Suchergebnisse

Abstract
Heavy metals in drinking water can threat human health and may induce several diseases. The association between heavy metals exposure and chronic kidney disease (CKD) has been indicated by few epidemiological studies. We conducted a systematic review of the epidemiologic publications of the association between exposure to heavy metals through drinking water and CKD. Keywords related to heavy metals and kidney diseases on MeSH were identified and searched in PubMed, Google Scholar, Scopus, Ovid-Medline and Web of Science until July 2020. 14 publications met our inclusion criteria and included in the current review. The included articles were conducted on the association between arsenic, cadmium, lead and chromium in drinking water and CKD. Our study could not find strong evidence between heavy exposure to through drinking water and CKD, except for arsenic. The negative association was found between arsenic and lead and glomerular filtration rate (eGFR). The positive correlation was observed between cadmium exposure and urinary N-acetyl-β-d-glucosaminidase (NAG) concentrations, and also arsenic and chromium exposure and kidney injury molecule (KIM-1). Assessment of studies showed an association between arsenic, cadmium, lead and chromium and albuminuria and proteinuria, without CKD outcomes. Current systematic study showed few evidence for exposure to arsenic, cadmium, lead and chromium through drinking water and incidence of kidney problems. However, more epidemiological studies are required to confirm this association.

Abstract

Objective
Numerous evidence indicates the association between polychlorinated biphenyls (PCBs), an endocrine disrupter, with thyroid hormone disruption, contradictory findings also exist. Herein, we tried to address this question by performing a scoping review.


Content
The search was performed on PubMed, Scopus, Web of Science, and Google Scholar databases from 2010 onwards. Animal studies on PCBs' effect on thyroid function were searched. The SYRCLE's RoB scale assessed the risk of bias. I2 and Q tests are used for investigating heterogeneity. A random-effects model with the pooled standard means difference (SMD) and 95 % confidence interval (CI) was performed for the TSH, TT4, TT3, and FT4 outcomes using Comprehensive Meta-Analyses (CMA) Software version 3. Also, we conducted subgroup analyses based on the different types of PCB. The initial search identified 1,279 publications from the main databases 26 of them fulfilled our eligibility criteria for the study, and then five studies among selected studies had sufficient data for analysis. Meta-analysis of data revealed that Aroclor 1260 (SDM: −0.47, 95 % CI: −0.92, −0.01, p=0.044) and PCB 126 (SDM: 0.17, 95 % CI: −0.40, 0.75, p=0.559) significantly increased TSH concentration in the exposed groups vs. the control groups. Related to the effects of PCBs on the TT4, our findings indicated a significant reduction the TT4 concentration of animals exposed to Aroclor 1260 (SDM: −5.62, 95 % CI: −8.30, −2.94, p=0.0001), PCB 118 (SDM: −6.24, 95 % CI: −7.76, −4.72, p=0.0001), PCB 126 (SDM: −1.81, 95 % CI: −2.90, −0.71, p=0.001), and PCB 153 (SDM: −1.32, 95 % CI: −2.29, −0.35, p=0.007) vs. the controls. Our meta-analysis indicated a significant increase in TT3 concentration following exposure to PCB 118 and PCB 153 (SDM: −0.89, 95 % CI: −1.36, −0.42, p=0.0001, and SDM: −1.45, 95 % CI: −2.15, −0.75, p=0.0001, respectively). Aroclor 1254 and PCB 126 significantly decreased TT3 concentration (SDM: 1.25, 95 % CI: 0.29, 2.21, p=0.01 and SDM: 3.33, 95 % CI: 2.49, 4.18, p=0.0001, respectively). PCB 126 significantly decreased FT4 in the exposed groups vs. the control groups (SDM: −7.80, 95 % CI: −11.51, −5.35, p=0.0001).


Summary
Our findings showed an association between PCBs exposure and hypothyroidism in rodents, fish, and chicken embryos.


Outlook
Regarding to the most evidence of hypothyroidism effects of PCBs in animal species, it is necessary to consider large cohort studies to address the association between PCBs exposure and thyroid function impairment in humans.