Journal of the Pancreas Open Access

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Mini Review - (2024) Volume 25, Issue 1

Environmental Triggers and Pancreatic Disease: Unraveling Etiological Links
Ana Pires*#
1The Discoveries Centre for Regenerative and Precision Medicine, Portugal
#Equally contribution
*Correspondence: Ana Pires, The Discoveries Centre for Regenerative and Precision Medicine, Portugal, Email:

Published: 20-Feb-2024, DOI: 10.35841/1590-8577-25.1.844




Pancreatic diseases, encompassing conditions such as pancreatic cancer, chronic pancreatitis, and pancreatic cysts, pose significant health challenges worldwide. While genetic factors play a crucial role, environmental triggers also contribute substantially to disease development and progression. Understanding the complex interplay between environmental exposures and pancreatic disease is essential for elucidating underlying mechanisms, identifying at-risk populations, and implementing preventive strategies. This review explores the diverse environmental factors implicated in pancreatic diseases, examining their etiological links and implications for clinical management [1].

Pancreatic cancer is characterized by its aggressive nature and poor prognosis, with environmental exposures playing a significant role in disease pathogenesis. Cigarette smoking is the most well-established environmental risk factor for pancreatic cancer, accounting for approximately 20-25% of cases. Tobacco smoke contains carcinogenic compounds that induce DNA damage, promote inflammation, and alter pancreatic cell physiology, contributing to tumor initiation and progression. Additionally, dietary factors such as high consumption of red and processed meats, saturated fats, and sugar-sweetened beverages have been linked to an increased risk of pancreatic cancer [2].

These dietary components may promote chronic inflammation, insulin resistance, and oxidative stress, creating a pro-carcinogenic microenvironment within the pancreas. Chronic pancreatitis, characterized by persistent inflammation and fibrosis of the pancreas, represents a significant risk factor for pancreatic cancer development. Alcohol abuse is the leading cause of chronic pancreatitis in Western countries, accounting for approximately 70% of cases. Chronic alcohol consumption leads to pancreatic injury, acinar cell damage, and ductal obstruction, culminating in inflammation and fibrosis [3].

Furthermore, exposure to occupational carcinogens such as polycyclic aromatic hydrocarbons (PAHs), found in certain industrial settings like metalworking and coal mining, has been associated with an increased risk of pancreatic cancer. PAHs exert their carcinogenic effects through the formation of DNA adducts and the generation of reactive oxygen species, contributing to genomic instability and malignant transformation [4].

Chronic pancreatitis results from a complex interplay of genetic predisposition, environmental factors, and lifestyle choices. While alcohol abuse is the predominant environmental trigger, other factors such as cigarette smoking, obesity, and dietary habits also contribute to disease development. Cigarette smoking increases the risk of chronic pancreatitis by promoting pancreatic inflammation, impairing pancreatic blood flow, and altering the composition of pancreatic secretions. Similarly, obesity and dietary factors such as high-fat and high-calorie diets exacerbate pancreatic inflammation and oxidative stress, accelerating the progression of chronic pancreatitis [5].

Exposure to environmental toxins and pollutants has emerged as a potential risk factor for chronic pancreatitis. Industrial chemicals, heavy metals, and pesticides have been implicated in pancreatic toxicity, leading to cellular injury, inflammation, and fibrosis. Moreover, infectious agents such as hepatitis viruses and Helicobacter pylori may contribute to pancreatic inflammation and fibrosis through direct infection or immune-mediated mechanisms. Understanding the impact of environmental exposures on pancreatic health is essential for implementing preventive measures and reducing the burden of chronic pancreatitis on affected individuals and healthcare systems [6].

Pancreatic cysts are fluid-filled lesions that vary in etiology, ranging from benign pseudocysts to premalignant or malignant neoplasms. While the majority of pancreatic cysts are asymptomatic and incidental findings on imaging studies, a subset may progress to invasive pancreatic cancer. Environmental factors such as smoking, obesity, and dietary habits influence the development and progression of pancreatic cysts through their effects on inflammation, oxidative stress, and metabolic dysfunction. Cigarette smoking, in particular, has been associated with an increased risk of developing pancreatic cysts, with heavier smokers exhibiting a higher prevalence of cystic lesions [7].

