DNA damage response in workers exposed to low-dose ionising radiation

• Published in: Occupational and environmental medicine (London, England) Vol. 75; no. 10; pp. 724 - 729
• Main Authors: Gaetani, Simona, Monaco, Federica, Bracci, Massimo, Ciarapica, Veronica, Impollonia, Giulia, Valentino, Matteo, Tomasetti, Marco, Santarelli, Lory, Amati, Monica
• Format: Journal Article
• Language: English
• Published: England BMJ 01.10.2018; BMJ Publishing Group LTD
• Subjects: Bioassays; Biomarkers; Cancer; Carcinogenic agents; Carcinogens; Chronic exposure; Comet assay; Damage accumulation; Damage assessment; Damage detection; Deoxyribonucleic acid; DNA; DNA damage; DNA glycosylase; DNA repair; DNA-formamidopyrimidine glycosylase; Dosimetry; Drug dosages; Enzymes; Exposure; Families & family life; Family medical history; Genetics; Genomes; Health risks; Hormesis; Hospitals; Ionizing radiation; Laboratories; Lymphocytes; Medical personnel; Mutagenesis; Mutation; Nuclear medicine; Occupational exposure; OGG1 protein; ORIGINAL ARTICLE; Population studies; Radiation damage; Radiation dosage; Repair; Therapeutic applications; Thyroid cancer; Workers; Italy; Dna damage response; occupational exposure; ionizing radiation; ogg1-dependent Dna repair activity
• ISSN: 1351-0711; 1470-7926; 1470-7926
• DOI: 10.1136/oemed-2018-105094

ObjectiveMedical personnel using radiation for diagnosis and therapeutic purposes are potentially at risk of cancer development. In this study, the effect of ionising radiation (IR) exposure was evaluated as DNA damage response (DDR) in the circulating cells of occupationally exposed subjects.MethodsThe study population consisted of IR-exposed workers included both in group B (effective dose ranging between 0.04 and 6 mSv/year) and group A (probable effective dose exceeding 6 mSv/year), and the control group consisted of healthy individuals who had never been occupationally exposed to IR or other known carcinogenic agents. DNA damage (single-strand breaks, oxidised purine and pyrimidine bases) and DNA repair (t1/2, half time to repair DNA damage, amount of repaired DNA and DNA repair activity) were measured in lymphocytes using the comet assay. To evaluate the influence of IR doses and genetic predisposition to cancer, the enrolled population was stratified according to IR exposure level and family history of cancer.ResultsIncreased DNA repair activity was found in IR-exposed group, and only subjects highly exposed to IR doses accumulated DNA damage in their circulating cells, thus supporting the hypothesis of ‘radiation hormesis’. A significant increase in DNA damage accumulation and a reduced 8-oxoguanine glycosylase 1-dependent DNA repair activity were found in IR-exposed subjects with cancer cases across their family.ConclusionOur results indicate that chronic exposure to a low dose of IR in occupational settings induces DDR in exposed subjects and may be mutagenic in workers with family history of cancer, suggesting that periodic surveillance might be advisable, along with exposure monitoring.