Bioaccumulation of perfluoroalkyl substances in greenhouse vegetables with long-term groundwater irrigation near fluorochemical plants in Fuxin, China.

The levels of perfluoroalkyl substances (PFASs) have been growing progressively in the groundwater beneath a fluorochemical industrial park (FIP) in Fuxin of China recently, however, little information is available about whether long-term irrigation with local groundwater could have a potential effect on the bioaccumulation of PFASs in greenhouse vegetables near the FIP. In the present study, groundwater, soil, and vegetable samples were collected from Fuxin with five sampling campaigns during a period of 40 days, and ten target analytes of PFASs in all the samples were analyzed via high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). As the dominant PFAS contaminants, perfluorooctanoic acid (PFOA) and perfluorobutane sulfonate (PFBS) in groundwater samples were determined with the maximum levels of 2.47 and 32.4 µg L-1, respectively. Furthermore, perfluorobutanoic acid (PFBA), PFOA, and PFBS were the major PFASs in greenhouse samples of soil (up to 6.1, 6.8, and 46 ng g dry weight (dw)-1), tomato (up to 87, 1.7, and 13 ng g dw-1), and cucumber (up to 63, 2.6, and 15 ng g dw-1), which were significantly correlated with those in groundwater samples, indicating PFAS contaminations could be introduced into soil and vegetables in the greenhouse through long-term groundwater irrigation. In addition, all the levels of three main PFAS analytes in soil and vegetables presented an overall increasing trend over the period of vegetable growth. The bioaccumulation efficiencies for PFAS contaminants from soil to vegetables were negatively associated with the carbon chain length in PFASs. According to the reference dose (RfD) for PFBA, PFOA, and PFBS from the Minnesota Department of Health (MDH), daily intakes of those three analytes by rural residents in Fuxin were lower than the respective RfD via consumption of greenhouse tomatoes and cucumbers so far. However, long-term surveillance would be focused on greenhouse vegetables near the Fuxin FIP to prevent potential health risks of local residents from increasing PFAS contaminations.

Perfluoroalkyl substances in groundwater and home-produced vegetables and eggs around a fluorochemical industrial park in China.

High-level contaminations of perfluoroalkyl substances (PFASs) were determined in both surface water and groundwater around a fluorochemical industrial park (FIP) in Fuxin, China, over the past few years. Yet little is known about whether groundwater PFAS contaminations in Fuxin could be introduced into home-produced vegetables and eggs in local residences via the application of groundwater for the irrigation or feeding purposes. In the present study, ten PFAS analytes were analyzed via high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) to investigate the extent of PFAS contaminations in the groundwater, soil, and home-produced vegetable and egg samples derived from Fuxin. As the predominant PFAS contaminants, perfluorobutane sulfonate (PFBS) and perfluorooctanoic acid (PFOA) were observed in groundwater beneath the Fuxin FIP with the maximum concentrations of 21.2 and 2.51 µg/L, respectively, which were 24-fold and 5-fold higher individually compared to those reported previously. Both of them were also higher than the updated health advisories for PFBS and PFOA in drinking water issued by the Minnesota Department of Health and the US Environmental Protection Agency. In addition, short-chain PFASs involving perfluorobutanoic acid (PFBA) and PFBS were found to be the major contaminants in both home-produced vegetables and eggs from the residential gardens around the FIP. Statistically significant relationships were determined between the levels of PFBA, PFOA, and PFBS in local groundwater and those observed in home-produced vegetables (p = 0.003, p = 0.025, and p < 0.001), suggesting potential entry of those PFAS contaminants into home-produced vegetables via irrigation with groundwater beneath the FIP.

Phthalate Metabolites in Urine Samples from School Children in Taipei, Taiwan.

