Iron-rich air pollution nanoparticles: An unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress.

Exposure to particulate air pollution is a major environmental risk factor for cardiovascular mortality and morbidity, on a global scale. Both acute and chronic cardiovascular impacts have so far been attributed to particulate-mediated oxidative stress in the lung and/or via 'secondary' pathways, including endothelial dysfunction, and inflammation. However, increasing evidence indicates the translocation of inhaled nanoparticles to major organs via the circulation. It is essential to identify the composition and intracellular targets of such particles, since these are likely to determine their toxicity and consequent health impacts. Of potential major concern is the abundant presence of iron-rich air pollution nanoparticles, emitted from a range of industry and traffic-related sources. Bioreactive iron can catalyse formation of damaging reactive oxygen species, leading to oxidative stress and cell damage or death. Here, we identify for the first time, in situ, that exogenous nanoparticles (~15-40 nm diameter) within myocardial mitochondria of young, highly-exposed subjects are dominantly iron-rich, and co-associated with other reactive metals including aluminium and titanium. These rounded, electrodense nanoparticles (up to ~ 10 x more abundant than in lower-pollution controls) are located within abnormal myocardial mitochondria (e.g. deformed cristae; ruptured membranes). Measurements of an oxidative stress marker, PrPC and an endoplasmic reticulum stress marker, GRP78, identify significant ventricular up-regulation in the highly-exposed vs lower-pollution controls. In shape/size/composition, the within-mitochondrial particles are indistinguishable from the iron-rich, combustion- and friction-derived nanoparticles prolific in roadside/urban environments, emitted from traffic/industrial sources. Incursion of myocardial mitochondria by inhaled iron-rich air pollution nanoparticles thus appears associated with mitochondrial dysfunction, and excess formation of reactive oxygen species through the iron-catalyzed Fenton reaction. Ventricular oxidative stress, as indicated by PrPC and GRP78 up-regulation, is evident even in children/young adults with minimal risk factors and no co-morbidities. These new findings indicate that myocardial iron overload resulting from inhalation of airborne, metal-rich nanoparticles is a plausible and modifiable environmental risk factor for cardiac oxidative stress and cardiovascular disease, on an international scale.

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond.

Air pollution (indoors and outdoors) is a major issue in public health as epidemiological studies have highlighted its numerous detrimental health consequences (notably, respiratory and cardiovascular pathological conditions). Over the past 15 years, air pollution has also been considered a potent environmental risk factor for neurological diseases and neuropathology. This review examines the impact of air pollution on children's brain development and the clinical, cognitive, brain structural and metabolic consequences. Long-term potential consequences for adults' brains and the effects on multiple sclerosis (MS) are also discussed. One challenge is to assess the effects of lifetime exposures to outdoor and indoor environmental pollutants, including occupational exposures: how much, for how long and what type. Diffuse neuroinflammation, damage to the neurovascular unit, and the production of autoantibodies to neural and tight-junction proteins are worrisome findings in children chronically exposed to concentrations above the current standards for ozone and fine particulate matter (PM2.5), and may constitute significant risk factors for the development of Alzheimer's disease later in life. Finally, data supporting the role of air pollution as a risk factor for MS are reviewed, focusing on the effects of PM10 and nitrogen oxides.

Diurnal variations of airborne pollen concentration and the effect of ambient temperature in three sites of Mexico City.

