Increasing evidence from experimental research suggests that exposure to microcystins (MCs) may induce lipid metabolism disorder. However, population-based epidemiological studies of the association between MCs exposure and the risk of dyslipidemia are lacking. Therefore, we conducted a population-based cross-sectional study involving 720 participants in Hunan Province, China, and evaluated the effects of MCs on blood lipids. After adjusting the lipid related metals, we used binary logistic regression and multiple linear regression models to examine the associations among serum MCs concentration, the risk of dyslipidemia and blood lipids (triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C)). Moreover, the additive model was used to explore the interaction effects on dyslipidemia between MCs and metals. Compared to the lowest quartile of MCs exposure, the risk of dyslipidemia [odds ratios (OR) = 2.27, 95% confidence interval (CI): 1.46, 3.53] and hyperTG (OR = 3.01, 95% CI: 1.79, 5.05) in the highest quartile was significantly increased, and showed dose–response relationships. MCs were positively associated with TG level (percent change, 9.43%; 95% CI: 3.53%, 15.67%) and negatively associated with HDL-C level (percent change, −3.53%; 95% CI: −5.70%, −2.10%). In addition, an additive antagonistic effect of MCs and Zn on dyslipidemia was also reported [relative excess risk due to interaction (RERI) = −1.81 (95% CI: −3.56, −0.05)], and the attributable proportion of the reduced risk of dyslipidemia due to the antagonism of these two exposures was 83% (95% CI: −1.66, −0.005). Our study first indicated that MCs exposure is an independent risk factor for dyslipidemia in a dose–response manner.

Systemic immune inflammation index (SII) and systemic inflammation response index (SIRI) have recently emerged as more comprehensive indicators of systemic inflammation. However, few studies have been conducted to evaluate the effect of serum cotinine levels and weight-adjusted waist index (WWI) with SII and SIRI. This study aims to evaluate the independent and combined impact of serum cotinine levels and WWI with SII and SIRI. This study enrolled 9,099 adults based on the National Health and Nutrition Examination Survey 2013-2016. Generalized linear models were employed to assess the associations between cotinine exposure and WWI with SII and SIRI. Moreover, smoothing curve fitting was conducted to investigate the potential nonlinear relationships between the WWI with SII and SIRI levels. Additionally, subgroup analyses and interaction tests were conducted. The combined associations of the WWI and cotinine with systemic inflammatory indices were further assessed. High serum cotinine exposure was associated with increased SII and SIRI. The WWI was positively correlated with SII and SIRI. Smoothing curve fitting demonstrated a nonlinearly increasing dose-response connection between WWI and SII and SIRI. Stratified analyses also showed a positive association of cotinine levels and WWI with the systemic inflammatory indices across subgroups. Furthermore, a positive joint association was observed between serum cotinine level and WWI with SII and SIRI. These findings suggest that serum cotinine levels and WWI may be positively related to SII and SIRI. Serum cotinine levels and WWI may have a positive combined effect.