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. 2019 Jul 29;18:69. doi: 10.1186/s12940-019-0508-0

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Co-exposure effects of smoking and urine PAH metabolites on risk of CYP1A1 hypomethylation and high 8-OHdG. The statuses of smoking were stratified by non-smokers and smokers. The levels of urine PAH metabolites were stratified by the highest tertile into low exposure (< 67th percentile) and high exposure (≥ 67th percentile). The levels of CYP1A1 methylation were stratified by the median (3.03) into CYP1A1 hypomethylation (< 3.03) and CYP1A1 hypermethylation (≥ 3.03). The levels of urine 8-OHdG were stratified by the median (204.05 mmol/mol Cr) into low 8-OHdG (< 204.05 mmol/mol Cr) and high 8-OHdG (≥ 204.05 mmol/mol Cr). Adjusted for sex, age, years of working, drinking status, education and central heating