In 2011, Taiwan authorities reported that two phthalates, including di-(2-ethylhexyl) phthalate and di-iso-nonyl phthalate, were intentionally introduced into a variety of foods and beverages during the course of 15 years. However, little is known about body burdens of phthalate contaminations in local residents, especially children recently living in Taiwan. In the present study, five target phthalate metabolite analytes-including mono-methyl phthalate, mono-ethyl phthalate, mono-n-butyl phthalate (MBP), mono-benzyl phthalate (MBzP), and mono-(2-ethylhexyl) phthalate (MEHP)-in spot urine samples were analyzed by way of high performance liquid chromatography-tandem mass spectrometry-mass spectrometry. All of the urine samples were collected from 225 healthy school children between 12 and 15 years of age (average 13.6) in the Taipei area, Taiwan, between 2009 and 2010. As the dominant urinary phthalate metabolites in Taiwanese school children, MEHP and MBP contributed 61 and 29 % of all of the target analytes, respectively. MEHP had the highest median of 29.8 µg/g creatinine (range of 13.1-72.8), which was greater than those reported for school children in the other countries during the same period, whereas MBP had a median of 14.3 µg/g creatinine (range 7.91-27.8). Statistically, urinary concentrations of MBP, MBzP, and MEHP were determined to have significantly positive correlations with the ages of Taiwanese school children (p < 0.05). Furthermore, urinary levels of MBzP in male children were considerably greater than those in female children (p = 0.006).

Induction of p53-mediated apoptosis in splenocytes and thymocytes of C57BL/6 mice exposed to perfluorooctane sulfonate (PFOS).

Perfluorooctane sulfonate (PFOS) is a persistent environmental contaminant found in human and wildlife tissues. It has been reported that PFOS can cause atrophy of the immune organs and apoptosis of immunocytes in rodents. However, the mechanism behind such cause is still unclear. To understand the model of cell death and its mechanism on lymphoid cells in vivo, we conducted a dose/response experiment in which 4 groups of male adult C57BL/6 mice (12 mice per group) were dosed daily by oral gavage with PFOS at 0, 0.0167, 0.0833, or 0.8333mg/kg/day, yielding targeted Total Administered Dose (TAD) of 0, 1, 5, or 50mg PFOS/kg, respectively, over 60days. The results showed that spleen and thymus weight were significantly reduced in the highest PFOS-dose-group (TAD 50mg PFOS/kg) compared to the control group, whereas liver weight was significantly increased. We analyzed the cell death via apoptosis with an annexin-V/propidium iodide assay by flow cytometry, and observed that both the percentage of apoptosis and the expression of the pro-apoptotic proteins p53 in splenocytes and thymocytes increased in a dose-related manner after PFOS treatment. We also observed that PFOS induced p53-dependent apoptosis through the cooperation between the Bcl-xl down regulation without changing the Bcl-2 and Bax expression. The down regulation of Bcl-xl was strongly indicating mitochondrial involvement in apoptosis. It is confirmed by the release of cytochrome c and activation of caspase-3. All of these findings establish an important role of p53 and mitochondrial function in PFOS induced toxic environment in the host.

Subchronic effects of perfluorooctanesulfonate exposure on inflammation in adult male C57BL/6 mice.

Previous studies indicate that exposure to perfluorooctanesulfonate (PFOS), a ubiquitous and highly persistent environmental contaminant, induces immunotoxicity in mice. However, few studies have specifically assessed the effects of PFOS on inflammation. This study utilized a standard 60-day oral exposure period to assess the effects of PFOS on the response of inflammatory cytokines [tumor necrosis factor α (TNF-α), interleukin-1 ß (IL-1ß), and interleukin-6 (IL-6)]. Adult male C57BL/6 mice were dosed daily by oral gavage with PFOS at 0, 0.0083, 0.0167, 0.0833, 0.4167, 0.8333 or 2.0833 mg/kg/day to yield a targeted Total Administered Dose (TAD) over 60 days of 0, 0.5, 1, 5, 25, 50, or 125 mg PFOS/kg, respectively. The percentage of peritoneal macrophages (CD11b+ cells) was significantly increased at concentrations ≥ 1 mg PFOS/kg TAD in a dose-dependent manner. Ex vivo IL-1ß production by peritoneal macrophages was elevated substantially at concentrations of ≥ 5 mg PFOS/kg TAD. Moreover, PFOS exposure markedly enhanced the ex vivo production of TNF-α, IL-1ß and IL-6 by peritoneal and splenic macrophages when stimulated either in vitro or in vivo with lipopolysaccharide (LPS). The serum levels of these inflammatory cytokines observed in response to in vivo stimulation with LPS were elevated substantially by exposure to PFOS. PFOS exposure elevated the expression of pro-inflammatory cytokines TNF-α, IL-1ß, IL-6, and proto-oncogene, c-myc, in the spleen. These data suggest that exposure to PFOS modulates the inflammatory response, and further research is needed to determine the mechanism of action.

Target analysis and suspect screening of per- and polyfluoroalkyl substances in paired samples of maternal serum, umbilical cord serum, and placenta near fluorochemical plants in Fuxin, China.

