Co-exposure health risk of benzo[a]pyrene with aromatic VOCs: Monoaromatic hydrocarbons inhibit the glucuronidation of benzo[a]pyrene.

Occupational workers and residents near petrochemical industry facilities are exposed to multiple contaminants on a daily basis. However, little is known about the co-exposure effects of different pollutants based on biotransformation. The study examined benzo[a]pyrene (BaP), a representative polycyclic aromatic hydrocarbon related to the petrochemical industry, to investigate changes in toxicity and co-exposure mechanism associated with different monoaromatic hydrocarbons (MAHs). A central composite design method was used to simulate site co-exposure scenarios to reveal biotransformation of BaP when co-exposed with benzene, toluene, chlorobenzene, or nitrobenzene in microsome systems. BaP metabolism depended on MAH concentration, and association of MAH with microsome concentration/incubation time. Particularly, MAH co-exposure negatively affected BaP glucuronidation, an important phase Ⅱ detoxification process. BaP metabolite intensities decreased to 43%-80% for OH-BaP-G, and 32%-71% for diOH-BaP-G in co-exposure system with MAHs, compared with control group. Furthermore, glucuronidation was affected by competitive and time-dependent inhibition. Co-exposure significantly decreased gene expression of UGT 1A10 and BCRP/ABCG2 in HepG2 cells, which are involved in BaP detoxification through metabolism and transmembrane transportation. Therefore, human co-exposure to multiple contaminants may deteriorate toxic effects of these chemicals by disturbing metabolic pathways. This study provides a reference for assessing toxic effects and co-exposure risks of pollutants.

A review of disrupted biological response associated with volatile organic compound exposure: Insight into identification of biomarkers.

Volatile organic compounds (VOCs) are widespread harmful atmospheric pollutants, which have long been concerned and elucidated to be one of the risks of acute and chronic diseases for human, such as leukemia and cancer. Although numerous scientific studies have documented the potential adverse outcomes caused by VOC exposure, the mechanisms which biological response pathways of these VOC disruption remain poorly understood. Therefore, the identification of biochemical markers associated with metabolism, health effects and diseases orientation can be an effective means of screening biological targets for VOC exposure, which provide evidences to the toxicity assessment of compounds. The current review aims to understand the mechanisms underlying VOCs-elicited adverse outcomes by charactering various types of biomarkers. VOCs-related biomarkers from three aspects were summarized through in vitro, animal and epidemiological studies. i) Unmetabolized and metabolized VOC biomarkers in human samples for assessing exposure characteristics in different communities; ii) Adverse endpoint effects related biomarkers, mainly including (anti)oxidative stress, inflammation response and DNA damage; iii) Omics-based molecular biomarkers alteration in gene, protein, lipid and metabolite aspects associated with biological signaling pathway disorders response to VOC exposure. Further research, advanced machine learning and bioinformation approaches combined with experimental results are urgently needed to ascertain the selection of biomarkers and further illuminate toxic mechanisms of VOC exposure. Finally, VOCs-induced disease causes can be predicted with proven results.

Combined exposure of MAHs and PAHs enhanced amino acid and lipid metabolism disruption in epithelium leading asthma risk.

Monoaromatic hydrocarbons (MAHs) and polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants from industry, with multiple adverse effects on respiratory system. However, the underlying mechanisms of their mixture to induce asthma is still unclear. Here, we examined mixture of 8 MAHs, mixture of 16 PAHs and a total mixture (MIX) on human bronchial epithelial (16-HBE) cells. Exposure to MIX resulted in increased expressions of asthma alarm cytokines (TSLP, IL-25 and IL-33), indicating potential asthma risk. Exposure to MIX led to significant upregulation of transcriptional level of oxidative stress and inflammation biomarkers through aryl hydrocarbon receptor activation, including SOD-2, NQO-1, IL-1ß, IL-6 and IL-8 with 3.1, 19.9, 3.5, 23.4, 18.7, 28.1-fold change, indicated asthma related epithelial cell lesions. A total of 25, 49 and 59 differential metabolites were identified in cells response to MAH, PAH and MIX exposure, respectively, and enrichment analysis demonstrated MIX exposure disturbing alanine, aspartate and glutamate metabolism, glutathione metabolism, methionine metabolism and sphingolipid metabolism, involved in antioxidative defense and inflammation response. Combined exposure of MAHs and PAHs may result in increased toxic risks, and provide evidence to asthma onset and deterioration.

Phytoremediation of cadmium-contaminated wetland soil with Typha latifolia L. and the underlying mechanisms involved in the heavy-metal uptake and removal.

The effects of Typha latifolia L. on the remediation of cadmium (Cd) in wetland soil were studied using greenhouse pot culture, with soil Cd concentrations of 0, 1, and 30 mg/kg. The T. latifolia showed excellent tolerance to the low and high concentrations of Cd in soil. A higher bioaccumulation of Cd was observed in roots, with bioconcentration factor values of 51.6 and 9.30 at 1 and 30 mg/kg of Cd stress, respectively; Cd concentration in T. latifolia was 77.0 and 410.7 mg/kg, and Cd content was 0.11 and 0.22 mg/plant at the end of the test period. The soil enzyme activities (urease, alkaline phosphatase, and dehydrogenase) exposed to 0, 1, and 30 mg/kg Cd were measured after 0-, 30-, 60-, and 90-day cultivation period and showed an increasing trend with exposure time. Metabolite changes were analyzed using liquid chromatography-mass spectrometry, combined with principal component analysis and orthogonal partial least squares discrimination analysis. Among 102 metabolites, 21 compounds were found and identified, in response to treatment of T. latifolia with different Cd concentrations. The results showed that T. latifolia had a good remedial effect on Cd-contaminated soil. The metabolites of T. latifolia changed with different Cd concentration exposures, as a result of metabolic response of plants to Cd-contaminated soils. Analysis of metabolites could better reveal the pollution remediation mechanism involved in different Cd uptake and accumulate properties.