Short-chain Chlorinated Paraffins Exposure Research Articles

Tracking and optimizing toxic chemical exposure pathways through food trade: A case study in SCCPs contaminated seafood in China

Abstract Food safety is related to human health and sustainable development. International food trade poses food safety risks through the collateral transport of toxic chemicals that are detrimental to human health. Domestic interprovincial trade has similar effects within countries but has not been comprehensively investigated previously. Here we assessed the effects of interprovincial trade on food safety and human dietary exposure to short-chain chlorinated paraffins (SCCPs), a group of emerging persistent toxic chemicals, in seafood across China by synthesizing data from field observation and various models. Our findings indicate that there is a higher level of SCCPs exposure risk in coastal provinces compared to inland provinces. Approximately 70.3% of human exposure to SCCPs through seafood consumption in China was embodied in the interprovincial seafood trade in 2021. Specifically, the domestic trade led to a remarkable increase in SCCPs exposure in the coastal provinces in South China, attributable to low SCCPs pollution in these provinces and imported seafood from those provinces with high SCCPs pollution. In contrast, human exposure to SCCPs decreased in those coastal provinces in East China due to importing seafood from those provinces with low SCCPs concentrations. The interprovincial seafood trade routes were optimized by linear programming to minimize human exposure to SCCPs considering both shipping cost and health risk constraints. The optimized trade routes reduced the national per capita SCCPs exposure through seafood consumption by over 12%. This study highlights the importance of interprovincial food trade in the risk assessment of toxic chemicals.

Developmental toxicity of short-chain chlorinated paraffins on early-stage chicken embryos in a shell-less (ex-ovo) incubation system

Short-chain chlorinated paraffins (SCCPs) are listed as a category of globally controlled persistent organic pollutants (POPs) by the Stockholm Convention in 2017. However, SCCP toxicity, particularly their developmental toxicity in avian embryos, has not been well studied. In this study, we observed the early development of chicken embryos (Gallus gallus domesticus) by applying a shell-less (ex-ovo) incubation system developed in our previous studies. After exposing embryos at Hamburger Hamilton stage (HHS) 1 to SCCPs (control, 0.1% DMSO; SCCPs-L, 200 ng/g; SCCPs-M, 2000 ng/g; SCCPs-H, 20,000 ng/g), we observed the development of embryos from the 3rd to 9th incubation day. Exposure to SCCPs-M and -H induced a significant reduction in survival, with an LD50 of 3100 ng/g on the 9th incubation day. Significant dose-dependent decreases in body length were observed from days 4–9. We also found that SCCPs-H decreased the blood vessel length and branch number on the 4th incubation day. Additionally, SCCPs-H significantly reduced the heart rate on the 4th and 5th incubation days. These findings suggest that SCCPs may have potential of developmental and cardiovascular toxicity during the early stages of chicken embryos. Quantitative PCR of the mRNA of genes related to embryonic development showed that SLC16A10 (a triiodothyronine transporter) level decreased in the SCCPs-H group, showing a significant positive correlation with the body length of embryos. THRA level, a thyroid hormone receptor, was significantly decreased in the SCCPs-H group, whereas that of DIO3 level, a deiodinase was significantly increased. These results suggest that SCCPs exposure induces developmental delays via the thyroxine signaling pathway. Analysis of thyroid hormones (THs) in blood plasma also indicated a significant reduction in thyroxine (T4) levels in the SCCPs-H group on the 9th incubation day of embryos. In conclusion, SCCPs induce developmental toxicity by disrupting thyroid functions at the early-life stage of chicken embryos.

