Barriers to care among persons living with HIV/AIDS in urban and rural areas

Phenols constitute an important toxic component of the main stream (MS) of cigarette smoke. The content of volatile fraction of that group of compounds in MS depends on the tobacco type and conditions in which cigarettes are smoked, as well as on the filters applied. The purpose of the research was to determine the content of volatile in steam phenols in the MS of selected brands of cigarettes produces in Poland, as well as imported ones, and the assessment of the toxicity of doses of the phenols that smokers were exposed to. Cigarettes conditioned in constant humidity were smoked in standard conditions in the simulator of smoking, designed by the authors, while MS was absorbed in Zaitcev washers, filled with methanol. The absorbed phenols were distilled in steam and extracted with ethyl acetate. Then the phenols were separated by the method of overpressure thin-layer chromatography on DC Alufolien Polyamid 11F254 Merck chromatoplates, in the developing system chloroform-methanol 99:1 v/v, were induced with sodium diazofluoroborate, and after eultuion the separated phenol, and o-cresol were determined, as well as the non-separated mixture of p- and m-cresols, by the spectrophotometric method. The determined contents of phenols in MS were assessed regarding their toxicity applying the criteria of environmental exposure. When calculating the results, the efficiencies of the applied in the analytical procedures processes of absorption, distillation and extraction of the investigated phenols previously determined experimentally, were taken into consideration. The content of determined compounds in the brands of the cigarettes examined was in the case of phenols, changing within the range from 41.25 +/- 1.15 to 7.60 +/- 0.93 (the average of 20.31 +/- 9.61 micrograms per cigarette); in the case oo-cresol it was within the range from 28.16 +/- 0.95 to 5.72 +/- 0.53 (the average of 11.56 +/- 6.7), while for the non-separated p- and m-cresols the range was from 21.12 +/- 0.5 to 7.31 +/- 0.45 (the average amounted to 11.48 +/- 4.98 micrograms per cigarette The conclusions of the study were the brands of cigarettes significantly influences the content of the phenols examined in the cigarette smoke the phenols determined coexist in the MS of examined cigarettes in similar proportions the doses of phenols inhaled by a smoker during a day with the MS of examined brands of cigarettes participate essentially in the toxicity of the cigarette smoke and smoking 20 cigarettes a day causes the smoker's organism to be exposed to incomparably larger doses of phenols than those from unpolluted atmospheric air.     

Transgenic mice carrying the human KRAS oncogene under the control of a thyroglobulin promoter: KRAS expression in thyroids analyzed by in situ hybridization

Indonesia as a developing country has air pollution which is mainly caused by motor vehicle emissions and industrial smoke. The most important indoor air pollution is cigarette smoke. The prevalence of smoking among Indonesian men is 45.7%. Of the population, 10.8% are ex-smokers and 43.5% are non-smokers. Among the female population, only 1.8% smoke. There are some important factors that influence the air pollution in Indonesia; this paper identifies the real problems and their impact. The paper reviews various studies that have been carried out in Indonesia which were related to ambient air quality, industrial air pollutants levels (SO2, NOx, Ox, Pb, CO, HC) in large cities in Indonesia have exceeded the acceptable level, especially in industrial trade and heavy traffic areas. The more cigarettes inhaled and the deeper the inhalation, especially the kretek cigarettes, the risk of ling function abnormality becomes greater. Smoking high dose kretek cigarettes, that is > or = 116 cigarettes/day x years, the risk of abnormal lung function is 13-fold that of a non-smoker; if added with the deep inhalation of smoke, the risk becomes 20-fold. Smoking increases the risk of occupational lung disease. The level of dust in some industrial areas exceeded the standard level and correlated with respiratory problems. The existence of industry caused by air pollution in the environment increased the incidence of obstructive airway diseases. We conclude that the main cause of air pollution in Indonesia is motor vehicle emissions, followed by industrial smoke. Cigarette smoke is also related to abnormal lung function.     

Reducing craving for cigarettes while decreasing smoke intake using capsaicin-enhanced low tar cigarettes.

