Numerous studies have demonstrated the important role played by indoor dust in human exposure to polybrominated diphenyl ethers (PBDEs), particularly in children, who spend most of their time indoors. Few data have been available for PBDEs in house dust in China. In this study, dust samples were collected randomly from 46 houses in Guangzhou, South China, for the first time to investigate levels and pattern profiles of PBDEs and to estimate human exposure to PBDEs for adults and toddlers (6 months to 2 years old). Using gas chromatography–mass spectrometry in selected ion monitoring mode, congeners—including BDE28, 47, 66, 85, 99, 100, 153, 154, 183, and 209—were determined. The results show that BDE209 is the predominant congener in house dust, comprising 90.7% to 99.8% (mean 97.4%) of the total concentration. Of ∑tri-hepta BDEs, BDE47, 99, and 183 were the most abundant congeners, with mean contributions of 23.3%, 25.2%, and 21.9%, respectively. The intake of ∑tri-hepta BDEs via dust ingestion was 0.16–3.82 ng/d for adults and 2.1–7.64 ng/d for toddlers, accounting for 0.65% to 13.6% and 18.6% to 45.5%, respectively, of the total (based on data in our previous work) (Chen et al. 2008). With respect to intake of BDE209, the values increased to 11 to 264 ng/d for adults and to 145 to 527 ng/d for toddlers. Risk assessment indicated that PBDEs may possibly affect the health of toddlers in Guangzhou, South China. Further studies are needed to investigate the bioavailability and metabolism of PBDEs in humans to improve risk evaluation.

Fifty-two house dust samples were randomly collected in Guangzhou and Haikou City, to analyze the concentrations of Sigma10 PBDEs (sum of BDE 28, 47, 66, 85, 99, 100, 153, 154, 183 and 209), the PBDE composition profiles, and possible influencing factors, and estimate human exposure to PBDEs via dust ingestion for adults and toddlers. The results showed that PBDEs were found in all samples, with the Sigma10 PBDEs concentrations ranging from 544.2 ng/g to 9 654 ng/g, and with median (mean) of 2 547 (3 096) ng/g. The PBDE levels in Guangzhou samples were obviously higher than those in Haikou. No significant correlations between PBDE levels and residential characteristics (number of TVs, computers, and polyurethane foam-contained furniture, time of using TVs and computers) were observed. BDE209, with a mean concentration of 3 021 ng/g, was the dominated congener, contributing 73.70%-99.74% to the Sigma10 PBDEs, with a mean contribution of 96.85%. BDE 47, 99 and 183 were the most abundant congeners of Sigma9 PBDEs (BDE 209 excluded), with a mean contribution of 24.48%, 23.99%, and 21.66%, respectively. There is no notable difference in PBDE composition between Guangzhou and Haikou samples. The estimated exposure for adults and toddlers to PBDEs ranged from 10.59 ng/d to 254.7 ng/d and from 140.1 ng/d to 509.3 ng/d, respectively. Due to their increased dust ingestion rates, toddlers in took more PBDEs via dust ingestion than adults. Dust ingestion was an important human exposure route for PBDEs, especially for toddlers.

Dust samples were collected randomly from forty-six houses, twelve offices, seventeen outdoor sites, two televisions and two computers in Guangzhou City to determine the concentrations, distribution and possible sources of PBDEs in indoor dust. Concentration of Σ_(10)PBDEs (sum of BDE28,47, 66, 85, 99,100, 153,154, 183, and 209) varied from 564.3 to 9654ng/g (median 2686ng/g, mean 3407ng/g) for house dust, and from 1737 to 4408 ng/g (median: 3133ng/g; mean: 3179ng/g) for office dust. BDE209 was the dominant congener detected, with an average contribution of 97.4% and 99.0% to Σ_(10)PBDEs for house dust and office dust, respectively, whereas BDE47, 99 and 183 were the most abundant congeners of Σ_9PBDEs (BDE209 excluded). Σ_(10)PBDEs concentration in indoor dust was higher than that in the outdoor dust, indicating possible indoor emission sources for PBDEs indoors. The predominant commercial products source for PBDEs in indoor dust was Deca-BDE formulations, followed by Penta-BDE, and the contribution of Octa-BDE was minimal.

