Exposure to widespread drinking water chemicals, blood inflammation markers, and colorectal cancer

Environment International

Pilar Amiano¹  Ana Espinosa¹  Manolis Kogevinas¹  Roel Vermeulen²  Jelle Vlaanderen³  Gemma Castaño-Vinyals³  Inés Gómez-Acebo⁴  Esther Gracia-Lavedan⁴  Cristina M. Villanueva⁵  Paolo Vineis⁵  Antonio José Molina⁵ 

[1] CIBER epidemiología y salud pública (CIBERESP), Madrid, Spain;Corresponding author at: ISGlobal - Institut de Salut Global de Barcelona, Barcelona Biomedical Research Park (PRBB), Doctor Aiguader, 88, 08003 Barcelona, Spain.;IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain;Universitat Pompeu Fabra (UPF), Barcelona, Spain;ISGlobal, Barcelona, Spain;

关键词: Drinking water;    Trihalomethanes;    Nitrate;    Inflammation;    Immune response;    Colorectal cancer;   

DOI  :  

来源: DOAJ

【 摘 要 】

Background: Trihalomethanes (THMs) and nitrate are widespread chemicals in drinking water associated with colorectal cancer risk but mechanisms are not well understood. Objectives: We explored the association between exposure to THMs and nitrate in drinking water and inflammation markers, and the link with colorectal cancer risk. Methods: A subset of 198 colorectal cancer cases and 205 controls from the multicase-control study MCC-Spain were included. Average concentration of THMs (chloroform, bromodichloromethane, dibromochloromethane, bromoform) and nitrate in tap water at the residence was estimated from age 18 until 2 years before the interview (“long term”) and for a recent period (3 years before diagnosis). Serum levels of EGF, eotaxin, G-CSF, IL-17E, IL-1rA, IL-8, IP-10, MDC, MPO, periostin, VEGF, and C-reactive protein (CRP) were measured. We estimated the linear association between inflammation markers and exposure among controls, and the odds ratio of colorectal cancer associated with THM and nitrate exposure, and inflammation markers. A mediation analysis was conducted to identify inflammation markers in the pathway between THM/nitrate exposure and colorectal cancer. Results: Serum concentrations of EGF, IL-8, IL-17E and eotaxin increased with recent residential levels of brominated THMs, chloroforom and/or total THM. No associations were observed for nitrate and for long-term residential THM levels. All residential exposures except chloroform were positively associated with colorectal cancer. Serum concentrations of VEGF and periostin were positively associated with colorectal cancer, while EGF was inversely associated. One protein-exposure combination (periostin-recent ingested brominated THMs) slightly mediated the association with colorectal cancer risk. Discussion: Results suggest that estimated THM exposure is involved in inflammation processes. However, the study design was limited to stablish etiologically relevant associations between the protein levels and colorectal cancer risk. The lack of association between nitrate exposure and inflammation markers suggests other biological mechanisms are involved in the link with colorectal cancer.

【 授权许可】

Unknown