Differential Effects Of Smoking Research Articles

Differential effects of cigarette smoking on cardiovascular disease in females: A narrative review and call to action

ObjectiveCigarette smoking continues to be a major driver in the incidence and progression of cardiovascular disease (CVD). As females become an increasingly larger fraction of those who smoke it is imperative that the sex-specific effects of smoking be further explored and acted upon. MethodsThis narrative review describes current evidence on the differential effects of smoking on CVD in females and the need to improve treatment. ResultsEvidence to date suggests that smoking has disproportionately negative effects on the cardiovascular (CV) system in females, especially in those who are younger. Usually, the onset of CVD is later in females than males, but smoking decreases or eliminates this gap. Females are also more likely to develop types of CVD closely tied to smoking, such as ST-elevated myocardial infarctions, with even higher rates among those who are younger. Possible mechanisms for these worse outcomes in females include a complex interplay between nicotine, other products of combusted cigarettes, and hormones. Sex differences also exist in treatment for smoking. In females, Varenicline appears more effective than either Bupropion or nicotine replacement therapy while in males, all three therapies show similar efficacy. Disparities in smoking are also apparent in secondary prevention settings. Females and males are entering secondary prevention with equal rates of smoking, with potentially higher levels of exposure to the byproducts of smoking in females. ConclusionsThese disproportionately negative outcomes for females who smoke require additional research and these persisting rates of smoking suggest a need for female-specific approaches for treating smoking.

Differential Effect of Smoking on Gene Expression in Head and Neck Cancer Patients.

Smoking is a well-known behavior that has an important negative impact on human health, and is considered to be a significant factor related to the development and progression of head and neck squamous cell carcinomas (HNSCCs). Use of high-dimensional datasets to discern novel HNSCC driver genes related to smoking represents an important challenge. The Cancer Genome Atlas (TCGA) analysis was performed in three co-existing groups of HNSCC in order to assess whether gene expression landscape is affected by tobacco smoking, having quit, or non-smoking status. We identified a set of differentially expressed genes that discriminate between smokers and non-smokers or based on human papilloma virus (HPV)16 status, or the co-occurrence of these two exposome components in HNSCC. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways classification shows that most of the genes are specific to cellular metabolism, emphasizing metabolic detoxification pathways, metabolism of chemical carcinogenesis, or drug metabolism. In the case of HPV16-positive patients it has been demonstrated that the altered genes are related to cellular adhesion and inflammation. The correlation between smoking and the survival rate was not statistically significant. This emphasizes the importance of the complex environmental exposure and genetic factors in order to establish prevention assays and personalized care system for HNSCC, with the potential for being extended to other cancer types.

Differential effects of smoking and COPD upon circulating myeloid derived suppressor cells

Chronic obstructive pulmonary disease (COPD) is characterized by an enhanced and persistent innate and acquired immune response to tobacco smoking. Myeloid-derived suppressor cells (MDSCs) modulate T-cell responses by down-modulating the T cell receptor ζ chain (TCR ζ) through the catabolism of l-arginine. The effects of smoking on MDSCs and their potential participation in COPD immunopathogenesis have not been explored so far. To investigate it, we compared the level of circulating Lineage-/HLA-DR-/CD33+/CD11b+ MDSCs, the serum concentration of arginase I (ARG I) and the expression of peripheral T-cell receptor ζ chain (TCR ζ) in never smokers, smokers with normal spirometry and COPD patients. Flow cytometry was used to quantify circulating MDSCs and TCR ζ expression. Serum ARG I levels were determined by ELISA. The main findings of this study were that: (1) current smoking upregulates and activates circulating MDSCs both in smoker controls and COPD patients; and, (2) at variance with the smokers with normal spirometry, in patients with COPD this effect persists after quitting smoking and is accompanied by a significant and specific down-regulation of the TCR ζ chain expression in circulating T lymphocytes. Smoking modulates circulating MDSCs. Their regulation appears altered in patients with COPD.

Disparities in health care utilization by smoking status in Canada

To examine the association between smoking status and the utilization of health care services in Canada. The study uses data from the 2007 Canadian Community Health Survey, which contains information on the number of visits to general practitioner (GP), specialists (SP) and the number of nights spent in a hospital. The finite mixture estimation method is used in order to account for heterogeneity among smokers. Multivariate regression results indicate differential effects of smoking on health care utilization for at least two different groups of health care users: low and high users. In particular, we find that among the low-use group, smokers use less GP and SP services than never smokers. However, for the low-use and high-use groups, smokers have more hospitalizations than never smokers. The incidence of hospitalization is higher for the low-use group after controlling for need, socio-demographic characteristics and province fixed effects. Former smokers who recently quit use more health care services. Tobacco consumption elevates the use of health care services, especially among the high-use group.

