Irma Rosas

Bio: Irma Rosas is an academic researcher from National Autonomous University of Mexico. The author has contributed to research in topics: Aerosol & Environmental exposure. The author has an hindex of 34, co-authored 93 publications receiving 3260 citations. Previous affiliations of Irma Rosas include Texas A&M University.

Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition.

Abstract: Exposure to urban airborne particulate matter (PM) is associated with adverse health effects. We previously reported that the cytotoxic and proinflammatory effects of Mexico City PM10 (less than or equal to 10 micro m mean aerodynamic diameter) are determined by transition metals and endotoxins associated with these particles. However, PM2.5 (less than or equal to 2.5 micro m mean aerodynamic diameter) could be more important as a human health risk because this smaller PM has the potential to reach the distal lung after inhalation. In this study, we compared the cytotoxic and proinflammatory effects of Mexico City PM10 with those of PM2.5 using the murine monocytic J774A.1 cell line in vitro. PMs were collected from the northern zone or the southeastern zone of Mexico City. Elemental composition and bacterial endotoxin on PMs were measured. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) production by J774A.1 cells was measured in the presence or absence of recombinant endotoxin-neutralizing protein (rENP). Both northern and southeastern PMs contained endotoxin and a variety of transition metals. Southeastern PM10 contained the highest endotoxin levels, 2-fold higher than that in northern PM10. Northern and southeastern PM2.5 contained the lowest endotoxin levels. Accordingly, southeastern PM10 was the most potent in causing secretion of the proinflammatory cytokines TNF-alpha and IL-6. All PM2.5 and PM10 samples caused cytotoxicity, but northern PMs were the most toxic. Cytokine secretion induced by southeastern PM10 was reduced 50-75% by rENP. These results indicate major differences in PM10 and PM2.5. PM2.5 induces cytotoxicity in vitro through an endotoxin-independent mechanism that is likely mediated by transition metals. In contrast, PM10 with relatively high levels of endotoxin induces proinflammatory cytokine release via an endotoxin-dependent mechanism.

Recent Advances in Particulate Matter and Nanoparticle Toxicology: A Review of the In Vivo and In Vitro Studies

Abstract: Epidemiological and clinical studies have linked exposure to particulate matter (PM) to adverse health effects, which may be registered as increased mortality and morbidity from various cardiopulmonary diseases. Despite the evidence relating PM to health effects, the physiological, cellular, and molecular mechanisms causing such effects are still not fully characterized. Two main approaches are used to elucidate the mechanisms of toxicity. One is the use of in vivo experimental models, where various effects of PM on respiratory, cardiovascular, and nervous systems can be evaluated. To more closely examine the molecular and cellular mechanisms behind the different physiological effects, the use of various in vitro models has proven to be valuable. In the present review, we discuss the current advances on the toxicology of particulate matter and nanoparticles based on these techniques.

Biologic effects induced in vitro by PM10 from three different zones of Mexico City.

Abstract: Exposure to urban airborne particles is associated with an increase in morbidity and mortality There is little experimental evidence of the mechanisms involved and the role of particle composition We assessed cytotoxicity (crystal violet assay), apoptosis [terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) or annexin V assay], DNA breakage (comet assay), and production of proinflammatory mediators [tumor necrosis factor Alpha (TNF-Alpha), interleukin 6 (IL-6), prostaglandin E2 (PGE2)] (enzyme-linked immunosorbent assay), and E-selectin (flow cytometry) in cell lines exposed to particulate matter < 10 microm in size (PM10) obtained from the northern, central, and southern zones of Mexico City Particle concentrations ranged from 25 to 160 microg/cm(2) We used epithelial, endothelial, fibroblastic, and monocytic cells and assessed DNA damage in Balb-c cells, TNF-Alpha and IL-6 production in mouse monocytes, and PGE2 in rat lung fibroblasts We determined the expression of E-selectin in human endothelial cells and evaluated the cytotoxic potential of the PM10 samples in all cell types PM10 from all three zones of Mexico City caused cell death, DNA breakage, and apoptosis, with particles from the north and central zones being the most toxic All of these PM10 samples induced secretion of proinflammatory molecules, and particles from the central zone were the most potent Endothelial cells exposed to PM10 from the three zones expressed similar E-selectin levels Mexico City PM10 induced biologic effects dependent on the zone of origin, which could be caused by differences in the mixture or size distribution within particle samples Our data suggest that particle composition as well as particle size should be considered in assessing the adverse effects of airborne particulate pollution

Analysis of the relationships between environmental factors (aeroallergens air pollution and weather) and asthma emergency admissions to a hospital in Mexico City

Abstract: There have been several studies of the relationships between environmental factors, particularly air pollution, and attacks of asthma. Most of these studies have ignored the potential confounding effects of aeroallergens such as pollens and fungal spores. We report a statistical analysis of the relationships between emergency admissions for asthma to a hospital in Mexico City and daily average airborne concentrations of pollen, fungal spores, air pollutants (O3, NO2, SO2, and particulates) and weather factors. Asthma admissions had a seasonal pattern with more during the wet season (May-October) than the dry season (November-April). There were few statistical associations between asthma admissions and air pollutants for the three age groups studied (children under 15 years, adults, and seniors [adults over 59 years]) in either season. Grass pollen was associated with child and adult admissions for both the wet and dry seasons, and fungal spores were associated with child admissions during both the wet and dry seasons. The analysis was done with environmental data averaged over the day of admission and the 2 previous days. Our results suggest that aeroallergens may be statistically associated more strongly with asthma hospital admissions than air pollutants and may act as confounding factors in epidemiologic studies.