The levels of legacy per- and polyfluoroalkyl substances (PFASs) have been growing in the environmental matrices and blood of residents living around the fluorochemical industrial park (FIP) in Fuxin of China over the past decade. Although some recent studies have reported occurrence of novel PFAS alternatives in biotic and abiotic matrices near fluorochemical facilities worldwide, little is known about novel PFAS congeners in maternal sera, umbilical cord sera, and placentas from the female residents close to the FIP and their related health risks. In this study, 50 paired samples of maternal and cord serum as well as placenta were derived from Fuxin pregnant women at delivery, and 21 target analytes of legacy PFASs in all the samples were analyzed via high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS), revealing that PFBS, PFBA, and PFOA were the dominant PFAS contaminants observed in the whole samples. Based upon the suspect screening through high-resolution mass spectrometry (HRMS), 49 novel PFASs assigned to 11 classes were further identified in the Fuxin samples, of which, 20 novel congeners in 4 classes were reported in human blood and placentas for the first time. Moreover, the coefficients for mother-placenta transfer (Rm/p), placenta-newborn transfer (Rp/n), and mother-newborn transfer (Rm/n) of legacy PFASs could be calculated with median values of 1.7, 1.1, and 2.0, respectively, and Rm/p, Rp/n, and Rm/n for each novel PFAS identified were also estimated with the median values of 0.9, 1.2, and 0.8 individually. Accordingly, novel PFASs contributed 90% of all the legacy and novel PFASs in maternal sera and even occupied 96% of the whole PFASs in both placentas and cord sera. In addition, significant associations were determined among the neonate birth outcomes and serum concentrations of thyroid hormone, sex hormone, and glucocorticoid, together with the levels of certain legacy and novel PFASs in cord sera.

Human nails analysis as biomarker of exposure to perfluoroalkyl compounds.

Extensive human exposure to perfluoroalkyl compounds (PFAA) together with their persistence and various toxicities have arisen increasing concern. A noninvasive method would improve exposure assessment for large population, especially the children susceptible to contaminants. The aim of the study was to assess the use of PFAA measurements in human nails as a biomarker of exposure to PFAAs. Fingernail, toenail, and blood samples were collected from 28 volunteers. The PFAA concentrations were determined by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Six PFAA were detected in nails, with perfluorooctane sulfonate (PFOS) being the compound with the highest median concentration (33.5 and 26.1 ng/g in fingernail and toenail, respectively). Followed was perfluorononanoate (PFNA), with the median concentrations of 20.4 and 16.8 ng/g, respectively, in fingernail and toenail. Other PFAA detected were perfluorooctanoate (PFOA), perfluorodecanoate (PFDA), perfluorododecanoate (PFDoA), and perfluorotetradecanoate (PFTA), with median levels ranging between 0.19 and 8.94 ng/g. PFOS and PFNA concentrations in fingernail significantly correlated with those in serum. Fingernail PFOS and PFNA levels were 2.8 and 24.4 times, respectively, higher than the serum levels. The accumulation of PFAA in nails, together with its advantages in noninvasive sampling and ability of reflecting long-term exposure, made nails PFAA an attractive biomarker of exposure.

Perfluorooctane sulfonate increased hepatic expression of OAPT2 and MRP2 in rats.

The toxicity of perfluorooctane sulfonate (PFOS), a persistent organic compound, is of great concern. Several studies have reported that PFOS decreases circulating thyroid hormone (TH) concentrations. However, the mechanisms involved remain to be determined. Female rats were exposed to (1) vehicle; (2) PFOS (0.2, 1.0, and 3.0 mg/kg); (3) propylthiouracil (PTU, 10 mg/kg); or (4) PTU (10 mg/kg) + PFOS (3.0 mg/kg) by gavage once a day for 5 consecutive days. Parameters including contents of total T4 (TT4) and total T3 (TT3) in both serum and bile, serum concentrations of transthyretin and thyroglobulin, as well as transcripts of transporters involved in hepatic uptake and efflux of T4 were determined in control and PFOS-exposed groups. TT4 and TT3 were also analyzed in PTU and PTU + PFOS groups in order to reflect the different hormone effects between PFOS, PTU, and PFOS + PTU. Results showed that serum TT4 and TT3 decreased, while bile TT4 and TT3 remained stable following PFOS exposure. Exposure to 3.0 mg/kg of PFOS significantly enhanced hepatic organic anion transporter OATP2 mRNA expression (1.43 times of control). Treatment with PFOS increased hepatic expression of multidrug resistance--associated protein MRP2, approximately 1.80 and 1.69 times of control in 1.0 and 3.0 mg/kg groups, respectively. Spearman's correlation coefficients revealed that MRP2 mRNA expression correlated well with serum TT4 level (r = -0.528, P = 0.012). Serum thyroglobulin and transthyretin levels remained stable. Serum TT3, bile TT4, and bile TT3 were significantly different between PFOS and PTU groups. No significant differences of TT4 and TT3 in both serum and bile were observed between PTU and PTU + PFOS (P > 0.05). In conclusion, PFOS increased hepatic expression of OAPT2, which could possibly enhance hepatic uptake and metabolism of T4 in rats. PFOS-induced TT4 deficiency is mainly due to the extrathyroidal metabolism of T4, which is probably different from the classic goitrogen, PTU.

