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BACKGROUND: Midlife residential exposure to greenspace may slow cognitive decline by increasing opportunities for physical activity and social connection, restoring attention, or reducing stress or adverse environmental exposures. However, prospective studies on the association between greenness and cognitive decline are sparse. OBJECTIVE: We investigated the prospective association between greenness at midlife and cognitive decline later in life. We explored effect measure modification by apolipoprotein E (APOE)-ε4 carrier status, neighborhood socioeconomic status (NSES), and rural/urban regions. METHODS: The Nurses' Health Study (푁 = 121,700) started in 1976 with married female nurses, 30-55 years of age, located across 11 US states. We examined 16,962 nurses who were enrolled in a substudy starting in 1995-2001 (mean age=74y) through 2008. We assessed average summer residential greenness in a 270-m buffer using Landsat Normalized Difference Vegetation Index data from 1986-1994. Starting in 1995-2001, participants underwent up to four repeated measures of five cognitive tests. A global composite score was calculated as the average of all 퓏-scores for each task to evaluate overall cognition. We used linear mixed models to evaluate the association of average greenness exposure at midlife with cognitive decline in later life, adjusted for age, education, NSES, and depression. RESULTS: In adjusted models, higher midlife greenness exposure [per interquartile range (IQR): 0.18] was associated with a 0.004-unit (95% CI: 0.001, 0.006) slower annual rate of cognitive decline. For comparison, we found that 1 year of age is related to a -0.006 mean annual difference for global cognition in the full sample; thus, higher midlife greenness appeared equivalent to slowing cognitive decline by ∼8 months. In analysis exploring gene-environment interactions, we found that among APOE-ε4 carriers, an IQR increase in greenness was associated with a rate of decline that was slower by 0.01 units of global composite score (95% CI: 0.0004, 0.02). This association was attenuated among APOE-ε4 noncarriers. We did not observe associations between greenness and baseline or annual rate of cognitive decline of verbal memory. DISCUSSION: Higher midlife greenness exposure is associated with slower cognitive decline later in life. Future research is necessary to confirm these findings. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

BACKGROUND: It remains unclear whether in utero and childhood exposure to air pollution affects pubertal development, particularly age of menarche in girls. OBJECTIVE: The aim of this study was to determine whether residential ambient particulate matter (PM) exposure in utero and during childhood is associated with age of menarche. METHODS: We studied 5,201 girls in the Growing Up Today Study 2 (2004-present) who were 10-17 y of age at enrollment (47.7% premenarchal; 52.3% postmenarchal). Exposure to three size fractions of PM [fine PM with aerodynamic diameter ≤ 2.5 μm (PM2.5), PM with aerodynamic diameters between 2.5 μm and 10 μm (PM2.5-10), and PM with aerodynamic diameter 10 μm (PM10)] was assigned based on maternal residential address, updated every 2 y, using nationwide spatiotemporal models. We estimated average PM exposure in utero, and time-varying windows: annual average exposure in the prior 1 and 2 y and cumulative average from birth. Age of menarche was self-reported on three surveys administered in 2004, 2006, and 2008. We calculated hazard ratios (HR) for menarche for an interquartile range (IQR) increase in PM exposure using Cox proportional hazard models adjusting for potential confounders. RESULTS: Girls attained menarche at 12.3 y of age on average. In the adjusted model, higher residential exposure to ambient PM2.5 during all time windows was associated with earlier age of menarche. The HRs of menarche for each IQR (4 μg/m³) increase in exposure to PM2.5 during the in utero period, 1 y prior to menarche, and throughout childhood were 1.03 [95% confidence interval (CI): 1.00, 1.06], 1.06 (95% CI: 1.02, 1.10) and 1.06 (95% CI: 1.02, 1.10), respectively. Effect estimates for PM10 exposure were similar, albeit attenuated, for all time windows. PM2.5-10 exposure was not associated with age of menarche. DISCUSSION: Among a large, nationwide, prospective cohort of U.S. girls, higher exposure to PM2.5 and PM10 in utero and throughout childhood was associated with an earlier age of menarche. Our results suggest that PM2.5 and PM10 may have endocrine-disrupting properties that could lead to altered timing of menarche. [ABSTRACT FROM AUTHOR]

Adverse neighborhood social and natural (green space) environments may contribute to the etiology of prostate cancer (CaP), but mechanisms are unclear. We examined associations between neighborhood environment and prostate intratumoral inflammation in 967 men diagnosed with CaP with available tissue samples from 1986–2009 in the Health Professionals Follow-up Study. Exposures were linked to work or residential addresses in 1988. We estimated indices of neighborhood socioeconomic status (nSES) and segregation (Index of Concentration at the Extremes (ICE)) using US Census tract–level data. Surrounding greenness was estimated using seasonal averaged Normalized Difference Vegetation Index (NDVI) data. Surgical tissue underwent pathological review for acute and chronic inflammation, corpora amylacea, and focal atrophic lesions. Adjusted odds ratios (aORs) for inflammation (ordinal) and focal atrophy (binary) were estimated using logistic regression. No associations were observed for acute or chronic inflammation. Each interquartile-range increase in NDVI within 1,230 m of the participant's work or home address (aOR = 0.74, 95% confidence interval (CI): 0.59, 0.93), in ICE-income (aOR = 0.79, 95% CI: 0.61, 1.04), and in ICE-race/income (aOR = 0.79, 95% CI: 0.63, 0.99) was associated with lower odds of postatrophic hyperplasia. Interquartile-range increases in nSES (aOR = 0.76, 95% CI: 0.57, 1.02) and ICE-race/income (aOR = 0.73, 95% CI: 0.54, 0.99) were associated with lower odds of tumor corpora amylacea. Histopathological inflammatory features of prostate tumors may be influenced by neighborhood. [ABSTRACT FROM AUTHOR]

