Ambient particulate matter, ozone, and neurologic symptoms in U.S. Gulf states adults.
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ABSTRACT:
SUBMITTER: Werder EJ
PROVIDER: S-EPMC8367062 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundStyrene is an established neurotoxicant at occupational levels, but effects at levels relevant to the general population have not been studied. We examined the neurologic effects of environmental styrene exposure among U.S. Gulf coast residents.MethodsWe used National Air Toxics Assessment (NATA) 2011 estimates of ambient styrene concentrations to assign exposure levels for 21,962 non-diabetic Gulf state residents, and additionally measured blood styrene concentration in a subset of participants (n = 874). Neurologic symptoms, as well as detailed covariate information, were ascertained via telephone interview. We used log-binomial regression to estimate prevalence ratios (PR) and 95% confidence intervals (95% CI) for cross-sectional associations between both ambient and blood styrene levels and self-reported neurologic symptoms. We estimated associations independently for ten unique symptoms, as well as for the presence of any neurologic, central nervous system (CNS), or peripheral nervous system (PNS) symptoms. We also examined heterogeneity of associations with estimated ambient styrene levels by race and sex.ResultsOne-third of participants reported at least one neurologic symptom. The highest quartile of estimated ambient styrene was associated with one or more neurologic (PR, 1.12; 95% CI: 1.07,1.18), CNS (PR, 1.17; 95% CI: 1.11,1.25), and PNS (PR, 1.16; 95% CI: 1.09,1.25) symptom. Results were less consistent for biomarker analyses, but blood styrene level was suggestively associated with nausea (PR, 1.78; 95% CI: 1.04, 3.03). In stratified analyses, we observed the strongest effects among non-White participants.ConclusionsIncreasing estimated ambient styrene concentration was consistently associated with increased prevalence of neurologic symptoms. Associations between blood styrene levels and some neurologic symptoms were suggestive. Environmental styrene exposure levels may be sufficient to elicit symptomatic neurotoxic effects.
| S-EPMC6712572 | biostudies-literature
Project description:The contribution of precursor emissions from 17 mobile source sectors to ambient ozone and fine particulate matter levels across the U.S. were evaluated, using the CAMx photochemical model, to identify which mobile source sectors are projected to have the largest impacts on air pollution in 2025. Both onroad and nonroad sectors contribute considerably to projected air pollution across much of the country. Summer ozone season ozone contributions between 2 and 5 ppb, which are among the highest levels presented on the maps of mobile source sectors, are largely found in the southeast United States from the onroad sectors, most notably light-duty and heavy-duty vehicles, and along the coastline from the Category 3 (C3) marine sector. Annual average PM2.5 contributions between 0.5 to 0.9 μg/m3, which are among the highest levels presented on the maps of mobile source sectors, are found throughout the Midwest and along portions of the east and west coast from onroad sectors as well as nonroad diesel and rail sectors. Additionally, contributions of precursor emissions to ambient ozone and PM2.5 levels were evaluated to understand the range of impacts from precursors in the various mobile source sectors. For most mobile source sectors, in most locations, NOX emissions contributed more to ozone than VOC emissions, and secondary PM2.5 contributed more to ambient PM2.5 than primary PM2.5. The largest ozone levels on the maps showing contributions from mobile source NOX emissions tended to be between 2 and 5 ppb, while the largest ozone levels on the maps showing contributions from mobile source VOC emissions tended to be between 0.9 and 2 ppb, except for southern California where ozone contributions from VOC emissions from onroad light duty vehicles were between 2 and 5 ppb. The largest contributions to ambient PM2.5 on the maps showing primary and secondary contributions from mobile source sectors tended to be between 0.1 and 0.5 μg/m3. The contribution from primary PM2.5 extended over localized areas (urban-scale) and the contribution from secondary PM2.5 extended over more regional (multi-state) areas.
