Meredith S K, Bugler J, Clark R L
MRC Clinical Trials Unit, 222 Euston Road, London NW1 2DA, UK.
Occup Environ Med. 2000 Dec;57(12):830-6. doi: 10.1136/oem.57.12.830.
To examine the quantitative relation between exposure to isocyanates and occupational asthma, and to explore the role of atopy and smoking in occurrence of the disease.
A case-referent study was undertaken of cases from two manufacturing companies (A and B) from which referents without disease could be selected and reliable exposure measurements were available. In company A, 27 cases mainly attributed to toluene diisocyanate (TDI) were matched to 51 referents on work area, start and duration of employment, sex, and age. Exposures were estimated from existing measurements by job category. In company B there were seven cases attributed to 4,4'-diphenylmethane diisocyanate (MDI) in two areas of the plant; 12 non-cases from the same areas were used as referents. Personal exposure measurements were available for all cases and 11 referents.
No difference in peak exposures between cases and referents was found in either plant; but in both, time weighted average (TWA) exposures at the time of onset of asthma were higher for cases. In A, the mean TWA exposure for cases was 1.5 (95% confidence interval (95% CI) 1.2 to 1.8) ppb compared with 1.2 (1.0 to 1.4) ppb for referents. From a matched analysis, the odds ratio (OR) associated with 8 hour TWA exposure to isocyanates greater than 1.125 ppb (the median concentration for the referent group) was 3.2 (95% CI 0.96 to 10.6; p=0.06). Occupational asthma was associated with a pre-employment history of atopic illness (OR 3. 5, p=0.04) and, less strongly, with smoking (OR 2.1, p=0.14). In B, small numbers limited analysis, but three of seven cases had at least one TWA exposure measurement greater than 5 ppb compared with one of 11 referents (OR 7.5, p=0.09).
Asthma can occur at low concentrations of isocyanates, but even at low concentrations, the higher the exposure the greater the risk. By contrast with other studies, smoking and atopy seemed to increase the odds of occupational asthma due to isocyanates, but did not affect the estimate of risk associated with exposure.
研究异氰酸酯暴露与职业性哮喘之间的定量关系，并探讨特应性体质和吸烟在该病发生中的作用。
对两家制造公司（A和B）的病例进行病例对照研究，从中可以选择无疾病的对照者，并且有可靠的暴露测量数据。在公司A中，将27例主要归因于甲苯二异氰酸酯（TDI）的病例与51名对照者按工作区域、开始工作时间和工作时长、性别及年龄进行匹配。根据现有的按工种分类的测量数据估算暴露情况。在公司B中，该工厂两个区域有7例归因于4,4'-二苯基甲烷二异氰酸酯（MDI）的病例；将来自相同区域的12名非病例用作对照者。所有病例和11名对照者均有个人暴露测量数据。
在两家工厂中，病例组和对照组的峰值暴露均无差异；但在两家工厂中，哮喘发作时病例组的时间加权平均（TWA）暴露均更高。在公司A中，病例组的平均TWA暴露为1.5（95%置信区间（95%CI）1.2至1.8）ppb，而对照组为1.2（1.0至1.4）ppb。通过匹配分析，8小时TWA暴露于异氰酸酯大于1.125 ppb（对照组的中位数浓度）的比值比（OR）为3.2（95%CI 0.96至10.6；p=0.06）。职业性哮喘与就业前的特应性疾病史相关（OR 3.5，p=0.04），与吸烟的相关性较弱（OR 2.1，p=0.14）。在公司B中，由于样本量小限制了分析，但7例病例中有3例至少有一次TWA暴露测量值大于5 ppb，而11名对照者中有1例（OR 7.5，p=0.09）。
异氰酸酯低浓度时也可发生哮喘，但即使在低浓度下，暴露越高风险越大。与其他研究不同的是，吸烟和特应性体质似乎增加了因异氰酸酯导致职业性哮喘的几率，但不影响与暴露相关的风险估计。
