Objective To investigate the correlationbetween the genepolymorphisms of interleukin and the susceptibility to pneumonoconiosis. Methods Literatures reporting the correlation between the gene polymorphisms of interleukin and the susceptibility to pneumonoconiosis in the PubMed, the Cochrane Library, Embase, CNKI, Wanfang Data, Weipu Database (VIP), and Chinese Biomedical Database (CBM) and other databases, which were published from the establishment of the databases to January 8, 2022 were screened.Two researchers independently extracted data and assessed the risk of bias. Using RevMan 5.2 and Stata 14.0, allelic model, dominant model, recessive model, co-dominant models (2 models), and over-dominant model were used in the meta-analysis on the correlation between interleukin-associated gene polymorphisms and susceptibility to pneumoconiosis. Results A total of 29 eligiblestudies, involving 5 315 pneumoconiosis cases and 5 332 controls were included in the current study. There were 8 literatures reporting the IL-1β-511C/T polymorphism, and the data revealed that the recessive model (=1.57, 95%=1.06-2.33, =0.024), and co-dominant model (TT vs CC) (=1.80, 95%=1.03-3.13, =0.039) of the IL-1β-511C/T polymorphism were significantly correlated with the susceptibility to pneumonoconiosis. There were 6 literatures reporting the IL-1RA+2018T/C polymorphism, and the data revealed that the allele model(=1.65, 95%=1.21-2.27, =0.002), dominant model(=1.65, 95%=1.11-2.46, =0.013), recessive model(=2.14, 95%=1.50-3.06, =0.000), and co-dominant model (TT vs CC) (=2.29, 95% =1.58-3.32, =0.000) of the IL-1RA+2018T/C polymorphism were significantly correlated with the susceptibility to pneumonoconiosis. There were 4 literatures reporting the IL-1α-889C/T polymorphism, and the data revealed that the dominant model(=1.75, 95%=1.02-3.01, =0.042), and co-dominant model (CT vs CC)(=1.79, 95%=1.21-2.636, =0.004) of the IL-1α-889C/T polymorphism were significantly correlated with the susceptibility to pneumonoconiosis. There were 3 literatures reporting the IL-1α +4845G/T polymorphism, and the data revealed that the allele model(=1.59, 95%=1.03-2.56, =0.038) of the IL-1α+4845G/T polymorphism was significantly correlated with the susceptibility to pneumonoconiosis. There were 4 literatures reporting the IL-6 -634C/G polymorphism, and the data revealed that the allele model(=0.60, 95%=0.47-0.75), dominant model(=0.47, 95% =0.35-0.64), co-dominant model(=0.63, 95%=0.42-0.94) (=0.36, 95%=0.24-0.54) and over-dominant model (=2.51, 95%=1.71-3.69) of the IL-6 -634C/G polymorphism were significantly correlated with the susceptibility to pneumonoconiosis. There were 2 literatures reporting the IL-8 -781C/T, IL-8-Met31Arg T/G and IL-8 -251A/T polymorphisms, and the data revealed their significant correlation with thesusceptibility to pneumonoconiosis. There was no significant correlation between IL-1β +3953C/T, IL-6 -174G/C and IL-10 -592A/C polymorphisms with the susceptibility topneumoconiosis. Conclusion IL-1RA +2018T/C and IL-6 -634 C/G polymorphisms were significantly correlated with the susceptibility to pneumoconiosis. IL-1α +4845G/T, IL-1β -511C/T and IL-1α -889C/T polymorphisms may be correlated with the susceptibility to pneumoconiosis. IL-1β +3953C/T and IL-6 -174G/C were not correlated with the susceptibility to pneumoconiosis. Our findings should be further validated in multi-center studies with a large sample size.