Nylander L A, Dement J M
Division of Industrial Hygiene, National Institute of Occupational Health, Solna, Sweden.
Am J Ind Med. 1993 Nov;24(5):619-47. doi: 10.1002/ajim.4700240511.
Occupational exposure to wood dust (alone or chemically treated) is associated with an increased risk of developing adenocarcinoma of the nasal cavity. The specific causative agents, i.e., wood dust alone (natural products), wood dust with additives used in the processing or manufacturing of wood products, and/or physical determinants of wood dust and the associated risk factors, are not known or understood. The strongest association of exposure to wood dust and development of nasal cancer is observed in those occupations where workers are exposed to hard wood dust and chemical additives are not used. The time between first occupational exposure to wood dust and the development of adenocarcinoma of the nasal cavity averages 40 years (range 7-70 years). The epidemiological data available are not sufficient to make a definitive assessment between wood dust exposure and increased risk for cancer other than nasal cancer. The toxicity, mutagenicity, and carcinogenicity of wood dust to laboratory animals or in vitro with animal or microbial cells have not been thoroughly studied. Thus there is no direct experimental evidence on the potential hazards of wood dust. Data are insufficient or lacking on 1) wood dust exposure levels in ambient air and worker's breathing zone, and the deposition in the nasal cavity; 2) hard vs. soft wood dusts; 3) particle size and shape; 4) chemical composition of wood dust and the extent of contamination with chemical additives; and 5) interaction between inhaled wood dust, chronic irritation, and tobacco smoking. These data are required so that one can understand the association between wood dust exposure and nasal cavity tumors, along with demographic differences in cancer rates, and to develop strategies for intervention and reduction of disease causing agents in order to reduce risk to wood industry workers.
职业接触木屑(单独或经过化学处理)与鼻腔腺癌发病风险增加有关。具体的致病因素,即单独的木屑(天然产物)、木材加工或制造过程中使用添加剂的木屑,和/或木屑的物理特性以及相关风险因素,目前尚不明确。在那些工人接触硬木屑且未使用化学添加剂的职业中,观察到木屑接触与鼻腔癌发病之间的关联最为强烈。首次职业接触木屑至鼻腔腺癌发病的平均时间为40年(范围7 - 70年)。现有的流行病学数据不足以对木屑接触与除鼻腔癌之外的其他癌症风险增加之间做出明确评估。木屑对实验动物或在体外对动物或微生物细胞的毒性、致突变性和致癌性尚未得到充分研究。因此,关于木屑潜在危害没有直接的实验证据。在以下方面的数据不足或缺乏:1)环境空气中和工人呼吸带的木屑接触水平以及在鼻腔中的沉积;2)硬木屑与软木屑;3)颗粒大小和形状;4)木屑的化学成分以及化学添加剂的污染程度;5)吸入的木屑、慢性刺激与吸烟之间的相互作用。需要这些数据以便了解木屑接触与鼻腔肿瘤之间的关联,以及癌症发病率的人口统计学差异,并制定干预策略和减少致病因子,以降低木材行业工人的风险。