Rotating night work, lifestyle factors, obesity and promoter methylation in BRCA1 and BRCA2 genes among nurses and midwives

PLoS One. 2017 Jun 8;12(6):e0178792. doi: 10.1371/journal.pone.0178792. eCollection 2017.


Some recent evidence suggests that environmental and lifestyle factors may modify DNA methylation. We hypothesized that rotating night work and several modifiable factors may be associated with the methylation of the promoter regions within two tumor suppressor and DNA repair genes: BRCA1 and BRCA2. The methylation status of BRCA1 and BRCA2 was determined via qMSP reactions using DNA samples derived from blood leucocytes of 347 nurses and midwives working rotating nights and 363 working during the days. The subjects were classified into unmethylated vs methylated BRCA1 and BRCA2 when the methylation index was 0% or >0%, respectively. The adjusted odds ratios with 95% confidence intervals were calculated for night work status, smoking, obesity, physical activity and alcohol drinking. Current night shift work or night work history was not associated with methylation status of the promoter sites within BRCA1 and BRCA2 genes. We observed weak associations between smoking and the methylation status of BRCA1 with OR = 1.50 (95%CI: 0.98-2.29) for current smoking, OR = 1.83, 95CI: 1.08-3.13 for smoking longer than 31 years, and 0.1>p>0.05 for trends for the number of cigarettes per day, smoking duration and packyears. In conclusion, no links between night shift work and methylation of the promoter region within the BRCA1, and BRCA2 genes were observed in this exploratory analysis. The findings of our study weakly support the hypothesis that smoking may contribute to epigenetic events.

MeSH terms

  • BRCA1 Protein / genetics*
  • BRCA2 Protein / genetics*
  • DNA Methylation / genetics*
  • Female
  • Humans
  • Life Style
  • Male
  • Midwifery / statistics & numerical data*
  • Nurses / statistics & numerical data*
  • Promoter Regions, Genetic / genetics*
  • Work Schedule Tolerance / physiology


  • BRCA1 Protein
  • BRCA1 protein, human
  • BRCA2 Protein
  • BRCA2 protein, human

Grant support

This project was supported by the Norway Grants, under the Polish-Norwegian Research Programme (Grant no. PNRF – 243 – AI – 1/07 and Pol-Nor/196940/22/2013-clockshift) (BP). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.