Sub-chronic effect of perfluorooctanesulfonate (PFOS) on the balance of type 1 and type 2 cytokine in adult C57BL6 mice.

As a ubiquitous and highly persistent environmental contaminant, the clear mechanisms to explain any perfluorooctanesulfonate (PFOS)-induced immunotoxicity are still unknown. This study here sought to examine the ability of PFOS to potentially perturb T-helper (T(H))-1 and T(H)-2 cell cytokine secreting activities, as well as to cause shifts in antibody isotype levels, and possible mechanisms involved in PFOS-induced immunotoxicity. Adult male C57BL/6 mice were exposed to PFOS daily via gavage for 60 days [0, 0.5, 1, 5, 25, or 50 mg/kg total administered dose (TAD)]. One day after the final exposure, the ex vivo production of the T(H)1-type cytokines (IL-2 and IFN-γ), T(H)2-type (IL-4), and IL-10 cytokines by isolated splenocytes, serum levels of immunoglobulin (Ig) were assessed via ELISA or ELISPOT. The results showed that IL-4 secretion was increased at exposure ≥5 mg PFOS/kg TAD in a dose-dependent manner. PFOS exposure increased IL-10 but decreased IL-2 and IFN-γ formation markedly at 50 mg PFOS/kg TAD. Serum levels of sheep red blood cells (SRBC)-specific IgM synthesis decreased significantly with PFOS exposure in a dose-related manner; serum SRBC-specific IgG, IgG1, and IgE levels increased with 50 mg PFOS/kg TAD regimens. These results indicated that, after a long-term exposure to PFOS, a host's immune state is likely to be characterized by a shift toward a more T(H)2-like state that, in turn, may lead to enhancement of their humoral response and suppression of their cellular response at levels of upper range for occupationally exposed workers or approximately 150-fold for general human population.

Immunotoxic changes associated with a 7-day oral exposure to perfluorooctanesulfonate (PFOS) in adult male C57BL/6 mice.

Perfluorooctanesulfonate (PFOS) is a widespread contaminant in the environment, as well as in wildlife and in humans. Toxicity tests in rodents have raised concerns about potential developmental, reproductive, and systemic effects of PFOS. However, there is little information about the effect of PFOS on immune system. In this study, adult male C57BL/6 mice were given by gavage 0, 5, 20 or 40 mg PFOS/kg day(-1) for 7 days. The results showed that PFOS exposure decreased food intake and body weight and increased liver mass and serum corticosterone levels in a dose-dependent manner. Flow cytometry analysis showed that the number of lymphocytic subpopulation cells decreased significantly in 20 or 40 mg PFOS/kg day(-1) group in comparison with normal C57BL/6 mice. Treatment with PFOS also markedly depressed the natural killer (NK) cell activity, lymphocyte proliferation and the plaque-forming cell (PFC) response. These results indicate that PFOS exposure can affect the immunity function in mice.

Chronic effects of perfluorooctanesulfonate exposure on immunotoxicity in adult male C57BL/6 mice.

