Short-term effects of airport-associated ultrafine particle exposure on lung function and inflammation in adults with asthma.

BACKGROUND

Exposure to ultrafine particles (UFP, particles with aerodynamic diameter < 100 nm) is associated with reduced lung function and airway inflammation in individuals with asthma. Recently, elevated UFP number concentrations (PN) from aircraft landing and takeoff activity were identified downwind of the Los Angeles International Airport (LAX) but little is known about the health impacts of airport-related UFP exposure.

METHODS

We conducted a randomized crossover study of 22 non-smoking adults with mild to moderate asthma in Nov-Dec 2014 and May-Jul 2015 to investigate short-term effects of exposure to LAX airport-related UFPs. Participants conducted scripted, mild walking activity on two occasions in public parks inside (exposure) and outside (control) of the high UFP zone. Spirometry, multiple flow exhaled nitric oxide, and circulating inflammatory cytokines were measured before and after exposure. Personal UFP PN and lung deposited surface area (LDSA) and stationary UFP PN, black carbon (BC), particle-bound PAHs (PB-PAH), ozone (O), carbon dioxide (CO) and particulate matter (PM) mass were measured. Source apportionment analysis was conducted to distinguish aircraft from roadway traffic related UFP sources. Health models investigated within-subject changes in outcomes as a function of pollutants and source factors.

RESULTS

A high two-hour walking period average contrast of ~34,000 particles·cm was achieved with mean (std) PN concentrations of 53,342 (25,529) and 19,557 (11,131) particles·cm and mean (std) particle size of 28.7 (9.5) and 33.2 (11.5) at the exposure and control site, respectively. Principal components analysis differentiated airport UFPs (PN), roadway traffic (BC, PB-PAH), PM mass (PM, PM), and secondary photochemistry (O) sources. A standard deviation increase in the 'Airport UFPs' factor was significantly associated with IL-6, a circulating marker of inflammation (single-pollutant model: 0.21, 95% CI = 0.08-0.34; multi-pollutant model: 0.18, 0.04-0.32). The 'Traffic' factor was significantly associated with lower Forced Expiratory Volume in 1 s (FEV) (single-pollutant model: -1.52, -2.28 to -0.77) and elevated sTNFrII (single-pollutant model: 36.47; 6.03-66.91; multi-pollutant model: 64.38; 6.30-122.46). No consistent associations were observed with exhaled nitric oxide.

CONCLUSIONS

To our knowledge, our study is the first to demonstrate increased acute systemic inflammation following exposure to airport-related UFPs. Health effects associated with roadway traffic exposure were distinct. This study emphasizes the importance of multi-pollutant measurements and modeling techniques to disentangle sources of UFPs contributing to the complex urban air pollution mixture and to evaluate population health risks.