A platform for research: civil engineering, architecture and urbanism
A platform for research: civil engineering, architecture and urbanism
A prospective study of the associations among fine particulate matter, genetic variants, and the risk of colorectal cancer
Highlights PM2.5 exposure was associated with an increased risk of colorectal cancer. Five genetic loci had the interaction with PM2.5 exposure on colorectal cancer risk. Genetic variants may modify the effect of PM2.5 exposure on colorectal cancer risk.
Abstract Background Fine particulate matter (PM2.5) is suspected to increase the risk of colorectal cancer, but the mechanism remains unknown. We aimed to investigate the association between PM2.5 exposure, genetic variants and colorectal cancer risk in the Prostate, Lung, Colon and Ovarian (PLCO) Cancer Screening trial. Methods We included a prospective cohort of 139,534 cancer-free individuals from 10 United States research centers with over ten years of follow-up. We used a Cox regression model to assess the association between PM2.5 exposure and colorectal cancer incidence by calculating the hazard ratio (HR) and 95% confidence interval (CI) with adjustment for potential confounders. The polygenic risk score (PRS) and genome-wide interaction analysis (GWIA) were used to evaluate the multiplicative interaction between PM2.5 exposure and genetic variants in regard to colorectal cancer risk. Results After a median of 10.43 years of follow-up, 1,666 participants had been diagnosed with colorectal cancer. PM2.5 exposure was significantly associated with an increased risk of colorectal cancer (HR = 1.27; 95% CI = 1.17–1.37 per 5 μg/m3 increase). Five independent susceptibility loci reached statistical significance at P < 1.22 × 10−8 in the interaction analysis. Furthermore, a joint interaction was observed between PM2.5 exposure and the PRS based on these five loci with colorectal cancer risk (P = 3.11 × 10−29). The Gene Ontology analysis showed that the vascular endothelial growth factor (VEGF) receptor signaling pathway was involved in the biological process of colorectal cancer. Conclusions Our large-scale analysis has shown for the first time that long-term PM2.5 exposure potential increases colorectal cancer risk, which might be modified by genetic variants.
A prospective study of the associations among fine particulate matter, genetic variants, and the risk of colorectal cancer
Highlights PM2.5 exposure was associated with an increased risk of colorectal cancer. Five genetic loci had the interaction with PM2.5 exposure on colorectal cancer risk. Genetic variants may modify the effect of PM2.5 exposure on colorectal cancer risk.
Abstract Background Fine particulate matter (PM2.5) is suspected to increase the risk of colorectal cancer, but the mechanism remains unknown. We aimed to investigate the association between PM2.5 exposure, genetic variants and colorectal cancer risk in the Prostate, Lung, Colon and Ovarian (PLCO) Cancer Screening trial. Methods We included a prospective cohort of 139,534 cancer-free individuals from 10 United States research centers with over ten years of follow-up. We used a Cox regression model to assess the association between PM2.5 exposure and colorectal cancer incidence by calculating the hazard ratio (HR) and 95% confidence interval (CI) with adjustment for potential confounders. The polygenic risk score (PRS) and genome-wide interaction analysis (GWIA) were used to evaluate the multiplicative interaction between PM2.5 exposure and genetic variants in regard to colorectal cancer risk. Results After a median of 10.43 years of follow-up, 1,666 participants had been diagnosed with colorectal cancer. PM2.5 exposure was significantly associated with an increased risk of colorectal cancer (HR = 1.27; 95% CI = 1.17–1.37 per 5 μg/m3 increase). Five independent susceptibility loci reached statistical significance at P < 1.22 × 10−8 in the interaction analysis. Furthermore, a joint interaction was observed between PM2.5 exposure and the PRS based on these five loci with colorectal cancer risk (P = 3.11 × 10−29). The Gene Ontology analysis showed that the vascular endothelial growth factor (VEGF) receptor signaling pathway was involved in the biological process of colorectal cancer. Conclusions Our large-scale analysis has shown for the first time that long-term PM2.5 exposure potential increases colorectal cancer risk, which might be modified by genetic variants.
A prospective study of the associations among fine particulate matter, genetic variants, and the risk of colorectal cancer
Chu, Haiyan (author) / Xin, Junyi (author) / Yuan, Qi (author) / Wu, Yanling (author) / Du, Mulong (author) / Zheng, Rui (author) / Liu, Hanting (author) / Wu, Shaowei (author) / Zhang, Zhengdong (author) / Wang, Meilin (author)
2020-11-26
Article (Journal)
Electronic Resource
English
Can fine particulate matter explain the paradoxical ozone associations?
| Online Contents | 2008
Can fine particulate matter explain the paradoxical ozone associations?
| Online Contents | 2008