Although CD5(+) B-1 B cells have been recognized as an infrequent B cell subset in mice for many years, attempts to identify their histologic location in normal mouse spleen have proven difficult due to both their paucity and low level expression of CD5. In this study we have studied V(H)11/D(H)/J(H) gene-targeted mice, V(H)11t, that develop elevated numbers of CD5(+) V(H)11/V(k)9 B cells with an anti-phosphatidylcholine (anti-PtC) autoreactive specificity, allowing B-1 B cell detection by anti-PtC Id-specific Abs in spleen section staining. Using this approach we found that anti-PtC B-1 cells first appear within the white pulp in neonates, expand in association with follicular dendritic cells (FDC), and localize more centrally than other (non-B-1) IgD(high) follicular B cells in adults. Among neonatal B cells, CD5(+) B-1 cells in both normal and V(H)11t mouse spleen and peritoneal cavity express the highest levels of CXCR5, which is important for FDC development. Injection of purified spleen or peritoneal B-1 cells into RAG knockout mice resulted in B-1 cell follicle formation in spleen, inducing FDC development and plasma cell generation. These results indicate that B-1 B cells are the first B cells to express fully mature levels of CXCR5, thereby promoting the development of FDC.

A natural serum autoantibody specific for the Thy-1 glycoprotein (anti-Thy-1 autoantibody [ATA]) is produced by B-1 cells that are positively selected by self-antigen. Here, using ATA micro kappa transgenic mice we show that cells with this B cell receptor are negatively selected during bone marrow (BM) development. In a Thy-1 null environment, BM ATA B cells progress to a normal follicular stage in spleen. However, in a self-antigen-positive environment, development is arrested at an immature stage in the spleen, concomitant with induction of CD5. Such cells are tolerant and short-lived, different from B-1. Nonetheless, ATA-positive selection was evident by self-antigen-dependent high serum ATA production, comprising approximately 90% of serum immunoglobulin M in ATA micro kappa mice. Splenectomy did not eliminate ATA production and transfer of tolerant splenic B cells did not induce it. These findings demonstrate that B-1 positive selection, resulting in the production of natural serum ATA, arises independently from the major pathway of BM B cell development and selection.

Abstract CD1d-dependent accumulation of αβ T cells bearing a canonical Vα14Jα281 α-chain (Vα14+ T cells) is thought to model positive selection of lipid-specific T cells, based on their ability to recognize CD1d-presented self glycolipid(s). However, it has been difficult to demonstrate self ligand specificity in this system, as most Vα14+ T cells do not exhibit significant autoreactivity despite high reactivity to α-galactosylceramide presented by CD1d (α-GalCer/CD1d). To assess the role of TCRβ chain in determining the α-GalCer/CD1d vs autoreactive specificity of Vα14+ T cells, we conducted TCRα or TCRβ chain transduction experiments. In this study we demonstrate, by combining different TCRβ chains with the Vα14 α-chain in retrovirally transduced T cell lines, that the Vα14 α-chain plays a primary role, necessary but not sufficient for imparting α-GalCer/CD1d recognition. β-Chain usage alone is not the sole factor that controls the extent of autoreactivity in Vα14+ T cells, since transduction of TCRαβ chains from a high CD1d autoreactive Vα14+ T cell line conferred the α-GalCer/CD1d specificity without induction of autoreactivity. Thus, heterogeneity of Vα14+ T cell reactivity is due to both β-chain diversity and control mechanism(s) beyond primary TCR structure.

CD1d-dependent accumulation of alphabeta T cells bearing a canonical Valpha14Jalpha281 alpha-chain (Valpha14+ T cells) is thought to model positive selection of lipid-specific T cells, based on their ability to recognize CD1d-presented self glycolipid(s). However, it has been difficult to demonstrate self ligand specificity in this system, as most Valpha14+ T cells do not exhibit significant autoreactivity despite high reactivity to alpha-galactosylceramide presented by CD1d (alpha-GalCer/CD1d). To assess the role of TCRbeta chain in determining the alpha-GalCer/CD1d vs autoreactive specificity of Valpha14+ T cells, we conducted TCRalpha or TCRbeta chain transduction experiments. In this study we demonstrate, by combining different TCRbeta chains with the Valpha14 alpha-chain in retrovirally transduced T cell lines, that the Valpha14 alpha-chain plays a primary role, necessary but not sufficient for imparting alpha-GalCer/CD1d recognition. beta-Chain usage alone is not the sole factor that controls the extent of autoreactivity in Valpha14+ T cells, since transduction of TCRalphabeta chains from a high CD1d autoreactive Valpha14+ T cell line conferred the alpha-GalCer/CD1d specificity without induction of autoreactivity. Thus, heterogeneity of Valpha14+ T cell reactivity is due to both beta-chain diversity and control mechanism(s) beyond primary TCR structure.