Previous studies have examined the association between prenatal nitrogen dioxide (NO2)—a traffic emissions tracer—and fetal growth based on ultrasound measures. Yet, most have used exposure assessment methods with low temporal resolution, which limits the identification of critical exposure windows given that pregnancy is relatively short. Here, we used NO2 data from an ensemble model linked to residential addresses at birth to fit distributed lag models that estimated the association between NO2 exposure (resolved weekly) and ultrasound biometric parameters in a Massachusetts-based cohort of 9,446 singleton births from 2011–2016. Ultrasound biometric parameters examined included biparietal diameter (BPD), head circumference, femur length, and abdominal circumference. All models adjusted for sociodemographic characteristics, time trends, and temperature. We found that higher NO2 was negatively associated with all ultrasound parameters. The critical window differed depending on the parameter and when it was assessed. For example, for BPD measured after week 31, the critical exposure window appeared to be weeks 15–25; 10-parts-per-billion higher NO2 sustained from conception to the time of measurement was associated with a lower mean z score of −0.11 (95% CI: −0.17, −0.05). Our findings indicate that reducing traffic emissions is one potential avenue to improving fetal and offspring health. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

BACKGROUND: Several studies have evaluated whether the distribution of natural environments differs between marginalized and privileged neighborhoods. However, most studies restricted their analyses to a single or handful of cities and used different natural environment measures. OBJECTIVES: We evaluated whether natural environments are inequitably distributed based on socioeconomic status (SES) and race/ethnicity in the contiguous United States. METHODS: We obtained SES and race/ethnicity data (2015–2019) for all U.S. Census tracts. For each tract, we calculated the Normalized Different Vegetation Index (NDVI) for 2020, NatureScore (a proprietary measure of the quantity and quality of natural elements) for 2019, park cover for 2020, and blue space for 1984–2018. We used generalized additive models with adjustment for potential confounders and spatial autocorrelation to evaluate associations of SES and race/ethnicity with NDVI, NatureScore, park cover, and odds of containing blue space in all tracts (푛=71,532) and in urban tracts (푛=45,338). To compare effect estimates, we standardized NDVI, NatureScore, and park cover so that beta coefficients presented a percentage increase or decrease of the standard deviation (SD). RESULTS: Tracts with higher SES had higher NDVI, NatureScore, park cover, and odds of containing blue space. For example, urban tracts in the highest median household income quintile had higher NDVI [44.8% of the SD (95% CI: 42.8, 46.8)] and park cover [16.2% of the SD (95% CI: 13.5, 19.0)] compared with urban tracts in the lowest median household income quintile. Across all tracts, a lower percentage of non-Hispanic White individuals and a higher percentage of Hispanic individuals were associated with lower NDVI and NatureScore. In urban tracts, we observed weak positive associations between percentage non-Hispanic Black and NDVI, NatureScore, and park cover; we did not find any clear associations for percentage Hispanics. DISCUSSION: Multiple facets of the natural environment are inequitably distributed in the contiguous United States. [ABSTRACT FROM AUTHOR]

BACKGROUND: Communities with lower socioeconomic status and higher prevalence of racial/ethnic minority populations are often more exposed to environmental pollutants. Although studies have shown associations between aircraft noise and property values and various health outcomes, little is known about how aircraft noise exposures are sociodemographically patterned. OBJECTIVE: Our aim was to describe characteristics of populations exposed to aviation noise by race/ethnicity, education, and income in the United States. METHODS: Aircraft noise contours characterized as day-night average sound level (DNL) were developed for 90 U.S. airports in 2010 for DNL ≥45 dB(A) in 1-dB(A) increments. We compared characteristics of exposed U.S. Census block groups at three thresholds (≥45, ≥55, and ≥65 dB(A)), assigned on the basis of the block group land area being =50% within the threshold, vs. unexposed block groups near study airports. Comparisons were made across block group race/ethnicity, education, and income categories within the study areas (푛 ≥ 4,031-74,253). We performed both multinomial and other various multivariable regression approaches, including models controlling for airport and models with random intercepts specifying within-airport effects and adjusting for airport-level means. RESULTS: Aggregated across multiple airports, block groups with a higher Hispanic population had higher odds of being exposed to aircraft noise. For example, the multinomial analysis showed that a 10-percentage point increase in a block group’s Hispanic population was associated with an increased odds ratio of 39% (95% CI: 25%, 54%) of being exposed to =65 dB(A) compared with block groups exposed to <45 dB(A). Block groups with higher proportions of residents with only a high school education had higher odds of being exposed to aircraft noise. Results were robust across multiple regression approaches; however, there was substantial heterogeneity across airports. DISCUSSION: These results suggest that across U.S. airports, there is indication of sociodemographic disparities in noise exposures. [ABSTRACT FROM AUTHOR]

BACKGROUND: Atrial fibrillation (AF) is associated with substantial morbidity and mortality. Short-term exposures to air pollution have been associated with AF triggering; less is known regarding associations between long-term air pollution exposures and AF incidence. OBJECTIVES: Our objectivewas to assess the association between long-term exposures to air pollution and distance to road on incidence of AF in a cohort of U.S.women. METHODS: We assessed the association of high resolution spatiotemporal model predictions of long-term exposures to particulate matter (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and distance to major roads with incidence of AF diagnosis, identified through Medicare linkage, among 83,117 women in the prospective Women's Health Initiative cohort, followed from enrollment in Medicare through December 2012, incidence of AF, or death. Using time-varying Cox proportional hazards models adjusted for age, race/ethnicity, study component, body mass index, physical activity, menopausal hormone therapy, smoking, diet quality, alcohol consumption, educational attainment, and neighborhood socioeconomic status, we estimated the relative risk of incident AF in association with each pollutant. METHODS: We assessed the association of high resolution spatiotemporal model predictions of long-term exposures to particulate matter (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and distance to major roads with incidence of AF diagnosis, identified through Medicare linkage, among 83,117 women in the prospective Women's Health Initiative cohort, followed from enrollment in Medicare through December 2012, incidence of AF, or death. Using time-varying Cox proportional hazards models adjusted for age, race/ethnicity, study component, body mass index, physical activity, menopausal hormone therapy, smoking, diet quality, alcohol consumption, educational attainment, and neighborhood socioeconomic status, we estimated the relative risk of incident AF in association with each pollutant. RESULTS: A total of 16,348 incident AF cases were observed over 660,236 person-years of follow-up. Most exposure–response associations were nonlinear. NO2 was associated with risk of AF in multivariable adjusted models [Hazard Ratio (HR)=1.18; 95% confidence interval (CI): 1.13, 1.24, comparing the top to bottom quartile, 푝-for-trend= <0.0001]. Women living closer to roadways were at higher risk of AF (e.g., HR=1.07; 95% CI: 1.01, 1.13 for living within 50 m of A3 roads, compared with =1,000 m, 푝-for-trend=0.02), but we did not observe adverse associations with exposures to PM10, PM2.5, or SO2. There were adverse associations with PM10 (top quartile HR=1.10; 95% CI: 1.05, 1.16, 푝-for-trend= <0.0001) and PM2.5 (top quartile HR=1.09; 95% CI: 1.03, 1.14, 푝-for-trend=0:002) in sensitivity models adjusting for census region. DISCUSSION: In this study of postmenopausal women, NO2 and distance to road were consistently associated with higher risk of AF. [ABSTRACT FROM AUTHOR]

