Professor Paul Fowler

Professor Paul Fowler
BSc (Hons 1st) Zoology, Aberdeen 1982. PhD, Aberdeen 1986, FRSB

Chair in Translational Medical Sciences
Director of Institute of Medical Science

Professor Paul Fowler
Professor Paul Fowler

Contact Details

work +44 (0)1224 437528
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The University of Aberdeen Room 2:62:1
Institute of Medical Sciences
School of Medicine, Medical Sciences & Nutrition
University of Aberdeen
AB25 2ZD

PA: Wendy Henderson
Tel:+44 (0)1224 437464

Research Publications - Google Scholar

I am a signatory of the The 2013 Berlaymont Declaration on Endocrine Disrupters.

Recent Highlights

Human Fetal Publications

Communication of Science

The Naked Scientists / BBC feature: Is Modern Life Affecting Fertility?

Related Links



Professor Fowler received his BSc Hons and PhD in Zoology at the University of Aberdeen. He later moved to Obstetrics & Gynaecology, University of Aberdeen, to work on ovarian hormones and antiprogesterones.  In 2000 he moved to the Institute of Medical Sciences, University of Aberdeen as a Professor of Translational Medical Sciences and is currently the Director of the Institute of Medical Sciences in the School of Medicine, Medical Sciences & Nutrition at Aberdeen..

Professor Fowler has spent much of his career working on elucidating mechanisms in the regulation of reproduction and has over 100 peer-reviewed publications, book chapters and editorials. At each stage he has made contributions in the use of technologies to answer reproductive questions, including: remote telemetry of body-testis temperature differentials, MRI analysis of body composition and mammary gland, phage library and protein purification techniques to investigate reproductive proteins and proteomic and microarray techniques to study fetal development and endometriosis. Since the turn of the century, his research has focused on the effects of environmental exposures and endocrine disruption on fetal development and subsequent health in both human and animal models. His group is one of the few to work on the normal first and second trimester human fetus and uses maternal smoking as a model to understand how adverse in-utero environment disturbs fetal development in our own species.


Research Interests

Since the breakthrough epidemiological studies of the 1980s it has been clear that adult human health is dependent upon fetal development and fetal programming (‘early life programming’). Fetal growth restriction, for example, can lead to hypertension, type 2 diabetes, obesity and cardiovascular disease in the adult. Dysfunctional changes in the fetus can arise through other mechanisms, such as maternal cigarette smoking or environmental pollutant exposure and the health trajectory of an individual is likely to depend upon the pollutant burden carried at birth. Fetal pollutant exposure has clear adverse effects on development but we currently have very little knowledge about levels of fetal exposure to “real-life” complex pollutant cocktails and developmental consequences. This fundamental lack of knowledge is a major impasse to developing strategies for reducing fetal pollutant burdens and predicting likely health outcomes. Available data is limited, and often indirect (i.e. animal models or surrogates of exposure), but all studies suggest that fetal pollutant exposure affects lifelong health outcomes and, thereby, impacts on the general economy.

Fetal reproductive development and the environment

(a) Human fetal development and its disruption

Better understanding of events during key stages in reproductive development in the human are key to determining the risks posed by exogenous chemicals, diet and lifestyle on reproductive health in humans, from breast cancer to infertility, testicular cancer to endometriosis, sperm counts to developmental defects. This kind of data is also key to translating the applicability and importance of findings in animal models to the human. Cigarette smoke contains well over 4,000 pollutant chemicals, including potentially toxic elements (PTEs, e.g. cadmium) persistent organic pollutants (POPs, e.g. dioxin) and, of course, nicotine. Many of these chemicals are endocrine-disrupting compounds (EDCs, e.g. nicotine reduces steroidogenesis). Thus, cigarette smoking provides a unique “real-life” model to study endocrine disruption in humans. Since up to 30% of women are smokers and few give up the habit, even when pregnant, it remains a major health challenge. Furthermore, fetal exposure to cigarette smoke chemicals constitutes one of the few models we can use to determine what effects environmental chemicals might have on our own species. This is one of the major models used in my research.

