A global meta-analysis of particulate and gaseous air pollutants in relation to COVID-19 mortality and hospitalization

Roles of pollution in the prevalence and exacerbations of allergic diseases in Asia

Long-term air pollution exposure is associated with increased mortality, but the association with incidence of fatal and nonfatal coronary heart disease is less certain. Moreover, it is unknown how chronic exposure to air pollution affects prognosis among survivors of a first coronary event. This study evaluated the association between long-term traffic-related air pollution exposure and incidence of nonfatal and fatal coronary events, as well as subsequent hospital readmission and mortality among myocardial infarction survivors. The study population comprised all residents of Rome aged 35-84 years during the period 1998-2000. Residential nitrogen dioxide (NO2) exposure as a marker of traffic pollution was assessed by a land-use regression model in 1995-1996 (R = 0.69). A total of 11,167 incident coronary events were observed (4654 fatal, including 3598 out-of-hospital coronary deaths, and 6513 nonfatal). The cohort of 6513 survivors was followed 4.0-7.5 years for readmission or mortality, starting 28 days from the date of first event. Relative risks per 10 mug/m of NO2 exposure, adjusted for age, sex, and socioeconomic status, were calculated by Poisson regression (population-based incidence) and Cox regression (cohort analysis). The relative risk for incidence in coronary events per 10 mug/m of NO2 was 1.03 (95% confidence interval = 1.00-1.07). Stronger associations were found for fatal cases (1.07; 1.02-1.12) and out-of-hospital deaths (1.08; 1.02-1.13). Using NO2 exposure at the time of the first event, there was no association of air pollution exposure with either subsequent hospital readmission or mortality among survivors of the first coronary event. Long-term air pollution exposure increases the risk of coronary heart disease, particularly fatal events. Hospital readmission or subsequent mortality among survivors was not associated with traffic air pollution.

Air Pollution and Coronary Risk in Kidney Transplant Recipients

Approximately 5 million fatalities occur annually due to stroke, along with its substantial effects on patient well-being and functional impairment. Research has established a connection between extended exposure to air pollutants and ischemic stroke. However, the link between short-term exposure to air pollutants and stroke remains less definitive. A comprehensive search was conducted on MEDLINE, Scopus, the Cochrane Central Register of Controlled Trials (CENTRAL), and Web of Sciences databases up until February 2023, without any language restrictions. The inclusion criteria encompassed observational or interventional studies that examined the correlation between short-term exposure to air pollutants (carbon monoxide [CO], sulfur dioxide [SO2], nitrogen dioxide [NO2], ozone [O3]) and particulate matter with diameters of less than 1 µm, less than 2.5 µm, or less than 10 µm (PM1, PM2.5, and PM10), with the incidence and mortality of ischemic stroke. Short-term exposure was defined as exposure occurring within 5 days of the onset of stroke. A total of 18,035,408 cases of ischemic stroke were included in the analysis, derived from 110 observational studies. Asia accounted for most included studies, representing 58.8% of the total. By contrast, Europe and the Americas contributed 24.6% and 16.7% of the studies, respectively. Notably, none of the included studies were conducted in Africa. Stroke incidence was significantly associated with an increase in the concentration of NO2 (RR = 1.28; 95% CI 1.21-1.36), O3 (RR = 1.05; 95% CI 1.03-1.07), CO (RR = 1.26; 95% CI 1.21-1.32), SO2 (RR = 1.15; 95% CI 1.11-1.19), PM1 (RR = 1.09; 95% CI 1.06-1.12), PM2.5 (RR = 1.15; 95% CI 1.13-1.17), and PM10 (RR = 1.14; 95% CI 1.12-1.16). Moreover, an increase in the concentration of NO2 (RR = 1.33; 95% CI 1.07-1.65), SO2 (RR = 1.60; 95% CI 1.05-2.44), PM2.5 (RR = 1.09; 95% CI 1.04-1.15), and PM10 (RR = 1.02; 95% CI 1.00-1.04) was associated with an increase in stroke mortality. There is a strong and significant correlation between gaseous and particulate air pollutants and the occurrence and mortality rates of stroke. This close temporal association underscores the importance of implementing global initiatives to develop policies aimed at reducing air pollution. By doing so, alleviate the burden of ischemic stroke and its consequences.

