Finotto S, Fabbri L M, Rado V, Mapp C E, Maestrelli P
Institute of Occupational Medicine, University of Padova, Italy.
Br J Ind Med. 1991 Feb;48(2):116-21. doi: 10.1136/oem.48.2.116.
Occupational asthma induced by toluene diisocyanate (TDI) shares several features with allergic asthma, but the mechanism of action of TDI is poorly understood. Ten sensitised subjects, previously shown to develop a dual or late asthmatic reaction after inhaling TDI were examined. In each subject, forced expiratory volume in one second (FEV1) was measured and venous blood was taken before, and 30 minutes and eight, 24, 48, and 72 hours after exposure to TDI (0.005-0.015 ppm for 10-30 minutes). Filtered air was used as a control. Differential leucocyte counts were determined and phenotypic analysis was performed by immunofluorescence on mononuclear cells using monoclonal antibodies (anti-CD3, anti-CD4, anti-CD8, and anti-HLA-DR). Five subjects developed a dual asthmatic reaction and five had a late reaction. Percentage of CD8 positive lymphocytes increased significantly eight hours after exposure to TDI (from 27 +/- 3 (SEM) % to 42.1 +/- 5%) in the subjects with an isolated late reaction. A delayed significant further increase in suppressor/cytotoxic T lymphocytes was seen in seven of the 10 subjects 48 hours after active exposure (from 27 +/- 2% to 42 +/- 4.8%), irrespective of the type of asthmatic reaction developed after exposure to TDI. Eosinophil percentage increased from 2.5% +/- 1.0 to 6.4% +/- 1.2 24 hours after exposure to TDI and the increase was sustained for up to 48 hours (4.7 +/- 1.1%). No significant variations of FEV1 or cell percentages were seen in the controls. In conclusion, the events triggered by exposure to TDI in sensitised subjects included changes in lung function and systemic effects which lasted longer than bonchoconstriction and concerned suppressor/cytotoxic lymphocytes and eosinophils. These results suggest that TDI induced late asthmatic reactions may be associated with an immunological response to TDI or to its products.
甲苯二异氰酸酯(TDI)诱发的职业性哮喘与过敏性哮喘有一些共同特征,但TDI的作用机制尚不清楚。对10名先前已证明在吸入TDI后会出现双相或迟发性哮喘反应的致敏受试者进行了检查。在每位受试者中,测量了一秒用力呼气量(FEV1),并在接触TDI(0.005 - 0.015 ppm,持续10 - 30分钟)之前、之后30分钟以及8、24、48和72小时采集静脉血。以过滤空气作为对照。测定了白细胞分类计数,并使用单克隆抗体(抗CD3、抗CD4、抗CD8和抗HLA - DR)通过免疫荧光对单核细胞进行表型分析。5名受试者出现双相哮喘反应,5名出现迟发性反应。在出现孤立迟发性反应的受试者中,接触TDI 8小时后,CD8阳性淋巴细胞百分比显著增加(从27±3(SEM)%增至42.1±5%)。在10名受试者中有7名在主动接触后48小时出现抑制性/细胞毒性T淋巴细胞的延迟显著进一步增加(从27±2%增至42±4.8%),无论接触TDI后发生的哮喘反应类型如何。接触TDI 24小时后,嗜酸性粒细胞百分比从2.5%±1.0增至6.4%±1.2,且这种增加持续长达48小时(4.7±1.1%)。在对照组中未观察到FEV1或细胞百分比的显著变化。总之,致敏受试者接触TDI引发的事件包括肺功能变化和全身效应,这些效应持续时间长于支气管收缩,涉及抑制性/细胞毒性淋巴细胞和嗜酸性粒细胞。这些结果表明,TDI诱发的迟发性哮喘反应可能与对TDI或其产物的免疫反应有关。