A paucity of data exists to corroborate the few studies that report immune suppression after exposure to perfluorooctanesulfonate (PFOS). In this study, adult male C57BL/6 mice were exposed to PFOS daily via gavage for 60 days [0, 0.5, 5, 25, 50, or 125 mg/kg total administered dose (TAD)]. The results showed that liver mass was significantly increased at > or =5 mg PFOS/kg TAD and in a dose-dependent manner. Lymphocyte proliferation and natural killer cell activity were altered in male mice. Plaque forming cell (PFC) response was suppressed beginning at 5 mg/kg TAD. Based on the liver mass and PFC response, the no observed adverse effect level and lowest observed adverse effect level for male mice exposed PFOS for 60 days was 0.5 and 5 mg/kg TAD, respectively. Measured PFOS serum concentrations at these dose levels were 0.674 +/- 0.166 and 7.132 +/- 1.039 mg/l, respectively. These results indicate that PFOS exposure can affect the immunity function in mice at levels approximately 50-fold for highly exposed human populations.

Effects of perfluorooctane sulfonate on rat thyroid hormone biosynthesis and metabolism.

The potential toxicity of perfluorooctane sulfonate (PFOS), an environmentally persistent organic pollutant, is of great concern. The present study examines the ability of PFOS to disturb thyroid function and the possible mechanisms involved in PFOS-induced thyroid hormone alteration. Male Sprague-Dawley rats were exposed to 1.7, 5.0, and 15.0 mg/L of PFOS in drinking water for 91 consecutive days. Serum was collected for analysis of total and free thyroxine (T4), total triiodothyronine (T3), and thyrotrophin (TSH). Thyroid and liver were removed for the measurement of endpoints closely related to thyroid hormone biosynthesis and metabolism following PFOS exposure. Determined endpoints were the messenger RNA (mRNA) levels for two isoforms of uridine diphosphoglucuronosyl transferases (UGT1A6 and UGT1A1) and type 1 deiodinase (DIO1) in liver, sodium iodide symporter (NIS), TSH receptor (TSHR), and DIO1 in thyroid as well as the activity of thyroid peroxidase (TPO). Serum total T4 level decreased significantly at all applied dosages, whereas total T3 level increased markedly only at 1.7 mg/L of PFOS. No statistically significant toxic effects of PFOS on serum TSH were observed. Hepatic UGTIA1, but not UGT1A6, mRNA was up-regulated at 5.0 and 15.0 mg/L of PFOS. Treatment with PFOS lowered hepatic DIO1 mRNA at 15.0 mg/L but increased thyroidal DIO1 mRNA dose dependently. The activity of TPO, NIS, and TSHR mRNA in thyroid were unaffected by PFOS treatment. These results indicate that increased hepatic T4 glucuronidation via UGT1A1 and increased thyroidal conversion of T4 to T3 via DIO1 were responsible in part for PFOS-induced hypothyroxinemia in rats.

[Effects of perfluorooctane sulfonate on learning and memory of rat pups].

OBJECTIVE: To study the effects of prenatal and postnatal perfluorooctane sulfonate (PFOS) exposure on spatial learning and memory, N-methyl-D-aspartate receptor 2B (NR2B) mRNA and protein level in frontal cortex and hippocampus of rat pups and to explore the mechanism of developmental neurotoxicity induced by PFOS. METHODS: Twenty-eight pregnant rats were randomly divided into three groups in proportion of 3:2:2, including control group (C), low dose group (L) and high dose group (H) by means of randomized number table, which respectively received 0, 7.2, 14.4 mg/kg PFOS feed from pregnancy day 0 to postnatal day (PND) 30 by free feedings. The animal models of prenatal and postnatal non-exposure (CC), prenatal exposure (LC and HC), postnatal exposure (CL and CH), and prenatal and postnatal exposure (LL and HH) to PFOS were established by cross-fostering method. The spatial learning and memory were measured by water maze experiment,the NR2B mRNA levels in frontal cortex of rat pups was determined with semi-quantitative RT-PCR, NR2B protein express in cerebral cortex (frontal and temporal cortex) and hippocampus (CA1, CA3, CA4 and DG regions) of rat pups was detected by immunohistochemistry. RESULTS: The escape latency of CL, CH, LL and HH groups pups in water maze experiment were (99.83 +/- 25.77) s, (111.30 +/- 17.82) s, (106.40 +/- 18.71) s, (107.70 +/- 16.85) s, and longer as compared with CC group [(54.90 +/- 26.69) s] (q value were 4.349, 4.773, 6.026 and 5.641, respectively, P <0.01). The number of errors of HH group rat pups entering dead end was (22.30 +/- 7.56) at the training day 4, and it was significantly higher than that of CC group (9.80 +/- 4.64) (q = 5.173, P < 0.01). The NR2B mRNA levels of frontal cortex of pups in HC group at PND1, and LC group, HC group and HH group at PND14 were (0.167 +/- 0.008), (0.364 +/- 0.035), (0.341 +/- 0.030) and (0.328 +/- 0.045) respectively,which were significantly lower than CC group (0.271 +/- 0.060) and (0.465 +/- 0.067) (q values were 3.547, 3.739, 4.597 and 5.006, respectively, P< 0.05 ). The results of immunohistochemistry indicated that NR2B protein express of the hippocampus CA1 region of pups in LC group was (0.091 +/- 0.005), and showed significant lower than CC group which was (0.123 +/- 0.009) at PND1 (q = 5.209, P <0.05). At PND14, the effect of PFOS extended to cerebral cortex and hippocampus regions. At PND28, the effects of PFOS were showed in hippocampus CA1, CA3 and temporal cortex regions. CONCLUSION: Prenatal and postnatal exposure to PFOS should result in the spatial learning and memory damage,and the mechanism might be possibly involved in the decrease of NR2B level in cerebral cortex and hippocampal formation regions.