BACKGROUND: Increased respiration during physical activity may increase air pollution dose, which may attenuate the benefits of physical activity on cardiovascular disease (CVD) risk and overall mortality. OBJECTIVES: We aimed to examine the multiplicative interaction between long-term ambient residential exposure to fine particulate matter <2.5 microns (PM2.5) and physical activity in the association with CVD risk and overall mortality. METHODS: We followed 104,990 female participants of the U.S.-based prospective Nurses' Health Study from 1988 to 2008. We used Cox proportional hazards models to assess the independent associations of 24-months moving average residential PM2.5 exposure and physical activity updated every 4 y and the multiplicative interaction of the two on CVD (myocardial infarction and stroke) risk and overall mortality, after adjusting for demographics and CVD risk factors. RESULTS: During 20 years of follow-up, we documented 6,074 incident CVD cases and 9,827 deaths. In fully adjusted models, PM2.5 exposure was associated with modest increased risks of CVD [hazard ratio (HR) for fifth quintile =16.5 µg/m³ compared to first quintile <10.7 µg/m³: 1.09, 95% confidence interval (CI): 0.99, 1.20; ??trend = 0.05] and overall mortality (HR fifth compared to first quintile: 1.10, 95% CI: 1.02, 1.19; ??trend = 0.07). Higher overall physical activity was associated with substantially lower risk of CVD [HR fourth quartile, which was =24.4 metabolic equivalent of task (MET)-h/wk, compared to first quartile (<3.7 MET-h=wk): 0.61, 95% CI: 0.57, 0.66; ??trend < 0.0001] and overall mortality (HR fourth compared to first quartile: 0.40, 95% CI: 0.37, 0.42; ??trend < 0.0001). We observed no statistically significant interactions between PM2.5 exposure and physical activity (overall, walking, vigorous activity) in association with CVD risk and overall mortality. DISCUSSION: In this study of U.S. women, we observed no multiplicative interaction between long-term PM2.5 exposure and physical activity; higher physical activity was strongly associated with lower CVD risk and overall mortality at all levels of PM2.5 exposure. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent evidence suggests that higher levels of residential greenness may contribute to better mental health. Despite this, few studies have considered its impact on depression, and most are cross-sectional. OBJECTIVE: The objective of this study was to examine surrounding residential greenness and depression risk prospectively in the Nurses' Health Study. METHODS: A total of 38,947 women (mean age throughout follow-up 70 y [range 54-91 y]) without depression in 2000 were followed to 2010. Residential greenness was measured using the satellite-based Normalized Difference Vegetation Index (NDVI) and defined as the mean greenness value within [Formula: see text] and [Formula: see text] radii of the women's residences in July of each year. Incidence of depression was defined according to the first self-report of either physician-diagnosed depression or regular antidepressant use. We used Cox proportional hazards models to examine the relationship between greenness and depression incidence and assessed physical activity as a potential effect modifier and mediator. RESULTS: Over 315,548 person-years, 3,612 incident depression cases occurred. In multivariable-adjusted models, living in the highest quintile of residential greenness within [Formula: see text] was associated with a 13% reduction in depression risk ([Formula: see text] [95% confidence interval (CI): 0.78, 0.98]) compared with the lowest quintile. The association between greenness and depression did not appear to be mediated by physical activity, nor was there evidence of effect modification by physical activity. CONCLUSIONS: In this population of mostly white women, we estimated an inverse association between the highest level of surrounding summer greenness and the risk of self-reported depression. [ABSTRACT FROM AUTHOR]

BACKGROUND: Particulate matter (PM) air pollution has been associated with decreased pulmonary function, but the exposure-response 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 = 2:5 lm (PM2:5) 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 PM2:5 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 PM2:5 were 0.19 (0.22) lg=m3 and 6.67 (5.80) lg=m3, respectively. Increasing indoor exposures to BC were associated with decreases in pre-bronchodilator forced expiratory volume in 1 s ðFEV1Þ and forced vital capacity (FVC), and FEV1=FVC. For example, in multivariable adjusted models, each IQR increase in indoor BC from the weekly integrated filter was associated with a 17:87mL [95% confidence interval (CI): -33:76, -1:98] decrease in pre-bronchodilator FEV1. Increases in indoor PM2:5 were associated with decreases in FEV1 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 PM2:5 was only associated with decreases in FVC and increases in FEV1=FVC, and neither indoor nor ambient BC or PM2:5 were associated with post-bronchodilator pulmonary function. CONCLUSIONS: Low-level exposures to indoor BC and PM2:5, but not ambient exposures, were consistently associated with decreases in prebronchodilator pulmonary function. There was no association between exposures and post-bronchodilator pulmonary function. [ABSTRACT FROM AUTHOR]

Background: High mammographic density is a strong, well-established breast cancer risk factor. Three studies conducted in various smaller geographic settings reported inconsistent findings between air pollution and mammographic density. We assessed whether particulate matter (PM) exposures (PM2.5, PM2.5-10, and PM10) and distance to roadways were associated with mammographic density among women residing across the United States.Methods: The Nurses' Health Studies are prospective cohorts for whom a subset has screening mammograms from the 1990s (interquartile range 1990-1999). PM was estimated using spatio-temporal models linked to residential addresses. Among 3258 women (average age at mammogram 52.7 years), we performed multivariable linear regression to assess associations between square-root-transformed mammographic density and PM within 1 and 3 years before the mammogram. For linear regression estimates of PM in relation to untransformed mammographic density outcomes, bootstrapped robust standard errors are used to calculate 95% confidence intervals (CIs). Analyses were stratified by menopausal status and region of residence.Results: Recent PM and distance to roadways were not associated with mammographic density in premenopausal women (PM2.5 within 3 years before mammogram β = 0.05, 95% CI -0.16, 0.27; PM2.5-10 β = 0, 95%, CI -0.15, 0.16; PM10 β = 0.02, 95% CI -0.10, 0.13) and postmenopausal women (PM2.5 within 3 years before mammogram β = -0.05, 95% CI -0.27, 0.17; PM2.5-10 β = -0.01, 95% CI -0.16, 0.14; PM10 β = -0.02, 95% CI -0.13, 0.09). Largely null associations were observed within regions. Suggestive associations were observed among postmenopausal women in the Northeast (n = 745), where a 10-μg/m3 increase in PM2.5 within 3 years before the mammogram was associated with 3.4 percentage points higher percent mammographic density (95% CI -0.5, 7.3).Conclusions: These findings do not support that recent PM or roadway exposures influence mammographic density. Although PM was largely not associated with mammographic density, we cannot rule out the role of PM during earlier exposure time windows and possible associations among northeastern postmenopausal women. [ABSTRACT FROM AUTHOR]

