Search

Key points: Cigarette smoke components directly alter muscle fatigue resistance and intracellular muscle fibre Ca2+ handling independent of a change in lung structure. Changes in muscle vascular structure are associated with a depletion of satellite cells. Sarcoplasmic reticulum Ca2+ uptake is substantially impaired in myofibres during fatiguing contractions in mice treated with cigarette smoke extract. Abstract: Cigarette smokers exhibit exercise intolerance before a decline in respiratory function. In the present study, the direct effects of cigarette smoke on limb muscle function were tested by comparing cigarette smoke delivered to mice by weekly injections of cigarette smoke extract (CSE), or nose‐only exposure (CS) 5 days each week, for 8 weeks. Cigarette smoke delivered by either route did not alter pulmonary airspace size. Muscle fatigue measured in situ was 50% lower in the CSE and CS groups than in control. This was accompanied by 34% and 22% decreases in soleus capillary‐to‐fibre ratio of the CSE and CS groups, respectively, and a trend for fewer skeletal muscle actin‐positive arterioles (P = 0.07). In addition, fewer quiescent satellite cells (Nes+Pax7+) were associated with soleus fibres in mice with skeletal myofibre VEGF gene deletion (decreased 47%) and CS exposed (decreased 73%) than with control fibres. Contractile properties of isolated extensor digitorum longus and soleus muscles were impaired. In flexor digitorum brevis myofibres isolated from CSE mice, fatigue resistance was diminished by 43% compared to control and CS myofibres, and this was accompanied by a pronounced slowing in relaxation, an increase in intracellular Ca2+ accumulation, and a slowing in sarcoplasmic reticulum Ca2+ uptake. These data suggest that cigarette smoke components may impair hindlimb muscle vascular structure, fatigue resistance and myofibre calcium handling, and these changes ultimately affect contractile efficiency of locomotor muscles independent of a change in lung function. [ABSTRACT FROM AUTHOR]

Key points: Chronic obstructive pulmonary disease (COPD) is largely caused by smoking, and patient limb muscle exhibits a fast fibre shift and atrophy. We show that this fast fibre shift is associated with type grouping, suggesting recurring cycles of denervation–reinnervation underlie the type shift. Compared to patients with normal fat‐free mass index (FFMI), patients with low FFMI exhibited an exacerbated fibre type shift, marked accumulation of very small persistently denervated muscle fibres, and a blunted denervation‐responsive transcript profile, suggesting failed denervation precipitates muscle atrophy in patients with low FFMI. Sixteen weeks of passive tobacco smoke exposure in mice caused neuromuscular junction degeneration, consistent with a key role for smoke exposure in initiating denervation in COPD. Abstract: A neurological basis for the fast fibre shift and atrophy seen in limb muscle of patients with chronic obstructive pulmonary disease (COPD) has not been considered previously. The objective of our study was: (1) to determine if denervation contributes to fast fibre shift and muscle atrophy in COPD; and (2) to assess using a preclinical smoking mouse model whether chronic tobacco smoke (TS) exposure could initiate denervation by causing neuromuscular junction (NMJ) degeneration. Vastus lateralis muscle biopsies were obtained from severe COPD patients [n = 10 with low fat‐free mass index (FFMI), 65 years; n = 15 normal FFMI, 65 years) and healthy age‐ and activity‐matched non‐smoker control subjects (CON; n = 11, 67 years), to evaluate morphological and transcriptional markers of denervation. To evaluate the potential for chronic TS exposure to initiate these changes, we examined NMJ morphology in male adult mice following 16 weeks of passive TS exposure. We observed a high proportion of grouped fast fibres and a denervation transcript profile in COPD patients, suggesting that motor unit remodelling drives the fast fibre type shift in COPD patient limb muscle. A further exacerbation of fast fibre grouping in patients with low FFMI, coupled with blunted reinnervation signals, accumulation of very small non‐specific esterase hyperactive fibres and neural cell adhesion molecule‐positive type I and type II fibres, suggests denervation‐induced exhaustion of reinnervation contributes to muscle atrophy in COPD. Evidence from a smoking mouse model showed significant NMJ degeneration, suggesting that recurring denervation in COPD is probably caused by decades of chronic TS exposure. [ABSTRACT FROM AUTHOR]

Smoking not only increases the risk of lung cancer but is strongly related to the onset of cardiovascular disease. Particularly, passive smoking due to sidestream smoke is a critical public health problem. To assess active and passive exposure to tobacco smoke, we developed a simple and sensitive method, consisting of on-line in-tube solid phase microextraction (SPME) coupled with liquid chromatography-tandem mass spectrometry (LC–MS/MS), to determine nicotine and its metabolite cotinine in hair samples. These compounds were separated within 5 min using a Polar-RP80A column and detected in the positive ion mode by multiple reaction monitoring. The optimum in-tube SPME conditions were 25 draw/eject cycles of 40 μL of sample at a flow rate of 200 μL/min using a Carboxen 1006 capillary column as an extraction device. The extracted compounds in the stationary phase on the inner wall of the capillary could be dissolved easily into the mobile phase and transferred to an LC column. Using the in-tube SPME LC–MS/MS method, the calibration curves were linear in the 5–1000 pg/mL ranges for nicotine and cotinine, and the detection limits (signal to noise ratio of 3) were 0.45 and 0.13 pg/mL, respectively. The intra-day and inter-day precisions were below 3.4% and 6.0% ( n  = 5), respectively. This method was utilized successfully to analyze pg/mg levels of nicotine and cotinine in 1 mg of hairs without interference peaks, and good recoveries were obtained. The concentration of cotinine in hair was two orders of magnitude lower than that of nicotine, but a good positive correlation was found between the concentrations of these compounds. This method can automate the extraction, concentration and analysis of samples, and is useful for the assessment of long-term exposure to tobacco smoke. [ABSTRACT FROM AUTHOR]

This systematic review explored associations between smoking and health outcomes involving the musculoskeletal system. AMSTAR criteria were followed. A comprehensive search of PubMed, Web of Science, and Science Direct returned 243 articles meeting inclusion criteria. A majority of studies found smoking has negative effects on the musculoskeletal system. In research on bones, smoking was associated with lower BMD, increased fracture risk, periodontitis, alveolar bone loss, and dental implant failure. In research on joints, smoking was associated with increased joint disease activity, poor functional outcomes, and poor therapeutic response. There was also evidence of adverse effects on muscles, tendons, cartilage, and ligaments. There were few studies on the musculoskeletal health outcomes of secondhand smoke, smoking cessation, or other modes of smoking, such as waterpipes or electronic cigarettes. This review found evidence that suggests tobacco smoking has negative effects on the health outcomes of the musculoskeletal system. There is a need for further research to understand mechanisms of action for the effects of smoking on the musculoskeletal system and to increase awareness of healthcare providers and community members of the adverse effects of smoking on the musculoskeletal system. [ABSTRACT FROM AUTHOR]

Introduction: Oral cancers are among the most common cancers in the Indian subcontinent and tobacco is the most common implicated etiologic agent for these cancers. Over last two decades, significant changes have occurred in the lifestyle of people in the subcontinent. Antitobacco legislations have made developed and awareness about the harmful effects of tobacco and related products have increased. We hypothesized that this would lead to change in tobacco use pattern and hence impact the trends of oral cancer in India. Methodology: We analyzed the hospital records of patients having buccal mucosa and tongue cancers at a tertiary care cancer center. We noted the trends of patients presenting with these cancers 4 yearly, over a period of 16 years and in this way tried to assess the impact of legislation and awareness activities upon cancer incidence and trends. Results: This study has shown that the number of patients presenting with tongue and buccal mucosa cancers has not decreased over the years. Increase in buccal mucosa cancers is marginally more than that of the tongue cancer. Proportion of males with respect to females presenting with these cancers has increased. There has been no significant decline in the younger patients presenting with these cancers. Common age of presentation of tongue cancers has come down. Conclusion: The findings of this study highlight the ineffectiveness of current laws and awareness programs in reducing the menace of oral cancer. [ABSTRACT FROM AUTHOR]

Objective: Strong expectations regarding positive effects of smoking may reduce the likelihood of successfully quitting. The Smoking Effects Questionnaire (SEQ) assesses the importance of seven expected positive and negative effects of smoking. SEQ was used to predict responses to contingent monetary rewards for smoking abstinence among smokers with substance use disorders (SUD).Methods: Smokers (N = 184) in residential (i.e., 24 h/day) treatment for SUD received 19 consecutive days of either contingent vouchers (CV) for smoking abstinence (twice-daily carbon monoxide [CO] readings) or non-contingent vouchers (NV) plus counseling to motivate smoking cessation. Analyses investigated effects of smoking expectancies on days of smoking within-treatment and number of cigarettes/day at 1 month post-treatment.Results: Higher positive expectancies for reduced negative affect, weight control, stimulation and positive social effects from smoking were related to more days of smoking during treatment only for participants in the CV condition. Post-treatment, expecting positive social and stimulating effects from smoking were related to more smoking only among CV participants. In both conditions, negative expectancies were largely unrelated to smoking outcomes.Conclusions: The moderation of CV by positive smoking expectancies suggests that those who rate positive expectancies as more important may require a complementary treatment or different incentives to reduce smoking. The SEQ was probably unassociated with smoking in NV due to little reduction in smoking behavior. Helping smokers with SUD develop alternative ways to produce positive effects sought from smoking may be important to improve initial smoking outcomes. [ABSTRACT FROM AUTHOR]

