Mary Prunicki

All Publications

• Traffic-related Air Pollution is Associated with Glucose Dysregulation, Blood Pressure, and Oxidative Stress in Children. Environmental research Mann, J. K., Lutzker, L., Holm, S. M., Margolis, H. G., Neophytou, A. M., Eisen, E. A., Costello, S., Tyner, T., Holland, N., Tindula, G., Prunicki, M., Nadeau, K., Noth, E. M., Lurmann, F., Hammond, S. K., Balmes, J. R. 2021: 110870

  Abstract

  BACKGROUND: Metabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood.OBJECTIVES: To assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects.METHODS: We studied 299 children (ages 6-8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) - the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO2, elemental carbon, and fine particulate matter (PM2.5) - were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome.RESULTS: The study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m3 increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 mug/m3 increase in 6-month average PM2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO2 was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane.DISCUSSION: Our results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children.

  View details for DOI 10.1016/j.envres.2021.110870

  View details for PubMedID 33587949

• Immune biomarkers link air pollution exposure to blood pressure in adolescents. Environmental health : a global access science source Prunicki, M., Cauwenberghs, N., Ataam, J. A., Movassagh, H., Kim, J. B., Kuznetsova, T., Wu, J. C., Maecker, H., Haddad, F., Nadeau, K. 2020; 19 (1): 108

  Abstract

  BACKGROUND: Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents.METHODS: We randomly recruited 100 adolescents (mean age, 16years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant's home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders.RESULTS: Using PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P≤0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P≤0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation.CONCLUSIONS: For the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

  View details for DOI 10.1186/s12940-020-00662-2

  View details for PubMedID 33066786

• Wildfire smoke exposure is associated with decreased methylation of the PDL2 gene Prunicki, M., Miller, S., Hopkins, A., Poulin, M., Movassagh, H., Yan, L., Nadeau, K. AMER ASSOC IMMUNOLOGISTS. 2020

  View details for Web of Science ID 000589972401240

• Pollution-Associated Exposure Signature in Teenagers Haddad, F., Cauwenberghs, N., Movassagh, H., Maecker, H., Arthur, J., Wu, J., Nadeau, K., Prunicki, M. MOSBY-ELSEVIER. 2020: AB82

  View details for Web of Science ID 000517092700253

• Immunologic effects of forest fire exposure show increases in IL-1β and CRP. Allergy Prunicki, M. M., Dant, C. C., Cao, S. n., Maecker, H. n., Haddad, F. n., Kim, J. B., Snyder, M. n., Wu, J. n., Nadeau, K. n. 2020

  View details for DOI 10.1111/all.14251

  View details for PubMedID 32112439

• Advances and novel developments in environmental influences on the development of atopic diseases. Allergy Alkotob, S. S., Cannedy, C. n., Harter, K. n., Movassagh, H. n., Paudel, B. n., Prunicki, M. n., Sampath, V. n., Schikowski, T. n., Smith, E. n., Zhao, Q. n., Traidl-Hoffmann, C. n., Nadeau, K. C. 2020

  Abstract

  Although genetic factors play a role in the etiology of atopic disease, the rapid increases in the prevalence of these diseases over the last few decades suggest that environmental, rather than genetic factors are the driving force behind the increasing prevalence. In modern societies, there is increased time spent indoors, use of antibiotics, and consumption of processed foods and decreased contact with farm animals and pets, which limit exposure to environmental allergens, infectious parasitic worms, and microbes. The lack of exposure to these factors is thought to prevent proper education and training of the immune system. Increased industrialization and urbanization has brought about increases in organic and inorganic pollutants. In addition, Caesarian birth, birth order, increased use of soaps and detergents, tobacco smoke exposure and psychosomatic factors are other factors that have been associated with increased rate of allergic diseases. Here, we review current knowledge on the environmental factors that have been shown to affect the development of allergic diseases and the recent developments in the field.

