Effects of short- and long-term exposure to air pollution and meteorological factors on Meniere's disease.
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ABSTRACT:
SUBMITTER: Choi HG
PROVIDER: S-EPMC8352931 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:This paper assesses the effect of short-term exposure to particulate matter (PM) air pollution on human cognitive performance via a double cross over experimental design. Two distinct experiments were performed, both of which exposed subjects to low and high concentrations of PM. Firstly, subjects completed a series of cognitive tests after being exposed to low ambient indoor PM concentrations and elevated PM concentrations generated via candle burning, which is a well-known source of PM. Secondly, a different cohort underwent cognitive tests after being exposed to low ambient indoor PM concentrations and elevated ambient outdoor PM concentrations via commuting on or next to roads. Three tests were used to assess cognitive performance: Mini-Mental State Examination (MMSE), the Stroop Color and Word test, and Ruff 2 & 7 test. The results from the MMSE test showed a statistically robust decline in cognitive function after exposure to both the candle burning and outdoor commuting compared to ambient indoor conditions. The similarity in the results between the two experiments suggests that PM exposure is the cause of the short-term cognitive decline observed in both. The outdoor commuting experiment also showed a statistically significant short-term cognitive decline in automatic detection speed from the Ruff 2 and 7 selective attention test. The other cognitive tests, for both the candle and commuting experiments, showed no statistically significant difference between the high and low PM exposure conditions. The findings from this study are potentially far reaching; they suggest that elevated PM pollution levels significantly affect short term cognition. This implies average human cognitive ability will vary from city to city and country to country as a function of PM air pollution exposure.
| S-EPMC6546704 | biostudies-literature
Project description:Studies have reported associations between long-term air pollution exposures and cardiovascular mortality. The biological mechanisms connecting them remain uncertain.We examined associations of fine particles (PM2.5) and ozone with serum markers of cardiovascular disease risk in a cohort of midlife women. We obtained information from women enrolled at six sites in the multi-ethnic, longitudinal Study of Women's Health Across the Nation, including repeated measurements of high-sensitivity C-reactive protein, fibrinogen, tissue-type plasminogen activator antigen, plasminogen activator inhibitor type 1, and factor VIIc (factor VII coagulant activity). We obtained residence-proximate PM2.5 and ozone monitoring data for a maximum five annual visits, calculating prior year, 6-month, 1-month, and 1-day exposures and their relations to serum markers using longitudinal mixed models.For the 2,086 women studied from 1999 to 2004, PM2.5 exposures were associated with all blood markers except factor VIIc after adjusting for age, race/ethnicity, education, site, body mass index, smoking, and recent alcohol use. Adjusted associations were strongest for prior year exposures for high-sensitivity C-reactive protein (21% increase per 10 ?g/m³ PM2.5, 95% confidence interval [CI]: 6.6, 37), tissue-type plasminogen activator antigen (8.6%, 95% CI: 1.8, 16), and plasminogen activator inhibitor (35%, 95% CI: 19, 53). An association was also observed between year prior ozone exposure and factor VIIc (5.7% increase per 10 ppb ozone, 95% CI: 2.9, 8.5).Our findings suggest that prior year exposures to PM2.5 and ozone are associated with adverse effects on inflammatory and hemostatic pathways for cardiovascular outcomes in midlife women.
| S-EPMC4841679 | biostudies-literature
Project description:Previous studies have suggested an increased risk of ischemic heart disease related to air pollution. This study aimed to explore both the short-term and long-term effects of air pollutants on the risk of ischemic heart disease after adjusting for meteorological factors. The Korean National Health Insurance Service-Health Screening Cohort from 2002 to 2013 was used. Overall, 2155 participants with ischemic heart disease and 8620 control participants were analyzed. The meteorological data and air pollution data, including SO2 (ppm), NO2 (ppm), O3 (ppm), CO (ppm), and particulate matter (PM)10 (μg/m3), were analyzed using conditional logistic regression. Subgroup analyses were performed according to age, sex, income, and region of residence. One-month exposure to SO2 was related to 1.36-fold higher odds for ischemic heart disease (95% confidence interval [95% CI] 1.06-1.75). One-year exposure to SO2, O3, and PM10 was associated with 1.58- (95% CI 1.01-2.47), 1.53- (95% CI 1.27-1.84), and 1.14 (95% CI 1.02-1.26)-fold higher odds for ischemic heart disease. In subgroup analyses, the ≥ 60-year-old group, men, individuals with low income, and urban groups demonstrated higher odds associated with 1-month exposure to SO2. Short-term exposure to SO2 and long-term exposure to SO2, O3, and PM10 were related to ischemic heart disease.