The association between total daily mortality and air pollution was investigated for a 1-year period (January 1995 to December 1995) in Inchon, Korea. The purpose of this study was to evaluate the relative importance of particulate and gaseous air pollution as predictors of daily mortality. Concentration of total suspended particulates (TSP), inhalable particles (PM10), and gaseous pollutants, such as sulfur dioxide, nitrogen dioxide, ozone, carbon monoxide, were measured daily during the study period. A generalized additive model was used to regress daily death counts on each air pollutant, controlling for time trend and meteorologic influences such as temperature or relative humidity. Total mortality was found to increase 1.2% (95% CI: 0.2 to 2.2%) for each 10 microg/m3 increase in 6-day moving average of TSP, and 1.2% (95% CI 0.2 to 2.1%) for each 10 microg/m3 increase in 5-day moving average of PM10. The association is similar in magnitude to associations between particulate air pollution and mortality found in several other communities in America and Europe. Associations with gaseous pollutants were all statistically insignificant in the generalized additive model. The relative risk of death increased at particulate levels that were well below the current Korean Ambient Air Quality Standard.

Epidemiologic studies report associations between particulate air pollution and increased mortality from pulmonary diseases. This study was performed to examine whether the exposure to ambient gaseous and particulate air pollution leads to an alteration of the differential white blood cell count in patients with chronic pulmonary diseases like chronic bronchitis, chronic obstructive pulmonary disease, and asthma. A prospective panel study was conducted in Erfurt, Eastern Germany, with 12 repeated differential white blood cell counts in 38 males with chronic pulmonary diseases. Hourly particulate and gaseous air pollutants and meteorological data were acquired. Mixed models with a random intercept adjusting for trend, meteorology, weekday, and other risk variables were used.In this explorative analysis, we found an immediate decrease of polymorphonuclear leukocytes in response to an increase of most gaseous and particulate pollutants. Lymphocytes increased within 24 h in association with all gaseous pollutants but showed only minor effects in regard to particulate air pollution. Monocytes showed an increase associated with ultrafine particles, and nitrogen monoxide. The effect had two peaks in time, one 0–23 h before blood withdrawal and a second one with a time lag of 48–71 h. The increase of particulate and gaseous air pollution was associated with multiple changes in the differential white blood cell count in patients with chronic pulmonary diseases.

Most of the evidence regarding the association between particulate air pollution and emergency room visits or hospital admissions for respiratory conditions and asthma comes from the USA. European time-series analyses have suggested that gaseous air pollutants are important determinants of acute hospitalization for respiratory conditions, at least as important as particulate mass. The association between daily mean levels of suspended particles and gaseous pollutants (sulphur dioxide, nitrogen dioxide, carbon monoxide, ozone) was examined. The daily emergency hospital admissions for respiratory conditions in the metropolitan area of Rome during 1995-1997 were also recorded. Daily counts of hospital admissions for total respiratory conditions (43 admissions day(-1)), acute respiratory infections including pneumonia (18 day(-1)), chronic obstructive pulmonary disease (COPD) (13 day(-1)), and asthma (4.5 day(-1)) among residents of all ages and among children (0-14 yrs) were analysed. The generalized additive models included spline smooth functions of the day of study, mean temperature, mean humidity, influenza epidemics, and indicator variables for day of the week and holidays. Total respiratory admissions were significantly associated with same-day level of NO2 (2.5% increase per interquartile range (IQR) change, 22.3 microg x m(-3)) and CO (2.8% increase per IQR, 1.5 mg x m(-3)). No effect was found for particulate matter and SO2, whereas O3 was associated with admissions only among children (lag 1, 5.5% increase per IQR, 23.9 microg x m3). The effect of NO2 was stronger on acute respiratory infections (lag 0, 4.0% increase) and on asthma among children (lag 1, 10.7% increase). The admissions for all ages for asthma and COPD were associated only with same-day level of CO (5.5% and 4.3% increase, respectively). Multipollutant models confirmed the role of CO on all respiratory admissions, including asthma and COPD, and that of NO2 on acute respiratory infections. Among children, O3 remained a strong indicator of acute respiratory infections. Carbon monoxide and photochemical pollutants (nitrogen dioxide, ozone) appear to be determinants of acute respiratory conditions in Rome. Since carbon monoxide and nitrogen dioxide are good indicators of combustion products from traffic related sources, the detected effect may be due to unmeasured fine and ultrafine particles.

