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The Biology of Shift Work and the Role of Lighting in the Workplace
Published in Agnieszka Wolska, Dariusz Sawicki, Małgorzata Tafil-Klawe, Visual and Non-Visual Effects of Light, 2020
Agnieszka Wolska, Dariusz Sawicki, Małgorzata Tafil-Klawe
Saksvik et al. [2011] reviewed the published literature regarding the relationship between individual differences and different measures of shift work tolerance. They concluded that young age, male gender, low scores on morningness, high scores on flexibility, low scores on languidity, low scores on neuroticism, high scores on extraversion and internal locus of control, and some genetic predispositions are related to higher shift work tolerance. Morningness/eveningness (the biological chronotype) seems to be a genetically linked trait. This term refers to the period during the day when subjects are most awake and active. “Morning larks” (morning chronotype) are individuals who are most functional in the early morning hours. “Night owls” (evening chronotype) are more active during the late afternoon or evening hours. A shift of circadian deep temperature curves was also observed between both chronotypes, with the minimum occurring earlier in morningness. Morning and evening preferences are linked to the period of the circadian clock “and a length polymorphism of the PER3 clock gene” regulating sleep and wakefulness [Taniyama et al. 2015; Wickwire et al. 2017]. The last study from the Hattamaru team [Hattamaru et al. 2019], who examined clock gene expression in Japanese shift-working men, suggests that night shift work affects the rhythms and levels of circadian PER3 and Nr1d2 expression dependent on the shift schedule or type of shift.
The potential interaction of environmental pollutants and circadian rhythm regulations that may cause leukemia
Published in Critical Reviews in Environmental Science and Technology, 2022
Francisco Alejandro Lagunas-Rangel, Błażej Kudłak, Wen Liu, Michael J. Williams, Helgi B. Schiöth
Burnt tobacco smoke is estimated to contain more than 3,800 chemicals of which more than half are considered potential toxins or carcinogens (including benzene) (IARC, 2004). Chronic exposure to cigarette smoke damages the cells of the hematopoietic niche, resulting in abnormal hematopoiesis, where proliferative signals increase and stimulate the expansion of HSPCs (Siggins et al., 2014). Chronic exposure to cigarette smoke caused a dysregulation of circadian clock genes, with nuclear receptor subfamily 1 group D member 1 (NR1D1) and nuclear receptor subfamily 1 group D member 2 (NR1D2) (genes that code for REV-ERBa), PER3, and PER2 up-regulated, while BMAL1 and RORC were down-regulated, resulting in increased proliferation but also a greater susceptibility to oxidative stress, inflammation, and cell damage (Hwang et al., 2014; Tsutsumi et al., 2020). This countercyclical change with respect to BMAL1 of several CCGs has been suggested to be due to the alteration in the redox potential in cells and tissues after exposure to cigarette smoke, which consequently alters DNA-binding activity and, in turn, the transcriptional activity of BMAL1-containing transcription factors (Gebel et al., 2006). In addition to these changes, a reduction in SIRT1 and an increase in the levels of acetylated BMAL1 were also found facilitating the recruitment of CRY1 to CLOCK-BMAL1, and thus promoting transcriptional repression (Hirayama et al., 2007; Hwang et al., 2014).