Recent advancements in in vitro exposure systems and cell culture technology enable direct exposure to cigarette smoke (CS) of human organotypic bronchial epithelial cultures. MucilAir organotypic bronchial epithelial cultures were exposed, using a Vitrocell exposure system, to mainstream aerosols from the 3R4F cigarette or from a recently developed novel tobacco vapor product (NTV). The exposure aerosol dose was controlled by dilution flow and the number of products smoked; there were five exposure conditions for 3R4F smoke and three for NTV vapor. The amount of nicotine delivered to the tissues under each condition was analyzed and that of the total particulate matter (TPM) was estimated using nicotine data. The nicotine dose was similar for the two products at the highest dose, but the estimated TPM levels from the NTV were 3.7 times the levels from the 3R4F. Following 3R4F smoke exposure, a dose dependent increase was observed in cytotoxicity, cytokine secretion, and differential gene expression. However, no changes were detected in these endpoints following NTV vapor exposure, suggesting the biological effects of NTV vapor are lower than those of conventional combustible CS. Our study design, which includes collection of biological data and dosimetry data, is applicable to assessing novel tobacco products. [ABSTRACT FROM AUTHOR]

Background Methodologic challenges related to the concomitant use (co-use) of substances and changes in policy and potency of marijuana contribute to ongoing uncertainty about risks to fetal neurodevelopment associated with prenatal marijuana use. In this study, we examined two biomarkers of fetal neurodevelopmental risk—birth weight and length of gestation—associated with prenatal marijuana use, independent of tobacco (TOB), alcohol (ALC), other drug use (OTH), and socioeconomic risk (SES), in a pooled sample ( N  = 1191) derived from 3 recent developmental cohorts (2003–2015) with state-of-the-art substance use measures. We examined differential associations by infant sex, and multiplicative effects associated with co-use of MJ and TOB. Methods Participants were mother-infant dyads with complete data on all study variables derived from Growing Up Healthy ( n  = 251), Behavior and Mood in Babies and Mothers (Cohorts 1 and 2; n  = 315), and the Early Growth and Development Study ( N  = 625). We estimated direct effects on birth weight and length of gestation associated with MJ, TOB, and co-use (MJ x TOB), using linear regression analysis in the full sample, and in male ( n  = 654) and female ( n  = 537) infants, separately. Results Mean birth weight and length of gestation were 3277 g ( SD  = 543) and 37.8 weeks (SD = 2.0), respectively. Rates of prenatal use were as follows: any use, n  = 748 (62.8%); MJ use, n  = 273 (22.9%); TOB use, n  = 608 (51.0%); co-use of MJ and TOB, n  = 230 (19.3%); ALC use, n  = 464 (39.0%); and OTH use n  = 115 (9.7%.) For all infants, unique effects on birth weight were observed for any MJ use [ B ( SE ) = −84.367(38.271), 95% C.I. −159.453 to −9.281, p  = .028], any TOB use [ B ( SE ) = −0.99.416(34.418), 95% C.I. −166.942 to −31.889, p  = .004], and each cigarette/day in mean TOB use [ B ( SE ) = −12.233(3.427), 95% C.I. −18.995 to −5.510, p  < .001]. Additional effects of co-use on birth weight, beyond these drug-specific effects, were not supported. In analyses stratified by sex, while TOB use was associated with lower birth weight in both sexes, MJ use during pregnancy was associated with lower birth weight of male infants [ B ( SE ) = −153.1 (54.20); 95% C.I. −259.5 to −46.7, p  = .005], but not female infants [ B ( SE ) = 8.3(53.1), 95% C.I. −96.024 to 112.551, p  = .876]. TOB, MJ, and their co-use were not associated with length of gestation. Conclusions In this sample, intrauterine co-exposure to MJ and TOB was associated with an estimated 18% reduction in birth weight not attributable to earlier delivery, exposure to ALC or OTH drugs, nor to maternal SES. We found evidence for greater susceptibility of male fetuses to any prenatal MJ exposure. Examination of dose-dependence in relationships found in this study, using continuous measures of exposure, is an important next step. Finally, we underscore the need to consider (a) the potential moderating influence of fetal sex on exposure-related neurodevelopmental risks; and (b) the importance of quantifying expressions of risk through subtle alterations, rather than dichotomous outcomes. [ABSTRACT FROM AUTHOR]

Oral microbiota is a vital part of human microbiota, including bacterial, protozoa, viral and fungal species. Beneficial microbes form biofilms to form a first-line defense against harmful microorganisms. Tobacco smoking is considered a major environmental factor affecting the orodental microbiota. Smokers harbor more pathogenic microbes than non-smokers. In fact, cigarette smoking exposes the oral cavity to a large number of toxicants, perturbing the oral microbial ecology through various mechanisms. In Saudi Arabia, research on the impact of tobacco smoking on oral microbiota is still lacking. Therefore, this case-control study is an important addition to the literature in terms of tobacco use and its effects on oral microbiota and oral hygiene. 130 men were recruited for this study, including 65 smokers and 65 non-smokers. The following parameters were recorded for all 130 participants - age, weight, height and education. The aim of this study was to investigate and compare the effect of tobacco smoking on the oral microbiome of smokers and non-smokers. The majority of the smokers were young adults between the ages of 21 and 30 inclusive (n=27). The results show that excessive microorganism growth was seen in smokers to a greater degree than non-smokers (38.5% of smokers vs. 8.8% of non-smokers). Not surprisingly, a significant majority (85.3%) of non-smokers had moderate microorganism growth compared to only 53.8% of smokers. cigarette smoking facilitates excessive growth of oral microorganisms, predisposing smokers to various periodontal diseases. In fact, smoking perturbs the balance of oral microbiota, producing a viable environment for microbes to cause diseases. Further large scale prospective studies are required to determine the exact mechanism that causes tobacco to affect oral microbiota. [ABSTRACT FROM AUTHOR]

Temperatures above the optimum are sensed as heat stress (HS) by all living organisms and represent one of the major environmental challenges for plants. Plants can cope with HS by activating specific defense mechanisms to minimize damage and ensure cellular functionality. One of the most common effects of HS is the overproduction of reactive oxygen and nitrogen species (ROS and RNS). The role of ROS and RNS in the regulation of many plant physiological processes is well established. On the contrary, in plants very little is known about the physiological role of peroxynitrite (ONOO−), the RNS species generated by the interaction between NO and O2−. In this work, the role of ONOO− on some of the stress responses induced by HS in tobacco BY-2 cultured cells has been investigated by measuring these responses both in the presence and in the absence of 2,6,8-trihydroxypurine (urate), a specific scavenger of ONOO−. The obtained results suggest a potential role for ONOO− in some of the responses induced by HS in tobacco cultured cells. In particular, ONOO− seems implicated in a form of cell death showing apoptotic features and in the regulation of the levels of proteins involved in the response to stress. [ABSTRACT FROM AUTHOR]

Background: To what extent steroid hormones contribute to lung cancer in male and female never smokers and smokers is unclear. We examined expression of hormone receptors in lung tumors by sex and smoking.Methods: Patients with primary non-small cell lung cancer were recruited into an Intergroup study in the United States and Canada, led by SWOG (S0424). Tumors from 813 cases (450 women and 363 men) were assayed using immunohistochemistry for estrogen receptor (ER)-α, ER-β, progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Linear regression was used to examine differences in expression by sex and smoking status. Cox proportional hazard models were used to estimate survival associated with the receptors. All statistical tests were two-sided.Results: In ever smokers, postmenopause and oral contraceptive use were associated with lower nuclear ER-β (P = .02) and total (nuclear + cytoplasmic) PR expression (P = .02), respectively. Women had lower cytoplasmic ER-α (regression coefficient [β], or differences in H-scores = -15.8, P = .003) and nuclear ER-β (β = -12.8, P = .04) expression than men, adjusting for age, race, and smoking. Ever smokers had both higher cytoplasmic ER-α (β = 45.0, P < .001) and ER-β (β = 25.9, P < .001) but lower total PR (β = -42.1, P < .001) than never smokers. Higher cytoplasmic ER-α and ER-β were associated with worse survival (hazard ratio = 1.73, 95% confidence interval [CI] = 1.15 to 2.58, and HR = 1.59, 95% CI = 1.08 to 2.33, respectively; quartiles 4 vs 1).Conclusions: Lower expression of nuclear ER-β in women supports the estrogen hypothesis in lung cancer etiology. Increasing cytoplasmic ER-α and ER-β and decreasing PR protein expression may be mechanisms whereby smoking disrupts hormone pathways. [ABSTRACT FROM AUTHOR]

Abstract: Single nucleotide polymorphisms (SNPs) may modulate individual susceptibility to carcinogens. We designed a genome‐wide association study to characterize individuals presenting extreme phenotypes of high and low risk to develop tobacco‐induced non‐small cell lung cancer (NSCLC), and we validated our results. We hypothesized that this strategy would enrich the frequencies of the alleles that contribute to the observed traits. We genotyped 2.37 million SNPs in 95 extreme phenotype individuals, that is: heavy smokers that either developed NSCLC at an early age (extreme cases); or did not present NSCLC at an advanced age (extreme controls), selected from a discovery set (n = 3631). We validated significant SNPs in 133 additional subjects with extreme phenotypes selected from databases including >39,000 individuals. Two SNPs were validated: rs12660420 (pcombined = 5.66 × 10−5; ORcombined = 2.80), mapping to a noncoding transcript exon of PDE10A; and rs6835978 (pcombined = 1.02 × 10−4; ORcombined = 2.57), an intronic variant in ATP10D. We assessed the relevance of both proteins in early‐stage NSCLC. PDE10A and ATP10DmRNA expressions correlated with survival in 821 stage I–II NSCLC patients (p = 0.01 and p < 0.0001). PDE10A protein expression correlated with survival in 149 patients with stage I–II NSCLC (p = 0.002). In conclusion, we validated two variants associated with extreme phenotypes of high and low risk of developing tobacco‐induced NSCLC. Our findings may allow to identify individuals presenting high and low risk to develop tobacco‐induced NSCLC and to characterize molecular mechanisms of carcinogenesis and resistance to develop NSCLC. [ABSTRACT FROM AUTHOR]

