-
1.
Independent and Opposing Associations of Habitual Exercise and Chronic PM2.5 Exposures on Hypertension Incidence.
Guo, C, Zeng, Y, Chang, LY, Yu, Z, Bo, Y, Lin, C, Lau, AK, Tam, T, Lao, XQ
Circulation. 2020;(7):645-656
Abstract
BACKGROUND We investigated the joint associations of habitual physical activity (PA) and long-term exposure to fine particulate matter (PM2.5) with the development of hypertension in a longitudinal cohort in Taiwan. METHODS We selected 140 072 adults (≥18 years of age) without hypertension who joined a standard medical screening program with 360 905 medical examinations between 2001 and 2016. PM2.5 exposure was estimated at each participant's address using a satellite data-based spatiotemporal model with 1 km2 resolution. Information on habitual PA and a wide range of covariates was collected using a standard self-administered questionnaire. We used the Cox regression model with time-dependent covariates to examine the joint associations. RESULTS The mean age of all observations was 41.7 years, and 48.8% were male. The mean value for systolic and diastolic blood pressure was 112.5 and 68.7mm Hg, respectively. Approximately 34.2% of all observations were inactive (0 metabolic equivalence values-hours), 29.8% had moderate-PA (median [interquartile range]; 3.75 [3.38 to 4.38] metabolic equivalence values-hours), and 36.0% had high-PA (15.7 [10.3 to 24.8] metabolic equivalence values-hours). The mean±SD of PM2.5 was 26.1±7.3 μg/m3. The prevalence of cardiovascular disease, diabetes mellitus, and cancer was 2.1%, 2.9%, and 1.5%, respectively. After adjusting for a wide range of covariates (including a mutual adjustment for PA or PM2.5), a higher PA level was associated with a lower risk of hypertension (hazard ratio [HR] for the moderate- and high-PA was 0.93 [95% CI, 0.89-0.97] and 0.92 [95% CI, 0.88-0.96], respectively, as compared with the inactive-PA), whereas a higher level of PM2.5 was associated with a higher risk of hypertension (HR for the moderate- and high-PM2.5 was 1.37 [95% CI, 1.32-1.43] and 1.92 [95% CI, 1.81-2.04], respectively, as compared with the low-PM2.5 group]. No significant interaction was observed between PA and PM2.5 (HR 1.01 [95% CI, 1.00-1.02]). CONCLUSIONS A high-PA and low PM2.5 exposure were associated with a lower risk of hypertension. The negative association between PA and hypertension remained stable in people exposed to various levels of PM2.5, and the positive association between PM2.5 and hypertension was not modified by PA. Our results indicated that PA is a suitable hypertension prevention strategy for people residing in relatively polluted regions.
-
2.
Air pollution in relation to very short-term risk of ST-segment elevation myocardial infarction: Case-crossover analysis of SWEDEHEART.
Sahlén, A, Ljungman, P, Erlinge, D, Chan, MY, Yap, J, Hausenloy, DJ, Yeo, KK, Jernberg, T
International journal of cardiology. 2019;:26-30
Abstract
OBJECTIVE Studies have related air pollution to myocardial infarction (MI) events over days or weeks, with few data on very short-term risks. We studied risk of ST-segment elevation MI (STEMI) within hours of exposure to air pollution while adjusting for weather. METHODS We performed a case-crossover study of STEMI cases in Stockholm, Sweden (Jan 2000-June 2014) based on SWEDEHEART. Exposures during hazard periods up to 24 h prior to admission were compared to bidirectionally sampled control periods. Risks attributable to sulphur dioxide (SO2), nitrogen dioxide (NO2), ozone and particulate pollutants (PM2.5, PM10) were studied in conditional logistic regression models for interquartile range increments. RESULTS Risk of STEMI (n = 14,601) was associated with NO2 (strongest at 15-h lag) and with PM2.5 (strongest at 20-h lag), in single-pollutant models adjusting for air temperature and humidity (NO2: odds ratio (OR; 95% confidence interval) 1.065 (1.031-1.101); PM2.5: 1.026 (1.001-1.054)). After adjusting models for atmospheric pressure (significantly associated with STEMI risk at 14-24-h lags), NO2 remained highly statistically significant (1.057 (1.022-1.094)) but not PM2.5 (1.024 (0.997-1.052)). No associations were seen for SO2, ozone or PM10. CONCLUSION Risk of STEMI rises within hours of exposure to air pollutants, with strongest impact of NO2. These findings are complementary to earlier reports which have not acknowledged widely the importance of very short-term fluctuations in air pollution.