In recent years, significant attention has been given to polycyclic aromatic hydrocarbons (PAHs) exposures given their mutagenic and carcinogenic properties. However, levels of exposure and the key determinants of exposure are not well defined for the trucking industry. We measured ultrafine particle characteristics at 10 trucking terminals of varying operating size and location in the Northeast region of the United States using particle concentration counter and a surface area analyzer. Multivariate mixed-effects linear regression models were used to assess determinants of the concentration of total bound PAHs (tPAH), the total aerosol active surface area (AS), and the ratio tPAH/AS overall and individually within docks, trucking cabs, and administrative offices. Associations between PAH measures with integrated measures of elemental carbon (EC), organic carbon (OC), and particulate matter (PM)2.5 were assessed by Spearman rank correlation. In adjusted models, tPAH, AS, and tPAH/AS average concentrations (95% confidence interval) were significantly higher in truck cabs compared to office locations (1.26 (ng m-3) (1.18, 1.35); 0.99 (mm² mm-3) (0.91, 1.08); 0.26 (ng mm-2) (0.18, 0.33), respectively). In the loading dock, AS concentrations were significantly higher than in the office (0.67 (0.61, 0.71), while the tPAH/AS was not (-0.63 (-0.67, -0.58). In each location, average tPAH concentrations were moderately but significantly correlated with EC (r = 0.47-0.63) and with tPAH/AS (r = 0.34-0.40) in the truck cabs and loading docks. In conclusion, key predictors of tPAH, AS, and tPAH/AS within the trucking industry are work location (in particular truck cabs and terminal docks) and terminal characteristics (size). The association of tPAH and tPAH/AS with EC concentrations in dockworkers and pick-up and delivery drivers is consistent with occupational exposure attributable to vehicle exhaust. Therefore, measurement of tPAH, AS, and tPAH/AS to characterize ultrafine particles and bound PAH concentrations provide additional information regarding exposures in the trucking industry not captured by integrated measures by EC, OC, and PM2.5. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to air pollution has been implicated in a number of adverse health outcomes, and the effect of particulate matter (PM) on the brain is beginning to be recognized. OBJECTIVES: We aimed to examine whether exposure to PM air pollution is related to risk of Parkinson's disease (PD) in the Health Professionals Follow-up Study (HPFS), a large prospective cohort of U.S. men. METHODS: We prospectively followed 50,352 men in the HPFS, a large prospective cohort of U.S. men, and identified 550 incident PD cases. Cumulative average exposure to various size fractions of PM [PM10 (≤10 μm microns in diameter), PM2:5 (≤2:5 μm in diameter), and PM2:5-10 (between 2.5 and 10 μm in diameter)] up to 2 years before the onset of PD was estimated using a spatiotemporal model by linking each participant's place of residence throughout the study with location-specific PM levels. We used multivariable Cox proportional hazards models to independently estimate the risk of PD associated with each size fraction of PM. RESULTS: In models adjusted for age, smoking, region, and population density, we did not observe statistically significant associations between exposure to PM and PD risk. In analyses considering cumulative average PM exposure, the comparing the top to the bottom quintile of PM exposure was 0.85 [95% confidence interval (CI): (0.63, 1.15)] for PM 10, 0.97 [95% CI: (0.72, 1.32)] for PM2:5, and 0.88 [95% CI: (0.64, 1.22)] for hazard ratio (HR) PM2:5-10. The results did not change markedly when restricted to men who did not move during the study or when stratified by smoking status or population density. CONCLUSIONS: In this study, we found no evidence that exposure to air pollution is a risk factor for PD in men. [ABSTRACT FROM AUTHOR]

BACKGROUND: Animal and epidemiologic studies suggest that exposure to light at night (LAN) may disrupt circadian patterns and decrease nocturnal secretion of melatonin, which may disturb estrogen regulation, leading to increased breast cancer risk. OBJECTIVES: We examined the association between residential outdoor LAN and breast cancer incidence using data from the nationwide U.S.-based Nurses' Health Study II cohort. METHODS: We followed 109,672 women from 1989 through 2013. Cumulative LAN exposure was estimated using time-varying satellite data for a composite of persistent nighttime illumination at ~1 km² scale for each residence during follow-up. Incident invasive breast cancer cases were con- firmed by medical record review. We used Cox proportional hazard models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for anthropometric, reproductive, lifestyle, and socioeconomic risk factors. RESULTS: Over 2,187,425 person-years, we identified 3,549 incident breast cancer cases. Based on a fully adjusted model, the estimated HR for incident breast cancer with an interquartile range (IQR) (31:6 nW/cm²/sr) increase in cumulative average outdoor LAN was 1.05 (95% CI: 1.00, 1.11). An association between LAN and breast cancer appeared to be limited to women who were premenopausal at the time of a case [HR=1:07 (95% CI: 1.01, 1.14) based on 1,973 cases vs. HR=1:00 (95% CI: 0.91, 1.09) based on 1,172 cases in postmenopausal women; p-interaction=0:08]. The LAN--breast cancer association was observed only in past and current smokers at the end of follow-up [HR=1:00 (95% CI: 0.94, 1.07) based on 2,215 cases in never smokers; HR=1:10 (95% CI: 1.01, 1.19) based on 1,034 cases in past smokers vs. HR=1:21 (95% CI: 1.07, 1.37) for 300 cases in current smokers; p-interaction=0:08]. CONCLUSIONS: Although further work is required to confirm our results and to clarify potential mechanisms, our findings suggest that exposure to residential outdoor light at night may contribute to invasive breast cancer risk. [ABSTRACT FROM AUTHOR]