| S-EPMC7930275 | biostudies-literature
Project description:We investigated associations between ambient air pollution and microvessel function measured by peripheral arterial tonometry between 2003 and 2008 in the Framingham Heart Study Offspring and Third Generation Cohorts. We measured particulate matter with aerodynamic diameter ?2.5 µm (PM2.5), black carbon, sulfates, particle number, nitrogen oxides, and ozone by using fixed monitors, and we determined moving averages for 1-7 days preceding vascular testing. We examined associations between these exposures and hyperemic response to ischemia and baseline pulse amplitude, a measure of arterial tone (n = 2,369). Higher short-term exposure to air pollutants, including PM2.5, black carbon, and particle number was associated with higher baseline pulse amplitude. For example, higher 3-day average PM2.5 exposure was associated with 6.3% higher baseline pulse amplitude (95% confidence interval: 2.0, 10.9). However, there were no consistent associations between the air pollution exposures assessed and hyperemic response. Our findings in a community-based sample exposed to relatively low pollution levels suggest that short-term exposure to ambient particulate pollution is not associated with vasodilator response, but that particulate air pollution is associated with baseline pulse amplitude, suggesting potentially adverse alterations in baseline vascular tone or compliance.
| S-EPMC4143083 | biostudies-literature
Project description:Elevated blood pressure (BP) has been proposed as a possible pathophysiological mechanism linking exposure to ambient air pollution and the increased risk of cardiovascular mortality and morbidity. In this study, we investigated the hourly relationship between ambient air pollutants and BP. BP measurements were extracted from the electronic health record database of the Seoul National University Bundang Hospital from February 2015 to June 2017. A total of 98,577 individual BP measurements were matched to the hourly levels of air pollutants. A generalized additive model was constructed for hour lags of 0-8 of air pollutants adjusting for age, sex, meteorological variables, and time trend. Systolic BP was shown to be significantly lower at 2-4?hours and 3-5?hours after increased levels of SO2 and CO, respectively (0.24?mmHg and 0.26?mmHg for an interquartile range, respectively). In contrast, O3 and NO2 were associated with significantly increased systolic BP at 3-5 lag hours and at 0-2 lag hours, respectively. BP elevation in association with O3 and NO2 was shown to be significantly greater in hypertensive patients than normotensive subjects. Our findings suggest that short-term exposure to air pollution may be associated with elevated BP.
| S-EPMC6937254 | biostudies-literature
Project description:BACKGROUND:Studies of air pollution exposure and arterial stiffness have reported inconsistent results and large studies employing the reference standard of arterial stiffness, carotid-femoral pulse-wave velocity (CFPWV), have not been conducted. AIM:To study long-term exposure to ambient fine particles (PM2.5), proximity to roadway, and short-term air pollution exposures in relation to multiple measures of arterial stiffness in the Framingham Heart Study. METHODS:We assessed central arterial stiffness using CFPWV, forward pressure wave amplitude, mean arterial pressure and augmentation index. We investigated long-and short-term air pollution exposure associations with arterial stiffness with linear regressions using long-term residential PM2.5 (2003 average from a spatiotemporal model using satellite data) and proximity to roadway in addition to short-term averages of PM2.5, black carbon, particle number, sulfate, nitrogen oxides, and ozone from stationary monitors. RESULTS:We examined 5842 participants (mean age 51?±?16, 54% women). Living closer to a major roadway was associated with higher arterial stiffness (0.11?m/s higher CFPWV [95% CI: 0.01, 0.22] living <50?m vs 400???1000?m). We did not observe association between arterial stiffness measures and long-term PM2.5 or short-term levels of PM2.5, particle number, sulfate or ozone. Higher levels of black carbon and nitrogen oxides in the previous days were unexpectedly associated with lower arterial stiffness. CONCLUSIONS:Long-term exposure to PM2.5 was not associated with arterial stiffness but positive associations with living close to a major road may suggest that pollutant mixtures very nearby major roads, rather than PM2.5, may affect arterial stiffness. Furthermore, short-term air pollution exposures were not associated with higher arterial stiffness.