The oxidative stress and cellular apoptosis by environmental factor including cigarette smoke induces alveolar airway remodeling leading to chronic obstructive pulmonary disease (COPD). Recently, the receptor for advanced glycan end products (RAGE) which is highly expressed in alveolar epithelium is emerging as a biomarker for COPD susceptibility or progression. However, it still remains unknown how RAGE plays a role in cigarette smoke extract (CSE)-exposed human alveolar type II epithelial cell line. Therefore, we determined the efficacy of RAGE-specific antagonist FPS-ZM1 in response to CSE-induced lung epithelial cells. CSE induced the elevated generation of RONS and release of pro-inflammatory cytokines, and impaired the cellular antioxidant defense system. Further, CSE induced the alteration of RAGE distribution via the activation of redox-sensitive DAMP (Damage-associated molecular patterns) signaling through Nrf2 in cells. Although pre-treatment with SB202190 (p38 inhibitor) or SP600125 (JNK inhibitor) failed to recover the alteration of RAGE distribution, treatment of FPS-ZM1 significantly exhibited anti-inflammatory and anti-oxidative/nitrosative effects, also inhibited the activation of redox-sensitive DAMP signaling through Nrf2 (nuclear factor erythroid 2-related factor 2) migration in the presence of CSE. Taken together, our data demonstrate that RAGE and Nrf2 play a pivotal role in maintenance of alveolar epithelial integrity. [ABSTRACT FROM AUTHOR]

Data from National Health and Nutrition Examination Survey for 2013-2014 were used to compute rates of exposure (ROE) to environmental tobacco smoke (ETS) from various indoor environments among US children and nonsmoking adolescents and adults. In a typical week in USA, 473,000 infants (ROE, 11%), 3.36 million children aged 1-5 years (ROE, 16.4%), and 4.59 million children aged 6-11 years (ROE, 18.6%) are exposed to ETS from indoor environments only. ROE among children was found to be highest by inhaling tobacco smoke inside home, riding in a car, and when visiting other people’s homes. In a typical week, 4.1 million nonsmoking adolescents (ROE, 29.2%) were being exposed to ETS. For every one adolescent smoker, 2.4 nonsmoker adolescents were being subjected to ETS exposure. Both non-Hispanic White (NHW) and non-Hispanic Black (NHB) nonsmoking adolescents had higher ROE (p < 0.01) than Hispanics (HISP) and non-Hispanic Asians (NHAS). Also, in a typical week, 16.8 million nonsmoking adults (ROE, 29.2%) were being exposed to ETS. For every adult smoker, 0.7 nonsmoker adult was subjected to ETS exposure. Both NHW and NHB nonsmoking adults had higher ROE (p < 0.01) than HISP and NHAS and males had higher ROE than females (p < 0.01). [ABSTRACT FROM AUTHOR]

The transdermal fentanyl patch is widely used to treat cancer-related pain despite its wide inter- and intrapatient variability in pharmacokinetics. The aim of this study was to investigate whether smoking and body size (i.e. body mass index) influence fentanyl exposure in patients with cancer. These are factors that typically change during treatment and disease trajectories. We performed an explorative cohort study in patients with cancer using transdermal fentanyl patches (Durogesic®), by taking a blood sample for pharmacokinetic analysis one day after applying a patch in patients with a stable fentanyl dose. A total of 88 patients were evaluable. Although no statistically significant difference was found, the plasma concentrations of non-smokers was 28% (95% CI [-14%; +89-%]) higher than those of smokers normalizing for a dose of 25μg/min. Patients with a low BMI (< 20 kg/m2) had almost similar (10% (95% CI [-39%; +97%]) higher) plasma concentrations compared to patients with a high BMI (> 25 kg/m2). A wider variation in fentanyl plasma concentrations was found in this study than anticipated. Due to this variation, studies in larger patient cohorts are needed to further investigate the effect of smoking on plasma concentration of fentanyl and thereby clarify the clinical significance of our findings. [ABSTRACT FROM AUTHOR]

Exposure to cigarette smoke (CS) causes vessel damage and mechanism of this damage has not yet been clearly identified. Therefore, in this study we aimed to investigate whether vessel damage due to the CS exposure will be prevented by the alpha-linolenic acid (ALA) or not which has anti-inflammatory effect in mice. For this reason, mice were grouped as controls (with and without CS) and ALA (with and without CS). The CS application continued 5 days a week for two months. At the end of two months, the mice were killed by cervical dislocation and their blood and thoracic aortas were isolated. ALA Treatment increased acetylcholine relaxations. CS decreased acetylcholine relaxation. CS with ALA treatment increased acetylcholine relaxations versus just CS treatment. CS caused rising in cyclooxigenase-2 and phospholipase A2 levels. This rise is inhibited with ALA treatment. CS decreased eNOS levels. But this result was not statistically significant. Furthermore, according to electron microscopic study CS damaged both smooth muscle and endothelium. While ALA treatment prevented smooth muscle damage it didn’t prevent endothelial damage. Using cigarette and CS exposure is a risk factor for cardiovascular disease. Our study showed that this disease. [ABSTRACT FROM AUTHOR]

Cigarette smoking (CS) has some detrimental effects that occur via oxidative stress (OS). The aim of this work was to demonstrate the pathological and immunohistochemical effects of CS and the protective effects of a strong antioxidant alpha lipoic acid (ALA) on CS-induced genital system changes in a rat model. Twenty-eight female rats were randomly allocated to three groups as control, CS-exposed, and CS-exposed and ALA-treated. Reproductive tract organs were collected for biochemical and pathological examinations. In the CS group, OS markers increased in the tissues of both the ovary and fallopian tubes. Decreased follicle numbers in the ovary, marked cilial loss in the fallopian tubes, and pathologic changes in the uterus were observed in the CS group. Positive calcitonin gene–related peptide (CGRP), caspase 3α, hypoxia-inducible factor 1α (HIF-1α), tumor necrosis factor-α (TNF-α) immunoreactions were observed in uterine tissues and HIF-1α immunoreactions in tubal and uterine epithelial cells of the CS group. ALA reversed all these findings effectively. CS has negative effects on the female reproductive system via HIF-1α in tuba uterina and HIF-1α, HIF-2α, TNF-α, caspase 3, and CGRP in the uterus, and ALA could protect against the negative effects of CS on the female reproductive system. [ABSTRACT FROM AUTHOR]

This paper examined knowledge about the health effects of smoking among health equity groups following the 2012 introduction of refreshed pictorial health warning labels (HWLs) in Canada. Data are from the 2012/2013 Youth Smoking Survey a representative school-based survey of 47,203 adolescents in Grades 6–12 in nine provinces. Regression models examined overall knowledge about eight health effects of smoking included in the HWLs. Less than one-third of adolescents (32.2%) knew that smoking causes vision loss/blindness and 33.7% knew that smoking causes bladder cancer. Whereas knowledge was high for lung cancer (93.9%), knowledge about other health effects ranged from 52.9% for chronic bronchitis/emphysema to 77.6% for gum or mouth disease. Non-smoking adolescents who were: susceptible to future smoking, male, ethnic minorities, and who had less spending money were significantly less likely to be knowledgeable of the health effects of smoking. There were fewer disparities in knowledge about the health effects of smoking among smokers. Smokers who bought loose or bagged cigarettes rather than cigarettes in packages or cartons were significantly less likely to be knowledgeable about the health effects of smoking. There are significant disparities in knowledge about the health effects of smoking by health equity groups particularly among non-smoking adolescents. Warning labels have the potential to reduce disparities in knowledge about the health effects of smoking when exposure to the warning labels is universal. Complementary strategies such as mass media campaigns are needed to address disparities in knowledge. [ABSTRACT FROM AUTHOR]

Smoking increases HIV-related and non-HIV-related morbidity and mortality for persons with HIV infection. We estimated changes in cigarette smoking among adults with HIV and adults in the general U.S. population from 2009 to 2014 to inform HIV smoking cessation programs. Among HIV-positive adults, rates of current smoking declined from 37.6% (confidence interval [CI]: 34.7-40.6) in 2009 to 33.6% (CI: 29.8-37.8) in 2014. Current smoking among U.S. adults declined from 20.6% (CI: 19.9-21.3) in 2009 to 16.8% (CI: 16.2-17.4) in 2014. HIV-positive adults in care were significantly more likely to be current smokers compared with the general U.S. population; they were also less likely to quit smoking. For both HIV-positive adults in care and the general population, disparities were noted by racial/ethnic, educational level, and poverty-level subgroups. For most years, non-Hispanic blacks, those with less than high school education, and those living below poverty level were more likely to be current smokers and less likely to quit smoking compared with non-Hispanic whites, those with greater than high school education, and those living above poverty level, respectively. To decrease smoking-related causes of illness and death and to decrease HIV-related disparities, smoking cessation interventions are vital as part of routine care with HIV-positive persons. Clinicians who care for HIV-positive persons who smoke should utilize opportunities to discuss and implement smoking cessation strategies during routine clinical visits. [ABSTRACT FROM AUTHOR]

