Acute Effects Of Ozone Research Articles

Short-Term Exposure Effect of Ambient Fine Particulate Matter, Ozone and Cold Temperature on Emergency Room Visits for Asthma Patients

(1) Background: The acute effects of ozone, cold temperature and particulate matter less than 2.5 μm (PM2.5) in size related to asthma attacks are well known worldwide. The adverse effects of ozone and cold temperature on asthma morbidity in Taiwan are still inconclusive. (2) Methods: This retrospective study included patients who had asthma emergency room visits (ERVs) from 1 January 2016 to 31 December 2019 in a regional hospital in Taiwan. The short-term negative effects were estimated using Distributed Lag Non-Linear Models (DLNMs) for the relative risks (RRs) of asthma ERVs associated with PM2.5, ozone and cold temperature exposures within 5 days. (3) Results: There was a significant association between a 10 ppm increase in PM2.5 exposure and asthma ERVs at a 2-day lag (RR 1.166, 95% confidence interval (C.I.): 1.051-1.294). There was a significant association between ozone and asthma ERVs at a 1-day lag (RR 1.179, 95% C.I.: 1.034-1.345). The ambient temperature in cold weather compared with the temperature of minimum asthma ERV showed an RR of 1.214, 95% C.I.: 1.009-1.252 at a 1-day lag. (4) Conclusions: This study provides evidence that short-term exposure to fine suspended particulates, ozone and inverse temperature is associated with asthma exacerbation.

Short-term Effect of Ambient Ozone on Daily Emergency Room Visits in Beijing, China

Little is known about the acute effects of ozone on morbidity risk in China. We conducted a time-series study to examine the association between ozone and daily emergency room visits (ERVs) in Beijing, China. We identified 7,088,309 ERVs between January 1, 2014 and December 31, 2015. A generalized additive model with Poisson regression incorporating penalized spline functions was employed to analyze ERVs in association with daily 8-h maximum ozone concentrations. An increase of 10 μg/m3 of same-day ozone concentration was significantly associated with a 0.24% (95% CI, 0.21%–0.26%), 0.31% (95% CI, 0.27%–0.35%), and 0.43% (95% CI, 0.36%–0.50%) increase in daily ERVs for the whole study period, days when the daily 8-h maximum ozone met the Chinese Ambient Air Quality Standards (CAAQS) Grade II standard, and days that met the CAAQS Grade I standard, respectively. These results were robust when considering the potential confounding effects of PM2.5, PM10, NO2, SO2, and CO. In conclusion, our findings suggested significant effects of ozone exposure on daily ERVs in Beijing. Improving air quality with even lower ozone level than the current CAAQS could yield important public health.

Acute effect of multiple ozone metrics on mortality by season in 34 Chinese counties in 2013-2015.

Although numerous multicentre studies have estimated the association between ozone exposure and mortality, there are currently no nationally representative multicentre studies of the ozone-mortality relationship in China. To investigate the effect on total (nonaccidental) and cause-specific mortality of short-term exposure to ambient ozone, and examine different exposure metrics. The effects of short-term exposure to ozone were analysed using various metrics (daily 1-h maximum, daily 8-h maximum and daily average) on total (nonaccidental) and cause-specific (circulatory and respiratory) mortality from 2013 to 2015 in 34 counties in 10 cities across China. We used distributed lag nonlinear models for estimating county-specific relative risk of mortality and combined the county-specific relative rates by conducting a random-effects meta-analysis. In all-year analyses, a 10 μg m-3 increase in daily average, daily 1-h maximum and daily 8-h maximum ozone at lag02 corresponded to an increase of 0.6% (95% CI: 0.33, 0.88), 0.26% (95% CI: 0.12, 0.39) and 0.37% (95% CI: 0.2, 0.55) in total (nonaccidental) mortality, 0.66% (95% CI: 0.28, 1.04), 0.31% (95% CI: 0.11, 0.51) and 0.39% (95% CI: 0.16, 0.62) in circulatory mortality, and 0.57% (95% CI: -0.09, 1.23), 0.11% (95% CI: -0.22, 0.44) and 0.22% (95% CI: -0.28, 0.72) in respiratory mortality, respectively. These estimates had a different seasonal pattern by cause of death. In general, the seasonal patterns were consistent with the times of year when ozone concentrations are highest. Our findings suggest that in China, the acute effects of ozone are more closely related to daily average exposure than any other metric.