(096) Chronic Oral Exposure to Short Chain - Chlorinated Paraffins Induced Testicular Toxicity by Promoting NRF2-mediated Oxidative Stress

Abstract Introduction Chlorinated paraffins (CPs) are important additives in a variety of chemical processing. Based on the lengths of the carbon chains, CPs are classified into short-chain CPs (SCCPs, C10-13), medium-chain CPs (MCCPs, C14-17) and long-chain CPs (LCCPs, C18-30) with the chlorine content ranging from 30%-70%. SCCPs were listed in the persistent organic pollutants (POPs) by Stockholm Convention due to its toxicity, bioaccumulation potential, long range transport potential and environmental persistence. Numerous studies have analyzed the toxicities of SCCPs in various organisms, with the toxic effects including lethality and carcinogenicity, developmental toxicity, endocrine disrupting effect and immunomodulatory effect. Objectives As a widespread environmental contaminant, short chain chlorinated paraffins (SCCPs) has attracted great attention. However, the toxicity of SCCPs on male reproductive system remains ambiguous. In this study, we investigated the toxic effects of SCCPs on testis. Methods We treated mice with 1,10 or 100 mg/kg bm/d SCCPs by gavage once a day for 35 days. The tissues and blood samples were collected after treatment. The weight of mice and testes were measured. The organ index is the body weight divided by the weight of the testis. The left testes were used for protein extraction, RNA extraction and measurement of SOD, CAT, GST and MDA. The left epididymis was used for analysis of sperm parameters. The right testis and epididymis were fixed in Bouin’s solution for H&E and TUNEL staining. GC2 cell (mouse spermatocyte) treated with SCCPs was used to examined the cell viability by CCK8 kits. Cellular ROS generation was evaluated by 2',7'Dichlorodihydrofluorescein diacetate (DCFH-DA). We used Apoptosis Detection Kit to detect the cell apoptosis by dual staining cells with Annexin V-fluorescein isothiocyanate (FITC) and propidium iodide (PI). Results SCCPs resulted in disorderly arranged seminiferous epithelium and increased apoptotic cells in testes. Both in vivo and in vitro experiments indicated that the oxidative stress was induced after SCCPs exposure, and dysfunction of nuclear factor erythroid-related factor (NRF2) signaling pathway played a role in this process. Moreover, resveratrol, an NRF2 activator, could alleviate the damage of SCCPs on spermatogenetic cells in vitro. Our study indicated that oxidative stress is the key point for explaining the testicular toxicity caused by SCCPs, and NRF2 could be used as a potential target for clinical treatment to alleviate the reproductive toxicity induced by SCCPs. Conclusions Our study is the first to evaluate the toxic effects of SCCPs on male reproductive system, which is associated with overproduction of ROS. This study also indicates that NRF2/ARE pathway plays the vital role in the toxic effects of SCCPs in spermatogenesis, thus providing a target for the prophylaxis and treatment. Disclosure No

Gut Microbiota from Short-Chain Chlorinated Paraffin-Exposed Mice Promotes Astrocyte Activation by Disrupting the Intestinal Tight Junction via Zonulin Upregulation.

Short-chain chlorinated paraffins (SCCPs) are novel toxicants in food and are reported to possess neurotoxicity. Here, we investigated the mechanism of SCCP-induced astrocyte activation and neuroinflammation. SCCP gavage induced astrocyte activation and neuronal cell death with the changes of gut microbiome and metabolites. Antibiotic cocktail administration to deplete the gut microbiome ameliorated the astrocyte activation and inflammation induced by SCCPs. In fecal microbiota transplantation (FMT) assays, mice that received transplanted gut microbiome from SCCP-treated mice showed increased astrocyte activation and elevated inflammatory response. In addition, SCCP exposure promotes zonulin expression and tight junction injury, and antibiotic cocktail administration inhibited that in the intestinal tract. Increased zonulin and tight junction injury were also observed in SCCPs_FMT mice. The zonulin inhibition protected the tight junction in the intestinal tract from SCCP exposure and suppressed astrocyte activation. In summary, this study proposes a novel possibility for SCCP-induced astrocyte activation and neurotoxicity by the gut microbiome-mediated zonulin expression and tight junction.

