Long-term aircraft noise exposure and risk of hypertension in postmenopausal women.

BACKGROUND: Studies of the association between aircraft noise and hypertension are complicated by inadequate control for potential confounders and a lack of longitudinal assessments, and existing evidence is inconclusive. OBJECTIVES: We evaluated the association between long-term aircraft noise exposure and risk of hypertension among post-menopausal women in the Women's Health Initiative Clinical Trials, an ongoing prospective U.S. METHODS: Day-night average (DNL) and night equivalent sound levels (Lnight) were modeled for 90 U.S. airports from 1995 to 2010 in 5-year intervals using the Aviation Environmental Design Tool and linked to participant geocoded addresses from 1993 to 2010. Participants with modeled exposures ≥45 A-weighted decibels (dB [A]) were considered exposed, and those outside of 45 dB(A) who also did not live in close proximity to unmodeled airports were considered unexposed. Hypertension was defined as systolic/diastolic blood pressure ≥140/90 mmHg or inventoried/self-reported antihypertensive medication use. Using time-varying Cox proportional hazards models, we estimated hazard ratios (HRs) for incident hypertension when exposed to DNL or Lnight ≥45 versus <45 dB(A), controlling for sociodemographic, behavioral, and environmental/contextual factors. RESULTS/DISCUSSION: There were 18,783 participants with non-missing DNL exposure and 14,443 with non-missing Lnight exposure at risk of hypertension. In adjusted models, DNL and Lnight ≥45 db(A) were associated with HRs of 1.00 (95% confidence interval [CI]: 0.93, 1.08) and 1.06 (95%CI: 0.91, 1.24), respectively. There was no evidence supporting a positive exposure-response relationship, and findings were robust in sensitivity analyses. Indications of elevated risk were seen among certain subgroups, such as those living in areas with lower population density (HRinteraction: 0.84; 95%CI: 0.72, 0.98) or nitrogen dioxide concentrations (HRinteraction: 0.82; 95%CI: 0.71, 0.95), which may indicate lower ambient/road traffic noise. Our findings do not suggest a relationship between aircraft noise and incident hypertension among older women in the U.S., though associations in lower ambient noise settings merit further investigation.

Long-term aircraft noise exposure and risk of hypertension in the Nurses' Health Studies.

BACKGROUND: Aircraft noise can affect populations living near airports. Chronic exposure to aircraft noise has been associated with cardiovascular disease, including hypertension. However, previous studies have been limited in their ability to characterize noise exposures over time and to adequately control for confounders. OBJECTIVES: The aim of this study was to examine the association between aircraft noise and incident hypertension in two cohorts of female nurses, using aircraft noise exposure estimates with high spatial resolution over a 20-year period. METHODS: We obtained contour maps of modeled aircraft noise levels over time for 90 U.S. airports and linked them with geocoded addresses of participants in the Nurses' Health Study (NHS) and Nurses' Health Study II (NHS II) to assign noise exposure for 1994-2014 and 1995-2013, respectively. We used time-varying Cox proportional hazards models to estimate hypertension risk associated with time-varying noise exposure (dichotomized at 45 and 55 dB(A)), adjusting for fixed and time-varying confounders. Results from both cohorts were pooled via random effects meta-analysis. RESULTS: In meta-analyses of parsimonious and fully-adjusted models with aircraft noise dichotomized at 45 dB(A), hazard ratios (HR) for hypertension incidence were 1.04 (95% CI: 1.00, 1.07) and 1.03 (95% CI: 0.99, 1.07), respectively. When dichotomized at 55 dB(A), HRs were 1.10 (95% CI: 1.01, 1.19) and 1.07 (95% CI: 0.98, 1.15), respectively. After conducting fully-adjusted sensitivity analyses limited to years in which particulate matter (PM) was obtained, we observed similar findings. In NHS, the PM-unadjusted HR was 1.01 (95% CI: 0.90, 1.14) and PM-adjusted HR was 1.01 (95% CI: 0.89, 1.14); in NHS II, the PM-unadjusted HR was 1.08 (95% CI: 0.96, 1.22) and the PM-adjusted HR was 1.08 (95% CI: 0.95, 1.21). Overall, in these cohorts, we found marginally suggestive evidence of a positive association between aircraft noise exposure and hypertension.

Modification of associations between indoor particulate matter and systemic inflammation in individuals with COPD.

