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Background: Ultraviolet B (UV-B) radiation plays a multifaceted role in human health, inducing DNA damage and representing the primary source of vitamin D for most humans; however, current U.S. UV exposure models are limited in spatial, temporal, and/or spectral resolution. Area-to-point (ATP) residual kriging is a geostatistical method that can be used to create a spatiotemporal exposure model by downscaling from an area- to point-level spatial resolution using fine-scale ancillary data. Methods: A stratified ATP residual kriging approach was used to predict average July noon-time erythemal UV (UVEry) (mW/m2) biennially from 1998 to 2012 by downscaling National Aeronautics and Space Administration (NASA) Total Ozone Mapping Spectrometer (TOMS) and Ozone Monitoring Instrument (OMI) gridded remote sensing images to a 1 km spatial resolution. Ancillary data were incorporated in random intercept linear mixedeffects regression models. Modeling was performed separately within nine U.S. regions to satisfy stationarity and account for locally varying associations between UVEry and predictors. Cross-validation was used to compare ATP residual kriging models and NASA grids to UV-B Monitoring and Research Program (UVMRP) measurements (gold standard). Results: Predictors included in the final regional models included surface albedo, aerosol optical depth (AOD), cloud cover, dew point, elevation, latitude, ozone, surface incoming shortwave flux, sulfur dioxide (SO2), year, and interactions between year and surface albedo, AOD, cloud cover, dew point, elevation, latitude, and SO2. ATP residual kriging models more accurately estimated UVEry at UVMRP monitoring stations on average compared to NASA grids across the contiguous U.S. (average mean absolute error [MAE] for ATP, NASA: 15.8, 20.3; average root mean square error [RMSE]: 21.3, 25.5). ATP residual kriging was associated with positive percent relative improvements in MAE (0.6-31.5%) and RMSE (3.6-29.4%) across all regions compared to NASA grids. Conclusions: ATP residual kriging incorporating fine-scale spatial predictors can provide more accurate, high-resolution UVEry estimates compared to using NASA grids and can be used in epidemiologic studies examining the health effects of ambient UV. [ABSTRACT FROM AUTHOR]

Background: Exposure to air pollution, including traffic-related pollutants, has been associated with a variety of adverse health outcomes, including increased cardiopulmonary morbidity and mortality, and increased lung cancer risk. Methods: To better understand the cellular responses induced by air pollution exposures, we performed genomewide gene expression microarray analysis using whole blood RNA sampled at three time-points across the work weeks of 63 non-smoking employees at 10 trucking terminals in the northeastern US. We defined genes and gene networks that were differentially activated in response to PM2.5 (particulate matter ≤ 2.5 microns in diameter) and elemental carbon (EC) and organic carbon (OC). Results: Multiple transcripts were strongly associated (padj < 0.001) with pollutant levels (48, 260, and 49 transcripts for EC, OC, and PM2.5, respectively), including 63 that were statistically significantly correlated with at least two out of the three exposures. These genes included many that have been implicated in ischemic heart disease, chronic obstructive pulmonary disease (COPD), lung cancer, and other pollution-related illnesses. Through the combination of Gene Set Enrichment Analysis and network analysis (using GeneMANIA), we identified a core set of 25 interrelated genes that were common to all three exposure measures and were differentially expressed in two previous studies assessing gene expression attributable to air pollution. Many of these are members of fundamental cancer-related pathways, including those related to DNA and metal binding, and regulation of apoptosis and also but include genes implicated in chronic heart and lung diseases. Conclusions: These data provide a molecular link between the associations of air pollution exposures with health effects. [ABSTRACT FROM AUTHOR]

