Road traffic noise and breast cancer: DNA methylation in four core circadian genes

Abstract Background Transportation noise has been linked with breast cancer, but existing literature is conflicting. One proposed mechanism is that transportation noise disrupts sleep and the circadian rhythm. We investigated the relationships between road traffic noise, DNA methylation in circadian...

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Main Authors: Jesse D. Thacher, Anastasiia Snigireva, Ulrike Maria Dauter, Mathilde N. Delaval, Anna Oudin, Kristoffer Mattisson, Mette Sørensen, Signe Borgquist, Maria Albin, Karin Broberg
Format: Article
Language:English
Published: BMC 2024-11-01
Series:Clinical Epigenetics
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Online Access:https://doi.org/10.1186/s13148-024-01774-z
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author Jesse D. Thacher
Anastasiia Snigireva
Ulrike Maria Dauter
Mathilde N. Delaval
Anna Oudin
Kristoffer Mattisson
Mette Sørensen
Signe Borgquist
Maria Albin
Karin Broberg
author_facet Jesse D. Thacher
Anastasiia Snigireva
Ulrike Maria Dauter
Mathilde N. Delaval
Anna Oudin
Kristoffer Mattisson
Mette Sørensen
Signe Borgquist
Maria Albin
Karin Broberg
author_sort Jesse D. Thacher
collection DOAJ
description Abstract Background Transportation noise has been linked with breast cancer, but existing literature is conflicting. One proposed mechanism is that transportation noise disrupts sleep and the circadian rhythm. We investigated the relationships between road traffic noise, DNA methylation in circadian rhythm genes, and breast cancer. We selected 610 female participants (318 breast cancer cases and 292 controls) enrolled into the Malmö, Diet, and Cancer cohort. DNA methylation of CpGs (N = 29) in regulatory regions of circadian rhythm genes (CRY1, BMAL1, CLOCK, and PER1) was assessed by pyrosequencing of DNA from lymphocytes collected at enrollment. To assess associations between modeled 5-year mean residential road traffic noise and differentially methylated CpG positions, we used linear regression models adjusting for potential confounders, including sociodemographics, shiftwork, and air pollution. Linear mixed effects models were used to evaluate road traffic noise and differentially methylated regions. Unconditional logistic regression was used to investigate CpG methylation and breast cancer. Results We found that higher mean road traffic noise was associated with lower DNA methylation of three CRY1 CpGs (CpG1, CpG2, and CpG12) and three BMAL1 CpGs (CpG2, CpG6, and CpG7). Road traffic noise was also associated with differential methylation of CRY1 and BMAL1 promoters. In CRY1 CpG2 and CpG5 and in CLOCK CpG1, increasing levels of methylation tended to be associated with lower odds of breast cancer, with odds ratios (OR) of 0.88 (95% confidence interval (CI) 0.76–1.02), 0.84 (95% CI 0.74–0.96), and 0.80 (95% CI 0.68–0.94), respectively. Conclusions In summary, our data suggest that DNA hypomethylation in CRY1 and BMAL1 could be part of a causal chain from road traffic noise to breast cancer. This is consistent with the hypothesis that disruption of the circadian rhythm, e.g., from road traffic noise exposure, increases the risk of breast cancer. Since no prior studies have explored this association, it is essential to replicate our results. Graphical abstract
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spelling doaj-art-623326945bf6458ca01fcb852fa8b8ed2024-12-01T12:31:51ZengBMCClinical Epigenetics1868-70832024-11-0116111110.1186/s13148-024-01774-zRoad traffic noise and breast cancer: DNA methylation in four core circadian genesJesse D. Thacher0Anastasiia Snigireva1Ulrike Maria Dauter2Mathilde N. Delaval3Anna Oudin4Kristoffer Mattisson5Mette Sørensen6Signe Borgquist7Maria Albin8Karin Broberg9Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund UniversityInstitute of Environmental Medicine, Karolinska InstitutetInstitute of Environmental Medicine, Karolinska InstitutetJoint Mass Spectrometry Centre (JMSC), Cooperation Group Comprehensive Molecular Analytics, Helmholtz MunichDivision of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund UniversityDivision of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund UniversityWork, Environment and Cancer, Danish Cancer InstituteDepartment of Oncology, Aarhus University Hospital, Aarhus UniversityDivision of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund UniversityDivision of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund UniversityAbstract Background Transportation noise has been linked with breast cancer, but existing literature is conflicting. One proposed mechanism is that transportation noise disrupts sleep and the circadian rhythm. We investigated the relationships between road traffic noise, DNA methylation in circadian rhythm genes, and breast cancer. We selected 610 female participants (318 breast cancer cases and 292 controls) enrolled into the Malmö, Diet, and Cancer cohort. DNA methylation of CpGs (N = 29) in regulatory regions of circadian rhythm genes (CRY1, BMAL1, CLOCK, and PER1) was assessed by pyrosequencing of DNA from lymphocytes collected at enrollment. To assess associations between modeled 5-year mean residential road traffic noise and differentially methylated CpG positions, we used linear regression models adjusting for potential confounders, including sociodemographics, shiftwork, and air pollution. Linear mixed effects models were used to evaluate road traffic noise and differentially methylated regions. Unconditional logistic regression was used to investigate CpG methylation and breast cancer. Results We found that higher mean road traffic noise was associated with lower DNA methylation of three CRY1 CpGs (CpG1, CpG2, and CpG12) and three BMAL1 CpGs (CpG2, CpG6, and CpG7). Road traffic noise was also associated with differential methylation of CRY1 and BMAL1 promoters. In CRY1 CpG2 and CpG5 and in CLOCK CpG1, increasing levels of methylation tended to be associated with lower odds of breast cancer, with odds ratios (OR) of 0.88 (95% confidence interval (CI) 0.76–1.02), 0.84 (95% CI 0.74–0.96), and 0.80 (95% CI 0.68–0.94), respectively. Conclusions In summary, our data suggest that DNA hypomethylation in CRY1 and BMAL1 could be part of a causal chain from road traffic noise to breast cancer. This is consistent with the hypothesis that disruption of the circadian rhythm, e.g., from road traffic noise exposure, increases the risk of breast cancer. Since no prior studies have explored this association, it is essential to replicate our results. Graphical abstracthttps://doi.org/10.1186/s13148-024-01774-zDNA methylationEnvironmental noiseRoad traffic noiseTrafficBreast cancerSleep
spellingShingle Jesse D. Thacher
Anastasiia Snigireva
Ulrike Maria Dauter
Mathilde N. Delaval
Anna Oudin
Kristoffer Mattisson
Mette Sørensen
Signe Borgquist
Maria Albin
Karin Broberg
Road traffic noise and breast cancer: DNA methylation in four core circadian genes
Clinical Epigenetics
DNA methylation
Environmental noise
Road traffic noise
Traffic
Breast cancer
Sleep
title Road traffic noise and breast cancer: DNA methylation in four core circadian genes
title_full Road traffic noise and breast cancer: DNA methylation in four core circadian genes
title_fullStr Road traffic noise and breast cancer: DNA methylation in four core circadian genes
title_full_unstemmed Road traffic noise and breast cancer: DNA methylation in four core circadian genes
title_short Road traffic noise and breast cancer: DNA methylation in four core circadian genes
title_sort road traffic noise and breast cancer dna methylation in four core circadian genes
topic DNA methylation
Environmental noise
Road traffic noise
Traffic
Breast cancer
Sleep
url https://doi.org/10.1186/s13148-024-01774-z
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