Risk of Chronic Bronchitis in Twin Pairs Discordant for Smoking

It is well known that smoking is a major risk factor for lung disease and respiratory symptoms. We examined the association between smoking and the risk of chronic bronchitis in a large twin sample. In a population-based questionnaire study of 13,649 twins, aged 50-71years, from the Danish Twin Registry, we identified 1,146 twin pairs, discordant for a lifetime history smoking. We performed co-twin control analysis to examine the impact of smoking on the risk of chronic bronchitis. The prevalence of chronic bronchitis was 9.7%. In the total sample, high age, living without a spouse, and smoking remained statistically significant predictors with an up to tenfold increased risk of chronic bronchitis in the heaviest smokers compared with never-smokers, after multivariate adjustment. Among twin pairs discordant for smoking, chronic bronchitis was significantly more common in the smoking twin compared with the nonsmoking co-twin. There was no differential effect of smoking on the risk of chronic bronchitis in monozygotic and dizygotic twins. The risk of chronic bronchitis increases with age and increasing tobacco consumption. The results indicate a direct relationship between smoking and development of chronic bronchitis, but other environmental factors, such as exposure to household smoking in childhood and living without a spouse, also play a role.

P50 amplitude reduction: a nicotinic receptor-mediated deficit in first-degree relatives of schizophrenia patients

Impaired P50 gating is a putative index of genetically mediated nicotinic dysfunction in schizophrenia. However, assessment is confounded, in patients, by differential effects of smoking, symptoms, and treatment. This double-blind placebo-controlled study was designed to tease apart the relationships among P50, acute and chronic nicotine exposure, and familial risk. Experiment 1: To assess the putative effects of genetic vulnerability without other confounds, 14 unaffected relatives of schizophrenia patients and 15 controls, all nonsmokers, were tested with/without 7 mg transdermal nicotine. Family members had reduced P50 amplitude to an initial auditory stimulus, but normal P50 gating. Nicotine decreased P50 amplitude in controls; family members had a mixed response: eight decreased and six increased P50 amplitude with nicotine. Experiment 2: To assess chronic nicotine use and short-term withdrawal as a model of nicotinic dysfunction, 26 healthy smokers (14 abstinent for >12 h) received 21 mg transdermal nicotine. Chronic nicotine use, alone, did not alter P50 amplitude or gating. Short-term withdrawal resulted in decreased P50 amplitude, with no effect on P50 gating. Nicotine increased P50 amplitude in abstinent smokers and decreased it in nonabstinent smokers. Familial vulnerability to schizophrenia reduces P50 amplitude. Nicotinic modulation of this deficit mirrors the effect of nicotine during smoking abstinence and suggests an "inverted-U" relationship between P50 amplitude and endogenous nicotinic activity. P50 amplitude may, therefore, be a sensitive marker of nicotinic dysfunction in individuals with familial risk for schizophrenia, which is mediated through mechanisms (e.g., α₄β₂ receptors) that are distinct from those (e.g., α₇ receptors) that mediate P50 gating.

Prevalence of obesity and abdominal obesity in the Lausanne population.

BackgroundObesity can be defined using body mass index (BMI) or waist (abdominal obesity). Little information exists regarding its prevalence and determinants in Switzerland. Hence, we assessed the levels of obesity as defined by BMI or waist circumference in a Swiss population-based sample.MethodsCross-sectional, population-based non-stratified random sample of 3,249 women and 2,937 men aged 35–75 years living in Lausanne, Switzerland. Overall participation rate was 41%.ResultsIn men, the prevalences of overweight (BMI ≥25 kg/m2) and obesity (BMI ≥30 kg/m2) were 45.5% and 16.9%, respectively, higher than in women (28.3% and 14.3%, respectively). The prevalence of abdominal obesity (waist ≥102 in men and ≥88 cm in women) was higher in women than in men (30.6% vs. 23.9%). Obesity and abdominal obesity increased with age and decreased with higher educational level in both genders. In women, the prevalence of obesity was lower among former and current smokers, whereas in men the prevalence of obesity was higher in former smokers but did not differ between current and never smokers. Multivariate analysis showed age to be positively related, and education and physical activity to be negatively related with obesity and abdominal obesity in both genders, whereas differential effects of smoking were found between genders.ConclusionThe prevalence of abdominal obesity is higher than BMI-derived obesity in the Swiss population. Women presented with more abdominal obesity than men. The association between smoking and obesity levels appears to differ between genders.