Summary: Objective: We aimed to evaluate differences in serum thyroid‐stimulating hormone (TSH) levels according to smoking status and urine iodine concentration (UIC) in a healthy Korean population using data from the Sixth Korean National Health and Nutrition Examination Survey (KNHANES VI). Study design: Sixth Korean National Health and Nutrition Examination Survey (2013‐2015) is a nationwide, cross‐sectional survey of the Korean population. Patients: Research subjects were selected by two‐stage stratified cluster sampling of the population and housing census data. A total of 5639 subjects aged >18 years, who were not pregnant, and had undergone thyroid function testing during the survey period, were included. Measurement: The level of serum TSH according to smoking status, iodine intake and presence of TPOAb were evaluated. Results: In the reference population, mean serum TSH level in current smokers (1.87 mIU/L, 95% CI, 0.52‐5.37 mIU/L) was significantly lower than that in nonsmokers (2.33 mIU/L, 95% CI, 0.79‐6.69 mIU/L, P < .001). The rate of thyroperoxidase antibody (TPOAb) positivity was higher in never smoker (7.7%) than past smokers (5.1%) and current smokers (4.7%), but sex‐specific rate of TPOAb was not different according to smoking status. The lower serum TSH levels in current smokers were more apparent in iodine‐deficient subjects (UIC < 100 μg/L), and this change was diminished in subjects with UICs between 100 and 299 μg/L. The difference in serum TSH levels in current smokers disappeared in subjects with UICs ≥ 300 μg/L. Conclusions: Smoking is associated with a left‐shift in serum TSH level that is more apparent in iodine‐deficient subjects. Smoking status is not associated with the presence of TPOAb or iodine intake. The results suggest that smoking has a direct effect on thyroid function that is not mediated by autoimmune processes in the thyroid gland. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the frequency and trend of tobacco use among the doctors of Medical University. Study Design: Cross-sectional survey. Period: 06 Months from Aug 2016 to Jan 2017. Setting: Medical College and Tertiary Care Hospital affiliated with Medical University of Larkana, Sindh, Pakistan. Methods: Collection of data through the modified questionnaire of IUATLD, on a total of 140 doctors of Medical University, Larkana. Results: A total of 140 respondents, 116 were male and 24 were females. Out of 116 males, 65 (56%) were smokers and out of 24 females, 04(16.66%) were smokers. Sixty four (45.7%) were current smokers, 5(3.6%) were ex-smokers and 71(50.7%) were non-smokers. Majority 37(26.4%) of smokers start smoking between the age of 21-30 years. Most frequent form of tobacco used is cigarettes. Non-smokers were affected by passive smoking in their environment. Majority of smokers use caffeinated drink with smoking cigarettes. 23(16.4%) smokers need proper guideline of smoking cessation plan. Conclusion: Mostly male doctors involved in smoking as compared to female doctors. Most of them lie in the moderate addiction index. There is a extreme need for special trainings in the educational institutes for both the students and teachers so that to make it smoke free zone. [ABSTRACT FROM AUTHOR]

Background: Cigarette smoking is common in persons living with hepatitis C (hepatitis C+), but national statistics on this harmful practice are lacking. A better understanding of smoking behaviors in hepatitis C+ individuals may help in the development of targeted treatment strategies.Methods: We extracted data from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2014. Hepatitis C+ were compared with hepatitis C- adults in the entire sample and in the subset of current smokers. Measures included demographics, current smoking, cigarettes/day, nicotine dependence, other tobacco use, substance use, and medical and psychiatric comorbidities.Results: Complete smoking and hepatitis C virus (HCV) data were available for 39,472 (90.1%) of 43,793 adult participants in NHANES during the study years. Hepatitis C+ smoked at almost triple the rate of hepatitis C- adults (62.4% vs 22.9%), with no significant difference between hepatitis C+ men and women (64.5% vs 58.2%). Hepatitis C+ smokers were more likely to smoke daily than hepatitis C- smokers (87.5% vs 80.0%), but had similar levels of nicotine dependence. Hepatitis C+ smokers were more likely to be older (mean age: 47.1 vs 41.5 years), male (69.4% vs 54.4%), Black (21.2% vs 12.1%), less educated (any college: 31.8% vs 42.9%), poor (mean family monthly poverty index: 1.80 vs 2.47), uninsured (43.9% vs 30.4%), use drugs (cocaine: 11.1% vs 3.2%; heroin: 4.0% vs 0.6%), and be depressed (33.2% vs 13.5%). Multivariate analyses revealed significant associations of both hepatitis C infection and cigarette smoking with current depression and hypertension.Conclusions: There is a cigarette smoking epidemic embedded within the hepatitis C epidemic in the United States. The sociodemographic profile of hepatitis C+ smokers suggests that the implementation of effective tobacco treatment will be challenging. Thoughtful treatment strategies that are mindful of the unique characteristics of this group are needed. [ABSTRACT FROM AUTHOR]

Although the relationship between cigarette smoke and lung cancer has been widely studied, the molecular mechanism for cigarette smoke-induced lung cancer remains largely unclear. The present study investigated the roles of hypoxia-inducible factor (HIF)-1α and miR-21 in the malignant transformation of human bronchial epithelial (HBE) cells induced by cigarette smoke extract (CSE). In case of acute and chronic treatment of HBE cells, CSE increased the levels of HIF-1α, p-Akt, p-NF-κB, and miR-21 and decreased PTEN levels. The increased miR-21 levels induced by CSE were prevented by down-regulation of HIF-1α. Further, elevated miR-21 suppressed PTEN levels, which decreased the levels of p-Akt and p-NF-κB. However, those changes were attenuated in cells co-transfected with HIF-1α siRNA and an miR-21 mimic. Silencing of HIF-1α or NF-κB decreased colony formation and the invasion and migration capacities of CSE-transformed HBE cells; however, up-regulation of miR-21 reversed these effects. These results indicate that the oncogenic capacity of HIF-1α in regulation of miR-21-inhibited PTEN in a manner dependent on the Akt/NF-κB pathway, a process that is involved in the CSE-induced malignant transformation of HBE cells. Thus, the present research has established a new mechanism for cigarette smoke-induced lung carcinogenesis. [ABSTRACT FROM AUTHOR]

Background: Smoking is one of the leading causes of preventable death globally. Smoking generally has negative health effects because smoke inhalation inherently poses challenges to various physiologic processes such as respiration. Apparently smoking is the wrong choice which numerous adults getting addicted to in their young age. Hence, this survey was conducted to create awareness about the effect of smoking among adolescents. Aim: The aim of this study was to conduct a survey on knowledge, attitude, and perception of smoking habits in college students in rural area (Kanchipuram District). Materials and Methods: This study is the questionnaire-based survey. The survey questionnaire comprises questions about knowledge, attitude, and perception of smoking habits in college students in rural area (Kanchipuram District).This survey was administered to the participants through the survey planet link. The result obtained was statistically analyzed. The survey was conducted among 101 students. Result: Many adolescents have proved to show addictive toward the smoking habit. The college teens have been very susceptible to such hazardous habit of smoking. Conclusion: Smoking is a very dangerous and addictive habit; hence, knowledge and awareness regarding its consequence should be effectively brought into practice. [ABSTRACT FROM AUTHOR]

Background: Smoking is one of the leading causes of preventable death globally. Smoking generally has negative health effects because smoke inhalation inherently poses challenges to various physiologic processes such as respiration. Smoking is an unhealthy and dangerous habit which numerous adolescents are getting addicted to in their young lives. Hence, this survey was conducted to create awareness about the effect of smoking among adolescents. Aim: The aim of this survey is to create awareness about smoking in adolescents among rural areas. Materials and Method: The survey was undertaken among 200 adolescent school children of around 13-19 age groups of St. Claret Matriculation Higher secondary school, Thiruninravur, and informed concern was obtained from the participants. Of 200 students, 69 were willing to participate in the study. The survey instrument was a pre-prepared questionnaire eliciting information about the attitude and perception on smoke. The obtained responses were tabulated and analyzed. Result: From the survey, it is recorded that about 40.4% of the participants started smoking at the age of 13-15, which we call it as the initiation of the teenage. Majority of the adolescents start up with this habit because of the bad influences from their peers, family members, and also of curiosity and venturesomeness which take the individuals life into risk, making it difficult for them to quit smoking. Conclusion: Parental influences were a major factor leading to smoking behavior in the studied population. About 60% of the students are willing to quit the habit. Hence, d-addiction programs should be initiated among students to prevent further progression of smoking habits. [ABSTRACT FROM AUTHOR]