Background: Long-term exposure to particulate matter less than 2.5 μm in diameter (PM2.5) has been consistently associated with risk of all-cause mortality. The methods used to assess exposure, such as area averages, nearest monitor values, land use regressions, and spatio-temporal models in these studies are subject to measurement error. However, to date, no study has attempted to incorporate adjustment for measurement error into a long-term study of the effects of air pollution on mortality. Methods: We followed 108,767 members of the Nurses' Health Study (NHS) 2000-2006 and identified all deaths. Biennial mailed questionnaires provided a detailed residential address history and updated information on potential confounders. Time-varying average PM2.5 in the previous 12-months was assigned based on residential address and was predicted from either spatio-temporal prediction models or as concentrations measured at the nearest USEPA monitor. Information on the relationships of personal exposure to PM2.5 of ambient origin with spatio-temporal predicted and nearest monitor PM2.5 was available from five previous validation studies. Time-varying Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95 percent confidence intervals (95%CI) for each 10 μg/m3 increase in PM2.5. Risk-set regression calibration was used to adjust estimates for measurement error. Results: Increasing exposure to PM2.5 was associated with an increased risk of mortality, and results were similar regardless of the method chosen for exposure assessment. Specifically, the multivariable adjusted HRs for each 10 μg/m3 increase in 12-month average PM2.5 from spatio-temporal prediction models were 1.13 (95%CI:1.05, 1.22) and 1.12 (95%CI:1.05, 1.21) for concentrations at the nearest EPA monitoring location. Adjustment for measurement error increased the magnitude of the HRs 4-10% and led to wider CIs (HR = 1.18; 95%CI: 1.02, 1.36 for each 10 μg/m3 increase in PM2.5 from the spatio-temporal models and HR = 1.22; 95%CI: 1.02, 1.45 from the nearest monitor estimates). Conclusions: These findings support the large body of literature on the adverse effects of PM2.5, and suggest that adjustment for measurement error be considered in future studies where possible. [ABSTRACT FROM AUTHOR]

Background: Experimental evidence suggests that inhaled particles from vehicle exhaust have systemic effects on inflammation, endothelial activation and oxidative stress. In the present study we assess the relationships of short-term exposures with inflammatory endothelial activation and oxidative stress biomarker levels in a population of trucking industry workers.Methods: Blood and urine samples were collected pre and post-shift, at the beginning and end of a workweek from 67 male non-smoking US trucking industry workers. Concurrent measurements of microenvironment concentrations of elemental and organic carbon (EC & OC), and fine particulate matter (PM2.5) combined with time activity patterns allowed for calculation of individual exposures. Associations between daily and first and last-day average levels of exposures and repeated measures of intercellular and vascular cell adhesion molecule-1 (ICAM-1 & VCAM-1), interleukin 6 (IL-6) and C-reactive protein (CRP) blood levels and urinary 8-Hydroxy-2'-Deoxyguanosine (8-OHdG) were assessed using linear mixed effects models for repeated measures.Results: There was a statistically significant association between first and last-day average PM2.5 and 8-OHdG (21% increase, 95% CI: 2, 42%) and first and last-day average OC and IL-6 levels (18% increase 95% CI: 1, 37%) per IQR in exposure. There were no significant findings associated with EC or associations suggesting acute cross-shift effects.Conclusion: Our findings suggest associations between weekly average exposures of PM2.5 on markers of oxidative stress and OC on IL-6 levels. [ABSTRACT FROM AUTHOR]

Geospatial artificial intelligence (geoAI) is an emerging scientific discipline that combines innovations in spatial science, artificial intelligence methods in machine learning (e.g., deep learning), data mining, and high-performance computing to extract knowledge from spatial big data. In environmental epidemiology, exposure modeling is a commonly used approach to conduct exposure assessment to determine the distribution of exposures in study populations. geoAI technologies provide important advantages for exposure modeling in environmental epidemiology, including the ability to incorporate large amounts of big spatial and temporal data in a variety of formats; computational efficiency; flexibility in algorithms and workflows to accommodate relevant characteristics of spatial (environmental) processes including spatial nonstationarity; and scalability to model other environmental exposures across different geographic areas. The objectives of this commentary are to provide an overview of key concepts surrounding the evolving and interdisciplinary field of geoAI including spatial data science, machine learning, deep learning, and data mining; recent geoAI applications in research; and potential future directions for geoAI in environmental epidemiology. [ABSTRACT FROM AUTHOR]

