Ambient PM Exposure and Tuberculosis Reactivation: a Cross-sectional Study in an Intermediate Burden City

Overview

Journal Epidemiol Infect

Publisher Cambridge University Press

Specialties Infectious Diseases
Public Health

Date 2025 Jan 2

PMID 39743772

Authors

Leonia Hiu Wan Lau

Ngai Sze Wong

Chi Chiu Leung

Chi Kuen Chan

Lai-Bun Tai

Alexis Kai Hon Lau

Changqing Lin

Shui Shan Lee

Affiliations

Soon will be listed here.

Abstract

Hong Kong is an intermediate tuberculosis (TB) endemicity city dominated by reactivation diseases. A cross-sectional study on the clinical and epidemiologic data of newly diagnosed TB cases was conducted in such a setting, to examine the association between ambient PM and TB reactivation. After the exclusion of cases most likely resulting from recent infection, four distinct TB population phenotypes were delineated by latent class analysis based on their reactivation risk and clinical profiles ( = 2,153): '' (26%), '' (34%), '' (19%) and '' (21%). Overall, exposure to high concentrations of ambient PM 6 and 12 months before the notification was significantly associated with '' membership (OR = 1.07 and 1.11, respectively) compared with ''. Such association was less evident for other phenotypes. The differential pattern of association between ambient PM exposure and TB population phenotypes suggested the role of ambient PM in TB reactivation.

References

Paynter S, Hayward A, Wilkinson P, Lozewicz S, Coker R . Patient and health service delays in initiating treatment for patients with pulmonary tuberculosis: retrospective cohort study. Int J Tuberc Lung Dis. 2004; 8(2):180-5. View

Leung C, Yew W, Chan T, Tam C, Chan C, Chan C . Seasonal pattern of tuberculosis in Hong Kong. Int J Epidemiol. 2005; 34(4):924-30. DOI: 10.1093/ije/dyi080. View

Strzelak A, Ratajczak A, Adamiec A, Feleszko W . Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases: A Mechanistic Review. Int J Environ Res Public Health. 2018; 15(5). PMC: 5982072. DOI: 10.3390/ijerph15051033. View

Lin P, Flynn J . Understanding latent tuberculosis: a moving target. J Immunol. 2010; 185(1):15-22. PMC: 3311959. DOI: 10.4049/jimmunol.0903856. View

Jassal M, Bakman I, Jones B . Correlation of ambient pollution levels and heavily-trafficked roadway proximity on the prevalence of smear-positive tuberculosis. Public Health. 2013; 127(3):268-74. DOI: 10.1016/j.puhe.2012.12.030. View

Lee S, Chan D, Wong N, Lui G, To K, Kam J . Distribution of molecular strains of in an intermediate burden Asia Pacific city. Epidemiol Infect. 2021; 149:e134. PMC: 8193765. DOI: 10.1017/S0950268821001199. View

Torres M, Carranza C, Sarkar S, Gonzalez Y, Osornio Vargas A, Black K . Urban airborne particle exposure impairs human lung and blood immunity. Thorax. 2019; 74(7):675-683. PMC: 7162557. DOI: 10.1136/thoraxjnl-2018-212529. View

Mao J, Chen H, Li C, Lu J, Gu Y, Feng J . Population impact of fine particulate matter on tuberculosis risk in China: a causal inference. BMC Public Health. 2023; 23(1):2285. PMC: 10657490. DOI: 10.1186/s12889-023-16934-8. View

Ernst J . The immunological life cycle of tuberculosis. Nat Rev Immunol. 2012; 12(8):581-91. DOI: 10.1038/nri3259. View

10.

Kumar P . Adult pulmonary tuberculosis as a pathological manifestation of hyperactive antimycobacterial immune response. Clin Transl Med. 2016; 5(1):38. PMC: 5052244. DOI: 10.1186/s40169-016-0119-0. View

11.

Ronacher K, Joosten S, van Crevel R, Dockrell H, Walzl G, Ottenhoff T . Acquired immunodeficiencies and tuberculosis: focus on HIV/AIDS and diabetes mellitus. Immunol Rev. 2015; 264(1):121-37. DOI: 10.1111/imr.12257. View

12.

Deiuliis J, Kampfrath T, Zhong J, Oghumu S, Maiseyeu A, Chen L . Pulmonary T cell activation in response to chronic particulate air pollution. Am J Physiol Lung Cell Mol Physiol. 2011; 302(4):L399-409. PMC: 3289266. DOI: 10.1152/ajplung.00261.2011. View

13.

Ma Q, Huang D, Zhang H, Wang S, Chen X . Exposure to particulate matter 2.5 (PM2.5) induced macrophage-dependent inflammation, characterized by increased Th1/Th17 cytokine secretion and cytotoxicity. Int Immunopharmacol. 2017; 50:139-145. DOI: 10.1016/j.intimp.2017.06.019. View

14.

Giefing-Kroll C, Berger P, Lepperdinger G, Grubeck-Loebenstein B . How sex and age affect immune responses, susceptibility to infections, and response to vaccination. Aging Cell. 2015; 14(3):309-21. PMC: 4406660. DOI: 10.1111/acel.12326. View

15.

Houben R, Dodd P . The Global Burden of Latent Tuberculosis Infection: A Re-estimation Using Mathematical Modelling. PLoS Med. 2016; 13(10):e1002152. PMC: 5079585. DOI: 10.1371/journal.pmed.1002152. View

16.

Lin P, Flynn J . The End of the Binary Era: Revisiting the Spectrum of Tuberculosis. J Immunol. 2018; 201(9):2541-2548. PMC: 6217958. DOI: 10.4049/jimmunol.1800993. View

17.

Sarkar S, Rivas-Santiago C, Ibironke O, Carranza C, Meng Q, Osornio-Vargas A . Season and size of urban particulate matter differentially affect cytotoxicity and human immune responses to Mycobacterium tuberculosis. PLoS One. 2019; 14(7):e0219122. PMC: 6622489. DOI: 10.1371/journal.pone.0219122. View

18.

Zhao Q, Chen H, Yang T, Rui W, Liu F, Zhang F . Direct effects of airborne PM2.5 exposure on macrophage polarizations. Biochim Biophys Acta. 2016; 1860(12):2835-43. DOI: 10.1016/j.bbagen.2016.03.033. View

19.

Behr M, Edelstein P, Ramakrishnan L . Revisiting the timetable of tuberculosis. BMJ. 2018; 362:k2738. PMC: 6105930. DOI: 10.1136/bmj.k2738. View

20.

Ai J, Ruan Q, Liu Q, Zhang W . Updates on the risk factors for latent tuberculosis reactivation and their managements. Emerg Microbes Infect. 2016; 5:e10. PMC: 4777925. DOI: 10.1038/emi.2016.10. View