Long-term exposure to low concentrations of air pollution and decline in lung function in people with idiopathic pulmonary fibrosis: Evidence from Australia

Background and Objective

Little is known about the association between ambient air pollution and idiopathic pulmonary fibrosis (IPF) in areas with lower levels of exposure. We aimed to investigate the impact of air pollution on lung function and rapid progression of IPF in Australia.

Methods

Participants were recruited from the Australian IPF Registry (n = 570). The impact of air pollution on changes in lung function was assessed using linear mixed models and Cox regression was used to investigate the association with rapid progression.

Results

Median (25th–75th percentiles) annual fine particulate matter (<2.5 μm, PM_2.5) and nitrogen dioxide (NO₂) were 6.8 (5.7, 7.9) μg/m³ and 6.7 (4.9, 8.2) ppb, respectively. Compared to living more than 100 m from a major road, living within 100 m was associated with a 1.3% predicted/year (95% confidence interval [CI] −2.4 to −0.3) faster annual decline in diffusing capacity of the lungs for carbon monoxide (DLco). Each interquartile range (IQR) of 2.2 μg/m³ increase in PM_2.5 was associated with a 0.9% predicted/year (95% CI −1.6 to −0.3) faster annual decline in DLco, while there was no association observed with NO₂. There was also no association between air pollution and rapid progression of IPF.

Conclusion

Living near a major road and increased PM_2.5 were both associated with an increased rate of annual decline in DLco. This study adds to the evidence supporting the negative effects of air pollution on lung function decline in people with IPF living at low-level concentrations of exposure.     

Comparison of total-breath and single-breath diffusing capacity in healthy volunteers and COPD patients

BACKGROUND: The measurement of single-breath diffusing capacity (Dlco(SB)) assumes that diffusing capacity per liter of alveolar volume (Dlco/VA) determined in a 750-mL gas sample represents the diffusing capacity (Dlco) of the entire lung. Fast-responding gas analyzers provide the opportunity to verify this assumption because of the possibility to measure CO and CH(4) fractions continuously throughout the entire expiration. Continuous gas sampling provides more information per measurement, but this information cannot be expressed in the traditional parameters. Our goals were to find new parameters to express the extra information of the continuous gas sampling, and to compare these new parameters with the traditional parameters. METHODS: We compared a new method to determine Dlco with the traditional method in 62 healthy volunteers and 26 COPD patients. Traditionally, Dlco(SB) is determined by multiplying Dlco/VA with alveolar volume, both calculated from gas concentrations in a 750-mL gas sample. The new method calculates total-breath Dlco (Dlco(TB)) by integration of Dlco/VA against exhaled volume. RESULTS: In healthy volunteers, Dlco/VA shows a slight upward slope during exhalation, while in COPD patients Dlco/VA shows a horizontal line. Total-breath total lung capacity (TLC) is larger than single-breath TLC both in healthy volunteers and in COPD patients, leading to a Dlco(TB) that is significantly larger than Dlco(SB) in both groups (p < 0.001). CONCLUSION: The assumption that a 750-mL gas sample represents the entire lung seems to be correct for Dlco/VA but not for the CH(4) fraction in case of ventilation inhomogeneity.