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      Assessing the effects of exposure to sulfuric acid aerosol on respiratory function in adults

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          Abstract

          \(\textbf{Background:}\) Sulfuric acid aerosol is suspected to be a major contributor to mortality and morbidity associated with air pollution. \(\textbf{Objective:}\) To determine if exposure of human participants to anticipated levels of sulfuric acid aerosol (\(\sim 100\mu g/m^3 \)) in the near future would have an adverse effect on respiratory function. \(\textbf{Methods:}\) We used data from 28 adults exposed to sulfuric acid for 4 hours in a controlled exposure chamber over a 3 day period with repeated measures of pulmonary function (FEV1) recorded at 2 hour intervals. Measurements were also recorded after 2 and 24 hours post exposure. We formulated a linear mixed effect model for FEV1 with fixed effects (day of treatment, hour, day-hour interaction, and smoking status), a random intercept and an AR1 covariance structure to estimate the effect of aerosol exposure on FEV1. We further assessed whether smoking status modified the exposure effects and compared the analysis to the method used by Kerr et al.,1981. \(\textbf{Results:}\) The effect of day 3 exposure is negatively associated with lung function (coefficient (\(\beta\)), -0.08; 95% CI, -0.16 to -0.01). A weak negative association is observed with increasing hours of exposure (\(\beta\), -0.01; 95% CI, -0.03 to 0.00). Among the smokers, we found a significant negative association with hours of exposure (\(\beta\), -0.02; 95% CI, -0.03 to -0.00), day 3 exposure (\(\beta\), -0.11; 95% CI, -0.14 to -0.02) and a borderline adverse effect for day 2 treatment (\(\beta\), -0.06; 95% CI, -0.14 to 0.03) whilst no significant association was observed for nonsmokers. \(\textbf{Conclusions:}\) Anticipated deposits of sulfuric acid aerosol in the near would adversely affect respiratory function. The effect observed in smokers is significantly more adverse than in nonsmokers.

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          Evidence for large upward trends of ultraviolet-B radiation linked to ozone depletion.

          Spectral measurements of ultraviolet-B radiation made at Toronto since 1989 indicate that the intensity of light at wavelengths near 300 nanometers has increased by 35 percent per year in winter and 7 percent per year in summer. The wavelength dependence of these trends indicates that the increase is caused by the downward trend in total ozone that was measured at Toronto during the same period. The trend at wavelengths between 320 and 325 nanometers is essentially zero.
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            Air Pollution Exposure and Cardiovascular Disease

            Ambient air pollution (AAP) and particulate matters (PM) have been closely associated with adverse health effects such as respiratory disease and cardiovascular diseases. Previous studies have examined the adverse health effects associated with short- and long-term exposure to AAP and outdoor PM on respiratory disease. However, the effect of PM size (PM2.5 and PM10) on cardiovascular disease has not been well studied. Thus, it remains unclear how the size of the inhalable particles (coarse, fine, or ultrafine) affects mortality and morbidity. Airborne PM concentrations are commonly used for ambient air quality management worldwide, owing to the known effects on cardiorespiratory health. In this article, we assess the relationship between cardiovascular diseases and PM, with a particular focus on PM size. We discuss the association of PM2.5 and PM10, nitrogen dioxide (NO2), and elemental carbon with mortality and morbidity due to cardiovascular diseases, stroke, and altered blood pressure, based on epidemiological studies. In addition, we provide evidence that the adverse health effects of AAP and PM are more pronounced among the elderly, children, and people with preexisting cardiovascular and respiratory conditions. Finally, we critically summarize the literature pertaining to cardiovascular diseases, including atherosclerosis and stroke, and introduce potential studies to better understand the health significance of AAP and PM on cardiovascular disease.
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              Characterisation of chemical species in PM2.5 and PM10 aerosols in Brisbane, Australia

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                Author and article information

                Journal
                10 June 2019
                Article
                1906.04296
                7fdb4ef8-05a6-4482-8bf5-33c4171b77aa

                http://arxiv.org/licenses/nonexclusive-distrib/1.0/

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