Acute lung injury after massive household endotoxin exposure

Frostbite is the occurrence of localized tissue freezing and injury. It results following cold exposure of sufficient magnitude or duration to cause acute tissue damage. Although there are several conditions that predispose to frostbite, all are at risk if subject to sufficient cold exposure. We discuss a case of frostbite presenting with bullae localized to the neck resulting from extreme cold encountered while snowmobiling at night in Minnesota, an entity known by some local practitioners as "polaris vulgaris."     

Relationship of burn-induced lung lipid peroxidation on the degree of injury after smoke inhalation and a body burn

OBJECTIVE: We compared the effect of a modest smoke inhalation injury, a burn injury alone, and a smoke inhalation injury plus a body burn, on the degree of lung oxidant-induced lipid peroxidation and lung injury. DESIGN: Prospective animal study with concurrent controls. SETTING: An animal laboratory. SUBJECTS: Forty-four adult yearling female sheep (weight range 45 to 50 kg). INTERVENTIONS: Forty-four sheep were prepared with lung and prefemoral (soft tissue) lymph fistulas. Twelve breaths of cooled smoke with tidal volume of 10 mL/kg body weight were given to 24 sheep, producing a peak blood carboxyhemoglobin of 25% to 30%. Twelve sheep also received a 15% total body surface third-degree burn. Sheep were killed at 4 or 24 hrs. MEASUREMENTS AND MAIN RESULTS: Circulating lipid peroxidation was monitored as conjugated dienes and tracheobronchial mucosal and lung parenchyma as malondialdehyde. Antioxidant defenses were monitored by catalase activity. Lung physiologic and histologic changes were compared. We noted intense airways inflammation in both smoke inhalation groups and lung parenchymal inflammation in all groups. Lung lymph flow was modestly increased (two-fold) in the smoke inhalation groups. Alveolar water content was not significantly increased after any injury. PaO2 was decreased at 24 hrs after the smoke insult alone. Parenchymal malondialdehyde content did not increase with the smoke insult alone, but did increase from a control value of 110 +/- 20 to 270 +/- 24 nmol/g tissue by 4 hrs in the combined burn and smoke injury group, while catalase activity decreased. Airway mucosal malondialdehyde did not increase in any group. CONCLUSIONS: We conclude that alveolar capillary permeability is not increased early after a moderate smoke injury or smoke injury with burn. Lipid peroxidation is not increased in large airway or lung parenchyma with early after-smoke exposure. The addition of a burn significantly increases lung parenchymal lipid peroxidation, but the oxidant changes do not correspond with the degree of early lung dysfunction.     

Acute effects of cigarette smoking on fetal cardiovascular and uterine Doppler parameters

The purpose of this study was to assess the effects of smoking one cigarette (nicotine mean 0.63 +/- 0.17 mg) on uterine- and foetal cardiovascular Doppler parameters in healthy pregnant smokers. All pregnancies (n = 16; mean gestational age: 36 +/- 4 weeks) had been uneventful and all foetuses were appropriate for gestational age with normal baseline Doppler parameters and normal foetal outcome (birthweight: 3254 +/- 340 grams). Measurements, performed immediately before and after smoking, included pulsatility index (PI) of umbilical artery (UA), middle cerebral artery (MCA), foetal descending aorta and uterine artery as well as maternal and foetal heart rate. The ratio of UA/MCA PI was used to assess centralisation. Changes in foetal cardiac output were determined by: time-velocity integral times heart rate, at aortic and pulmonary valve level. Foetal heart rate (p < 0.0005, paired t-test) and maternal heart rate (p < 0.05) increased significantly. All other parameters did not change significantly. However, in one additional woman with labile hypertension and increased baseline uterine artery PI (1.9), smoking of one cigarette caused a substantial rise in uterine artery PI to 3.25 ten minutes after smoking. Middle cerebral artery PI decreased from 2.2 to 1.18 with an unchanged cardiac output and umbilical artery PI raising the UA/MCA PI ratio from 0.51 to 0.81, suggesting a brain sparing effect. Smoking of one cigarette raised maternal and foetal heart rate. There was no evidence of other cardiovascular effects or centralisation in healthy foetuses of normal pregnancies, but this might not be true in foetus of pathologic pregnancies.     