RATIONALE: Little is known about personal characteristics and systemic responses to particulate pollution in patients with COPD. OBJECTIVES: Assess whether diabetes, obesity, statins and non-steroidal anti-inflammatory medications (NSAIDs) modify associations between indoor black carbon (BC) and fine particulate matter ≤2.5 µm in diameter (PM2.5) on systemic inflammation and endothelial activation. METHODS: 144 individuals with COPD without current smoking and without major in-home combustion sources were recruited at Veterans Affairs Boston Healthcare System. PM2.5 and BC were measured in each participant's home seasonally for a week (up to 4 times; 482 observations) and plasma biomarkers of systemic inflammation [C-reactive protein (CRP); interleukin-6 (IL-6)] and endothelial activation [soluble vascular adhesion molecule-1 (sVCAM-1)] measured. Linear mixed effects regression with a random intercept was used, and effect modification assessed with multiplicative interaction terms and stratum specific estimates. RESULTS: Median (25%ile, 75%ile) indoor BC and PM2.5 were 0.6 (0.5,0.7) µg/m3 and 6.8 (4.8,10.4) µg/m3, respectively. Although p-values for effect modification were not statistically significant, there were positive associations (%-increase/interquartile range; 95% CI) between CRP and BC greater among non-statin (18.8%; 3.6-36.3) than statin users (11.1%; 2.1-20.9). There were also positive associations greater among non-statin users between PM2.5 and CRP. For IL-6, associations with BC and PM2.5 were also greater among non-statin users. Associations between CRP and BC were greater (20.3%; 4.5-38.5) in persons with diabetes than without diabetes (10.3%; 0.92-20.6) with similar effects of PM2.5. There were no consistent associations that differed based on obesity. Effect modification was not observed for NSAID use, or with any factor considered with sVCAM-1. CONCLUSIONS: Associations between indoor BC and PM2.5 and CRP were greater in patients with diabetes and those not taking statins, and with IL-6 if not taking statins. These results suggest that these characteristics may modify the systemic response to indoor BC and PM2.5 in persons with COPD.

Short-term exposures to particulate matter gamma radiation activities and biomarkers of systemic inflammation and endothelial activation in COPD patients.

BACKGROUND: We hypothesized that particulate matter (PM) gamma activity (gamma radiation associated with PM) is associated with systemic effects. OBJECTIVE: Examine short-term relationships between ambient and indoor exposures to PM gamma activities with systemic inflammation and endothelial activation in chronic obstructive pulmonary disease (COPD) patients. METHODS: In 85 COPD patients from Eastern Massachusetts, USA from 2012 to 2014, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured seasonally up to four times. We used US EPA RadNet data measuring ambient gamma radiation attached to PM adjusted for background radiation, and estimated in-home gamma radiation exposures using the ratio of in-home-to-ambient sulfur in PM2.5. Linear mixed-effects regression models were used to determine associations between moving averages of PM gamma activities through the week before phlebotomy with these biomarkers. We explored ambient and indoor PM2.5, black carbon (BC), and NO2 as confounders. RESULTS: Ambient and indoor PM gamma activities measured as energy spectra classes 3 through 9 were positively associated with CRP and IL-6. For example, averaged from phlebotomy day through previous 6 days, each IQR increase in indoor PM gamma activity for each spectra class, was associated with an CRP increase ranging from 7.45% (95%CI: 2.77, 12.4) to 13.4% (95%CI: 5.82, 21.4) and for ambient exposures were associated with an increase of 8.75% (95%CI: -0.57, 18.95) to 14.8% (95%CI: 4.5, 26.0). Indoor exposures were associated with IL-6 increase of 3.56% (95%CI: 0.31, 6.91) to 6.46% (95%CI:1.33, 11.85) and ambient exposures were associated with an increase of 0.03% (95%CI: -6.37, 6.87) to 3.50% (95%CI: -3.15, 10.61). There were no positive associations with sVCAM-1. Sensitivity analyses using two-pollutant models showed similar effects. CONCLUSIONS: Our results demonstrate that short-term exposures to environmental PM gamma radiation activities were associated with systemic inflammation in COPD patients.

Indoor black carbon and biomarkers of systemic inflammation and endothelial activation in COPD patients.

