Air pollution and cold temperatures drive bronchiectasis mortality in vulnerable populations

By Dr. Priyom Bose, Ph.D.Reviewed by Benedette Cuffari, M.Sc.Nov 26 2024

New research underscores how air pollution and temperature extremes amplify risks for bronchiectasis patients, pointing to critical measures for safeguarding vulnerable groups.

Study: Association of short-term exposure to ambient air pollution and temperature with bronchiectasis mortality: a nationwide time-stratified case-crossover study. Image Credit: Shutterstock AI / Shutterstock.com

A recent eBioMedicine study investigates how short-term exposure to ambient air pollution and temperature affects bronchiectasis mortality rates in China.

What is bronchiectasis?

Bronchiectasis is a long-term chronic lung condition associated with irreversible bronchial dilation that impairs mucus clearance. Typically, bronchiectasis patients persistently produce sputum, as well as frequent coughs and recurrent respiratory infections, with affected individuals almost twice as likely to die than the general population.

Exposure to air pollutants increases the risk of various respiratory diseases, including asthma, chronic obstructive pulmonary disease (COPD), and pneumonia. Oxidative stress and inflammatory responses in the airways affect the airway epithelial barrier and reduce lung function. Air pollutant exposure may also exacerbate bronchiectasis symptoms.

In addition to air pollutants, extreme hot and cold temperatures may also adversely affect patients with pre-existing structural lung lesions, such as those due to COPD and cystic fibrosis. To date, few studies have provided epidemiological evidence on the relationships between air pollutants and non-optimal temperatures with bronchiectasis, which could play a key role in improving public health management for patients with bronchiectasis.

About the study

The current nationwide, time-stratified, and case-crossover study was conducted in China to elucidate how short-term exposure to air pollution and non-optimum ambient temperature influence bronchiectasis mortality.

To this end, data on bronchiectasis deaths between 2013 and 2019 were obtained from the National Death Registration and Reporting Information System (DRIS), which is maintained by the Center for Chronic and Noncommunicable Disease Control and Prevention of China.

Detailed information, including age, sex, marital status, profession, residential code, disease prognosis, diagnosis date, and ethnicity, was obtained for each bronchiectasis death. Any duplicate data was removed before analysis. Notably, each patient had a distinct and independent primary cause of death.

The case period was defined as the date of bronchiectasis death, with three or four corresponding control periods selected for each date. For example, if the bronchiectasis death occurred on Thursday, January 22, 2015, the corresponding control periods were Thursday, January 1, 8, 15, and 29, 2015.

A daily concentration of particulate matter 2.5 micrometers (µm) or smaller (PM_2.5), ozone (O₃), PM₁₀, and nitrogen dioxide (NO₂) were analyzed using high-resolution prediction models. More specifically, random forest models containing fixed-site measurements, multi-angle implementation of atmospheric correction aerosol optical depth (MAIAC AOD), meteorological parameters, altitude, and population density were used to determine the daily concentrations of PM_2.5 and PM₁₀.

Study findings

Short-term exposure to PM_2.5, PM_2.5–10, O_3, and low temperature increased the risk of bronchiectasis mortality; however, no association was observed for NO₂. These findings were based on 19,320 bronchiectasis death cases, 56% of which occurred in men, 92% of whom were of Han nationality, and 75% were 65 years of age or older.

On the day of bronchiectasis death, the mean concentrations of PM_2.5, PM_2.5–10, NO₂, and O₃ were estimated to be 46.0, 28.2, 33.7, and 81.8 μg/m³, respectively. The mean humidity and temperature of the day were 72.5% and 16.1 °C, respectively. A weak to moderate correlation between air pollutants and meteorological factors was observed, which varied from 0.01 to 0.56.

O₃ exhibited the strongest association with bronchiectasis mortality, followed by PM_2.5–10 and PM_2.5. The exposure-response relationship curves indicated a linear growth, with greater exposure to higher concentrations of air pollutants increasing the risk of bronchiectasis mortality.

Stratified analyses showed a stronger relationship between air pollutants and bronchiectasis mortality among males and older adults. Air pollutant exposure also had a greater impact among people who resided in the north and during the cold season.

The association between short-term exposure to air temperature and bronchiectasis mortality occurred about three days after exposure. This association gradually increased and peaked at around lag day six, eventually attenuating and becoming almost insignificant by lag day 11.

An inverse J-shaped relationship between air temperature and bronchiectasis mortality was observed, in which low temperature, rather than high temperature, accelerated bronchiectasis mortality. A temperature reduction of 10 °C was associated with a 12% increased risk of bronchiectasis mortality.

Stratified analyses revealed that low temperature was more likely to affect bronchiectasis mortality in women during the cold season in southern China and among older adults. Interactions between four air pollutants and temperature did not influence bronchiectasis mortality at different lag days.

Conclusions

Short-term exposure to air pollution and low temperatures increases the risk of bronchiectasis mortality. Therefore, to alleviate the disease burden, it is essential to reduce air pollution levels and adapt to non-optimum temperatures.