Ambient air pollution exposure and risk of chronic kidney disease: A systematic review of the literature and meta-analysis

Abstract Ambient air pollution has been identified as one of the leading causes of global burden of disease. The relationship between ambient air pollution exposure and risk of chronic kidney disease (CKD) has stimulated increasing scientific interest in the past few years. However, evidence from human epidemiological studies is still limited and inconsistent. We performed an updated systematic review and meta-analysis to clarify the potential association comprehensively. Selected electronic databases were searched for related English language studies until March 1, 2020 with a final follow-up in December 31, 2020. Risk of bias assessment for individual studies were assessed using the OHAT (Office of Health Assessment and Translation) risk-of-bias rating tool. Confidence rating and level-of-evidence conclusions were developed for bodies of evidence for a given ambient air pollutant. Summary effect estimates were calculated using random-effects meta-analyses when three or more studies are identified for the same air pollutant–CKD combination. A total of 13 studies were finally identified in our study. The meta-analytic estimates (ORs) for risk of CKD were 1.15 (95% CI: 1.07, 1.24) for each 10 μg/m3 increase in PM2.5, 1.25 (95% CI: 1.11, 1.40) for each 10 μg/m3 increase in PM10, 1.10 (95% CI: 1.03, 1.17) for each 10 ppb increase in NO2, 1.06 (95% CI: 0.98, 1.15) for each 1 ppb increase in SO2 and 1.04 (95% CI: 1.00, 1.08) for each 0.1 ppm increase in CO, respectively. The level of evidence was appraised as moderate for four of the five tested air pollutant–CKD combinations using an adaptation of the GRADE (Grading of Recommendations Assessment, Development and Evaluation) tool. In conclusion, this study suggests that certain ambient air pollutant exposure was significantly associated with an increased risk of CKD. Given the limitations, the results of this study should be interpreted with caution, and further well-designed epidemiological studies are needed to draw a definite evidence of a causal relationship.