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Short-term air pollution exposure aggravates Parkinson's disease in a population-based cohort.

ABSTRACT: Increasing experimental evidence has suggested air pollution as new risk factor for neurological disease. Although long-term exposure is reportedly related to neurological disease, information on association with short-term exposure is scarce. We examined the association of short-term exposure to particles <2.5??m (PM_2.5), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), ozone (O₃), and carbon monoxide (CO) with PD aggravation in Seoul from the National Health Insurance Service-National Sample Cohort, Korea during 2002-2013. PD aggravation cases were defined as emergency hospital admissions for primarily diagnosed PD and analyzed with a case-crossover analysis, designed for rare acute outcomes. Pollutants concentrations on case and control days were compared and effect modifications were explored. A unit increase in 8-day moving average of concentrations was significantly associated with PD aggravation. The association was consistent for PM_2.5 (odds ratio [95% confidence interval]: 1.61 [1.14-2.29] per 10??g/m³), NO₂ (2.35 [1.39-3.97] per 10?ppb), SO₂ (1.54 [1.11-2.14] per 1?ppb), and CO (1.46 [1.05-2.04] per 0.1?ppm). The associations were stronger in women, patients aged 65-74 years, and cold season, but not significant. In conclusion, short-term air pollution exposure increased risk of PD aggravation, and may cause neurological disease progression in humans.

SUBMITTER: Lee H

PROVIDER: S-EPMC5353743 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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Short-term air pollution exposure aggravates Parkinson's disease in a population-based cohort.

Lee Hyewon H Myung Woojae W Kim Doh Kwan DK Kim Satbyul Estella SE Kim Clara Tammy CT Kim Ho H

Scientific reports 20170316

Increasing experimental evidence has suggested air pollution as new risk factor for neurological disease. Although long-term exposure is reportedly related to neurological disease, information on association with short-term exposure is scarce. We examined the association of short-term exposure to particles <2.5 μm (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO) with PD aggravation in Seoul from the National H ...[more]

PMID: 28300224

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Project description:Previous studies revealed that chronic exposure to air pollution can significantly increase the risk of the development of Parkinson's disease (PD), but this relationship is inconclusive as large-scale prospective studies are limited and the results are inconsistent. Therefore, the purpose of this study was to ascertain the adverse health effects of air pollution exposure in a nationwide population using a longitudinal approach.We conducted a nested case-control study using the National Health Insurance Research Dataset (NHIRD), which consisted of 1,000,000 beneficiaries in the National Health Insurance Program (NHI) in the year 2000 and their medical records from 1995 to 2013 and using public data on air pollution concentrations from monitoring stations across Taiwan released from the Environmental Protection Administration to identify people with ages ≥ 40 years living in areas with monitoring stations during 1995-1999 as study subjects. Then, we excluded subjects with PD, dementia, stroke and diabetes diagnosed before Jan. 1, 2000 and obtained 54,524 subjects to follow until Dec. 31, 2013. In this observational period, 1060 newly diagnosed PD cases were identified. 4240 controls were randomly selected from those without PD using a matching strategy for age, sex, the year of PD diagnosis and the year of entering the NHI program at a ratio of 1:4. Ten elements of air pollution were examined, and multiple logistic regression models were used to measure their risks in subsequent PD development.The incidence of PD in adults aged ≥ 40 years was 1.9%, and the median duration for disease onset was 8.45 years. None of the chemical compounds (SO2, O3, CO, NOx, NO, NO2, THC, CH4, or NMHC) significantly affected the incidence of PD except for particulate matter. PM10 exposure showed significant effects on the likelihood of PD development (T3 level: > 65μg/m3 versus T1 level: ≤ 54μg/m3; OR = 1.35, 95% CI = 1.12-1.62, 0.001 ≤ P < 0.01). In addition, comorbid conditions such as dementia (ORs = 3.53-3.93, Ps < 0.001), stroke (ORs = 2.99-3.01, Ps < 0.001), depression (ORs = 2.51-2.64, Ps < 0.001), head injury (ORs = 1.24-1.29, 0.001 ≤ Ps < 0.01 or 0.01 ≤ Ps < 0.05), sleep disorder (OR = 1.23-1.26, 0.001 ≤ Ps < 0.01), and hypertension (ORs = 1.18-1.19, 0.01 ≤ Ps < 0.05) also significantly increased the risk for PD development.Although PM10 plays a significant role in PD development, the associated chemical/metal compounds that are capable of inducing adverse biological mechanisms still warrant further exploration. Because of a link between comorbid conditions and PM exposure, research on the causal relationship between long-term exposure to PM and the development of PD should be considered with caution because other possible modifiers or mediators, comorbid diseases in particular, may be involved.

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.

Project description:The US Environmental Protection Agency is required to reexamine its National Ambient Air Quality Standards (NAAQS) every 5 years, but evidence of mortality risk is lacking at air pollution levels below the current daily NAAQS in unmonitored areas and for sensitive subgroups.To estimate the association between short-term exposures to ambient fine particulate matter (PM2.5) and ozone, and at levels below the current daily NAAQS, and mortality in the continental United States.Case-crossover design and conditional logistic regression to estimate the association between short-term exposures to PM2.5 and ozone (mean of daily exposure on the same day of death and 1 day prior) and mortality in 2-pollutant models. The study included the entire Medicare population from January 1, 2000, to December 31, 2012, residing in 39?182 zip codes.Daily PM2.5 and ozone levels in a 1-km × 1-km grid were estimated using published and validated air pollution prediction models based on land use, chemical transport modeling, and satellite remote sensing data. From these gridded exposures, daily exposures were calculated for every zip code in the United States. Warm-season ozone was defined as ozone levels for the months April to September of each year.All-cause mortality in the entire Medicare population from 2000 to 2012.During the study period, there were 22?433?862 million case days and 76?143?209 control days. Of all case and control days, 93.6% had PM2.5 levels below 25 ?g/m3, during which 95.2% of deaths occurred (21?353?817 of 22?433?862), and 91.1% of days had ozone levels below 60 parts per billion, during which 93.4% of deaths occurred (20?955?387 of 22?433?862). The baseline daily mortality rates were 137.33 and 129.44 (per 1 million persons at risk per day) for the entire year and for the warm season, respectively. Each short-term increase of 10 ?g/m3 in PM2.5 (adjusted by ozone) and 10 parts per billion (10-9) in warm-season ozone (adjusted by PM2.5) were statistically significantly associated with a relative increase of 1.05% (95% CI, 0.95%-1.15%) and 0.51% (95% CI, 0.41%-0.61%) in daily mortality rate, respectively. Absolute risk differences in daily mortality rate were 1.42 (95% CI, 1.29-1.56) and 0.66 (95% CI, 0.53-0.78) per 1 million persons at risk per day. There was no evidence of a threshold in the exposure-response relationship.In the US Medicare population from 2000 to 2012, short-term exposures to PM2.5 and warm-season ozone were significantly associated with increased risk of mortality. This risk occurred at levels below current national air quality standards, suggesting that these standards may need to be reevaluated.

Dataset Information

Short-term air pollution exposure aggravates Parkinson's disease in a population-based cohort.

Publications

Short-term air pollution exposure aggravates Parkinson's disease in a population-based cohort.

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