• Journal of Yeungnam Medical Science
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• v.35 no.2
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• pp.156-164
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• 2018

Environmental contaminants are one of the important causal factors for development of various human diseases. In particular, the perinatal period is highly vulnerable to environmental toxicants and resultant dysregulation of fetal development can cause detrimental health outcomes potentially affecting life-long health. Perfluoroalkyl compounds (PFCs), emerging environmental pollutants, are man-made organic molecules, which are widely used in diverse industries and consumer products. PFCs are non-degradable and bioaccumulate in the environment. Importantly, PFCs can be found in cord blood and breast milk as well as in the general population. Due to their physicochemical properties and potential toxicity, many studies have evaluated the health effects of PFCs. This review summarizes the epidemiological and experimental studies addressing the association of PFCs with neurotoxicity and immunotoxicity. While the relationships between PFC levels and changes in neural and immune health are not yet conclusive, accumulative studies provide evidence for positive associations between PFC levels and the incidence of attention deficit hyperactivity disorder and reduced immune response to vaccination both in children and adults. In conclusion, PFCs have the potential to affect human health linked with neurological disorders and immunosuppressive responses. However, our understanding of the molecular mechanism of the effects of PFCs on human health is still in its infancy. Therefore, along with efforts to develop methods to reduce exposure to PFCs, studies on the mode of action of these chemicals are required in the near future.

• Environmental Engineering Research
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• v.25 no.3
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• pp.281-289
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• 2020

Environmental fate of ionizable organic pollutants such as perfluoroalkyl acids (PFAAs) are of increasing interest but has not been well understood because of uncertain values for parameters related with atmospheric interphase partitioning behavior. In the present study, not only the values for air-water partition coefficient (K_AW) and dissociation constant (pKa) of PFAAs were induced by adjusting to in situ measurements of air-water distribution coefficient between vapor phase and rainwater but also gas-particle partition coefficients were also estimated using three-phase partitioning model of ionizable organic pollutants, in situ measurements of PFAAs in aerosol and air vapor phase, and obtained parameter values. The pKa values of PFAAs we obtained were close to the minimum values suggested in literature except for perfluorooctane sulfonic acids, and COSMOtherm-modeled K_AW values were assessed to more appropriate among suggested values. When applying parameter values we obtained, it was predicted that air particle-associated fate and transport of PFAAs could be negligible and PFAAs could distribute ubiquitously along the transection from urban to rural region by pH-dependent phase transfer in air. Our study is expected to have some implications in prediction of the environmental redistribution of other ionizable organic compounds.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.55 no.5
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• pp.514-523
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• 2022

Concentrations of perfluoroalkyl substances (PFASs) were measured in seawater, sediment, and biota collected from Gunsan coast, Korea to investigate their occurrence, distribution, and risk of exposure to humans through seafood consumption. The total concentrations of PFASs in seawater, sediment, and biota ranged from 5.97 to 74.9 ng/L, 0.01 to 13.3 ng/g dry weight, and 0.02 to 5.73 ng/g wet weight, respectively. Predominant PFAS compounds differed across matrices, indicating that the distribution of PFASs in multiple environmental samples is governed by their carbon-chain length. The concentrations of PFASs in seawater were significantly negatively correlated with salinity (P<0.01), suggesting terrestrial input (including land-used PFASs) as the major source of PFAS contamination in coastal environments. The estimated daily intakes (EDIs) of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) through seafood consumption were 0.05 and 0.06 ng/kg body weight/day, respectively. The EDIs of PFOA and PFOS measured in this study were lower those the proposed by the United States Environmental Protection Agency and Canada guidelines, indicating limited health risk for Korean population from PFASs through consumption of seafood from Gunsan coastal environment.

• Textile Coloration and Finishing
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• v.28 no.3
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• pp.134-155
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• 2016

Perfluorinated chemicals are highly diverse and widely used. More than 160 substances are pre-registered under REACH and approximately 140 substances are in the existing chemicals list of Korea from this chemical group. Chemical structures of PFCs that are globally prohibited and still in uses are identified with OECD's classification of PFCs with an overall review on their uses in consumer products including textile products. Case examples for current domestic situation on use of PFCs as a major component of water-repelling agents in textile products as well as a brief summary of eight major PFC manufacturers' situation are presented from our survey study along the supply chains and the most recent report of EPA stewardship programme, respectively.

• Environmental Analysis Health and Toxicology
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• v.25 no.2
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• pp.153-159
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• 2010

Perfluorooctane sulfonic acid (PFOS) and Perfluorooctanoic acid (PFOA) are the principal chemicals known as perfluoroalkyl acids (PFAs). Despite the widespread use of these compounds, relatively little is known about their fate and effects. The purpose of this study was to determine the toxic effects of PFOS and PFOA on Daphnia magna. In the acute toxicity test, D. magna were exposed for 48 hours at concentrations of 0, 30, 45, 67.5, 101.25 and 151.88 mg/L PFOS, and 0, 100, 160, 225, 337.5 and 506.25 mg/L PFOA, respectively. In the case of chronic toxicity test, D. magna were exposed through water for 21 days at concentrations of 0, 0.375, 0.75, 1.5, 3 and 6 mg/L PFOS, and 0, 1.25, 2.5, 5, 10 and 20 mg/L PFOA, respectively. Acute toxicity was assessed on the basis of immobility, while chronic toxicity was assessed on the basis of fecundity. The acute toxicity test on PFOS and PFOA showed that the values of $EC_{50}$ were 50.90 mg/L and 253.47 mg/L, respectively. In the chronic test, fecundity was reduced significantly at 1.5 mg/L of PFOS and 10 mg/L of PFOA, respectively. These results indicated that PFOS is more toxic to zooplankton than PFOA, and both chemicals have some hazard demonstrates risk for acute or chronic toxicity to freshwater organism.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.4
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• pp.399-406
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• 2016

Early life neuronal exposure to environmental toxicants has been suggested to be an important etiology of neurodegenerative disease development. Perfluorohexanesulfonate (PFHxS), one of the major perfluoroalkyl compounds, is widely distributed environmental contaminants. We have reported that PFHxS induces neuronal apoptosis via ERK-mediated pathway. Imperatorin is a furanocoumarin found in various edible plants and has a wide range of pharmacological effects including neuroprotection. In this study, the effects of imperatorin on PFHxS-induced neuronal apoptosis and the underlying mechanisms are examined using cerebellar granule cells (CGC). CGC were isolated from seven-day old rats and were grown in culture for seven days. Caspase-3 activity and TUNEL staining were used to determine neuronal apoptosis. PFHxS-induced apoptosis of CGC was significantly reduced by imperatorin and PD98059, an ERK pathway inhibitor. PFHxS induced a persistent increase in intracellular calcium, which was significantly blocked by imperatorin, NMDA receptor antagonist, MK801 and the L-type voltage-dependent calcium channel blockers, diltiazem and nifedipine. The activation of caspase-3 by PFHxS was also inhibited by MK801, diltiazem and nifedipine. PFHxS-increased ERK activation was inhibited by imperatorin, MK801, diltiazem and nifedipine. Taken together, imperatorin protects CGC against PFHxS-induced apoptosis via inhibition of NMDA receptor/intracellular calcium-mediated ERK pathway.