No information is available on the long-term effects on thyroid and growth hormones of children exposed to phthalate-tainted products, despite the infamous 2011 Taiwan phthalate episode. We investigated estimated daily intake levels and their long-term effects on serum thyroid and growth hormone levels in children.We recruited 166 children (2–18 years old) in three visits who provided specimens and filled out a questionnaire from the Risk Assessment of Phthalate Incident in Taiwan (RAPIT) project study from 2012 to 2016. Morning spot urine samples were analyzed for nine phthalate metabolites. Serum thyroid (triiodothyronine [T₃], thyroxine [T₄], and free T₄) and growth hormone (insulin-like growth factor-1 [IGF-1] and its binding protein 3 [IGF-BP3]) levels were measured. A generalized estimating equation model was used to evaluate associations between phthalate metabolite levels and children’s thyroid and growth hormone levels.The median metabolite levels of monomethyl phthalate (MMP), Σdibutyl phthalate (DBP), and Σdi-(2-ethylhexyl) phthalate (DEHP) at visits 1, 2, and 3 were 6.59, 10.5, and 21.0 ng/mL, 0.15, 0.24, and 0.20 nmol/mL, and 0.15, 0.17, and 0.12 nmol/mL, respectively. After adjusting for potential confounding factors, we found that levels of urinary MMP were negatively associated with T₃ (β = −0.013, p = 0.047), T₄ (β = −0.016, p = 0.006), free T₄ (β = −0.012, p = 0.002), and IGF-BP3 (β = −0.025, p = 0.003). Urinary mono-ethyl phthalate (MEP) was negatively associated with IGF-1 (β = −0.027, p = 0.029) and IGF-BP3 (β = −0.016, p = 0.018). In addition, serum free T₄ was positively associated with urinary mono-2-ethyl-5-hydroxy hexyl phthalate (MEHHP) (β = 0.016, p = 0.043), mono-2-ethyl-5-oxohexyl phthalate (MEOHP) (β = 0.015, p = 0.024), and ΣDEHPm (β = 0.019, p = 0.020).Our findings support the hypothesis that specific phthalates disturb the hemostasis of thyroid and growth hormone levels in children exposed to phthalate-tainted products.

Substantial pieces of evidence support the potential of exogenous toxins in disrupting neuroimmune homeostasis. It appears that mycotoxins are one of the noticeable sources of naturally occurring substances dysregulating the immune system, which involves the physiology of many organs, such as the central nervous system (CNS). The induction of inflammatory responses in microglial cells and astrocytes, the CNS resident cells with immunological characteristics, could interrupt the hemostasis upon even with low-level exposure to mycotoxins. The inevitable widespread occurrence of a low level of mycotoxins in foods and feed is likely increasing worldwide, predisposing individuals to potential neuroimmunological dysregulations. This paper reviews the current understanding of mycotoxins’ neuro-immunotoxic features under low-dose exposure and the possible ways for detoxification and clearance as a perspective.

The wide use of phthalates, as phthalates are used in the manufacturing of not only plastics but also many others goods, has become a main concern in the current century because of their potency to induce deleterious effects on organism health. The toxic effects of phthalates such as reproductive toxicity, cardiotoxicity, hepatotoxicity, nephrotoxicity, teratogenicity, and tumor development have been widely indicated by previous experimental studies. Some of the important mechanisms of toxicity by phthalates are the induction and promotion of inflammation, oxidative stress, and apoptosis. Awareness of the involved molecular pathways of these mechanisms will permit the detection of exact molecular targets of phthalates to protect or treat their toxicity. Up to now, various transcription factors and signaling pathways have been associated with phthalate-induced toxicity which by influencing on nuclear surface and the expression of different genes can alter cell hemostasis. In different studies, the role of nuclear factor erythroid 2–related factor 2 (Nrf2), nuclear factor-κB (NF-κB), and phosphatidylinositol-3-kinase (PI3K)/AKT signaling pathways in processes of oxidative stress, inflammation, apoptosis, and cancer has been shown following exposure to phthalates. In the present review, we aim to survey experimental studies (in vitro and in vivo) in order to show firstly the most involved receptors and also the importance and the role of the mentioned signaling pathways in phthalate-induced toxicity, and with considering this point, the future studies can focus on these molecular targets as a strategic method to reduce environmental chemicals-induced toxicity especially phthalates toxic effects.

Chlorpyrifos, an organophosphate insecticide, disturbs blood glucose hemostasis in experimental models and causes metabolic disorders. However, there are controversial findings of its impact on the BS level. The present meta-analysis aimed to investigate blood gluocse levels in rats exposed to chlorpyrifos. Present systematic review and meta-analysis study was done by searching in the online databases, including Google Scholar, Web of Science, PubMed, and Scopus. Data were analyzed by performing “random effects meta-regression.” Findings were expressed as standardized mean value and 95% confidence interval (CI). Heterogeneity between studies was assessed using I-square and Q test. Meta-analysis of 7 animal studies indicated the dose-dependence manner of chlorpyrifos exposure on the blood glucose levels. The subgroup analysis indicated that exposure to low doses of chlorpyrifos significantly increased the blood glucose levels in exposed animals versus the nonexposed (0.11; 95% CI: − 1.14, 1.36, z = 2.25, p = 0.03, I2 = 90.1%, p < 0.001) and high doses markedly decreased blood glucose levels in exposed rats versus the nonexposed (7.34; 95%CI: − 9.35, − 5.32, z = 6.41, p < 0.001, I2 = 96.9%, p < 0.001). The random effects and pooled analysis indicated that the blood glucose levels were 4.22-fold lower in exposed animals versus the nonexposed ones (95% CI: − 5.59,− 2.85; Z = 3.97; p < 0.001); therefore, heterogeneity was significant (I2 = 96.5%, p < 0.001). The present finding indicated the association between chlorpyrifos exposure and a decrease in blood glucose levels. However, more studies should be designed to clarify this effect of chlorpyrifos exposure on blood glucose levels and involved mechanisms.