Acetaldehyde (AA) has been classified as a probable human carcinogen by the International Agency for Research on Cancer (IARC, WHO) and by the US Environmental Protection Agency due to its ability to cause tumours following inhalation or alcohol consumption in animals. Humans are constantly exposed to AA through inhalation from the environment through cigarette smoke, vehicle fumes and industrial emissions as well as by persistent alcohol ingestion. Individuals with deficiencies in the enzymes that are involved in the metabolism of AA are more susceptible to its toxicity and constitute a vulnerable human population. Studies have shown that AA induces DNA damage and cytogenetic abnormalities. A study was undertaken to elucidate the clastogenic effects induced by AA and any preceding DNA damage that occurs in normal human lung fibroblasts as this will further validate the detrimental effects of inhalation exposure to AA. AA exposure induced DNA damage, involving DNA double strand breaks, which could possibly occur at the telomeric regions as well, resulting in a clastogenic effect and subsequent genomic instability, which contributed to the cell cycle arrest. The clastogenic effect induced by AA in human lung fibroblasts was evidenced by micronuclei induction and chromosomal aberrations, including those at the telomeric regions. Co-localisation between the DNA double strand breaks and telomeric regions was observed, suggesting possible induction of DNA double strand breaks due to AA exposure at the telomeric regions as a new mechanism beyond the clastogenic effect of AA. From the cell cycle profile following AA exposure, a G2/M phase arrest and a decrease in cell viability were also detected. Therefore, these effects due to AA exposure via inhalation may have implications in the development of carcinogenesis in humans.

乙醛 (AA) 已被国际癌症研究机构 (IARC, WHO) 和美国环境保护署列为可能的人类致癌物，因为它能够在动物吸入或饮酒后引起肿瘤。人类通过从环境中吸入香烟烟雾、汽车烟雾和工业排放物以及持续摄入酒精而不断接触 AA。参与 AA 代谢的酶缺乏的个体更容易受到其毒性的影响，并构成脆弱的人群。研究表明，AA 会导致 DNA 损伤和细胞遗传学异常。进行了一项研究，以阐明由 AA 引起的致裂体效应以及发生在正常人肺成纤维细胞中的任何先前的 DNA 损伤，因为这将进一步验证吸入暴露于 AA 的有害影响。AA 暴露诱导 DNA 损伤，包括 DNA 双链断裂，这也可能发生在端粒区域，导致断裂效应和随后的基因组不稳定，从而导致细胞周期停滞。AA 在人肺成纤维细胞中诱导的致裂体效应由微核诱导和染色体畸变（包括端粒区域的畸变）证明。观察到 DNA 双链断裂和端粒区域之间的共定位，表明由于端粒区域的 AA 暴露可能诱导 DNA 双链断裂，这是一种超越 AA 致裂效应的新机制。从 AA 暴露后的细胞周期曲线中，还检测到 G2/M 期停滞和细胞活力降低。因此，通过吸入接触 AA 引起的这些影响可能对人类致癌作用的发展产生影响。