Air pollution and hospital admissions for respiratory and cardiovascular diseases in Hong Kong.
(49/1280)
OBJECTIVE: To investigate short term effects of concentrations of pollutants in ambient air on hospital admissions for cardiovascular and respiratory diseases in Hong Kong. METHODS: Retrospective ecological study. A Poisson regression was performed of concentrations of daily air pollutant on daily counts of emergency hospital admissions in 12 major hospitals. The effects of time trend, season, and other cyclical factors, temperature, and humidity were accounted for. Autocorrelation and overdispersion were corrected. Daily concentrations of nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3), and particulate matter < 10 microns in aerodynamic diameter (PM10) were obtained from seven air monitoring stations in Hong Kong in 1994 and 1995. Relative risks (RR) of respiratory and cardiovascular disease admissions (for an increase of 10 micrograms/m3 in concentration of air pollutant) were calculated. RESULTS: Significant associations were found between hospital admissions for all respiratory diseases, all cardiovascular diseases, chronic obstructive pulmonary diseases, and heart failure and the concentrations of all four pollutants. Admissions for asthma, pneumonia, and influenza were significantly associated with NO2, O3, and PM10. Relative risk (RR) for admissions for respiratory disease for the four pollutants ranged from 1.013 (for SO2) to 1.022 (for O3), and for admissions for cardiovascular disease, from 1.006 (for PM10) to 1.016 (for SO2). Those aged > or = 65 years were at higher risk. Significant positive interactions were detected between NO2, O3, and PM10, and between O3 and winter months. CONCLUSIONS: Adverse health effects are evident at current ambient concentrations of air pollutants. Further reduction in air pollution is necessary to protect the health of the community, especially that of the high risk group. (+info)
Laboratory evaluation of welder's exposure and efficiency of air duct ventilation for welding work in a confined space.
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CO2 arc welding in a confined space was simulated in a laboratory by manipulating a welding robot which worked in a small chamber to experimentally evaluate the welder's exposure to welding fumes, ozone and carbon monoxide (CO). The effects of the welding arc on the air temperature rise and oxygen (O2) concentration in the chamber were also investigated. The measuring points for these items were located in the presumed breathing zone of a welder in a confined space. The time averaged concentrations of welding fumes, ozone and CO during the arcing time were 83.55 mg/m3, 0.203 ppm and 0.006%, respectively, at a welding current of 120A-200A. These results suggest serious exposure of a welder who operates in a confined space. Air temperature in the chamber rose remarkably due to the arc heat and the increase in the welding current. No clear decrease in the O2 concentration in the chamber was recognized during this welding operation. A model of air duct ventilation was constructed in the small chamber to investigate the strategy of effective ventilation for hazardous welding contaminants in a confined space. With this model we examined ventilation efficiency with a flow rate of 1.08-1.80 m3/min (ventilation rate for 0.40-0.67 air exchanges per minute) in the chamber, and proved that the exposure level was not drastically reduced during arcing time by this air duct ventilation, but the residual contaminants were rapidly exhausted after the welding operation. (+info)
Laboratory measurement of hazardous fumes and gases at a point corresponding to breathing zone of welder during a CO2 arc welding.
(51/1280)
Concentrations of fumes, ozone (O3), carbon monoxide (CO), nitric oxide (NO), manganese (Mn) and total and hexavalent chromium (Cr) as well as size distribution of fumes were measured at a point corresponding to the welder's breathing zone during CO2-arc welding, using a welding robot and three kinds of wires. Concentrations of fumes, O3, CO, Mn and total-Cr were found to exceed their corresponding occupational exposure limit (OEL) values, while the concentrations of NO and Cr(VI) were below those OEL levels. Airborne concentration of Mn exceeded its OEL value, and the Mn content was 8 times higher in welding fumes than in the wire. Using an additive equation of OEL and exposure concentration of each hazardous component, health risk in welders with combined exposure to welding fumes and gases was assessed as 18.6 to 46.0 times of OEL, which exceeded the unity. This finding suggests that effective protection of welders from the exposure can be attained by use of the supplied-air respirator or combined use of a dust respirator and a local exhaust system. (+info)
Studies on the biological effects of ozone: 10. Release of factors from ozonated human platelets.
