What Is the Real Impact of Smoking on Diseases Alleged to Benefit from It?

Position Statement on Tobacco Exposures in Children and Families

The 1964 report of the US Surgeon General on smoking and health made an authoritative case that tobacco smoking was a cause of premature deaths from lung cancer and chronic bronchitis. It justified the practice of drawing causal inferences from epidemiological studies, specified influential criteria for doing so, and made use of an early form of meta-analysis.

Cigarette smoking is emerging as a strong risk factor in the otherwise unknown etiology of chronic inflammatory diseases. Whether the same applies also to smokeless tobacco remains unknown. Nicotine is a powerful modifier of the inflammatory response. By comparing risks associated with tobacco smoking and with smokeless tobacco, the role of nicotine in the development of chronic inflammation may be evaluated. To assess and compare the risks of rheumatoid arthritis (RA), ulcerative colitis (UC), Crohn's disease (CD), sarcoidosis, and multiple sclerosis (MS) associated with cigarette smoking and with the use of Swedish moist snuff. We performed a cohort study of 277,777 males within a cohort of Swedish construction workers who had provided information about tobacco use in 1978-1993. Cross-linkage to the nationwide Swedish Hospital Discharge Register provided information about the occurrence of RA, UC, CD, sarcoidosis, and MS through 2004. Age-adjusted relative risks (RRs) associated with smoking and moist snuff, respectively, were estimated by Cox regression. Ever-smoking was associated with an increased risk for RA (RR, 2.1; 95% confidence interval [CI], 1.7-2.5), CD (RR, 1.5; 95% CI, 1.2-1.8), MS (RR, 1.9; 95% CI, 1.4-2.6), and UC (RR, 1.3; 95% CI, 1.1-1.5, confined to ex-smokers), and a decreased risk of sarcoidosis (RR, 0.5; 95% CI, 0.4-0.5). By contrast, ever-use of moist snuff, adjusted for smoking, was not associated with RA (RR, 1.0; 95% CI, 0.9-1.2), UC (RR, 1.1; 95% CI, 0.9-1.2), CD (RR, 0.9; 95% CI, 0.8-1.1), sarcoidosis (RR, 1.1; 95% CI, 0.8-1.5), or MS (RR, 1.0; 95% CI, 0.8-1.4). Smokeless tobacco does not increase the risk of chronic inflammatory diseases, suggesting that inhaled nonnicotinic components of cigarette smoke are more important than nicotine itself in the etiology of these diseases.

Inflammatory bowel disease in children and adolescents: Working Group Report of the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition.

The Spectrum of Smoking-Related Interstitial Lung Disorders: The Never-Ending Story of Smoke and Disease

Cigarette smoking and rheumatoid arthritis

The Greatest International Killer

Endometriosis, polycystic ovary syndrome (PCOS) and uterine fibroids have been proposed as endometrial cancer risk factors; however, disentangling their relationships with endometrial cancer is complicated due to shared risk factors and comorbidities. Using genome-wide association study (GWAS) data, we explored the relationships between these non-cancerous gynecological diseases and endometrial cancer risk by assessing genetic correlation, causal relationships and shared risk loci. We found significant genetic correlation between endometrial cancer and PCOS, and uterine fibroids. Adjustment for genetically predicted body mass index (a risk factor for PCOS, uterine fibroids and endometrial cancer) substantially attenuated the genetic correlation between endometrial cancer and PCOS but did not affect the correlation with uterine fibroids. Mendelian randomization analyses suggested a causal relationship between only uterine fibroids and endometrial cancer. Gene-based analyses revealed risk regions shared between endometrial cancer and endometriosis, and uterine fibroids. Multi-trait GWAS analysis of endometrial cancer and the genetically correlated gynecological diseases identified a novel genome-wide significant endometrial cancer risk locus at 1p36.12, which replicated in an independent endometrial cancer dataset. Interrogation of functional genomic data at 1p36.12 revealed biologically relevant genes, including WNT4 which is necessary for the development of the female reproductive system. In summary, our study provides genetic evidence for a causal relationship between uterine fibroids and endometrial cancer. It further provides evidence that the comorbidity of endometrial cancer, PCOS and uterine fibroids may partly be due to shared genetic architecture. Notably, this shared architecture has revealed a novel genome-wide risk locus for endometrial cancer.