Chronic oral exposure to short chain chlorinated paraffins induced testicular toxicity by promoting NRF2-mediated oxidative stress

As a widespread environmental contaminant, short chain chlorinated paraffins (SCCPs) has attracted great attention. However, the toxicity of SCCPs on male reproductive system remains ambiguous. In this study, we treated mice with SCCPs by gavage and investigated the toxic effects of SCCPs on testis. According to the results, the sperm parameters of mice were significantly reduced after exposure to 1, 10, 100 mg/kg body mass per day SCCPs for 35 days. SCCPs resulted in disorderly arranged seminiferous epithelium and increased apoptotic cells in testes. Both in vivo and in vitro experiments indicated that the oxidative stress was induced after SCCPs exposure, and dysfunction of nuclear factor erythroid-related factor (NRF2) signaling pathway played a role in this process. Moreover, resveratrol, an NRF2 activator, could alleviate the damage of SCCPs onmale reproductive system. Our study indicated that oxidative stress is the key point for explaining the testicular toxicity caused by SCCPs, and NRF2 could be used as a potential target for clinical treatment to alleviate the reproductive toxicity induced by SCCPs.

Exposure to short-chain chlorinated paraffins induces astrocyte activation via JAK2/STAT3 signaling pathway

In the last few decades, short-chain chlorinated paraffins (SCCPs) have become the most heavily produced monomeric organohalogen compounds, and have been reported to induce multiple organ toxicity. However, the effects of SCCPs on the central nervous system are unknown. In the present study, we show that SCCP exposure induced astrocyte proliferation and increased the expression of two critical markers of astrocyte activation, glial fibrillary acidic protein and inducible nitric oxide synthase, in vivo and in vitro. SCCP exposure also increased inflammatory factory gene expression. Moreover, SCCP treatment triggered Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signalling, as shown by increased phosphorylation and STAT3 translocation to the nucleus. Both JAK2 and STAT3 inhibition effectively attenuated SCCP-induced astrocyte activation. Finally, JAK2 inhibition significantly rescued STAT3 phosphorylation and nuclear translocation. Taken together, JAK2/STAT3 pathway activation contributed to SCCP-induced astrocyte activation. These data will help elucidate the molecular mechanism underlying SCCP-induced neurotoxicity.

Cross-Model Comparison of Transcriptomic Dose-Response of Short-Chain Chlorinated Paraffins.

Short-chain chlorinated paraffins (SCCPs) have attracted attention because of their toxicological potential in humans and wildlife at environmentally relevant doses. However, limited information is available regarding mechanistic differences across species in terms of the biological pathways that are impacted by SCCP exposure. Here, a concentration-dependent reduced human transcriptome (RHT) approach was conducted to evaluate 15 SCCPs in HepG2 cells and compared with our previous results using a reduced zebrafish transcriptome (RZT) approach in zebrafish embryos (ZFEs). Generally, SCCPs induced a broader suite of biological pathways in ZFEs than HepG2 cells, and all of the 15 SCCPs were more potent in HepG2 cells compared to ZFEs. Despite these general differences, the transcriptional potency of SCCPs in both model systems showed a significant linear relationship (p = 0.0017, r2 = 0.57), and the average ratios of transcriptional potency for each SCCP in RZT to that in RHT were ∼100,000. C10H14Cl8 was the most potent SCCP, while C10H17Cl5 was the least potent in both ZFEs and HepG2 cells. An adverse outcome pathway network-based analysis demonstrated model-specific responses, such as xenobiotic metabolism that may be mediated by different nuclear receptor-mediated pathways between HepG2 cells (e.g., CAR and AhR activation) and ZFEs (e.g., PXR activation). Moreover, induced transcriptional changes in ZFEs associated with pathways and molecular initiating events (e.g., activation of nicotinic acetylcholine receptor) suggest that SCCPs may disrupt neural development processes. The cross-model comparison of concentration-dependent transcriptomics represents a promising approach to assess and prioritize SCCPs.