  View details for DOI 10.1111/all.14624

  View details for PubMedID 33037680

• Immunology of COVID-19: mechanisms, clinical outcome, diagnostics and perspectives - a report of the European Academy of Allergy and Clinical Immunology (EAACI). Allergy Sokolowska, M. n., Lukasik, Z. n., Agache, I. n., Akdis, C. A., Akdis, D. n., Akdis, M. n., Barcik, W. n., Brough, H. n., Eiwegger, T. n., Eliaszewicz, A. n., Eyerich, S. n., Feleszko, W. n., Gomez Casado, C. n., Hoffmann-Sommergruber, K. n., Janda, J. n., Jiménez-Saiz, R. n., Jutel, M. n., Knol, E. n., Kortekaas Krohn, I. n., Kothari, A. n., Makowska, J. n., Moniuszko, M. n., Morita, H. n., O'Mahony, L. n., Nadeau, K. n., Ozdemir, C. n., Pali-Schöll, I. n., Palomares, O. n., Papaleo, F. n., Prunicki, M. n., Schmidt-Weber, C. B., Sediva, A. n., Schwarze, J. n., Shamji, M. H., Tramper-Stranders, G. n., van, W. n., de Veen, n. n., Untersmayr, E. n. 2020

  Abstract

  With the worldwide spread of the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) resulting in declaration of a pandemic by the World Health Organization (WHO) on March 11, 2020, the SARS-CoV-2-induced Coronavirus disease-19 (COVID-19) has become one of the main challenges of our times. The high infection rate and the severe disease course led to major safety and social restriction measures worldwide. There is an urgent need of unbiased expert knowledge guiding the development of efficient treatment and prevention strategies. This report summarizes current immunological data on mechanisms associated with the SARS-CoV-2 infection and COVID-19 development and progression to the most severe forms. We characterize the differences between adequate innate and adaptive immune response in mild disease and the deep immune dysfunction in the severe multi-organ disease. The similarities of the human immune response to SARS-CoV-2 and the SARS-CoV and MERS-CoV are underlined. We also summarize known and potential SARS-CoV-2 receptors on epithelial barriers, immune cells, endothelium and clinically involved organs such as lung, gut, kidney, cardiovascular and neuronal system. Finally, we discuss the known and potential mechanisms underlying the involvement of comorbidities, gender and age in development of COVID-19. Consequently, we highlight the knowledge gaps and urgent research requirements to provide a quick roadmap for ongoing and needed COVID-19 studies.

  View details for DOI 10.1111/all.14462

  View details for PubMedID 32584441

• The impact of prescribed fire versus wildfire on the immune and cardiovascular systems of children ALLERGY Prunicki, M., Kelsey, R., Lee, J., Zhou, X., Smith, E., Haddad, F., Wu, J., Nadeau, K. 2019; 74 (10): 1989–91

  View details for DOI 10.1111/all.13825

  View details for Web of Science ID 000493013400015

• Mass Cytometry Reveals Monocytes are Associated with Air Pollution and Blood Pressure in Minority Children Prunicki, M., Nadeau, K., Lee, J., Zhou, X., Movassagh, H., Wu, J. MOSBY-ELSEVIER. 2020: AB128

  View details for Web of Science ID 000517092700407

• COVID-19 Solutions Are Climate Solutions: Lessons From Reusable Gowns Frontiers in Public Health Baker, N. M., Bromley-Dulfano, R., Chan, J., Gupta, A., Herman, L., Jain, N., Taylor, A. L., Lu, J., Pannu, J., Patel, L., Prunicki, M. 2020

  View details for DOI 10.3389/fpubh.2020.590275

• Cumulative Lifetime Burden of Cardiovascular Disease From Early Exposure to Air Pollution. Journal of the American Heart Association Kim, J. B., Prunicki, M. n., Haddad, F. n., Dant, C. n., Sampath, V. n., Patel, R. n., Smith, E. n., Akdis, C. n., Balmes, J. n., Snyder, M. P., Wu, J. C., Nadeau, K. C. 2020; 9 (6): e014944