Association between cigarette smoking and FHIT gene alterations in lung cancer

Epidemiologic data have strongly indicated that cigarette smoking is linked to the development of lung cancer. However, little is known of the molecular targets of carcinogens contained in tobacco smoke. To identify genetic lesions characteristic of tobacco damage, we undertook a molecular analysis of microsatellite alterations within the FHIT gene and FRA3B, as well as at an independent locus on chromosome 10, D10S197, in lung tumors from heavy smokers and in tumors from never smokers. Loss of heterozygosity affecting at least one locus of the FHIT gene was observed in 41 of 51 tumors in the smokers group (80%) but in only 9 of 40 tumors in nonsmokers (22%). The comparison between the frequency of losses in FHIT in smokers and nonsmokers was statistically significant (P = 0.0001), whereas no difference in loss of heterozygosity rate was observed at D10S197 locus. These findings suggest that FHIT is a candidate molecular target of carcinogens contained in tobacco smoke.     

Acetonitrile as a possible marker of current cigarette smoking

Volatile nitriles are present in cigarette smoke. We tested the hypothesis that the presence of any of four nitriles in the blood can serve as a marker of recent cigarette smoking. We determined the sensitivity and specificity of these nitriles as indicators of daily cigarette smoking in 24 smokers (Group A) and 18 non-smokers (Group B), as well as the correlation between intensity of daily smoking and the blood concentration of acetonitrile. A new head space GLC assay method was used. Of the four nitriles, only acetonitrile was present in the blood of any study subject. Acetonitrile was moderately sensitive (67%) and entirely specific (100%) for self-reported daily smoking. There was fair correlation between blood acetonitrile concentration and the average daily number of cigarettes smoked (r2 = 0.39; P = 0.001), and the mean blood acetonitrile concentration was significantly higher (P = 0.03) among subjects with higher (> 10 cigarettes per day) current cigarette exposure (148.3 +/- 18.0 micrograms/l) than among smokers with low or minimal (1-10 cigarettes per day) exposure (43.3 +/- 6.0 micrograms/l). Thus, acetonitrile in blood appears to be highly specific and a moderately sensitive marker of cigarette smoking with a dose-effect relationship. As such, acetonitrile shows promise as a marker of current cigarette exposure.     

A model for the effect of cigarette smoking on lung cancer incidence in Connecticut

Population based data on smoking history derived from NCHS surveys were used to develop a model for lung cancer incidence in Connecticut. Trends in smoking prevalence suggest that, while the prevalence in men increased earlier than women, more male smokers have quit than their female counterparts. These trends in smoking prevalence suggest striking gender differences in a period effect for the smoking prevalence. Estimates of the proportion of current smokers, ex-smokers, and the mean duration of smoking were used in a model for the lung cancer incidence rates. The form for the relationship between smoking history and the incidence rate for these subgroups was based on information from cohort studies. The models represented a mixture of the smoking subgroups where the effect of smoking was considered to be either a multiplicative effect on the underlying age distribution, or a separate effect in which the level of exposure was the sole contribution to risk among smokers. The multiplicative model explained more than 80 per cent of the deviance for the period and cohort effects, while the non-multiplicative model could only account for trends in females. Hence, these results suggest that a sizeable portion of the period and cohort contributions to the lung cancer incidence trends in Connecticut can be attributed to the multiplicative model that utilizes this smoking information, although the lack of more detailed information is a limiting factor in developing the model.     

Historical changes in cigarette smoking and smoking-related beliefs after 2 decades in a midwestern community.