PCDDs/PCDFs and PCBs in water samples from the Three Gorge Reservoir.

The Three Gorge Reservoir (TGR) is the largest reservoir in China and its water quality is an important health concern, we have determined the concentrations of PCDDs/PCDFs and PCBs in the water samples collected at three seasons: August 2004, January 2005 and August 2005. The results showed that the average WHO-TEQ of total dioxins-like compounds (PCDDs/PCDFs+PCBs) was 0.06558 pg l(-1), ranged from 0.0008 to 0.32439 pg l(-1), which are much lower than other reported water sources. The main dioxins (PCDDs/PCDFs) are hepta- and octa-chlorinated dibenzo-p-dioxins (CDDs) and chlorinated dibenzofurans (CDFs). Since the levels of dioxins may change after the last water-store stage, the present study provides important data to compare the water quality in the TGR in the future.

Toxic effect of serial perfluorosulfonic and perfluorocarboxylic acids on the membrane system of a freshwater alga measured by flow cytometry.

Flow cytometric measurements were used to investigate the toxic effect of perfluorobutanoic sulfonate (PFBS), perfluorooctane sulfonate (PFOS), perfluorohexanoic acid (PFHxA), perfluorooctanoic acid (PFOA), perfluorododecanoic acid (PFDoA), and perfluorotetradecanoic acid (PFTeA) on some membrane systems of the freshwater alga species Scenedesmus obliquus. Among the test compounds, PFOS, PFDoA, and PFTeA inhibited algal growth rate in a concentration-dependent manner while PFBS, PFHxA, and PFOA did not inhibit algal growth within the test concentration ranges. An enhancement of the mitochondrial membrane potential (MMP) and cell membrane permeability in S. obliquus was observed caused by exposure to PFOS, PFOA, PFDoA, and PFTeA. Both carbon chain length and acid group influenced the toxicity of PFAAs, where the toxicity increased with increasing carbon chain length for the compounds belonging to the same class. The observed effective concentrations lie in the micromole range and the test compounds disrupted membrane properties at concentrations below those associated with algal growth inhibition. Flow cytometry is proved to be a useful technique for toxicity testing with microalgae and provide additional information regarding the mode of action of PFAAs to algal species.

[Comparative study on the acute toxicity of pulmonary caused by nanosized and microsized powders of silicon dioxide].

