Erika Garcia

Prof. Erika Garcia

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Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 2020 in Annals of the American Thoracic Society
Verified
Journal Article
Open access
GTGeorge Thurston
George Thurston
John BalmesJohn Balmes
John Balmes
EGErika Garcia
Erika Garcia
FGFrank D. Gilliland
Frank D. Gilliland
MRMary B. Rice
Mary B. Rice
CWCarl W. White
Carl W. White
Although it is well accepted that air pollution exposure exacerbates preexisting airway disease, it has not been firmly established that long-term pollution exposure increases the risk of new-onset asthma or chronic obstruction pulmonary disease (COPD). This Workshop brought together experts on mechanistic, epidemiological, and clinical aspects of airway disease to review current knowledge regarding whether air pollution is a causal factor in the development of asthma and/or COPD. Speakers presented recent evidence in their respective areas of expertise related to air pollution and new airway disease incidence, followed by interactive discussions. A writing committee summarized their collective findings. The Epidemiology Group found that long-term exposure to air pollution, especially metrics of traffic-related air pollution such as nitrogen dioxide and black carbon, is associated with onset of childhood asthma. However, the evidence for a causal role in adult-onset asthma or COPD remains insufficient. The Mechanistic Group concluded that air pollution exposure can cause airway remodeling, which can lead to asthma or COPD, as well as asthma-like phenotypes that worsen with long-term exposure to air pollution, especially fine particulate matter and ozone. The Clinical Group concluded that air pollution is a plausible contributor to the onset of both asthma and COPD. Available evidence indicates that long-term exposure to air pollution is a cause of childhood asthma, but the evidence for a similar determination for adult asthma or COPD remains insufficient. Further research is needed to elucidate the exact biological mechanism underlying incident childhood asthma, and the specific air pollutant that causes it.

1 November 2022 in American Journal of Respiratory and Critical Care Medicine
Verified
Journal Article
Open access
MRMostafijur Rahman
Mostafijur Rahman
RMRob McConnell
Rob McConnell
HSHannah Schlaerth
Hannah Schlaerth
JKJoseph Ko
Joseph Ko
SSSam Silva
Sam Silva
EGErika Garcia
Erika Garcia
Rationale: Extremes of heat and particulate air pollution threaten human health and are becoming more frequent because of climate change. Understanding the health impacts of coexposure to extreme heat and air pollution is urgent. Objectives: To estimate the association of acute coexposure to extreme heat and ambient fine particulate matter (PM2.5) with all-cause, cardiovascular, and respiratory mortality in California from 2014 to 2019. Methods: We used a case-crossover study design with time-stratified matching using conditional logistic regression to estimate mortality associations with acute coexposures to extreme heat and PM2.5. For each case day (date of death) and its control days, daily average PM2.5 and maximum and minimum temperatures were assigned (0- to 3-day lag) on the basis of the decedent’s residence census tract. Measurements and Main Results: All-cause mortality risk increased 6.1% (95% confidence interval [CI], 4.1–8.1) on extreme maximum temperature-only days and 5.0% (95% CI, 3.0–8.0) on extreme PM2.5-only days, compared with nonextreme days. Risk increased by 21.0% (95% CI, 6.6–37.3) on days with exposure to both extreme maximum temperature and PM2.5. Increased risk of cardiovascular and respiratory mortality on extreme coexposure days was 29.9% (95% CI, 3.3–63.3) and 38.0% (95% CI, −12.5 to 117.7), respectively, and were more than the sum of individual effects of extreme temperature and PM2.5 only. A similar pattern was observed for coexposure to extreme PM2.5 and minimum temperature. Effect estimates were larger over age 75 years. Conclusions: Short-term exposure to extreme heat and air pollution alone were individually associated with increased risk of mortality, but their coexposure had larger effects beyond the sum of their individual effects.

21 May 2019 in JAMA
Verified
Journal Article
Open access
PDF file
EGErika Garcia
Erika Garcia
KBKiros T. Berhane
Kiros T. Berhane
TITalat Islam
Talat Islam
RMRob McConnell
Rob McConnell
RURobert Urman
Robert Urman
FGFrank D. Gilliland
Frank D. Gilliland
Asthma is the most common pediatric chronic disease, estimated to have affected 14% of children globally in 2002-2003.1 There has been much interest in the effect of outdoor air pollution on asthma risk given its ubiquity and high levels in urban areas, which, compared with rural areas, have higher rates of asthma.2 Globally, outdoor air pollution has been recognized as a major public health concern and was estimated to have contributed 6.8% of the annual disability-adjusted life-years lost in 2016.3 Although ambient air pollution exposure has been causally linked to asthma exacerbations in children,4 evidence has been limited for a role in asthma development.2,4 There has been support for a link with close proximity to busy roads,4-6 but studies of regional pollutants, such as ozone, nitrogen dioxide, and particulate matter (PM), have provided less robust evidence.