Arsenic Concentrations in Water, Soil, Milk and Forage in Comarca Lagunera, Mexico

Abstract: Arsenic levels were determined in seventy three samples of well water, and in fifty samples of soil, forage and cow's milk collected at the most important dairy farms of the Comarca Lagunera located in Coahuila and Durango, Mexico, region naturally rich in As. The total inorganic arsenic concentration in well water ranged from 7 to 740 μg L-1 and about ninety percent of the total arsenic was found as As(V). The agricultural soil texture of the sampled area was sandy clay loam type with total arsenic levels up to 30 μg g-1, however, the extractable arsenic was not higher than 12% of the total and it was higher in the 0–30 cm depth horizon. In alfalfa, the most important crop, the total aresenic ranged from 0.24 to 3.16 μg g-1, with 40% of it accumulated at the root level. Significant correlations (p=0.05) were obtained between arsenic (III), (V) and total inorganic arsenic in groundwater with arsenic in soil (0–30 cm depth), and with arsenic in alfalfa (leaves and roots). It was also found a good correlation between extractable arsenic in soil with As concentrations in alfalfa (roots). Arsenic concentrations found in milk ranged from <0.9 to 27.4 ng g-1. The cow's milk biotransfer factor for arsenic was up to 6 × 10-4, applying a pharmacokinetic approach. It was associated with the exposure not only to food but also to water arsenic.

Atmospheric pollution profiles in Mexico City in two different seasons

Abstract: A CO2-laser-based photoacoustic spectrometer was used to determine the temporal concentration profile of atmospheric ethene in Mexico City. Ethene measurements were conducted at the facilities of our institute, which is located in the north of the city and next to an avenue with heavy traffic density. Ambient air from outside our laboratory was continuously pumped into the spectrometer. This campaign was performed for 24 h a day, from November 24–30, 2001. The maximum ethene levels ranged between 26 and 81 ppbV. As expected, the lowest concentrations were monitored on weekends. These data were analyzed in combination with ozone and nitrogen oxides profiles, which were permanently monitored by an air-pollution-monitoring government network. Information on the seasonal variability of ethene was obtained by comparing the results of this campaign with data obtained in the winter of 2001. In general, the ethene concentration in November was about 30% higher than in February. On weekdays, the mean dose of human...

Variability of Absorption and Optical Properties of Key Aerosol Types Observed in Worldwide Locations

Abstract: Aerosol radiative forcing is a critical, though variable and uncertain, component of the global climate. Yet climate models rely on sparse information of the aerosol optical properties. In situ measurements, though important in many respects, seldom provide measurements of the undisturbed aerosol in the entire atmospheric column. Here, 8 yr of worldwide distributed data from the AERONET network of ground-based radiometers were used to remotely sense the aerosol absorption and other optical properties in several key locations. Established procedures for maintaining and calibrating the global network of radiometers, cloud screening, and inversion techniques allow for a consistent retrieval of the optical properties of aerosol in locations with varying emission sources and conditions. The multiyear, multi-instrument observations show robust differentiation in both the magnitude and spectral dependence of the absorption—a property driving aerosol climate forcing, for desert dust, biomass burning, urban‐industrial, and marine aerosols. Moreover, significant variability of the absorption for the same aerosol type appearing due to different meteorological and source characteristics as well as different emission characteristics are observed. It is expected that this aerosol characterization will help refine aerosol optical models and reduce uncertainties in satellite observations of the global aerosol and in modeling aerosol impacts on climate.

TLR4 mutations are associated with endotoxin hyporesponsiveness in humans.

Abstract: There is much variability between individuals in the response to inhaled toxins, but it is not known why certain people develop disease when challenged with environmental agents and others remain healthy. To address this, we investigated whether TLR4 (encoding the toll-like receptor-4), which has been shown to affect lipopolysaccharide (LPS) responsiveness in mice 1,2 , underlies the variability in airway responsiveness to inhaled LPS in humans 3 . Here we show that common, co-segregating missense mutations (Asp299Gly and Thr399Ile) affecting the extracellular domain of the TLR4 receptor are associated with a blunted response to inhaled LPS in humans. Transfection of THP-1 cells demonstrates that the Asp299Gly mutation (but not the Thr399Ile mutation) interrupts TLR4-mediated LPS signalling. Moreover, the wild-type allele of TLR4 rescues the LPS hyporesponsive phenotype in either primary airway epithelial cells or alveolar macrophages obtained from individuals with the TLR4 mutations. Our findings provide the first genetic evidence that common mutations in TLR4 are associated with differences in LPS responsiveness in humans, and demonstrate that gene-sequence changes can alter the ability of the host to respond to environmental stress. We investigated the genetic basis for the physiologic response to inhaled endotoxin or LPS for several reasons. First, endotoxin is associated with the development and progression of asthma and other forms of airway disease. In the domestic setting, the concentration of endotoxin is associated with the clinical severity of asthma 4 , and, among exposed workers, endotoxin is the most significant component of the bioaerosol that is associated with the development 5 and progression 6 of airway disease. Endotoxin may also have a role in the pathophysiological consequences of air pollution 7 . Second, the ability of the host to respond to endotoxin is highly variable. Differences between individuals have been reported in the release and synthesis of cytokines by human monocytes stimulated with LPS in vitro 8 , and a patient with recurrent bacterial infections has been reported to be refractory to the in vivo and in vitro effects of LPS (ref. 9). We have recently found that normal, healthy, non-asthmatic subjects demonstrate a reproducible airway response to an incremental LPS inhalation challenge test; some subjects developed airflow obstruction when challenged with low concentrations of LPS and others were unaffected by high concentrations of inhaled LPS (ref. 3). Third, the