Health impacts of artificial turf: Toxicity studies, challenges, and future directions.

Many communities around the country are undergoing contentious battles over the installation of artificial turf. Opponents are concerned about exposure to hazardous chemicals leaching from the crumb rubber cushioning fill made of recycled tires, the plastic carpet, and other synthetic components. Numerous studies have shown that chemicals identified in artificial turf, including polycyclic aromatic hydrocarbons (PAHs), phthalates, and per- and polyfluoroalkyl substances (PFAS), are known carcinogens, neurotoxicants, mutagens, and endocrine disruptors. However, few studies have looked directly at health outcomes of exposure to these chemicals in the context of artificial turf. Ecotoxicology studies in invertebrates exposed to crumb rubber have identified risks to organisms whose habitats have been contaminated by artificial turf. Chicken eggs injected with crumb rubber leachate also showed impaired development and endocrine disruption. The only human epidemiology studies conducted related to artificial turf have been highly limited in design, focusing on cancer incidence. In addition, government agencies have begun their own risk assessment studies to aid community decisions. Additional studies in in vitro and in vivo translational models, ecotoxicological systems, and human epidemiology are strongly needed to consider exposure from both field use and runoff, components other than crumb rubber, sensitive windows of development, and additional physiological endpoints. Identification of potential health effects from exposures due to spending time at artificial turf fields and adjacent environments that may be contaminated by runoff will aid in risk assessment and community decision making on the use of artificial turf.

Perfluorooctanoic Acid Disrupts Ovarian Steroidogenesis and Folliculogenesis in Adult Mice.

Perfluorooctanoic acid (PFOA) is a synthetic fluorosurfactant used in the manufacturing of fluorotelomers. Although PFOA is no longer produced in the United States, it is environmentally persistent and found in imported food packaging, cookware, and textiles. Previous studies have identified developmental toxicity of PFOA, but little is known about the effects of PFOA on the adult ovary. Thus, this study examined the effects of PFOA on hormone levels, ovarian steroidogenic gene expression, and folliculogenesis in mice in vitro and in vivo. For the in vitro studies, antral follicles from adult female mice were cultured with vehicle control or 1, 10, or 100 µg/ml PFOA for 96 h. For the in vivo studies, adult CD-1 female mice were orally dosed with vehicle control or 1, 5, 10, or 20 mg/kg/day PFOA for 10 days. Gene expression of steroidogenic enzymes, levels of sex steroid hormones, and follicle counts were analyzed. In vitro, PFOA (100 µg/ml) significantly decreased follicle growth, estradiol and estrone levels, and gene expression of StaR, Cyp11a1, and Hsd3b1 compared with controls. In vivo, exposure to PFOA significantly decreased progesterone and pregnenolone levels (5 mg/kg), increased testosterone levels (1 mg/kg), and increased gene expression of Cyp19a1 (1 mg/kg) compared with controls. Exposure to PFOA also significantly altered follicle counts by decreasing primordial follicles and increasing preantral and antral follicles (5 and 10 mg/kg) compared with controls. Collectively, these data show that PFOA disrupts adult ovarian function in a nonmonotonic matter and may pose a risk for premature ovarian failure.

Endocrine disrupting chemicals and reproductive disorders in women, men, and animal models.

This chapter covers the known effects of endocrine disrupting chemicals (EDCs) on reproductive disorders. The EDCs represented are highly studied, including plasticizers (bisphenols and phthalates), chemicals in personal care products (parabens), persistent environmental contaminants (polychlorinated biphenyls), and chemicals in pesticides or herbicides. Both female and male reproductive disorders are reviewed in the chapter. Female disorders include infertility/subfertility, irregular reproductive cycles, early menopause, premature ovarian insufficiency, polycystic ovarian syndrome, endometriosis, and uterine fibroids. Male disorders include infertility/subfertility, cryptorchidism, and hypospadias. Findings from both human and animal studies are represented.

Predicting Properties of Iron(III) TAML Activators of Peroxides from Their III/IV and IV/V Reduction Potentials or a Lost Battle to Peroxidase.