RATIONALE: Evidence linking traffic-related particle exposure to systemic effects in chronic obstructive lung disease (COPD) patients is limited. OBJECTIVES: Assess relationships between indoor black carbon (BC), a tracer of traffic-related particles, and plasma biomarkers of systemic inflammation and endothelial activation. METHODS: BC was measured by reflectance in fine particle samples over a mean of 7.6 days in homes of 85 COPD patients up to 4 times seasonally over a year. After the completion of sampling, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular adhesion molecule-1 (sVCAM-1) were measured. Current smokers and homes with major sources of BC were excluded; therefore, indoor BC was primarily a measure of infiltrated outdoor BC. Mixed effects regression models with a random intercept for each participant were used to assess BC effects at different times (1-9 days before phlebotomy) and in the multi-day sample. RESULTS: Measured median BC was 0.19 µg/m3 (interquartile range, IQR=0.22 µg/m3). Adjusting for season, race, age, BMI, heart disease, diabetes, ambient temperature, relative humidity, a recent cold or similar illness, and blood draw time, there was a positive relationship between BC and CRP. The largest effect size was for BC averaged over the previous seven days (11.8% increase in CRP per IQR; 95%CI = 1.8-22.9). Effects were greatest among non-statin users and persons with diabetes. There were positive effects of BC on IL-6 only in non-statin users. There were no associations with sVCAM-1. CONCLUSIONS: These results demonstrate exposure-response relationships between indoor BC with biomarkers of systemic inflammation in COPD patients, with stronger relationships in persons not using statins and with diabetes.

In the Wrong Place with the Wrong SNP: The Association Between Stressful Neighborhoods and Cardiac Arrest Within Beta-2-adrenergic Receptor Variants.

BACKGROUND: Sudden cardiac arrest has been linked independently both to stressful neighborhood conditions and to polymorphisms in the ADRB2 gene. The ADRB2 gene mediates sympathetic activation in response to stress. Therefore, if neighborhood conditions cause cardiac arrest through the stress pathway, the ADRB2 variant may modify the association between neighborhood conditions, such as socioeconomic deprivation and incidence of cardiac arrest. METHODS: The Cardiac Arrest Blood Study Repository is a population-based repository of specimens and other data from adult cardiac arrest patients residing in King County, Washington. Cases (n = 1,539) were 25- to 100-year-old individuals of European descent who experienced out-of-hospital cardiac arrest from 1988 to 2004. Interactions between neighborhood conditions and the ADRB2 genotype on cardiac arrest risk were assessed in a case-only study design. Gene-environment independence was assessed in blood samples obtained from King County residents initially contacted by random-digit dialing. RESULTS: Fewer than 4% of study subjects resided in socioeconomically deprived neighborhoods. Nonetheless, the case-only analysis indicated the presence of supramultiplicative interaction of socioeconomic deprivation and the homozygous Gln27Glu variant (case-only odds ratio: 1.8 [95% confidence interval: 1.0, 2.9]). Interactions between population density and the homozygous Gln27Glu variant were weaker (case-only odds ratio: 1.2 [95% confidence interval: 0.97, 1.5]). CONCLUSIONS: Findings support a supramultiplicative interaction between the Gln27Glu ADRB2 variant and socioeconomic deprivation among individuals of European descent. This result is consistent with the hypothesis that the elevation in cardiac arrest risk associated with socioeconomic deprivation operates through the stress pathway.

Aircraft noise exposure and body mass index among female participants in two Nurses' Health Study prospective cohorts living around 90 airports in the United States.

OBJECTIVE: Aircraft noise exposure is linked to cardiovascular disease risk. One understudied candidate pathway is obesity. This study investigates the association between aircraft noise and obesity among female participants in two prospective Nurses' Health Study (NHS and NHSII) cohorts. METHODS: Aircraft day-night average sound levels (DNL) were estimated at participant residential addresses from modeled 1 dB (dB) noise contours above 44 dB for 90 United States (U.S.) airports in 5-year intervals 1995-2010. Biennial surveys (1994-2017) provided information on body mass index (BMI; dichotomized, categorical) and other individual characteristics. Change in BMI from age 18 (BMI18; tertiles) was also calculated. Aircraft noise exposures were dichotomized (45, 55 dB), categorized (<45, 45-54, ≥55 dB) or continuous for exposure ≥45 dB. Multivariable multinomial logistic regression using generalized estimating equations were adjusted for individual characteristics and neighborhood socioeconomic status, greenness, population density, and environmental noise. Effect modification was assessed by U.S. Census region, climate boundary, airline hub type, hearing loss, and smoking status. RESULTS: At baseline, the 74,848 female participants averaged 50.1 years old, with 83.0%, 14.8%, and 2.2% exposed to <45, 45-54, and ≥55 dB of aircraft noise, respectively. In fully adjusted models, exposure ≥55 dB was associated with 11% higher odds (95% confidence interval [95%CI]: -1%, 24%) of BMIs ≥30.0, and 15% higher odds (95%CI: 3%, 29%) of membership in the highest tertile of BMI18 (ΔBMI 6.7 to 71.6). Less-pronounced associations were observed for the 2nd tertile of BMI18 (ΔBMI 2.9 to 6.6) and BMI 25.0-29.9 as well as exposures ≥45 versus <45 dB. There was evidence of DNL-BMI trends (ptrends ≤ 0.02). Stronger associations were observed among participants living in the West, arid climate areas, and among former smokers. DISCUSSION: In two nationwide cohorts of female nurses, higher aircraft noise exposure was associated with higher BMI, adding evidence to an aircraft noise-obesity-disease pathway.

