Effects of household air pollution and HIV on lung disease

Charles “Chuck” Kim, MD

I am currently a second year resident in internal medicine at the University of Colorado, Denver. Eight months ago, I spent a few weeks in the Petrache Lab at National Jewish for my research elective. I had the opportunity to get myself immersed into a research project that appealed to both of my interests in pulmonary medicine and global health. I have submitted an abstract for this project in the late breaking American Thoracic Society (ATS) submission and hope to present it at the ATS conference in May.

Household air pollution (HAP) is a global health concern with over 3 billion people all over the world using solid biomass to heat and cook in their homes. HAP is associated with increased risk of chronic obstructive pulmonary disease (COPD) and other pulmonary diseases. Some of the largest burden of HAP occur in Sub-Saharan Africa where coincidentally the bulk of the world’s burden of HIV/AIDS is also located. As HIV/AIDS is also known to be an independent risk factor for COPD and pulmonary vascular disease, we hypothesized that HIV status and HAP exposure would experience greater pulmonary symptoms and exhibit greater inflammation and vascular injury than those individuals without HIV or exposure to HAP. With such a large burden of both HAP and HIV around the world and recent efforts to reduce HAP exposure in the developing world, we found that this was a very clinically relevant and timely question to pursue.malawi_map-resized

Our investigation took us to the population of Malawi, a Sub-Saharan country, where they stand at the intersection of HIV and HAP with 10.6% of adults (15-49 years of age) with HIV and the average HAP levels far above WHO’s recommended levels. Our colleagues at the Wellcome Trust Tropical Centre at the University of Liverpool recruited subjects in Malawi with known HIV status. These subjects were given an extensive survey of pulmonary symptoms and exposure history to HAP. Ambulatory measurements of typical HAP exposures were also made. Serum samples were collected from each individual which were analyzed at our lab with the MSD® Multi-Spot assay to measure the levels of 41 different serum markers.

Clinical results showed that significant proportion of our subjects carried respiratory diagnoses and/or reported respiratory symptoms with breathlessness and cough being the most common symptoms. Subjects with HIV or HAP exposure were shown to have higher prevalence of chronic respiratory symptoms/diagnoses as compared to those without HIV or HAP exposures. Laboratory analysis showed serum IL-2 levels were significantly decreased in HIV+ subjects who had persistent respiratory symptoms as compared to other subjects. Serum IL-16 levels were also significantly decreased in HIV+ subjects with HAP exposure as compared to subjects without HIV or HAP exposures.

Our pilot study suggests that there is a high prevalence of respiratory symptoms in individuals with HIV and/or have high HAP exposure. A larger cohort of similar populations should be studied to see if there is a true synergy between HIV and HAP exposure with more clinical data such as pulmonary function tests. Furthermore, further studies need to be pursued on IL-2 (a cytokine that promotes CD4+ cell proliferation and survival) and IL-16 (a cytokine that inhibits HIV replication) to investigate if decreases in these cytokines can be useful biomarkers for the risk of development of COPD in this population.