| S-EPMC6192431 | biostudies-literature
Project description:BackgroundThe chemicals benzene, toluene, ethylbenzene, and xylenes (BTEX) are neuroactive. Exposures often co-occur because they share common sources. We examined neurologic effects of environmental BTEX exposure among U.S. Gulf coast residents taking into account concomitant exposures.MethodsWe measured blood concentrations of BTEX in 690 Gulf state residents. Neurologic symptoms were ascertained via telephone interview. We used log-binomial regression to estimate associations between blood BTEX levels and self-reported neurologic symptoms independently for the presence of any neurologic, central (CNS), or peripheral nervous system (PNS) symptoms. We estimated associations in single chemical models mutually adjusted for co-occurring BTEX and used weighted quantile sum regression to model associations between the combined BTEX mixture and neurologic symptoms.ResultsHalf (49%) of participants reported at least one neurologic symptom. Each BTEX chemical was associated with increased CNS and PNS symptoms in single-chemical models comparing the highest to lowest quartile of exposure. After adjusting for coexposures, benzene was associated with CNS symptoms among all participants (PR = 2.13, 95% CI: 1.27, 3.57) and among nonsmokers (PR = 2.30, 95% CI: 1.35, 3.91). After adjusting for coexposures, associations with toluene were apparent only for reporting multiple PNS symptoms (PR = 2.00, 95% CI: 0.96, 4.16). In mixture analyses, a one-quartile increase in BTEX exposure was associated with neurologic symptoms (OR = 1.47, 95% CI: 1.11, 1.98). The weighted quantile sum index weighted benzene most heavily, which was consistent with single chemical analyses.ConclusionsIncreasing blood benzene concentration was associated with increased prevalence of CNS symptoms. In this sample, BTEX-associated neurologic effects are likely driven by exposure to benzene and, to a lesser extent, toluene.
| S-EPMC6571161 | biostudies-literature
Project description:BackgroundThe associations of long-term exposure to air pollutants in the presence of asthmatic symptoms remain inconclusive and the joint effects of air pollutants as a mixture are unclear.ObjectiveWe aimed to investigate the individual and joint associations of long-term exposure to ambient fine particulate matter (PM2.5) and daily 8-hour maximum ozone concentrations (MDA8 O3) in the presence of asthmatic symptoms in Chinese adults.MethodsData were derived from the World Health Organization Study on Global Ageing and Adult Health (WHO SAGE) cohort study among adults aged 50 years or older, which was implemented in 1 municipality and 7 provinces across China during 2007-2018. Annual average MDA8 O3 and PM2.5 at individual residential addresses were estimated by an iterative random forest model and a satellite-based spatiotemporal model, respectively. Participants who were diagnosed with asthma by a doctor or taking asthma-related therapies or experiencing related conditions within the past 12 months were recorded as having asthmatic symptoms. The individual associations of PM2.5 and MDA8 O3 with asthmatic symptoms were estimated by a Cox proportional hazards regression model, and the joint association was estimated by a quantile g-computation model. A series of subgroup analyses was applied to examine the potential modifications of some characteristics. We also calculated the population-attributable fraction (PAF) of asthmatic symptoms attributed to PM2.5 and MDA8 O3.ResultsA total of 8490 adults older than 50 years were included, and the average follow-up duration was 6.9 years. During the follow-up periods, 586 (6.9%) participants reported asthmatic symptoms. Individual effect analyses showed that the risk of asthmatic symptoms was positively associated with MDA8 O3 (hazard ratio [HR] 1.12, 95% CI 1.01-1.24, for per quantile) and PM2.5 (HR 1.18, 95% CI 1.05-1.31, for per quantile). Joint effect analyses showed that per equal quantile increment of MDA8 O3 and PM2.5 was associated with an 18% (HR 1.18, 95% CI 1.05-1.33) increase in the risk of asthmatic symptoms, and PM2.5 contributed more (68%) in the joint effects. The individual PAFs of asthmatic symptoms attributable to PM2.5 and MDA8 O3 were 2.86% (95% CI 0.17%-5.50%) and 4.83% (95% CI 1.42%-7.25%), respectively, while the joint PAF of asthmatic symptoms attributable to exposure mixture was 4.32% (95% CI 1.10%-7.46%). The joint associations were greater in participants with obesity, in urban areas, with lower family income, and who used unclean household cooking fuel.ConclusionsLong-term exposure to PM2.5 and MDA8 O3 may individually and jointly increase the risk of asthmatic symptoms, and the joint effects were smaller than the sum of individual effects. These findings informed the importance of joint associations of long-term exposure to air pollutants with asthma.
