School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia
School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia.
Thorax. 2020 Oct;75(10):864-869. doi: 10.1136/thoraxjnl-2019-214478. Epub 2020 Jul 13.
Idiopathic pulmonary fibrosis (IPF) is a lung disease of unknown cause characterised by progressive scarring, with limited effective treatment and a median survival of only 2-3 years. Our aim was to identify potential occupational and environmental exposures associated with IPF in Australia.
Cases were recruited by the Australian IPF registry. Population-based controls were recruited by random digit dialling, frequency matched on age, sex and state. Participants completed a questionnaire on demographics, smoking, family history, environmental and occupational exposures. Occupational exposure assessment was undertaken with the Finnish Job Exposure Matrix and Australian asbestos JEM. Multivariable logistic regression was used to describe associations with IPF as ORs and 95% CIs, adjusted for age, sex, state and smoking.
We recruited 503 cases (mean±SD age 71±9 years, 69% male) and 902 controls (71±8 years, 69% male). Ever smoking tobacco was associated with increased risk of IPF: OR 2.20 (95% CI 1.74 to 2.79), but ever using marijuana with reduced risk after adjusting for tobacco: 0.51 (0.33 to 0.78). A family history of pulmonary fibrosis was associated with 12.6-fold (6.52 to 24.2) increased risk of IPF. Occupational exposures to secondhand smoke (OR 2.1; 1.2 to 3.7), respirable dust (OR 1.38; 1.04 to 1.82) and asbestos (OR 1.57; 1.15 to 2.15) were independently associated with increased risk of IPF. However occupational exposures to other specific organic, mineral or metal dusts were not associated with IPF.
The burden of IPF could be reduced by intensified tobacco control, occupational dust control measures and elimination of asbestos at work.
特发性肺纤维化（IPF）是一种病因不明的肺部疾病，其特征为进行性瘢痕形成，目前治疗方法有限，中位生存期仅为 2-3 年。本研究旨在确定澳大利亚特发性肺纤维化与潜在的职业和环境暴露因素之间的关系。
病例通过澳大利亚特发性肺纤维化登记系统招募。采用随机数字拨号法招募基于人群的对照，按照年龄、性别和州进行频率匹配。参与者完成了一份关于人口统计学、吸烟、家族史、环境和职业暴露的调查问卷。职业暴露评估采用芬兰职业暴露矩阵和澳大利亚石棉 JEM。多变量逻辑回归用于描述与特发性肺纤维化的关联，OR 和 95%CI 为比值比，调整了年龄、性别、州和吸烟状况。
我们招募了 503 例病例（平均年龄 71±9 岁，69%为男性）和 902 例对照（71±8 岁，69%为男性）。吸烟与特发性肺纤维化的风险增加有关：OR 2.20（95%CI 1.74 至 2.79），但在调整烟草因素后，使用大麻与风险降低相关：0.51（0.33 至 0.78）。家族性肺纤维化病史与特发性肺纤维化的风险增加 12.6 倍（6.52 至 24.2）有关。接触二手烟（OR 2.1；1.2 至 3.7）、可吸入粉尘（OR 1.38；1.04 至 1.82）和石棉（OR 1.57；1.15 至 2.15）与特发性肺纤维化的风险增加独立相关。然而，接触其他特定有机、矿物质或金属粉尘与特发性肺纤维化无关。
通过加强烟草控制、职业粉尘控制措施和消除工作场所中的石棉，可以降低特发性肺纤维化的负担。