Seasonal variation in the acute effects of ozone on premature mortality among elderly Japanese

We conducted a multicity time-series study using monitoring data to assess seasonal patterns of short-term ozone-mortality association among elderly aged 65years and over in Japan. Daily exposure to ambient ozone was computed using hourly measurements of photochemical oxidants available at multiple monitoring stations in each city. Effects of ozone on daily all-cause non-accidental, cardiovascular, and respiratory mortality were estimated using distributed lag linear models, controlling for confounding by temporal, day of the week, temperature, and flu epidemics. City-level effect estimates were combined using inverse variance meta-analysis. In spring and autumn, a 10-ppbv increase of daily maximum 8-h average ozone concentration in the previous 3days was associated with 0.69% (95% confidence interval (CI): 0.27-1.10), 1.07% (0.34-1.82), and 1.77% (0.78-2.77) increases in daily all-cause, cardiovascular, and respiratory mortality, respectively. Forward displacement of respiratory mortality was large during the cold season despite lower ozone concentration. Results were generally independent of fine particulate matter and nitrogen dioxide. Findings suggest significant mortality effects of short-term ozone exposure among the elderly during the moderate season. Those with underlying respiratory diseases were susceptible, even during winter.

Susceptibility Factors to Ozone-related Mortality

Acute effects of ozone on mortality have been extensively documented in clinical and epidemiological research. However, only a few studies have focused on subgroups of the population especially vulnerable to these effects. To estimate the association between exposure to ozone and cause-specific mortality, and to evaluate whether individual sociodemographic characteristics or chronic conditions confer greater susceptibility to the adverse effects of ozone. A case-crossover analysis was conducted in 10 Italian cities. Data on mortality were collected for the period 2001 to 2005 (April-September) for 127,860 deceased subjects. Information was retrieved on cause of death, sociodemographic characteristics, chronic conditions from previous hospital admissions, and location of death. Daily ozone concentrations were collected from background fixed monitors. We estimated a 1.5% (95% confidence interval [CI], 0.9-2.1) increase in total mortality for a 10 microg/m(3) increase in ozone (8-h, lag 0-5). The effect lasted several days for total, cardiac and respiratory mortality (lag 0-5), and it was delayed for cerebrovascular deaths (lag 3-5). In the subgroup analysis, the effect was more pronounced in people older than 85 years of age (3.5%; 95% CI, 2.4-4.6) than in 35- to 64-year-old subjects (0.8%; 95% CI, -0.8 to 2.5), in women (2.2%; 95% CI, 1.4-3.1) than in men (0.8%; 95% CI, -0.1 to 1.8), and for out-of-hospital deaths (2.1%; 95% CI, 1.0-3.2), especially among patients with diabetes (5.5%; 95% CI, 1.4-9.8). A greater vulnerability of elderly people and women was indicated; subjects who died at home and had diabetes emerged as especially affected.

Susceptibility Factors to Ozone-Related Mortality-A Population-Based Case-Crossover Analysis

ISEE-0133 Background and Objective: Acute effects of ozone on mortality have been extensively documented in clinical and epidemiological research. However, few studies have focused on subgroups of the population especially vulnerable to these effects. The objective of the study is to estimate the association between cause-specific mortality and exposure to ozone, and to evaluate whether individual socio-demographic or chronic conditions present greater susceptibility to adverse effects of ozone. Methods: A case-crossover analysis was conducted in 10 Italian cities to evaluate individual effect modifiers of the ozone-mortality association. Data on mortality and air pollution exposure were collected for the period 2001-2005 (April to September), for 129,026 deceased subjects. Individual information was retrieved on cause of death, socio-demographic characteristics, chronic conditions from previous hospital admissions, and place of death. Results: We estimated a 1.54% (95% confidence interval, CI, 0.92-2.15) increase in total mortality for 10 ug/m3 increase in ozone (8-hour, lag 0-5). The association had a prolonged lag for total, cardiac and respiratory mortality (lag 0-5), while there was a suggestion of a delayed effect on mortality from cerebrovascular causes (lag 3-5). No important confounding effect of PM10 or NO2 was found. In the subgroup analysis, the effect was more pronounced among the elderly over 85 years of age (3.51%, 95% CI 2.41-4.62), women (2.25%, 95% CI 1.37-3.14), and for people who died outside the hospital (2.10%, 95% CI 1.05-3.17), especially diabetics (5.53%, 95% CI 1.39-9.84). Conclusion: A strong effect of ozone on mortality has been found in Italian cities. Greater vulnerability was confirmed for women and elderly; other subgroups of the population emerged as especially affected, in particular chronically ill house-bound and diabetics.

Acute effects of ozone on pulmonary function of cyclists receiving antioxidant supplements.