-
3.
B vitamins attenuate the epigenetic effects of ambient fine particles in a pilot human intervention trial.
Zhong, J, Karlsson, O, Wang, G, Li, J, Guo, Y, Lin, X, Zemplenyi, M, Sanchez-Guerra, M, Trevisi, L, Urch, B, et al
Proceedings of the National Academy of Sciences of the United States of America. 2017;(13):3503-3508
-
-
Free full text
-
Abstract
Acute exposure to fine particle (PM2.5) induces DNA methylation changes implicated in inflammation and oxidative stress. We conducted a crossover trial to determine whether B-vitamin supplementation averts such changes. Ten healthy adults blindly received a 2-h, controlled-exposure experiment to sham under placebo, PM2.5 (250 μg/m3) under placebo, and PM2.5 (250 μg/m3) under B-vitamin supplementation (2.5 mg/d folic acid, 50 mg/d vitamin B6, and 1 mg/d vitamin B12), respectively. We profiled epigenome-wide methylation before and after each experiment using the Infinium HumanMethylation450 BeadChip in peripheral CD4+ T-helper cells. PM2.5 induced methylation changes in genes involved in mitochondrial oxidative energy metabolism. B-vitamin supplementation prevented these changes. Likewise, PM2.5 depleted 11.1% [95% confidence interval (CI), 0.4%, 21.7%; P = 0.04] of mitochondrial DNA content compared with sham, and B-vitamin supplementation attenuated the PM2.5 effect by 102% (Pinteraction = 0.01). Our study indicates that individual-level prevention may be used to complement regulations and control potential mechanistic pathways underlying the adverse PM2.5 effects, with possible significant public health benefit in areas with frequent PM2.5 peaks.
-
4.
The effect of nebulized NaHCO3 treatment on "RADS" due to chlorine gas inhalation.
Aslan, S, Kandiş, H, Akgun, M, Cakir, Z, Inandi, T, Görgüner, M
Inhalation toxicology. 2006;(11):895-900
Abstract
Chlorine is one of the most common substances involved in toxic inhalation. As with all irritant gases, the airway injuries caused by chlorine gas may result in clinical manifestations similar to those of asthma. In this study, we investigated the effect of nebulized sodium bicarbonate (NSB) on the treatment and quality of life (QoL) of victims exposed to chlorine gas. Forty-four consecutive patients with reactive airways dysfunction syndrome (RADS) due to chlorine inhalation (40 females and 4 males, age range 17-56 yr) were included in this study. Patients were placed in control and treatment groups in a sequential odd-even fashion based on their order of presentation. Treatment of all patients included corticosteroids and nebulized short-acting beta2-agonists. Then the control group (n = 22) received nebulized placebo (NP), and the NSB group (n = 22) received NSB treatment (4 cm3 of 4.20% sodium bicarbonate solution). A quality of life (QoL) questionnaire and pulmonary function tests (PFTs) were performed before and after treatments in both groups. The most common symptoms were dyspnea (82%) and chest tightness (82%). Baseline characteristics of both groups were similar. Compared to the placebo group, the NSB group had significantly higher FEV1 values at 120 and 240 min (p < .05). Significantly more improvement in QoL questionnaire scores occurred in the NSB group compared to the NP group (p < .001). Thus, NSB is a clinically useful treatment, as tested by PFTs and QoL questionnaire, for patients with RADS caused by exposure to chlorine gas.
-
5.
Nasal polyposis: prevalence of positive food and inhalant skin tests.
Collins, MM, Loughran, S, Davidson, P, Wilson, JA
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery. 2006;(5):680-3
Abstract
OBJECTIVES To investigate the etiology of nasal polyps and its relationship to allergy. The prevalence of positive food and inhalant skin tests in patients with nasal polyps and nonatopic controls was compared. STUDY DESIGN AND SETTING Prospective controlled study in tertiary referral rhinology clinic. RESULTS Seventy percent (70%) of the patients with nasal polyps had positive skin tests to an average of four foodstuffs, compared to 34 percent of controls (P = 0.006). Only 35 percent of the nasal polyp patients also had positive inhalant skin tests. Overall, the prevalence of positive inhalant skin tests was similar in the nasal polyp patients and controls. CONCLUSIONS These findings suggest that the positive skin tests to foods are not merely a reflection of the general atopic status of patients with nasal polyps. It may be that non-IgE-mediated hypersensitivities, such as to ingested foods, play a role on the basis of a significant number of patients with positive intradermal skin tests to foods. SIGNIFICANCE Evaluation of the allergic status of patients with polyposis is important. Dietary manipulation may be indicated, though its role needs further investigation.