Metabolomic mechanisms of short chain chlorinated paraffins toxicity in rats

Short chain chlorinated paraffins (SCCPs) have received increased interest worldwide since they were added to the list of controlled POPs in Annex A of the Stockholm Convention in 2017. Although many toxicological studies have already shown that SCCPs are hepatotoxic, nephrotoxic, and thyrotoxic to rodents, there have been few studies to date that have characterized changes in the metabolic pathways targeted by SCCPs. In this study, a UPLC-Q-TOF-MS based plasma metabolomics approach was used to investigate the toxicity of SCCPs in rats. Liver and kidney injury occurred rapidly after high-dose SCCP exposure, and the most relevant pathways affected were energy metabolism, amino acid metabolism, glycerophospholipid metabolism, nucleotide metabolism, and vitamin B metabolism. Exposure to SCCPs inhibited the tricarboxylic acid cycle and accelerated degradation. Fluctuating levels of phospholipids and nucleotides may have contributed to the neurotoxicity of SCCPs. In addition, the down regulation of folic acid induced by SCCPs may have led to malformations during the early development of laboratory animals. These results suggested that high exposure levels of SCCPs may have serious health risks and more research is needed to assess the health status of relevant occupational groups.

Effect of short-chain chlorinated paraffins (SCCPs) on lipid membranes: Combination of molecular dynamics and membrane damage experiments

In recent years, more attention has been paid to the biological effects of short-chain chlorinated paraffin (SCCP). Studies have shown that SCCPs exposure could cause metabolic damage and lipid metabolic damage. In the present work, based on E. coli membrane damage experiments and molecular dynamics (MD) simulation, the effects of SCCPs on the membrane structure and membrane properties were studied to explore the possible toxic damage effects of SCCPs on cell membrane. Experiments results showed that SCCPs had a significant inhibitory effect on E. coli. The E. coli cell membrane of the bacteria was broken and the macromolecules of the cell flowed out when exposed to SCCPs. SCCPs would lead to the decrease and depolarization of cell membrane potential, and then affect the integrity and permeability of cell membrane. The further molecular dynamic simulation revealed that SCCP molecules can easily enter the lipid DPPC membranes from the aqueous phase and tended to aggregate inside bilayer stably. The bound of SCCPs could lead to significant variations in DPPC bilayer with a less dense, more disorder and rougher layer, which thus made the damage of cell membrane. In a word, although the overall toxicity of SCCPs to cell was relatively weak, the damage to the cell membrane may be one of the mechanisms of its toxicity. Main finding of the workThe exposure of SCCPs could cause structural change of cell membrane in E. coli, which verified the damage to the cell membrane may be one of the mechanisms of its toxicity.

Effect of short-chain chlorinated paraffins on metabolic profiling of male SD rats

The toxic effect of high-dose of short-chain chlorinated paraffins (SCCPs) has been extensively studied, however the possible health risks induced by SCCPs at low-dose remain largely unknown. In this study, a comprehensive toxicology analysis of SCCPs was conducted with the exposure levels from the environmental dose to the Lowest Observed Adverse Effect Level (LOAEL) of 100 mg/kg/day. General toxicology analysis revealed inconspicuous toxicity of the environmental dose of SCCPs, high dose SCCP exposure inhibited the growth rate and increased the liver weight of rat. Metabolomics analysis indicated that SCCP-induced toxicity was triggered at environmentally relevant doses. First, inhibition of energy metabolism was observed with the decrease in blood glucose and the dysfunction of TCA cycle, which may have contributed to lower body weight gain in rats exposed to a high dose of SCCPs. Second, the increase of free fatty acids indicated the acceleration of lipid metabolism to compensate for the energy deficiency caused by hypoglycemia. Lipid oxidative metabolism inevitably leads to oxidative stress and stimulates the up-regulation of antioxidant metabolites such as GSH and GSSH. The up-regulation of polyunsaturated fatty acids (PUFAs) and phospholipids composed of arachidonic acid indicates the occurrence of inflammation. Dysfunction of lipid metabolism can be an indicator of SCCP-induced liver injury.

