Yu Chengdong, Xu Jiawei, Xu Siyi, Tang Lei, Zhang Xiaofang, Chen Wen, Yu Ting
Department of Medical Oncology, Jiangxi Cancer Hospital, Jiangxi Clinical Research Center for Cancer, Nanchang, China; Jiangxi Medical College, Nanchang University, Nanchang, China; Department of Breast Surgery, Jiangxi Cancer Hospital, Nanchang, China.
Department of Medical Oncology, Jiangxi Cancer Hospital, Jiangxi Clinical Research Center for Cancer, Nanchang, China; Jiangxi Medical College, Nanchang University, Nanchang, China.
Public Health. 2025 Jan;238:197-205. doi: 10.1016/j.puhe.2024.11.021. Epub 2024 Dec 14.
Previous studies have reported associations of noise and air pollution with breast cancer (BC) risk, but the causality remains unclear. This study aimed to explore the effects of noise and air pollution on BC from a genetic perspective.
Genetic association study.
We began our investigation by visualizing the development trends in this field through bibliometric analysis. Subsequently, we conducted Mendelian randomization analyses to assess the effects of noise (daytime and evening) and air pollution (NO, NO, PM, PM, and PM) on BC. Genetic variants extracted from genome-wide association studies (GWAS) robustly associated with noise and air pollution were used as instrumental variables. The GWAS data for BC in European and East Asian populations were obtained from the Breast Cancer Association Consortium and the Biobank Japan, respectively.
The effects of noise and air pollution on BC are receiving increasing attention. In the European population, genetically predicted exposure to NO (OR: 1.9381; 95% CI: 1.2873-2.9180; P = 0.0015) and PM (OR: 1.4187; 95% CI: 1.0880-1.8500; P = 0.0098) were positively associated with overall BC risk. Subtype analyses showed that PM was significantly related to the risks of both ER+ (OR: 1.6165; 95% CI: 1.1778-2.2186; P = 0.0030) and ER- (OR: 1.6228; 95% CI: 1.0175-2.5881; P = 0.0421) BC. Additionally, NO only increased the risk of ER+ BC (OR: 1.7429; 95% CI: 1.0679-2.8444; P = 0.0262), but not ER- BC. In East Asians, genetically predicted NO was positively related to BC risk (OR: 1.1394; 95% CI: 1.0082-1.2877; P = 0.0366).
Our study gave new evidence from a genetic standpoint underscoring that improving the environmental quality of residential areas is conducive to reducing BC risk.
既往研究报道了噪声和空气污染与乳腺癌（BC）风险之间的关联，但因果关系仍不明确。本研究旨在从遗传学角度探讨噪声和空气污染对乳腺癌的影响。
基因关联研究。
我们首先通过文献计量分析直观呈现该领域的发展趋势，从而开启研究。随后，我们进行孟德尔随机化分析，以评估噪声（白天和晚上）及空气污染（一氧化氮、二氧化氮、细颗粒物、可吸入颗粒物和细颗粒物）对乳腺癌的影响。从与噪声和空气污染密切相关的全基因组关联研究（GWAS）中提取的基因变异用作工具变量。欧洲和东亚人群乳腺癌的GWAS数据分别取自乳腺癌协会联盟和日本生物银行。
噪声和空气污染对乳腺癌的影响正受到越来越多的关注。在欧洲人群中，基因预测的一氧化氮暴露（比值比：1.9381；95%置信区间：1.2873 - 2.9180；P = 0.0015）和细颗粒物暴露（比值比：1.4187；95%置信区间：1.0880 - 1.8500；P = 0.0098）与总体乳腺癌风险呈正相关。亚组分析表明，细颗粒物与雌激素受体阳性（ER +）（比值比：1.6165；95%置信区间：1.1778 - 2.2186；P = 0.0030）和雌激素受体阴性（ER -）（比值比：1.6228；95%置信区间：1.0175 - 2.5881；P = 0.0421）乳腺癌的风险均显著相关。此外，一氧化氮仅增加ER +乳腺癌的风险（比值比：1.7429；95%置信区间：1.0679 - 2.8444；P = 0.0262），而不增加ER -乳腺癌的风险。在东亚人群中，基因预测的一氧化氮与乳腺癌风险呈正相关（比值比：1.1394；95%置信区间：1.0082 - 1.2877；P = 0.0366）。
我们的研究从遗传学角度提供了新证据，强调改善居住区环境质量有助于降低乳腺癌风险。