Background: Tobacco use related illness are common cause of premature deaths globally. WHO and CDC in 2011 estimated that 5 million deaths occur due to smoking relate illness globally and projected an increase to eight million in the estimated figure by 2030. Community outreach medical camps are conducted by various organizations across country and provide an unique opportunity to study the individuals attending these camps regarding their health related behaviour and knowledge. The current study was designed to study the smoking prevalence and knowledge of hazards of smoking and the motivation to quit of individuals attending community outreach medical camps. Method: It was a cross sectional descriptive study conducted at the various outreach camps held by a tertiary care hospital in Mumbai. Camps were held between Sep 2015 and Mar 2016. 302 person attending these outreach camps were interviewed. 86 current daily smokers were included in the study. Data was collected using questions recommended by Global Adult Tobacco Survey (GATS) Collaborative group. In person interviewer conducted interviews based on adapted GATS were administered during the outreach camps by the principal investigator. Only current tobacco users were included in the study and tobacco smoking pattern was assessed by asking about their current smoking status, age of initiation, the type of smoking product used (bidi/cigarette), the number of products smoked daily. Smoking Cessation was assessed by their motivation to quit smoking. Second hand smoke harm awareness was assessed by asking about knowledge of harmful effect of second hand smoke in non smokers. Awareness about dangers of smoking, and means to quit smoking were also assessed. Results: Among the study population preferred means of smoking tobacco was via cigarette (n=48;57.1%) while rest of subjects smoked bidi (n=36;42.9%). Majority of study subjects were mild smokers with smoking index < 100 (n=35;41.7%), while moderate smokers (n=29;34.5%) and heavy smokers (n=20;23.8%) also formed a sizeable chunk of the study population. 23 subjects (27.38%) had no knowledge about smoking related illness. Majority of those interviewed knew that smoking can result in Cancer (n=50; 59.5%). When asked about weather smoking results in harm to family members 26 subjects (31%) did not have the knowledge of smoking causing harm to family members. There was significantly more subjects with knowledge of harm to family members (p=0.010) and knowledge of means to quit smoking (p<0.001) in Middle SES group. However the motivation to quit smoking across two groups was not significantly different (p=0.010). Conclusion: Although awareness among smoking related illness is increasing there is need to concentrate on campaigns which make people aware of other ill effects of smoking and make them aware of supportive measures available to quit smoking. [ABSTRACT FROM AUTHOR]

Smoking has detrimental oral effects. The aim of this study was to review the literature related to the impact of smoking cessation on periodontal health, periodontal disease and periodontal treatment outcome as well as to review the smoking cessation strategies and the dentist's role in the smoking cessation effort. Smoking cessation seems to have a positive effect on the periodontium, to decrease the risk for incidence and progression of periodontitis and to lead to a non-significant trend for greater mean probing depth reductions after non-surgical treatment over a 12-month period. Smoking cessation effect on the periodontium should be further investigated. Dentists should inform their patients on the harmful effect of smoking and the beneficial effect of smoking cessation on oral health. They should advise, motivate and support their patients to quit smoking. Smoking-control strategies should be incorporated in dental practise. The dentist's role in the smoking cessation effort is important. Guidelines on smoking-control strategies applied in the dental office are required. [ABSTRACT FROM AUTHOR]

Background and Objective: Comprehension of the similarities and differences in the composition of the subgingival microbiota of patients with diabetes mellitus (DM), smokers or smokers with DM is an important step in developing therapies specific for these groups at risk for periodontitis. Therefore, the aim of this study was to compare the combined and individual effects of DM and smoking on the levels and prevalence of key subgingival periodontal pathogens in patients with chronic periodontitis. Material and Methods: One hundred patients with generalized chronic periodontitis were allocated into one of the following groups: DM (n = 25, non‐smokers with type 2 DM); S (n = 25, non‐diabetic smokers); SDM (n = 25, smokers with type 2 DM); and control (n = 25, non‐diabetic non‐smokers). Two subgingival biofilm samples from healthy sites (probing depth and clinical attachment level ≤3 mm and no bleeding) and 2 from diseased sites (probing depth and clinical attachment level ≥5 mm and bleeding on probing) were analyzed by quantitative polymerase chain reaction for Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Eubacterium nodatum, Parvimonas micra, Fusobacterium nucleatum ssp. and Prevotella intermedia. Results: There were no differences among groups in the mean counts of the bacterial species studied, considering all sampled sites (healthy plus diseased sites). There were also no differences among groups regarding the prevalence of any bacteria species in healthy and diseased sites (P > .05). The mean P. micra count was significantly higher in the healthy sites of both smoking groups, than in those of the control group (P < .05). Conclusion: The subgingival levels and prevalence of the bacterial species studied are not significantly different in subjects with chronic periodontitis presenting DM, smokers or smokers with DM. In addition, DM and smoking, jointly and individually, do not considerably affect the subgingival levels of target periodontal pathogens in patients with chronic periodontitis. [ABSTRACT FROM AUTHOR]

Smoking is an established risk factor for cardiovascular disease including coronary heart disease and stroke, however, data regarding smoking and sudden cardiac death have not been summarized in a meta-analysis previously. We therefore conducted a systematic review and meta-analysis to clarify this association. We searched the PubMed and Embase databases for studies of smoking and sudden cardiac death up to July 20th 2017. Prospective studies were included if they reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for smoking and sudden cardiac death. Summary RRs were estimated by use of a random effects model. Twelve prospective studies were included. The summary RR was 3.06 (95% CI 2.46-3.82, I2 = 41%, pheterogeneity = 0.12, n = 7) for current smokers and 1.38 (95% CI 1.20-1.60, I2 = 0%, pheterogeneity = 0.55, n = 7) for former smokers compared to never smokers. For four studies using non-current (never + former) smokers as the reference category the summary RR among current smokers was 2.08 (95% CI 1.70-2.53, I2 = 18%, pheterogeneity = 0.30). The results persisted in most of the subgroup analyses. There was no evidence of publication bias. These results confirm that smoking increases the risk of sudden cardiac death. Any further studies should investigate in more detail the effects of duration of smoking, number of cigarettes per day, pack-years, and time since quitting smoking and sudden cardiac death. [ABSTRACT FROM AUTHOR]

Background and purpose: We aimed to investigate the effect of smoking on the risk of intracranial aneurysm (IA) rupture (IAR), specifically relationship between the number of cigarettes smoked per day (CPD) or smoking index and the risk of IAR. Methods: We performed a single-center case-control study of consecutive patients evaluated or treated for IA at our institution from June 2015 to July 2016. Cases were patients with a ruptured IA. Two age- and sex-matched controls with an unruptured IA were included per case. Conditional logistic regression models were used to assess the relationship between both the CPD and smoking index (CPD × years of smoking) and IAR. results: The study population included 127 cases of IAR and 254 controls. The higher IAR risk was associated with cigarette smoking (both current and former) (OR, 2.3; 95% CI, 1.1-4.8; P = 0.029). Our subgroup analysis of smokers revealed a significant association between IAR risk and current smoking (OR, 2.8; 95% CI, 1.2-6.3; P = 0.012), current heavy smoking (CPD ≥ 20) (OR, 3.9; 95% CI, 1.4-11.0; P = 0.007), and a smoking index ≥800 (OR, 11.4; 95% CI, 2.3-24.5; P = 0.003). Former smoking was not significantly associated with IAR (OR, 1.1; 95% CI, 0.3-4.0; P = 0.929). conclusion: A dose-response relationship has been noted for intensity and duration of smoking consumption and increased risk of IAR. As smoking is modifiable, this finding is important to managing patients with IAs to quit or reduce smoking prior to lifethreatening subarachnoid hemorrhage. [ABSTRACT FROM AUTHOR]

The main purpose of this study is to examine the lifetime tobacco consumption and the degree of nicotine dependence related gray matter (GM) and white matter (WM) volume alterations in young adult-male smokers. Fifty-three long-term male smokers and 53 well-matched male healthy non-smokers participated in the study, and the smokers were respectively categorized into light and heavy tobacco consumption subgroups by pack-years and into moderate and severe nicotine dependence subgroups using the Fagerström Test for Nicotine Dependence (FTND). Voxel-based morphometry analysis was then performed, and ANCOVA analysis combined with subsequent post hoc test were used to explore the between-group brain volume abnormalities related to the smoking amount and nicotine dependence. Light and heavy smokers displayed smaller GM and WM volumes than non-smokers, while heavy smokers were found with more significant brain atrophy than light smokers in GM areas of precuneus, inferior and middle frontal gyrus, superior temporal gyrus, cerebellum anterior lobe and insula, and in WM areas of cerebellum anterior lobe. However, the contrary trend was observed regarding alterations associated with severity of nicotine dependence. Severe nicotine dependence smokers rather demonstrated less atrophy levels compared to moderate nicotine dependence smokers, especially in GM areas of precuneus, superior and middle temporal gyrus, middle occipital gyrus, posterior cingulate and insula, and in WM areas of precuneus, posterior cingulate, cerebellum anterior lobe and midbrain. The results reveal that the nicotine dependence displays a dissimilar effect on the brain volume in comparison to the cigarette consumption. Our study could provide new evidences to understand the adverse effects of smoking on the brain structure, which is helpful for further treatment of smokers. [ABSTRACT FROM AUTHOR]

Synthetic cannabinoids (SCs) are a significant public health concern given their widespread use and severe effects associated with intoxication. However, there is a paucity of controlled human studies investigating the behavioral and physiological effects and pharmacokinetics of these compounds. Designing a reliable method to administer consistent, concentration-dependent synthetic cannabinoids is an integral component of controlled study of these compounds. Further, optimizing methods to assess the parent compounds and metabolites in plasma is critical in order to be able to establish their pharmacokinetics after administration. To develop a reliable method to administer smokable, concentration-dependent SCs, cigarettes were prepared with plant matter adulterated with increasing concentrations of the first generation cannabinoids found in SC products, JWH-018 and JWH-073. Cigarettes were assessed 1–6 months after preparation using ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) to determine compound stability over time and concentration consistency throughout the cigarettes. Optimal conditions to detect metabolites in human plasma as a function of storage temperature (−4 °C to −80 °C) and time (24 h - 1 month) were also determined. Analyses verified that the method utilized to develop SC cigarettes yielded consistent, concentration-dependent products within 25% of the expected concentrations. JWH-018, JWH-073 and metabolites in spiked plasma were stable under the time and temperature conditions; concentrations were within ±20% of target values. These studies provide techniques and methods to conduct controlled investigations of the dose-dependent effects of first generation SCs to begin understanding risks associated with use. This article is part of the Special Issue entitled ‘Designer Drugs and Legal Highs.’ [ABSTRACT FROM AUTHOR]

