Swapna Upadhyay

About me

PhD, ERT, Associate Professor (Docent)

I hail from the city of joy, Kolkata, India. I have completed my bachelors and master’s degrees from the University of Calcutta India. I obtained my PhD in the field of toxicology (toxicokinetics) from the Technical University of Munich, Germany followed by post-doctoral research (2006-2010) at the German Research Center for Environmental Health, Helmholtz Zentrum Munich, Institute of Lung Biology and Disease. Later, I joined the Department of Environmental and Occupational Health, University of Pittsburgh (2010-2012). Between 2012-2015, I worked at the Indian Institute of Technology, Madras, India in the department of Biotechnology.

Since 2015, I have been associated with the Institute of Environmental Medicine (IMM), KI.

Current Research Funding (as PI):

• Swedish Research Council (VR)
• Swedish Heart Lung Foundation

Other Research Funding : 

• Forska Utan DjurFörsök/ Do Research without animal
• IMM Strategic Grant
• Karolinska Institutet KID funding
• European Respiratory Society

Research description

Our research activities orient around understanding the molecular mechanism of nanoparticles, air pollutants (gaseous mixtures, diesel exhaust particles), biomass smoke, and inhalable chemicals (eg. acrolein, diacetyl) related pulmonary toxicity using human bronchial-and alveolar mucosa models cultured at air-liquid-interface. We are engaged in developing physiologically relevant advanced in vitro lung models for toxicity testing with the aim to put in practice more rigorously the 3R principles in respiratory research. Another important area of our research is the identification of naturally occurring protective phytochemicals against air pollution induced adverse pulmonary effects (eg. oxidative stress, inflammation extracellular matrix degradation) under normal and predisposed (eg. chronic bronchitis) conditions.

Identification of putative naturally occurring bioactive compounds to protect against biomass particle exposure induced lung injury

Biomass smoke (BMS) due to e.g. indoor cocking/heating causing household air pollution is a large public health problem and directly linked to poverty. Deaths due to household air pollution (3·5–4 million per year worldwide) are highly concentrated in several Asian and African countries.  Biomass smoke exposure has been implicated in the development of chronic obstructive pulmonary disease (COPD) in the same order of magnitude as tobacco smoking.  Biomass particles (BMP) are a major component of biomass smoke. In this project we aim to investigate the molecular mechanisms involved in BMP mediated pulmonary injury. Additionally, we will screen naturally occurring phytochemicals present in regular diet for their potential protective effect by reversing/reducing BMP induced oxidative stress and/ or inflammation.

Assessment of pulmonary toxicity and risk due  to multi-flavoured electronic cigarette use

According to a Eurobarometer survey, about 30 million adults in the 27 European Union member states used or had used electronic-cigarette (E-cigs) in 2012. The use of E-cigs has increased tremendously since the millennium shift, and today there are hundreds of E-cig devices and more than seven thousand flavor variations on the market. Use of e-cigs are considered to be of potential health burden, particularly lung. Since the e-cig products are relatively new and evolving there exists an urgent need to establish a neutral integrative risk assessment strategy for evaluating the safety of E-cigs and e-liquids. The primary aim of this project is to develop a basis for pulmonary risk assessment of E-cigs combining epidemiological and molecular toxicity assessment following in vitro exposure experiments. Additionally, we will estimate the prevalence of E-cig users in a young population by using the well-established BAMSE birth-cohort and compare the use of E-cigs with the use of ordinary cigarettes and Swedish snus in its 24-years follow-up where E-cigs use is included in the questionnaire.

Molecular mechanism of air pollutant (diesel exhaust particle, NO2 and SO2) mediated chronic pulmonary effects:  treatment strategies for chronic obstructive pulmonary disease (COPD) and chronic bronchitis (CB).

Ambient air pollution is an established cause of morbidity and mortality – like tobacco smoke. Even more than passive smoking, air pollution is not a lifestyle choice but a ubiquitous involuntary environmental exposure, which can affect the population, from womb to death. WHO 2012, estimates that more than 6 million premature deaths were caused due to increased air pollution. Six common ambient air pollutants are particulate matter (PM: PM10, PM2.5 and ultrafine particles), ozone (O3), sulphur oxide (SOx), nitrogen oxides (NOx), carbon monoxide (CO), and lead. Epidemiological evidence suggests that air pollution contributes to the large global burden of chronic and acute respiratory diseases including asthma, chronic bronchitis (CB), COPD, pneumonia etc. However, detail molecular mechanism leading to onset of chronic respiratory (e.g. COPD) diseases still remains unclear or under explored. This study aims to mimic the real life exposure scenario by repeated exposure of bronchial and alveolar mucosa model to either or combination of both diesel particles and gaseous air pollutants (NOx and Sox). Additionally, we aim to evaluate details molecular mechanism of CB and COPD and the mechanisms of action of established and/or newly developed treatment strategies (anticholinergic drugs, phosphodiesteras inhibitor, 15-lipoxygenase-1 inhibitor).

Diacetyl exposure and popcorn lung diseases: 

Diacetyl (2,3 butanedione), is a volatile α-diketone, formed naturally in dairy products and as a by-product during fermentation by yeast and bacteria. Due to its characteristic butter like aroma, diacetyl has been extensively used as an artificial butter flavouring agent in food products such as microwave popcorn confectionery, baked goods and currently in flavoured electronic cigarette liquids. Occupational exposure of workers to diacetyl has been associated with a severe, irreversible pulmonary disease called bronchiolitis obliterans or popcorn lung. Despite the increasing recognition of diacetyl toxicity, the patho-mechanisms associated with diacetyl mediated pulmonary toxicity remain poorly understood. We hypothesize that exposure to diacetyl may alter expression of key oxidative stress, pro-inflammatory and tissue injury/repair markers. Therefore, in this project we are investigating the potential inflammatory and toxicological effects of diacetyl on human lung mucosa models. The results might contribute to increase the knowledge on molecular mechanisms of diacetyl and its toxicity as well this knowledge will be used for risk assessment.

Publications: (Please refer to the attached file below for complete list)

Pubmed:

https://www.ncbi.nlm.nih.gov/pubmed/?term=Swapna+Upadhyay

Google Scholar:

https://scholar.google.se/citations?user=ab7T4Y8AAAAJ&hl=en

Teaching portfolio

• Problem Based Learning (PBL) tutor in organ toxicology (2016-present): Heart and lung toxicology as well as air pollution.

• Activity based teaching: Climate Change and Cardio-pulmonary Health Impact

• Journal Club Tutor (2016-present)

• Laboratory Technique (2017-present): Application of molecular biology methods in toxicological research

• Master thesis supervision (7) 

 

Education

MSc (2000): University of Calcutta, India

PhD (2006): Technical University of Munich, Germany

 

Academic honours, awards and prizes

Awards/Fellowships:

• European Registered Toxicologist (ERT, 2019)
• Long-term European Respiratory Society (ERS) research fellowship (2015-2017).
• Council of Scientific and Industrial Research (CSIR); Government of India, Senior Research Associate (2012-2015).

Commissions of Trust:

• The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals: 15X. Occupational chemical exposure and chronic obstructive pulmonary disease (COPD): Swapna Upadhyay and Lena Palmberg (Under preparation)