Ambient PM2.5 air pollution exposure and hepatocellular carcinoma incidence in the United States.
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ABSTRACT:
SUBMITTER: VoPham T
PROVIDER: S-EPMC5940508 | biostudies-literature | 2018 Jun
REPOSITORIES: biostudies-literature
Publications
Ambient PM<sub>2.5</sub> air pollution exposure and hepatocellular carcinoma incidence in the United States.
VoPham Trang T Bertrand Kimberly A KA Tamimi Rulla M RM Laden Francine F Hart Jaime E JE
Cancer causes & control : CCC 20180425 6
<h4>Purpose</h4>To conduct the first epidemiologic study prospectively examining the association between particulate matter air pollution < 2.5 µm in diameter (PM<sub>2.5</sub>) exposure and hepatocellular carcinoma (HCC) risk in the U.S.<h4>Methods</h4>Surveillance, Epidemiology, and End Results (SEER) provided information on HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries across the U.S. Ambient PM<sub>2.5</sub> exposure was estimated by linking the SEER co ...[more]
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Project description: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.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.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).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.
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Project description:Importance:Ambient fine particulate matter (PM2.5) air pollution is associated with increased risk of several causes of death. However, epidemiologic evidence suggests that current knowledge does not comprehensively capture all causes of death associated with PM2.5 exposure. Objective:To systematically identify causes of death associated with PM2.5 pollution and estimate the burden of death for each cause in the United States. Design, Setting, and Participants:In a cohort study of US veterans followed up between 2006 and 2016, ensemble modeling was used to identify and characterize morphology of the association between PM2.5 and causes of death. Burden of death associated with PM2.5 exposure in the contiguous United States and for each state was then estimated by application of estimated risk functions to county-level PM2.5 estimates from the US Environmental Protection Agency and cause-specific death rate data from the Centers for Disease Control and Prevention. Main Outcomes and Measures:Nonlinear exposure-response functions of the association between PM2.5 and causes of death and burden of death associated with PM2.5. Exposures:Annual mean PM2.5 levels. Results:A cohort of 4?522?160 US veterans (4?243?462 [93.8%] male; median [interquartile range] age, 64.1 [55.7-75.5] years; 3?702?942 [82.0%] white, 667?550 [14.8%] black, and 145?593 [3.2%] other race) was followed up for a median (interquartile range) of 10.0 (6.8-10.2) years. In the contiguous United States, PM2.5 exposure was associated with excess burden of death due to cardiovascular disease (56?070.1 deaths [95% uncertainty interval {UI}, 51?940.2-60?318.3 deaths]), cerebrovascular disease (40?466.1 deaths [95% UI, 21?770.1-46?487.9 deaths]), chronic kidney disease (7175.2 deaths [95% UI, 5910.2-8371.9 deaths]), chronic obstructive pulmonary disease (645.7 deaths [95% UI, 300.2-2490.9 deaths]), dementia (19?851.5 deaths [95% UI, 14?420.6-31?621.4 deaths]), type 2 diabetes (501.3 deaths [95% UI, 447.5-561.1 deaths]), hypertension (30?696.9 deaths [95% UI, 27?518.1-33?881.9 deaths]), lung cancer (17?545.3 deaths [95% UI, 15?055.3-20?464.5 deaths]), and pneumonia (8854.9 deaths [95% UI, 7696.2-10?710.6 deaths]). Burden exhibited substantial geographic variation. Estimated burden of death due to nonaccidental causes was 197?905.1 deaths (95% UI, 183?463.3-213?644.9 deaths); mean age-standardized death rates (per 100?000) due to nonaccidental causes were higher among black individuals (55.2 [95% UI, 50.5-60.6]) than nonblack individuals (51.0 [95% UI, 46.4-56.1]) and higher among those living in counties with high (65.3 [95% UI, 56.2-75.4]) vs low (46.1 [95% UI, 42.3-50.4]) socioeconomic deprivation; 99.0% of the burden of death due to nonaccidental causes was associated with PM2.5 levels below standards set by the US Environmental Protection Agency. Conclusions and Relevance:In this study, 9 causes of death were associated with PM2.5 exposure. The burden of death associated with PM2.5 was disproportionally borne by black individuals and socioeconomically disadvantaged communities. Effort toward cleaner air might reduce the burden of PM2.5-associated deaths.