(i) Characterising normal events during human fetal development.

1st gene array study of the human fetal gonad : Gene expression analysis of human fetal ovarian primordial follicle formation. Fowler PA, Flannigan S, Mathers A, Gillanders K, Lea RG, Wood MJ, Maheshwari A, Bhattacharya S, Collie-Duguid ES, Baker PJ, Monteiro A, O'Shaughnessy PJ. J Clin Endocrinol Metab. 2009 Apr;94(4):1427-35.

(ii) Investigating how these events are affected by exposure to cigarette smoke chemicals.

1st fetal testis gene reduced by maternal cigarette smoking: Maternal smoking during pregnancy specifically reduces human fetal desert hedgehog gene expression during testis development. Fowler PA, Cassie S, Rhind SM, Brewer MJ, Collinson JM, Lea RG, Baker PJ, Bhattacharya S, O'Shaughnessy PJ. J Clin Endocrinol Metab. 2008 Feb;93(2):619-26.

(b) Effects of environmental chemicals: using animal models to understand risks

Domestic animals, like humans and all other animals, are exposed to environmental pollutants through exposure to contaminated food, water, air and soil. Environmental pollutants include a range of (mainly) anthropogenic chemicals which have the capacity to interfere, subtly, with hormonal systems and therefore with their capacity to reproduce, rear offspring and fight disease); these chemicals, which included heavy metals and organic compounds of many different classes are described as endocrine disrupting compounds (EDCs). The physiological insult associated with exposure to EDCs involves many different chemical types, each acting on different physiological systems. Furthermore, while environmental concentrations of most individual chemicals are very low and below the No Observable Effect Level (NOEL), in many cases they can act additively to induce a physiological change, even when concentrations of individual chemicals appear harmless.

Empirical evidence in support of this has been provided by our previous work involving exposure of sheep to low (environmental) levels of EDCs through grazing pastures fertilised with sewage sludge (contains high concentrations of multiple EDCs). This work has shown that maternal exposure to sewage sludge treated pasture was associated with perturbation of the fetal hypothalamus-pituitary and ovary, despite the fact that fetal and adult tissue concentrations of individual EDCs at the time of slaughter were minimally increased by such exposure and were at concentrations below the NOEL. Work funded by the Wellcome Trust and the European Union is addressing the effects of exposure during specific windows of time, before and during gestation, on patterns of tissue accumulation and associated physiological changes.

Current Research

Current Team

  • Dr Pan Filis (FREIA Post-doc)
  • Ms Natasha Walker (Glasgow Children’s Hospital Charity PhD student)
  • Ms Chiara Talia (EU MSCA-ITN PhD student)
  • Ms Aikaterini Zafeiri (EASTBIO PhD student)
  • Ms Carol Wallace (Research technician)

Recent Visiting Scientists

  • Mr Ajay Yadav, 3 months secondment as part of PROTECTED MSCA-ITN, Norwegian University of Life Sciences, Oslo, Norway
  • Ms Laetitia Lecante (3 months visit, Universite de Rennes 1, Rennes, France, PhD student)
  • Mr Glen Gauderat (3 months on Royal Society grant: Ecole Nationale Veterinaire de Toulouse, France, PhD student)
  • Ms Hanna Johansson (Technical University of Denmark, PhD student)
  • Dr Partha Roy (Indian Institute of Technology Roorkee)

MRC funded project (layperson summary)

