Reduced forced vital capacity in Aboriginal Australians: Biology or missing evidence?

Chronic lung disease is the third largest contributor to the burden of disease in Aboriginal and Torres Strait Islanders (collectively referred to as Aboriginal Australians) and is estimated to contribute to 6% of the mortality gap between Aboriginal and nonAboriginal Australians. The prevalence of selfreported chronic obstructive pulmonary disease (COPD) in the Aboriginal population has been reported to be ∼2.5 times higher than that of the non-Aboriginal population. Hospitalizations for COPD are five times higher in Aboriginal people compared with the non-Aboriginal population, are increasing and may reflect a more severe phenotype profile in the Aboriginal population. It is possible that the self-reported rates of COPD in Aboriginal people are lower than that actually occurring, due to a range of factors including barriers to accessing healthcare and/or a lack of accurate lung function measurements in this patient population. Spirometry plays an important role in the diagnosis and management of COPD. However, there are very few studies that have accurately defined the normal range of spirometry in Aboriginal people or conducted a detailed assessment of lung function in older Aboriginal Australians at risk of COPD. As such, policy and practice in this critical area of healthcare remains mired in the too hard basket. In this issue of Respirology, Cooksley et al. offer an important contribution to understanding the prevalence of COPD in the Aboriginal population. Following the internationally standardized Burden of Lung Disease (BOLD) protocols, the authors obtained preand post-bronchodilator spirometry and respiratory symptoms in 231 and 451 Aboriginal and nonAboriginal adults from the Kimberley region of Western Australia. These data represent the first comprehensive objective assessment of non-reversible obstruction in Aboriginal people and give us an insight into the complexities of the challenges facing us. As well recognized, the prevalence of current smoking in Aboriginal participants was significantly higher than that in the non-Aboriginal group from the same geographical region being 48.5% and 21.4%, respectively. Surprisingly, the history of smoking was not different between the Aboriginal and nonAboriginal people in the Kimberley region (68.3% and 64.7%) and was higher than that reported in the broader Australian BOLD study, highlighting the importance of appropriate geographically relevant controls when assessing the impact of chronic disease in Aboriginal populations. As expected, this high level of past and current smoking in Aboriginal people was associated with significantly increased respiratory symptoms, including shortness of breath, cough and sputum production, but not wheeze. Given this picture of significant smoking history and respiratory symptoms, it was startling to see that the level of post-bronchodilator airflow obstruction based on Global Initiative for Chronic Obstructive Lung Disease (GOLD) Stage 1 or higher in Aboriginal people from the Kimberley region was significantly lower (8.4%) than that of non-Aboriginal residents in the same area (16.0%), although these differences were not apparent at GOLD Stage 2 or higher. A further, even more, unexpected finding was the reporting that 74% of the Aboriginal group in this study had ‘low FVC’ compared with 9.7% of the nonAboriginal control population. The reasons for these differences highlight the complexities of both modern respiratory medicine and applying global respiratory models to Indigenous populations. The international approach of BOLD is to define airflow obstruction as being present with a forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC) < 0.7 for GOLD Stage 1 and higher, with more severe obstruction (GOLD Stage 2 or higher) being FEV1/FVC < 0.7 and FEV1 < 80% predicted. This approach has been repeatedly questioned, and the use of a fixed spirometry cut-off has been shown to lead to an overestimation of airflow obstruction that increases with age and can result in up to 20% misclassification in older individuals. It could be argued that as the same criteria for defining obstruction was used in all groups that the between group difference would not be significantly influenced by these factors, particularly as the statistical analysis adjusted for age and sex. However, in this study, the outcomes are further confounded by the use of the National Health and Nutrition Examination Survey III spirometry reference values without any ethnic adjustments. Therefore, the estimates of obstruction in this study are affected by the differences between both the true lower limit of normal of both FEV1/FVC and FEV1 and the arbitrary fixed cut-offs used by BOLD and any differences in spirometry outcomes between healthy Caucasian and Aboriginal peoples. There is a paucity of spirometry reference ranges for Aboriginal Australians; however, it has been reported that on average, healthy Aboriginal Australians have spirometry approximately 20–30% lower than that of bs_bs_banner