Indoor and ambient black carbon and fine particulate matter associations with blood biomarkers in COPD patients.

BACKGROUND: Systemic inflammation contributes to cardiovascular risk and chronic obstructive pulmonary disease (COPD) pathophysiology. Associations between systemic inflammation and exposure to ambient fine particulate matter (PM ≤ 2.5 µm diameter; PM2.5), and black carbon (BC), a PM2.5 component attributable to traffic and other sources of combustion, infiltrating indoors are not well described. METHODS: Between 2012 and 2017, COPD patients completed in-home air sampling over one-week intervals, up to four times (seasonally), followed by measurement of plasma biomarkers of systemic inflammation, C-reactive protein (CRP) and interleukin-6 (IL-6), and endothelial activation, soluble vascular adhesion molecule-1 (sVCAM-1). Ambient PM2.5, BC and sulfur were measured at a central site. The ratio of indoor/ambient sulfur in PM2.5, a surrogate for fine particle infiltration, was used to estimate indoor BC and PM2.5 of ambient origin. Linear mixed effects regression with a random intercept for each participant was used to assess associations between indoor and indoor of ambient origin PM2.5 and BC with each biomarker. RESULTS: 144 participants resulting in 482 observations were included in the analysis. There were significant positive associations between indoor BC and indoor BC of ambient origin with CRP [%-increase per interquartile range (IQR);95 % CI (13.2 %;5.2-21.8 and 11.4 %;1.7-22.1, respectively)]. Associations with indoor PM2.5 and indoor PM2.5 of ambient origin were weaker. There were no associations with IL-6 or sVCAM-1. CONCLUSIONS: In homes of patients with COPD without major sources of combustion, indoor BC is mainly attributable to the infiltration of ambient sources of combustion indoors. Indoor BC of ambient origin is associated with increases in systemic inflammation in patients with COPD, even when staying indoors.

Determinants of indoor carbonaceous aerosols in homes in the Northeast United States.

BACKGROUND: Little is known about sources of residential exposure to carbonaceous aerosols, which include black carbon (BC), the elemental carbon core of combustion particles, and organic compounds from biomass combustion (delta carbon). OBJECTIVE: Assess the impact of residential characteristics on indoor BC and delta carbon when known sources of combustion (e.g., smoking) are minimized. METHODS: Between November 2012-December 2014, 125 subjects (129 homes) in Northeast USA were recruited and completed a residential characteristics questionnaire. Every 3 months, participants received an automated sampler to measure fine particulate matter (PM2.5) in their home during a weeklong period (N = 371 indoor air samples) and were also questioned about indoor exposures. The samples were analyzed using a transmissometer at 880 nm (reflecting BC) and at 370 nm. The difference between the two wavelengths estimates delta carbon. Outdoor BC and delta carbon were measured using a central site aethalometer. RESULTS: Geometric mean indoor concentrations of BC and delta carbon (0.65 µg/m³ and 0.19 µg/m³, respectively), were greater than central site concentrations (0.53 µg/m³ and 0.02 µg/m³, respectively). Multivariable analysis showed that greater indoor concentrations of BC were associated with infrequent candle use, multi-family homes, winter season, lack of air conditioning, and central site BC. For delta carbon, greater indoor concentrations were associated with apartments, spring season, and central site concentrations. SIGNIFICANCE: In addition to outdoor central site concentrations, factors related to the type of housing, season, and home exposures are associated with indoor exposure to carbonaceous aerosols. Recognition of these characteristics should enable greater understanding of indoor exposures and their sources.

Association between Noise and Cardiovascular Disease in a Nationwide U.S. Prospective Cohort Study of Women Followed from 1988 to 2018.

