Abstract
BACKGROUND: The widespread distribution of air pollutants poses a major challenge to global public health, causing a range of health problems, including the incidence and progression of idiopathic pulmonary fibrosis (IPF). This study aims to provide insights into the specific effects of air pollutants on the risk of IPF through a systematic evaluation and meta-analysis approach. METHODS: The present study was conducted through a comprehensive search of four data-Embase, Web of Science, PubMed, and Cochrane Library-from their inception to 25th November 2024, limited to English-language literature. To assess the potential relationship between a wide range of air pollutants and IPF, a random effects model was used to estimate the risk factors in this study. In addition, subgroup analyses of the data according to age, sex, smoking habits, and geographic location were performed, with the aim of exploring the relationship between air pollutants and the risk of IPF in different populations. RESULT: A total of 17 papers covering 14 countries were included in this study, totaling 18 studies involving 858,557 participants and 25,968 event occurrences. Our systematic evaluation and meta-analysis showed an increased risk of IPF disease progression for every 5 µg/m(3) increase in PM(2.5) (RR = 1.08, 95% CI:1.01,1.15; I(2) = 63.51%; p = 0.01; 7 studies). The risk of IPF progression was increased for every 10 µg/m(3) increase in NO(2) ( RR = 1.32,95% CI:1.16,1.50; I(2) = 38.59%; p = 0.12; 7 studies). For every 10 µg/m(3) increase in O(3), there was an increased risk of IPF progression (RR = 1.19, 95% CI:1.03,1.38; I(2) = 29.05%; p = 0.24; 4 studies). For every 10 µg/m(3) increase in CO increase of 10 µg/m(3) was associated with an increased risk of IPF progression (RR = 1.28, 95% CI:1.01,1.63; I(2) = 20.03%; p = 0.29; 3 studies). For every 10 µg/m(3) increase in NO(X), the risk of IPF progression was increased (RR = 1.21, 95% CI:1.11, 1.33; I(2) = 13.69%; p = 0.31; 3 studies). For every 10 µg/m(3) increase in NO(2), there was an increased risk of IPF incidence (RR = 1.67, 95% CI:1.05,2.66; I(2) = 36.94%; p = 0.20; 3 studies). CONCLUSIONS: This study found that NO(2) and PM(2.5) increase the risk of IPF disease progression, while NO(X), CO, and O(3) also increase this risk, albeit with limited data. In addition, NO(2) increases the risk of IPF occurrence. Therefore, global health policies targeting reductions in air pollutants like NO(2) and PM(2.5) may reduce the risk of the occurrence and progression of IPF, with significant implications for the future prevention and treatment of IPF.