Spatial distribution and profile of atmospheric short-chain chlorinated paraffins in the Yangtze River Delta

Research on the atmospheric occurrence of short chain chlorinated paraffins (SCCPs) in industrialized areas is scarce. In this study, we investigated the concentrations, profile, and spatial distribution of SCCPs in the highly industrialized and developed areas of the Yangtze River Delta (YRD) in China using polyurethane foam passive air samplers. Sampling was performed during two separate periods in 2011. The concentrations of atmospheric SCCPs ranged from 6.1 to 63 ng m−3 in summer and 6.2–42 ng m−3 in winter. The C10 and C11 groups were the predominant carbon groups in all the samples. Different congener patterns between summer and winter were found, indicating that congeners in the air in winter may be influenced by local and external sources. The highest level of SCCPs was found in Suzhou, which is a highly industrialized area with many manufactories including electronic industries and plastic factories. Higher levels of SCCPs were found in the air than polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), and polybrominated diphenyl ether (PBDEs), suggesting that the production and use of SCCPs were much higher than prohibited or restricted persistent organic pollutants (e.g., PCBs, OCPs, and PBDEs). Future studies should investigate the different sources of atmospheric SCCPs by conducting a comprehensive assessment of SCCP exposure.

Dietary exposure and risk assessment of short-chain chlorinated paraffins in supermarket fresh products in Jinan, China.

Dietary intake is the major route for the exposure of residents to short-chain chlorinated paraffins (SCCPs). SCCPs are classified as persistent organic pollutants (POPs) by the Stockholm Convention since May 2017. This study assessed the general population's dietary exposure to SCCPs through supermarket products. Five food categories, which included 40 food species, were collected from five supermarkets in April 2019. The SCCP concentrations in all food matrices varied between 58.6 and 1977ngg-1 dry weight (dw), with the average and standard deviation (SD) value of 301±379ngg-1 dw. Generally, the SCCP concentrations in animal-origin food matrices were higher than those in plant-origin food matrices. The C10Cl7 congeners were predominant among the congener groups of SCCPs. The proportion of C10 congeners in the animal-origin food samples (29.8%) was lower than that in the plant-origin food samples (39.7%), and the C13 congeners showed a contrasting result. The estimated daily intake (EDI) of SCCPs through dietary intake for the residents was 3109ngkg-1 day-1, which is much lower than the standards of European Food Safety Authority (10mgkg-1 day-1) for SCCPs. Risk assessment based on the supermarket foods indicated that SCCP exposure through dietary intake does not cause adverse effects to human health according to the margin of exposure (MOE).

Concentrations of selected chemicals in indoor air from Norwegian homes and schools

Both building materials and consumer products have been identified as possible sources for potentially hazardous substances like phthalates, polychlorinated biphenyls (PCBs), organophosphorous flame retardants (OPFRs), polybrominated diphenyl ethers (PBDEs) and short chain chlorinated paraffins (SCCPs) in indoor air. Thus, indoor air has been suggested to contribute significantly to human exposure to these chemicals. There is lack of data on the occurrence of several of the aforementioned chemicals in indoor air. Therefore, indoor air (gas and particulate phase) was collected from 48 households and 6 classrooms in two counties in Norway. In both the households and schools, median levels of low molecular weight phthalates (785 ng/m3), OPFRs (55 ng/m3) and SCCPs (128 ng/m3) were up to 1000 times higher than the levels of PCBs (829 pg/m3) and PBDEs (167 pg/m3). Median concentrations of dimethyl phthalate (DMP), diethyl phthalate (DEP), di-isobutyl phthalate (DiBP) and SCCPs were 3–6 times higher in households compared to schools. The levels of OPFRs, PCBs and PBDEs were similar in households and schools. In univariate analysis, the indoor concentrations of different environmental chemicals were significantly affected by location of households (OPFRs), airing of living room (some PCBs and PBDEs), presence of upholstered chair/couch (OPFRs), pet animal hold (some PBDEs) and presence of electrical heaters (selected PCBs and PBDEs). Significant correlations were also detected for the total size of households with OPFRs, frequency of vacuuming the living room with selected PCBs and PBDEs, frequency of washing the living room with selected PCBs and the total number of TVs in the households with selected phthalates and SCCPs. Finally, intake estimates indicated that indoor air contributed more or equally to low molecular weight phthalates and SCCPs exposure compared to food consumption, whereas the contribution from indoor air was smaller than the dietary intake for the other groups of chemicals.