BACKGROUND: Long-term noise exposure is associated with cardiovascular disease (CVD), including acute cardiovascular events such as myocardial infarction and stroke. However, longitudinal cohort studies in the U.S. of long-term noise and CVD are almost exclusively from Europe and few modeled nighttime noise, when an individual is likely at home or asleep, separately from daytime noise. We aimed to examine the prospective association of outdoor long-term nighttime and daytime noise from anthropogenic sources with incident CVD using a U.S.-based, nationwide cohort of women. METHODS: We linked L50 nighttime and L50 daytime anthropogenic modeled noise estimates from a U.S. National Parks Service model (L50: sound pressure levels exceeded 50 percent of the time) to geocoded residential addresses of 114,116 participants in the Nurses' Health Study. We used time-varying Cox proportional hazards models to estimate risk of incident CVD, coronary heart disease (CHD), and stroke associated with long-term average (14-y measurement period) noise exposure, adjusted for potential individual- and area-level confounders and CVD risk factors (1988-2018; biennial residential address updates; monthly CVD updates). We assessed effect modification by population density, region, air pollution, vegetation cover, and neighborhood socioeconomic status, and explored mediation by self-reported average nightly sleep duration. RESULTS: Over 2,548,927 person-years, there were 10,331 incident CVD events. In fully adjusted models, the hazard ratios for each interquartile range increase in L50 nighttime noise (3.67 dBA) and L50 daytime noise (4.35 dBA), respectively, were 1.04 (95% CI: 1.02, 1.06) and 1.04 (95% CI: 1.02, 1.07). Associations for total energy-equivalent noise level (Leq) measures were stronger than for the anthropogenic statistical L50 noise measures. Similar associations were observed for CHD and stroke. Interaction analyses suggested that associations of L50 nighttime and L50 daytime noise with CVD did not differ by prespecified effect modifiers. We found no evidence that inadequate sleep (<5 h/night) mediated associations of L50 nighttime noise and CVD. DISCUSSION: Outdoor L50 anthropogenic nighttime and daytime noise at the residential address was associated with a small increase in CVD risk in a cohort of adult female nurses. https://doi.org/10.1289/EHP12906.

Pulmonary, inflammatory, and oxidative effects of indoor nitrogen dioxide in patients with COPD.

Introduction: Indoor nitrogen dioxide (NO2) sources include gas heating, cooking, and infiltration from outdoors. Associations with pulmonary function, systemic inflammation, and oxidative stress in patients with chronic obstructive pulmonary disease (COPD) are uncertain. Methods: We recruited 144 COPD patients at the VA Boston Healthcare System between 2012 and 2017. In-home NO2 was measured using an Ogawa passive sampling badge for a week seasonally followed by measuring plasma biomarkers of systemic inflammation (C-reactive protein [CRP] and interleukin-6 [IL-6]), urinary oxidative stress biomarkers (8-hydroxy-2'deoxyguanosine [8-OHdG] and malondialdehyde [MDA]), and pre- and postbronchodilator spirometry. Linear mixed effects regression with a random intercept for each subject was used to assess associations with weekly NO2. Effect modification by COPD severity and by body mass index (BMI) was examined using multiplicative interaction terms and stratum-specific effect estimates. Results: Median (25%ile, 75%ile) concentration of indoor NO2 was 6.8 (4.4, 11.2) ppb. There were no associations observed between NO2 with CRP, 8-OHdG, or MDA. Although the confidence intervals were wide, there was a reduction in prebronchodilator FEV1 and FVC among participants with more severe COPD (FEV1: -17.36 mL; -58.35, 23.60 and FVC: -28.22 mL; -91.49, 35.07) that was greater than in patients with less severe COPD (FEV1: -1.64 mL; -24.80, 21.57 and FVC: -6.22 mL; -42.16, 29.71). In participants with a BMI <30, there was a reduction in FEV1 and FVC. Conclusions: Low-level indoor NO2 was not associated with systemic inflammation or oxidative stress. There was a suggestive association with reduced lung function among patients with more severe COPD and among patients with a lower BMI.

Air Pollution and Temperature: a Systematic Review of Ubiquitous Environmental Exposures and Sudden Cardiac Death.

PURPOSE OF REVIEW: Environmental exposures have been associated with increased risk of cardiovascular mortality and acute coronary events, but their relationship with out-of-hospital cardiac arrest (OHCA) and sudden cardiac death (SCD) remains unclear. SCD is an important contributor to the global burden of cardiovascular disease worldwide. RECENT FINDINGS: Current literature suggests a relationship between environmental exposures and cardiovascular disease, but their relationship with OHCA/SCD remains unclear. A literature search was conducted in PubMed, Embase, Web of Science, and Global Health. Of 5138 studies identified by our literature search, this review included 30 studies on air pollution, 42 studies on temperature, 6 studies on both air pollution and temperature, and 1 study on altitude exposure and OHCA/SCD. Particulate matter air pollution, ozone, and both hot and cold temperatures are associated with increased risk of OHCA/SCD. Pollution and other exposures related to climate change play an important role in OHCA/SCD incidence.