Acute eosinophilic pneumonia (AEP) is commonly misdiagnosed as infectious pneumonia due to presence of fever and radiological features. However, development of peripheral eosinophilia within days of presentation should raise the concern of AEP especially in previously heathy adults with history of recent tobacco smoking. [ABSTRACT FROM AUTHOR]

The biology and life table of two populations of Chloridea virescens F. were evaluated under laboratory conditions (T= 24.02 ± 0.24°C; HR= 82.52 ± 0.72%). Both populations differed in the morphological characteristic of the last instar larvae and the organ of the plant of tobacco from which they were collected. They were separated into two groups: Group A, larvae from the leaves of the plant head and Group B, larvae from the capsules. From these larvae, adults were obtained that mated and after the oviposition initiated, a cohort of recently emerged larvae of both groups was selected. They were disposed on leaves of tobacco to continue their development until adult death. In each group, the number of eggs per laying, the duration of the each development phase, and the main population parameters were recorded. The biological parameters showed significant differences in the larval and pupal duration and the life cycle that favored the specimens of the Group A, as in the population parameters. The results indicated that these parameters in the Group B population were affected by the change of food; however, a high reproductive capacity was evident in both groups when the specimens fed on leaves of the plant head, and the potentiality of both populations as pest of this crop was confirmed. [ABSTRACT FROM AUTHOR]

We sought to test within- and between- family associations of smoking during pregnancy (SDP) and attention deficit-hyperactivity disorder (ADHD) symptoms using a structured interview based on the conventional Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) symptoms and the Strengths and Weaknesses of ADHD-Symptoms and Normal-Behavior (SWAN) scale, which is a population based measure that grew out of the notion that an ADHD diagnosis exists on the extreme end of a continuum of normative behaviors and includes both above- and below- average performance on attention and activity. We used a sibling-comparison approach in a sample of 173 families including siblings aged 7-16 years (52% male) drawn from the state of Missouri, USA, wherein mothers smoked during one pregnancy but not the other. There was a within-family effect of smoking during pregnancy on SWAN hyperactivity/impulsivity and SWAN total ADHD behaviors. The associations between SDP and DSM-IV-based ADHD symptom dimensions as well as SWAN inattention were explained by familial confounds. These findings suggest that SDP exerts a potentially causal effect on increased ADHD hyperactive/impulsive behaviors and that this SDP effect is best captured when hyperactivity/impulsivity is assessed more normatively across the population, rather than specifically assessing problematic behaviors via DSM symptoms. Thus, any potentially causal effect of SDP on ADHD symptom dimensions may be restricted to hyperactive/impulsive behaviors rather than inattention, and normative, non-DSM-IV based behavioral measures may provide a more sensitive test of mechanisms of SDP-ADHD symptom associations, particularly in non-clinical samples. [ABSTRACT FROM AUTHOR]

There are higher rates of menthol cigarette smoking within certain population subgroups. Limited research has examined menthol use among individuals in treatment for substance use disorders (SUD), a population with a high prevalence of cigarette smoking, poor smoking cessation outcomes, and high tobacco disease burden. Survey data were collected from 863 smokers sampled from 24 SUD treatment programs affiliated with the NIDA Clinical Trials Network (CTN) in the United States. Prevalence of menthol cigarette smoking was examined for the sample. Bivariate and multivariate analyses were used to examine demographic and tobacco use characteristics associated with menthol cigarette smoking. Overall, the prevalence of menthol smoking among individuals in SUD treatment was 53.3%. Smoking menthol versus non-menthol cigarettes was associated with being female (AOR=1.61, p=0.003), African American (AOR=7.89, p<0.001), Hispanic/Latino (AOR=3.39, p<0.001), and lower odds of having a college degree (AOR=0.49, p=0.015). Controlling for demographic factors, menthol smokers were more likely to report marijuana (AOR=3.33, p<0.007) as their primary drug compared to alcohol. Lastly, menthol smokers were more likely to report interest in getting help for quitting smoking (AOR=1.53, p=0.01), although they were not more likely to report making a past year quit attempt. In conclusion, use of menthol cigarettes was higher among smokers in SUD treatment than in general population smokers. Regulatory policies targeting the manufacture, marketing, or sale of menthol cigarettes may benefit vulnerable populations, including smokers in SUD treatment. [ABSTRACT FROM AUTHOR]

Introduction: Contemporary state-specific estimates of mortality caused by cigarette smoking are important for tobacco control advocacy and healthcare planning in the U.S., but are currently lacking.Methods: The population-attributable fraction (i.e., proportion of deaths in the population caused by smoking), number of deaths, and number of years of potential life lost because of active cigarette smoking were estimated for each state based on state-specific smoking prevalence data from the 2014 Behavioral Risk Factor Surveillance System, recently updated relative risks of smoking, and numbers of deaths from smoking-attributable diseases. Analyses were performed in 2017.Results: In 2014, active cigarette smoking caused an estimated 448,865 deaths (258,456 men and 190,409 women), representing 17.8% (95% CI=17.7%, 17.9%) of all deaths at age >35 years in the U.S. These deaths resulted in the premature loss of 6,387,021 years of life in 2014. Across states, population-attributable fractions ranged from 12.4% in Utah to 25.2% in Arkansas in men, and from 7.0% in Utah to 20.0% in Nevada in women. Cigarette smoking caused >20% of all deaths in seven states (Kentucky, Arkansas, Nevada, Tennessee, West Virginia, Oklahoma, and Missouri). California had the highest number of smoking-attributable deaths (n=38,182) and years of potential life lost (508,370 years), despite a relatively low population-attributable fraction (16.2%).Conclusions: Cigarette smoking continues to cause a substantial proportion of deaths in every state, with the highest population-attributable fractions in Nevada and the South. The continuing high burden in states with longstanding tobacco control, like California, highlights the need for enhanced tobacco control in all states. [ABSTRACT FROM AUTHOR]

Background: Given background sparsity of country-specific literature evidence, and the pervasive unhealthy lifestyle habits such as tobacco, alcohol use, and high sugar consumption among fishermen, the aim of this study was to assess the oral health status and associated lifestyle factors among Malaysian fishermen in Teluk Bahang, Penang.Subjects and Methods: In an analytical cross-sectional design, we used simple random sampling technique to select 242 multiracial Malaysian male fishermen aged between 18 and 75 years from five fishing villages located at Gurney Drive, Tanjong Tokong, Tanjong Bungah, Batu Ferringhi, and Teluk Bahang to participate in this study. During four consecutive weekends in January 2017, we conducted face-to-face interviews with participants using a pre-validated, interviewer-administered WHO oral health questionnaire. We categorized participants as having "good" or "poor" oral health based on a mean cutoff score of 14. Multivariate regression models were fitted to assess the oral health status and associated lifestyle factors among the study population, using SPSS version 22.Results: We achieved a response rate of 97.6%. Overall, the prevalence of poor oral health in this study was 47.5%. "Income" (RM/month), "type of fishing," "additional occupation," "age" (years), "frequency of pies, buns consumed," and "frequency of sweets, soft drinks consumed" were significant predictors of oral health status among the fishermen.Conclusion: Poor oral health is relatively highly prevalent among the fishermen in our study. The oral health status of fishermen in Teluk Bahang was consistent with the national average and significantly associated with their sociodemographic and lifestyle factors. Targeted interventions are required to arrest and reverse this trend. [ABSTRACT FROM AUTHOR]

Background and Objectives: Cigarette smoking is one of the major global health issues. Accurate measurement of smoking is essential for accepting patterns of adolescent smoking behavior and for the evaluation of health education programs aimed at reducing or preventing the habit. The aim of the present study was to estimate and compare the salivary thiocyanate levels in young adult smokers and nonsmokers and also to evaluate and correlate the cellular and nuclear changes in cytological smears with salivary thiocyanate levels. Materials and Methods: The study included a total of 70 individuals in the age range of 18–25 years comprising of 35 smokers and 35 nonsmokers. A volume of 2 ml unstimulated whole saliva samples were collected by spitting method and were carried in a vaccine carrier with ice pack to the laboratory to avoid biochemical changes. Each sample was analyzed on the same day of collection by spectrophotometric method. In addition, cytosmears were prepared using Cytobrush® plus and stained with rapid Papanicolaou stain for cytological evaluation. Results: Salivary thiocyanate levels were significantly higher in smokers than nonsmokers. When these levels were compared with pack-years, there was a progressive significant increase in salivary thiocyanate levels as the pack-years increased. Duration of habit showed no statistically significant effect on salivary thiocyanate levels. Cytological evaluation revealed increase in nuclear-cytoplasmic area ratio and number of micronuclei in smokers than nonsmokers. The correlation between salivary thiocyanate levels and cytological changes showed insignificant result. Conclusion: Salivary thiocyanate levels were significantly higher in smokers than controls and showed significant correlation with the number of pack years. Although the present study failed to reveal any significant correlation between salivary thiocyanate level and cytological alterations, few early alterations in the oral mucosa even in the absence of clinical manifestations were detected by exfoliative cytology. Salivary thiocyanate determination is a safe, inexpensive, noninvasive method to differentiate early smokers from nonsmokers. [ABSTRACT FROM AUTHOR]

