Jet engine exhaust is a significant source of ultrafine particles and aviation-related emissions can adversely impact air quality over large areas surrounding airports. We investigated outdoor and indoor ultrafine particle number concentrations (PNC) from 16 residences located in two study areas in the greater Boston metropolitan area (MA, USA) for evidence of aviation-related impacts. During winds from the direction of Logan International Airport, that is, impact-sector winds, an increase in outdoor and indoor PNC was clearly evident at all seven residences in the Chelsea study area (∼4–5 km from the airport) and three out of nine residences in the Boston study area (∼5–6 km from the airport); the median increase during impact-sector winds compared to other winds was 1.7-fold for both outdoor and indoor PNC. Across all residences during impact-sector and other winds, median outdoor PNC were 19 000 and 10 000 particles/cm³, respectively, and median indoor PNC were 7000 and 4000 particles/cm³, respectively. Overall, our results indicate that aviation-related outdoor PNC infiltrate indoors and result in significantly higher indoor PNC. Our study provides compelling evidence for the impact of aviation-related emissions on residential exposures. Further investigation is warranted because these impacts are not expected to be unique to Logan airport.

Exposure to traffic-generated ultrafine particles (UFP; particles <100 nm) is likely a risk factor for cardiovascular disease. We conducted a trial of high-efficiency particulate arrestance (HEPA) filtration in public housing near a highway. Twenty residents in 19 apartments living <200 m from the highway participated in a randomized, double-blind crossover trial. A HEPA filter unit and a particle counter (measuring particle number concentration (PNC), a proxy for UFP) were installed in living rooms. Participants were exposed to filtered air for 21 days and unfiltered air for 21 days. Blood samples were collected and blood pressure measured at days 0, 21 and 42 after a 12-hour fasting period. Plasma was analyzed for high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor necrosis factor alpha-receptor II (TNF-RII) and fibrinogen. PNC reductions ranging from 21% to 68% were recorded in 15 of the apartments. We observed no significant differences in blood pressure or three of the four biomarkers (hsCRP, fibrinogen, and TNF-RII) measured in participants after 21-day exposure to HEPA-filtered air compared to measurements after 21-day exposure to sham-filtered air. In contrast, IL-6 concentrations were significantly higher following HEPA filtration (0.668 pg/mL; CI = 0.465–0.959) compared to sham filtration. Likewise, PNC adjusted for time activity were associated with increasing IL-6 in 14- and 21-day moving averages, and PNC was associated with decreasing blood pressure in Lags 0, 1 and 2, and in a 3-day moving average. These negative associations were unexpected and could be due to a combination of factors including exposure misclassification, unsuccessful randomization (i.e., IL-6 and use of anti-inflammatory medicines), or uncontrolled confounding. Studies with greater reduction in UFP levels and larger sample sizes are needed. There also needs to be more complete assessment of resident time activity and of outdoor vs. indoor source contributions to UFP exposure. HEPA filtration remains a promising, but not fully realized intervention.

Few longitudinal studies have examined the association between ultrafine particulate matter (UFP, particles < 0.1 μm aerodynamic diameter) exposure and cardiovascular disease (CVD) risk factors. We used data from 791 adults participating in the longitudinal Boston Puerto Rican Health Study (Massachusetts, USA) between 2004 and 2015 to assess whether UFP exposure was associated with blood pressure and high sensitivity C-reactive protein (hsCRP, a biomarker of systemic inflammation). Residential annual average UFP exposure (measured as particle number concentration, PNC) was assigned using a model accounting for spatial and temporal trends. We also adjusted PNC values for participants’ inhalation rate to obtain the particle inhalation rate (PIR) as a secondary exposure measure. Multilevel linear models with a random intercept for each participant were used to examine the association of UFP with blood pressure and hsCRP. Overall, in adjusted models, an inter-quartile range increase in PNC was associated with increased hsCRP (β = 6.8; 95% CI = − 0.3, 14.0%) but not with increased systolic blood pressure (β = 0.96; 95% CI = − 0.33, 2.25 mmHg), pulse pressure (β = 0.70; 95% CI = − 0.27, 1.67 mmHg), or diastolic blood pressure (β = 0.55; 95% CI = − 0.20, 1.30 mmHg). There were generally stronger positive associations among women and never smokers. Among men, there were inverse associations of PNC with systolic blood pressure and pulse pressure. In contrast to the primary findings, an inter-quartile range increase in the PIR was positively associated with systolic blood pressure (β = 1.03; 95% CI = 0.00, 2.06 mmHg) and diastolic blood pressure (β = 1.01; 95% CI = 0.36, 1.66 mmHg), but not with pulse pressure or hsCRP. We observed that exposure to PNC was associated with increases in measures of CVD risk markers, especially among certain sub-populations. The exploratory PIR exposure metric should be further developed.