Inhalation bioacessibility and lung cell penetration of indoor PM2.5-bound PAEs and its implication in risk assessment.

Several studies have evaluated the human exposure of phthalate esters (PAEs) in PM2.5 via inhalation route, however, inhalation bioaccessibility and the lung cell penetration of PAEs were barely considered in risk assessment. In the present study, PM2.5 samples collected from indoor environments were investigated for inhalation bioaccessibility of PAEs using two simulated lung fluids (gamble's solution (GMB) and artificial lysosomal fluid (ALF)). The results showed that the inhalation bioaccessibility of PAEs (except for diethyl phthalate) under healthy state (GMB: 8.9%-62.8%) was lower than that under the inflammatory condition (ALF: 14.5%-67.6%). Lung cell permeation and metabolism of three selected PAEs (diethyl phthalate, di(n-butyl)phthalate and di-2-ethylhexyl phthalate) was tested using equivalent lung cell (A549) model. The inhalation bioavailability obtained by combination of the bioaccessibility of PAEs in indoor PM2.5 and permeability data of A549 cell ranged from 11.7% to 51.1% in health condition, and 13.5%-55.0% in inflammatory state. The calibration parameter (Fc) based on the inhalation bioavailability was established in present study and could provide a reference for a more accurate risk assessment of PM2.5-bound PAEs.

Inhalation bioacessibility and absorption of polycyclic aromatic hydrocarbons (PAHs) in indoor PM2.5 and its implication in risk assessment.

Inhalation bioaccessibility of polycyclic aromatic hydrocarbons (PAHs) in PM2.5 was assessed in numerous studies, however, the lung cell uptake and penetration of PAHs was seldom taken into account in risk assessment. In the present study, eighteen indoor PM2.5 samples collected from Guangzhou, China were analyzed for the inhalation bioavailability of PAHs combining the inhalation bioaccessibility and cell absorption of PAHs. Two simulated epithelial lung fluid mimicking the healthy condition (as represented by gamble's solution (GMB), pH = 7.4) and the inflammatory condition (as represented by artificial lysosomal fluid (ALF), pH = 4.5) were employed to evaluate the inhalation bioaccessibility. The results indicated that the bioaccessibility of PAHs under the inflammatory condition (1.28%-87.7%) was higher than that under healthy condition (0.88%-87.6%). Naphthalene, phenanthrene, pyrene and benzo[a]pyrene were selected for absorption assay of lung epithelial cells (A549). The absorption rate of PAHs ranged from 64.7 to 90.7% and it was inversely proportional to the number of aromatic rings. Taken together, the inhalation bioavailability based on the bioaccessibility of PAHs and the lung cell absorption ratio ranged from 9.9 to 56.9% under the healthy state, from 12.7 to 65.6% under inflammatory condition. The correction parameter (Fc) was thus established and can be used to improve the risk assessment of human exposure to PAHs via PM2.5 inhalation in future work.

Percutaneous Penetration and Metabolism of Plasticizers by Skin Cells and Its Implication in Dermal Exposure to Plasticizers by Skin Wipes.

Numerous studies focused on the human exposure to plasticizers via dermal contact; however, the percutaneous penetration of plasticizers was seldom considered in exposure assessment. In the present study, skin wipes of palms, back-of-hands, and forehead were collected from 114 participants (ages: 18-27). There was no significant difference between the levels of phthalates from palms and back-of-hand, while all phthalates collected from the forehead were significantly higher than those from palms and back-of-hand (p < 0.001); di(2-ethylhexyl)phthalate levels were substantially higher than other detected phthalates followed by di(n-butyl)phthalate and di(isobutyl)phthalate (DiBP), and for alternative plasticizers, bis-2-ethylhexyl terephthalate levels were substantially higher than acetyltributyl citrate and bis-2-ethylhexyladipate. Skin permeation and metabolism of phthalates was assessed using human skin equivalent models. The permeability coefficient (kp) values of phthalates were significantly negatively correlated with their log octanol-water partition coefficient (log Kow), while a significantly positive correlation was found between the log Kow and the cumulative amounts of phthalates in the cells. The proportion of phthalate intake via dermal exposure to skin wipes ranges from 1.3% (for dimethyl phthalate) to 8.6% (for DiBP) and suggests that dermal absorption is a significant route for adult phthalate exposure.

