PubMed · 13624442
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M MONCHOT. 1958. [Air pollution].. https://pubmed.ncbi.nlm.nih.gov/13624442/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Capturing the spatiotemporal distribution of pollutants in industrial parks remains challenging for regional air quality models because of their coarse resolution (3 km), resulting in uncertainties in local emission quantification. To address this, we developed the Integrated Multiscale Air Quality Modelling System for Industry (IAQMS-Industry), coupling the regional Nested Air Quality Prediction Modelling System (NAQPMS) with a city-scale chemical transport model. This framework integrates point-source locations and Gaussian plume dispersion to simulate particulate matter with a diameter smaller than 2.5 micrometres (PM2.5) at 100 m resolution. Applied to the Beijing Yi Zhuang and Tangshan industrial parks and evaluated against observations. The coupled model achieved a normalized mean bias (NMB) ranging from 3.1 % to 6.2 %, improving upon NAQPMS (-16.9 % to -7.7 %). Spatial analysis revealed that coarse regional grids underestimated the PM2.5​ concentrations at industrial sites by smoothing gradients, whereas IAQMS-Industry successfully resolved spatial patterns. Industrial point emissions accounted for 22.9 %-26.4 % of PM2.5 in the coupled model, which was significantly greater than the regional model estimates of 1.6 %-13.7 %. These findings indicate that regional models overestimate pollutant dispersion processes in industrial parks while underestimating local industrial impacts. By explicitly resolving point-source dynamics and linking them to regional transport, IAQMS-Industry provides a robust tool for designing targeted emission controls in industrial cities and balancing local air quality improvements with minimized regional pollution outflow. This study underscores the necessity of multiscale modelling for accurate source apportionment and informed environmental governance in industrial zones.
This study was undertaken to determine whether there is an association between air pollutants levels and increased number of hospital admissions for cardiovascular diseases (CVD) in Kaohsiung, Taiwan. Hospital admissions records for CVD and ambient air contaminant data collected from monitoring station in Kaohsiung were obtained for the period 1997-2000. The relative risk of hospital admission for CVD was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. In the single-pollutant model, on warm days (> or =25 degrees C) statistically significant positive associations were found between levels of particular matter of < 10 microm aerodynamic diameter (PM10), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). On cool days (< 25 degrees C), all pollutants except O3 were significantly associated with increased CVD admissions. For the two-pollutant model, CO and O3 were both significant in combination with each of the other four contaminants on warm days. PM10 and NO2 remained significantly associated with elevated CVD admissions on warm days. On cool days, CO and NO2 remained statistically significant in all the two-pollutant models. This study provides evidence that higher levels of ambient contaminants, particularly CO, increase the risk of increased hospital admissions for CVD.
Lung and skin are the organs directly exposed to environmental pollution. Ozone (O(3)) is a toxic, oxidant air pollutant, and exposure has been shown to induce antioxidant depletion as well as oxidation of lipids and proteins within the outermost skin layer (stratum corneum) and the lung respiratory tract lining fluids (RTLFs). To further define skin and lung responses to O(3) exposure, SKH-1 hairless mice were exposed to either 0.8 ppm of O(3) (a level occasionally reached in very polluted areas) or ambient air 6 h/day for 6 consecutive days. O(3) exposure resulted in the depletion of alpha-tocopherol in lung and plasma and induction in both skin and lung of heme oxygenase 1, cyclooxygenase 2, and proliferating cell nuclear antigen. O(3)-exposed animals showed a similar extent of upregulation of COX-2 and PCNA in lung and skin, whereas HO-1 was more responsive in skin than in lung (7-fold induction vs. 2-fold induction). In addition to these measures of response to oxidative stress, O(3) exposure led to the activation of nuclear factor kappaB measured as IkappaBalpha phosphorylation in both tissues. We conclude that in this model, O(3) at high pollutant levels is able to affect both lung and skin biology, inducing depletion of alpha-tocopherol and inducing stress-related responses in both skin epidermis and respiratory tract epithelium.