Mei-Hui Li

Toxicity of perfluorooctane sulfonate and perfluorooctanoic acid to plants and aquatic invertebrates.

Acute toxicities of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were tested on four freshwater species and three plant species. PFOS was more toxic than PFOA for all species tested in this study. Similar time‐response patterns of PFOS and PFOA toxicity were observed for each tested species. Values of the 48‐h LC50 of PFOS for all test species ranged from 27 to 233 mg/L and values of the 96‐h LC50 for three of the species ranged from 10 to 178 mg/L. Values of the 48‐h LC50 of PFOA for all test species ranged from 181 to 732 mg/L and values of the 96‐h LC50 for three of the species ranged from 337 to 672 mg/L. The most sensitive freshwater species to PFOS was green neon shrimp (Neocaridina denticulate) with a 96‐h LC50 of 10 mg/L. Of the aquatic organisms tested, the aquatic snail (Physa acuta) always has the highest resistance to PFOS or PFOA toxicity over each exposure period. Both PFOS and PFOA had no obvious adverse effect on seed germination for all three plant species. Five‐day EC50 of root elongation was more sensitive to LC50 of seed germination in this study. Based on EC10, EC50, and NOECs, the 5‐day root elongation sensitivity of test plants to both PFOS and PFOA was in the order of lettuce (Lactuca sativa) > pakchoi (Brassica rapa chinensis) > cucumber (Cucumis sativus). Based on the results of this study and other published literature, it is suggested that current PFOS and PFOA levels in freshwater may have no acute harmful ecological impact on the aquatic environment. However, more research on the long‐term ecological effects of PFOS and PFOA on aquatic fauna are needed to provide important information to adequately assess ecological risk of PFOS and PFOA.

Effects of nonylphenol on cholinesterase and carboxylesterase activities in male guppies (Poecilia reticulata).

Compared to the estrogenic effects of 4-nonylphenol (NP), there is little data available on other potential toxic effects of NP in aquatic animals. The effects of NP on cholinesterase (ChE) and carboxylesterase (CbE) activities of male guppies exposed to 10, 60, 150, or 300 μg L(-1) NP were examined after 1, 2, 4, and 7 days of treatment. A significant muscle ChE inhibition, that used acetylthiocholine iodide as a substrate, was noted in male guppies in all NP treatment groups after a 4-day exposure, and 60 and 150 μg L(-1) of NP treatment groups after a 7-day exposure. All guppies exposed to 300 μg L(-1) NP died during the 7-day treatment. However, there was no significant inhibition of muscle ChE that used butyrylthiocholine iodide as a substrate in male guppies for any NP treatments in different exposure times. There were no CbE activity differences in livers of male guppies among NP treatment groups after different exposure times. This is the first report showing the ChE activity inhibition by NP in fish. Further mechanistic studies are needed to define how NP directly or indirectly alters ChE activities at molecular level. The implication of ChE inhibition of NP on potential impacts of aquatic animals also warrants further research.

Environmental polychlorinated biphenyls: Acute toxicity of landfill soil extract to female prepubertal rats

Subsurface soil from a National Priorities List landfill containing about 2.5% polychlorinated biphenyls (PCBs) was extracted and the extract cleaned by Florisil® slurry and alumina column chromatography. The refined extract contained 48 mg/mL PCB, mainly trichlorobiphenyls and tetrachlorobiphenyls, traces of polychlorinated naphthalenes, 125 μg/mL 2,2-bis-p-chlorophenyl-1, 1-dichloroethylene (DDE), and low levels of chlorinated dibenzofurans. The refined extract was dissolved in corn oil and administered intraperitoneally to weanling (day 20) female rats on days 20 and 21; rats were terminated on day 22. Limited data indicated possible hematopoietic effects, including neutrophilia. There were no changes in relative uterus, kidney, or adrenal gland weights between total doses of 3 to 96 mg/kg total PCB. Relative liver weights increased significantly at 36 mg/kg and activities of P450s 1A1 (as ethoxyresorufin O-dealkylase) and 2B (as pentoxyresorufin O-dealkylase) increased at 12 mg/kg and plateaued at 36 (P450 1A1) or 48 (P450 2B) mg/kg. Serum total thyroxine (T4) declined significantly at doses of 36 mg/kg and greater; thyroid follicular epithelial cells were significantly larger within the same dose range, but the follicular colloid area decreased to less than 60% control values at 12 mg/kg and remained at this size through 72 mg/kg. Maximum mobilization of T4 apparently occurred at 12 mg/kg and attenuated measured declines in circulating levels. Even though a large proportion of proven and probable estrogenic chlorobiphenyls (CBs) were present, the lower amounts of more potent antiestrogenic aryl hydrocarbon (Ah) receptor agonists and/or decreased responsiveness because of low serum T4 levels may have antagonized the uterotropic response.