It is well known that if a woman smokes while pregnant there are bad consequences for the resulting offspring, especially slowed growth in the womb. However, other serious problems are also likely to occur in children exposed to their mothers’ cigarette smoke chemicals during pregnancy. These include an impaired immune system (e.g. increased asthma), poorer educational performance and a raised chance of developing obesity, diabetes and heart disease (called metabolic syndrome). Many of these effects also happen if the mother regularly drinks alcohol while pregnant, even if not to the extent of addiction. We do not know exactly how much the chance of somebody developing metabolic syndrome is altered if their mother smoked and/or drank while pregnant. However, a recent study of 74,000 women found that if their mothers smoked while pregnant, the women had a 53% higher chance of becoming obese. This would be a major added drain on the NHS and would mean that many more people would be likely to suffer these debilitating conditions since smoking and/or alcohol use during pregnancy continues in 20-40% of women. In 2006-07 costs to the English NHS of lifestyle and related conditions were: smoking £3.3 billion, alcohol £3.3 billion, overweight/obesity £5.1 billion and diabetes £3.5 billion annually.

Adult health is partly programmed by events during fetal life when the individual is still in the womb and an individual may be badly adjusted for life if the mother uses recreational drugs. Growth restriction is important in this process and the liver is one of the organs most affected by disturbed growth before birth. The fetal liver is a key organ, protecting the fetus from harmful chemicals and controlling fetal growth. Progress in understanding the effects of maternal drug use on fetal development suffers from two problems: firstly, our ignorance of the levels of drugs to which the fetus is exposed and, secondly, the mechanisms by which these drugs affect development. Two factors contribute to our ignorance. Firstly, very little research uses normal human fetuses. Secondly, there is a lack of low-cost means with which to measure how much/which chemicals (nicotine, alcohol, cannabis etc.) are getting into the human fetus during pregnancy. This project aims to resolve these issues using our uniquely large collection of normal, second trimester human fetal livers and by collecting both the liver and the placenta from further terminations of normal pregnancies.

We will use highly sophisticated methods at the National Institute on Drug Abuse (USA) to measure chemicals from tobacco, cannabis, cocaine and alcohol in the fetal liver and in matched pairs of fetal livers and placentas. This will tell us how much the fetus has been exposed to drugs taken by the mother and whether the placenta can be used to measure the fetal burden of drugs and chemicals from the mother. This would allow us to carry out much larger studies of newborn babies to measure exposure levels in the placenta and their contribution to adult ill-health.

At the same time as measuring drug levels in the fetal liver we will work out how those drugs have affected liver function. Then, by using cell culture, it will be possible to re-create the effects of drug exposure in the culture dish with a view to understanding the long-term consequences. We will also be able to find out more about how liver function develops and how it differs between male and female babies Overall, our aim is to relate changes in the control of fetal liver development to the effects of chemicals in cigarette smoke. This will allow us to understand liver mal-development turns to metabolic syndrome. The information from this study will allow us to measure, and to understand, the effects of exposing the developing fetus to its mother’s recreational drug use. This will enable treatments to be designed to reverse these effects and to lower the incidence of the modern scourge of metabolic syndrome.