(52/1280)
In a previous work we have shown that heparin, in the presence of ozone (O3), promotes a dose-dependent platelet aggregation, while after Ca2+ chelation with citrate, platelet aggregation is almost negligible. These results led us to think that aggregation may enhance the release of platelet components. We have here shown that indeed significantly higher amount of platelet-derived growth factor (PDGF), transforming growth factor beta1 (TGF-beta1) and interleukin-8 (IL-8) are released in a dose-dependent manner after ozonation of heparinised platelet-rich plasma samples. These findings may explain the enhanced healing of torpid ulcers in patients with chronic limb ischemia treated with O3 autohaemoteraphy (O3-AHT). (+info)
Prevention of renal injury after induction of ozone tolerance in rats submitted to warm ischaemia.
(53/1280)
On the basis that ozone (O3) can upregulate cellular antioxidant enzymes, a morphological, biochemical and functional renal study was performed in rats undergoing a prolonged treatment with O3 before renal ischaemia. Rats were divided into four groups: (1) control, a medial abdominal incision was performed to expose the kidneys; (2) ischaemia, in animals undergoing a bilateral renal ischaemia (30 min), with subsequent reperfusion (3 h); (3) O3 + ischaemia, as group 2, but with previous treatment with O3 (0.5 mg/kg per day given in 2.5 ml O2) via rectal administration for 15 treatments; (4) O2 + ischaemia, as group 3, but using oxygen (O2) alone. Biochemical parameters as fructosamine level, phospholipase A, and superoxide dismutases (SOD) activities, as well as renal plasma flow (RPF) and glomerular filtration rate (GFR), were measured by means of plasma clearance of p-amino-hippurate and inulin, respectively. In comparison with groups 1 and 3, the RPF and GFR were significantly decreased in groups 2 and 4. Interestingly, renal homogenates of the latter groups yielded significantly higher values of phospholipase A activity and fructosamine level in comparison with either the control (1) and the O3 (3) treated groups. Moreover renal SOD activity showed a significant increase in group 3 without significant differences among groups 1, 2 and 4. Morphological alterations of the kidney were present in 100%, 88% and 30% of the animals in groups 2, 4 and 3, respectively. It is proposed that the O3 protective effect can be ascribed to the substantial possibility of upregulating the antioxidant defence system capable of counteracting the damaging effect of ischaemia. These findings suggest that, whenever possible, ozone preconditioning may represent a prophylactic approach for minimizing renal damage before transplantation. (+info)
The Harvard Southern California Chronic Ozone Exposure Study: assessing ozone exposure of grade-school-age children in two Southern California communities.
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The Harvard Southern California Chronic Ozone Exposure Study measured personal exposure to, and indoor and outdoor ozone concentrations of, approximately 200 elementary school children 6-12 years of age for 12 months (June 1995-May 1996). We selected two Southern California communities, Upland and several towns located in the San Bernardino mountains, because certain characteristics of those communities were believed to affect personal exposures. On 6 consecutive days during each study month, participant homes were monitored for indoor and outdoor ozone concentrations, and participating children wore a small passive ozone sampler to measure personal exposure. During each sampling period, the children recorded time-location-activity information in a diary. Ambient ozone concentration data were obtained from air quality monitoring stations in the study areas. We present ozone concentration data for the ozone season (June-September 1995 and May 1996) and the nonozone season (October 1995-April 1996). During the ozone season, outdoor and indoor concentrations and personal exposure averaged 48.2, 11.8, and 18.8 ppb in Upland and 60.1, 21.4, and 25.4 ppb in the mountain towns, respectively. During the nonozone season, outdoor and indoor concentrations and personal exposure averaged 21.1, 3.2, and 6.2 ppb in Upland, and 35.7, 2.8, and 5.7 ppb in the mountain towns, respectively. Personal exposure differed by community and sex, but not by age group. (+info)
Interstrain variation in murine susceptibility to inhaled acid-coated particles.