OBJECTIVES: To identify whether acute lung function effects of ozone can be modulated by antioxidant vitamin supplementation. METHODS: Amateur cyclists (n = 26) were studied in the summer of 1994...

Acute Effects of Ozone on Heart Rate and Body Temperature in the Unanesthetized, Unrestrained Rat Maintained at Different Ambient Temperatures

AbstractThe present studies were conducted to investigate the concentration-response characteristics of acute ozone (O3) exposure on the cardiovascular and thermoregulatory function of the unanesthetized, unrestrained rat, and to examine the modulating effects produced by changes in ambient temperature (T a) on the induced toxic response. For all studies, groups of male Fischer 344 rats (n - 4-6/group) were implanted with radiotelemetry transmitters and allowed to recover overnight. The transmitters permitted continuous monitoring of electrocardiogram (ECG) and body core temperature (T co); heart rate (HR) was derived from the ECG signal. Frequency of breathing (f) was obtained in selected experiments using a barometric plethysmograph. All animals were monitored according to the following protocol: control (filtered air, 0.25 hr); exposure (O3, 2 hr); recovery (filtered air, 3–18 hr). For the concentration-response experiments, O3 concentration was varied from 0.25 to 1.0 ppm and all exposures were conduc...

Acute effects of ozone on EEG activity, sleep-wakefulness and heart rate in rats.

Effects of exposure to O3 on EEG activity, sleep-wakefulness and heart rate were examined using conscious rats which had been chronically implanted with electrodes for EEG, EMG and ECG recordings. Exposure to 0.5 ppm O3 for 6 hrs and 1.0 ppm O3 for 3 hrs suppressed amounts of wakefulness (W) and paradoxical sleep (PS) at the expense of an increase in slow-wave sleep (SWS), and lowered the amplitude of fast EEG waves and heart rate (HR). The lowered EEG amplitude and the suppressed PS recovered more rapidly during the post-exposure period than did the lowered HR. The ip administration of atropine sulfate blocked the suppressed W, the increased SWS and the lowered HR, while the lowered EEG amplitude and the suppressed PS were not blocked. These observations suggest that the O3-induced bradycardia results from enhanced activity of cardiac parasympathetic nerves and that the O3-induced changes in W and SWS result secondarily from some circulatory factor including the bradycardia.

A nonlinear pharmacologic model of the acute effects of ozone on the human lungs

A pharmacologic model describing the quantitative relationship between short-term exposure to ozone and pulmonary airway resistance is described. The model simulates the following processes: (1) removal of a fraction of inhaled ozone in the airways of the head; (2) ozone oxidation of membrane-bound fatty acids in the target tissue in the lower airways; (3) rupture of cell membranes, releasing inflammatory mediators into the intercellular space; (4) migration of inflammatory cells into the injured tissue, releasing additional mediators and thus amplifying the inflammatory effect of ozone in a positive feedback loop; (5) stimulation of irritant receptors by ozone directly and by inflammatory mediators leading to vagally mediated bronchoconstriction. Mathematically the model consists of a logistic equation determining losses in the head, and a set of four differential equations simulating the uptake of ozone in the target tissue and the ensuing inflammation and bronchoconstriction. The observed human response to ozone in chamber studies is nonlinear, and it was necessary to introduce a nonlinear feedback loop for inflammation in the model to replicate this. Despite limited data upon which to base the model, it successfully predicts the human response to ozone reported in a series of published short-term chamber studies and is superior to "effective dose" (the product of ozone concentration, minute ventilation, and exposure duration) used by other investigations to describe dose-response relationships. Nonlinear multicompartment pharmacologic models such as this one can exhibit very complex behavior making the estimation of model parameters difficult, but they hold promise because the physiologic processes under study are themselves complex nonlinear phenomena.

Acute effects of ozone on cat lungs. II. Structural.

Cats artificially ventilated with 0.26, 0.50, or 1.00 ppM O/sub 3/ for 4.7 to 6.6 hr showed variable but generally dose-related effects that included: focal desquamation of ciliated epithelium, cytoplasmic vacuolization of ciliated cells, condensed mitochondria with abnormal cristae configuration, swelling or denudation of cytoplasm of type 1 alveolar cells, swelling or breakage of capillary endothelium, and lysis of red blood cells. Type 2 pneumocytes were generally unaffected. Pulmonary resistance increased in most all animals exposed to > 0.5 ppM, but only 2 (of 7) exposed to 0.26 ppM showed an increase. Diffusing capacity was reduced in all exposed groups irrespective of dose.