Recent plenary and invited presentations

  • Preparing for a healthy life – maternal lifestyle and fetal programming. Toxalim, 12 October 2018, Toulouse, France.
  • Effect of prenatal exposure to environmental toxins on female reproduction. Fertility 2018, 4-6 January 2018, Liverpool, UK.
  • Evidence for EDC involvement in reproductive dysfunction in women. Invited seminar at PhD Course in Reproductive Toxicology, Centre for Reproductive Biology in Uppsala (CRU) and Swedish Toxicological Sciences Research Centre (SWETOX), 12-16 June 2016, Uppsala, Sweden.
  • Real-world chemical mixtures disturb fetal endocrine systems and gonad development humans and animal models. Symposium: “Mixtures, medicines and diet, where now for endocrine disrupting compounds?” ECE2016: European Congress of Endocrinology, 28-31 May 2016, Munich, Germany.
  • Effects of in-utero exposure to toxicants on the fetal gonad and liver. Invited seminar, BIOSIT, combined University of Rennes, CNRS & INSERM unit, 9 November 2015, Rennes, France.
  • Sex, drugs, oestrogens and the human fetus. Invited public talk, Aberdeen Medico-Chirurgical Society, 1 October 2015, Aberdeen, UK.
  • New insights into human fetal development: endogenous oestrogens, maternal smoking and gene methylation. 8th Copenhagen Workshop of Endocrine Disrupters, 27-30 April 2015, Copenhagen, Denmark.
  • Environmental factors in sex differences and metabolism. ESE basic Endocrinology Course in reproductive Endocrinology, 18-20 February 2015, Edinburgh, UK.
  • The exposed proteome. Understanding biology and disease: the application of proteomics. University of Aberdeen Symposium, 9 December 2014, Aberdeen, UK. Regulation and dysregulation of primordial follicle formation and activation. 3rd World Congress of Reproductive Biology, 2-4 September 2014, Edinburgh, UK.
  • Environmental chemicals and fetal development. 2ieme Journee des Jeunes Chercheurs de L’IRSET, February 4th 2014, University of Rennes, France.
  • On women and sheep: making and breaking the fetal ovary. INRA, 13 December 2013, Jouy-en-Josas, France.
  • The evidence for EDC involvement in reproductive dysfunction in women. International Workshop: Endocrine Disrupting Chemicals and Female Reproduction. 5-6 November 2013, Uppsala, Sweden.
  • Environment and endocrine disruptors in fetal reproductive development.  IfLS Conference: Reproductive Biology – from gametes to systems, and between generations. 17 September 2013, Southampton, UK.
  • Effects of chemicals on reproductive development. Subspecialist Trainees in Reproductive Medicine and Surgery (STIRMAS). 27 September 2013, Cambridge, UK.
  • Human fetal reproductive development and endocrinology: effects of maternal smoking. 7th Copenhagen Workshop of Endocrine Disrupters, 28-31 May 2013, Copenhagen, Denmark.
  • Impact of endocrine-disrupting compounds (EDCs) on female reproductive health. Fertility 2013, Liverpool, January 3-5 2013.
  • Effects of exposure to environmental chemicals during pregnancy on the development of the male and female reproductive access“. 17th International Congress on Animal Reproduction (ICAR 29012) in Vancouver, British Columbia, Canada, July 29 – August 2, 2012.
  • Environmental exposure in reproductive development and function of the female. World Congress on Reproductive Biology, Cairns Australia 9-11 October 2011.
  • Environmental effects on fetal reproductive development. Australia Society of Reproductive Biology, Cairns Australia 7-9 October 2011.
  • Effects of EDCs on the human foetus: lessons from smoking. 6th Copenhagen Workshop of Endocrine Disrupters, 25-30 April 2011, Copenhagen, Denmark.
  • Maternal smoking and sewage sludge: consequences for fetal gonadal development. Centre for Reproductive Biology Special Symposium: “Endocrine disruptors and reproductive health: separating fact from fiction.” 7 March 2011, University of Edinburgh.
  • Mixtures of environmental chemicals: concentrations and effects in the fetus. Covance Environmental Risk Assessment (ERA) Symposium, 2-3 March 2011, Brussels.
  • In-utero exposures to environmental chemicals and consequences for ovarian development. Gordon Research Conference: “Environmental Endocrine Disrupters", 30 May-4 June 2010, Les Diablerets, Switzerland.
  • Environmental endocrine disruption of the ovary. 37th Nordic Congress of Obstetrics & Gynecology, 15-18 June 2010, Copenhagen, Denmark.
  • Endocrine disruptors and gonadal development.  Symposium: Environmental factors and nosology of the endocrine system, 2-4 October 2009, Athens, Greece.
  • In-utero exposure to environmental chemicals and consequences ovarian development. 5th Copenhagen Workshop of Endocrine Disrupters, 20-22 May 2009, Copenhagen, Denmark.
  • The fetal ovary as a target for disruption. Danish Society of Obstetrics & Gynaecology, 17 April 2009, Copenhagen, Denmark
  • Is the fetus under chemical attack? St George’s University London, 26 March 2009.
  • Gender bending chemicals and the mammalian fetal gonad. XXth International Congress of Zoology, Paris 26-29 August 2008.

