The role of occupational exposure on chronic obstructive pulmonary disease in middle-aged adults

Abstract

Chronic Obstructive Pulmonary Disease (COPD) contributes significantly to the global burden of disease. COPD is characterized by the presence of fixed airflow obstruction (AO) as measured by spirometry and defined by irreversible reduction in the post-bronchodilator (BD) ratio between the forced expiratory volume in one second and forced vital capacity (FEV1/FVC). Chronic bronchitis, chronic respiratory symptoms and lung function decline over time are also significant predictors of COPD. However, they are also considered separate conditions as these may exist with normal lung function. Smoking is the main risk factor for COPD but a large number of people with COPD are never smokers, so other factors are contributing to the disease burden. Occupational exposure is one of the known important preventable risk factor for this disease. Understanding how occupational exposures contribute to the overall risk of COPD in the general population is essential to be able to gain a greater understanding of COPD etiology and to be able to identify high-risk occupational groups. Population-based studies have found evidence of a relationship between some occupational exposures and COPD. However, a critical review of literature presented in Chapter 2, identified that studies to date investigating these relationships have had some significant limitations including lack of post-BD measurement, limited use of lifetime work history and cumulative exposure assessment. Furthermore, some common occupational exposures with known respiratory impacts have not been investigated in relation to fixed AO with adequate consideration of asthma and lung function decline. Therefore, the aim of my doctoral work was to investigate the effects of occupational exposures on COPD using robust definitions of COPD, chronic bronchitis, and lung function decline and to explore if any effect modification existed.

My systematic review and meta-analyses (Chapter 3) identified an association between low exposure to mineral dust and high exposure to gases/fumes and COPD, and both low and high exposure to biological dust and mineral dust were associated with chronic bronchitis. This work further helped to identify some of the major gaps in the literature that I have addressed in my subsequent analysis.

In Chapter 4, I used data from the population-based Tasmanian Longitudinal Health Study (TAHS). Lifetime work history calendars were collected at age 45 years, and occupational exposures were assigned using the ALOHA plus Job Exposure Matrix and defined as ever exposed and cumulative exposure-unit years. Multivariable linear and logistic regressions were used to investigate the associations adjusting for possible confounders.

In Chapter 5, I examined the associations between occupational exposure and COPD defined by fixed AO, chronic bronchitis, and respiratory symptoms. I found consistent significant associations between ever exposure and cumulative exposure-unit years to pesticides and herbicides and fixed AO, chronic bronchitis, and respiratory symptoms. I also found evidence of effect modification by current asthma for the association between biological dust, mineral dust, and gases/fumes and fixed AO.

In Chapter 6, I examined the association between exposure to solvents and metals and COPD as defined by fixed AO and gas transfer factor. I found an association between ever exposure to metals and fixed AO. Interestingly I also found an association between increasing cumulative exposure-unit years to chlorinated solvents and fixed AO and fixed AO plus low DLco but only in women, not in men.

In Chapter 7, I investigated the association between occupational exposures and lung function decline between age 45 and 50 years. I found an association between both ever exposure and cumulative exposure-unit years to aromatic solvents and a greater decline in lung function. I also found that increasing cumulative exposure-unit years to aromatic solvents were associated with a greater lung function decline in women, but not in men.

Collectively these findings have strengthened and have filled some major gaps in our understanding of the links between overall occupational exposure and the development of COPD in an adult population. I have confirmed in my study that exposure to pesticides is a risk factor for COPD with solvents and metals exposure also linked to an increased risk of COPD. Importantly, my findings suggest that women are at a greater risk of COPD when exposed to solvents. These findings lead me to make several important public health recommendations. Firstly, workplaces need to be monitored to ensure exposure to pesticides and solvents is reduced via adequate ventilation, storage, and usage solutions. Secondly, occupational groups with regular and high exposure to these chemicals need to be encouraged to utilize personal protective equipment, together with routine monitoring. By implementation of these control measures, the burden of COPD caused by occupational exposures has the potential to be reduced.