Rates of cigarette smoking and smoking-related beliefs in 1980 and 2001 among 7th-11th graders in a midwestern community were compared. Smoking was less prevalent in 2001 than in 1980, with the greatest declines in experimental smoking and a smaller drop in regular smoking. Beliefs about smoking generally became more negative. Adolescents (particularly nonsmokers) viewed smoking as more addictive and as having more negative social consequences in 2001 than in 1980 and had more negative attitudes toward smoking in 2001. These results were replicated among parent-child pairs in which parents were measured when they were adolescents between 1980 and 1983 and their children were measured in 2001. These beliefs and attitudes partially mediated the effects of time on smoking. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The relationship between body mass and cigarette smoking using a biochemical index of smoking exposure

This study evaluated the relationship between smoking and body mass using objective indices of both smoking exposure (COHb) and body mass. The subjects were 4240 adults who participated in the Second National Health and Nutrition Examination Survey (NHANES II). Measurements of dietary intake, physical activity, demographics, body mass index (BMI) and blood carboxy-haemoglobin (COHb) were used in these analyses. After controlling for covariables of body mass, the results indicated that smokers displayed a significantly lower mass compared with non-smokers. Smokers with higher levels of COHb had lower BMIs than smokers at lower COHb levels. White smokers had lower BMIs with increasing COHb exposure whereas black smokers had BMIs at high COHb exposure similar to those of non-smokers. Results indicated that smokers weighed less than non-smokers and that the weight control 'benefits' of smoking were most pronounced in white subjects who were heavy smokers.     

An ecological view of cigarette smoking.

Considers the social, biological, and physical inputs, mediating systems, and behavioral outputs of smoking in an ecological model. Implications of this model in understanding changes in smoking patterns are discussed. Experimental data is presented in an analysis of some determinants of the decision to stop smoking. Findings indicate that the individual stops smoking, not out of fear of consequences (e.g., lung cancer), but because of expectations of benefits: the decision to stop is based on subjectively expected utility. Attempts to change utilities have been inconclusive but do tend to indicate the importance of smoking patterns and that, for many individuals, smoking is an important source of ego strength. It is suggested that within Western society cigarettes are a major source for the fulfillment of the dominant values of achieving and doing. The need to change the society's as well as the individual's view of the utility of smoking is discussed. (27 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Adverse influence of cigarette smoking on the endothelium

The effect of smoking on the blood vessel intima was examined by comparing indices of endothelial activity in serum from smokers with that from non-smokers. Serum from smokers contained higher levels of von Willebrand factor (p < 0.01), the smoking markers cotinine (p < 0.02) and thiocyanate (p < 0.01), and was more cytotoxic to endothelial cells in vitro (p < 0.02) than serum from non-smokers. The acute effects of smoking two unfiltered medium tar cigarettes was to briefly increase von Willebrand factor (p < 0.001) and cytotoxicity of serum to endothelial cells in vitro (p < 0.005), but lipid peroxides or thiocyanate were not increased by this short exposure to tobacco smoke. Although there were correlations between von Willebrand factor and smokers consumption of cigarettes (r = 0.28, p < 0.02), number of years smoking (r = 0.41, p < 0.001) and cotinine (r = 0.45, p < 0.01), the tissue culture of endothelial cells with physiological levels of thiocyanate or nicotine suggested that these two smoking markers were not cytotoxic. They are therefore unlikely to be directly responsible for increased von Willebrand factor in the serum of smokers. We suggest that smoking exerts a deleterious influence on the endothelium and that the mechanism is complex.     

Radioaerosol inhalation lung cine-scintigraphy: a preliminary report

"Radioaerosol inhalation lung cine-scintigraphy", a cinematographic display of the lungs following radioaerosol inhalation has been found to be extremely helpful not only to the visual assessment of mucociliary clearance in the lungs but also to the setting of regions of interest and to the interpretation and analysis of clearance curves over the regions of interest in the lungs. It is expected that this procedure offers an important means to the study of mucociliary clearance in health and disease in man.     

The natural history of cigarette smoking: Predicting young-adult smoking outcomes from adolescent smoking patterns.

Assessed the magnitude of risk that adolescent cigarette smoking carries for adult smoking, using longitudinal data from 4,156 Ss surveyed originally during Grades 6–12 and followed up after completion of high school. Even infrequent experimentation (i.e., smoking only a few cigarettes) in adolescence significantly raised the risk for adult smoking by a factor of 16 compared to nonsmoking adolescents. Relative risk was also increased by early onset of smoking and by a stable, uninterrupted course from experimentation to regular smoking. Data support the importance of primary prevention programs directed at adolescent populations. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Initiation of cigarette smoking: Is it related to parental smoking behavior?