Background: Findings from a recent prospective cohort study in California suggested increased risk of breast cancer associated with higher exposure to certain carcinogenic and estrogen-disrupting hazardous air pollutants (HAPs). However, to date, no nationwide studies have evaluated these possible associations. Our objective was to examine the impacts of mammary carcinogen and estrogen disrupting HAPs on risk of invasive breast cancer in a nationwide cohort.Methods: We assigned HAPs from the US Environmental Protection Agency's 2002 National Air Toxics Assessment to 109,239 members of the nationwide, prospective Nurses' Health Study II (NHSII). Risk of overall invasive, estrogen receptor (ER)-positive (ER+), and ER-negative (ER-) breast cancer with increasing quartiles of exposure were assessed in time-varying multivariable proportional hazards models, adjusted for traditional breast cancer risk factors.Results: A total of 3321 invasive cases occurred (2160 ER+, 558 ER-) during follow-up 1989-2011. Overall, there was no consistent pattern of elevated risk of the HAPs with risk of breast cancer. Suggestive elevations were only seen with increasing 1,2-dibromo-3-chloropropane exposures (multivariable adjusted HR of overall breast cancer = 1.12, 95% CI: 0.98-1.29; ER+ breast cancer HR = 1.09; 95% CI: 0.92, 1.30; ER- breast cancer HR = 1.14; 95% CI: 0.81, 1.61; each in the top exposure quartile compared to the lowest).Conclusions: Exposures to HAPs during adulthood were not consistently associated with an increased risk of overall or estrogen-receptor subtypes of invasive breast cancer in this nationwide cohort of women. [ABSTRACT FROM AUTHOR]

Background: Long-term exposure to particulate matter less than 2.5 μm in diameter (PM2.5) has been consistently associated with risk of all-cause mortality. The methods used to assess exposure, such as area averages, nearest monitor values, land use regressions, and spatio-temporal models in these studies are subject to measurement error. However, to date, no study has attempted to incorporate adjustment for measurement error into a long-term study of the effects of air pollution on mortality.Methods: We followed 108,767 members of the Nurses' Health Study (NHS) 2000-2006 and identified all deaths. Biennial mailed questionnaires provided a detailed residential address history and updated information on potential confounders. Time-varying average PM2.5 in the previous 12-months was assigned based on residential address and was predicted from either spatio-temporal prediction models or as concentrations measured at the nearest USEPA monitor. Information on the relationships of personal exposure to PM2.5 of ambient origin with spatio-temporal predicted and nearest monitor PM2.5 was available from five previous validation studies. Time-varying Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95 percent confidence intervals (95%CI) for each 10 μg/m(3) increase in PM2.5. Risk-set regression calibration was used to adjust estimates for measurement error.Results: Increasing exposure to PM2.5 was associated with an increased risk of mortality, and results were similar regardless of the method chosen for exposure assessment. Specifically, the multivariable adjusted HRs for each 10 μg/m(3) increase in 12-month average PM2.5 from spatio-temporal prediction models were 1.13 (95%CI:1.05, 1.22) and 1.12 (95%CI:1.05, 1.21) for concentrations at the nearest EPA monitoring location. Adjustment for measurement error increased the magnitude of the HRs 4-10% and led to wider CIs (HR = 1.18; 95%CI: 1.02, 1.36 for each 10 μg/m(3) increase in PM2.5 from the spatio-temporal models and HR = 1.22; 95%CI: 1.02, 1.45 from the nearest monitor estimates).Conclusions: These findings support the large body of literature on the adverse effects of PM2.5, and suggest that adjustment for measurement error be considered in future studies where possible. [ABSTRACT FROM AUTHOR]

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

Background: Radon and its decay products, a source of ionizing radiation, are primarily inhaled and can deliver a radiation dose to breast tissue, where they may continue to decay and emit DNA damage-inducing particles. Few studies have examined the relationship between radon and breast cancer.Methods: The Nurses' Health Study II (NHSII) includes U.S. female registered nurses who completed biennial questionnaires since 1989. Self-reported breast cancer was confirmed from medical records. County-level radon exposures were linked with geocoded residential addresses updated throughout follow-up. Time-varying Cox regression models adjusted for established breast cancer risk factors were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).Results: From 1989 to 2013, 3966 invasive breast cancer cases occurred among 112,639 participants. Increasing radon exposure was not associated with breast cancer risk overall (adjusted HR comparing highest to lowest quintile = 1.06, 95% CI: 0.94, 1.21, p for trend = 0.30). However, women in the highest quintile of exposure (≥74.9 Bq/m3) had a suggested elevated risk of ER-/PR- breast cancer compared to women in the lowest quintile (<27.0 Bq/m3) (adjusted HR = 1.38, 95% CI: 0.97, 1.96, p for trend = 0.05). No association was observed for ER+/PR+ breast cancer.Conclusions: Although we did not find an association between radon exposure and risk of overall or ER+/PR+ breast cancer, we observed a suggestive association with risk of ER-/PR- breast cancer. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC), the most commonly occurring type of primary liver cancer, has been increasing in incidence worldwide. Vitamin D, acquired from sunlight exposure, diet, and dietary supplements, has been hypothesized to impact hepatocarcinogenesis. However, previous epidemiologic studies examining the associations between dietary and serum vitamin D reported mixed results. The purpose of this study was to examine the association between ambient ultraviolet (UV) radiation exposure and HCC risk in the U.S.Methods: The Surveillance, Epidemiology, and End Results (SEER) database provided information on HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries across the U.S. Ambient UV exposure was estimated by linking the SEER county with a spatiotemporal UV exposure model using a geographic information system. Poisson regression with robust variance estimation was used to calculate incidence rate ratios (IRRs) and 95% confidence intervals (CIs) for the association between ambient UV exposure per interquartile range (IQR) increase (32.4 mW/m2) and HCC risk adjusting for age at diagnosis, sex, race, year of diagnosis, SEER registry, and county-level information on prevalence of health conditions, lifestyle, socioeconomic, and environmental factors.Results: Higher levels of ambient UV exposure were associated with statistically significant lower HCC risk (n = 56,245 cases; adjusted IRR per IQR increase: 0.83, 95% CI 0.77, 0.90; p < 0.01). A statistically significant inverse association between ambient UV and HCC risk was observed among males (p for interaction = 0.01) and whites (p for interaction = 0.01).Conclusions: Higher ambient UV exposure was associated with a decreased risk of HCC in the U.S. UV exposure may be a potential modifiable risk factor for HCC that should be explored in future research. [ABSTRACT FROM AUTHOR]

