Tracking pesticide exposure to operating workers for risk assessment in seed coating with tebuconazole and carbofuran.

BACKGROUND: Coating seed with pesticides is an effective way to control plant pests, however, factory-based coating processes may carry a potential risk to operational workers of chemical exposure. To study the risk, carbofuran and tebuconazole were used to coat corn seed and their subsequent distribution on the bodies of workers was measured at manufacturers XFS and LS (Shanxi, China). Clothing was collected from workers during operations and analyzed using high-performance liquid chromatography. RESULTS: At XFS, dermal exposure to carbofuran was 4.83, 3.31 and 1.48 mg kg-1 , and exposure to tebuconazole was 6.88, 5.16 and 1.72 mg kg-1 for coating, packing and transport workers, respectively. At LS, dermal exposure to carbofuran was 2.32, 0.46 and 0.55 mg kg-1 , and exposure to tebuconazole was 1.69, 0.46 and 0.70 mg kg-1 , for coating, packing and transport workers, respectively. The level of pesticide exposure was significantly higher for seed-coating workers than for packing and transport workers. The main area of exposure was the hands for all workers and the lower limbs for packers; exposure was relatively uniform for pesticide handlers. Occupational risk was assessed based on margin of exposure (MOE). In seed-coating, the MOE was greater than 100 for tebuconazole, indicating no potential risk, but ranged from 0.25 to 2.88 for carbofuran, indicating the risk of a health impact. CONCLUSION: The level of exposure varied depending on type of operation undertaken and body parts of workers' body, but the risk of a health impact was highly associated with pesticide toxicity. This provides a guideline for workers in pesticide manufacturing to ensure safe operation of the seed-coating process. © 2021 Society of Chemical Industry.

Solid tumor-targeted infiltrating cytotoxic T lymphocytes retained by a superantigen fusion protein.

Successful immune-mediated regression of solid tumors is difficult because of the small number of cytotoxic T lymphocytes (CTLs) that were traffic to the tumor site. Here, the targeting of tumor-specific infiltrating CTLs was dependent on a fusion protein consisting of human epidermal growth factor (EGF) and staphylococcal enterotoxin A (SEA) with the D227A mutation. EGF-SEA strongly restrained the growth of murine solid sarcoma 180 (S180) tumors (control versus EGF-SEA, mean tumor weight: 1.013 versus 0.197 g, difference  = 0.816 g). In mice treated with EGF-SEA, CD4+, CD8+ and SEA-reactive T lymphocytes were enriched around the EGFR expressing tumor cells. The EGF receptors were potentially phosphorylated by EGF-SEA stimulation and the fusion protein promoted T cells to release the tumoricidal cytokines interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Intratumoral CTLs secreted cytolytic pore-forming perforins and granzyme B proteins near the surface of carcinomas, causing the death of many tumor cells. We additionally show that labeled EGF-SEA was directly targeted to the tumor tissue after intravenous (i.v.) injection. The findings demonstrate that antibody-like EGF-SEA plays an important role in arresting CTLs in the solid tumor site and has therapeutic potential as a tumor-targeting agent.