Obesity and metabolic syndrome, characterized by insulin resistance and dyslipidemia, contribute to pancreatic cyst formation through their effects on adipokine secretion, chronic inflammation, and pancreatic stellate cell activation. High-calorie diets rich in saturated fats and processed sugars exacerbate metabolic dysfunction and promote pancreatic cyst growth and malignant transformation. Additionally, exposure to environmental toxins and pollutants, including heavy metals, pesticides, and industrial chemicals, may increase the risk of developing pancreatic cysts by inducing pancreatic injury, inflammation, and fibrosis [8].

Despite significant advances in understanding the environmental determinants of pancreatic diseases, several challenges remain. The complex interplay between genetic susceptibility, environmental exposures, and lifestyle factors complicates risk assessment and disease prevention efforts. Moreover, the heterogeneity of pancreatic diseases necessitates multidisciplinary approaches integrating epidemiological, clinical, and molecular data to identify high-risk populations and implement targeted interventions [9].

Longitudinal studies are needed to elucidate the cumulative effects of environmental exposures on pancreatic health and to identify modifiable risk factors that can be targeted for preventive interventions. Furthermore, public health initiatives aimed at reducing tobacco use, promoting healthy dietary habits, and minimizing exposure to environmental toxins are essential for mitigating the burden of pancreatic diseases on population health [10].


Environmental triggers play a significant role in the etiology of pancreatic diseases, including pancreatic cancer, chronic pancreatitis, and pancreatic cysts. Cigarette smoking, alcohol consumption, dietary factors, occupational exposures, and environmental toxins exert diverse effects on pancreatic health, contributing to disease initiation, progression, and complications. Understanding the complex interplay between genetic and environmental factors is essential for identifying at-risk populations, implementing preventive measures, and improving clinical management strategies for pancreatic diseases. Continued research efforts aimed at unraveling the etiological links between environmental exposures and pancreatic diseases are essential for reducing the global burden of these devastating conditions.


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  1. Dedrick S, Sundaresh B, Huang Q, Brady C, Yoo T, Cronin C, et al. The role of gut microbiota and environmental factors in type 1 diabetes pathogenesis. Front Endocrinol (Lausanne). 2020;11:78. [PMID: 32174888]
  2. Esposito S, Toni G, Tascini G, Santi E, Berioli MG, Principi N. Environmental factors associated with type 1 diabetes. Front Endocrinol (Lausanne). 2019;10:592. [PMID: 35937815]
  3. Kohil A, Al-Asmakh M, Al-Shafai M, Terranegra A. The interplay between diet and the epigenome in the pathogenesis of type-1 diabetes. Front Nutr. 2021;7:612115. [PMID: 33585535]
  4. Raza F, Evans L, Motallebi M, Zafar H, Pereira-Silva M, Saleem K, et al. Liposome-based diagnostic and therapeutic applications for pancreatic cancer. Acta Biomater. 2023;157:1-23. [PMID: 36521673]
  5. style="text-align: right;">Andreone L, Gimeno ML, Perone MJ. Interactions between the neuroendocrine system and T lymphocytes in diabetes. Front Endocrinol (Lausanne). 2018;9:229. [PMID: 29867762]
    Indexed at, Google Scholar, Cross Ref
  6. Limanaqi F, Vicentini C, Saulle I, Clerici M, Biasin M. The role of endoplasmic reticulum aminopeptidases in type 1 diabetes mellitus. Life Sci. 2023:121701. [PMID: 37059356]
  7. Olmos-Ortiz A, Flores-Espinosa P, Díaz L, Velázquez P, Ramírez-Isarraraz C, Zaga-Clavellina V. Immunoendocrine dysregulation during gestational diabetes mellitus: The central role of the placenta. Int J Mol Sci. 2021;22(15):8087. [PMID: 34360849]
  8. de Azevedo JC, de Medeiros Fernandes TA, Cavalcante GA, de Medeiros IA, Lanza DC, de Araújo JM, et al. Biology and Natural History of Type 1 Diabetes Mellitus. Curr Pediatr Rev. 2023;19(3):253-75. [PMID: 36045526]
  9. Dunne JL, Richardson SJ, Atkinson MA, Craig ME, Dahl-Jørgensen K, Flodström-Tullberg M, et al. Rationale for enteroviral vaccination and antiviral therapies in human type 1 diabetes. Diabetologia. 2019;62:744-53. [PMID: 30675626]
  10. Houeiss P, Luce S, Boitard C. Environmental triggering of type 1 diabetes autoimmunity. Front Endocrinol (Lausanne). 2022;13:933965. [PMID: 35937815]

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