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Project description:This study aimed to investigate whether long-term exposure to airborne hydrocarbons, including volatile organic compounds, increases the risk of developing retinal vein occlusion (RVO) among the population of Taiwan. A retrospective cohort study involving 855,297 people was conducted. Cox proportional hazards regression analysis fitted the multiple pollutant models for two targeted pollutants, including total hydrocarbons (THC), nonmethane hydrocarbons (NMHC) were used, and the risk of RVO was estimated. The chi-squared test and one-way analysis of variance were used to test differences in demographics and comorbidity distribution among tertiles of the targeted pollutants. Before controlling for multiple pollutants, hazard ratios for the overall population were 19.88 (95% CI: 17.56-22.50) at 0.51-ppm increases in THC and 4.33 (95% CI: 3.97-4.73) at 0.27-ppm increases in NMHC. The highest adjusted hazard ratios for different multiple pollutant models of each targeted pollutant were statistically significant (all p values were ?0.05) for all patients at 29.67 (95% CI: 25.57-34.42) for THC and 16.24 (95% CI: 14.14-18.65) for NMHC. Our findings suggest that long-term exposure to THC and NMHC contribute to RVO development.
| S-EPMC6759191 | biostudies-literature
Project description:BackgroundEpidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent.MethodsIn 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.ResultsOf 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89-3.14 per 10-5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors.ConclusionWe found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.
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Project description:Background: Circadian misalignment may increase the risk of developing hepatocellular carcinoma (HCC). The aim of this study was to examine the association between distance from time zone meridian, a proxy for circadian misalignment, and HCC risk in the United States adjusting for known HCC risk factors.Methods: Surveillance, Epidemiology, and End Results (SEER) provided information on 56,347 HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries in the United States. Distance from time zone meridian was estimated using the location of each SEER county's Center of Population in 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 distance from time zone meridian and HCC risk adjusting for individual-level age at diagnosis, sex, race/ethnicity, year of diagnosis, SEER registry, and county-level prevalence of health conditions, lifestyle factors, shift work occupation, socioeconomic status, and demographic and environmental factors.Results: A 5-degree increase in longitude moving east to west within a time zone was associated with a statistically significant increased risk for HCC (IRR, 1.07; 95% CI, 1.01-1.14, P = 0.03). A statistically significant positive association was observed among those <65 years old, while no association was observed among individuals ?65 years old (Pfor interaction < 0.01).Conclusions: Circadian misalignment from residing in the western region of a time zone may impact hepatocarcinogenesis.Impact: Circadian misalignment may be an independent risk factor for HCC. Cancer Epidemiol Biomarkers Prev; 27(7); 719-27. ©2018 AACR.
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Project description:Olfactory dysfunction affects millions of people worldwide. This sensory impairment is associated with neurodegenerative disease and significantly decreased quality of life. Exposure to airborne pollutants has been implicated in olfactory decline, likely due to the anatomic susceptibility of the olfactory nerve to the environment. Historically, studies have focused on occupational exposures, but more recent studies have considered effects from exposure to ambient air pollutants.To examine all relevant human data evaluating a link between ambient pollution exposure and olfaction and to review supporting animal data in order to examine potential mechanisms for pollution-associated olfactory loss.We identified and reviewed relevant articles from 1950 to 2015 using PubMed and Web of Science and focusing on human epidemiologic and pathophysiologic studies. Animal studies were included only to support pertinent data on humans. We reviewed findings from these studies evaluating a relationship between environmental pollutant exposure and olfactory function.We identified and reviewed 17 articles, with 1 additional article added from a bibliography search, for a total of 18 human studies. There is evidence in human epidemiologic and pathologic studies that increased exposure to ambient air pollutants is associated with olfactory dysfunction. However, most studies have used proxies for pollution exposure in small samples of convenience. Human pathologic studies, with supporting animal work, have also shown that air pollution can contact the olfactory epithelium, translocate to the olfactory bulb, and migrate to the olfactory cortex. Pollutants can deposit at each location, causing direct damage and disruption of tissue morphology or inducing local inflammation and cellular stress responses.Ambient air pollution may impact human olfactory function. Additional studies are needed to examine air pollution-related olfactory impacts on the general population using measured pollution exposures and to link pollution exposure with olfactory dysfunction and related pathology. Citation: Ajmani GS, Suh HH, Pinto JM. 2016. Effects of ambient air pollution exposure on olfaction: a review. Environ Health Perspect 124:1683-1693;?http://dx.doi.org/10.1289/EHP136.
