D A Basketter

The Kings College, Brooklyn, New York, United States

Are you D A Basketter?

Claim your profile

Publications (412)1061.48 Total impact

  • Anne Marie Api, David Basketter, Jon Lalko
    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Quantitative risk assessment for skin sensitization is directed towards the determination of levels of exposure to known sensitizing substances that will avoid the induction of contact allergy in humans. A key component of this work is the predictive identification of relative skin sensitizing potency, achieved normally by the measurement of the threshold (the "EC3" value) in the local lymph node assay (LLNA). In an extended series of studies, the accuracy of this murine induction threshold as the predictor of the absence of a sensitizing effect has been verified by conduct of a human repeated insult patch test (HRIPT). Murine and human thresholds for a diverse set of 57 fragrance chemicals spanning approximately four orders of magnitude variation in potency have been compared. The results confirm that there is a useful correlation, with the LLNA EC3 value helping particularly to identify stronger sensitizers. Good correlation (with half an order of magnitude) was seen with three-quarters of the dataset. The analysis also helps to identify potential outlier types of (fragrance) chemistry, exemplified by hexyl and benzyl salicylates (an over-prediction) and trans-2-hexenal (an under-prediction).
    Cutaneous and ocular toxicology. 11/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Integrated testing strategies (ITS), as opposed to single definitive tests or fixed batteries of tests, are expected to efficiently combine different information sources in a quantifiable fashion to satisfy an information need, in this case for regulatory safety assessments. With increasing awareness of the limitations of each individual tool and the development of highly targeted tests and predictions, the need for combining pieces of evidence increases. The discussions that took place during this workshop, which brought together a group of experts coming from different related areas, illustrate the current state of the art of ITS, as well as promising developments and identifiable challenges. The case of skin sensitization was taken as an example to understand how possible ITS can be constructed, optimized and validated. This will require embracing and developing new concepts such as adverse outcome pathways (AOP), advanced statistical learning algorithms and machine learning, mechanistic validation and "Good ITS Practices".
    ALTEX. 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: During the last 50 years there has been a significant increase in Western societies of atopic disease and associated allergy. The balance between functional subpopulations of Th cells determines the quality of immune response provoked by antigen. One such subpopulation – Th2 cells – is associated with the production of IgE antibody and atopic allergy, whereas, Th1 cells antagonise IgE responses and the development of allergic disease. In seeking to provide a mechanistic basis for this increased prevalence of allergic disease one proposal has been the ‘hygiene hypothesis’ which argues that in westernised societies reduced exposure during early childhood to pathogenic microorganisms favours the development of atopic allergy.Pregnancy is normally associated with Th2 skewing, that persists for some months in the neonate before Th1/Th2 realignment occurs. In this review we consider the immunophysiology of Th2 immune skewing during pregnancy. In particular, we explore the possibility that altered and increased patterns of exposure to certain chemicals have served to accentuate this normal Th2 skewing and therefore promote further the persistence of a Th2 bias in neonates. Furthermore we propose that the more marked Th2 skewing observed in first pregnancy may, at least in part, explain he higher prevalence of atopic disease and allergy in the first born.This article is protected by copyright. All rights reserved.
