were 160 alcohol-dependent inpatients. Biological assessments, performed at admission, were plasma levels of GGT, apolipoprotein AI, aspartate aminotransferase, and mean corpuscular volume (MCV), and urine cotinine and caffeine indexes. Years of alcohol abuse and of smoking, alcohol and coffee intake, and smoking rate were estimated in a semistructured interview, and Fagerstr?m Tolerance Questionnaire was completed by inpatients. RESULTS: Coffee intake, but not caffeine, correlated negatively with biological markers of heavy drinking, after controlling for alcohol and tobacco intake. Years of smoking correlated positively to MCV, after controlling for alcohol and coffee intake. CONCLUSIONS: Concerning the effect of coffee, the most likely hypothesis is that noncaffeine coffee fractions have a protective effect on liver cells. Concerning the effect of smoking, one can propose that the increase of MCV with smoking could be a consequence of carbon monoxide inhalation, leading to hypoxemia, or of folate deficiency.     

Inhalation injury

Inhalation injury remains a primary determinant of patient survival, with 60% to 70% of burn center fatalities attributed to the pulmonary complications of inhalation injury. Substantial airway damage and pulmonary complications can result from the inhalation of toxic fumes and gases found in smoke. Partial to complete airway obstruction, pulmonary edema, pneumonia, and progressive pulmonary failure may occur. Early diagnosis of inhalation injury and vigorous pulmonary care and support are vitally important to patient survival. Bronchoscopy and xenon 133 ventilation-perfusion scans are two of the newer diagnostic tools used to identify burn patients with inhalation injury. Treatment measures for patients with inhalation injury and recommendations for nursing practice are discussed.     

Delirium risk factors in elderly hospitalized patients

BACKGROUND: The relation of parental smoking to wheezing and asthma occurring after the first year of life was assessed by a systematic quantitative review of case-control and longitudinal studies, complementing earlier reviews of cross sectional surveys and wheezing in early childhood. METHODS: Fifty one relevant publications were identified after consideration of 1593 abstracts selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified six studies of asthma incidence, seven of prognosis, 22 case-control studies, and 10 case series addressing disease severity. RESULTS: Maternal smoking was associated with an increased incidence of wheezing illness up to age 6 (pooled odds ratio 1.31, 95% CI 1.22 to 1.41), but less strongly thereafter (1.13, 95% CI 1.04 to 1.22). The long term prognosis of early wheezing illness was better if the mother smoked. The pooled odds ratio for asthma prevalence from 14 case-control studies was 1.37 (95% CI 1.15 to 1.64) if either parent smoked. Four studies suggest that parental smoking is more strongly associated with wheezing among non-atopic children. Indicators of disease severity including symptom scores, attack frequency, medication use, hospital attendance, and life threatening bronchospasm were in general positively related to household smoke exposure. CONCLUSIONS: The excess incidence of wheezing in smoking households appears to be largely non-atopic "wheezy bronchitis" with a relatively benign prognosis, but among children with established asthma, parental smoking is associated with more severe disease. This apparent paradox may be reconciled if environmental tobacco smoke is considered a co-factor provoking wheezing attacks, rather than a cause of the underlying asthmatic tendency.     

Determination of nicotine, cotinine and caffeine in meconium using high-performance liquid chromatography

A high-performance liquid chromatographic method with diode-array detection for the determination of nicotine and its metabolites, cotinine and caffeine, in meconium is described. This method is suitable to assess foetus exposure to tobacco smoke. The analytes were extracted by solid-phase extraction before chromatography. From among 30 meconium samples 11 were positive for cotinine (20-86 ng/g) and 27 for caffeine (10-45 ng/g). No nicotine was present in the samples because of its rapid metabolism into cotinine.     

