Comparative Carcinogenic Risk Assessment of Polycyclic Aromatic Hydrocarbons Accumulation in Normal and Cancerous Lung Tissues of Patients from Northern Thailand
High-molecular-weight carcinogens significantly accumulate in human lungs in Northern Thailand, reflecting substantial environmental exposure, while tissue lipid content modulates toxin bioaccumulation, underscores an urgent need for targeted public health strategies addressing both environmental pollution and tobacco use.
Abstract
Lung cancer mortality is a critical issue in Northern Thailand, where incidence rates significantly exceed the national average. Key risk factors include tobacco smoking and seasonal air pollution from biomass burning, which releases carcinogenic polycyclic aromatic hydrocarbons (PAHs). This study aims to analyze the accumulation of 16 priority PAHs in human lung tissues to explore links between environmental exposure, smoking habits, and cancer development. Tissue samples (normal, para-cancerous, and adenocarcinoma) were collected from 30 surgical participants (15 lung cancer patients, 15 non-cancer controls) at Chiang Mai University Hospital. Compounds were extracted via ultrasonication and quantified using gas chromatography-mass spectrometry. Carcinogenic potency was evaluated using Benzo[a]pyrene equivalents, with concentrations compared across tissue types and patient groups using generalized estimating equations. High-molecular-weight PAHs were the dominant species, accounting for over 50% of total accumulation in all tissues, aligning with regional biomass burning profiles. Total concentrations and carcinogenic potency were significantly higher in smokers, particularly within normal lung tissues. Furthermore, high-molecular-weight PAH concentrations positively correlated with tissue cholesterol levels (R = 0.66). Source analysis indicated exposure primarily from pyrogenic sources, alongside petroleum emissions. In conclusion, high-molecular-weight carcinogens significantly accumulate in human lungs in Northern Thailand, reflecting substantial environmental exposure, while tissue lipid content modulates toxin bioaccumulation. Smoking facilitates compound retention in normal tissues, underscoring an urgent need for targeted public health strategies addressing both environmental pollution and tobacco use.
An increase in formaldehyde concentration in the air is associated with a gain in breast cancer incidence, especially at the early stages, and it is advisable to strengthen formaldehyde monitoring, implement molecular epidemiological screening of these polymorphisms and active detection of breast cancer in genetically determined risk groups.
O. N. Gulyaeva, Ivan E. Tereshkin, V. Kislitsyna et al.· Hygiene and Sanitation· 0 citations
Polycyclic aromatic hydrocarbons (PAHs) are environmental and occupational risk factors for some cancers. We conducted a systematic review and meta-analysis on the risk of upper gastrointestinal cancers, including esophageal and gastric cancers, among workers exposed to PAHs. We searched PubMed, EMBASE, and SCOPUS through December 2024, as well as International Agency for Research on Cancer Monographs and reference lists, for cohort and nested case-control studies. Relative risks (RRs) and odds ratios were pooled using random-effects models. Heterogeneity was assessed with the I2 statistic. Subgroup analyses were conducted by sex, region, industry type, study quality, and publication year. Duration of exposure-response was evaluated using meta-regression. Twenty-seven studies met the inclusion criteria, comprising diverse high-exposure occupations including coke production, aluminum production, metalworking, and chimney sweeping. Overall, occupational PAH exposure was associated with an increased risk of upper gastrointestinal cancers [relative risk (RR) = 1.23, 95% confidence interval (CI): 1.10-1.38]. For esophageal cancer, the pooled RR was 1.31 (95% CI: 1.05-1.63), with higher risk estimates observed in high-exposure occupations. Gastric cancer showed a modestly elevated risk (RR = 1.19, 95% CI: 1.05-1.35). Meta-regression indicated a positive association between duration of exposure and esophageal cancer risk (RR per year = 1.03, 95% CI: 1.01-1.06), but not for gastric cancer. No evidence of publication bias was detected (P = 0.66 for esophageal and P = 0.33 for gastric cancer). Occupational PAH exposure is modestly associated with upper gastrointestinal cancer risk, particularly esophageal cancer. Residual confounding and other sources of bias cannot be excluded, preventing conclusions in terms of causality.
M. S. Seyyedsalehi, Anna Vrtev, Marco Lanza et al.· European Journal of Cancer P...· 0 citations
Long-term exposure to selected pollutants was associated with variations in PD-L1 expression and EGFR status, suggesting that environmental factors may contribute to tumor heterogeneity, but causal relationships cannot be established.