    British Journal of Dermatology 10/2014; · 3.76 Impact Factor
  • Ian Kimber, Rebecca J Dearman, David A Basketter
    [Show abstract] [Hide abstract]
    ABSTRACT: Sensitization of the respiratory tract by chemicals resulting in rhinitis and asthma is an important occupational health issue. Occupational asthma is associated with significant morbidity and can be fatal. Tests for the identification and characterization of chemicals with the potential to cause sensitization of the respiratory tract are lacking. In spite of sustained interest there are no validated or widely accepted methods available, and this presents toxicologists with a considerable challenge. One important constraint on the development of appropriate testing strategies has been uncertainty and controversy about the immunological mechanisms through which chemicals may induce sensitization of the respiratory tract. By analogy with protein respiratory allergy it is legitimate to consider that IgE antibody-dependent mechanisms may play a pivotal role. However, although many aspects of chemical respiratory allergy are consistent with reactions caused by IgE antibody, uncertainty remains because among patients with occupational asthma caused by chemical respiratory allergens there are commonly a proportion, and sometimes a significant proportion, of subjects that lack detectable IgE antibody. Here we consider the relevance of IgE antibody responses for the development of a chemical respiratory allergy to diisocyanates. A case is made that IgE antibody responses are, either directly or indirectly, closely associated with occupational asthma to the diisocyanates (and to other chemical respiratory allergens). As such the argument is advanced here that IgE antibody represents an appropriate readout for the characterization of chemical respiratory allergens, and that uncertainty about mode of action should no longer represent a hurdle in the development of suitable test methods. Copyright © 2014 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 07/2014; · 2.60 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Background: Hexyl cinnamal (HCA) is a widely used fragrance chemical, the low skin-sensitizing potency of which has made it a common choice for the use as a positive control for predictive toxicology assays. However, HCA is commonly negative in current candidate in vitro alternatives test methods. Objective: To review the evidence that HCA is a classifiable skin sensitizer against the standards set by the Globally Harmonized Scheme (GHS), and determine whether it represents an appropriate choice for a positive control substance for predictive testing. Methods: Using the GHS criteria, mechanistic data, and in vitro, in vivo and human evidence relating to HCA and skin sensitization have been reviewed. Results: The chemistry of HCA is consistent with potential for skin sensitization and predictive in vivo test data support this conclusion. However, the human data are relatively sparse, consistent with HCA possessing a low capacity to induce skin sensitization under conditions of consumer exposures. Conclusions: Using GHS criteria (and applying a precautionary approach) HCA would classify as a weaker skin sensitizer than predicted by the local lymph node assay (LLNA). However, given the human experience, it is necessary to consider whether HCA is the most appropriate choice for use as a positive regulatory control.
    Cutaneous and ocular toxicology. 07/2014;
  • David Basketter, Ian Kimber
    [Show abstract] [Hide abstract]
    ABSTRACT: The identification, characterisation, risk assessment and risk management of materials that cause allergic sensitisation is an important requirement for human health protection. It has been proposed that for some chemical and protein allergens, and in particular for those that cause sensitisation of the respiratory tract (associated with occupational asthma), it may be appropriate to regard them as Substances of Very High Concern (SVHC) under the provisions of REACH (Registration, Evaluation, Authorisation and restriction of CHemicals). We have argued previously that categorisation of sensitising agents as SVHC should be used only in exceptional circumstances. In the present article, the subject of SVHC is addressed from another perspective. Here the information that would be required to provide a compelling case for categorisation of a skin sensitising substance as a SVHC is considered. Three skin sensitising chemicals have been identified to serve as working examples. These are chromate, a potent contact allergen, and the skin sensitisers formaldehyde and isoeugenol. The key criterion influencing the decision regarding a skin sensitiser being categorized as SVHC is the extent to which impacts on the quality of life are reversible. Consequently, SVHC categorisation for skin sensitising chemicals should be used only in exceptional circumstances.
    Regulatory toxicology and pharmacology : RTP. 05/2014;
  • David A Basketter, G Frank Gerberick, Ian Kimber
    [Show abstract] [Hide abstract]
    ABSTRACT: Toxicology endeavors to predict the potential of materials to cause adverse health (and environmental) effects and to assess the risk(s) associated with exposure. For skin sensitizers, the local lymph node assay was the first method to be fully and independently validated, as well as the first to offer an objective end point with a quantitative measure of sensitizing potency (in addition to hazard identification). Fifteen years later, it serves as the primary standard for the development of in vitro/in chemico/in silico alternatives.
    Dermatitis 03/2014; · 0.93 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The skin has a sophisticated and highly orchestrated immune system. The ability of proteins encountered at skin surfaces to access that immune system remains controversial, however. In this article the question considered is whether proteins encountered epicutaneously (on the skin) at abraded or tape-stripped skin surfaces, but also at sites where the skin is intact, can engage with the cutaneous immune system to provoke and regulate responses. The available evidence suggests that epicutaneous exposure to foreign proteins is able to elicit immune and allergic responses, and that encounter with protein via this route may favour the development of selective Th2 responses and allergic sensitisation. It is also clear that proteins can modify immunological function when delivered topically and that intact skin may provide an effective route of exposure for active immunotherapy of allergic disease. An appreciation that epicutaneously applied proteins can interact with the skin immune system, even when delivered at intact skin sites, opens up important opportunities for immunotherapy, local immune modulation and the treatment of inflammatory skin diseases. It also indicates that this route of exposure must be considered as part of the safety assessment and risk management of protein-induced allergic sensitisation.