Despite recently reported associations between air pollution and acute psychiatric outcomes, the association with depression onset has not, to our knowledge, been previously examined. We conducted a prospective cohort study among 41,844 women in the Nurses' Health Study, in the United States. The women had an average age of 66.6 (standard deviation, 7.6) years, were depression-free in 1996, and were followed through 2008. May-September ozone exposures were predicted by interpolating concentrations from the 5 nearest monitors. One-, 2-, and 5-year average concentrations of particulate matter with an aerodynamic diameter less than or equal to 2.5 µm (PM2.5) were predicted at each participant's residence using a spatiotemporal model. We defined depression as report of doctor's diagnosis or use of antidepressant medication. We estimated adjusted hazard ratios with timevarying Cox models. Hazard ratios for both pollutants were elevated (per 10-parts-per-billion increase in ozone, hazard ratio (HR) = 1.06; 95% confidence interval (CI): 1.00, 1.12; per 10-µg/m³ increase in 1-year PM2.5, HR = 1.08; 95% CI: 0.97, 1.20). Associations were stronger when only antidepressant use was used to define cases (for ozone, HR = 1.08; 95% CI: 1.02, 1.14; for PM2.5, HR = 1.12; 95% CI: 1.00, 1.25). To our knowledge, these results represent the first identification of a possible association between both long-term ozone and PM2.5 exposure and depression onset. Although the stronger association specifically with antidepressant use may reflect that this endpoint better captures the onset time and milder cases, our findings should be interpreted with caution. [ABSTRACT FROM AUTHOR]

BACKGROUND: Green, natural environments may ameliorate adverse environmental exposures (e.g., air pollution, noise, and extreme heat), increase physical activity and social engagement, and lower stress. OBJECTIVES: We aimed to examine the prospective association between residential greenness and mortality. METHODS: Using data from the U.S.-based Nurses' Health Study prospective cohort, we defined cumulative average time-varying seasonal greenness surrounding each participant's address using satellite imagery [Normalized Difference Vegetation Index (NDVI)]. We followed 108,630 women and observed 8,604 deaths between 2000 and 2008. RESULTS: In models adjusted for mortality risk factors (age, race/ethnicity, smoking, and individual-and area-level socioeconomic status), women living in the highest quintile of cumulative average greenness (accounting for changes in residence during follow-up) in the 250-m area around their home had a 12% lower rate of all-cause nonaccidental mortality [95% confidence interval (CI); 0.82, 0.94] than those in the lowest quintile. The results were consistent for the 1,250-m area, although the relationship was slightly attenuated. These associations were strongest for respiratory and cancer mortality. The findings from a mediation analysis suggested that the association between greenness and mortality may be at least partly mediated by physical activity, particulate matter < 2.5 µm, social engagement, and depression. CONCLUSIONS: Higher levels of green vegetation were associated with decreased mortality. Policies to increase vegetation may provide opportunities for physical activity, reduce harmful exposures, increase social engagement, and improve mental health. Planting vegetation may mitigate the effects of climate change; in addition, evidence of an association between vegetation and lower mortality rates suggests it also might be used to improve health. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies have suggested associations between elevated blood pressure and short-term air pollution exposures, but the evidence is mixed regarding long-term exposures on incidence of hypertension. OBJECTIVES: We examined the association of hypertension incidence with long-term residential exposures to ambient particulate matter (PM) and residential distance to roadway. METHODS: We estimated 24-month and cumulative average exposures to PM[sub 10], PM[sub 2.5], and PM[sub 2.5-10] and residential distance to road for women participating in the prospective nationwide Nurses' Health Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for incident hypertension from 1988 to 2008 using Cox proportional hazards models adjusted for potential confounders. We considered effect modification by age, diet, diabetes, obesity, region, and latitude. RESULTS: Among 74,880 participants, 36,812 incident cases of hypertension were observed during 960,041 person-years. In multivariable models, 10-µg/m³ increases in 24-month average PM[sub 10], PM[sub 2.5], and PM[sub 2.5-10] were associated with small increases in the incidence of hypertension (HR: 1.02, 95% CI: 1.00, 1.04; HR: 1.04, 95% CI: 1.00, 1.07; and HR: 1.03, 95% CI: 1.00, 1.07, respectively). Associations were stronger among women < 65 years of age (HR: 1.04, 95% CI: 1.01, 1.06; HR: 1.07, 95% CI: 1.02, 1.12; and HR: 1.05, 95% CI: 1.01, 1.09, respectively) and the obese (HR: 1.07, 95% CI: 1.04, 1.12; HR: 1.15, 95% CI: 1.07, 1.23; and HR: 1.13, 95% CI: 1.07, 1.19, respectively), with p-values for interaction < 0.05 for all models except age and PM[sub 2.5-10]. There was no association with roadway proximity. CONCLUSIONS: Long-term exposure to particulate matter was associated with small increases in risk of incident hypertension, particularly among younger women and the obese. [ABSTRACT FROM AUTHOR]

BACKGROUND: Pulmonary embolism (PE) is the most serious manifestation of venous thromboembolism and a leading cause of sudden death. Several studies have suggested associations of venous thromboembolism with short-term particulate matter (PM) exposure; evidence on long-term PM and traffic exposure is mixed. OBJECTIVES: We examined the association of long-term exposure to PM2.5, PM2.5-10, and PM10 (PM with diameter of ≤ 2.5, 2.5-10, and < 10 μm) and distance to roadways with overall incident PE and with PE subtypes in a cohort of U.S. women. METHODS: The study included 115,745 women from the Nurses' Health Study, followed from 1992 through 2008. Incident PE cases were self-reported biennially. Nonidiopathic PE were cases for which the medical record revealed an underlying health condition related to PE (i.e., surgery, trauma, or malignancy); idiopathic PE were cases with no such history. We used spatiotemporal models combining spatial smoothing and geographic covariates to quantify exposure at residential addresses, and Cox proportional hazards models to calculate hazard ratios (HR) and 95% confidence intervals (CIs). RESULTS: PM2.5 averaged over 1 month (HR = 1.22; 95% CI: 1.04, 1.44) or 12 months (HR = 1.17; 95% CI: 0.93, 1.48) was associated with incident PE, after adjusting for known risk factors and PM2.5-10. Equivalent analyses restricted to PE subtypes showed a positive association for PM2.5 with nonidiopathic PE, but not with idiopathic PE. We did not find evidence of an association between distance to roadways and PE risk. CONCLUSIONS: We provide evidence that PM in the prior 1 and 12 months is associated with PE risk. Our results also suggest that women with underlying health conditions may be more susceptible to PE after PM exposure. [ABSTRACT FROM AUTHOR]