Indoor (residential) and ambient particulate matter associations with urinary oxidative stress biomarkers in a COPD cohort.

OBJECTIVES: Oxidative stress contributes to chronic obstructive pulmonary disease (COPD) pathophysiology. Associations between indoor (residential) exposure to particulate matter ≤2.5 µm in diameter (PM2.5) and one of its components, black carbon (BC), and oxidative stress are ill-defined. METHODS: Between 2012 and 2017, 140 patients with COPD completed in-home air sampling over one week intervals, followed by collection of urine samples to measure oxidative stress biomarkers, malondialdehyde (MDA), a marker of lipid peroxidation, and 8-hydroxy-2' -deoxyguanosine (8-OHdG), a marker of oxidative DNA damage. Ambient (central site) BC and PM2.5 were measured, and the ratio of indoor/ambient sulfur in PM2.5, a surrogate for residential ventilation and particle infiltration, was used to estimate indoor BC and PM2.5 of outdoor origin. Mixed effects linear regression models with a participant-specific random intercept were used to assess associations with oxidative biomarkers, adjusting for personal characteristics. RESULTS: There were positive associations (% increase per IQR; 95 % CI) of directly measured indoor BC with total MDA (6.96; 1.54, 12.69) and 8-OHdG (4.18; -0.67, 9.27), and similar associations with both indoor BC of outdoor origin and ambient BC. There were no associations with directly measured indoor PM2.5, but there were positive associations between indoor PM2.5 of outdoor origin and total MDA (5.40; -0.91, 12.11) and 8-OHdG (8.02; 2.14, 14.25). CONCLUSIONS: In homes with few indoor combustion sources, directly measured indoor BC, estimates of indoor BC and PM2.5 of outdoor origin, and ambient BC, were positively associated with urinary biomarkers of oxidative stress. This suggests that the infiltration of particulate matter from outdoor sources, attributable to traffic and other sources of combustion, promotes oxidative stress in COPD patients.

Associations between Aircraft Noise Exposure and Self-Reported Sleep Duration and Quality in the United States-Based Prospective Nurses' Health Study Cohort.

BACKGROUND: Sleep disruption is linked with chronic disease, and aircraft noise can disrupt sleep. However, there are few investigations of aircraft noise and sleep in large cohorts. OBJECTIVES: We examined associations between aircraft noise and self-reported sleep duration and quality in the Nurses' Health Study, a large prospective cohort. METHODS: Aircraft nighttime equivalent sound levels (Lnight) and day-night average sound levels (DNL) were modeled around 90 U.S. airports from 1995 to 2015 in 5-y intervals using the Aviation Environmental Design Tool and linked to geocoded participant residential addresses. Lnight exposure was dichotomized at the lowest modeled level of 45 A-weighted decibels [dB(A)] and at multiple cut points for DNL. Multiple categories of both metrics were compared with <45 dB(A). Self-reported short sleep duration (<7 h/24-h day) was ascertained in 2000, 2002, 2008, 2012, and 2014, and poor sleep quality (frequent trouble falling/staying asleep) was ascertained in 2000. We analyzed repeated sleep duration measures using generalized estimating equations and sleep quality by conditional logistic regression. We adjusted for participant-level demographics, behaviors, comorbidities, and environmental exposures (greenness and light at night) and examined effect modification. RESULTS: In 35,226 female nurses averaging 66.1 years of age at baseline, prevalence of short sleep duration and poor sleep quality were 29.6% and 13.1%, respectively. In multivariable models, exposure to Lnight ≥45 dB(A) was associated with 23% [95% confidence interval (CI): 7%, 40%] greater odds of short sleep duration but was not associated with poor sleep quality (9% lower odds; 95% CI: -30%, 19%). Increasing categories of Lnight and DNL ≥45 dB(A) suggested an exposure-response relationship for short sleep duration. We observed higher magnitude associations among participants living in the West, near major cargo airports, and near water-adjacent airports and among those reporting no hearing loss. DISCUSSION: Aircraft noise was associated with short sleep duration in female nurses, modified by individual and airport characteristics. https://doi.org/10.1289/EHP10959.

Associations between long-term aircraft noise exposure, cardiovascular disease, and mortality in US cohorts of female nurses.