A cyclic voltammetry study of a series of iron(III) TAML activators of peroxides of several generations in acetonitrile as solvent reveals reversible or quasireversible FeIII/IV and FeIV/V anodic transitions, the formal reduction potentials (E°') for which are observed in the ranges 0.4-1.2 and 1.4-1.6 V, respectively, versus Ag/AgCl. The slope of 0.33 for a linear E°'(IV/V) against E°'(III/IV) plot suggests that the TAML ligand system plays a bigger role in the FeIII/IV transition, whereas the second electron transfer is to a larger extent an iron-centered phenomenon. The reduction potentials appear to be a convenient tool for analysis of various properties of iron TAML activators in terms of linear free energy relationships (LFERs). The values of E°'(III/IV) and E°'(IV V-1 ) correlate 1) with the pKa values of the axial aqua ligand of iron(III) TAMLs with slopes of 0.28 and 0.06 V, respectively; 2) with the Stern-Volmer constants KSV for the quenching of fluorescence of propranolol, a micropollutant of broad concern; 3) with the calculated ionization potentials of FeIII and FeIV TAMLs; and 4) with rate constants kI and kII for the oxidation of the resting iron(III) TAML state by H2 O2 and reactions of the active forms of TAMLs formed with donors of electrons S, respectively. Interestingly, slopes of log kII versus E°'(III/IV) plots are lower for fast-to-oxidize S than for slow-to-oxidize S. The log kI versus E°'(III/IV) plot suggests that the manmade TAML catalyst can never be as reactive toward H2 O2 as a horseradish peroxidase enzyme.

Subchronic and Low Dose of Tributyltin Exposure Leads to Reduced Ovarian Reserve, Reduced Uterine Gland Number, and Other Reproductive Irregularities in Female Mice.

Tributyltin (TBT) chloride is an endocrine disrupting chemical associated with reproductive complications. Studies have shown that TBT targets the reproductive tract, impairing ovarian folliculogenesis, and uterine morphophysiology. In this investigation, we assessed whether subchronic and low dose of TBT exposure results in abnormal ovarian follicular reserve and other irregularities in female mice. TBT was administered to female mice (500 ng/kg/day for 12 days via gavage), and reproductive tract morphophysiology was assessed. We further assessed reproductive tract inflammation and oxidative stress. Improper functioning of the reproductive tract in TBT mice was observed. Specifically, irregular estrous cyclicity and abnormal ovarian morphology coupled with reduction in primordial and primary follicle numbers was observed, suggesting ovarian reserve depletion. In addition, improper follicular development and a reduction in antral follicles, corpora lutea, and total healthy ovarian follicles together with an increase in cystic follicles were apparent. Evidence of uterine atrophy, reduction in endometrial gland number, and inflammation and oxidative stress were seen in TBT mice. Further, strong negative correlations were observed between testosterone levels and primordial, primary, and total healthy ovarian follicles. Thus, these data suggest that the subchronic and low dose of TBT exposure impaired ovarian follicular reserve, uterine gland number, and other reproductive features in female mice.

Mechanisms of action of agrochemicals acting as endocrine disrupting chemicals.

Agrochemicals represent a significant class of endocrine disrupting chemicals that humans and animals around the world are exposed to constantly. Agrochemicals can act as endocrine disrupting chemicals through a variety of mechanisms. Recent studies have shown that several mechanisms of action involve the ability of agrochemicals to mimic the interaction of endogenous hormones with nuclear receptors such as estrogen receptors, androgen receptors, peroxisome proliferator activated receptors, the aryl hydrocarbon receptor, and thyroid hormone receptors. Further, studies indicate that agrochemicals can exert toxicity through non-nuclear receptor-mediated mechanisms of action. Such non-genomic mechanisms of action include interference with peptide, steroid, or amino acid hormone response, synthesis and degradation as well as epigenetic changes (DNA methylation and histone modifications). This review summarizes the major mechanisms of action by which agrochemicals target the endocrine system.