Investigated 2 theories of parent-child smoking patterns: (a) that although there is a direct relationship between the cigarette smoking of parents and their teen-aged children, the observed influences are only transitory and do not endure to adulthood, and (b) the identification theory which predicts that a young adult's smoking behavior is directly related to his parents' smoking behavior. The smoking behavior and family stability of 251 undergraduates and their parents were studied. Results support the identification interpretation of the father-son smoking pattern, as father-son smoking behaviors were directly related in intact families. The variable of family intactness was a highly relevant moderator of the parent-son smoking pattern. The mother and daughter smoking patterns remained enigmatic. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: a multivariate analysis

OBJECTIVES: This study sought to determine whether the reopening of the infarct-related vessel is related to clinical characteristics or cardiovascular risk factors, or both. BACKGROUND: In acute myocardial infarction, thrombolytic therapy reduces mortality by restoring the patency of the infarct-related vessel. However, despite the use of thrombolytic agents, the infarct-related vessel remains occluded in up to 40% of patients. METHODS: We studied 295 consecutive patients with an acute myocardial infarction who underwent coronary angiography within 15 days (mean [+/- SD] 6.7 +/- 3.2 days) of the onset of symptoms. Infarct-related artery patency was defined by Thrombolysis in Myocardial Infarction trial flow grade > or = 2. Four cardiovascular risk factors--smoking, hypertension, hypercholesterolemia and diabetes mellitus--and eight different variables-age, gender, in-hospital death, history of previous myocardial infarction, location of current myocardial infarction, use of thrombolytic agents, time interval between onset of symptoms, thrombolytic therapy and coronary angiography--were recorded in all patients. RESULTS: Thrombolysis in current smokers and anterior infard location on admission were the three independent factors highly correlated with the patency of the infarct-related vessel (odds ratios 3.2, 3.0 and 1.9, respectively). In smokers, thrombolytic therapy was associated with a higher reopening rate of the infard vessel, from 35% to 77% (p < 0.001). Nonsmokers did not benefit from thrombolytic therapy, regardless of infarct location. CONCLUSIONS: These observational data, if replicated, suggest that in patients with acute myocardial infarction, thrombolytic therapy may be most effective in current smokers, whereas nonsmokers and ex-smokers may require other management strategies, such as emergency percutaneous transluminal coronary angioplasty.     

Association between cigarette smoking and lipid peroxidation in a controlled feeding study

BACKGROUND: Cigarette smoke may promote atherogenesis by producing oxygen-derived free radicals that damage lipids. However, evidence in support of this hypothesis is inconsistent because most studies did not control for aspects of diet (antioxidants and lipid substrate) that may confound the association between smoking and measures of lipid peroxidation. METHODS AND RESULTS: The relationships between cigarette smoking and two measures of lipid peroxidation, breath ethane (an in vivo assay) and thiobarbituric acid-reactive substances (TBARS, an in vitro assay), were examined in 123 adults (11% of whom were smokers) participating in a controlled feeding study. After 3 weeks of controlled feeding on a common diet (36% total fat, 14% saturated fats, 6% polyunsaturated fats, and 12% monounsaturated fats), breath and fasting serum samples were collected for measurement of ethane and TBARS, respectively. Baseline characteristics of smokers and nonsmokers were similar, including several indices related to diet and nutritional status (albumin, cholesterol, body mass index, and oxygen radical-absorbing capacity). Cigarette smokers had significantly higher breath ethane (8.88 versus 1.71 pmol/L; P<.0001) and TBARS (24.0 versus 20.7 micromol/mL; P=.008) than nonsmokers. The interval between breath collection and the time the last cigarette was smoked was significantly and inversely correlated with breath ethane. Neither measure of lipid peroxidation was associated with measures of serum cholesterol or albumin, body mass index, or serum oxygen radical-absorbing capacity. CONCLUSIONS: Cigarette smokers have higher rates of in vivo and in vitro lipid peroxidation. These results support the hypothesis that the atherogenic effects of smoking are mediated in part by free radical damage to lipids.