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Previous epidemiological studies have reported increased risks of certain cancers in relation to pesticide exposures. Although the biologic mechanisms underlying these associations are not well understood, altered telomere length has been hypothesized to play a role. We examined associations between occupational use of specific pesticides and leukocyte telomere length in the Biomarkers of Exposure and Effect in Agriculture study, a molecular epidemiological investigation of pesticide applicators in Iowa and North Carolina. Relative telomere length (RTL) was measured using quantitative polymerase chain reaction in leukocytes from 1539 male pesticide applicators ≥50 years of age. We evaluated lifetime use of 47 pesticides in terms of self-reported ever use and intensity-weighted lifetime days (IWLDs), a metric integrating lifetime days of use and other factors influencing exposure. Multivariable linear regression was used to estimate percent difference in geometric mean RTL in relation to ever (vs. never) use, IWLDs of use, and timing of use [recent (last 12 months) and former vs. never use]. Mean RTL was significantly longer among ever users of the insecticides lindane (percent difference = 2.20%, 95%CI: 0.45%, 3.99%) and aldicarb (percent difference = 3.27%, 95%CI: 0.23%, 6.40%). Longer RTL was also associated with increasing IWLDs of lindane (highest quartile vs. never use: percent difference = 4.51%, 95%CI: -0.22%, 9.46%; p-trend = 0.048) and the insecticide diazinon (4.77%, 95%CI: 0.17%, 9.58%; p-trend = 0.055), and with recent use of the insecticide dichlorvos (vs. never use: 8.15%, 95%CI: 1.31%, 15.46%). Increasing IWLDs of the insecticide heptachlor and the herbicide 2,4,5-TP and recent use of the herbicide metolachlor were significantly associated with shorter RTL. Our findings provide novel evidence suggesting that use of certain pesticides is associated with altered leukocyte telomere length. Notably, diazinon and lindane have previously been associated with increased risks of lung and lymphoid malignancies, respectively, and longer leukocyte telomere length has been implicated in the development of these cancers.
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http://dx.doi.org/10.1016/j.envres.2025.121174 | DOI Listing |
Exp Gerontol
September 2025
Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA; Salk Institute for Biological Studies, La Jolla, CA, 92037, USA; Department of Molecular Biology, University of Utah, Salt Lake City, UT, USA; Department of Biochemistry, University of Utah, Salt Lake Ci
Aging is the greatest risk factor for cardiovascular diseases (CVD) and is characterized by inflammation, oxidative stress, and cellular senescence. Cellular senescence is a state of persistent cell cycle arrest triggered by stressors such as DNA damage and telomere attrition. Senescent endothelial cells (ECs) can impair vascular function and promote inflammation, thereby contributing to CVD progression.
View Article and Find Full Text PDFKardiologiia
September 2025
National Medical Research Center for Therapy and Preventive Medicine, Moscow.
Atrial fibrillation (AF) is the most common form of cardiac arrhythmia, the prevalence of which increases with age. Slowing down senescence is one of the urgent challenges of modern science. Therefore, it is important to identify individuals with markers of premature cellular senescence for further development of pharmacological agents capable of slowing it.
View Article and Find Full Text PDFChron Respir Dis
September 2025
Department of Pulmonology, II.Medical Clinic and Polyclinic, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Case presentationDescription of a patient with a progressive destructive lung disease resembling pleuroparenchymal fibroelastosis, liver cirrhosis and bone marrow changes. Genetic workup identified a rare heterozygous coding variant in the (telomerase reverse transcriptase) gene c.472 C>T; p.
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Polyploidy, a conserved mechanism involved in normal development and tissue homeostasis, plays a paradoxical role in cancer by facilitating both tumor progression and therapeutic vulnerability. Although polyploidization may confer survival advantages to cancer cells, its controlled induction could represent an effective anticancer strategy. Aurora B kinase, a critical regulator of mitosis, plays a pivotal role in ensuring chromosomal integrity and preventing polyploidy.
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