A comprehensive review published in Genes and Environment examines the complex relationship between tobacco smoking and prostate cancer, highlighting that while the link to disease incidence remains inconsistent, smoking is robustly associated with increased mortality and more aggressive disease progression. The study, authored by Ishvaria Sundaresan, Nallasivam Palanisamy, and Radha Saraswathy, synthesizes global and regional evidence to position smoking as a significant modifiable risk factor. The authors note that prostate cancer remains the most common malignancy in men worldwide, with causes ranging from genetic abnormalities to environmental and lifestyle factors. This review specifically narrows its focus to how smoking influences both the initiation and the progression of the disease, offering a perspective that includes recent findings from India, a region with distinct regional patterns and growing evidence of tobacco-related health impacts.
The methodology involved a systematic review of literature from PubMed, Scopus, and Web of Science, utilizing search terms related to smoking and prostate cancer. The selection criteria prioritized relevancy, developing research, and accessibility, while excluding non-human studies. The review examines worldwide patterns but places particular emphasis on tobacco use in India, where cultural, societal, and economic variables contribute to high tobacco consumption. According to the Global Adult Tobacco Survey cited in the review, nearly 267 million adults in India, or 29% of the adult population, consume various forms of tobacco, including smoked and smokeless products. This high prevalence underscores the need to contextualize smoking risks within specific demographic and regional frameworks to accurately assess the prostate cancer burden.
Prostate cancer is the second most frequent cancer in men and the sixth leading cause of cancer deaths globally, with an estimated 1.4 million new cases in 2020. The review highlights significant geographical disparities in incidence, with North America and Western Europe reporting the highest rates, likely due to improved screening methods such as the prostate-specific antigen (PSA) test. In contrast, Asian countries generally report lower incidence rates, which may be related to dietary habits, genetics, or limited screening access. The authors project that global prostate cancer diagnoses will reach 2.3 million by 2040, accompanied by 740,000 deaths. These projections emphasize the growing public health challenge, driven by aging populations, lifestyle changes, and improved detection capabilities that continue to influence prevalence rates worldwide.
The biological mechanisms linking smoking to prostate cancer
The biological mechanisms linking smoking to prostate cancer are multifaceted, involving hormonal disruptions, oxidative stress, and DNA damage. Cigarette smoke contains numerous carcinogens, including polycyclic aromatic hydrocarbons and nitrosamines, which can induce genetic mutations. The review details how specific chemicals in tobacco, such as cadmium, interact with the androgen receptor, a key player in prostate cancer development. Cadmium, a heavy metal present in cigarette smoke, can mimic hormonal activity similar to testosterone, potentially enhancing the response of the androgen receptor in prostate cells. This interaction may promote cellular proliferation and increase the risk of malignancy. Additionally, smoking disrupts the balance between androgens and estrogens, with elevated levels of bioavailable testosterone and reduced estradiol creating an internal environment that may favor prostate cancer growth.
Epidemiological evidence regarding the link between smoking and prostate cancer incidence is less consistent than data on mortality outcomes. Large-scale cohort and case-control studies have often reported weak or null associations between smoking and the risk of developing the disease. This discrepancy is partly attributable to the influence of PSA screening, which has led to the widespread overdiagnosis of indolent tumors, thereby obscuring true etiological relationships. Some cohorts have even reported a lower incidence among smokers, a finding that the authors suggest may reflect detection bias, residual confounding, or lower screening rates in this demographic. Current smokers are substantially less likely to obtain recommended PSA screening compared to former or never smokers, which may delay detection and worsen outcomes for those who do develop the disease.
In contrast, the association between smoking and prostate cancer-specific mortality is more robust. Recent meta-analyses and systematic reviews indicate that current smokers have a 24% to 42% higher risk of dying from prostate cancer compared to non-smokers. A meta-analysis by Islami et al. found a 25% higher risk of mortality for current smokers, while another by Al-Fayez et al. reported a 42% greater chance of death. These studies reveal a clear dose-response relationship, where the risk of mortality increases with the number of cigarettes smoked. The review emphasizes that mortality outcomes more accurately reflect clinically significant disease burden and public health impact than incidence rates, suggesting that smoking may accelerate disease progression and compromise treatment efficacy rather than solely initiating the cancer.
The review also addresses the impact of smoking
The review also addresses the impact of smoking on disease aggressiveness and treatment outcomes. Smokers are more likely to develop high-grade prostate cancer and experience poorer survival rates compared to non-smokers. Continuing to smoke after diagnosis is linked to more aggressive disease, higher recurrence rates, and increased mortality. The authors note that smoking may hinder early detection attempts and compromise the efficacy of treatments such as radiation therapy. Patients who smoke during radiation treatment show poorer response rates and a higher risk of adverse effects. Therefore, the review suggests that smoking cessation prior to therapy is crucial to optimize response and minimize complications, highlighting the tangible benefits of quitting in reducing prostate cancer mortality.
Smoking cessation is strongly associated with both a reduced risk of developing prostate cancer and improved outcomes in men already diagnosed with the disease. A meta-analysis of 13 studies reported that current smokers have a 28% higher risk of developing prostate cancer compared to non-smokers, whereas former smokers showed only a 10% increased risk. This indicates a substantial benefit from cessation, with long-term quitting, typically for 10 years or more, reducing the risk to a level comparable with that of men who have never smoked. The protective effects of quitting may be mediated by changes in sex hormone levels, reduced DNA damage, and improved immune function. These biological mechanisms suggest that cessation can alter the internal environment of the prostate, potentially lowering the likelihood of disease development and improving overall prognosis.
The review highlights the importance of integrating smoking cessation support into routine healthcare, particularly for men at risk or diagnosed with prostate cancer. Public health campaigns can highlight prostate-specific risks associated with smoking, encouraging men to quit or never start. Healthcare providers can offer targeted advice and support to those at risk, particularly heavy smokers and those with occupational exposure to harmful chemicals. The authors recommend that public health messaging accurately convey that smoking cessation offers tangible benefits in reducing prostate cancer mortality, even if its effect on incidence remains modest. Integrating cessation programs into clinical practice can help lower smoking rates and enhance patient outcomes, addressing the complex interplay between lifestyle decisions and genetic predisposition.
Future research should prioritize longitudinal studies with detailed
Future research should prioritize longitudinal studies with detailed exposure assessment and molecular characterization to elucidate the pathways linking smoking to aggressive prostate cancer phenotypes. The review calls for large-scale, multiethnic longitudinal studies and clinical trials to establish a cause-and-effect relationship and provide conclusive insights into genetic factors. Integrating genomic data with environmental exposures will enhance risk stratification and inform targeted prevention and treatment strategies. The authors also suggest investigating the impact of second-hand smoke exposure and the influence of e-cigarettes and other types of tobacco usage. By combining genetic, molecular, and epidemiological insights, researchers can develop personalized prevention and treatment strategies that address the full scope of smoking’s impact on prostate cancer biology.
Subject of Research: Smoking and the risk of prostate cancer: a review of risk and disease progression
Article Title: Smoking and the risk of prostate cancer: a review of risk and disease progression
Article References: Sundaresan, I., Palanisamy, N., & Saraswathy, R. (2025). Smoking and the risk of prostate cancer: a review of risk and disease progression. Genes and Environment, 47(1), Article 17. https://doi.org/10.1186/s41021-025-00338-8
DOI:10.1186/s41021-025-00338-8
Keywords: Smoking, risk, prostate, cancer, review, disease, progression, scientific research
News. Review Links Smoking to Prostate Cancer Mortality. Scienmag
