Abstract
Multiple diseases and disorders are connected with occupational and environmental exposure risk. It is also well-established that chemicals and chemical mixtures have an influence on the immune cells of humans. This is an important field of research that has been pursued extensively in relation to autoimmune illnesses, allergy/asthma, and lung cancer, but Prostate Carcinoma has received rare reports. Chronic chemical exposure is known to produce inflammation, which is one of the most prominent characteristics of all malignancies. Changes in the ratio of pro-inflammatory to anti-inflammatory molecules are thought to be a key factor in the emergence of inflammation. Prostate gland cells express the pro-inflammatory cytokine interleukin-18 (IL-18), which is a major facilitator of immunological responses. Conversely, interleukin-10 (IL-10) is an anti-inflammatory cytokine that is linked to immune responses and inhibits the development of an inflammatory environment. Our goal is to investigate the inflammatory status of IL-18 (pro-) and IL-10 (anti-) in a variety of occupationally exposed populations in patients with Benign Prostate Hyperplasia (BPH) and patients with Prostate Carcinoma. The present study was conducted with 664 subjects, comprising 285 Prostate Carcinoma patients, 94 BPH patients and 285 controls. The subjects of BPH and Prostate Carcinoma were screened and confirmed on the basis of Prostate Serum Antigen (PSA) and pathological biopsy. All subjects were categorized as per their occupational exposure into various groups. The pro-inflammatory and anti-inflammatory Interleukins (IL-18 and IL-10) and serum PSA levels were analysed by using corresponding quantitative ELISA kits. The results showed that as compared to control participants, the serum PSA levels were higher in the Prostate Carcinoma and BPH groups. When mean levels of IL-18 were compared between various occupational groups, Tanners (tanning industry), Agriculture, and Ordnance workers had significantly higher levels (P < 0.05) of IL-18 than sedentary workers. The pro-inflammatory cytokine (IL-18) levels were also found to be aggravated in Prostate Carcinoma compared to BPH and controls. According to the findings of the current study, the levels of inflammatory cytokines (IL-18 and IL-10) in various occupational groups of BPH, Prostate Carcinoma, and controls were altered. Long-term occupational exposure may have a negative influence on inflammation levels and the immune system; therefore, preventative measures should be explored for improved health.
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References
Ledda C, Loreto C, Zammit C, Marconi A, Fago L, Matera S, et al. Non infective occupational risk factors for hepatocellular carcinoma: a review. Mol Med Rep. 2017;15:511–33.
Dai Y, Ren D, Bassig BA, Vermeulen R, Hu W, Niu Y, et al. Occupational exposure to diesel engine exhaust and serum cytokine levels. Environ Mol Mutagen. 2018;59(2):144–50.
Brouwers MM, van Tongeren M, Hirst AA, Bretveld RW, Roeleveld N. Occupational exposure to potential endocrine disruptors: further development of a job exposure matrix. Occup Environ Med. 2009;66:607–14.
World Health Organisation (WHO), United Nations Environment Program (UNEP). State of the Science of Endocrine Disrupting Chemicals 2012;1/296.
Spinder N, Bergman JEH, van Tongeren M, Boezen HM, Kromhout H, de Walle HEK. Maternal occupational exposure to endocrine-disrupting chemicals and urogenital anomalies in the offspring. Hum Reprod. 2021;37(1):142–51.
Prins GS. Endocrine disruptors and prostate carcinoma risk. Endocr Relat Cancer. 2008;15(3):649–56.
Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell. 2010;140(6):883–99.
Pathak VM, Verma VK, Rawat BS, Kaur B, Babu N, Sharma A, et al. Current status of pesticide effects on environment, human health and it’s eco-friendly management as bioremediation: a comprehensive review. Front Microbiol. 2022;13:962619.
Terme M, Ullrich E, Aymeric L, Meinhardt K, Desbois M, Delahaye N, et al. IL-18 induces PD-1-dependent immunosuppression in cancer. Cancer Res. 2011;71:5393–9.
Dwivedi S, Goel A, Mandhani A, Khattri S, Sharma P, Misra S, et al. Functional genetic variability at promoters of pro-(IL-18) and anti-(IL-10) inflammatory affects their mRNA expression and survival in prostate carcinoma patients: Five year follow-up study. Prostate. 2015;75(15):1737–46.
Mattiuzzi C, Lippi G. Current cancer epidemiology. J Epidemiol Glob Health. 2019;9(4):217–22.
Zhao H, Wu L, Yan G, Chen Y, Zhou M, Wu Y, et al. Inflammation and tumor progression: signaling pathways and targeted intervention. Signal Transduct Target Ther. 2021;6(1):263.
Dwivedi S, Shukla KK, Gupta G, Sharma P. Non-invasive biomarker in prostate carcinoma: a novel approach. Indian J Clin Biochem. 2013;28(2):107–9.