The effects on smoking behavior and subjective evaluation of adding capsaicin (a pungent principle of chili pepper) to a low tar and nicotine cigarette were studied in 12 cigarette smokers. In a 4-hr session, Ss inhaled smoke from 3 types of cigarettes: low tar and nicotine with capsaicin added; low tar and nicotine without capsaicin (control); and commercial high tar and nicotine. Ss puffed significantly less on the capsaicin cigarettes than on the other 2 types of cigarettes and reported greater reduction in cigarette craving after smoking capsaicin cigarettes than after smoking control low nicotine cigarettes. Estimated nicotine intake and respiratory tract sensations for the capsaicin cigarettes were also significantly higher than for the control cigarettes. Results support the view that respiratory tract sensations are important in reducing smokers' craving for cigarettes and in modulating smoking behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Behavioral filter vent blocking on the first cigarette of the day predicts which smokers of light cigarettes will increase smoke exposure from blocked vents.

Filter vent blocking on best-selling light cigarettes increases smoke yield during standard machine testing but not in clinical investigations of smokers. The purpose of the study was to investigate the effect of (a) manipulating cigarette filter vent blocking and (b) blocking status of first cigarette of the day on carbon monoxide (CO) boost. Participants (n = 25; Marlboro Lights nonmenthol cigarette smokers, age range 21–60 years, minimum 15 daily cigarettes, and daily smoking for a minimum 5 years) completed the laboratory-based, within-subject, double-blind, cross-over design of 2 smoking sessions, one utilizing a smoking topography device, one without. Each session consisted of smoking 4 cigarettes; 2 with filter vents blocked and 2 with filter vents unblocked. Spent first daily cigarette filters collected between sessions were scored for evidence of filter vent blocking. Smoking cigarettes with blocked filter vents significantly increased CO boost in both laboratory sessions (p     

Distribution of major and minor alkaloids in tobacco, mainstream and sidestream smoke of popular Indian smoking products

Various Indian smoking products--cigarette, bidi, chutta and a brand of US cigarette--were analysed by gas chromatography-flame ionization detection (GC-FID) for the levels of nicotine and minor tobacco alkaloids in tobacco, mainstream smoke (MS) and sidestream smoke (SS) employing modified smoking standards, namely two puffs/min. The analysis clearly demonstrated relatively higher levels of nicotine and minor tobacco alkaloids in tobacco from bidi (37.7 mg/g) and chutta (34.5 mg/g) when compared with Indian and US cigarettes (14-16 mg/g) studied. Relatively lower levels (SS/MS) of nicotine in SS from bidi and chutta compared with Indian/US cigarettes, suggest that the contribution of nicotine in SS from a single bidi/chutta to environmental tobacco smoke (ETS) is very much less than that of a single Indian/US cigarette. Reduced levels of nicotine in SS of bidi/chutta result in relatively higher deliveries of nicotine in MS as reflected by higher MS/SS values. The observed differences are likely to be due to difference in tobacco processing, burning rate/temperature and design of the smoking product.     

Paced smoking in the laboratory and in the natural smoking setting: differential situation-specific effects in light and heavy smokers

The present study examined the situation-specific effects of smoking using a paced regimen of smoking to control the smoke intake. The subjects were first required to sham smoke and then actually smoke one of their cigarettes in two different test contexts: 1) in the laboratory where they had never previously smoked and 2) at home, alone in a quiet room where they regularly smoke. Light (< 10 cigarettes/day) and heavy smokers (> 15 cigarettes/day) were studied to test for a possible effect of the paced regimen itself. In the light smokers, smoking produced a larger increase in heart rate (HR) in the laboratory than in the natural smoking environment; however, in the heavy smokers the smoking had a larger effect in the normal smoking environment than in the laboratory. There were no significant group or test situation differences for baseline HR, skin conductance and finger temperature. The groups also did not differ in the intensity of drawing on the cigarette or inhaling, as indicated by a puff sensor and a respiratory belt, respectively. It was concluded that differences between the effects of a cigarette in a laboratory setting and in a natural smoking environment may reflect pharmacodynamic effects of smoking that are modified by the subjects' prior experience with smoking. The data are discussed with regard to conditioned tolerance to the effect of smoking.     

Placebo cigarettes in smoking research.

