Diesel exhaust particulate matter induces multinucleate cells and zinc transporter-dependent apoptosis in human airway cells

The cellular effects of biodiesel emissions particulate matter (BDEP) and petroleum diesel emissions particulate matter (PDEP) were compared using a human airway cell line, A549. At concentrations of 25 µg/ml, diesel particulate matter induced the formation of multinucleate cells. In cells treated with a mixture of 80% PDEP:20% BDEP, 52% of cells were multinucleate cells compared with only 16% of cells treated with 20% PDEP:80% BDEP with a background multinucleate rate of 7%. These results demonstrate a causal relation between the formation of multinucleate cells and exposure to exhaust particulate matter, in particular diesel exhaust. Exposure of A549 cells to PDEP induced apoptosis, seen by active caspase-3 expression and the presence of cleaved pancytokeratin. PDEP exhaust was a much stronger inducer of cellular death through apoptosis than BDEP. There was an eightfold increase in the expression of SLC30A3 (zinc transporter-3 or ZnT3) in cells exposed to 80% PDEP:20% BDEP compared to untreated cells. The increase in ZnT3 expression seen in apoptotic cells following PDEP suggests a role for this zinc transporter in the apoptotic pathway, possibly through controlling zinc fluxes. As exposure to diesel exhaust particles is associated with asthma and apoptosis in airway cells, diesel exhaust particles may directly contribute to asthma by inducing epithelial cell death through apoptotic pathway.

Major grass pollen allergen Lol p 1 binds to diesel exhaust particles : implications for asthma and air pollution

Background Grass pollen allergens are known to be present in the atmosphere in a range of particle sizes from whole pollen grains (approx. 20 to 55 μim in diameter) to smaller size fractions < 2.5 μ (fine particles, PM2.5). These latter particles are within the respirable range and include allergen-containing starch granules released from within the grains into the atmosphere when grass pollen ruptures in rainfall and are associated with epidemics of thunderstorm asthma during the grass pollen season. The question arises whether grass pollen allergens can interact with other sources of fine particles, particularly those present during episodes of air pollution.

Objective We propose the hypothesis that free grass pollen allergen molecules, derived from dead or burst grains and dispersed in microdroplets of water in aerosols, can bind to fine particles in polluted air.

Methods We used diesel exhaust carbon particles (DECP) derived from the exhaust of a stationary diesel engine, natural highly purified Lol p 1, immunogold labelling with specific monoclonal antibodies and a high voltage transmission electron -microscopic imaging technique

Results DECP are visualized as small carbon spheres, each 30–60 nm in diameter, forming fractal aggregates about 1–2μ in diameter. Here we test our hypothesis and show by in vitro experiments that the major grass pollen allergen, Lol p I. binds to one defined class of fine particles, DECP.

Conclusion DECP are in the respirable size range, can bind to the major grass pollen allergen Lol p I under in vitro conditions and represent a possible mechanism by which allergens can become concentrated in polluted air and thus trigger attacks of asthma.

Contribution of climate and air pollution to variation in coronary heart disease mortality rates in England

There are substantial geographic variations in coronary heart disease (CHD) mortality rates in England that may in part be due to differences in climate and air pollution. An ecological cross-sectional multi-level analysis of male and female CHD mortality rates in all wards in England (1999–2004) was conducted to estimate the relative strength of the association between CHD mortality rates and three aspects of the physical environment - temperature, hours of sunshine and air quality. Models were adjusted for deprivation, an index measuring the healthiness of the lifestyle of populations, and urbanicity. In the fully adjusted model, air quality was not significantly associated with CHD mortality rates, but temperature and sunshine were both significantly negatively associated (p<0.05), suggesting that CHD mortality rates were higher in areas with lower average temperature and hours of sunshine. After adjustment for the unhealthy lifestyle of populations and deprivation, the climate variables explained at least 15% of large scale variation in CHD mortality rates. The results suggest that the climate has a small but significant independent association with CHD mortality rates in England.

Applications of redundancy analysis for the detection of chemical response patterns to air pollution in lichen

The lichens Ramalina celastri (Spreng.) Krog & Swinsc., Punctelia microsticta (Müll. Arg.) Krog and Canomaculina pilosa (Stizenb.) Elix & Hale were transplanted simultaneously to 17 urban-industrial sites in a northwestern area of Córdoba city, Argentina. The transplantation sites were set according to different environmental conditions: traffic, industries, tree cover, building height, topographic level, position in the block and distances from the river and from the power plant. Three months later, chlorophyll a, chlorophyll b, phaeophytin a, soluble proteins, hydroperoxy conjugated dienes, malondialdehyde concentration and sulfur accumulation were determined, and a pollution index was calculated for each sampling site. Redundancy analysis was applied to detect the variation pattern of the lichen variables that can be 'best' explained by the environmental variables considered. The present study provides information about both the specific pattern response of each species to atmospheric pollution, and environmental conditions that determine it. As regards pollutants emission sources R. celastri showed a chemical response associated mainly with pollutant released by the power plant and traffic. P. microsticta and C. pilosa responded mainly to industrial sources. Regarding environmental conditions that affect the spreading of air pollutants and their incidence on the bioindicator, the topographic level and tree cover surrounding the sampling site were found to be important for R. celastri, tree cover surrounding the sampling site and the building height affected P. microsticta, while building height did so for C. pilosa.

Air pollution and infant mortality: evidence from the expansion of natural gas infrastructure

We examine the impact of widespread adoption of natural gas as a source of fuel on infant mortality in Turkey, using variation across provinces and over time in the intensity of natural gas utilisation. Our estimates indicate that the expansion of natural gas infrastructure has resulted in a significant decrease in the rate of infant mortality. Specifically, a one-percentage point increase in natural gas intensity – measured by the rate of subscriptions to natural gas services – would cause the infant mortality rate to decrease by 4%, which would translate into approximately 348 infant lives saved in 2011 alone.

Data quality issues in the GIS modelling of air pollution and cardiovascular mortality in Bangalore

Cardiovascular disease (CVD) is the world's number one cause of mortality. Research in recent years has begun to illustrate a significant association between CVD and air pollution. As most of these studies employed traditional statistics, cross-sectional or meta-analysis methods, a study undertaken by the authors was designed to investigate how a geographical information system (GIS) could be used to develop a more efficient spatio-temporal method of analysis than the currently existing methods mainly based on statistical inference. Using Bangalore, India, as a case study, demographic, environmental and CVD mortality data was sought from the city. However, critical deficiencies in the quality of the environmental data and mortality records were identified and quantified. This paper discusses the shortcomings in the quality of mortality data, together with the development of a framework based on WHO guidelines to improve the defects, henceforth considerably improving data quality.