Background: Occupational exposures to ultrafine particles in the plume generated during laser hair removal procedures, the most commonly performed light based cosmetic procedure, have not been thoroughly characterized. Acute and chronic exposures to ambient ultrafine particles have been associated with a number of negative respiratory and cardiovascular health effects. Thus, the aim of this study was to measure airborne concentrations of particles in a diameter size range of 10 nm to 1 μm in procedure rooms during laser hair removal procedures.Methods: TSI Model 3007 Condensation Particle Counters were used to quantify the particle count concentrations in the waiting and procedure rooms of a dermatology office. Particle concentrations were sampled before, during, and after laser hair removal procedures, and characteristics of each procedure were noted by the performing dermatologist.Results: Twelve procedures were sampled over 4 days. Mean ultrafine particle concentrations in the waiting and procedure rooms were 14,957.4 particles/cm3 and 22,916.8 particles/cm3 (p < 0.0001), respectively. Compared to background ultrafine particle concentrations before the procedure, the mean concentration in the procedure room was 2.89 times greater during the procedure (p = 0.009) and 2.09 times greater after the procedure (p = 0.007). Duration of procedure (p = 0.006), body part (p = 0.013), and the use of pre-laser lotion/type of laser (p = 0.039), were the most important predictors of ultrafine particle concentrations. Use of a smoke evacuator (a recommended form of local exhaust ventilation) positioned at 30.5 cm from the source, as opposed to the recommended 1-2 in., lowered particle concentrations, but was not a statistically significant predictor (p = 0.49).Conclusions: Laser hair removal procedures can generate high exposures to ultrafine particles for dermatologists and other individuals performing laser hair removal, with exposure varying based on multiple determinants. [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. Yet, no prospective study has examined the association between PM and risk of Parkinson Disease. Thus, our goal was assess if exposure to particulate matter air pollution is related to risk of Parkinson's disease (PD) in the Nurses' Health Study (NHS), a large prospective cohort of women.Methods: Cumulative average exposure to different size fractions of PM up to 2 years before the onset of PD, was estimated using a spatio-temporal model by linking each individual's places of residence throughout the study with location-specific air pollution levels. We prospectively followed 115,767 women in the NHS, identified 508 incident PD cases and used multivariable Cox proportional hazards models to estimate the risk of PD associated with each size fraction of PM independently.Results: In models adjusted for age in months, smoking, region, population density, caffeine and ibuprofen intake, we observed no statistically significant associations between exposure to air pollution and PD risk. The relative risk (RR) comparing the top quartile to the bottom quartile of PM exposure was 0.99 (95% Confidence Intervals (CI): 0.84,1.16) for PM10 (≤10 microns in diameter), 1.08 (95% CI: 0.81, 1.45) for PM2.5 (≤2.5 microns in diameter), and 0.92 (95% CI: 0.71, 1.19) for PM(10-2.5) (2.5 to 10 microns in diameter).Conclusions: In this study, we found no evidence that exposure to air pollution is a risk factor for PD. [ABSTRACT FROM AUTHOR]