There is limited research examining aircraft noise and cardiovascular disease (CVD) risk. The objective of this study was to investigate associations of aircraft noise with CVD among two US cohorts, the Nurses' Health Study (NHS) and Nurses' Health Study II (NHSII). Methods: Between 1994 and 2014, we followed 57,306 NHS and 60,058 NHSII participants surrounding 90 airports. Aircraft noise was modeled above 44 A-weighted decibels (dB(A)) and linked to geocoded addresses. Based on exposure distributions, we dichotomized exposures at 50 dB(A) and tested sensitivity of this cut-point by analyzing aircraft noise as categories (<45, 45-49, 50-54, ≥55) and continuously. We fit cohort-specific Cox proportional hazards models to estimate relationships between time-varying day-night average sound level (DNL) and CVD incidence and CVD and all-cause mortality, adjusting for fixed and time-varying individual- and area-level covariates. Results were pooled using random effects meta-analysis. Results: Over 20 years of follow-up, there were 4529 CVD cases and 14,930 deaths. Approximately 7% (n = 317) of CVD cases were exposed to DNL ≥50 dB(A). In pooled analyses comparing ≥50 with <50 dB(A), the adjusted hazard ratio for CVD incidence was 1.00 (95% confidence interval: 0.89, 1.12). The corresponding adjusted hazard ratio for all-cause mortality was 1.02 (95% confidence interval: 0.96, 1.09). Patterns were similar for CVD mortality in NHS yet underpowered. Conclusions: Among participants in the NHS and NHSII prospective cohorts who generally experience low exposure to aircraft noise, we did not find adverse associations of aircraft noise with CVD incidence, CVD mortality, or all-cause mortality.

Effects of particulate matter gamma radiation on oxidative stress biomarkers in COPD patients.

Inhalation of particulate matter (PM) radioactivity is an important pathway of ionizing radiation exposure. We investigated the associations between short-term exposures to PM gamma radioactivity with oxidative stress in COPD patients. Urinary concentrations of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA) of 81 COPD patients from Eastern Massachusetts were measured 1-4 times during 2012-2014. Daily ambient and indoor PM gamma activities (gamma-3 through gamma-9) were calculated based on EPA RadNet data and indoor-outdoor infiltration ratios. Linear mixed-effects models were used to examine the associations between biomarkers with PM gamma activities for moving averages from urine collection day to 7 days before. Our results indicate that ambient and indoor PM gamma activities were positively associated with 8-OHdG, with stronger effects for exposure windows closer to urine collection day. For per interquartile range increase in indoor PM gamma activities averaged over urine collection day and 1 day before, 8-OHdG increased from 3.41% (95% CI: -0.88, 7.88) to 8.87% (95% CI: 2.98, 15.1), adjusted for indoor black carbon. For MDA, the timing of greatest effects across the exposure week varied but was nearly all positive. These findings provide insight into the toxigenic properties associated with PM radioactivity and suggest that these exposures promote systemic oxidative stress.

Residential wood stove use and indoor exposure to PM2.5 and its components in Northern New England.

BACKGROUND: Residential wood stove use has become more prevalent in high-income countries, but only limited data exist on indoor exposure to PM2.5 and its components. METHODS: From 2014 to 2016, we collected 7-day indoor air samples in 137 homes of pregnant women in Northern New England, using a micro-environmental monitor. We examined associations of wood stove use with PM2.5 mass and its components [black carbon (BC), organic and elemental carbon and their fractions, and trace elements], adjusted for sampling season, community wood stove use, and indoor activities. We examined impact of stove age, EPA-certification, and wood moisture on indoor pollutants. RESULTS: Median (IQR) household PM2.5 was 6.65 (5.02) µg/m3 and BC was 0.23 (0.20) µg/m3. Thirty percent of homes used a wood stove during monitoring. In homes with versus without a stove, PM2.5 was 20.6% higher [although 95% confidence intervals (-10.6, 62.6) included the null] and BC was 61.5% higher (95% CI: 11.6, 133.6). Elemental carbon (total and fractions 3 and 4), potassium, calcium, and chloride were also higher in homes with a stove. Older stoves, non-EPA-certified stoves, and wet or mixed (versus dry) wood were associated with higher pollutant concentrations, especially BC. CONCLUSIONS: Homes with wood stoves, particularly those that were older and non-EPA-certified or burning wet wood had higher concentrations of indoor air combustion-related pollutants.

Effects of Indoor and Ambient Black Carbon and [Formula: see text] on Pulmonary Function among Individuals with COPD.