1 July 2021 in Journal of Allergy and Clinical Immunology
Verified
Journal Article
Closed access
EGErika Garcia
Erika Garcia
MRMary B. Rice
Mary B. Rice
DGDiane R. Gold
Diane R. Gold

30 January 2015 in Environmental Health
Verified
Journal Article
Open access
PDF file
EGErika Garcia
Erika Garcia
SHSusan Hurley
Susan Hurley
DNDavid O Nelson
David O Nelson
AHAndrew Hertz
Andrew Hertz
PRPeggy Reynolds
Peggy Reynolds
Studies suggest that higher breast cancer rates in urban areas persist after accounting for the prevalence of known risk factors, leading to speculation that urban environmental exposures, such as air pollution, may play a role in the etiology of breast cancer. Combining modeled ambient air concentrations with data from a large prospective cohort of California women with over 15 years of follow-up, we examined the relationship between breast cancer incidence and modeled concentrations of air pollutants shown to be mammary gland carcinogens (MGCs). The study population of 112,378 California Teachers Study participants included 5,676 women diagnosed with invasive breast cancer. Modeled annual average ambient air concentrations of 24 MGCs from the U.S. Environmental Protection Agency were linked to participants’ addresses. Cox proportional hazards models were used to estimate hazard rate ratios and 95% confidence intervals associated with residential MGC levels. MGCs were examined individually and as a combined summary variable for all participants, in selected subsets, and by tumor hormone responsiveness. Initial models yielded some evidence for increased risk for several compounds, including acrylamide, carbon tetrachloride, chloroprene, 4,4'-methylene bis(2-chloroaniline), propylene oxide, and vinyl chloride, but after adjustment for multiple comparisons, only results for propylene oxide and vinyl chloride remained statistically significant. In subset analyses, estrogen-receptor positive or progesterone-receptor positive (ER+/PR+) tumors were associated with higher ambient levels of acrylamide, benzidine, carbon tetrachloride, ethylidene dichloride, and vinyl chloride, while ER-/PR- tumors were associated with higher ambient levels of benzene. Interesting results for different compounds were observed within certain subsets of the population. While our initial models yielded several elevated risk estimates, after adjusting for multiple comparisons and breast cancer risk factors, most hazard ratios were no longer statistically significant. Our subset analyses, however, suggest that elevated risk may be associated with some compounds for certain subgroups of interest. A summary variable for all 24 MGCs did not offer any advantage over the models for individual compounds. Results must be interpreted cautiously, as estimated exposure was limited to modeled annual average ambient air concentrations, and could not account for other sources or routes other than inhalation.

Lawrence A PalinkasLawrence A Palinkas
Lawrence A Palinkas
MHMichael S. Hurlburt
Michael S. Hurlburt
CFCecilia Fernandez
Cecilia Fernandez
JLJessenia De Leon
Jessenia De Leon
KYKexin Yu
Kexin Yu
RMRob S. McConnell
Rob S. McConnell
Little is known of how low-income residents of urban heat islands engage their knowledge, attitudes, behaviors, and resources to mitigate the health impacts of heat waves. In this qualitative study, we conducted semi-structured interviews with 40 adults in two such neighborhoods in Los Angeles California to explore their adaptation resources and behaviors, the impacts of heat waves on physical and mental health, and threat assessments of future heat waves. Eighty percent of participants received advanced warning of heat waves from television news and social media. The most common resource was air conditioning (AC) units or fans. However, one-third of participants lacked AC, and many of those with AC engaged in limited use due primarily to the high cost of electricity. Adaptation behaviors include staying hydrated, remaining indoors or going to cooler locations, reducing energy usage, and consuming certain foods and drinks. Most of the participants reported some physical or mental health problem or symptom during heat waves, suggesting vulnerability to heat waves. Almost all participants asserted that heat waves were likely to increase in frequency and intensity with adverse health effects for vulnerable populations. Despite limited resources, low-income residents of urban heat islands utilize a wide range of behaviors to minimize the severity of health impacts, suggesting they are both vulnerable and resilient to heat waves.