Aims: Oral squamous cell carcinoma (OSCC) primarily occurs in older age group. However, in the recent years, incidence of oral cancer in young people has been on rise worldwide. Towards this end, we sought to analyze the clinical and histopathological characteristics of OSCC in patients less than 45 years of age. Materials and Methods: The clinical and histological features of patients diagnosed with squamous cell carcinoma of the oral cavity at two hospitals in the coastal Karnataka region of South India between 1996-2012 were reviewed. The tabulation and descriptive statistics of the study were carried out. Results: A total of 420 patients were treated for OSCC in the 17-year period (1996-2012), of which 86 (20.5 %) patients were under 45 years of age. The most common site of involvement among the young was tongue (29.07%) and buccal mucosa (27.9%) respectively. A total of 47 (54.65%) patients were either habitual chewers, smokers, or alcoholics. Pathological grading of cases classified tumors into well differentiated (34.88%), moderately differentiated (46.51%) and poorly differentiated (4.65%). Conclusions: The data from this study reveals that a significant proportion of the OSCC cases are observed in patients of 45 years or younger. Additionally, our study also indicated an increase in the usage of tobacco and pan chewing in young adults in comparison to older individuals in the two hospitals of South India. The data obtained from this analysis emphasizes the need for screening programs that are tailor-made for individuals at high risk of developing oral cancer and warrants tobacco awareness programs in the community. [ABSTRACT FROM AUTHOR]

Background: Cigarette smoking has severe adverse health consequences in adults and in the offspring of mothers who smoke during pregnancy. One of the most widely reported effects of smoking during pregnancy is reduced birth weight which is in turn associated with chronic disease in adulthood. Epigenome-wide association studies have revealed that smokers show a characteristic "smoking methylation pattern", and recent authors have proposed that DNA methylation mediates the impact of maternal smoking on birth weight. The aims of the present study were to replicate previous reports that methylation mediates the effect of maternal smoking on birth weight, and for the first time to investigate whether the observed mediation effects are sex-specific in order to account for known sex-specific differences in methylation levels. Methods: Methylation levels in the cord blood of 313 newborns were determined using the Illumina HumanMethylation450K Beadchip. A total of 5,527 CpG sites selected on the basis of evidence from the literature were tested. To determine whether the observed association between maternal smoking and birth weight was attributable to methylation, mediation analyses were performed for significant CpG sites. Separate analyses were then performed in males and females. Results: Following quality control, 282 newborns eventually remained in the analysis. A total of 25 mothers had smoked consistently throughout the pregnancy. The birthweigt of newborns whose mothers had smoked throughout pregnancy was reduced by >200g. After correction for multiple testing, 30 CpGs showed differential methylation in the maternal smoking subgroup including top "smoking methylation pattern" genes AHRR, MYO1G, GFI1, CYP1A1, and CNTNAP2. The effect of maternal smoking on birth weight was partly mediated by the methylation of cg25325512 (PIM1); cg25949550 (CNTNAP2); and cg08699196 (ITGB7). Sex-specific analyses revealed a mediating effect for cg25949550 (CNTNAP2) in male newborns. Conclusion: The present data replicate previous findings that methylation can mediate the effect of maternal smoking on birth weight. The analysis of sex-dependent mediation effects suggests that the sex of the newborn may have an influence. Larger studies are warranted to investigate the role of both the identified differentially methylated loci and the sex of the newborn in mediating the association between maternal smoking during pregnancy and birth weight. [ABSTRACT FROM AUTHOR]

We investigated the involvement of two avirulence genes, avrA ( ripAA in unified nomenclature) and popP1 ( ripP1 in unified nomenclature), of Japanese Ralstonia solanacearum strains in the pathogenicity to tobacco. One virulent strain OE1-1 and four hypersensitive response (HR)-eliciting strains, 8107, MAFF 211471, MAFF 211496, and MAFF 301520, were used. While 8107 and MAFF 211471 contain popP1 , other three strains do not. When popP1 of strain 8107 was transferred into the virulent strain OE1-1, the transconjugant strain had significantly reduced virulence but did not become a HR-eliciting strain. We deleted avrA and/or popP1 from the HR-eliciting strains; all deletion mutants still elicited a HR and did not become virulent to tobacco, although leaf lesion appearance was delayed on infection with avrA mutants. These results indicate that although avrA and popP1 could be functional as avirulence determinants, other unidentified factors are necessary for full virulence or HR elicitation by Japanese R. solanacearum strains. [ABSTRACT FROM AUTHOR]

Cognitive impairment in HIV-1 infection is associated with the induction of chronic proinflammatory responses in the brains of infected individuals. The risk of HIV-related cognitive impairment is increased by cigarette smoking, which induces brain inflammation in rodent models. To better understand the role of smoking and the associated immune response on behavioral and motor function in HIV infection, wild-type F344 and HIV-1 transgenic (HIV1Tg) rats were exposed to either smoke from nicotine-containing (regular) cigarettes, smoke from nicotine-free cigarettes, or to nicotine alone. The animals were then tested using the rotarod test (RRT), the novel object recognition test (NORT), and the open field test (OFT). Subsequently, brain frontal cortex from the rats was analyzed for levels of TNF-α, IL-1, and IL-6. On the RRT, impairment was noted for F344 rats exposed to either nicotine-free cigarette smoke or nicotine alone and for F344 and HIV1Tg rats exposed to regular cigarette smoke. Effects from the exposures on the OFT were seen only for HIV1Tg rats, for which function was worse following exposure to regular cigarette smoke as compared to exposure to nicotine alone. Expression levels for all three cytokines were overall higher for HIV1Tg than for F344 rats. For HIV1Tg rats, TNF-α, IL-1, and IL-6 gene expression levels for all exposure groups were higher than for control rats. All F344 rat exposure groups also showed significantly increased TNF-α expression levels. However, for F344 rats, IL-1 expression levels were higher only for rats exposed to nicotine-free and nicotine-containing CS, and no increase in IL-6 gene expression was noted with any of the exposures as compared to controls. These studies, therefore, demonstrate that F344 and HIV1Tg rats show differential behavioral and immune effects from these exposures. These effects may potentially reflect differences in the responsiveness of the various brain regions in the two animal species as well as the result of direct toxicity mediated by the proinflammatory cytokines that are produced by HIV proteins and by other factors that are present in regular cigarette smoke. [ABSTRACT FROM AUTHOR]

Atherosclerotic Cardiovascular Diseases are the leading cause of death worldwide. Aim. To estimate the prevalence of cardiovascular risk (CVR) categories in the adult population (aged 40-79 years) of Romania. Design. The present study was part of the epidemiological, cross-sectional PREDATORR study (PREvalence of DiAbeTes mellitus, prediabetes, overweight, Obesity, dyslipidemia, hyperuricemia and chronic kidney disease in Romania). Subjects and Methods. Exclusion criteria: age <40/or>79 years old and diagnosis of ischemic vascular disease. The CVR was evaluated using charts developed by the World Health Organization/International Society of Hypertension (WHO/ISH) available for Europe B (epidemiological subregion where Romania was included). The CVR was divided into 5 categories: <10%, 10-20%, 20-30%, 30-40%, > 40%. Results. A total of 1631 subjects (57.0±10.7 years, 45.1% males) were included in the present study. The age and sex-adjusted prevalence of CVR >40% was 2.9% (95%CI 2.8-3.1%), CVR 30-40% was 1.85% (95%CI 1.8-1.9%), CVR 20-30% was 5.8% (95%CI 5.6-6.0%) and 13.0% (95%CI 12.8-13.3%) of the adult Romanian population has a 10-20% CVR, these CVR categories being more frequent in male and older age. Diabetes, overweight/obesity and smoking were associated with high CVR categories. Conclusion. Romania is one of the countries with high CVR, requiring CVD prevention measures. [ABSTRACT FROM AUTHOR]

Adverse health effects of airborne particulate matter depend on parameters like particle size, particle surface and chemical composition. Major emission of indoor particles is caused by combustion processes like tobacco smoking and cooking. Nevertheless, the use of household electrical appliances, such as vacuum cleaners, flat irons or hair dryers, can produce particles as well. In this study the emissions of different hair dryers and flat irons were investigated using a test chamber. The particle number concentrations, particle volume concentrations, as well as the size distributions were measured. Particles were sampled and analyzed by electron microscopy, inductively coupled plasma mass spectrometry and gas chromatography mass spectrometry. Moreover different volatile organic compounds (VOCs) were measured. Each tested appliance, especially flat irons produced small particles with diameters far below 100 nm and might be a nonnegligible source for indoor particles. Copper was the main identified element in most of the particles emitted from hair dryers, but in the emission of two hair dryers silver-containing nanoparticles were found as well. Various VOCs were observed in the emission of both flat irons and hair dryers, while cyclic siloxanes were detected only in the emission of flat irons. The use of flat irons or hair dryers may significantly contribute to the personal particle exposure. [ABSTRACT FROM AUTHOR]