-
6.
[Particles in the outside air increase the risk of cardiovascular diseases].
Peters, A, ,
Gesundheitswesen (Bundesverband der Arzte des Offentlichen Gesundheitsdienstes (Germany)). 2005;:S79-85
Abstract
Evidence accumulated during the mid-1990 s that ambient particulate air pollution aerosol particles may not only exacerbate respiratory diseases but also be a risk factor for cardiovascular disease exacerbation. The aim of the studies described here was to assess the impact of the 1985 smog episode on the risk factor profile in the randomly selected population-based sample of the MONICA survey 1984/85 (S1). During a 13-day period in January 1985 sulphur dioxide concentrations increased four times and concentrations of total suspended atmospheric particles doubled. The impact of this time period on plasma viscosity, plasma C-reactive protein concentrations, heart rate and blood pressure was investigated. Regression models were used to assess these associations adjusting for individual risk factors such as gender, age, body mass index, serum total cholesterol and HDL-cholesterol, smoking, physical activity and medication for cardiovascular diseases and for weather conditions during the survey period. An increase in plasma viscosity, C-reactive protein and heart rate was estimated during the air pollution episode. There was also an increase in blood pressure, but this appeared to be attributable to the weather conditions during the air pollution episode. All the four outcomes were associated with the sulphur dioxide concentrations and the total suspended particle concentrations during the survey. These results indicate that ambient air pollution, particularly ambient particulate air pollution may induce systemic inflammation and modulate the autonomic function of the heart. These pathomechanisms may contribute to the observed associations between ambient air pollution concentrations and cardiovascular disease exacerbation such as hospitalisation and mortality due to cardiovascular diseases.
-
7.
Dermal, oral, and inhalation pharmacokinetics of methyl tertiary butyl ether (MTBE) in human volunteers.
Prah, J, Ashley, D, Blount, B, Case, M, Leavens, T, Pleil, J, Cardinali, F
Toxicological sciences : an official journal of the Society of Toxicology. 2004;(2):195-205
Abstract
Methyl tertiary butyl ether (MTBE), a gasoline additive used to increase octane and reduce carbon monoxide emissions and ozone precursors, has contaminated drinking water and can lead to exposure by oral, inhalation, and dermal routes. To determine its dermal, oral, and inhalation kinetics, 14 volunteers were exposed to 51.3 microg/ml MTBE dermally in tap water for 1 h, drank 2.8 mg MTBE in 250 ml Gatorade(R), and inhaled 3.1 ppm. MTBE for 1 h. Blood and exhaled breath samples were then obtained. Blood MTBE peaked between 15 and 30 min following oral exposure, at the end of inhalation exposure, and ~5 min after dermal exposure. Elimination by each route was described well by a three-compartment model (Rsq >0.9). The Akaike Information Criterion for the three-compartment model was smaller than the two-compartment model, supporting it over the two-compartment model. One metabolite, tertiary butyl alcohol (TBA), measured in blood slowly increased and plateaued, but it did not return to the pre-exposure baseline at the 24-h follow-up. TBA is very water-soluble and has a blood:air partition ratio of 462, reducing elimination by exhalation. Oral exposure resulted in a significantly greater MTBE metabolism into TBA than by other routes based on a greater blood TBA:MTBE AUC ratio, implying significant first-pass metabolism. The slower TBA elimination may make it a better biomarker of MTBE exposure, though one must consider the exposure route when estimating MTBE exposure from TBA because of first-pass metabolism. Most subjects had a baseline blood TBA of 1-3 ppb. Because TBA is found in consumer products and can be used as a fuel additive, it is not a definitive marker of MTBE exposure. These data provide the risk assessment process of pharmacokinetic information relevant to the media through which most exposures occur-air and drinking water.
-
8.
The effect of sulphurous air pollutant exposures on symptoms, lung function, exhaled nitric oxide, and nasal epithelial lining fluid antioxidant concentrations in normal and asthmatic adults.