Background: The International Agency for Research on Cancer (IARC) recently declared air pollution carcinogenic to humans. However, no study of air pollution and lung cancer to date has incorporated adjustment for exposure measurement error, and few have examined specific histological subtypes. Objectives: Our aim was to assess the association of air pollution and incident lung cancer in the Netherlands Cohort Study on Diet and Cancer and the impact of measurement error on these associations. Methods: The cohort was followed from 1986 through 2003, and 3,355 incident cases were identified. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals, for long-term exposures to nitrogen dioxide (NO2), black smoke (BS), PM2.5 (particulate matter with diameter ≤ 2.5 μm), and measures of roadway proximity and traffic volume, adjusted for potential confounders. Information from a previous validation study was used to correct the effect estimates for measurement error. Results: We observed elevated risks of incident lung cancer with exposure to BS [hazard ratio (HR) = 1.16; 95% CI: 1.02, 1.32, per 10 μg/m3], NO2 (HR = 1.29; 95% CI: 1.08, 1.54, per 30 μg/m3), PM2.5 (HR = 1.17; 95% CI: 0.93, 1.47, per 10 μg/m3), and with measures of traffic at the baseline address. The exposures were positively associated with all lung cancer subtypes. After adjustment for measurement error, the HRs increased and the 95% CIs widened [HR = 1.19 (95% CI: 1.02, 1.39) for BS and HR = 1.37 (95% CI: 0.86, 2.17) for PM2.5]. Conclusions: These findings add support to a growing body of literature on the effects of air pollution on lung cancer. In addition, they highlight variation in measurement error by pollutant and support the implementation of measurement error corrections when possible. [ABSTRACT FROM AUTHOR]

Background: Epidemiologic studies of postnatal PCB exposure and behavior have not reported consistent evidence of adverse associations, possibly because of challenges in exposure estimation. We previously developed a pharmacokinetic model to improve estimation of children's PCB exposure. Objectives: We aimed to assess whether estimated serum PCB levels in infancy are associated with attention deficit/hyperactivity disorder (ADHD)-related behaviors at 8 years of age among children whose cord serum PCB levels were previously shown to be associated with ADHDrelated behaviors. Methods: We used a pharmacokinetic model to estimate monthly serum polychlorinated biphenyl (PCB)-153 levels in 441 infants (ages 1-12 months) based on parameters such as breastfeeding and cord serum PCB‑153 levels. Behavior was evaluated at age 8 using the Conners' Rating Scale for Teachers (CRS-T). Associations between PCB‑153 levels and ADHD-related CRS-T indices were assessed using multivariable quantile regression at the 50th and 75th percentiles of CRS-T scores, where higher percentiles reflect more adverse behaviors. Results: Cord serum PCB-153 levels (median, 38 ng/g lipids) were associated with ADHD-related behaviors, although statistical significance was observed with quantile regression models only at the 75th percentile. Associations with postnatal exposure estimates were attenuated. For example, hyperactive-impulsive behavior scores at age 8 years were 0.9 points (95% CI: 0.2, 2.5), 0.5 points (95% CI: 0.3, 2.3), and 0.3 points (95% CI: -0.2, 1.5) higher in association with interquartile range increases in serum PCB-153 at birth, 2 months, and 12 months of age, respectively. Conclusions: Associations between estimated postnatal PCB-153 exposures and ADHD-related behaviors at 8 years of age were weaker than associations with PCB-153 concentrations measured in cord serum at birth. [ABSTRACT FROM AUTHOR]

Background: Autism spectrum disorder (ASD) is a developmental disorder with increasing prevalence worldwide, yet has unclear etiology. Objective: We explored the association between maternal exposure to particulate matter (PM) air pollution and odds of ASD in her child. Methods: We conducted a nested case–control study of participants in the Nurses’ Health Study II (NHS II), a prospective cohort of 116,430 U.S. female nurses recruited in 1989, followed by biennial mailed questionnaires. Subjects were NHS II participants’ children born 1990–2002 with ASD (n = 245), and children without ASD (n = 1,522) randomly selected using frequency matching for birth years. Diagnosis of ASD was based on maternal report, which was validated against the Autism Diagnostic Interview-Revised in a subset. Monthly averages of PM with diameters ≤ 2.5 μm (PM2.5) and 2.5–10 μm (PM10–2.5) were predicted from a spatiotemporal model for the continental United States and linked to residential addresses. Results: PM2.5 exposure during pregnancy was associated with increased odds of ASD, with an adjusted odds ratio (OR) for ASD per interquartile range (IQR) higher PM2.5 (4.42 μg/m3) of 1.57 (95% CI: 1.22, 2.03) among women with the same address before and after pregnancy (160 cases, 986 controls). Associations with PM2.5 exposure 9 months before or after the pregnancy were weaker in independent models and null when all three time periods were included, whereas the association with the 9 months of pregnancy remained (OR = 1.63; 95% CI: 1.08, 2.47). The association between ASD and PM2.5 was stronger for exposure during the third trimester (OR = 1.42 per IQR increase in PM2.5; 95% CI: 1.09, 1.86) than during the first two trimesters (ORs = 1.06 and 1.00) when mutually adjusted. There was little association between PM10–2.5 and ASD. Conclusions: Higher maternal exposure to PM2.5 during pregnancy, particularly the third trimester, was associated with greater odds of a child having ASD. [ABSTRACT FROM AUTHOR]