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Project description:Exposure to higher levels of ambient air pollution is a known risk factor for cardiovascular disease but long-term effects of pollution exposure on the pulmonary vessels are unknown.MethodsAmong 2428 Framingham Heart Study participants who underwent chest computed tomography (CT) between 2008 and 2011, pulmonary vascular volumes were calculated by image analysis, including the total vascular volume and small vessel volume (cross-sectional area <5 mm2; BV5 defined as small vessel volume). Using spatiotemporal models and participant home address, we assigned 1-year (2008) and 5-year (2004-2008) average concentrations of fine particulate matter (PM2.5), elemental carbon (EC), and ground-level ozone (O3), and distance to major roadway. We examined associations of 1- and 5-year exposures, and distance to road, with CT vascular volumes using multivariable linear regression models.ResultsThere was a consistent negative association of higher O3 with lower small vessel volumes, which persisted after adjustment for distance to road. Per interquartile range (IQR) of 2008 O3, BV5 was 0.34 mL lower (95% confidence intervals [CI], -0.61 to -0.06; P = 0.02), with similar results for 5-year exposure. One-year EC exposure and closer proximity to road were weakly associated with small vessel volumes; BV5 was 0.18 mL higher per IQR of 2008 EC (95% CI, -0.05 to 0.42; P = 0.13) and 0.40 mL higher per IQR closer proximity to road (95% CI: -0.10 to 0.89; P = 0.12). PM2.5 was not associated with small vascular volumes; BV5 was 0.26 mL lower per IQR of 2008 PM2.5 (95% CI: -0.68 to 0.16; P = 0.22).ConclusionsAmong community-dwelling adults living in the northeastern United States, higher exposure to O3 was associated with lower small pulmonary vessel volumes on CT.
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Project description:This research examined the relationship between colon cancer risks and pollution in various areas of Thailand, using satellites to gather quantities of aerosols in the atmosphere. Bayesian hierarchical spatio-temporal model and the Poisson log-linear model were used to examine the incidence rates of colon cancer standardized by national references; from the database of the National Health Security Office, Ministry of Public Health of Thailand and NASA's database from aerosol diagnostics model. Modern-Era Retrospective Analysis for Research and Applications, Version 2 (MERRA-2) was used to explore disease-gender-specific spatio-temporal patterns of colon cancer incidences and accumulated air pollution-related cancers in Thailand between 2010 and 2016. A total of 59,605 patients were selected for the study. Due to concerns regarding statistical reliability between aerosol diagnostics model and colon cancer incidences, the posterior probabilities of risk appeared the most in dust PM2.5. It could be interpreted as relative risk in every increase of 10 ?g/m3 in black carbon, organic carbon, and dust-PM2.5 levels were associated respectively with an increase of 4%, 4%, and 15% in the risks of colon cancer. A significant increase in the incidence of colon cancer with accumulated ambient air quality raised concerns regarding the prevention of air pollution. This study utilized data based on the incidences of colon cancer; the country's database and linked cancer data to pollution. According to the database from NASA's technology, this research has never been conducted in Thailand.
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