The transepithelial transport mechanism of polybrominated diphenyl ethers in human intestine determined using a Caco-2 cell monolayer.

Oral ingestion plays an important role in human exposure to polybrominated diphenyl ethers (PBDEs). The uptake of PBDEs primarily occurs in the small intestine. The aim of the present study is to investigate the transepithelial transport characteristics and mechanisms of PBDEs in the small intestine using a Caco-2 cell monolayer model. The apparent permeability coefficients of PBDEs indicated that tri- to hepta-BDEs were poorly absorbed compounds. A linear increase in transepithelial transport was observed with various concentrations of PBDEs, which suggested that passive diffusion dominated their transport at the concentration range tested. In addition, the pseudo-first-order kinetics equation can be applied to the transepithelial transport of PBDEs. The rate-determining step in transepithelial transport of PBDEs was trans-cell transport including the trans-pore process. The significantly lower transepithelial transport rates at low temperature for bidirectional transepithelial transport suggested that an energy-dependent transport mechanism was involved. The efflux transporters (P-glycoprotein, multidrug resistance-associated protein, and breast cancer resistance protein) and influx transporters (organic cation transporters) participated in the transepithelial transport of PBDEs. In addition, the transepithelial transport of PBDEs was pH sensitive; however, more information is required to understand the influence of pH.

Human health risk assessment of multiple contaminants due to consumption of animal-based foods available in the markets of Shanghai, China.

To assess the health risks due to food consumption, the human daily intake and uptake of organochlorine pesticides, polychlorinated biphenyls, polybrominated diphenyl ethers, polycyclic aromatic hydrocarbons, and toxic trace elements (mercury, chromium, cadmium, lead, and arsenic) were estimated based on the animal-based foods collected from markets in Shanghai, China. The estimated daily intake and uptake considering the contaminant bioaccessibility via single food consumption were 9.4-399 and 4.2-282 ng/kg body weight/day for adults, and 10.8-458 and 4.8-323 ng/kg body weight/day for children, respectively. These values were 0.2-104 and 0.05-58.1, and 0.2-119 and 0.06-66.6 ng/kg body weight/day via multiple food consumption for adults and children, respectively. According to the United States Environmental Protection Agency risk assessment method, the non-cancer and cancer health risks posed by the contaminants were estimated using the hazard quotient and the lifetime cancer risk method, respectively. The results showed that the combined hazard quotient values for multiple contaminants via single or multiple food consumption were below 1, suggesting that the residents in Shanghai would not experience a significant non-cancer health risk. Among the contaminants investigated, the potential non-cancer risk of methylmercury was highest. However, the combined cancer risk posed by multiple contaminants in most foods exceeded the accepted risk level of 10(-6), and inorganic arsenic was the main contributor. The risks caused by polybrominated diphenyl ethers for cancer and non-cancer effects were negligible. The cancer risk of inorganic arsenic is a matter of concern in animal-based foods from Shanghai markets.

Polybrominated biphenyl ethers in breast milk and infant formula from Shanghai, China: temporal trends, daily intake, and risk assessment.

To investigate the temporal trend of polybrominated diphenyl ethers (PBDEs) in breast milk and assess the risks to breast- and formula-fed infants, breast milk and infant formula samples were collected from Shanghai, China. The PBDE concentrations decreased from 14.8 to 4.85 pmol/g lipid weight during 2006-2012, with a rate of decrease by half approximately every four years. Although there were no significant correlations between the total PBDEs in breast milk and age, parity, and pre-pregnant BMI of mothers, there were significant differences between primiparous and multiparous mothers for tri- to hepta-BDEs. PBDEs in breast milk were much higher than those in infant formula (equivalent to 91.9 vs. 5.25 pg/mL). Among the different brand infant formulas, there were no significant differences in their PBDE concentrations. The estimated daily intake of PBDEs by breast- and formula-fed infants suggested that breast-fed infants are exposed to much more PBDEs than formula-fed ones (12.9 vs. 0.72 ng/kg-bw/day). However, the hazard quotient values were much smaller than one, indicating that the ingested PBDEs did not exert obvious adverse effects on both breast- and formula-fed infants considering non-carcinogenic effect endpoint. This is the first report on temporal trend of PBDEs in breast milk from China.