BACKGROUND: Particulate matter (PM) air pollution has been associated with decreased pulmonary function, but the exposure­response relationship in chronic obstructive pulmonary disease (COPD) patients is uncertain, and most studies have only focused on exposures to ambient pollution. OBJECTIVES: We aimed to assess associations between pulmonary function and indoor and ambient PM [Formula: see text] ([Formula: see text]) and black carbon (BC). METHODS: Between November 2012 and December 2014, 125 patients with COPD (mean age, 73.4 y) who were not currently smoking and without known indoor BC sources were recruited. Indoor BC and [Formula: see text] were measured in each home for a week in each season, up to four times a year, followed by in-person spirometry pre- and post-bronchodilator. Ambient exposures were available from a central site monitor. Multivariable adjusted mixed effects regression models were used to assess associations scaled per interquartile range (IQR) of exposure. RESULTS: There were 367 study visits; the median (IQR) indoor BC and [Formula: see text] were 0.19 (0.22) [Formula: see text] and 6.67 (5.80) [Formula: see text], respectively. Increasing indoor exposures to BC were associated with decreases in pre-bronchodilator forced expiratory volume in 1 s [Formula: see text] and forced vital capacity (FVC), and [Formula: see text]. For example, in multivariable adjusted models, each IQR increase in indoor BC from the weekly integrated filter was associated with a [Formula: see text] [95% confidence interval (CI): [Formula: see text], [Formula: see text]] decrease in pre-bronchodilator [Formula: see text]. Increases in indoor [Formula: see text] were associated with decreases in [Formula: see text] and FVC of smaller magnitude than those for indoor BC; however, the results were less precise. Ambient BC was not associated with pre-bronchodilator pulmonary function, ambient [Formula: see text] was only associated with decreases in FVC and increases in [Formula: see text], and neither indoor nor ambient BC or [Formula: see text] were associated with post-bronchodilator pulmonary function. CONCLUSIONS: Low-level exposures to indoor BC and [Formula: see text], but not ambient exposures, were consistently associated with decreases in pre-bronchodilator pulmonary function. There was no association between exposures and post-bronchodilator pulmonary function. https://doi.org/10.1289/EHP3668.

Indoor black carbon of outdoor origin and oxidative stress biomarkers in patients with chronic obstructive pulmonary disease.

OBJECTIVES: We assessed relationships between indoor black carbon (BC) exposure and urinary oxidative stress biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), in participants with chronic obstructive pulmonary disease (COPD). METHODS: Eighty-two participants completed in-home air sampling for one week prior to providing urine samples up to four times in a year. Weekly indoor and daily outdoor concentrations were used to estimate indoor daily lags and moving averages. There were no reported in-home BC sources, thus indoor levels closely represented outdoor BC infiltration. Mixed effects regression models with a random intercept for each participant were used to assess relationships between indoor BC and 8-OHdG and MDA, adjusting for age, race, BMI, diabetes, heart disease, season, time of urine collection, urine creatinine, and outdoor humidity and temperature. RESULTS: There were positive effects of BC on 8-OHdG and MDA, with the greatest effect the day before urine collection (6.9% increase; 95% CI 0.9-13.3%, per interquartile range: 0.22 µg/m3) for 8-OHdG and 1 to 4 days before collection (8.3% increase; 95% CI 0.03-17.3% per IQR) for MDA. Results were similar in models adjusting for PM2.5 not associated with BC and NO2 (10.4% increase, 95% CI: 3.5-17.9 for 8-OHdG; 8.1% increase, 95% CI: -1.1-18.1 for MDA). Effects on 8-OHdG were greater in obese participants. CONCLUSIONS: We found positive associations between BC exposure and 8-OHdG and MDA, in which associations with 8-OHdG were stronger in obese participants. These results suggest that exposure to low levels of traffic-related pollution results in lipid peroxidation and oxidative DNA damage in individuals with COPD.

Drosophila melanogaster p24 trafficking proteins have vital roles in development and reproduction.

p24 proteins comprise a family of type-I transmembrane proteins of ~24kD that are present in yeast and plants as well as metazoans ranging from Drosophila to humans. These proteins are most commonly localized to the endoplasmic reticulum (ER)-Golgi interface and are incorporated in anterograde and retrograde transport vesicles. Little is known about how disruption of p24 signaling affects individual tissue function or whole animals. Drosophila melanogaster express nine p24 genes, grouped into four subfamilies. Based upon our mRNA and protein expression data, Drosophila p24 family members are expressed in a variety of tissues. To identify functions for particular Drosophila p24 proteins, we used RNA interference (RNAi) to reduce p24 expression. Ubiquitous reduction of most p24 genes resulted in complete or partial lethality during development. We found that reducing p24 levels in adults caused defects in female fecundity (egg laying) and also reduced male fertility. We attributed reduced female fecundity to decreased neural p24 expression. These results provide the first genetic analysis of all p24 family members in a multicellular animal and indicate vital roles for Drosophila p24s in development and reproduction, implicating neural expression of p24s in the regulation of female behavior.