Ambient fine particulate matter (PM2.5) air pollution is associated with lung cancer risk. However, less is known regarding air pollution associations with lung cancer subtypes, and it is unclear if air pollution plays a role in lung cancer survival. To address this, participants in the American Cancer Society's Cancer Prevention Study-II Nutrition cohort (n=122,442) were linked to residential annual concentrations of particulate matter and gaseous pollutants. Extended Cox regression was used to model time-varying pollutant exposures with risk of lung cancer by subtype and risk of death after diagnosis (hazard ratio per pollutant 5th %-mean difference [95% confidence interval]). From 1992 to 2017, 4282 lung cancers were diagnosed. PM2.5 was associated with lung cancer incidence (1.06 [1.02-1.11]) as were nitrogen dioxide, ozone, and sulfur dioxide (4-7% increase). PM2.5 was associated with all lung cancer subtypes whereas nitrogen dioxide was particularly associated with adenocarcinoma (1.07 [1.00-1.14]), and ozone with large cell carcinoma (1.13 [0.97-1.33]). Among 3656 lung cancer patients with detailed diagnosis information, there were few associations with pollutant exposure in the past year and overall mortality or lung cancer death specifically. Sulfur dioxide was associated with lung cancer death among localized stage cancers (1.18 [1.00-1.40]), while coarse particulates were associated with lung cancer death in regional stage cases with elevated but not statistically significant findings in current smokers. Both particulate and gaseous air pollutants were associated with incident lung cancer subtypes. Recent air pollution exposure was associated with shorter survival after lung cancer for select groups only.

Use of GLM approach to assess the responses of tropical trees to urban air pollution in relation to leaf functional traits and tree characteristics

Although particulate air pollution has been associated with increased numbers of daily deaths in dozens of cities around the world, issues still remain about the association. Some have questioned the complex modeling used to control for season in Poisson regression or the role of gaseous air pollutants as potential confounders of the association. I examined the association between deaths and particulate matter with an aerodynamic diameter less than or equal to 10 microm (PM10) using a case-crossover design. In this approach, the pollution on the day of each death is contrasted with the pollution level on control days when the subject did not die. Season and gaseous air pollutants were controlled by matching. Control days were chosen within the same month of the same year to control for season, and matched on either sulfur dioxide (SO2; within 1 ppb), nitrogen dioxide (within 1 ppb), maximum ozone (within 2 ppb), or carbon monoxide (within 0.03 ppm). The analysis was conducted in 14 U.S. cities that have daily PM10 monitoring. After matching, there were about 400,000 deaths in each analysis. Results were combined across cities using a maximum likelihood method. PM10 was a significant predictor of mortality when controlling for gaseous air pollutants, with effect sizes ranging from a 0.45% increase per 10 microg/m3 increment of PM10 [95% confidence interval (CI), 0.12-0.79%] when matched on maximum hourly ozone levels, to a 0.81% increase per 10 microg/m3 increment of PM10 (95% CI, 0.47-1.16%) when matched on 24-hr average SO2.

Air pollution and daily mortality: Associations with particulates and acid aerosols

