Liss G M, Bernstein D, Genesove L, Roos J O, Lim J
Health and Safety Studies Unit, Ontario Ministry of Labour, Toronto.
J Allergy Clin Immunol. 1993 Aug;92(2):237-47. doi: 10.1016/0091-6749(93)90167-e.
Two groups of workers with occupational asthma caused by tetrachlorophthalic anhydride (TCPA) have been reported on; in only one report was specific anti-TCPA antibody demonstrated. We received a request to investigate respiratory problems among workers at a plant where solenoid coils are manufactured with the use of epoxy resin and where a new TCPA hardener had been introduced in 1988. In response, we conducted a cross-sectional evaluation of 52 current workers and assayed serum samples from 49 workers for TCPA-human serum albumin-specific IgE and IgG by ELISA. Mean airborne TCPA concentrations ranged from 0.21 to 0.39 mg/m3 in 1989 and May 1990 but were considerably lower (less than 0.009 to 0.13 mg/m3) by July 1990 when ventilation was introduced. Workers were classified in four departments as molders (most directly working with TCPA), those intermittently exposed to TCPA, coil assemblers, and office workers. There was a high prevalence of reported work-related respiratory symptoms (from 27% to 39%). The mean decline in FEV1 over the shift in the molders (down 4.1%) was significantly different from the change in the office group (increased 2.5%). Intrashift change in FEV1 was inversely correlated with log personal TCPA concentration (r = -0.47). Of 49 current workers, 15 (31%) had elevated serum TCPA-human serum albumin-specific IgE antibody levels and 19 (39%) had elevated specific IgG levels. The prevalence of specific IgE was highest in the mold and intermittent groups (54%), in comparison with the coil assembly (25%) and office (0%) groups. Those workers who were IgE positive were significantly less likely to be current smokers and had worked significantly longer since 1988. Of those hired in 1988 or after, the proportion of workers who were IgE positive increased with duration of employment category (p value for trend 0.022). Since ventilation was installed and TCPA exposures reduced to less than 0.1 mg/m3, there has been a marked decrease in symptoms and no new cases of occupational asthma among newly hired workers at the plant.
已有两组因四氯邻苯二甲酸酐(TCPA)导致职业性哮喘的工人的报告;仅有一份报告证实了特异性抗TCPA抗体的存在。我们收到一项请求,要对一家制造电磁线圈的工厂的工人的呼吸问题展开调查,该工厂使用环氧树脂,且于1988年引入了一种新型TCPA硬化剂。作为回应,我们对52名在职工人进行了横断面评估,并通过酶联免疫吸附测定法(ELISA)检测了49名工人血清样本中的TCPA - 人血清白蛋白特异性IgE和IgG。1989年和1990年5月,空气中TCPA的平均浓度在0.21至0.39毫克/立方米之间,但到1990年7月引入通风设备后,浓度大幅降低(低于0.009至0.13毫克/立方米)。工人被分为四个部门,即成型工(最直接接触TCPA)、间歇性接触TCPA的工人、线圈装配工和办公室职员。报告的与工作相关的呼吸道症状患病率很高(从27%到39%)。成型工在轮班期间FEV1的平均下降幅度(下降4.1%)与办公室职员组的变化(上升2.5%)有显著差异。FEV1的轮班内变化与个人TCPA浓度的对数呈负相关(r = -0.47)。在49名在职工人中,15人(31%)血清TCPA - 人血清白蛋白特异性IgE抗体水平升高,19人(39%)特异性IgG水平升高。特异性IgE的患病率在成型工和间歇性接触组中最高(54%),相比之下,线圈装配组(25%)和办公室职员组(0%)则较低。那些IgE呈阳性的工人目前吸烟的可能性显著更低,且自1988年以来工作时间显著更长。在1988年或之后受雇的工人中,IgE呈阳性的工人比例随就业年限增加(趋势p值为0.022)。自从安装通风设备并将TCPA暴露降低到低于0.1毫克/立方米以来,该工厂新雇佣工人的症状明显减少,且未出现新的职业性哮喘病例。