-
1.
Smoking and COVID-19: Adding Fuel to the Flame.
Kashyap, VK, Dhasmana, A, Massey, A, Kotnala, S, Zafar, N, Jaggi, M, Yallapu, MM, Chauhan, SC
International journal of molecular sciences. 2020;(18)
Abstract
The coronavirus disease 2019 (COVID-19) pandemic, an infection caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2), has led to more than 771,000 deaths worldwide. Tobacco smoking is a major known risk factor for severe illness and even death from many respiratory infections. The effects of smoking on COVID-19 are currently controversial. Here, we provide an overview of the current knowledge on the effects of smoking on the clinical manifestations, disease progression, inflammatory responses, immunopathogenesis, racial ethnic disparities, and incidence of COVID-19. This review also documents future directions of smoking related research in COVID-19. The current epidemiological finding suggests that active smoking is associated with an increased severity of disease and death in hospitalized COVID-19 patients. Smoking can upregulate the angiotensin-converting enzyme-2 (ACE-2) receptor utilized by SARS-CoV-2 to enter the host cell and activate a 'cytokine storm' which can lead to worsen outcomes in COVID-19 patients. This receptor can also act as a potential therapeutic target for COVID-19 and other infectious diseases. The COVID-19 pandemic sheds light on a legacy of inequalities regarding gender, racial, and ethnic health disparities associated with active smoking, thus, smoking cessation may help in improving outcomes. In addition, to flatten the COVID-19 curve, staying indoors, avoiding unnecessary social contact, and bolstering the immune defense system by maintaining a healthy diet/living are highly desirable.
-
2.
Catalog of exogenous risk factors for bladder carcinogenesis.
Jahrreiss, V, Pradere, B, Laukhtina, E, Mori, K, Shariat, SF
Current opinion in urology. 2020;(3):449-456
Abstract
PURPOSE OF REVIEW The aim of this article is to provide an overview of recent findings regarding the risk factors for bladder cancer. RECENT FINDINGS Most of the available data derive from retrospective analysis. Smoking represents the most common and important risk factor. Occupational, dietary, and environmental exogenic carcinogen exposure, as well as several lifestyle factors, can increase the risk of developing bladder cancer. SUMMARY Bladder cancer is a common malignancy worldwide. Cigarette smoking, exposure to aromatic amines and arsenic are known risk factors for bladder cancer. Evidence on other modifiable risk factors such as carcinogen exposure derived from the diet or environment as well as occupational hazards is still weak. Medical conditions leading to chronic inflammation, altering insulin resistance, negatively modulating the immune system and/or genetic alterations may have a role in bladder cancer carcinogenesis. Further studies are, however, necessary to identify possible exogenic risk factors, as well as their interactions, that partake in the carcinogenesis of bladder cancer.
-
3.
The interaction between smoking, alcohol and the gut microbiome.
Capurso, G, Lahner, E
Best practice & research. Clinical gastroenterology. 2017;(5):579-588
Abstract
The gastrointestinal microbiome is a complex echosystem that establishes a symbiotic, mutually beneficial relation with the host, being rather stable in health, but affected by age, drugs, diet, alcohol, and smoking. Alcohol and smoking contribute to changes in the stomach and affect H pylori-related disorders including the risk of gastric cancer. In the small intestine and in the colon alcohol causes depletion of bacteria with anti-inflammatory activity, eventually resulting in intestinal damage with "leaky gut". These changes contribute to hepatic damage in both alcoholic and non-alcoholic liver disease and have been associated with other disorders. Lactobacillus GG and A. muciniphila exert a protective effect in this setting. Smoking leads to modifications of the gut microbiome linked with a protective effect toward ulcerative colitis and deleterious for Crohn's disease. The exact cause-effect relation between alcohol and smoking and changes of the gastrointestinal microbiome needs further exploration with high throughput methodologies, and controlled studies are necessary to define the role of microbiome modulation on the immune response and systemic activation of pro-inflammatory pathways.
-
4.
Smoking in inflammatory bowel disease: impact on disease course and insights into the aetiology of its effect.
Parkes, GC, Whelan, K, Lindsay, JO
Journal of Crohn's & colitis. 2014;(8):717-25
Abstract
The chronic intestinal inflammation that characterises Crohn's disease and ulcerative colitis arises from a complex interplay between host genotype, the immune system, and the intestinal microbiota. In addition, environmental factors such as smoking impact on disease onset and progression. Individuals who smoke are more likely to develop Crohn's disease, and smoking is associated with recurrence after surgery and a poor response to medical therapy. Conversely, smoking appears protective against ulcerative colitis and smokers are less likely to require colectomy. The mechanism by which smoking exerts its impact on disease and the rational for the dichotomous effect in patients with Crohn's disease and ulcerative colitis is not clear. Recent evidence suggests that smoking induces alterations to both the innate and acquired immune system. In addition, smoking is associated with a distinct alteration in the intestinal microbiota both in patients with active Crohn's disease and healthy subjects.