Press Releases


  • Grateful thanks to Dr Stewart Rhind (James Hutton Institute, Aberdeen, Scotland) for the years of friendship and collaboration before his untimely death.

Research Grants

  • van Duursen M,Van den Berg M, Fowler PA and 9 other partners, Female Reproductive toxicity of Endocrine disrupting chemicals (EDCs): a human evidence-based screening and Identification Approach (FREIA), European Commission, Horizon 2020, €6,107,832.

  • De Bari C, Haggarty P, Fowler PA, Roelofs A, Unlocking the joint morphogenetic code in mesenchymal stem cells from human synovium. Arthritis Research UK, £327,873.
  • Filis P, O'Shaughnessy PJ, Fowler PA, Can the human fetal plasma proteome be used to monitor "exposure" to increased maternal BMI during fetal life and predict resulting childhood disease? NHS Grampian Endowments, £11,935.
  • Fowler PA, Heys SD, Pathways to breast cancer - lessons from early life. NHS Grampian Endowment, £28.000.
  • Fowler PA, Effect of in-utero exposure to cigarette smoking to human fetal kidney development. (Summer studentship stipend to Serena Banh) Endocrine Society, £3,000.
  • Fowler PA, Filis P, Walker N, O’Shaughnessy PJ, Modelling the gateways to the human fetus by high-throughput placental molecular transporter protein measurements.NHS Grampian Endowments, £11,587.
  • Rae M, Duncan WC, Fowler PA, Sex-specific disease aetiology from developmental steroid insults: mechanistic understanding and biomarker development towards disease prevention.MRC, £636,511.
  • Connolly L, Fowler PA, Ropstad E, Oswald I, Kausel G, Erikson G, Muller M, Van der Burg B, Gozalbes R, PROTECTion against Endocrine Disruptors: detection, mixtures, health effects, risk assessment & communication. Horizon 2020 MSCA-ITN, €3,974,595.
  • Walker N, Bellingham M, Fowler PA, Maternal smoking, drinking and deprivation: when and how of placental damage. Yorkhill Children's Charity, £59,988.
  • Fowler PA, Gayrard V, Biomonitoring and effect biomarkers of fetal exposure to bisphenol A. International Exchange, Royal Society & Ecole Nationale Veterinaire de Toulouse, £14,755.
  • Fowler PA, Maternal smoking, drinking and deprivation: when and how of placental damage. Development Trust, £14,057.
  • Fowler PA, Filis P, Soffientini U, O'Shaughnessy PJ Placental Molecular transporters in early human pregnancy: identifying open gates to the fetus. NHS Grampian Endowments, £11,933.
  • Filis P, O’Shaughnessy PJ, Fowler PA, The impact of maternal smoking to the human fetal adrenal proteome. Society for Endocrinology Early Career Grant to P Filis, £9,870.
  • Fowler PA, Filis P, O’Shaughnessy PJ, Proteomic analysis of the effects of maternal smoking on the second trimester human fetal gonad. Society for Endocrinology summer studentship, £2,850.
  • Fowler PA, Douglas A, Hay D, Iredale J, Fairley S, O'Shaughnessy PJ, Huestis M, The human fetal liver: development and response to maternal drug use. MRC, £588,601.
  • Fowler PA, Filis P, O'Shaughnessy PJ, Does exposure to a complex cocktail of environmental chemicals during pregnancy and lactation alter metabolic and steroid hormone systems in the adult liver? Society for Reproduction & Fertility, Academic Schorlarship, £8,900
  • Bellingham M, Fowler PA, O'Shaughnessy PJ, Prenatal programming of adult disease by maternal smoking: the adrenal gland as a key player? Wellcome Trust Institutional Strategic Support Fund (Catalyst), £18,230.
  • Fowler PA, Bhattacharya S, O'Shaughnessy PJ, Gatekeepers to the cell: which ones operate customs posts in the fetal liver and does maternal smoking allow drugs to slip through? NHS Grampian Endowments, £9,356.
  • Fowler PA, Collinson JM, O’Shaughnessy PJ, Bioincubator system to model toxic effects on the human fetal testis, Chief Scientist Office, £62,078.
  • Fowler PA, Harkany T, O’Shaughnessy PJ, Fetal human gonadal cannabinoid receptors: expression and effects of maternal smoking., NHS Grampian Endowments, £6,713.
  • Fowler PA, Cotinot C, O’Shaughnessy PJ, Inter-species comparison of the onset ovarian follicle formation, Wellcome Trust summer studentship, £5,760
  • Fowler PA, Cotinot C, Fischer B, Lea RG, Pocar P, Sinclair K, Rhind SM, Reproductive effects of environmental chemicals in females (REEF), European Commission, Framework 7, £2,322,380. REEF
  • Fowler PA, Bhattacharya S, Rhind SM, O'Shaughnessy PJ, Does maternal smoking disrupt key developmental sex steroid hormones in the fetus? NHS Grampian Endowments, £10,834.
  • Fowler PA, Sharpe R, Cotinot C, Evans N, Rhind S, Effect of in-utero exposure to environmental chemicals via maternal pasture ingestion on fetal development., Wellcome Trust, £425,786.
  • Fowler PA, Maheshwari A, Bhattacharya S, Follicular assembly in the human fetal ovary, IMS Microarray Core Facility grant, UoA, £6,000.
  • Fowler PA, Wood M, Human fetal gonad: 2 summer research studentships, SRF, £2,640.
  • Skaare JU et al, including Fowler PA, The mechanisms behind toxic effects of POPS, NFR, £170,377.
  • Fowler PA, Bhattacharya S, Hamilton MPR, al-Gubory K, Identification of implantation-related proteins, NHS R&D, £18,500.
  • Fowler PA, Bhattacharya S, Cash P, Circulating biomarkers for endometriosis, University of Aberdeen Commercialisation Fund, £19,095.
  • Shanbhag S, Cruickshank M, Millier I, Murray G, Fowler PA, Molecular basis of granulosa cell tumours, NHS Grampian Endowments, £11,343.
  • Fowler PA, Bhattacharya S, Cash P, Establishing a relationship between endometrial proteins and endometriosis., CSO, £18,856.
  • Fowler PA, Bhattacharya S, Optimisation of an in-vitro model to investigate the human fetal testis, CSO, £15,571.
  • Huhtaniemi I, Fowler PA, Cash P, Charlton H, Novel biological actions of luteinizing hormone and its receptor, Wellcome Trust, £1,408,031.
  • Fowler PA and colleagues, Translational medicine funding: >£700,000.