Tunnicliffe, WS, Harrison, RM, Kelly, FJ, Dunster, C, Ayres, JG
Occupational and environmental medicine. 2003;(11):e15
-
-
Free full text
-
Abstract
AIMS: To explore the effects in normal and asthmatic adults of exposure to 200 ppb sulphur dioxide (SO2) and 200 microg/m3 and 2000 microg/m3 aerosols of ammonium bisulphate (AB) and sulphuric acid (SA) (MMD 0.3 microm). METHODS Exposures were placebo controlled, for one hour at rest, double blind in random order. DeltaFEV1 was the primary outcome; secondary outcomes included symptoms, ventilation, exhaled nitric oxide (NO) concentrations, and nasal lavage fluid ascorbic (AA) and uric acid (UA) concentrations. RESULTS There were no significant changes in spirometry or symptoms with any exposure in either group. SO2 exposure was associated with an increased respiratory rate relative to air exposure in the asthmatic group (SO2: 958.9 breaths/hour; air: 906.8 breaths/hour) but the mean volume breathed did not differ significantly (SO2: 318.8 litres; air: 311.4 litres). AB exposures were associated with a significant rise in [NO] in the asthmatic (+1.51 ppb, and +1.39 ppb), but not in the normal group. Mean pre- and post-exposure [AA] tended to be higher in the normal than in the asthmatic group. Within each group, [AA] did not change significantly with any exposure. Post-exposure [UA] were greater than pre-exposure concentrations for all exposures, significantly so in the normal group for all exposures except SO2. There were no significant differences in the mean change in [UA] for any exposure relative to air. CONCLUSIONS The pollutant exposure concentrations employed in this study were generally much greater than ambient. It is unlikely that short lived exposures at lower concentrations would show significant effects, but effects of longer term lower concentration exposures cannot be ruled out.
-
9.
Antioxidant supplementation and lung functions among children with asthma exposed to high levels of air pollutants.
Romieu, I, Sienra-Monge, JJ, Ramírez-Aguilar, M, Téllez-Rojo, MM, Moreno-Macías, H, Reyes-Ruiz, NI, del Río-Navarro, BE, Ruiz-Navarro, MX, Hatch, G, Slade, R, et al
American journal of respiratory and critical care medicine. 2002;(5):703-9
Abstract
To evaluate whether acute effects of ozone, nitrogen dioxide, and particulates with mass median diameter less than 10 micro m could be attenuated by antioxidant vitamin supplementation, we conducted a randomized trial using a double-blinded design. Children with asthma (n = 158) who were residents of Mexico City were randomly given a daily supplement of vitamins (50 mg/day of vitamin E and 250 mg/day of vitamin C) or a placebo and were followed from October 1998 to April 2000. Pulmonary function tests were carried out twice a week in the morning. During the follow-up observation period, the mean 1-hour maximum ozone level was 102 ppb (SD = 47), and the mean 24-hour average PM(10) level was 56.7 micro g/m(3) (SD = 27.4). In children with moderate and severe asthma, ozone levels 1 day before spirometry were inversely associated significantly with forced expiratory flow (FEF(25-75)) (-13.32 ml/second/10 ppb; p = 0.000), FEV(1) (-4.59 ml/10 ppb; p = 0.036), and peak expiratory flow (PEF) (-15.01 ml/second/10 ppb; p = 0.04) in the placebo group after adjusting for potential confounding factors. No association between ozone and lung functions was observed in the supplement group. We observed significant differences in lung function decrements between groups for FEF(25-75) and PEF. Our results suggest that supplementation with antioxidants might modulate the impact of ozone exposure on the small airways of children with moderate to severe asthma.
-
10.
The effect of sulphur dioxide exposure on indices of heart rate variability in normal and asthmatic adults.
Tunnicliffe, WS, Hilton, MF, Harrison, RM, Ayres, JG
The European respiratory journal. 2001;(4):604-8
Abstract
Sulphur dioxide (SO2) is an important air pollutant and causes bronchoconstriction in normal and asthmatic adults. This paper has explored the autonomic consequences of SO2 exposure using the spectral analysis of heart rate variability. Electrocardiogram recordings were made in 12 normal and 12 asthmatic adults undergoing pollutant exposures. Exposures were of a 1 h duration, double blind, in random order, > or = 2 weeks apart and included air and 200 parts per billion SO2. Spectral analysis of R-R intervals was performed. SO2 exposure was associated with an increase in total power (TP) and high (HF) and low frequency (LF) power in the normal subjects, and a reduction in these indices in the subjects with asthma. The difference in TP with SO2 exposure compared to air was +1730 ms2 in the normal group and -1021 ms2 asthmatic group (p<0.003). For HF the respective values were +964 ms2 and -539 ms2 (p=0.02) and for LF, +43 7 ms2 and -57 2 ms2 (p=0.01). No change in lung function or symptoms was observed in either group. This suggests that SO2 exposure at concentrations which are frequently encountered during air pollution episodes can influence the autonomic nervous system. This may be important in understanding the mechanisms involved in SO2 induced bronchoconstriction, and of the cardiovascular effects of air pollution.