Short-chain chlorinated paraffins (SCCPs) induced thyroid disruption by enhancement of hepatic thyroid hormone influx and degradation in male Sprague Dawley rats

Short-chain chlorinated paraffins (SCCPs) are known to disturb thyroid hormone (TH) homeostasis in rodents. However, the mechanism remains to be fully characterized. In this study, male Sprague Dawley rats received SCCPs (0, 1, 10, or 100mg/kg/day) via gavage once a day for consecutive 28days. Plasma and hepatic TH concentrations, thyrocyte structure, as well as thyroid and hepatic mRNA and protein levels of genes associated with TH homeostasis were examined. Moreover, we performed molecular docking to predict interactions between constitutive androstane receptor (CAR), a key regulator in xenobiotic-induced TH metabolism, with different SCCP molecules. Exposure to SCCPs significantly decreased the circulating free thyroxine (T4) and triiodothyronine (T3) levels, but increased thyroid-stimulating hormone (TSH) levels by a feedback mechanism. Decreased hepatic T4 and increased hepatic T3 levels were also seen after 100mg/kg/day SCCPs exposure. SCCPs didn't show any significant effects on the expression of thyroid TH synthesis genes or thyrocyte structure. However, stimulation effects were observed for mRNA and protein levels of hepatic uridine diphosphoglucuronosyl transferase (UGT) 1A1 and organic anion transporter 2, suggesting an accelerated TH metabolism in rat liver. The increased cytochrome P450 2B1 but not 1A1 mRNA and protein levels indicated that the CAR signaling was activated by SCCPs exposure. According to docking analysis, SCCPs form hydrophobic interactions with CAR and the binding affinity shows dependency on chlorine content. Overall, our data showed that CAR implicated enhancement of hepatic TH influx and degradation could be the main cause for SCCPs induced TH deficiency in male rats.

Developmental and metabolic responses of zebrafish (Danio rerio) embryos and larvae to short-chain chlorinated paraffins (SCCPs) exposure

Short-chain chlorinated paraffins (SCCPs) are highly toxic to aquatic organisms, but their toxicity is yet not well characterized. In this study, the developmental toxicity of SCCPs to zebrafish embryos/larvae was evaluated, and a metabolomics approach was adopted to explore the impact of SCCPs exposure on the metabolism in zebrafish embryos. Exposure to SCCPs at concentrations of 1–200μg/L did not produce an observable effect on the hatching rate and morphological deformities of zebrafish embryos/larvae. However, the survival rate of zebrafish larvae in SCCPs exposure groups decreased in a concentration-dependent manner. The 13-day 50% lethal concentration (LC50) value of SCCPs was calculated to be 34.4μg/L. Exposure to SCCPs induced a significant change of overall metabolism, even at environmentally relevant concentrations (1–5μg/L). The most relevant pathways affected by SCCPs exposure were glycerophospholipid metabolism, fatty acid metabolism and purine metabolism. Exposure to SCCPs at concentrations of 1–5μg/L had begun to accelerate the β-oxidation of unsaturated fatty acids and very long chain fatty acids, and affect the transformation of guanine to xanthine in the pathway of purine metabolism. Furthermore, when the exposure concentrations of SCCPs were increased to 50–200μg/L, the levels of phospholipids and amino acids were significantly raised; whereas the levels of fatty acids, carnitines and inosine were significantly decreased. In view of the significant effect on metabolism, the sub-chronic and chronic toxicity of SCCPs to fish should be concerned.