(55/1280)
Epidemiologic studies have demonstrated a positive correlation between concentration of acid aerosol and increased morbidity and mortality in many urban environments. To determine whether genetic background is an important risk factor for susceptibility to the toxic effects of inhaled particles, we studied the interstrain (genetic) and intrastrain (environmental) variance of lung responses to acid-coated particle (ACP) aerosol in nine strains of inbred mice. A flow-past nose-only inhalation system was used to expose mice to ACPs produced by the cogeneration of a carbon black aerosol-sulfur dioxide (SO(2)) mixture at high humidity. Three days after a single 4-h exposure to ACPs or filtered air, mice underwent bronchoalveolar lavage, and cell differentials and total protein were determined as indexes of inflammation and epithelial permeability, respectively. To determine the effect of ACPs on alveolar macrophage (AM) function, lavaged AMs were isolated from exposed animals and Fc receptor-mediated phagocytosis was evaluated. Compared with air-exposed animals, there was a slight but significant exposure effect of ACPs on the mean number of lavageable polymorphonuclear leukocytes in C3H/HeJ and C3H/HeOuJ mice. ACP exposure also caused a significant decrease in AM phagocytosis. Relative to respective air-exposed animals, Fc receptor-mediated phagocytosis was suppressed in eight of nine strains. The order of strain-specific effect of ACPs on phagocytosis was C57BL/6J > 129/J > SJL/J > BALB/cJ > C3H/HeOuJ > A/J > SWR/J > AKR/J. There was no effect of ACP exposure on AM phagocytosis in C3H/HeJ mice. The significant interstrain variation in AM response to particle challenge indicates that genetic background has an important role in susceptibility. The effects of ACPs on AM function, inflammation, and epithelial hyperpermeability were not correlated (i.e., no cosegregation). This model may have important implications concerning interindividual variation in particle-induced compromise of host defense. (+info)
Associations between ambient ozone, hydrocarbons, and childhood wheezy episodes: a prospective observational study in south east London.
(56/1280)
OBJECTIVES: To explore the hypothesis that hydrocarbon species and other air pollutants which accumulate at low and high concentrations of ozone are more directly associated with childhood wheezy episodes than ozone. METHODS: Prospective observational study over 1 year set in the Lewisham district of south east London. The daily attendance rate of children with acute wheeze at the accident and emergency department of Lewisham Hospital was related to local measurements of ozone, hydrocarbon species, nitrogen dioxide (NO2), sulphur dioxide (SO2) and small particulate matter with diameter < 10 microns (PM10). RESULTS: An inverse relation was found between the air pollutants and ozone. After seasonal and meteorological adjustment a non-linear U shaped trend was found between incidence of wheeze and ozone. The trend was significant in children < 2 years of age but not in older children. In the younger age group, after adjustment for season, temperature, wind speed, and respiratory infection, the incidence relative to that at the mean daily ozone concentration of 32.7 micrograms/m3, was estimated to increase by 65% (95% confidence interval (95% CI) 22% to 122%) at an ozone concentration of 5 micrograms/m3 (1.5 SDs below the mean) and by 63% (95% CI -6% to 184%) at 80 micrograms/m3 (2.5 SDs above the mean). For several hydrocarbons there were significant positive linear relations found, again in children < 2 years of age but not older children. For benzene, the incidence increased by 8% (95% CI 2 to 13%) per SD (SD 2.8 micrograms/m3) increase in benzene concentration. A same day association between incidence and ozone was found to be the most significant but for other pollutants a lag of 2 days gave the most significant associations. No significant association was found for the non-hydrocarbon pollutants including SO2, NO2, and PM10. CONCLUSIONS: A U shaped relation was found between ozone and the incidence of wheezy episodes in young children. Certain hydrocarbon pollutants accumulate in the atmosphere when ozone concentrations are low, and are associated with childhood wheezy episodes. However, the U shaped association of ozone on incidence cannot be explained by these other pollutants. The finding supports an earlier finding that incidences of wheeze are at a minimum when ozone concentrations are 30-40 micrograms/m3. (+info)