This review outlines the development and use of placebo cigarettes in smoking research. Research on effects of smoking has been disadvantaged by the lack of an adequate placebo condition. Recently, tobacco-based denicotinized cigarettes have been used in smoking research to distinguish effects of smoking due to the delivery of nicotine, other components of tobacco smoke, and the sensory process of smoking. Placebo cigarettes do not increase heart rate and blood pressure or produce electroencephalogram changes ordinarily associated with nicotine. However, placebo cigarettes reduce subjective measures of tobacco craving, desire to smoke, and tobacco withdrawal. These findings indicate that the effects of cigarette smoking are dependent on the delivery of nicotine, tar, other compounds of tobacco smoke, and the sensory stimuli. The next generation of research may begin to investigate the mechanisms that modulate these placebo effects. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of dietary protein and environmental temperature on growth performance and water consumption of male broiler chickens

The purpose of this study was to investigate whether smokers outside buildings with work-place smoking bans smoke "harder" than those smoking in social settings. An unobtrusive random observational study of smokers followed by structured interview was used, with 143 smokers taking smoking breaks outside their office buildings and 113 smokers in social settings. The main outcome measurements were number of puffs per cigarette and cigarette smoking duration. The mean number of puffs per cigarette for the office building group was 18.7% greater than that for the social settings group (10.7 +/- 3.2 vs. 8.7 +/- 2.7, t = 5.58, df = 253, p < 0.001); 74.8% of smokers outside offices took more than the mean number of puffs for the group compared to 42.5% of smokers in social settings (chi 2 df 1 = 26.31, p < 0.0001). Mean cigarette smoking duration was 30.4% shorter for the work-place group than the social settings group (3.9 +/- 1.2 minutes vs. 5.6 +/- 2.6 minutes). Of smokers outside offices, 55.2% had a cigarette smoking duration between 3 and 4.59 minutes, while 53.1% of smokers in social settings took > or = 5 minutes to smoke the observed cigarette (chi 2 df 2 = 31.55, p < 0.0001). Smokers who scored at the 75th percentile on the Fagerstrom Tolerance Scale took a mean 9.5 +/- 2.6 puffs per cigarette compared to 9.3 +/- 2.7 puffs by those who scored in the 25th percentile on the scale (t = 0.34, df = 145, p = 0.73). Regardless of degree of nicotine dependency, smokers leaving work-stations to smoke outside buildings smoked their cigarettes nearly 19% "harder" than cigarettes smoked in social settings. The individual and public health benefits of reduced smoking frequency engendered by work-place smoking bans may be lessened by policies which allow smokers to take smoking breaks.     

Metabolic activation and carcinogen-DNA adduct detection in human larynx

Putative carcinogen-DNA adducts in human larynx tissues (n = 25) from smoker and non/ex-smoker patients were examined by 32P-postlabeling and compared with the metabolic activation capacity of larynx microsomes and cytosols from the same tissues. Hydrophobic DNA adducts were evident only in smokers, and chromatographic profiles of the adducts were similar using either the butanol extraction or nuclease P1 enhancement method, which suggested that the adducts may be derived from polycyclic aromatic hydrocarbons but not aromatic amines. Immunoblots of larynx microsomes using anti-cytochrome P450 1A1/1A2, 2C, 3A4, 2E1, and 2A6 antibodies showed intensities ranging from 1-10% of that typically observed with human liver microsomes. Enzymatic assays of larynx microsomes showed appreciable activity for benzo(a)pyrene hydroxylation (P450 1A1 and 2C) but not for 4-aminobiphenyl N-oxidation (P450 1A2), which indicated that the observed immunoreactivity was for P450 1A1; this represents the highest level of this P450 yet detected in human extrahepatic tissues. Accordingly, total DNA adduct levels in the larynx correlated strongly with levels of P450 2C, 1A1, and 3A4 but not with P450 2E1 or 2A6. Larynx cytosols also showed appreciable aromatic amine N-acetyl-transferase activity for p-aminobenzoic acid (NAT-1) but not for sulfamethazine (NAT-2); however, NAT-1 activity was not correlated with total DNA adducts, which is again consistent with the lack of aromatic amine-DNA adducts detected by 32P-postlabeling. Thus, these results suggest that the DNA adducts detected in human larynx are largely derived from metabolic activation of polycyclic aromatic hydrocarbons in cigarette smoke by P450 2C, 3A4, and/or 1A1.     