The effect of solar UVB doses and vitamin D production, skin cancer action spectra, and smoking in explaining links between skin cancers and solid tumours

The report of differences between skin cancer rates and solid tumours in sunny versus less sunny countries [Tuohimaa P, Pukkala E, Scelo G, et al. Does solar exposure, as indicated by the non-melanoma skin cancers, protect from solid cancers: Vitamin D as a possible explanation. Eur J Cancer 2007; 43: 1701–12] raised some important questions regarding the roles of solar ultraviolet (UV) irradiance and cancer risk. The findings can likely be explained based on the effects of UVB dose on cancer risk, the action spectra of different skin cancers, the amount of skin exposed, and the differential effects of smoking on cancer risk. Solar UVB has been found inversely correlated with about 20 types of cancer in ecological and cohort studies in sunny countries. Vitamin D and calcium were recently found to greatly reduce cancer incidence in a prospective double-blind study. Epidemiological studies suggest that the action spectra for skin cancers vary, with solar UVB most important for squamous cell carcinoma, UVA most important for melanoma, and both important for basal cell carcinoma. These differences may explain the different standardised incidence ratios for solid tumours with respect to the different skin cancers in sunny countries. Smoking has been reported as a risk factor for non-melanoma skin cancers, but has been found inversely correlated with melanoma, which may explain some of the differences in standardised incidence ratios for solid tumours linked to smoking with respect to type of skin cancer. In Nordic countries, less skin is generally exposed (in head and neck regions, the most frequent sites of squamous cell carcinoma) resulting in reduced vitamin D production.

Differential effects of smoking on myocardial infarction risk according to to the Gln/Arg 192 variants of the human paraoxonase gene

Paraoxonase (PON1) seems to exert a major antioxidant effect by removing lipid peroxidation products. A common polymorphism of the PON1 gene modulates paraoxonase activity and has been related in some studies to coronary heart disease. PON1 genetic polymorphism includes PON1 Q, an isoform with a low activity toward paraoxon hydrolysis that has a glutamine at position 192, and PON1 R, the high-activity isoform with an arginine at position 192. In the present study, we investigated whether smoking, which is related to increased susceptibility to lipoprotein oxidation, has a differential effect by PON1-192 genotype on the risk of myocardial infarction (MI). One hundred fifty-six consecutive MI patients and 310 control subjects were studied. PON1 genotypes in the controls were distributed as follows: 154 (49.7%) QQ, 123 (39.7%) QR, and 33 (10.6%) RR. This distribution did not significantly differ from that of the MI patients: 84 (53.8%) QQ, 60 (38.5%) QR, and 12 (7.7%) RR. Subjects were classified into two groups, those who never smoked (n = 209) and those who were current smokers (n = 135) or ex-smokers (n = 122). In the latter, the variable "cigarette packs smoked per year" was defined as the number of packs smoked daily multiplied by the number of smoking years. As expected, smoking was significantly associated with an increased MI risk in the overall group. Subjects were then stratified by PON1 genotype. The packs smoked per year were significantly associated with an increased MI risk only in QQ homozygotes. This risk was higher among those in the higher tertile for cigarette packs smoked per year (odds ratio [OR] = 5.24, 95% confidence interval = 1.67 to 16.44, Pfor trend <.001). In contrast, the packs smoked per year were not significantly associated with MI risk in R-carrier subjects. We conclude that the risk of MI associated with smoking appears to be increased in subjects who are homozygous for the low-activity PON1 QQ genotype compared with R carriers, and this risk seems to be time- and dose-dependent.

Differential effects of cigarette smoking and alcohol consumption on the plasma levels of carotenoids in middle-aged Japanese men.

Although several studies have reported that cigarette smoking and alcohol consumption are inversely associated with the plasma level of beta‐carotene even after adjustment for dietary carotene intake, their effects on other carotenoids have not been examined extensively. The authors examined the associations of smoking and alcohol with plasma levels of the five principal carotenoids (beta‐carotene, alpha‐carotene, lutein, lycopene, and zeaxanthin). The subjects were 634 apparently healthy men aged 40–49 years who were sampled randomly from five areas in Japan with varying rates of mortality from gastric cancer. Multiple linear regression analysis controlling for age, serum total cholesterol, serum triglycerides, body mass index, and consumption frequencies of green vegetables, yellow vegetables and fruit, showed that both smoking and alcohol had a significant inverse association with the plasma levels of beta‐carotene and alpha‐carotene; only smoking reduced the level of lutein, and neither smoking nor alcohol significantly affected the level of lycopene or zeaxanthin. With regard to the reduction of beta‐carotene and alpha‐carotene, the effect of smoking was smaller in drinkers than in nondrinkers, and the effect of alcohol was smaller in smokers than in nonsmokers, and significant interactions between smoking and alcohol were observed (P=0.034 for beta‐carotene and 0.026 for alpha‐carotene). The results indicate that the differential effects of smoking and alcohol should be considered when the health effects of plasma carotenoids are examined.

Semen characteristics of tobacco users in India.

Qualitative analysis of semen samples have been compared between 79 different types of tobacco addicts (smokers, chewers, and multiple addicts) with 21 nonaddicts (never consumed any form of tobacco). The percentage of motile sperm and total sperm count of the tobacco chewers are significantly low (p < .05). The frequency of abnormal sperm is also significantly high (p < .001) for smoking and multiple addict groups. Differential effects of smoking and chewing tobacco on sperm characteristics are discussed.