Developmental exposure to decabrominated diphenyl ether (BDE‐209): Effects on sperm oxidative stress and chromatin dna damage in mouse offspring

Polybrominated diphenyl ethers (PBDEs) are used as brominated flame retardants and have been found in human milk in recent years. This study investigates whether prenatal exposure to decabrominated diphenyl ether (BDE‐209) induces sperm dysfunction in male offspring. Pregnant CD‐1 mice were gavaged once daily with corn oil (control), 10, 500, and 1500 mg kg−1 body weight of BDE‐209 from day 0 of gestation to day 17. The outcomes of male reproductive parameters were assessed on postnatal day 71. Anogenital distance, sperm‐head abnormalities, and testicular histopathology were significantly affected in male offspring prenatally exposed to 1500 mg kg−1. Significant increases in the tendency for sperm DNA denaturation (αT) induction and the DNA fragmentation index (DFI) were found in those exposed to 10, 500, and 1500 mg kg−1 (P < 0.05). We observed a significant increase of sperm hydrogen peroxide (H2O2) generation in the 10 and 1500 mg/kg/day groups compared to the control group (P < 0.05). Although our findings suggested that the mechanisms underlying BDE‐209‐induced sperm DNA damage and H2O2 generation might not be represented as a dose‐response relationship, we found that the greater the excess production of sperm H2O2, the greater the sperm αT (r = 0.65, P = 0.0155) and DFI (r = 0.53, P = 0.002). In conclusion, developmental exposure to BDE‐209 induced sperm‐head abnormality, oxidative stress, chromatin DNA damage, and testicular histopathological changes. These findings suggest that BDE‐209‐induced male reproductive effects might involve the formation of sperm H2O2 which attacks nucleic acids via H2O2 generation.

Survival, mobility, and membrane-bound enzyme activities of freshwater planarian, Dugesia japonica, exposed to synthetic and natural surfactants

Surfactants are a major class of emerging pollutants widely used in large quantities in everyday life and commonly found in surface waters worldwide. Freshwater planarian was selected to examine the effects of different surfactants by measuring mortality, mobility, and membrane-bound enzyme activities. Among the 10 surfactants tested, the acute toxicities of betaine and polyethylene glycol (PEG-200) to planarians were relatively low, with a median lethal concentration (LC50) greater than 10,000 mg/L. The toxicity to planarians of the other eight surfactants based on 48-h LC50 could be arranged in the descending order of cetylpyridinum chloride (CPC) > 4-tert-octylphenol (4-tert-OP) > ammonium lauryl sulfate > benzalkonium chloride > saponin > sodium lauroylsarcosinate > dioctyl sulfosuccinate > dodecyl trimethyl ammonium bromide (DTAB). Both CPC and 4-tert-OP were very toxic to planarians, with 48-h LC50 values <1 mg/L. The median effective concentrations (EC50s) of planarian mobility were in the 0.1 to 50 mg/L range and were in the same range as the 24-h LC50 of planarians exposed to different surfactants, except for DTAB. In addition, significant inhibition of cholinesterase activity activities was found in planarians exposed to 4-tert-OP at 2.5 and 5 mg/L and to saponin at 10 mg/L after 2-h treatments. This result suggests that planarian mobility responses can be used as an alternative indicator for acute toxicity of surfactants after a very short exposure period.

Acute toxicity of 30 pharmaceutically active compounds to freshwater planarians, Dugesia japonica

Pharmaceutically active compounds are produced worldwide and consumed in large quantities, so these chemicals are frequently detected in limnic environments posing potential ecological risks. Thirty pharmaceutically active compounds were selected for examination of their acute toxicity for freshwater planarians (Dugesia japonica). Among the 30 compounds tested, diclofenac, mefenamic acid, naproxen, propranolol HCl, and diphenhydramine HCl had a 48-h nominal LC50 below10 mg L−1, and for 18 chemicals, it exceeded 100 mg L−1. The 96-h nominal LC50 was below 10 mg L−1 for diclofenac, mefenamic acid, naproxen, propranolol HCl, diltiazem HCl, diphenhydramine HCl, hydroxyzine HCl, and triprolidine HCl, and for 15 chemicals, it exceeded 100 mg L−1. Among different therapeutic groups, analgesics were most toxic to planarians, and antibiotics were least toxic. Antihistamines and beta blockers varied in their acute toxicity to planarians. At the current environmental levels, none of the tested pharmaceutically active compounds may have acutely harmful impacts on aquatic invertebrates. To answer the question whether chronic, long-term exposure to pharmaceutically active compounds may entail ecological risks for aquatic ecosystems, further investigations with different end points in multiple species tests are needed.