| S-EPMC10436124 | biostudies-literature
Project description:BackgroundMetals have been shown to have a wide range of neurologic effects across the life course, but most studies consider neurodevelopment or neurodegenerative diseases in older adults. We investigated exposure to metals during adulthood in association with subclinical neurologic endpoints, considering the metals individually and as a mixture, and potential interactions among exposures.MethodsWe measured blood levels of cadmium, lead, mercury, manganese, and selenium in 1007 Gulf state residents and estimated cross-sectional associations between ranked levels of blood metals and the presence of self-reported neurologic symptoms. Single pollutant models were mutually adjusted for other metals and we used quantile g-computation to evaluate associations with exposure to the combined mixture. In stratified analyses, we assessed heterogeneity by smoking and blood selenium.ResultsThe highest quartile of cadmium was associated with a higher prevalence of central nervous system symptoms (prevalence ratio [PR] = 1.50; 95% confidence interval [CI] = 1.13, 1.99), with stronger associations among nonsmokers (PR = 1.63; 95% CI = 1.11, 2.38) and those with low selenium (PR = 2.29, 95% CI = 1.50, 3.49). Selenium also modified associations between lead and peripheral nervous system symptoms, with increased symptoms in the low selenium group at all quartiles of exposure (P-trend = 0.07). Conversely, those with the highest co-exposure to mercury and selenium had reduced neurologic symptoms (PR = 0.73, 95% CI = 0.55, 0.96). Results of the mixture analysis were consistent with single chemical results.ConclusionsCadmium exhibited the most consistent relationship with increased neurologic symptoms, though lead was an important exposure in subgroup analyses. Selenium may modify subclinical neurotoxic effects of metals at non-occupational levels in adults.
| S-EPMC7727467 | biostudies-literature
Project description:BackgroundEpidemiological studies report fairly consistent associations between various air pollution metrics and autism spectrum disorder (ASD), with some elevated risks reported for different prenatal and postnatal periods.ObjectivesTo examine associations between ASD and ambient fine particulate matter (PM2.5) and ozone concentrations during the prenatal period through the second year of life in a case-control study.MethodsASD cases (n = 428) diagnosed at Cincinnati Children's Hospital Medical Center were frequency matched (15:1) to 6420 controls from Ohio birth records. We assigned daily PM2.5 and ozone estimates for 2005-2012 from US EPA's Fused Air Quality Surface Using Downscaling model to each participant for each day based on the mother's census tract of residence at birth. We calculated adjusted odds ratios (aORs) using logistic regression across continuous and categorical exposure window averages (trimesters, first and second postnatal years, and cumulative measure), adjusting for maternal- and birth-related confounders, both air pollutants, and multiple temporal exposure windows.ResultsWe detected elevated aORs for PM2.5 during the 2nd trimester, 1st year of life, and a cumulative period from pregnancy through the 2nd year (aOR ranges across categories: 1.41-1.44, 1.54-1.84, and 1.41-1.52 respectively), and for ozone in the 2nd year of life (aOR range across categories: 1.29-1.42). Per each change in IQR, we observed elevated aORs for ozone in the 3rd trimester, 1st and 2nd years of life, and the cumulative period (aOR range: 1.19-1.27) and for PM2.5 in the 2nd trimester, 1st year of life, and the cumulative period (aOR range: 1.11-1.17).DiscussionWe saw limited evidence of linear exposure-response relationships for ASD with increasing air pollution, but the elevated aORs detected for PM2.5 in upper exposure categories and per IQR unit increases were similar in magnitude to those reported in previous studies, especially for postnatal exposures.
| S-EPMC7232936 | biostudies-literature
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Keywords: gene expression
2007-12-01 | GSE9465 | GEO
Project description:Short-term effects of air pollution exposure on respiratory disease mortality are well established. However, few studies have examined the effects of long-term exposure, and among those that have, results are inconsistent.To evaluate long-term association between ambient ozone, fine particulate matter (PM2.5, particles with an aerodynamic diameter of 2.5 ?m or less), and chronic lower respiratory disease (CLRD) mortality in the contiguous United States.We fit Bayesian hierarchical spatial Poisson models, adjusting for five county-level covariates (percentage of adults aged ?65 years, poverty, lifetime smoking, obesity, and temperature), with random effects at state and county levels to account for spatial heterogeneity and spatial dependence.We derived county-level average daily concentration levels for ambient ozone and PM2.5 for 2001-2008 from the U.S. Environmental Protection Agency's down-scaled estimates and obtained 2007-2008 CLRD deaths from the National Center for Health Statistics. Exposure to ambient ozone was associated with an increased rate of CLRD deaths, with a rate ratio of 1.05 (95% credible interval, 1.01-1.09) per 5-ppb increase in ozone; the association between ambient PM2.5 and CLRD mortality was positive but statistically insignificant (rate ratio, 1.07; 95% credible interval, 0.99-1.14).This study links air pollution exposure data with CLRD mortality for all 3,109 contiguous U.S. counties. Ambient ozone may be associated with an increased rate of death from CLRD in the contiguous United States. Although we adjusted for selected county-level covariates and unobserved influences through Bayesian hierarchical spatial modeling, the possibility of ecologic bias remains.
| S-EPMC4937454 | biostudies-literature
Project description: Not available
| S-EPMC6444659 | biostudies-literature