OBJECTIVE: To compare the acute pulmonary toxicities of nanosized and microsized silicon dioxide particles. METHODS: All 125 healthy male Wistar rats were divided into 25 groups randomly according to the weight. Experimental animals were exposed to microsized SiO2 at the doses of 100 mg/m3 (group A) and 300 mg/m3 (group B), and to the nanosized SiO2 at the same dose levels (group A' and B') by inhalation for 2 hours. Compositions in bronchoalveolar lavage fluids (BALF) and contents of hydroxyproline in blood sera and lung tissues were detected and then compared at 6, 12, 24, 48, 72 hours after administration. RESULTS: The total cellular score (TCS) in BALF of group A'[(55.00 +/- 8.30) x 10(4)/ ml] and B'[(52.50 +/- 9.02) x 10(4)/ml] at 6 hours were significantly higher than those in control groups [(34.88 +/- 12.53) x 10(4)/ml]; TCS in BALF of group A' [(55.00 +/- 8.30) x 10(4)/ml]at 6 hours and group A' [(39.75 +/- 12.08) x 10(4)/ml] at 24 hours were significantly higher than those in isodose group of microsized SiO2 [(32.38 +/- 13.07) x 10(4)/ml, (24.13 +/- 10.97) x 10(4)/ml) ]; total protein (TPr) in BALF of group A' [(0.34 +/- 0.09)g/L] and B' [(0.38 +/- 0.16) g/L] at 48 hours were significantly higher than those in isodose group of microsized SiO2 [(0.20 +/- 0.07) g/L, (0.21 +/- 0.05) g/L]. Lactate dehydrogenase (LDH) in BALF of group A' [(1.66 +/- 0.22) x 10(3) U/L] at 72 hours were significantly higher than those in isodose group of microsized SiO2 [(1.38 +/- 0.17) x 10(3) U/L]. Alkaline phosphatase (AKP) in BALF of group B' [(5.14 +/- 1.47) U/100 ml] at 6 hours and group B' [(5.86 +/- 2.41) U/100 ml] at 24 hours were significantly higher than those in isodose group of microsized SiO2 [(3.64 +/- 0.36) U/100 ml, (3.30 +/- 2.19) U/100 ml]. Hydroxyproline (HyP) in tissues of lung of group A' [(0.532 +/- 0.053) microg/mg, (0.484 +/- 0.046) microg/mg, (0.591 +/- 0.096) microg/mg, (0.551 +/- 0.084) microg/mg] at 6, 12, 48, 72 hours and group B' [(0.508 +/- 0.081) microg/mg, (0.565 +/- 0.053) microg/mg ] at 12, 72 hours were significantly higher than those in isodose group of microsized SiO2 [(0.345 +/- 0.074) microg/mg, (0.368 +/- 0.095) microg/mg, (0.431 +/- 0.036) microg/mg, (0.399 +/- 0.080) microg/mg, (0.396 +/- 0.039) microg/mg, (0.465 +/- 0.062) microg/mg]. CONCLUSION: Nanosized and microsized SiO2 should have some differences on acute pulmonary toxicities in our experiment condition.

[Effects of perfluorooctane sulfonate on Glu, PKC and PKA activities in mouse brain].

OBJECTIVE: To study the effects of perfluorooctane sulfonate (PFOS) on contents of glutamate and activity of protein kinase C (PKC) and A (PKA) and ultrastructure injury in the brain of male mice and to explore the mechanism of neurotoxicity and patho-alteration resulted from PFOS. METHODS: 44 male mice were randomly divided into four groups, who were respectively orally given 0, 5, 10, 20 mg/kg PFOS for 10 days. The Glu consents in the brain of the mice was measured with spectrophotometer and protein kinases activity were measured with non-radioactive assay of protein kinase and the changes of cerebral cortex ultrastructure were observed. RESULTS: Contents of Glu in 10 and 20 mg/kg groups were (1.57 +/- 0.11) and (1.62 +/- 0.16) mmol/g prot respectively,which was significantly increased compared with the corresponding controlled group [(1.45 +/- 0.13) mmol/g prot] (F = 39.59, P < 0.05). PKC activity in 5, 10 and 20 mg/kg BW groups were (29.05 +/- 2.89), (33.65 +/- 3.82) and (34.20 +/- 3.16) pmol x min(-1) x (mg prot)-1 respectively, which was significantly increased compared with the corresponding control group [(24.53 +/- 2.88) pmol x min(-1) x (mg prot)-1] (F = 7.75, P < 0.05). Compared with the corresponding control group, PKA in 5, 10 and 20 mg/kg BW groups increased by (24.12 +/- 3.86)%, (34.02 +/- 3.04)% and (33.42 +/- 3.71)% with a statistical significance (F = 26.27, P < 0.01). The exposed mice had cerebral cortex ultrastructure injury of cell nucleus envelope hollow. CONCLUSION: Exposure to PFOS increases Glu contents and activity of PKC and PKA in mouse brain and induce the cerebral cortex ultrastructural injury, a possible mechanism of the neurotoxicity caused by PFOS.

Human exposure to perfluoroalkyl substances near a fluorochemical industrial park in China.