Acute toxicity of benzophenone-type UV filters and paraben preservatives to freshwater planarian, Dugesia japonica

Fourteen benzophenone-type UV filters and four paraben preservatives were selected to examine their acute toxicities on Dugesia japonica. The 48-h LC50 values for planarians exposed to benzophenone-type UV filters can be ranked as oxybenzone > mexenone > 5-chloro-2-hydroxybenzophenone > 2,4-dihydroxybenzophenone > 2-hydroxybenzophenone > dioxybenzone > benzophenone > 2,2′,4,4′-tetrahydroxybenzophenone > 4-hydroxybenzophenone > 3-hydroxybenzophenone > 4,4′-dihydroxybenzophenone > 2,2′-dihydroxy-4,4′-dimethoxybenzophenone > 2,3,4-trihydroxybenzophenone > sulisobenzone with a range from 0.9 to 145 mg L−1 with a similar sequence for the 96 h LC50 values, ranging from 0.5 to 77 mg L−1. The 48 and 96 LC50 values for planarians exposed to paraben preservatives can be ranked as butylparaben > propylparaben > ethylparaben > methylparaben. Among all the tested chemicals, oxybenzone was the most toxic and sulisobenzone the least toxic chemical to planarian at each exposure period. Most benzophenone-type UV filters are toxic to aquatic animals with 48 h LC50 values less than 10 mg L−1, except for 2,2′-dihydroxy-4,4′-dimethoxybenzophenone, 2,3,4-trihydroxybenzophenone, and sulisobenzone. Because of their common occurrence in aquatic environment, more studies on aquatic toxicities of benzophenone-type UV filters and paraben preservativs are needed to provide important information to adequately assess their ecological risk.

Bioaccumulation and Toxicodynamics of Cadmium to Freshwater Planarian and the Protective Effect of N-Acetylcysteine

Although toxic responses of freshwater planarians after exposure to environmental toxicants can be observed through external toxicological end points, physiological responses inside the bodies of treated planarians have rarely been investigated. The present study was designed, using cadmium (Cd) as a reference toxicant, to determine its bioaccumulation and toxicodynamics in the freshwater planarian, Dugesia japonica, after acute toxicity was obtained. Accumulated Cd concentrations, metallothionein levels, and the oxidative status in planarians were determined after exposure to Cd. Furthermore, we hypothesized that the acute death of Cd-treated planarians was associated with increased oxidative stress. After Cd-treated planarians were coexposed to antioxidant, N-acetylcysteine (NAC), we found that NAC protected planarians from Cd lethality by maintaining the oxidative status and decreasing the bioaccumulation of Cd. The results of the present study support planarians being used as a practical model for toxicological studies of environmental contaminants in the future.

Acute toxicity of industrial endocrine-disrupting chemicals, natural and synthetic sex hormones to the freshwater planarian, Dugesia japonica

Many chemicals commonly occurring in surface water are found to be hormonally active. Fourteen compounds including four sex hormones, three synthetic hormones, one non-steroidal anti-androgen, and six industrial endocrine-disrupting chemicals were selected to examine their acute toxicities on the freshwater planarian, Dugesia japonica. Among all test chemicals, diethylstilbestrol had the highest toxicity. Relatively, the toxicities of the synthetic hormones were higher than the natural ones. Among the six industrial endocrine-disrupting chemicals tested, bisphenol A was the most toxic, with a 48-h LC50 of 8.3 mg L−1. Overall, the natural or synthetic hormones, other than estrone and estriol, were more acutely toxic to planarians than the industrial endocrine disruptors tested. The acute toxicities of the test chemicals to Dugesia japonica were in the same order of magnitude as those to Daphnia magna based on available published data. Despite this study used non-environmentally relevant levels, such kinds of chemicals do not exist singly in the aquatic environment, but typically act in synergistic and/or additive ways in the complex environmental mixtures, and the total estrogen equivalents are much higher than a single chemical. This study stands as a starting point for other acute and chronic assays, namely using mixtures.

Disturbances to neurotransmitter levels and their metabolic enzyme activity in a freshwater planarian exposed to cadmium

Using specific neurobehaviors as endpoints, previous studies suggested that planarian neurotransmission systems could be targets of Cd neurotoxicity. However, direct evidence for disturbed neurotransmission systems by Cd in treated planarians is still lacking. In planarians, dopamine (DA) and serotonin (5-HT) play critical roles in neuromuscular function, but little is known about their metabolic degradation. Therefore, in this study, we attempted to determine the appearances of DA, 5-HT, and their metabolic products in the freshwater planarian Dugesia japonica, characterize the activity of enzymes involved in their metabolism, and investigate the effects of Cd on planarian 5-HTergic and DAergic neurotransmission systems. Only DA, 5-HT, and 5-hydroxyindole-3-acetic acid (5-HIAA) were found in planarian tissues. Further enzymatic study revealed the activity of planarian monoamine oxidase (MAO) but not catechol-O-methyl transferase (COMT). These findings suggest that planarian MAO catalyzes the metabolism of 5-HT into 5-HIAA. However, DA metabolites from the MAO-involved metabolic pathway were not found, which might be due to a lack of COMT activity. Finally, in Cd-treated planarians, tissue levels of 5-HT and DA were decreased and MAO activity altered, suggesting that planarian neurotransmission systems are disturbed following Cd treatment.