Introduction: Nicotine dependence (ND) is a chronic, relapsing mental disorder characterized by compulsive cigarette seeking and smoking. Although the cerebellum plays an increasingly implicated role in ND, the exact cerebellar alterations in ND remain unclear. Identifying the localization of these cerebellar abnormalities in ND may help to further understand the role of the cerebellum in ND. Thus, we investigated the structural and functional alterations in the cerebellum in a large sample of smokers using the spatially unbiased infratentorial template (SUIT).Methods: High-resolution structural magnetic resonance imaging (MRI) data were acquired from 85 smokers and 41 nonsmokers. We applied voxel-based morphometry (VBM) and the SUIT cerebellar atlas to compare the cerebellar gray matter (GM) volume between smokers and nonsmokers. Using resting-state functional MRI data, we also performed seed-based functional connectivity (FC) analysis to examine the functional correlates of the GM volume changes.Results: Both VBM and lobular analyses revealed smaller GM volume in the bilateral Crus I in smokers. The GM volume of the left Crus I was inversely correlated with the severity of nicotine dependence as assessed by Fagerström Test for Nicotine Dependence (r = -.268, p = .013). We also found reduced FC between the bilateral Crus I and brain regions involved in the default mode network and motor system, as well as the frontal and temporal cortex in smokers.Conclusions: Our results indicate that decreased cerebellar GM volume and corticocerebellar FC are associated with ND, and these may underlie the core ND phenotypes, including automatized smoking behavior, cognitive, and emotional deficits.Implications: As smoking remains a worldwide public health problem, identifying the related neural alterations may help to understand the pathophysiology of ND. Based on previous findings in the cerebellum, we investigated the localization of the GM differences and related FC changes in ND subjects. Our findings highlight altered corticocerebellar circuits in ND, suggesting an association between the cerebellum and the phenotypes of ND. [ABSTRACT FROM AUTHOR]

Background: Water-pipe smoking (WPS) is the most widespread tobacco use in the Middle-East, and is rapidly spreading globally. Smoke from WP contains most of the compounds present in cigarette smoke, although in different proportions. WPS is associated with the risk of several human diseases; however, its impact on the early stage of normal development has not been investigated yet. Thus, in this investigation, we assess the effect of WPS on the embryo at the early stage of development.Methods: Chicken embryos at 3 days of incubations were used in this study. Meanwhile, we explored the outcome of WPS on angiogenesis using the chorioallantoic membrane (CAM) of the chicken embryos. Finally, quantitative real-time polymerase chain reaction was used to study the regulation of some key control genes of cell proliferation, apoptosis, and migration.Results: Our data reveal that WPS inhibits angiogenesis of the CAM and in embryos in comparison with their matched controls; in addition, WPS-exposed embryos show slight reduction in their sizes. We also noted that around 80% of WPS-exposed embryos die before 10 days of incubation. More significantly, WPS induces upregulations of BCL-2, Caspase-8, ATF-3, INHIB-A, and Cadherin 6 genes, which are important key regulators of cell apoptosis, proliferation, and migration.Conclusion: Our data reveal, for the first time, that WPS has very toxic effects during the early stage of embryogenesis. Thus, we believe that further studies are required to elucidate the pathogenic effect of WPS on human health especially on the embryo at the early stage of its development.Implications: This investigation addresses an important gap on the outcome of WPS during the early stage of embryogenesis. Data of this study point out that WPS can have a very toxic effect on the embryo at this stage. Additionally, results from this report display for the first time that WPS can damage normal angiogenesis of the embryo thus provoking a significant number of embryonic death. Moreover, this study reveals that this effect can occur via the deregulation of several genes related to cell apoptosis, proliferation, and migration. [ABSTRACT FROM AUTHOR]

Introduction: National data suggest tobacco smoke is positively associated with higher glycated hemoglobin (HbA1c) among adults. Our objective was to examine the association between serum cotinine and HbA1c among adolescents without known diabetes. Methods: We assessed adolescents 12-19 years old (N = 11 550) who participated in the 1999-2012 National Health and Nutrition Examination Survey. We applied sampling weights while performing multiple linear regression analyses. Results: The prevalence of serum cotinine indicative of no tobacco smoke exposure (TSE, <0.05 ng/mL) was 43.2%, passive TSE (0.05-2.99 ng/mL) was 38.9%, and active TSE (>3 ng/mL) was 17.9% in our sample. Mean (± standard error) HbA1c in participants with no TSE was 5.16% (±0.01), passive TSE was 5.16% (±0.01), and active TSE was 5.14% (±0.01). No differences in HbA1c were found between TSE groups including sex, age, race/ethnicity, education, income, and physical activity or the fully adjusted model with waist circumference. We found cotinine × sex (p = .01) and cotinine × age (p = .02) interactions. There was an association between cotinine and HbA1c for males but not females. Within males, participants with cotinine ≥3 ng/mL (5.26 ± 0.02) had higher mean HbA1c than those with cotinine 0.05-2.99 ng/mL and <0.05 ng/mL (both 5.20 ± 0.01, p ≤ .02). The negative association between age and HbA1c was stronger for participants with cotinine ≥3 ng/mL than participants with cotinine <0.05 ng/mL. Conclusion: No linear association was found between HbA1c and serum cotinine in adolescents overall after adjusting for potential confounders. Differences between TSE groups were found in males. Future research in adolescents should examine chronic TSE over time to examine the potential for development of type 2 diabetes. Implications: TSE has been associated with increased risk for the development of type 2 diabetes among adults. It is unclear if this relationship holds in adolescents. We examined the association between serum cotinine and HbA1c in adolescents without known diabetes who completed the 1999-2012 National Health and Nutrition Examination Survey. Although no association was found between serum cotinine and HbA1c overall while controlling for potential confounding factors, we observed interaction effects that are indicative of TSE influencing HbA1c differentially by sex and age. Reducing TSE in adolescents should be a priority for future tobacco control efforts. [ABSTRACT FROM AUTHOR]

Introduction: Genetic variants associated with nicotine dependence have previously been identified, primarily in European-ancestry populations. No genome-wide association studies (GWAS) have been reported for smoking behaviors in Hispanics/Latinos in the United States and Latin America, who are of mixed ancestry with European, African, and American Indigenous components.Methods: We examined genetic associations with smoking behaviors in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) (N = 12 741 with smoking data, 5119 ever-smokers), using ~2.3 million genotyped variants imputed to the 1000 Genomes Project phase 3. Mixed logistic regression models accounted for population structure, sampling, relatedness, sex, and age.Results: The known region of CHRNA5, which encodes the α5 cholinergic nicotinic receptor subunit, was associated with heavy smoking at genome-wide significance (p ≤ 5 × 10-8) in a comparison of 1929 ever-smokers reporting cigarettes per day (CPD) > 10 versus 3156 reporting CPD ≤ 10. The functional variant rs16969968 in CHRNA5 had a p value of 2.20 × 10-7 and odds ratio (OR) of 1.32 for the minor allele (A); its minor allele frequency was 0.22 overall and similar across Hispanic/Latino background groups (Central American = 0.17; South American = 0.19; Mexican = 0.18; Puerto Rican = 0.22; Cuban = 0.29; Dominican = 0.19). CHRNA4 on chromosome 20 attained p < 10-4, supporting prior findings in non-Hispanics. For nondaily smoking, which is prevalent in Hispanic/Latino smokers, compared to daily smoking, loci on chromosomes 2 and 4 achieved genome-wide significance; replication attempts were limited by small Hispanic/Latino sample sizes.Conclusions: Associations of nicotinic receptor gene variants with smoking, first reported in non-Hispanic European-ancestry populations, generalized to Hispanics/Latinos despite different patterns of smoking behavior.Implications: We conducted the first large-scale genome-wide association study (GWAS) of smoking behavior in a US Hispanic/Latino cohort, and the first GWAS of daily/nondaily smoking in any population. Results show that the region of the nicotinic receptor subunit gene CHRNA5, which in non-Hispanic European-ancestry smokers has been associated with heavy smoking as well as cessation and treatment efficacy, is also significantly associated with heavy smoking in this Hispanic/Latino cohort. The results are an important addition to understanding the impact of genetic variants in understudied Hispanic/Latino smokers. [ABSTRACT FROM AUTHOR]

Introduction: Smoking prevalence, cigarettes per day (CPD), and lung cancer incidence differ between Northern Plains (NP) and Southwest (SW) American Indian populations. We used cotinine as a biomarker of tobacco smoke exposure to biochemically characterize NP and SW smokers and nonsmokers and to investigate factors associated with variation in tobacco exposure.Methods: American Indians (N = 636) were recruited from two different tribal populations (NP and SW) as part of a study conducted as part of the Collaborative to Improve Native Cancer Outcomes P50 project. For each participant, a questionnaire assessed smoking status, CPD, second-hand smoke exposure, and traditional ceremonial tobacco use; plasma and/or salivary cotinine was measured.Results: Cotinine levels were (mean ± 95% confidence interval [CI]) 81.6 ± 14.1 and 21.3 ± 7.3 ng/ml among NP smokers and non-mokers, respectively, and 44.8 ± 14.4 and 9.8 ± 5.8 ng/ml among SW smokers and nonsmokers, respectively. Cotinine levels correlated with CPD in both populations (p < .0001). Cotinine ≥15 ng/ml was measured in 73.4% of NP smokers and 47.8% of SW smokers and in 19.0% of NP nonsmokers and 10.9% of SW nonsmokers. Ceremonial traditional tobacco use was associated with higher cotinine among NP smokers only (p = 0.004). Second-hand smoke exposure was associated with higher cotinine among NP non-smokers (P < 0.02). More secondhand smoke exposure was associated with smoking more CPD in both populations (p = 0.03-0.29). Linear regression modeling mirrored these findings.Conclusions: High prevalence of smoking in the Northern Plains and high cotinine levels among nonsmokers in both regions highlights the tribal populations' risk for tobacco-related disease.Implications: There is a high prevalence of smoking in Northern Plains American Indians. Among Northern Plains and Southwest nonsmokers, relatively high cotinine levels, representative of high tobacco exposure, suggest considerable exposure to second-hand smoke. It is critical to highlight the extent of second-hand smoke exposure among the Northern Plains and Southwest American Indians and to enhance efforts to initiate smoke-free policies in tribal communities, which are not subject to state-level polices. [ABSTRACT FROM AUTHOR]