| S-EPMC6221919 | biostudies-literature
Project description:There is strong evidence that short-run fluctuations in air pollution negatively impact infant health and contemporaneous adult health, but there is less evidence on the causal link between long-term exposure to air pollution and increased adult mortality. This project estimates the impact of long-term exposure to air pollution on mortality by leveraging quasi-random variation in pollution levels generated by wind patterns near major highways. I combine geocoded data on the residence of every decedent in Los Angeles over three years, high-frequency wind data, and Census short form data. Using these data, I estimate the effect of downwind exposure to highway-generated pollutants on the age-specific mortality rate by using orientation to the nearest major highway as an instrument for pollution exposure. I find that doubling the percentage of time spent downwind of a highway increases mortality among individuals 75 or older by 3.8%-6.5%. These estimates are robust and imply significant loss of life years.
| S-EPMC7445412 | 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.
| S-EPMC5817954 | biostudies-literature
Project description:ImportancePsoriasis is a chronic inflammatory disease with a relapsing-remitting course. Selected environmental factors such as infections, stressful life events, or drugs may trigger disease flares. Whether air pollution could trigger psoriasis flares is still unknown.ObjectiveTo investigate whether short-term exposure to environmental air pollution is associated with psoriasis flares.Design, setting, and participantsThis observational study with both case-crossover and cross-sectional design retrospectively analyzed longitudinal data from September 2013 to January 2020 from patients with chronic plaque psoriasis consecutively attending the outpatient dermatologic clinic of the University Hospital of Verona. For the case-crossover analysis, patients were included who had at least 1 disease flare, defined as Psoriasis Area and Severity Index (PASI) increase of 5 or greater between 2 consecutive assessments in a time frame of 3 to 4 months. For the cross-sectional analysis, patients were included who received any systemic treatment for 6 or more months, with grade 2 or higher consecutive PASI assessment.Main outcomes and measuresWe compared the mean and cumulative (area under the curve) concentrations of several air pollutants (carbon monoxide, nitrogen dioxide, other nitrogen oxides, benzene, coarse particulate matter [PM; 2.5-10.0 μm in diameter, PM10] and fine PM [<2.5 μm in diameter, PM2.5]) in the 60 days preceding the psoriasis flare and the control visits.ResultsA total of 957 patients with plaque psoriasis with 4398 follow-up visits were included in the study. Patients had a mean (SD) age of 61 (15) years and 602 (62.9%) were men. More than 15 000 measurements of air pollutant concentration from the official, open-source bulletin of the Italian Institute for Environmental Protection and Research (ISPRA) were retrieved. Among the overall cohort, 369 (38.6%) patients with psoriasis flare were included in the case-crossover study. We found that concentrations of all pollutants were significantly higher in the 60 days before psoriasis flare (median PASI at the flare 12; IQR, 9-18) compared with the control visit (median PASI 1; IQR, 1-3, P < .001). In the cross-sectional analysis, exposure to mean PM10 over 20 μg/m3 and mean PM2.5 over 15 μg/m3 in the 60 days before assessment were associated with a higher risk of PASI 5 or greater point worsening (adjusted odds ratio [aOR], 1.55; 95% CI, 1.21-1.99; and aOR, 1.25; 95% CI, 1.0-1.57, respectively). Sensitivity analyses that stratified for trimester of evaluation, with various lag of exposure and adjusting for type of treatment, yielded similar results.Conclusions and relevanceThe findings of this case-crossover and cross-sectional study suggest that air pollution may be a trigger factor for psoriasis flare.
| S-EPMC8851365 | biostudies-literature
Project description:This study is aimed at defining the relationship between a set of environmental factors and childhood HFMD and then at estimating the related effect. The 16 environmental factors included meteorological, air pollution, and sunspot. A traditional TSR modified by using susceptible-infectious-recovery models and distribution lag nonlinear model was applied to estimate the short-term effects of daily environmental factors on children HFMD occurrence in 2014-2018 with adjustment of potential confounding factors. A total of 70,027 children aged 0-15 years with HFMD were enrolled. No significant effect was observed for daily sunspot numbers and average visibility. We found positive effects of the ambient average temperature, with an approximately m-shaped curve of the overall cumulative relationship, peaking at 25.6 °C with a relative risk (RR) of 1.45 (95% confidence intervals 1.21-1.73). The largest RR value of hot effect was achieved on the current day and then decreased by 2 days (total group, male group, and scatter group) or 1 day (female group and nursery group), and the effect lasted about 6 to 8 days from the lag 4 or lag 6 day. A greater association of temperature with HFMD for the female group and the scattered group was observed. This study suggests that ambient average temperature might be a risk factor for children HFMD in Tianjin. Further studies are warranted to confirm these findings.
| S-EPMC7311115 | biostudies-literature