Isolated, solvent-extracted lignin from candlenut (Aleurites moluccana) biomass was subjected to catalytic depolymerization in methanol with an added pressure of H₂, using a porous metal oxide catalyst (PMO) derived from a Cu-doped hydrotalcite-like precursor. The Cu-PMO was effective in converting low-molecular weight lignin into simple mixtures of aromatic products in high yield, without char formation. Gel permeation chromatography was used to track changes in molecular weight as a result of the catalytic treatments and product mixtures were characterized by ¹H and ¹³C NMR spectroscopy. In the temperature range 140–220 °C, unusual C9 catechols were obtained with high selectivity. Lignin conversion of >90% and recovery of methanol-soluble products in yields of was >70% was seen at 180 °C with optimized catalyst and biomass loadings. At 140 °C, 4-(3-hydroxypropyl)-catechol was the major product and could be isolated in high purity.

The global plasticizer market is projected to increase from $17 billion in 2022 to $22.5 billion in 2027. Various emerging/alternative plasticizers entered the market following the ban on several phthalate plasticizers because of their harmful effects. However, there are limited data (especially peer-reviewed) on emerging plasticizers’ toxicity and environmental impact. This review compiles available data on toxicity, exposure, environmental effects, and safe production of emerging plasticizers. It identifies gaps in scientific research and provides evidence that emerging plasticizers are potential cases of regrettable substitution. Several alternative plasticizers, such as acetyl tributyl citrate (ATBC), diisononyl cyclohexane-1,2 dicarboxylate (DINCH), tris-2-ethylhexyl phosphate (TEHP), tricresyl phosphate (TCP), tris-2-ethylhexyl phosphate (TPHP), bis-2-ethylhexyl terephthalate (DEHT), and tris-2-ethylhexyl trimellitate (TOTM), show potential endocrine-disrupting properties and other toxic characteristics. Some chemicals like bis-2-ethylhexyl adipate (DEHA), diisobutyl adipate (DIBA), ATBC, DINCH, bis-2-ethylhexyl sebacate (DOS), diethylene glycol dibenzoate (DEGDB), DEHT, and phosphate esters showed the potential to cause toxicity in aquatic species. Plus, there is great lack of information on compounds like diisononyl adipate (DINA), dibutyl adipate (DBA), diisodecyl adipate (DIDA), dipropylene glycol dibenzoate (DPGDB), dibutyl sebacate (DBS), alkylsulfonic phenyl ester (ASE), trimethyl pentanyl diisobutyrate (TXIB), DEGDB and bis-2-ethylhexyl sebacate (DOS). Some compounds like epoxidized soybean oil (ESBO), castor-oil-mono-hydrogenated acetate (COMGHA), and glycerin triacetate (GTA) are potentially safer or less toxic. Alternative plasticizers such as adipates (log K_ow 4.3–10.1), cyclohexane dicarboxylic acids (log K_ow 10), phosphate esters (log K_ow 2.7–9.5), sebacates (log K_ow 6.3–10.1), terephthalates (log K_ow 8.4), and vegetable oil derivatives (log K_ow 6.4–14.8) have log K_ow values that are comparable to phthalate plasticizers (log K_ow 7.5–10.4), indicating potential bioaccumulation and health consequences. Field studies have demonstrated that phosphate esters can undergo bioaccumulation and biomagnification, but there is a lack of bioaccumulation studies for other compounds. We also discuss the metabolism of emerging plasticizers, though data are limited. Our article highlights that numerous alternative compounds display potential health and ecological risks, indicating they might not be suitable substitutes for legacy plasticizers. There is also a lack of scientific data on most emerging plasticizers. This way, we call for increased research and timely regulatory action to prevent global contamination and health risks. Finally, this study presents a scientifically robust protocol to avoid harmful substitutions and ensure the production of safer chemicals.

Bisphenol A (BPA) and phthalates are important chemical building blocks in the plastics industry. They are also ubiquitous contaminants in the human body, wildlife, and the environment ( CDC and NCEH, 2018; Teuten et al., 2009). Despite longstanding questions over their safety, BPA and phthalates are still used in consumer products around the globe because it has been difficult to develop economical and safe replacements ( Lowell Center for Sustainable Production, 2011; Ritter, 2011). One reason for their continued use is that during initial toxicity testing over 50 years ago, BPA and phthalates were not identified as harmful using traditional toxicological methods. Historically, toxicity was evaluated using high-dose testing under the assumption of a linear dose response curve. However, this paradigm of “the dose makes the poison” does not hold for BPA, phthalates, and other endocrine disrupting chemicals. The unique properties of BPA and phthalates, including low-dose effects, nonmonotonic dose response curves (NMDRCs), and quick metabolism, disobey traditional principles of toxicology ( Vandenberg et al., 2012). Our journey to understand and incorporate these properties into toxicological methods has triggered a paradigm shift within the field of toxicology ( Kuhn, 1970).

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.