Chemical and biological studies of a new cigarette that primarily heats tobacco. Part 1. Chemical composition of mainstream smoke

A new-technology cigarette has been developed. While the new cigarette burns some tobacco, it does not use tobacco as the fuel to sustain combustion and provide heat to the cigarette. Rather, the new cigarette primarily heats tobacco thereby reducing products of smoke formation mechanisms such as tobacco combustion, tobacco pyrolysis and pyrosynthesis. The mainstream smoke composition from a cigarette based on the new design (TOB-HT) has been characterized in comparative chemical testing with two reference cigarettes using the FTC puffing regimen. Thermal properties, UV absorption characteristics, elemental composition and materials balance studies all suggest a simplified smoke aerosol. Twenty-five smoke constituents ("target compounds") identified by the scientific community as compounds that may contribute to the diseases statistically associated with smoking have also been measured. Mainstream smoke concentrations of most target compounds are significantly lower with the TOB-HT cigarette when compared with reference cigarettes in the ultra-light "tar" and light "tar" categories. Taken together, chemical analysis results suggest simplified TOB-HT smoke chemistry with marked reductions in specific chemicals reported to be biologically active.     

Smoking behavior and smoking history of tobacco chippers.

Nicotine produces dependence in almost all cigarette smokers. 65 chippers (anomalous smokers who smoke regularly but at very low levels [1–5 cigarettes/day]) were compared with 72 matched regular smokers (20–40 cigarettes/day). Despite having smoked an average of 46,000 cigarettes in 19 yrs of smoking, chippers demonstrated little sign of nicotine dependence. They reported frequent casual abstinence from smoking without withdrawal symptoms, smoked their 1st cigarette of the day hours after waking, and scored low on a modified Fagerstrom Tolerance Questionnaire, a measure of tobacco dependence. Although most chippers had never smoked heavily, a small subgroup of chippers reported previous extended periods of heavy smoking, which suggests that some people may be able to overcome dependence while continuing to smoke. These "converted chippers" could not be distinguished from "native chippers" on the basis of their current smoking behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mechanisms underlying cerebrovascular effects of cigarette smoking in rats in vivo

BACKGROUND AND PURPOSE: The effects of acute smoking on cerebral circulation are controversial. This study was designed (1) to clarify any differences between the effects of cigarette smoking and nicotine infusion and between the effects of single- and multiple-cigarette smoking on cerebral vessels and (2) to probe the mechanism(s) underlying the vascular responses. METHODS: In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, pial vessel diameters were measured with the use of a cranial window preparation. We studied the effects of (1) 60 puffs per minute of mainstream cigarette smoke from cigarettes having 2 nicotine levels (0.1 and 1 mg per cigarette), (2) administration of nicotine (0.05 mg per body IV), and (3) repeated smoking (four 1 mg nicotine-containing cigarettes at 30-minute intervals) (n=6 each). RESULTS: Inhalation of smoke from a 0.1 or 1 mg nicotine-containing cigarette for 1 minute caused pial arterioles to constrict at 30 seconds (7.2% and 7.3%, respectively) and then to dilate (peak at 5 to 10 minutes; 4.6% and 17.9%, respectively). Nicotine infusion caused pial vasodilation (35.7%) without an initial vasoconstriction. Repeated smoking suppressed the pial vasodilation but not the initial vasoconstriction. The vasodilation induced by a single cigarette was greatly inhibited by pretreatment with mecamylamine or glibenclamide and attenuated by propranolol or Nomega-nitro-L-arginine methyl ester; the initial vasoconstriction was inhibited by seratrodast, a thromboxane A2 receptor antagonist (n=6 in each case). CONCLUSIONS: Single-cigarette smoking had a significant biphasic effect on cerebral arteriolar tone. The vasodilation was attenuated by repeated smoking. The vasodilation is most likely an effect of nicotine, at least in part mediated via sympathetic activation, NO production, and K+ channel activation. The vasoconstriction is partially due to thromboxane A2 induced by cigarette smoke.     

Cigarette smoking, nicotine addiction, and relaxation.

Shock endurance was used to measure the amount of anxiety experienced in a stressful situation by nonsmokers, smokers allowed to smoke cigarettes containing low levels or moderately high levels of nicotine, and smokers not allowed to smoke. Ss were 51 university students. Smokers deprived of cigarettes and those who smoked cigarettes containing low levels of nicotine behaved more anxiously than nonsmokers and Ss allowed to smoke high-nicotine cigarettes, but the high-nicotine smokers behaved no less anxiously than nonsmokers. Results support the hypothesis that the calming effect of smoking is due to the action of nicotine in ending withdrawal symptoms in addicted smokers rather than to a sedative property of cigarette smoking. (12 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Leaving work to smoke