Short-chain chlorinated paraffins (SCCPs) in a freshwater food web from Dianshan Lake: Occurrence level, congener pattern and trophic transfer

Short-chain chlorinated paraffins (SCCPs) are new group of persistent organic pollutants (POPs) listed in the Stockholm Convention. The Yangtze River Delta is among the industrially most developed areas in China, supporting a large production and consumption of chlorinated paraffins (CPs). Despite this, there is very limited data on the environmental exposure of SCCPs from the region. This study analyzed SCCPs in 14 wild aquatic organisms from Dianshan Lake, Shanghai, China. The concentrations of total SCCPs ranged from 10 to 1300μgg−1 lipid weight, with significantly higher levels (p<0.05) in benthic (benthic fish and invertebrates) than in non-benthic species (pelagic and mesopelagic fish). The abundance of C10 congeners was much higher in the benthic species compared to in the non-benthic species. The calculated trophic magnification factors (TMFs) of SCCP congeners varied from 1.19 (C10H12Cl10) to 1.57 (C13H20Cl8). The TMFs were significantly correlated (p<0.01) with carbon-chain length in a positive linear relationship and with Log Kow in a parabolic curve relationship. Considering the high concentrations of SCCPs in wild aquatic organisms and the trophic magnification observed in the freshwater food web, further studies should be undertaken to assess the environmental fate of SCCPs and the public health risk in the Yangtze River Delta.

Occurrence, sources and human exposure assessment of SCCPs in indoor dust of northeast China

Short-chain chlorinated paraffins (SCCPs) are widely used chemicals in household products and might cause adverse human health effects. However, limited information is available on the occurrence of SCCPs in indoor environments and their exposure risks on humans. In this study the concentrations, profiles and human exposure of SCCPs in indoor dust from five different indoor environments, including commercial stores, residential apartments, dormitories, offices and laboratories were characterized. The SCCPs levels ranged from 10.1 to 173.0 μg/g, with the median and mean concentration of 47.2 and 53.6 μg/g, respectively. No significant difference was found on concentrations among the five microenvironments. The most abundant compounds in indoor dust samples were homologues of C13 group, Cl7 group and N20 (N is the total number of C and Cl) group. In the five microenvironments, commercial stores were more frequently exposed to shorter carbon chained and higher chlorinated homologues. Three potential sources for SCCPs were identified by the multiple linear regression of factor score model and correspondence analysis. The major sources of SCCPs in indoor dust were technical mixtures of CP–42 (42% chlorine, w/w) and CP–52 b (52% chlorine, w/w). The total daily exposure doses and hazard quotients (HQ) were calculated by the human exposure models, and they were all below the reference doses and threshold values, respectively. Monte Carlo simulation was applied to predict the human exposure risk of SCCPs. Infants and toddlers were at risk of SCCPs based on predicted HQ values, which were exceeded the threshold for neoplastic effects in the worst case. Our results on the occurrences, sources and human exposures of SCCPs will be useful to provide a better understanding of SCCPs behaviors in indoor environment in China, and to support environmental risk evaluation and regulation of SCCPs in the world.

