Novel in vitro method for measuring the mass fraction of bioaccessible atmospheric polycyclic aromatic hydrocarbons using simulated human lung fluids.

The bioaccessibility of organic pollutants is a key factor in human health risk assessments. We developed a novel in vitro method for determining the mass fraction of bioaccessible atmospheric polycyclic aromatic hydrocarbons (PAHs) using an air-washing device containing simulated human lung fluid. The experimental parameters were optimized based on the deposition fractions (DFs) of PAHs in human lung fluids. The DFs were measured for PAHs based on the mass of compounds in the mainstream and exhaled cigarette smoke. The mass fractions of bioaccessible PAHs were measured by passing the mainstream cigarette smoke through the air-washing device, and they were calculated via a simple mass balance equation based on the PAHs in the fluid and mainstream cigarette smoke. The DFs of individual PAHs ranged from 20.5% to 78.1%, and the bioaccessible mass fractions varied between 45.5% and 99.8%. The octanol-water partition coefficients (KOW) significantly influenced both the DFs and bioaccessible mass fractions of PAHs, and the optimized in vitro method could be used to estimate the bioavailable atmospheric PAHs. This in vitro method can potentially be used to measure the mass fraction of bioaccessible atmospheric PAHs and to assess the health risk related to human exposure to airborne PAHs.

Polybrominated diphenyl ethers in the air and comparison of the daily intake and uptake through inhalation by Shanghai residents with those through other matrices and routes.

To obtain a comprehensive understanding of the main source and route of human exposure to polybrominated diphenyl ethers (PBDEs), the daily intake and uptakes through inhalation, ingestion, and dermal contact for Shanghai residents were estimated on the basis of the PBDE concentrations in the air obtained in the present study and previous data reported in the literature. The PBDE concentrations in the gas and particle phases collected in Shanghai were 0.99-57.5 and 0.1-234 pg/m(3), respectively. The contamination levels of PBDEs in the air in Shanghai were similar to or slightly lower than the data from other regions. The estimated total daily intakes of PBDEs through the three routes were 607 and 1,636 ng/day for children and adults, respectively, while they decreased to 63.0 and 93.1 ng/day when the uptake efficiency (which is the fraction of contaminants that reaches the systemic circulation) of PBDEs was added to calculation. The results showed that dust is the main source of human exposure to PBDEs when PBDE uptake efficiency was not considered. It accounted for 66.2-79.2 % of the total PBDE intake. However, food is the main source, which accounted for 66.6-75.1 %, when the uptake efficiency was added to calculation. Among the three routes, dermal contact (53.1-76.6 %) is the main pathway, whereas ingestion (84.7-92.9 %) is the main one when the uptake efficiency was considered. Furthermore, risk assessment showed that the PBDE exposure amount would not cause obvious non-cancer and cancer risks to local residents.

Effect of arsenic trioxide on inhibition of restenosis after rabbit vascular injury and its mechanism.

OBJECTIVE: To investigate the effect and mechanism of arsenic trioxide (As(2)O(3)) on the prevention of restenosis after vascular injury. METHODS: Apoptosis induction of As(2)O(3) on cultured rabbit vascular smooth muscle cells (VSMCs) in vitro was observed. Thirty-two New Zealand white rabbits were randomly divided into 2- and 4-wk study groups, and their controls. 10% As(2)O(3) at 2.5 mg x Kg(-1) x d(-1) or 0.9% sodium chloride was intraperitoneally infused for 3 days before left common carotid arteries were denudated with a balloon. After denudation 2- and 4-wk animals were sacrificed for morphometry and immunohistochemical studies on carotid arteries, and for histopathology on liver and kidney. RESULTS: It was shown via cellular morphology and DNA fragments in electrophoresis that promotion of As(2)O(3) on cultured vascular smooth muscle cell apoptosis was dependent upon its concentration and duration. Compared with the control animals, the mean vascular intimal proliferation areas were reduced in 2-wk study animals (P < 0.05) and no difference was shown in 4-wk (P > 0.05), while the mean vascular luminal areas were all enlarged in both study groups (all P < 0.05). The downregulated bcl-2 expression (all P < 0.05 in 2- and 4-wk) and the upregulated bax expression (P < 0.01 in 2-wk; P < 0.05 in 4-wk) were detected by immunohistochemistry, in comparison with control groups. Gene bcl-2 and bax protein expression were consistent with the suppression of intimal proliferation and the enlargement of luminal areas in corresponding sections. CONCLUSION: As(2)O(3) induces apoptosis of VSMCs and inhibits experimental restenosis effectively after artery injury, via downregulation of bcl-2 and upregulation of bax expression.