The 1980 report that inhaled formaldehyde induced nasal squamous cell carcinomas in rats had a significant societal impact and resulted in extensive research in the fields of rodent nasal pathology and human cancer risk assessment. This article presents an overview of the evolution of these events. It is concluded that the nasal passages of humans and rats are fundamentally identical biological target organs. Nevertheless, in the case of human health risk assessment, minor differences between these species may be critically important. Special attention should be paid to interspecies differences in nasal dosimetry and local metabolism; thus, chemical toxicity data derived from rats require careful interpretation when used for human risk assessments. In the case of formaldehyde, it is recommended that low-concentration (< or = 2 ppm airborne exposure) extrapolation, where no tissue damage is observed, be uncoupled from the responses at high concentrations (> or = 6 ppm), where epithelial degeneration, regenerative cell replication, and inflammation appear to be essential driving forces in formaldehyde carcinogenesis. The presence of treatment-related nasal lesions in rats following exposure to chemicals should always be treated as an indication of a potential human health risk, whether exposure is by the inhalation, oral, or dermal route.

译文

1980报告说,吸入甲醛诱导的大鼠鼻鳞状细胞癌具有重大的社会影响,并导致在啮齿动物鼻病理学和人类癌症风险评估领域的广泛研究。本文概述了这些事件的演变。结论人和大鼠的鼻腔通道是基本相同的生物靶器官。然而,就人类健康风险评估而言,这些物种之间的微小差异可能至关重要。应特别注意鼻剂量测定和局部代谢的种间差异; 因此,从大鼠获得的化学毒性数据在用于人类风险评估时需要仔细解释。在甲醛的情况下,建议低浓度 (< or = 2 ppm空气传播暴露) 外推,在没有观察到组织损伤的情况下,与高浓度 (> or = 6 ppm) 的反应分离,在高浓度 (> or = 6 ppm),上皮变性,再生细胞复制,炎症似乎是甲醛致癌的重要驱动力。无论是通过吸入,口服还是通过皮肤途径暴露,都应始终将暴露于化学物质后的大鼠中与治疗相关的鼻部病变视为潜在的人类健康风险的指示。

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