Description: Exposure to high levels of particulate matter from wildfire smoke during pregnancy may negatively affect birth outcomes including birth weight, preterm delivery, and intrauterine growth restriction or later health during infancy, regardless of subsequent exposure levels or background ambient air pollution levels. We will investigate the effect of wildfire generated PM 10 and PM 2.5 on these birth outcomes, using California vital statistics records for 2003-2004 and exposures estimates created at the zipcode level for the week of the wildfires in eight counties in southern California. These estimates will be derived in a GIS framework using a combination of existing data from an extensive monitoring network, light extinction data, meteorological conditions, and smoke information extracted from MODIS satellite images. Exact addresses from records will be converted to mapping coordinates and assigned an exposure estimate for wildfire PM and for background ambient PM throughout the pregnancy. Logistic regression will then be used to determine whether an association exists with wildfire PM exposure for each of the outcomes of interest. Given previous evidence linking ambient PM to birth outcomes, we expect that peak exposures to extremely high levels of PM during critical developmental stages in pregnancy may also negatively affect birth outcomes, even after taking into account background ambient air pollution exposure.

Award Amount: $15,475

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Exposure to Airborne Allergens and Endotoxins During Pregnancy and the Risk of Preterm Delivery

Description: Studies of air pollution and pregnancy outcomes have focused mainly on pollutants of outdoor origin, such as pollution from vehicle exhaust and industrial sources. However, there is a growing literature that implicates indoor air as a major source of pollution exposure affecting birth outcomes, mostly in studies of cigarette smoking or biomass cooking fuels in rural areas. Because pregnant women in the United States spend a large majority of their time indoors, it is important to determine whether indoor air pollution is a risk factor for preterm delivery. The UCLA Environment and Pregnancy Outcomes Study (EPOS) is a case-control survey of 2,543 Los Angeles (LA) County mothers who gave birth in 2003. The survey collected data on indoor sources of air pollution and allergens to study the effects on adverse birth outcomes. Survey questions asked about potential sources of allergens (pets), indoor combustion sources (smoking, gas appliances, and cooking methods) and housing characteristics that may affect indoor air exposures (ventilation and carpeting). Dust wipe samples were collected at the homes of these babies at the time of the survey (approximately 3-6 months post-delivery). Here we are proposing to analyze a sample of 50 of these wipes for animal allergens and bacterial endotoxin. We will use these data to validate our survey measures of indoor sources of allergen exposure and housing characteristics that may affect a mother's indoor exposure. Additionally, we will develop indoor air pollution measures based on survey data on multiple pollutant sources, and evaluate whether these measures affect the risk of delivering preterm. Finally, we wish to evaluate the joint effects of indoor and outdoor air pollution on preterm birth. This study will provide key validation data for our indoor allergen air pollution measures, and provide a basis for us to seek grant funding to study how in utero and early childhood exposures to indoor and outdoor air pollutants affect a child's risk of developing respiratory symptoms and diseases, such as asthma.

Award Amount: $ 9,788

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Description: We propose to validate new approaches for the characterization of airborne allergens by (i) conducting a year-long evaluation of a newly developed computer-vision system for pollen counting and identification, and (ii) fabricating, calibrating, and conducting preliminary field tests of a new sampling system that is optimized for the analysis of allergens that are found in airborne respirable-sized fragments. A Burkard pollen sampler will be operated on the roof of a building on the Caltech campus to collect pollen samples at regular intervals, at least twice per week. A computerized microscope will be used to capture images from the Burkard tapes for computer identification using software developed at Caltech. Computerized pollen counts will be performed on all samples. Traditional manual pollen counts will also be performed periodically in order to evaluate the accuracy of the computerized pollen count. The second activity will produce a prototype of a novel impaction system that has been designed based upon computational fluid dynamics simulations with the objective of collecting size-resolved samples of atmospheric aerosols into low surface area vials that minimize blanks and sample extraction difficulties. This particle trap impactor will then be calibrated to determine its collection efficiency characteristics. Preliminary evaluation of its utility for bioaerosol sampling will be undertaken during a single pollen season. This pilot study will enable completion and validation of two technologies that should prove very useful in the study of allergic disease.

 

Award Amount: $25,000

Description: Emphysema is a devastating pulmonary disease with high mortality and morbidity, particularly in the smoking population. However, only 15% of smoking population develops emphysema. Therefore, emphysema is thought to be caused by many genetic factors, in combination with harmful environmental factors including cigarette smoke. Our previous studies found that (1) abrogation of intracellular TGF-ß-Smad3 pathway resulted in early abnormal alveolarization, followed by subsequent centrilobular emphysema in mice; (2) short term exposure (three weeks) of side stream smoke in young Smad3 (a TGF-ß downstream component) null mutant mice also exacerbated early onset of emphysematic pathology. Thus, we hypothesize that Thus, we hypothesize that deficiency of TGF-ß signaling in lung epithelial cells and/or inflammatory system makes predisposition to emphysema, in particular with cigarette smoke exposure. The proposed studies will generate preliminary data and potential publication on the relationship between abnormally developed lung caused by genetic mutation and cigarette smoke-induced early onset emphysema.These will further help to seek NIEHS R01 funding to expand the studies on cigarette smoke exposure in childhood and genetic susceptibility to emphysema.

Award Amount: $25,000

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Description: There is no doubt that environmental exposures have significant effects on human diseases. Yet the mechanisms behind these effects are uncertain. In this pilot project, we revisit an old hypothesis with more modern molecular tools. Many mutagens are also mitogens, and the primary mode of damage by many significant environmental agents may be mediated by increased cell proliferation. However, it has been extremely difficult to document increased proliferation because direct counting of cell division is impossible. We propose that many environmental agents increase cell proliferation and result in greater mitotic ages (total numbers of divisions since the zygote) in exposed individuals. In this pilot project, we propose to use a novel epigenetic mitotic clock or odometer to measure the mitotic ages of buccal cells. At certain CpG sites, DNA methylation appears to primarily represent replication errors; the greater the number of cell divisions, the higher the level of clock DNA methylation. Individuals exposed to certain environmental agents should have cells with greater mitotic ages.

Award Amount: $25,000

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