An early rise in urine N-telopeptide predicts the growth response of normal prepubertal short children to growth hormone therapy

The effects of growth hormone (GH) therapy on biochemical markers of bone turnover were investigated in 11 short prepubertal children without GH deficiency by measuring serum osteocalcin, a marker for bone formation, and urinary concentrations of pyridinium cross-linked amino acids of collagen (PCL), and the peptide-bound pyridinoline residue N-telopeptide (NT), which are specific markers for bone resorption. GH treatment for three months increased bone turnover in this group of children: urinary PCL concentrations increased from 69 +/- 6.2 to 114 +/- 9.3 nmol/mmol Cr (p < 0.01), and urinary NT levels increased from 512 +/- 65 to 766 +/- 74 pmol BCE/mumol Cr (p = 0.058). Serum osteocalcin concentrations increased from 13.64 +/- 2.57 ng/ml to 26.45 +/- 1.39 ng/ml (p < 0.01). The increment in 12-hour urinary concentrations of PCL was highly correlated with the increment in 12-hour urinary NT levels (r = 0.92, p < 0.01). Stepwise multiple regression analysis revealed that the urinary concentrations of NT after 3 months of GH therapy were the best predictor of growth after 12 months of treatment (r = 0.78, F = 7.9, p = 0.037).     

Concentration-response relationships for fentanyl and sufentanil in patients undergoing coronary artery bypass grafting

BACKGROUND: Concentration-response relationships for sufentanil and fentanyl are undefined in patients undergoing coronary artery bypass grafting. METHODS: Separate studies of sufentanil and fentanyl were performed in lorazepam-premedicated patients undergoing coronary artery bypass grafting. Patients were assigned randomly to groups with different prebypass effect-site opioid concentrations targeted by computer-assisted infusion. The target sufentanil concentrations were 0.4 ng/ml (group LS, n = 11), 0.8 ng/ml (group MS, n = 10), and 1.2 ng/ml (group HS, n = 11); the target fentanyl concentrations were 5 ng/ml (group LF, n = 7), 10 ng/ml (group MF, n = 7), and 15 ng/ml (group HF, n = 6). Propofol at a dose of 1 mg/kg was administered at induction of anesthesia and isoflurane was used for hemodynamic control Hemodynamics, end-tidal isoflurane concentration, and opioid concentration in arterial blood were measured at specific intervals. RESULTS: Intraoperative opioid concentrations were constant, averaging 0.71 +/- 0.13, 1.25 +/- 0.21, and 2.03 +/- 0.46 ng/ml for groups LS, MS, and HS, respectively, and 7.3 +/- 1.1, 13.2 +/- 2.2, and 24.4 +/- 5.8 ng/ml for groups LF, MF, and HF, respectively (all mean +/- SD). Isoflurane requirements were significantly greater in group LS than in groups MS and HS and greater in group LF than in groups MF and HF. The serum opioid and end-tidal isoflurane concentrations were correlated significantly. There were no intergroup differences in hemodynamics. CONCLUSIONS: Serum sufentanil and fentanyl concentrations of 0.71 +/- 0.13 ng/ml and 7.3 +/- 1.3 ng/ml, respectively, are on the steep parts of the concentration-response relationships and facilitate prebypass hemodynamic control in patients undergoing coronary artery bypass grafting with opioid-isoflurane anesthesia. Concentrations of sufentanil > or = 1.25 +/- 0.21 ng/ml and of fentanyl > or = 13.3 +/- 2.2 ng/ml minimize isoflurane requirements but do not improve hemodynamic control.     

Analysis of nicotine and cotinine in the hair of hospitality workers exposed to environmental tobacco smoke

The purpose of this study was to determine if hair nicotine and cotinine levels reflect relative exposure to environmental tobacco smoke (ETS) in subjects who worked in the hospitality industry, where public smoking was permitted. Hair samples from 26 subjects were analyzed by gas chromatograph/mass spectrometry techniques for nicotine and cotinine. An exposure gradient was shown for nicotine but not cotinine. Among nonsmokers, those working in bars where there are no public smoking restrictions had the highest hair nicotine levels, which were close to levels found in smokers. Nicotine measured in hair is useful as a biological marker for exposure to ETS from multiple sources. Bar workers in particular are exposed to high levels of ETS, which may adversely affect the health of nonsmokers.