Background: A body of literature has suggested an elevated risk of lung cancer associated with particulate matter and traffic-related pollutants. Objective: We examined the relation of lung cancer incidence with long-term residential exposures to ambient particulate matter and residential distance to roadway, as a proxy for traffic-related exposures. Methods: For participants in the Nurses’ Health Study, a nationwide prospective cohort of women, we estimated 72‑month average exposures to PM2.5, PM2.5–10, and PM10 and residential distance to road. Follow-up for incident cases of lung cancer occurred from 1994 through 2010. Cox proportional hazards models were adjusted for potential confounders. Effect modification by smoking status was examined. Results: During 1,510,027 person-years, 2,155 incident cases of lung cancer were observed among 103,650 participants. In fully adjusted models, a 10‑μg/m3 increase in 72‑month average PM10 [hazard ratio (HR) = 1.04; 95% CI: 0.95, 1.14], PM2.5 (HR = 1.06; 95% CI: 0.91, 1.25), or PM2.5-10 (HR = 1.05; 95% CI: 0.92, 1.20) was positively associated with lung cancer. When the cohort was restricted to never-smokers and to former smokers who had quit at least 10 years before, the associations appeared to increase and were strongest for PM2.5 (PM10: HR = 1.15; 95% CI: 1.00, 1.32; PM2.5: HR = 1.37; 95% CI: 1.06, 1.77; PM2.5-10: HR = 1.11; 95% CI: 0.90, 1.37). Results were most elevated when restricted to the most prevalent subtype, adenocarcinomas. Risks with roadway proximity were less consistent. Conclusions: Our findings support those from other studies indicating increased risk of incident lung cancer associated with ambient PM exposures, especially among never- and long-term former smokers. [ABSTRACT FROM AUTHOR]

Background: Exposure to metals has been implicated in the pathogenesis of Parkinson disease (PD). Objectives: We sought to examine in a large prospective study of female nurses whether exposure to airborne metals was associated with risk of PD. Methods: We linked the U.S. Environmental Protection Agency (EPA)’s Air Toxics tract-level data with the Nurses’ Health Study, a prospective cohort of female nurses. Over the course of 18 years of follow-up from 1990 through 2008, we identified 425 incident cases of PD. We examined the association of risk of PD with the following metals that were part of the first U.S. EPA collections in 1990, 1996, and 1999: arsenic, antimony, cadmium, chromium, lead, manganese, mercury, and nickel. To estimate hazard ratios (HRs) and 95% CIs, we used the Cox proportional hazards model, adjusting for age, smoking, and population density. Results: In adjusted models, the HR for the highest compared with the lowest quartile of each metal ranged from 0.78 (95% CI: 0.59, 1.04) for chromium to 1.33 (95% CI: 0.98, 1.79) for mercury. Conclusions: Overall, we found limited evidence for the association between adulthood ambient exposure to metals and risk of PD. The results for mercury need to be confirmed in future studies. [ABSTRACT FROM AUTHOR]

Previous studies evaluating the association of prenatal exposure to diethylstilbestrol (DES), a potent endocrine disruptor, with incidence of uterine leiomyomata (UL) have had conflicting results. We evaluated the association between prenatal DES exposure and incident UL in women in the Nurses' Health Study II from 1989 to 2009. Women were aged 25–42 years at enrollment and had a prenatal exposure window corresponding to DES use. The analytical sample was larger than previous studies and included 102,164 premenopausal women with intact uteri, no prior history of UL or cancer, and prenatal DES exposure. Multivariable-adjusted Cox proportional hazard models were used to estimate the relationship between DES exposure and UL risk. During 1,273,342 person-years of follow-up, there were 11,831 incident cases of UL. Women with prenatal exposure to DES had a higher incidence of UL compared with unexposed women, with an adjusted hazard ratio of 1.12 (95% confidence interval: 0.98, 1.27). Risk was strongest for women exposed to DES in the first trimester, when exposure corresponds to early stages of fetal Müllerian development (adjusted hazard ratio = 1.21, 95% confidence interval: 1.02, 1.43). These results suggest that first-trimester DES exposure may be associated with an increased risk of UL, but they must be interpreted with concern for detection and recall biases. [ABSTRACT FROM AUTHOR]

Background: Particulate matter and proximity to large roadways may promote disease mechanisms, including systemic inflammation, hormonal alteration, and vascular proliferation, that may contribute to the development and severity of endometriosis. Objective: Our goal was to determine the association of air pollution exposures during adulthood, including distance to road, particulate matter < 2.5 μm, between 2.5 and 10 μm, and < 10 μm, (PM2.5, PM10-2.5, PM10), and timing of exposure with risk of endometriosis in the Nurses' Health Study II. Methods: Proximity to major roadways and outdoor levels of PM2.5, PM10-2.5, and PM10 were determined for all residential addresses from 1993 to 2007. Multivariable-adjusted time-varying Cox proportional hazard models were used to estimate the relation between these air pollution exposures and endometriosis risk. Results: Among 84,060 women, 2,486 incident cases of surgically confirmed endometriosis were identified over 710,230 person-years of follow-up. There was no evidence of an association between endometriosis risk and distance to road or exposure to PM2.5, PM10-2.5, or PM10 averaged over follow-up or during the previous 2- or 4-year period. Conclusions: Traffic and air pollution exposures during adulthood were not associated with incident endometriosis in this cohort of women. [ABSTRACT FROM AUTHOR]

Objective: Air pollution contains many toxicants known to affect neurological function and to have effects on the fetus in utero. Recent studies have reported associations between perinatal exposure to air pollutants and autism spectrum disorder (ASD) in children. We tested the hypothesis that perinatal exposure to air pollutants is associated with ASD, focusing on pollutants associated with ASD in prior studies. Methods: We estimated associations between U.S. Environmental Protection Agency-modeled levels of hazardous air pollutants at the time and place of birth and ASD in the children of participants in the Nurses' Health Study II (325 cases, 22,101 controls). Our analyses focused on pollutants associated with ASD in prior research. We accounted for possible confounding and ascertainment bias by adjusting for family-level socioeconomic status (maternal grandparents' education) and census tract-level socioeconomic measures (e.g., tract median income and percent college educated), as well as maternal age at birth and year of birth. We also examined possible differences in the relationship between ASD and pollutant exposures by child's sex. Results: Perinatal exposures to the highest versus lowest quintile of diesel, lead, manganese, mercury, methylene chloride, and an overall measure of metals were significantly associated with ASD, with odds ratios ranging from 1.5 (for overall metals measure) to 2.0 (for diesel and mercury). In addition, linear trends were positive and statistically significant for these exposures (p < .05 for each). For most pollutants, associations were stronger for boys (279 cases) than for girls (46 cases) and significantly different according to sex. Conclusions: Perinatal exposure to air pollutants may increase risk for ASD. Additionally, future studies should consider sex-specific biological pathways connecting perinatal exposure to pollutants with ASD. INSET: CORRECTION. [ABSTRACT FROM AUTHOR]