Teaching Responsibilities

  • BM4004: Advanced Molecules, Membranes & Cells
  • DB3006: Principles of Developmental & Reproductive Biology
  • MB5026: MSc Principles of Reproductive Biology
  • MB5524: MSc Applied Developmental Biology

Honours and MSc students undertake research projects in my lab.

Further Info

External Responsibilities

I am a co-author of the EFSA (European Food Safety Authority) Scientific Opinion on the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs as a member of the Toxicology Working Group.

3 documents available for download:


European Commission: Science in Society - How gender analysis contributes to research - REEF Project as a case study in Gendered Innovation.

Admin Responsibilities

  • Director of the Institute of Medical Sciences, 2015 - 2020
  • Lead, Cell, Developmental & Cancer Biology Research Programme, 2011 - 2015
  • Member, European Advisory Committee
  • Member, Division of Applied Medicine Executive
  • Member, Schools of Medicine & Dentistry and Medical Sciences Joint Research Committee
  • Member, Athena Swann CLSM assessment team


I work to foster research at Aberdeen via my responsibility for the management, monitoring and generic training of laboratory postgraduate researchers in the School of Medicine under the aegis of the Graduate School, College of Medicine & Life Sciences.

Membership of Professional Societies



I am a long-term member of Fauna & Flora International