-
5.
Environment and the inflammatory bowel diseases.
Frolkis, A, Dieleman, LA, Barkema, HW, Panaccione, R, Ghosh, S, Fedorak, RN, Madsen, K, Kaplan, GG, ,
Canadian journal of gastroenterology = Journal canadien de gastroenterologie. 2013;(3):e18-24
Abstract
Inflammatory bowel diseases (IBD), which consists of Crohn disease and ulcerative colitis, are chronic inflammatory conditions of the gastrointestinal tract. In genetically susceptible individuals, the interaction between environmental factors and normal intestinal commensal flora is believed to lead to an inappropriate immune response that results in chronic inflammation. The incidence of IBD have increased in the past century in developed and developing countries. The purpose of the present review is to summarize the current knowledge of the association between environmental risk factors and IBD. A number of environmental risk factors were investigated including smoking, hygiene, microorganisms, oral contraceptives, antibiotics, diet, breastfeeding, geographical factors, pollution and stress. Inconsistent findings among the studies highlight the complex pathogenesis of IBD. Additional studies are necessary to identify and elucidate the role of environmental factors in IBD etiology.
-
6.
Discovering the route from inflammation to pancreatic cancer.
Momi, N, Kaur, S, Krishn, SR, Batra, SK
Minerva gastroenterologica e dietologica. 2012;(4):283-97
-
-
Free full text
-
Abstract
Pancreatic cancer (PC) remains a complex malignancy with the worst prognosis, lack of early diagnostic symptoms and resistance to conventional chemo- and radiotherapies. A better understanding of the etiology and early developmental events of PC requires profound attention. The evolution of fully blown PC from initial pancreatic injury is a multi-factorial phenomenon with a series of sequential events. The initial acute infection or tissue damage triggers inflammation that, in conjunction with innate immunity, establishes a state of homeostasis to limit harm to the body. Recurrent pancreatic injuries due to genetic susceptibility, smoking, unhealthy diet, and alcohol abuse induces a pro-inflammatory milieu, consisting of various types of immune cells, cytokines, chemokines, growth factors and restructured extracellular matrix, leading to prolonged inflammatory/chronic conditions. Cells having sustained DNA damage and/or mutagenic assault take advantage of this prolonged inflammatory response and aid in the initiation and development of neoplastic/fibrotic events. Eventually, many tumor-stromal interactions result in a chaotic environment accompanied by a loss of immune surveillance and repair response, thereby leading to PC. A better understanding of the inflammatory markers defining this "injury-inflammation-cancer" pathway would help to identify novel molecular targets for early screening and therapeutic intervention for this lethal malignancy.
-
7.
Recent advances in the epidemiologic investigation of risk factors for asthma: a review of the 2011 literature.
Antó, JM
Current allergy and asthma reports. 2012;(3):192-200
Abstract
The present review aims to identify and summarize epidemiologic investigations published during 2011 on the environmental risk factors for asthma. Potentially eligible papers were identified by a MEDLINE search. In total, 1,130 items were retrieved. Based on a broad definition of environment, the following topics were included: obesity, diet, vitamin D, air pollution, farming environment, and social factors. Some of the more relevant contributions included evidence that 1) obesity precedes asthma, 2) fruit consumption is longitudinally associated with a lower risk of asthma and atopy, 3) a comprehensive statewide smoking ban was followed by a reduction in hospital admissions for asthma, 4) asthma is one of the diseases showing the largest burdens due to environmental tobacco smoke, 5) traffic-related urban air pollution is associated with bronchial inflammation as measured by fractional exhaled nitric oxide and uncontrolled asthma, 6) aeroallergens and desert dust may contribute to the short-term effects of air pollution and asthma, and 7) maternal exposure to air pollution before and during pregnancy may alter the immune competence in offspring.
-
8.
Postsurgical recurrence of ileal Crohn's disease: an update on risk factors and intervention points to a central role for impaired host-microflora homeostasis.
