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.
Abstract
Background/Objectives: Air pollution is progressively acknowledged not only as a carcinogenic exposure, but also as a potential modulator of tumor immune activation and molecular heterogeneity in lung cancer. However, integrated analyses combining long-term environmental exposure, molecular biomarkers and immune phenotype remain limited, especially in Eastern European populations. Methods: We conducted a regional retrospective study including patients diagnosed with lung cancer in Constanța County, Romania. Prolonged atmospheric pollution exposure over an average period of 15 years was estimated using historic environmental monitoring data. Tumor samples were assessed for histopathological subtype, PD-L1 expression and EGFR status, while ALK and KRAS alterations were descriptively analyzed because of the limited number of positive cases. Multivariate ordinal and binary logistic regression models and predicted probability analyses were used to evaluate the association between chronic pollution exposure, PD-L1 expression and EGFR positivity. Results: Chronic NO2 exposure was significantly associated with increased PD-L1 expression (OR = 1.035, p = 0.017), suggesting an association between NO2 exposure and an immune-related tumor phenotype. Similar trends were observed for PM10, NO and NOx exposures. Exploratory associations were observed between EGFR positivity and carbon monoxide exposure. Conclusions: Chronic atmospheric pollution was associated with differences in the immune and molecular profile of lung cancer. 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. However, causal relationships cannot be established from this retrospective observational study.
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
Background: Environmental exposures are biologically plausible contributors to thyroid cancer outcomes, but population-based evidence is heterogeneous and often focuses on incidence rather than stage at diagnosis. Objective: This study aimed to evaluate whether ecological state-year environmental indicators add predictive information for advanced-stage thyroid cancer at diagnosis in a large SEER-based cohort (U.S. National Cancer Institute’s Surveillance, Epidemiology, and End Results Program). Methods: We conducted a retrospective registry-linked analysis of 368,726 SEER thyroid cancer cases with valid combined summary stage. Advanced stage was defined as regional or distant disease and occurred in 118,509 cases (32.14%). Environmental variables were linked as state-year indicators using five-year moving averages from the years preceding diagnosis. Regularized logistic regression, gradient boosting, and Extra Trees models evaluated incremental predictive performance. Results: Adding environmental variables to demographic, socioeconomic, histology, and laterality predictors produced small random-split improvements across model families. However, after SEER registry was added before environmental variables, the remaining environmental increment was minimal. Registry-group holdout validation did not support improved geographic generalizability from the environmental feature set. Conclusions: State-year environmental indicators carried limited predictive information for advanced thyroid cancer stage, and much of this information overlapped with registry and geographic structure. These findings clarify both the potential and limitations of ecological environmental linkage in SEER-based prediction studies.
Increasing PM2.5, NO2, NOx, and CO exposures were suggestively associated with increased CRC incidence, particularly among female and Latino participants and for left colon and rectal cancers.
U. Ihenacho, Chiu‐Cheng Tseng, Jun Wu et al.· Environmental Research· 0 citations
Mixture exposure showed a significant positive association with chronic obstructive pulmonary disease risk, and these substances disrupt pulmonary homeostasis through concurrent molecular activation and lipid-metabolic disturbance, evidenced by triglyceride-glucose index mediation.
Yansong Hu, Huanyu Cui, Yakun Wang et al.· BMC Pulmonary Medicine· 0 citations
The findings do not strongly support an association with invasive ovarian cancer, but suggest that air pollution, as indicated by NO₂ concentrations, may increase the risk of borderline tumours.
Lysandre Viau, S. Buteau, Anita Koushik· Cancer Epidemiology, Biomark...· 0 citations
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.