Denisa-Gabriela Ion-Andrei, Andre Barde, Cristina Cioti et al.· Biomedicines· 0 citations
Prostate cancer (PCa) remains one of the most common malignancies in men worldwide, yet modifiable environmental contributors remain incompletely defined. Aromatic hydrocarbons (AHs), particularly benzene and polycyclic aromatic hydrocarbons (PAHs), are widespread pollutants in ambient air, occupational settings, tobacco smoke, and high-temperature cooking emissions. In this review, we synthesize evidence from population-based and occupational epidemiology, dietary exposure proxies, animal carcinogenesis models, organoid systems, and cell-based mechanistic studies to assess the biological plausibility of AH-related prostate carcinogenesis. Human studies support modest but recurrent associations between long-term exposure to traffic-related mixtures, benzene-containing emissions, PAH-generating cooking practices, and increased PCa risk, with stronger duration–response signals in occupational settings. Experimental evidence further indicates that benzo[a]pyrene and related PAHs can induce prostatic mutagenesis, oxidative and genotoxic stress, endocrine perturbation, epigenetic remodeling, and immunosuppressive changes in the tumor microenvironment. The most coherent mechanisms involve AhR–AR crosstalk, CYP1A1/1B1-mediated bioactivation, ROS generation, DNA-adduct formation, DNMT1/HDAC6-associated epigenetic regulation, JAK2/STAT3-linked survival signaling, epithelial–mesenchymal transition, and IDO/TDO–kynurenine–AhR-mediated immune suppression. Collectively, current evidence supports a biologically plausible framework in which AH exposure may contribute to PCa initiation and progression and may intersect with pathways implicated in therapy resistance, although causal inference remains constrained by exposure misclassification, mixture complexity, and limited longitudinal biomarker data. Future studies should integrate precise exposure assessment with prostate-specific molecular studies, organoid systems, animal models, and prospective human cohorts.
Hao Wu, Hongliang Cao, Zihao Ye et al.· Frontiers in Cell and Develo...· 0 citations
Communities residing near petrochemical complexes are chronically exposed to complex volatile organic compound (VOC) mixtures, but routine surveillance is often restricted to limited sentinel panels, which may lead to the underestimation of true health risks. This study assessed age-stratified probabilistic carcinogenic and noncarcinogenic inhalation risks near the Map Ta Phut Industrial Estate, Thailand, the world’s eighth-largest petrochemical hub.
During 2021–2023, six routinely monitored VOCs, namely, benzene, toluene, ethylbenzene, xylene, 1,3-butadiene, and vinyl chloride, were measured at two residential stations and one industrial fence-line station. An expanded 20-VOC panel was additionally analyzed at the fence-line station to capture broader industrial emissions. In this study, Thai-specific anthropometric data and the carcinogenic equivalence quotient framework were integrated into 10,000-iteration Monte Carlo simulations to estimate the excess lifetime cancer risk (ELCR) and hazard index (HI) for preschool children, school-aged children, adolescents, and adults. In addition, the annual number of VOC-attributable excess cancer cases in Rayong Province was also estimated.
The mean ELCRs were low at the community stations (4.10 × 10
− 7
to 3.08 × 10
− 6
) but increased markedly at the fence-line station (3.18 × 10
− 5
to 2.32 × 10
− 4
) and increased further under the expanded 20-VOC panel (5.00 × 10
− 5
to 3.61 × 10
− 4
). While the mean HI remained below 1.0 for the routine panel at all the stations, it exceeded 1.0 for all the age groups under the expanded 20-VOC panel (ranging from 2.04 to 4.83). Preschool children had the greatest noncarcinogenic burden, with a 95th -percentile HI of 10.8. Benzene and ethylbenzene were the main carcinogenic contributors at the two community stations, whereas vinyl chloride dominated both the carcinogenic and noncarcinogenic risks at the industrial fence line. The estimated number of adult VOC-attributable excess cancer cases increased from 2.79 in 2015 to 3.15 in 2023, accounting for 0.36% of the regional cancer burden.
Limited routine VOC monitoring may substantially underestimate petrochemical-related carcinogenic and noncarcinogenic risks. Age-stratified probabilistic assessment using an expanded VOC panel revealed substantial fence-line risks driven by specialty monomers, highlighting preschool children as a priority population for strengthened surveillance and site-specific risk management.
P. Sirinara, P. Chanpiwat, Natthaya Bunplod et al.· BMC Public Health· 0 citations
Introduction Prostate cancer is one of the most commonly diagnosed malignancies among men worldwide, with higher reported incidence in many high-income countries. Environmental factors are receiving increasing attention as potential contributors to cancer development. Microplastics, which are found in air, water, food, and personal care items, are one possible risk factor. Methodology Data from 22 nations were investigated to examine whether an association exists between exposure to microplastics and the rate of prostate cancer. Data on exposure were combined from several sources, such as stool particles, breathed air, drinking water, seafood intake, and personal care products. Statistical and machine learning methods, such as K-means clustering, principal component analysis, and random forest modeling, were applied to find the most important exposure variables linked to cancer risk. Results Stool microplastic concentrations and heavy metal burden showed the strongest model-based associations with prostate cancer incidence. Countries with higher external exposure indicators did not consistently show higher reported prostate cancer incidence. This pattern suggests that external exposure metrics alone may be insufficient to explain country-level variation. Internal retention and tissue-response pathways remain plausible hypotheses, but they require direct validation using individual-level and tissue-based data. Discussion The findings support the need to integrate exposure pathways, biomonitoring indicators, and biological-response markers when studying microplastic-related cancer risk. However, this study was limited by its ecological design, cross-sectional structure, and small sample size of 22 countries. Therefore, the results should be interpreted as exploratory and hypothesis-generating rather than causal. Further longitudinal and individual-level studies are required to validate these associations.
A. M. Elewa, Moustafa Gamal Snousy, F. M. Alghamdi et al.· Frontiers in Public Health· 0 citations