Cunningham, MF, Docherty, NG, Coffey, JC, Burke, JP, O'Connell, PR
World journal of surgery. 2010;(7):1615-26
Abstract
BACKGROUND A pressing need exists to identify factors that predispose to recurrence after terminal ileal resection for Crohn's disease (CD) and to determine effective prophylactic strategies. This review presents an up-to-date summary of the literature in the field and points to a role for bacterial overproliferation in recurrence. METHODS The literature (Medline, Embase, and the Cochrane Library, 1971-2009) on ileal CD and postoperative recurrence was searched, and 528 relevant articles were identified and reviewed. RESULTS Smoking is a key independent risk factor for recurrence. NOD2/CARD15 polymorphisms and penetrating phenotype are associated with aggressive disease and higher reoperation rates. Age at diagnosis, disease duration, gender, and family history are inconsistent predictors of recurrence. Prophylactic 5-aminosalicylic acid therapy and nitromidazole antibiotics are beneficial. Combination therapies with immunosuppressants are also effective. Anti-TNFalpha-based regimens show benefit but the evidence base is small. Corticosteroid, interleukin-10, and probiotic therapies are not effective. Wider, stapled anastomotic configurations are associated with reduced recurrence rates. Strictureplasty and laparoscopic approaches have similar long-term recurrence rates to open resection techniques. Length of resection and presence of microscopic disease at resection margins do not influence recurrence. A lack of consensus exists regarding whether the presence of granulomas or plexitis affects outcome. CONCLUSIONS Current evidence points to defects in mucosal immunity and intestinal dysbiosis of either innate (NOD2/CARD15) or induced (smoking) origin in postoperative CD recurrence. Prophylactic strategies should aim to limit dysbiosis (antibiotics, side-to-side anastomoses) or prevent downstream chronic inflammatory sequelae (anti-inflammatory, immunosuppressive, and immunomodulatory therapy).
-
9.
Vitamin C metabolites, independent of smoking status, significantly enhance leukocyte, but not plasma ascorbate concentrations.
Moyad, MA, Combs, MA, Vrablic, AS, Velasquez, J, Turner, B, Bernal, S
Advances in therapy. 2008;(10):995-1009
Abstract
INTRODUCTION The objective of this study was to test the effects of acute doses of vitamin C alone, calcium ascorbate with vitamin C metabolites, and placebo, on total plasma and leukocyte vitamin C concentrations over 24 hours. METHODS A double-blind, placebo-controlled, four-way crossover study was performed consisting of four separate phases lasting 24 hours each and utilizing one of four oral 1000-mg preparations within each phase (one of vitamin C alone, two separate vitamin C formulations of calcium ascorbate with vitamin C metabolites, and placebo). There was a 7-day washout between phases, and blood draws at seven time points within each phase of the study for a total of 28 serologic measurements per subject and 420 total measurements for the entire clinical trial. Vitamin C concentration in plasma and leukocytes were measured by high-performance liquid chromatography at baseline and at six sequential time periods over 24 hours. RESULTS Fifteen healthy males were enrolled, aged 18-39 years; nine were had never smoked and six were chronic smokers. No significant difference in plasma vitamin C levels was observed when comparing the different preparations. However, at 24 hours, calcium ascorbate with metabolites resulted in significantly higher concentrations of vitamin C in leukocytes (P<0.0001) compared with vitamin C alone. These results were similar for both metabolite formulations, and independent of smoking status. CONCLUSION Regardless of smoking status, vitamin C metabolites may enhance leukocyte utilization of vitamin C itself, despite no consistent difference in plasma levels among the different preparations. A larger clinical investigation is warranted to confirm these preliminary findings, and to determine the clinical relevance of this impact on overall immune function.
-
10.
Vitamin E supplementation may transiently increase tuberculosis risk in males who smoke heavily and have high dietary vitamin C intake.
Hemilä, H, Kaprio, J
The British journal of nutrition. 2008;(4):896-902
Abstract
Vitamin E and beta-carotene affect the immune function and might influence the predisposition of man to infections. To examine whether vitamin E or beta-carotene supplementation affects tuberculosis risk, we analysed data of the Alpha-Tocopherol Beta-Carotene Cancer Prevention (ATBC)Study, a randomised controlled trial which examined the effects of vitamin E (50 mg/d) and beta-carotene (20 mg/d) on lung cancer. The trial was conducted in the general community in Finland in 1985-93; the intervention lasted for 6.1 years (median). The ATBC Study cohort consists of 29,023 males aged 50-69 years, smoking at baseline, with no tuberculosis diagnosis prior to randomisation. Vitamin E supplementation had no overall effect on the incidence of tuberculosis (risk ratio (RR) = 1.18; 95% CI 0.87, 1.59) nor had beta-carotene (RR = 1.07; 95% CI 0.80, 1.45). Nevertheless, dietary vitamin C intake significantly modified the vitamin E effect. Among participants who obtained 90 mg/d or more of vitamin Cin foods (n 13,502), vitamin E supplementation increased tuberculosis risk by 72 (95% CI 4, 185)%. This effect was restricted to participants who smoked heavily. Finally, in participants not supplemented with vitamin E, dietary vitamin C had a negative association with tuberculosis risk so that the adjusted risk was 60 (95% CI 16, 81)% lower in the highest intake quartile compared with the lowest. Our finding that vitamin E seemed to transiently increase the risk of tuberculosis in those who smoked heavily and had high dietary vitamin C intake should increase caution towards vitamin E supplementation for improving the immune system.