Pollen is an important cause of allergic respiratory ailments in the Mexico City Metropolitan Area (MCMA). However, very little is known if ambient air temperature correlates with the early blooming of plants observed in other urban areas around the world. A research study was conducted during the dry season of 2012-2013 at three representative sites of the MCMA with different urban characteristics with the aim to understand the relationships between the profusion and diversity of pollen against temperature and other meteorological variables and degree of urbanization. Pollen samples were collected using a Hirst-type trap sampler in the sites: Merced (highly urbanized), Iztapalapa (medium-high urbanized) and Coyoacan (moderately urbanized). Urbanization levels were determined using a composite index based on population density, proportion of surface covered by construction and asphalt, and urban heat island intensity. A set of representative pollen sampling tapes were assayed under a light microscope at magnification of ×1,000 and converted to grains per cubic meter. The most representative pollen types found in the three sites were, regardless of urbanization levels were: Fraxinus, Cupressaceae/Taxodiaceae, Casuarina, Alnus, Myrtaceae, and Pinus. Total pollen concentration was greatest in the moderately urbanized area, although earlier blooming took place at the highly urbanized zone. Total pollen concentration in the medium-high urbanized site has the lowest because the green areas in this zone of MCMA are few. In a diurnal basis, the most abundant pollen types peaked near midday or in the afternoon evening at the three sites. A Spearman test showed a positive correlation among bihourly pollen concentrations, temperature and relative humidity in all sites, but wind speed just correlated in Iztapalapa and Coyoacan. The results obtained suggest that Urban Heat Island Intensity can disturb flowering periods and pollen concentrations, largely in the highly urbanized areas. A principal components analysis established that the concentrations of each pollen type differed across the urbanization gradients. Additionally, it was found that a large number of allergenic pollens are produced by ornamental trees, some only recently introduced by urban planners.

Study of the regional air quality south of Mexico City (Morelos state).

Results from the first study of the regional air quality in Morelos state (located south of Mexico City) are presented. Criteria pollutants concentrations were measured at several sites within Morelos in February and March of 2007 and 2009; meteorological data was also collected along the state for the same time periods; additionally, a coupled meteorology-chemistry model (Mesoscale Climate Chemistry Model, MCCM) was used to gain understanding on the atmospheric processes occurring in the region. In general, concentrations of almost all the monitored pollutants (O(3), NO(x), CO, SO(2), PM) remained below the Mexican air quality standards during the campaign; however, relatively high concentrations of ozone (8-hour average concentrations above the 60 ppb level several times during the campaigns, i.e. exceeding the World Health Organization and the European Union maximum levels) were observed even at sites with very low reported local emissions. In fact, there is evidence that a large percentage of Morelos vegetation was probably exposed to unhealthy ozone levels (estimated AOT40 levels above the 3 ppm h critical limit). The MCCM qualitatively reproduced ozone daily variations in the sites with an urban component; though it consistently overestimated the ozone concentration in all the sites in Morelos. This is probably because the lack of an updated and detailed emission inventory for the state. The main wind patterns in the region corresponded to the mountain-valley system (downslope flows at night and during the first hours of the day, and upslope flows in the afternoon). At times, Morelos was affected by emissions from surrounding states (Distrito Federal or Puebla). The results are indicative of an efficient transport of ozone and its precursors at a regional level. They also suggest that the state is divided in two atmospheric basins by the Sierras de Tepoztlán, Texcal and Monte Negro.

Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants.

Mexico City children are chronically exposed to significant concentrations of air pollutants and exhibit chronic respiratory-tract inflammation. Epidemiological, controlled human exposures, laboratory-based animal models, and in vitro/in vivo studies have shown that inflammatory, endothelial dysfunction, and endothelial damage mediators are upregulated upon exposure to particulate matter (PM). Endothelial dysfunction is a critical event in cardiovascular disease. The focus of this work was to investigate whether exposure to ambient air pollution including PM(2.5) produces systemic inflammation and endothelial injury in healthy children. We measured markers of endothelial activation, and inflammatory mediators in 52 children age 8.6+/-0.1 yr, residents of Mexico City (n: 28) or of Polotitlán (n: 24), a city with low levels of pollutants. Mexico City children had significant increases in inflammatory mediators and vasoconstrictors, including tumor necrosis factor (TNF)alpha, prostaglandin (PG) E2, C-reactive protein, interleukin-1beta, and endothelin-1. There was a significant anti-inflammatory response, and a downregulation of vascular adhesion molecule-1, intercellular adhesion molecule-1 and -2, and selectins sE and sL. Results from linear regression found TNF a positively associated with 24- and 48-h cumulative levels of PM(2.5), while the 7-d PM(2.5) value was negatively associated with the numbers of white blood cells in peripheral blood in highly exposed children. Systemic subclinical inflammation, increased endothelin- 1, and significant downregulation of soluble adhesion molecules are seen in Mexico City children. Children chronically exposed to fine PM above the standard could be at risk of developing cardiovascular diseases, atherosclerosis, stroke, and other systemic effects later in life.