Dwivedi S, Singh S, Goel A, Khattri S, Mandhani A, Sharma P, et al. Pro-(IL-18) and anti-(IL-10) inflammatory promoter genetic variants (intrinsic factors) with tobacco exposure (extrinsic factors) may influence susceptibility and severity of prostate carcinoma: a prospective study. Asian Pac J Cancer Prev. 2015;16(8):3173–81.
Dwivedi S, Goel A, Khattri S, Sharma P, Pant KK. Aggravation of inflammation by smokeless tobacco in comparison of smoked tobacco. Indian J Clin Biochem. 2015;30(1):117–9.
Dwivedi S, Goel A, Mandhani A, Khattri S, Pant KK. Tobacco exposure may enhance inflammation in prostate carcinoma patients: an explorative study in north Indian population. Toxicol Int. 2012;19(3):310–8. https://doi.org/10.4103/0971-6580.103681.
Cho Y, Lee J, Choi M, Choi W, Myong JP, Kim HR, et al. Work-related COPD after years of occupational exposure. Ann Occup Environ Med. 2015;19(27):6.
Lee IP, Suzuki K. Induction of aryl hydrocarbon hydroxylase activity in the rat prostate glands by 2, 3, 7, 8-tetrachlorodibenzop-dioxin. J Pharmacol Exp Ther. 1980;215:601–5.
Waalkes MP, Rehm S, Perantoni AO, Coogan TP. Cadmium exposure in rats and tumours of the prostate. IARC Sci Publ. 1992;118:391–400.
Dich J, Wiklund K. Prostate carcinoma in pesticide applicators in Swedish agriculture. Prostate. 1998;34:100–12.
Golden RJ, Noller KL, Titus-Ernstoff L, Kaufman RH, Mittendorf R, Stillman R, et al. Environmental endocrine modulators and human health: an assessment of the biological evidence. Crit Rev Toxicol. 1998;28:109–227.
Mitra S, Sarkar A, Sen S. Removal of chromium from industrial effluents using nanotechnology: a review. Nanotechnol Environ Eng. 2017;2:11. https://doi.org/10.1007/s41204-017-0022-y.
Grabinski CM, Methner MM, Jackson JM, Moore AL, Flory LE, Tilly T, et al. Characterization of exposure to byproducts from firing lead-free frangible ammunition in an enclosed, ventilated firing range. J Occup Environ Hyg. 2017;14(6):461–72.
Dalby O, Butler D, Birkett J. Analysis of gunshot residue and associated materials—a review. J Forensic Sci. 2010;55(4):924–43.
Engwa GA, Ferdinand PU, Nwalo FN, Unachukwu MN. Mechanism and health effects of heavy metal toxicity in humans. In: Karcioglu O, Arslan B, editors. Poisoning in the modern world—new tricks for an old dog? London: IntechOpen; 2019.
Alengebawy A, Abdelkhalek ST, Qureshi SR, Wang MQ. Heavy metals and pesticides toxicity in agricultural soil and plants: ecological risks and human health implications. Toxics. 2021;9(3):42.
Rea IM, Gibson DS, McGilligan V, McNerlan SE, Alexander HD, Ross OA. Age and age-related diseases: role of inflammation triggers and cytokines. Front Immunol. 2018;9:586.
Zhang JM, An J. Cytokines, inflammation, and pain. Int Anesthesiol Clin. 2007;45(2):27–37.
Sharma P, Dwivedi S. Prospects of molecular biotechnology in diagnostics: step towards precision medicine. Indian J Clin Biochem. 2017;32(2):121–3.
Funding
Shailendra Dwivedi is thankful to the Indian Council of Medical Research, New Delhi, for providing the grant of Senior Research Fellowship. The present research work was also supported by the grant from the Indian Council of Medical Research, New Delhi (2/2/204/2009-NCD-III), India.
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All authors were involved in the conception, design, and write-up of the article. SD, KKP, and SK planned the study, and AG was involved in providing samples with clinical guidance. PS and SD were involved in the analysis of the data.
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The study is performed on human participants, and the study was approved (Ref. code: XXXVII ECM/B-P12) by the institutional ethical committee of the King George Medical University, India. All personal identifiers (name, employer, contact) were removed from the data set, and analysis was carried out at the institute level.
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Dwivedi, S., Sharma, P., Goel, A. et al. Occupational and Environmental Exposure Influences the Inflammatory (Pro-and Anti-) Status in Benign Prostate Hyperplasia and Prostate Carcinoma Patients: A Retrospective Analysis. Ind J Clin Biochem 39, 241–247 (2024). https://doi.org/10.1007/s12291-023-01112-9
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DOI: https://doi.org/10.1007/s12291-023-01112-9