    European journal of dermatology : EJD. 02/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Allergic contact dermatitis is a disease that to a great extent can be limited or even avoided. Limitation of allergic contact dermatitis can be realized by the predictive identification of sensitizing chemicals (hazard identification), measurement of their relative sensitizing potency (hazard characterization) and subsequent use of proper risk assessment/management strategies in relation to the anticipated skin exposure. Several in vivo methods exist that are known to be reliable predictors of chemicals that can behave as skin sensitizers. One particular method, the local lymph node assay, also produces vital information on the relative potency of identified sensitizers. This potency information can be applied to quantitative risk assessment for skin sensitization, although the completion of quantitative risk assessment is dependent also on access to information on human skin exposure. However, the challenge in 2013 is how to obtain the same type of information on the potency of skin sensitising chemicals using only in vitro and in silico methods. With the impending elimination of in vivo tests, the in vitro test development focus has been on the essential mechanistic steps of sensitization induction, including hapten–peptide binding, dendritic cell migration/maturation and T-lymphocyte priming. Several in vitro methods appear close to successful validation for hazard identification. What has to be addressed is how information from such in vitro assays is integrated, together with data on epidermal bioavailability, to deliver hazard characterization in the form of assessment of sensitizer potency. More than a single protocol, a battery of different in vitro tests will be probably necessary to optimize the detection of skin sensitizers.
    Expert Review of Dermatology 01/2014; 8(4).
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Although adoption of skin sensitization in vivo assays for hazard identification is likely to be successful in the next few years, this does not replace their use in potency prediction. Notably, measurement of potency of skin sensitizers in the local lymph node assay has been important. However, this local lymph node assay potency measure has not been formally assessed against a range of substances of known human sensitizing potential, because the latter is lacking. Accordingly, criteria for human data have been established that characterize 6 categories of human sensitizing potency, with 1 the most potent and 5 the least potent; category 6 represents true nonsensitizers. The literature has been searched, and 131 chemicals assigned into these categories according to their intrinsic potency judged only by the available human information. The criteria and data set generated provide a basis for examination of the capacity of nonanimal approaches for the determination of human sensitization potency.
    Dermatitis 01/2014; · 0.93 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Allergic sensitisation of the respiratory tract by chemicals is associated with rhinitis and asthma and remains an important occupational health issue. Although less than 80 chemicals have been confirmed as respiratory allergens the adverse health effects can be serious, and in rare instances can be fatal, and there are, in addition, related socioeconomic issues. The challenges that chemical respiratory allergy pose for toxicologists are substantial. No validated methods are available for hazard identification and characterisation, and this is due in large part to the fact that there remains considerable uncertainty and debate about the mechanisms through which sensitization of the respiratory tract is acquired. Despite that uncertainty, there is a need to establish some common understanding of the key events and processes that are involved in respiratory sensitisation to chemicals and that might in turn provide the foundations for novel approaches to safety assessment. In recent years the concept of Adverse Outcome Pathways (AOP) has gained some considerable interest among the toxicology community as a basis for outlining the key steps leading to an adverse health outcome, while also providing a framework for focusing future research, and for developing alternative paradigms for hazard characterisation. Here we explore application of the same general principles to an examination of the induction by chemicals of respiratory sensitization. In this instance, however, we have chosen to adopt a reverse engineering approach and to model a possible AOP for chemical respiratory allergy working backwards from the elicitation of adverse health effects to the cellular and molecular mechanisms that are implicated in the acquisition of sensitisation.