Dermal bioaccessibility and absorption of polycyclic aromatic hydrocarbons (PAHs) in indoor dust and its implication in risk assessment.

Numerous studies have focused on assessing the risk of human exposure to polycyclic aromatic hydrocarbons (PAHs) in indoor dust via dermal contact. However, the dermal bioaccessibility and dermal absorption of PAHs in indoor dust have seldom been reported. In the present study, the effects of temperature, sweat ratio, solid-liquid ratio and incubation time on the dermal bioaccessibility of PAHs were examined. Naphthalene, phenanthrene, pyrene and benzo[a]pyrenewere selected for examination in an absorption assay with keratinocyte cells. The results showed the release of PAHs from indoor dust fitted a first-order one-compartment model. Naphthalene had the highest rate of release, which was consistent with the bioaccessibility assay results. In addition, the absorption rate of naphthalene and phenanthrene by keratinocytes was higher than that of pyrene and benzo[a]pyrene, with the latter being of higher molecular weight. These results indicated that low molecular weight PAHs were much more easily absorbed via dermal contact than were high molecular weight PAHs. The dermal bioavailability of PAHs in indoor dust was estimated by multiplying the bioaccessibility of PAHs in indoor dust by the ratio of dermal absorption by skin cells, and ranged from 0.12 to 51.0%. These data will be useful in risk assessments.

The comparison of transcriptomic response of green microalga Chlorella sorokiniana exposure to environmentally relevant concentration of cadmium(II) and 4-n-nonylphenol.

The transcriptomic response of green microalga Chlorella sorokiniana exposure to environmentally relevant concentration of cadmium(II) (Cd) and 4-n-nonylphenol (4-n-NP) was compared in the present study. Cd and 4-n-NP exposure showed a similar pattern of dys-regulated pathways. The photosystem was affected due to suppression of chlorophyll biosynthesis via down-regulation of Mg-protoporphyrin IX chelatase subunit ChlD (CHLD) and divinyl chlorophyllide a 8-vinyl-reductase (DVR) in Cd group and via down-regulation of DVR in 4-n-NP group. Furthermore, the reactive oxygen species (ROS) could be induced through down-regulation of solanesyl diphosphate synthase 1 (SPS1) and homogentisate phytyltransferase (HPT) in Cd group and via down-regulation of HPT in 4-n-NP group. Additionally, Cd and 4-n-NP would both cause the dys-regulation of carbohydrate metabolism and protein synthesis. On the other hand, there are some different responses or detoxification mechanism of C. sorokiniana to 4-n-NP stress compared to Cd exposure. The increased ROS would cause the DNA damage and protein destruction in Cd exposure group. Simultaneously, the RNA transcription was dys-regulated and a series of changes in gene expressions were observed. This included lipid metabolism, protein modification, and DNA repair, which involved in response of C. sorokiniana to Cd stress or detoxification of Cd. For 4-n-NP exposure, no effect on lipid metabolism and DNA repair was observed. The nucleotide metabolism including pyrimidine metabolism and purine metabolism was significantly up-regulated in the 4-n-NP exposure group, but not in the Cd exposure group. In addition, 4-n-NP would induce the ubiquitin-mediated proteolysis and proteasomal degradation to diminish the misfolded protein caused by ROS and down-regulation of heat shocking protein 40. In sum, the Cd and 4-n-NP could cause the same toxicological effects via the common pathways and possess similar detoxification mechanism. They also showed different responses in nucleotide metabolism, lipid metabolism, and DNA repair.