Night Shift Work, DNA Methylation and Telomere Length: An Investigation on Hospital Female Nurses

Increased breast cancer risk has been reported in some night shift (NS) workers but underlying biological mechanisms are still unclear. We assessed the association between NS work and DNA methylation of tumor suppressor ( , , , ) and estrogen receptor ( , ) genes, methylation of repetitive elements...

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Published inInternational journal of environmental research and public health Vol. 16; no. 13; p. 2292
Main Authors Carugno, Michele, Maggioni, Cristina, Crespi, Eleonora, Bonzini, Matteo, Cuocina, Simone, Dioni, Laura, Tarantini, Letizia, Consonni, Dario, Ferrari, Luca, Pesatori, Angela Cecilia
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 28.06.2019
MDPI
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Summary:Increased breast cancer risk has been reported in some night shift (NS) workers but underlying biological mechanisms are still unclear. We assessed the association between NS work and DNA methylation of tumor suppressor ( , , , ) and estrogen receptor ( , ) genes, methylation of repetitive elements ( , ), and telomere length (TL). Forty six female nurses employed in NS for at least two years were matched by age (30-45 years) and length of service (≥1 year) with 51 female colleagues not working in NS. Each subject underwent a semi-structured interview and gave a blood sample. We applied linear regression and spline models adjusted for age, BMI, smoking habit, oral contraceptive use, parity and marital status/age at marriage. Currently working in NS was associated with hypomethylation (β: -1.85 (95%CI: -3.03; -0.67), = 0.003). In current and former NS workers we observed (-0.93 (-1.73; -0.12), = 0.03) and (-1.14 (-1.71; -0.58), <0.001) hypomethylation. We found an increase between TL and number of years in NS in subjects employed in NS <12 years (0.06 (0.03; 0.09), <0.001), while a decrease if employed in NS ≥12 years (-0.07 -0.10; -0.04), <0.001). Our findings show NS-associated markers potentially involved in cellular aging, genomic instability, and cancer development.
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ISSN:1660-4601
1661-7827
1660-4601
DOI:10.3390/ijerph16132292