BERKELEY, CA (UroToday.com) - Globally, prostate cancer is a leading cause of cancer death, only surpassed by lung cancer, however, the etiology of prostate cancer is still unknown. Chronic inflammation has been suspected as an important environmental factor that can cause cancer. A recent study revealed that the cause of chronic inflammation in cancer patients was chronic infection in 20%, tobacco smoking and inhaled pollutants in 30%, and dietary factors in 35%. Individual risk and incidence of prostate cancer may result from the interaction of genetic susceptibility with exposure to environmental factors such as infectious agents, tobacco, occupational exposure, dietary carcinogens, and/or hormonal imbalances leading to injury to the prostate as well as to the development of chronic inflammation. Inflammation is now regarded as an important hallmark of cancer.
The objective of this study was to explore the pro-inflammatory levels in prostate carcinoma patients by evaluating the serum levels of novel cytokine interleukin-18 (IL-18) expression in a tobacco exposed population. A total of 578 (n = 284 biopsy proven prostate cancer patients, n = 294 controls (with and without tobacco exposure) were enrolled. Serum IL-18 (Interleukin-18) level was determined by ELISA. Tobacco exposure increased the inflammation in prostate carcinoma patients, in the stratified group, as it has been suspected as a risk factor in various cancers, but this study further revealed its role of influencing inflammation, especially in prostate carcinoma.
Exposure to diverse exogenous agents, such as chemicals in a working environment, and over a long time period, may influence the physiological and biochemical metabolism. This study was conducted in the densely populated north-Indian region to evaluate the association of various modes of tobacco consumption with inflammation in prostate cancer patients by examining the serum IL-18 pro-inflammatory levels. Our study offers evidence that tobacco chewing and smoking may be important contributors to inflammation.
Exposure Factors
The exposure factors were recorded in cases and controls, which included tobacco use (smoking and chewing form tobacco) and alcohol intake. Tobacco habit was classified into smokers and chewers (use of non-smoking tobacco as powder or in beetle leaf or areca nut, catechu) and non users (as those who were not smoking, chewing and drinking). A detailed description of tobacco products exposure and their corresponding IL-18 levels have been presented in the original manuscript.
The Interleukin-18 (Pro-inflammatory) trends and tobacco exposure
Tobacco Smokers
The current study showed the relationship between various modes of smoking on IL-18 levels as compared to the control population. We found that the IL-18 levels in tobacco smokers were high compared to controls. The IL-18 levels differed according to the mode of tobacco exposure, and the highest level was seen in bidi smokers, followed by cigarette smokers, chillum, hookah (bidis > cigarette>chillum>hookah).Within the control group, IL-18 levels with statistically high in tobacco smokers as compared to non-users. Similarly, significantly high levels of IL-18 were found in cigarette and bidi smokers as compared to non-users while it was not significant with chillum and hookah smokers. In men with cancer, the IL-18 levels differed significantly (P < 0.05) among cigarette, bidi, hookah, chillum smokers as compared to non-users. On comparing the IL-18 levels between cancer patients and controls with the same mode of exposure, statistically significant (P < 0.0001) differences in levels were found in cancer patients who were bidi and cigarette smokers than control bidi and cigarette users.
Tobacco Chewers
The relation between IL-18 levels with various forms of chewed tobacco also showed unique trends. Among tobacco chewer groups, mean IL-18 levels showed a specific trend with the levels being highest in khaini chewers, followed by gutkha and betel quid chewers (khaini > gutkha > betel quid chewers). The levels of IL-18 were statistically significantly raised in cancer patients (who chewed tobacco in any form) as compared to controls. However, on comparing non-user controls with betel quid and gutkha user controls then the difference was not statistically significant.
Tobacco Exposure in Combination with Alcohol
The mean level of IL-18 was highest in men who consumed all three (chewing and smoking tobacco and alcohol (CSA)). This was followed by men who were smokers and alcohol consumers (SA) followed by men who consumed alcohol only, and then followed by chewers and alcohol consumers (CA) (CSA > SA > alcohol (only) > CA). The IL-18 levels in cancer patients were significantly higher in men who were CSA users, SA users, and men who were drinkers as compared to cancer patients who were non-users. On comparing the IL-18 levels between cancer patients and controls with the same exposure, men in CSA and SA groups showed significant differences (P < 0.01) from controls.The IL-18 levels were significantly higher (P < 0.05) in men who were chewers and smokers as compared to non-users, for stages III and IV cancer.
Limitations
This study may be enhanced by including a larger sample size and some parameters like various occupational exposures, dietary factors, living area as rural, urban, and industrial, etc., but we tried to reduce biases by including patients from all occupational sites who came for treatment during the study period.
Conclusions
Tobacco exposure has been determined to be an important risk factor in the development of various cancers, and this study provides further evidence that tobacco use seems to influence inflammation, especially in prostate carcinoma.
Written by:
Shailendra Dwivedi,1 Apul Goel,2 Sanjay Khattri,1 and Kamlesh Kumar Pant1, # as part of Beyond the Abstract on UroToday.com. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc... of their research by referencing the published abstract.
1 Department of Pharmacology and Therapeutics, Chhatrapati Sahuji Maharaj Medical University (Erstwhile KGMU), Lucknow, India
2 Department of Urology, Chhatrapati Sahuji Maharaj Medical University (Erstwhile KGMU), Lucknow, India
#Corresponding Author:
Kamlesh Kumar Pant
Department of Pharmacology and Therapeutics,King George Medical University (Erstwhile CSMMU), Lucknow, India
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