Ambient particulate matter has been associated consistently with an increased risk for mortality largely due to cardiovascular diseases.1 Although the relative risk estimates from epidemiological studies are small, they apply to almost the entire population of the United States. Consequently, exposure to ambient particles produces considerable burden of disease, and its mitigation offers the benefit of improving life expectancy.2 Articles see pp 941 and 949 Over the past decade, research has substantiated the understanding of the pathophysiological mechanisms linking ambient particles to the cardiovascular system3,4 once it was noted that ambient air pollution elicits systemic inflammatory responses in the general population.5 An update of the American Heart Association statement on air pollution and cardiovascular disease3 is under way. Mechanisms considered for active and secondhand smoke as well as ambient air pollution are strikingly similar.4,6,7 They include progression of atherosclerotic plaques to vulnerable forms, prothrombotic states, endothelial dysfunction, and altered autonomic nervous system control (Figure). Increased systemic oxidative stress is considered the key mechanism responsible for most of these pathophysiological changes. Increased risks for cardiovascular disease in general and coronary artery disease in particular have been documented for active and secondhand smoke as well as ambient particulate matter. Deep venous thrombosis has been added to this list recently.8 Figure. Overview on pathomechanism linking ambient air pollution,4 secondhand smoke,7 and active smoking to acute coronary syndromes. Nevertheless, the public health relevance of particulate matter in the light of the smoking literature remains hotly debated. Smokers are exposed to considerably higher cumulative doses of particulate matter than the general nonsmoking population. Mortality due to low doses of ambient particles may be considered counterintuitive compared with doses of particles tolerated by smoking individuals. A systematic assessment of the exposure-response function ranging from low doses of inhaled particles …

PP-30-034 Background/Aims: Numerous epidemiological studies have reported the association between ambient pollutants in North American, European, and Asian cities. However, few studies explored the effects of air pollutants on daily mortality in Tianjin city. The aim is to study the association between sulfur dioxide and nitrogen dioxide and daily mortality in urban population in Tianjin. Methods: We collected daily concentration of inhalable particulate matter, sulfur dioxide and nitrogen dioxide, daily mean temperature and relative humidity, and daily cause-specific death counts. We used generalized additive models to explore the relationship between sulfur dioxide and nitrogen dioxide and daily mortality, after adjusting the effects of long-term and seasonal trend, and weather conditions, and analyzed the potential effect of particulate matter and model parameters on relative risk estimates. Results: Daily concentrations of SO2 and NO2 were significantly associated with daily nonaccidental and cardiovascular mortality, and not associated with daily respiratory mortality. An increase of 10 μg/m3 in SO2 was associated with 0.56% (95% CI: 0.23%–0.89%) nonaccidental morality and 0.49% (0.06%–0.93%) cardiovascular morality. An increase of 10 μg/m3 in NO2 was associated with 0.94% (95% CI: 0.17%–1.70%) nonaccidental morality and 1.29% (0.29%–2.30%) cardiovascular morality. Conclusion: The findings suggest that exposure to SO2 and NO2 was significantly associated with daily cardiovascular and respiratory mortality in urban population in Tianjin.

Gaseous air pollution and acute myocardial infarction mortality in Hong Kong: A time-stratified case-crossover study

Exposure surrogates, such as air quality measured at a fixed-site monitor (FSM) or residence, are typically used for health estimates. However, people spend various amounts of time in different microenvironments, including the home, office, outdoors and in transit, where they are exposed to different magnitudes of particle and gaseous air pollutants. Health risks caused by air pollution exposure differ among individuals due to differences in activity, microenvironmental concentration, as well as the toxicity of pollutants. We evaluated individual and combined added health risks (AR) of exposure to PM2.5, NO2, and O3 for 21 participants in their daily life based on real-world personal exposure measurements. Exposure errors from using surrogates were quantified. Inter- and intra-individual variability in health risks and key contributors in variations were investigated using linear mixed-effects models and correlation analysis, respectively. Substantial errors were found between personal exposure concentrations and ambient concentrations when using air quality measurements at either FSM or the residence location. The mean exposure errors based on the measurements taken at either the FSM or residence as exposure surrogates was higher for NO2 than PM2.5, because of the larger spatial variability in NO2 concentrations in urban areas. The daily time-integrated AR for the combined PM2.5, NO2, and O3 (TIARcombine) ranged by a factor of 2.5 among participants and by a factor up to 2.5 for a given person across measured days. Inter- and intra-individual variability in TIARcombine is almost equally important. Several factors were identified to be significantly correlated with daily TIARcombine, with the top five factors, including PM2.5, NO2 and O3 concentrations at ‘home indoor’, O3 concentrations at ‘office indoor’ and ambient PM2.5 concentrations. The results on the contributors of variability in the daily TIARcombine could help in targeting interventions to reduce daily health damage related to air pollutants.