Objectives. We evaluated the association between the county sprawl index, a measure of residential density and street accessibility, and physical activity and body mass index (BMI). Methods. We conducted a multilevel cross-sectional analysis in a sample of Nurses' Health Study participants living throughout the United States in 2000 to 2001 (n = 136 592). Results. In analyses adjusted for age, smoking status, race, and husband's education, a 1-SD (25.7) increase in the county sprawl index (indicating a denser, more compact county) was associated with a 0.13 kilograms per meters squared (95% confidence interval [CI] = -0.18, -0.07) lower BMI and 0.41 (95% CI = 0.17, 0.65) more metabolic equivalent (MET) hours per week of total physical activity, 0.26 (95% CI = 0.19, 0.33) more MET hours per week of walking, and 0.47 (95% CI = 0.34, 0.59) more MET hours per week of walking, bicycling, jogging, and running. We detected potential effect modification for age, previous disease status, husband's education level (a proxy for socioeconomic status), and race. Conclusions. Our results suggest that living in a dense, compact county may be conducive to higher levels of physical activity and lower BMI in women. [ABSTRACT FROM AUTHOR]

Background: Diesel exhaust has been considered to be a probable lung carcinogen based on studies of occupationally exposed workers. Efforts to define lung cancer risk in these studies have been limited in part by lack of quantitative exposure estimates. Objective: We conducted a retrospective cohort study to assess lung cancer mortality risk among U.S. trucking industry workers. Elemental carbon (EC) was used as a surrogate of exposure to engine exhaust from diesel vehicles, traffic, and loading dock operations. Methods: Work records were available for 31,135 male workers employed in the unionized U.S. trucking industry in 1985. A statistical model based on a national exposure assessment was used to estimate historical work-related exposures to EC. Lung cancer mortality was ascertained through the year 2000, and associations with cumulative and average EC were estimated using proportional hazards models. Results: Duration of employment was inversely associated with lung cancer risk consistent with a healthy worker survivor effect and a cohort composed of prevalent hires. After adjusting for employment duration, we noted a suggestion of a linear exposure-response relationship. For each 1,000-μg/m3 months of cumulative EC, based on a 5-year exposure lag, the hazard ratio (HR) was 1.07 [95% confidence interval (CI): 0.99, 1.15] with a similar association for a 10-year exposure lag [HR = 1.09 (95% CI: 0.99, 1.20)]. Average exposure was not associated with relative risk. Conclusions: Lung cancer mortality in trucking industry workers increased in association with cumulative exposure to EC after adjusting for negative confounding by employment duration. [ABSTRACT FROM AUTHOR]

BACKGROUND: The association of all-cause mortality and cardiovascular outcomes with air pollution exposures has been well established in the literature. The number of studies examining chronic exposures in cohorts is growing, with more recent studies conducted among women finding risk estimates of greater magnitude. Questions remain regarding sex differences in the relationship of chronic particulate matter (PM) exposures with mortality and cardiovascular outcomes. OBJECTIVES: In this study we explored these associations in the all-male Health Professionals Follow-Up Study prospective cohort. METHODS: The same spatiotemporal exposure estimation models, similar outcomes, and biennially updated covariates were used as those previously applied in the female Nurses' Health Study cohort. RESULTS: Among 17,545 men residing in the northeastern and midwestern United States, there were 2,813 deaths, including 746 cases of fatal coronary heart disease (CHD). An interquartile range change (4 µg/m3) in average exposure to PM ≤ 2.5 µm in diameter in the 12 previous months was not associated with all-cause mortality [hazard ratio (HR) = 0.94; 95% confidence interval (CI), 0.87-1.00] or fatal CHD (HR = 0.99; 95% CI, 0.87-1.13) in fully adjusted models. Findings were similar for separate models of exposure to PM ≤10 µm in diameter and PM between 2.5 and 10 µm in diameter and for copollutant models. CONCLUSIONS: Among this cohort of men with high socioeconomic status living in the midwestern and northeastern United States, the results did not support an association of chronic PM exposures with all-cause mortality and cardiovascular outcomes in models with time-varying covariates. Whether these findings suggest sex differences in susceptibility or the protective impact of healthier lifestyles and higher socioeconomic status requires additional investigation. [ABSTRACT FROM AUTHOR]

The dietary supplements industry disproportionately markets potentially harmful products promising weight loss, cleansing/detoxing, and boosted energy and immunity to women. The COVID-19 pandemic heightened consumer concerns around health and body weight, which may have increased women's risks of using supplements, particularly if they had a higher weight and experienced weight discrimination. This study aimed to estimate inequities in prevalence and change in use of weight-loss, cleanse/detox, immunity, and energy supplements in the first year of the pandemic and to assess the extent to which the relationship between weight and supplement use differs across discrimination experiences. We drew upon longitudinal data from cisgender women in the U.S. COVID-19 Pandemic Substudy of the Nurses' Health Study II and 3 and Growing Up Today Study cohorts, collected over 5 waves from April/May 2020 to April 2021 (N = 51,814). Modified Poisson generalized estimating equation models, adjusted for age, cohort, race/ethnicity, wave, and Census region, estimated the relative excess risk due to interaction (RERI) between weight status and weight discrimination on prevalence of supplement use. Weight status categories were derived from body mass index (BMI), and weight discrimination was assessed using the attributions item of the Everyday Discrimination Scale. Baseline prevalence of supplement use was 2.7% for weight-loss, 3.3% for cleanse/detox, 4.2% for energy, and 22.6% for immune. Respondents with BMIs of 25–29.9 kg/m2 and 30–34.9 kg/m2 who experienced weight discrimination had RERI values of 0.89 (95% CI 0.14, 1.65) and 1.00 (95% CI 0.25, 1.75) for weight-loss and 0.57 (95% CI 0.13, 1.02) and 0.60 (95% CI 0.19, 1.01) for energy supplements, respectively, indicating this group had excess risk of use compared to lower BMI respondents who experienced no weight discrimination. The findings demonstrate the disproportionate impact of weight discrimination on use of potentially harmful supplements among cisgender women with higher weights during the pandemic. • Disproportionate use of potentially harmful dietary supplements is well-documented • We assessed the influence of weight discrimination on supplement use among women • High weight women reporting weight discrimination have excess risk of supplement use • Excess risk was specific to potentially harmful weight-loss and energy supplements • Experiencing weight discrimination influenced supplement use during the pandemic [ABSTRACT FROM AUTHOR]