Severe perfluoroalkyl substance (PFAS) contaminations have been observed in both surface water and groundwater in the vicinity of Fuxin, China, over the past years, attributing to the fast-growing fluorochemical industries locally. However, little is known about the overall daily intake of PFAS contaminations by Fuxin residents recently. In the present study, ten target PFAS analytes in the blood serum samples collected from 100 non-occupationally exposed healthy residents in Fuxin, with an average age of 47.6 years, together with 14 drinking water samples obtained from the public water system (PWS) of Fuxin were analyzed via high-performance liquid chromotography-tandem mass spectrometry (HPLC-MS/MS). As the dominant PFAS contaminant, the serum concentrations of perfluorooctanoic acid (PFOA) in Fuxin residents ranged between <0.05 and 160 ng/mL, with a median concentration of 9.4 ng/mL, which was higher than those reported previously for Fuxin and other areas worldwide. In drinking water samples, PFOA had a median value of 8.5 ng/L, ranging from 7.7 to 8.8 ng/L. Based upon the simplified one-compartment pharmacokinetic model, the total daily intake of PFOA for individuals residing in Fuxin ranged from 0.30 to 1.76 ng/kg bw/day, with a median of 0.79 ng/kg bw/day; furthermore, daily consumption of drinking water from the PWS in Fuxin appeared to contribute 35% of overall PFOA burden in local residents, which was approximately 3-fold higher compared to that estimated for Fuxin residents in 2009.

[Comparative study of nanosized and microsized silicon dioxide on spermatogenesis function of male rats].

OBJECTIVE: To compare the effects of nanosized and microsized silicon dioxide on spermatogenesis function of male rats exposed by inhalation. METHODS: 45 male rats were randomly divided into control group and four experimental groups which were exposed by 100 mg/m3 or 300 mg/m3 nanosized and microsized silicon dioxide in inhalation chambers 2 hours every other day. Age-matched rats were exposed to room air with the same condition and served as controls. 65 days later, the testicular and epididymal viscera coefficients, the quantity and quality of sperm were examined and the histopathological assessment was done. The changes in biochemical parameters in serum and testes were also measured. RESULTS: Nanosized silicon dioxide could induce histopathological changes of testes in rats, and the effect was higher than that of microsized particles at the same concentration. Nanosized silicon dioxide could reduce the sperm counts of rats and the testicular LDH-C4 activities, increase MDA levels in the testes and the effect was higher than that of microsized particles at the same concentration. Nanosized silicon dioxide could lead to the reduction of sperm motility, testicular LDH-C4 activities and 8-hydroxydeoxyguanosine (8-OHdG) concentration in serum elevation in particles-exposed rats compared with the control animals, but there are no significant difference compared with that of microsized particles at the same concentration. CONCLUSION: The present findings suggest a different effect of impairment of sperm production and maturation induced by inhalation of nanosized and microsized silicon dioxide, and nanosized silicon dioxide exerted more severe reaction.

[Comparison of perfluorooctane sulfonate and perfluorooctane acid in serum of non-occupational human from Shenyang and Chongqing areas].

OBJECTIVE: The purpose of this investigation was to illustrate the perfluorooctane sulfonate (PFOS) and perfluorooctane acid (PFOA) levels in serum of non-occupational exposure human from Shenyang and Chongqing areas and to compare the distributing character and region difference of PFOS and PFOA in those two region human. METHODS: Sera samples of non-occupational human from Shenyang and Chongqing areas were collected, and the concentration of PFOS and PFOA in serum were measured by High Performance Liquid Chromatography/Mass Selective Detector (HPLC/MS-MIS). RESULTS: The average Shenyang and Chongqing fluorochemical concentrations, respectively, were as follows: PFOS, 22.40 microg/L vs 7.40 microg/L, PFOA, 4.32 microg/L vs 1.00 microg/L. Statistical analysis indicated that serum concentrations of PFOS and PFOA were significantly (P < 0.01) higher in Shenyang human than in Chongqing human. Furthermore, there are sex differences in PFOS and PFOA concentrations in serum at all location. In Shenyang the concentration of PFOS in females were significantly (P < 0.05) higher than in males. The correlations of PFOS (r = 0.298) and PFOA (r = 0.271) with age were significant in females from Chongqing area, and especially the correlations were higher in older females (age t 50) than the groups of age < 13 and 13 - 50 years old. CONCLUSION: This finding suggests that there are predominant regional differences and distributing character for both PFOS and PFOA concentrations in Shenyang and Chongqing areas, and the concentrations of PFOS and PFOA in serum were correlated with age and sex.