Work-place smoking bans have not only reduced work-day cigarette consumption but also been associated with going outside to smoke during working hours. We examined the extent of "exiled smoking", estimated how much work-day cigarette consumption can be attributed to it, and examined proximal predictors of both these two variables. Some 794 smokers from 42 medium-sized work-places were surveyed as the baseline for an intervention study. A self-completed questionnaire assessed smoking behaviour on work and non-working days, leaving work to smoke, and beliefs and opinions about smoking and smoking bans. Multiple regressions were used to examine predictors of leaving work to smoke, and of the amount smoked when doing so. Smokers reported consuming an average of 5.4 cigarettes during work breaks, 3.5 of which were associated with deliberately seeking opportunities to smoke; 39% reported leaving work to smoke one or more times per day during non-break periods. Indices of addiction were significant predictors of both leaving work to smoke and of cigarette consumption while doing so. Leaving work to smoke is in part an activity of addicted smokers, presumably to maintain blood nicotine levels. There is the potential to further reduce rates of cigarette consumption associated with work-place smoking bans if this "exiled smoking" can be reduced. This may be easier to achieve in light smokers.     

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.     

Cigarette mentholation increases smokers' exhaled carbon monoxide levels.

12 male smokers participated in 3 controlled-dose smoking sessions spaced 1 wk apart. In each session, Ss inhaled 1,200 cc of cigarette smoke. Menthol dosage varied across sessions, such that Ss smoked experimental cigarettes that had been injected with 0, 4, or 8 mg of menthol. Exhaled CO levels increased concomitantly with menthol dosage. There were no differences in smoking topography across the 3 conditions. The ability of menthol to increase the toxicity of cigarette smoke by raising CO levels is discussed. Results suggest that menthol cigarette preference may account for some of the racial differences in smoking behavior and smoking-related outcomes found in past literature. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Changes in tobacco use among adolescent smokers in substance abuse treatment.

Adolescents with substance use disorders (SUDs) smoke cigarettes more than youth in the general population. Little is known about changes in smoking patterns during and after outpatient SUD treatment. We examined whether receiving SUD treatment had a differential impact on cigarette smoking behaviors of mild (     

Dose-dependent induction of IL-12 but not IL-10 from human keratinocytes after exposure to ultraviolet light A

OBJECTIVE: Our purpose was to assess the risk of ectopic pregnancy among women who smoke cigarettes. STUDY DESIGN: We used data from a case-control study of ectopic pregnancy conducted from October 1988 to August 1990 at an inner-city hospital in Georgia. Cases were 196 non-Hispanic black women with a surgically confirmed ectopic pregnancy. Controls were non-Hispanic black women who had delivered either a live or a stillborn infant weighing at least 500 gm (n = 882) or who were pregnant and seeking an induced abortion (n = 237). RESULTS: After we adjusted for parity, douching history, history of infertility, and age, the odds ratio for ectopic pregnancy was 1.9 (95% confidence interval 1.4 to 2.7) for women who smoked during the periconception period compared with women who did not smoke at that time. After stratification by the amount of daily smoking during the periconception period, the odds ratio rose from 1.6 (95% confidence interval 0.9 to 2.9) for women who smoked 1 to 5 cigarettes to 1.7 (95% confidence interval 1.1 to 2.8) for women who smoked 6 to 10 cigarettes to 2.3 (95% confidence interval 1.3 to 4.0) for women who smoked 11 to 20 cigarettes, and to 3.5 (95% confidence interval 1.4 to 8.6) for women who smoked >20 cigarettes per day. CONCLUSION: In this inner-city population, cigarette smoking was an independent, dose-related risk factor for ectopic pregnancy among black women. The public health and medical care communities should inform the public of this additional risk associated with cigarette smoking and intensify intervention strategies to reduce cigarette smoking among women of reproductive age.     

Effects of cigarette smoking on perception of thermal pain.

The effects of cigarette smoking on pain perception were evaluated in 18 healthy smokers. Thermal pain stimuli were used to assess pain detection threshold and tolerance and to collect subjective ratings of the intensity and unpleasantness of painful stimuli. After overnight abstinence, pain perception was evaluated before and after 3 experimental treatments. Participants smoked normal cigarettes, smoked denicotinized cigarettes, or remained abstinent. Smoking normal cigarettes produced relative increases in pain tolerance compared with abstinence. Smoking denicotinized cigarettes produced intermediate effects on tolerance not different from the other 2 treatments. Effects were not detected for pain threshold or subjective pain ratings. Results suggest that cigarette smoking can have antinociceptive effects, which may depend both on nicotine and on other factors associated with smoking. (PsycINFO Database Record (c) 2010 APA, all rights reserved)