Objective: Gynaecologic benign diseases such uterine fibroids share similar pathogeneses with endometrial and ovarian cancers. Whether a history of uterine fibroids increases the risk of developing endometrial or ovarian cancers is controversial, due to uterine fibroids was self-reported in those studies.Methods: In our current case-control study, 268 women with endometrial cancer and 108 women with ovarian cancer were included. In addition, 500 women without gynaecological cancers were randomly selected as a control group. Uterine fibroids in both groups were clinically diagnosed by pelvic examination and ultrasound. Data on age, parity, gravida, stages of cancers and history of uterine fibroids, endometriosis and adenomyosis were collected from hospital database.Results: After adjusted age and parity, the odds of women with history of uterine fibroids or endometriosis were lower in women with endometrial cancer than controls (odds ratio: 0.148, 95% CI: 0.097, 0.225, or 0.360, 95% CI: 0094, 1.381, respectively). The odds of women with a history of uterine fibroids or endometriosis were lower in women with ovarian cancer than controls (odds ratio: 0.141, 95% CI: 0.085, 0.235, or 1.057, 95% CI: 0.377, 2.963, respectively). However, the odds of women with a history of adenomyosis were higher in women with endometrial or ovarian cancers than controls (odd ratio: 3.757, 95% CI: 1.858, 7.599 or 2.341, 95% CI: 1.086, 5.045, respectively).Conclusion: Our observational data suggested that uterine fibroids or endometriosis may be not associated with the increased risk of developing endometrial or ovarian cancer. However, a history of adenomyosis may do.

The prevalence rate of smoking among psychiatric patients has been shown to be higher than that among the general population, and this may have several neuropsychiatric implications. This cross-sectional study examines the prevalence, sociodemographic variables and pattern of smoking among psychiatric outpatients in Saudi Arabia. Over a period of 18 months (January 1996 to June 1997), 505 outpatients from five different hospitals were randomly selected to participate in the study. It was observed that 292 patients (57.83%) were current smokers, 199 (39.4%) were nonsmokers and 14 patients (2.77%) were ex-smokers. Besides revealing certain attitudes towards smoking and religious antismoking notions, it was observed that unemployment, low education status, rural background, and drug abuse were significantly associated with smoking. The prevalence rate of smoking revealed in this study is consistent with international data, and probably has implications similar to those reported in other studies. This study also found certain patterns of tobacco use in psychiatric outpatients characterized by certain sociodemographic variables and drug abuse.

The Tobacco Endgame-Eradicating a Worsening Epidemic: A Joint Opinion From the American Heart Association, World Heart Federation, American College of Cardiology, and the European Society of Cardiology.

Smoking increases the risk of developing seropositive rheumatoid arthritis (RA) by 50% on average, and is associated with a reduced response to RA drug treatments. This talk will focus on...