Short-chain chlorinated paraffins in soil, paddy seeds (Oryza sativa) and snails (Ampullariidae) in an e-waste dismantling area in China: Homologue group pattern, spatial distribution and risk assessment

Short-chain chlorinated paraffins (SCCPs) in multi-environmental matrices are studied in Taizhou, Zhejiang Province, China, which is a notorious e-waste dismantling area. The investigated matrices consist of paddy field soil, paddy seeds (Oryza sativa, separated into hulls and rice unpolished) and apple snails (Ampullariidae, inhabiting the paddy fields). The sampling area covered a 65-km radius around the contamination center. C10 and C11 are the two predominant homologue groups in the area, accounting for about 35.7% and 33.0% of total SCCPs, respectively. SCCPs in snails and hulls are generally higher than in soil samples (30.4–530 ng/g dw), and SCCPs in hulls are approximate five times higher than in corresponding rice samples (4.90–55.1 ng/g dw). Homologue pattern analysis indicates that paddy seeds (both hull and rice) tend to accumulate relatively high volatile SCCP homologues, especially the ones with shorter carbon chain length, while snails tend to accumulate relatively high lipophilic homologues, especially the ones with more substituted chlorines. SCCPs in both paddy seeds and snails are linearly related to those in the soil. The e-waste dismantling area, which covers a radius of approximate 20 km, shows higher pollution levels for SCCPs according to their spatial distribution in four matrices. The preliminary assessment indicates that SCCP levels in local soils pose no significant ecological risk for soil dwelling organisms, but higher risks from dietary exposure of SCCPs are suspected for people living in e-waste dismantling area.

Relative developmental toxicity of short-chain chlorinated paraffins in Zebrafish (Danio rerio) embryos

Short-chain chlorinated paraffins (SCCPs) are ubiquitous in the environment and might cause adverse environmental and human health effects. Little is known about the relative toxicity of different SCCP compounds especially during development. The objective of this study was to characterize and compare effects of seven SCCP groups at environmentally relevant levels, using a zebrafish (Danio rerio) model. Observations on malformation, survival rates at 96 h post fertilization (hpf), and hatching rates at 72 hpf indicated that the C10- groups (C10H18Cl4, 1,2,5,6,9,10-C10H16Cl6 and C10H15Cl7) were more toxic than the C12- groups (C12H22Cl4, C12H19Cl7 and 1,1,1,3,10,12,12,12-C12H18Cl8) and Cereclor 63L. The C10- groups were also more potent than C12- groups and Cereclor 63L in decreasing thyroid hormone levels. Among the three compounds within the C10- group, the compounds with less chlorine content had stronger effects on sub-lethal malformations but less effects on triiodothyronine (T3) and tetraiodothyronine (T4). Only C10H18Cl4 significantly decreased the mRNA expression of tyr, ttr, dio2 and dio3 at a dose-dependent manner suggesting that the specific mode of actions differ with different congeners. The mechanisms of disruption of thyroid status by different SCCPs could be different. C10H18Cl4 might inhibit T3 production through the inhibition effect on dio2. These results indicate that SCCP exposure could alter gene expression in the hypothalamic-pituitary-thyroid (HPT) axis and thyroid hormone levels. The mechanisms of disruption of thyroid status by different SCCPs could be different. Our results on the relative developmental toxicities of SCCPs will be useful to reach a better understanding of SCCP toxicity supporting environmental risk evaluation and regulation and used as a guidance for environmental monitoring of SCCPs in the future.

Distribution and congener profiles of short-chain chlorinated paraffins in indoor/outdoor glass window surface films and their film-air partitioning in Beijing, China.

Short-chain chlorinated paraffins (SCCPs) are a group of n-alkanes with carbon chain length of 10-13. In this work, paired indoor/outdoor samples of organic films on window glass surfaces from urban buildings in Beijing, China, were collected to measure the concentrations and congener distributions of SCCPs. The total SCCP levels ranged from 337 ng/m(2) to 114 μg/m(2), with total organic carbon (TOC) normalized concentrations of 365 μg/m(2)-365 mg/m(2). Overall, the concentrations of SCCPs on the interior films were higher than the concentrations on the exterior films, suggesting an important indoor environmental exposure of SCCPs to the general public. A significant linear relationship was found between the SCCP concentrations and TOC, with a correlation coefficient of R = 0.34 (p < 0.01). A film-air partitioning model suggests that the indoor gas-phase SCCPs are related to their corresponding window film levels.