  Abstract

  The disease burden associated with air pollution continues to grow. The World Health Organization (WHO) estimates ≈7 million people worldwide die yearly from exposure to polluted air, half of which-3.3 million-are attributable to cardiovascular disease (CVD), greater than from major modifiable CVD risks including smoking, hypertension, hyperlipidemia, and diabetes mellitus. This serious and growing health threat is attributed to increasing urbanization of the world's populations with consequent exposure to polluted air. Especially vulnerable are the elderly, patients with pre-existing CVD, and children. The cumulative lifetime burden in children is particularly of concern because their rapidly developing cardiopulmonary systems are more susceptible to damage and they spend more time outdoors and therefore inhale more pollutants. World Health Organization estimates that 93% of the world's children aged <15 years-1.8 billion children-breathe air that puts their health and development at risk. Here, we present growing scientific evidence, including from our own group, that chronic exposure to air pollution early in life is directly linked to development of major CVD risks, including obesity, hypertension, and metabolic disorders. In this review, we surveyed the literature for current knowledge of how pollution exposure early in life adversely impacts cardiovascular phenotypes, and lay the foundation for early intervention and other strategies that can help prevent this damage. We also discuss the need for better guidelines and additional research to validate exposure metrics and interventions that will ultimately help healthcare providers reduce the growing burden of CVD from pollution.

  View details for DOI 10.1161/JAHA.119.014944

  View details for PubMedID 32174249

• High dimensional immune biomarkers demonstrate differences in phenotypes and endotypes in food allergy and asthma. Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology Chinthrajah, R. S., Purington, N., Sampath, V., Andorf, S., Manohar, M., Prunicki, M., Zhou, X., Tupa, D., Nadeau, K. C. 2018

  View details for PubMedID 29705381

• Exposure to NO2, CO, and PM2.5 is linked to regional DNA methylation differences in asthma CLINICAL EPIGENETICS Prunicki, M., Stell, L., Dinakarpandian, D., de Planell-Saguer, M., Lucas, R. W., Hammond, S., Balmes, J. R., Zhou, X., Paglino, T., Sabatti, C., Miller, R. L., Nadeau, K. C. 2018; 10: 2

  Abstract

  DNA methylation of CpG sites on genetic loci has been linked to increased risk of asthma in children exposed to elevated ambient air pollutants (AAPs). Further identification of specific CpG sites and the pollutants that are associated with methylation of these CpG sites in immune cells could impact our understanding of asthma pathophysiology. In this study, we sought to identify some CpG sites in specific genes that could be associated with asthma regulation (Foxp3 and IL10) and to identify the different AAPs for which exposure prior to the blood draw is linked to methylation levels at these sites. We recruited subjects from Fresno, California, an area known for high levels of AAPs. Blood samples and responses to questionnaires were obtained (n = 188), and in a subset of subjects (n = 33), repeat samples were collected 2 years later. Average measures of AAPs were obtained for 1, 15, 30, 90, 180, and 365 days prior to each blood draw to estimate the short-term vs. long-term effects of the AAP exposures.Asthma was significantly associated with higher differentially methylated regions (DMRs) of the Foxp3 promoter region (p = 0.030) and the IL10 intronic region (p = 0.026). Additionally, at the 90-day time period (90 days prior to the blood draw), Foxp3 methylation was positively associated with NO2, CO, and PM2.5 exposures (p = 0.001, p = 0.001, and p = 0.012, respectively). In the subset of subjects retested 2 years later (n = 33), a positive association between AAP exposure and methylation was sustained. There was also a negative correlation between the average Foxp3 methylation of the promoter region and activated Treg levels (p = 0.039) and a positive correlation between the average IL10 methylation of region 3 of intron 4 and IL10 cytokine expression (p = 0.030).Short-term and long-term exposures to high levels of CO, NO2, and PM2.5 were associated with alterations in differentially methylated regions of Foxp3. IL10 methylation showed a similar trend. For any given individual, these changes tend to be sustained over time. In addition, asthma was associated with higher differentially methylated regions of Foxp3 and IL10.

  View details for PubMedID 29317916