e17561 Background: Contribution of local inflammation to the course of endometrial cancer (EC) is of interest since it may aggravate the disease. Methods: The study included 25 women aged 62+1.6 years with histologically verified EC (group 1a), 29 women aged 48+8.4 years with uterine fibroids (UF) (group 1b) and 13 non-cancer women aged 42+2.3 years (group 2, controls). Vaginal swabs were taken prior to antitumor treatment. Relative expression of genes encoding the synthesis of IL1B, IL10, IL18, TNFA, TLR4, GATA3, and CD68 in comparison with the reference gene B2M was determined by Real-time PCR using the ImmunoQuantex kit (Russia). An integral parameter of an inflammation index was calculated using binary logistics, and the ratios of the listed indicators were also calculated. 12 parameters were analyzed in total. Groups Ia and Ib were compared with healthy people (p1) and with each other (p2). Results: 4 of 12 studied parameters in EC patients differed from control; no differences were found in UF patients. 7 statistically significant differences were registered between EC and UF. Relative expression of the gene encoding the synthesis of IL10 was maximal in EC (2.8+0.2 vs. 1.8+0.3 in healthy women (p1= 0.006) and 1.8+0.2 in UF (p2= 0.002)). The IL10/IL18 ratio in EC statistically significantly exceeded the ratios in UF patients and in healthy women (61.4+21.7 (p1= 0.003), 46.3+32.2 (p2< 0.001) and 53.7+47.1 respectively). The TNFA/IL18 ratio in EC patients was also higher than in UF patients (1.1+0.7 vs. 0.5+0.2 (p2= 0.035)) due to higher TNFA levels (3.7+0.1 vs. 3.3+0.1 (p2= 0.006)), one of which effects includes stimulation of neoangiogenesis. The ratio of TLR4/GATA3, on the contrary, was lower in EC than in UF (0.7+0.3 and 1.5+0.9 respectively (p2= 0.001). Apparently, it characterized antimicrobial immunity because both of these genes are involved in the response to PAMP (TLR4) and in the genesis of intraepithelial lymphocytes related to innate immunity, as well as in the development of a humoral response via stimulation of Th2 (GATA3). The latter, in addition, is involved in the ontogenesis some organs, including the vagina and uterus. The highest TLR4/GATA3 ratio was found in UF, which, in our opinion, indicated the predominance of the inflammatory process in UF and local immunosuppression in EC. The inflammation index determined with the ImmunoQuantex test system did not differ between the studied groups of women. Conclusions: Some differences were observed in local reactions of immunity and inflammation in benign and malignant uterine tumors, involving the prevalence of immunosuppressive and angiogenic factors in EC and inflammatory factors in UF.

Cadmium (Cd) is a persistent and widespread environmental pollutant, which may constitute a potential risk factor for hormone-dependent tumors such as endometrial cancer. The vascular endothelium is an important target of cadmium toxicity, which may interfere with the coagulation cascade and fibrinolytic system. The aim of this research was to investigate whether in female patients with uterine endometrial cancer or myoma in comparison to healthy women, the concentration of cadmium in blood affects the process of coagulation and fibrinolysis. The study group comprised 91 women: 35 healthy (A-control), 39 with uterine myoma (B) and 17 with endometrial cancer (C), in which blood cadmium concentrations (BCd), coagulation and selected fibrinolysis parameters in plasma were assayed. In the women with myoma and especially in those with endometrial cancer disturbances in coagulation and fibrinolysis were detected when compared to the healthy women. In the group of women with endometrial cancer significant changes in prothrombin index, levels of fibrinogen, fibrin D-dimer and t-PA were observed. Whereas, in the patients with myoma significant changes in prothrombin time, index of vWillebrand Factor and fibrin D-dimer level were noted. Mean BCd concentrations in subsequent groups were as follows: B - 0.91±0.81; C - 0.78±0.45 μg Cd/l and did not differ significantly in comparison with the control group (0.86±0.35 μg Cd/l). However, in each study group smokers had approximately twice as high BCd as non-smokers. Studies also showed significant associations between BCd and fibrinogen level and thrombin time among the women with myoma and endometrial cancer, as well as in healthy women. Moreover, thrombin time significantly correlated with fibrinogen level in the women studied. In the patients with myoma and especially in these with endometrial cancer disturbances in coagulation and fibrinolysis parameters leading to hypercoagulability were detected. Exposure to cadmium can be one of the factors inducing these changes.

As the most preventable cause of death in the world today, understanding tobacco use among one of the fastest growing ethnic/racial groups is warranted. We explore cigarette and smokeless tobacco (SLT) use among South Asians in NJ and the Northeast using the Tobacco Use Supplement to the Current Population Survey. Overall, tobacco use rates among South Asians were similar or lower than the population. However, in NJ, South Asian males had the highest SLT rate (2.7%) and in the Northeast, White (AOR = 5.8, 95% CI = 3.7–9.4) and South Asian males (AOR = 4.0, 95% CI = 1.5–10.6) had significantly higher odds of current SLT use relative to non-White males. Tobacco use among South Asians was not homogeneous; Pakistanis are overrepresented among cigarette smokers while Indians are overrepresented among SLT users. Given the differential tobacco use among and within South Asian, disaggregating data to understand tobacco use behaviors is necessary to develop effective interventions for tobacco cessation.