LAUSR

BACKGROUND Except for known cardiovascular risk factors, long-term exposure to environmental endocrine disruptors (EEDs) - a class of exogenous chemicals, or a mixture of chemicals, that can interfere with any aspect of hormone action - has been shown to increase the risk of cardiovascular diseases (CVDs), which are still controversial. OBJECTIVE To conduct a comprehensive systematic review and meta-analysis to estimate the association between EEDs, including nonylphenol (NP), bisphenol A (BPA), polychlorinated biphenyl (PCB), organo-chlorine pesticide (OCP) and phthalate (PAE) exposure and CVD risk. METHODS The heterogeneity between different studies was qualitatively and quantitatively evaluated using Q test and I2 statistical magnitude, respectively. Subgroup analysis was performed using chemical homologs - a previously unused grouping method - to extract data and perform meta-analysis to assess their exposure to CVD. RESULTS Twenty-nine literatures were enrolled with a total sample size of 88891. The results indicated that exposure to PCB138 and PCB153 were the risk factors for CVD morbidity (odds ratio (OR) = 1.35, 95% confidence interval (CI): 1.10-1.66; OR = 1.35, 95% CI: 1.13-1.62). Exposure to organo-chlorine pesticide (OCP) (OR = 1.12, 95% CI: 1.00-1.24), as well as with phthalate (PAE) (OR = 1.11, 95% CI: 1.06-1.17) and BPA (OR = 1.19, 95% CI: 1.03-1.37) were positively associated with CVD risk, respectively. BPA exposure concentration had no correlation with total cholesterol (TC), or low-density lipoprotein (LDL), but exhibited a correlation with gender, waist circumference (WC), high-density lipoprotein (HDL), age, and body mass index (BMI) (standardized mean difference (SMD)) = 1.51; 95% CI: =(1.01-2.25); SMD = 0.16; 95% CI: (0.08-0.23); SMD = -0.19; 95% CI: (-0.27-0.12); SMD = -0.78; 95% CI: (-1.42-0.14); SMD = 0.08; 95% CI: (0.00-0.16). CONCLUSIONS EED exposure is a risk factor for CVD. Long-term exposure to EEDs can influence cardiovascular health in humans. A possible synergistic effect may exist between the homologs. The mechanism of which needs to be further explored and demonstrated by additional prospective cohort studies, results of in vitro and in vivo analyses, as well as indices affecting CVD.