    Toxicology 01/2014; · 4.02 Impact Factor
  • Source
    David Basketter, Ian Kimber
    [Show abstract] [Hide abstract]
    ABSTRACT: The identification, characterisation, risk assessment and risk management of materials that cause allergic sensitisation is an important requirement for human health protection. It has been proposed that for some chemical and protein allergens, and in particular for those that cause sensitisation of the respiratory tract (associated with occupational asthma), it may be appropriate to regard them as Substances of Very High Concern (SVHC) under the provisions of REACH (Registration, Evaluation, Authorisation and restriction of CHemicals). We have argued previously that categorisation of sensitising agents as SVHC should be used only in exceptional circumstances. In the present article, the subject of SVHC is addressed from another perspective. Here the information that would be required to provide a compelling case for categorisation of a skin sensitising substance as a SVHC is considered. Three skin sensitising chemicals have been identified to serve as working examples. These are chromate, a potent contact allergen, and the skin sensitisers formaldehyde and isoeugenol. The key criterion influencing the decision regarding a skin sensitiser being categorized as SVHC is the extent to which impacts on the quality of life are reversible. Consequently, SVHC categorisation for skin sensitising chemicals should be used only in exceptional circumstances.
    Regulatory Toxicology and Pharmacology 01/2014; · 2.13 Impact Factor
  • Ian Kimber, David A Basketter
    [Show abstract] [Hide abstract]
    ABSTRACT: Characterisation of the relative sensitizing potency of protein and chemical allergens remains challenging, particularly for materials causing allergic sensitization of the respiratory tract. There nevertheless remains an appetite, for priority setting and risk management, to develop paradigms that distinguish between individual respiratory allergens according to perceptions of the hazards and risks posed to human health. One manifestation thereof is recent listing of certain respiratory allergens as Substances of Very High Concern (SVHC) under the provisions of REACH (Registration, Evaluation, Authorisation and restriction of CHemicals). Although priority setting is a laudable ambition, it is important the process is predicated on evidence-based criteria that are transparent, understood and owned. The danger is that in the absence of rigorous criteria unwanted precedents can be created, and confidence in the process is compromised. A default categorisation of sensitisers as SVHC requiring assessment under the authorisation process is not desirable. We therefore consider here the value and limitations of selective assignment of certain respiratory allergens as being SVHC. The difficulties of sustaining such designations in a sound and equitable way is discussed in the context of the challenges that exist with respect to assessment of potency, and information available regarding the effectiveness of exposure-based risk management.
    Regulatory Toxicology and Pharmacology 01/2014; · 2.13 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In a previous EPAA-Cefic LRI workshop in 2011, issues surrounding the use and interpretation of results from the local lymph node assay were addressed. At the beginning of 2013 a second joint workshop focused greater attention on the opportunities to make use of non-animal test data, not least since a number of in vitro assays have progressed to an advanced position in terms of their formal validation. It is already recognised that information produced from non-animal assays can be used in regulatory decision-making, notably in terms of classifying a substance as a skin sensitiser. The evolution into a full replacement for hazard identification, where the decision is not to classify, requires the generation of confidence in the in vitro alternative, e.g. via formal validation, the existence of peer reviewed publications and the knowledge that the assay(s) are founded on key elements of the Adverse Outcome Pathway for skin sensitisation. It is foreseen that the validated in vitro assays and relevant QSAR models can be organised into formal testing strategies to be applied for regulatory purposes by the industry. To facilitate progress, the European Partnership for Alternative Approaches to animal testing (EPAA) provided the platform for cross-industry and regulatory dialogue, enabling an essential and open debate on the acceptability of an in vitro based integrated strategy. Based on these considerations, a follow up activity was agreed upon to explore an example of an Integrated Testing Strategy for skin sensitisation hazard identification purposes in the context of REACH submissions.
    Regulatory Toxicology and Pharmacology 10/2013; · 2.13 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract There is considerable interest in the immunobiological processes through which the development of allergic sensitization to chemicals is initiated and orchestrated. One of the most intriguing issues is the basis for the elicitation by chemical sensitizers of different forms of allergic reaction; that is, allergic contact dermatitis or sensitization of the respiratory tract associated with occupational asthma. Studies in rodents have revealed that differential forms of allergic sensitization to chemicals are, in large part at least, a function of the selective development of discrete functional sub-populations of CD4(+) and CD8(+) T-lymphocytes. Evidence for a similar association of chemical allergy in humans with discrete T-lymphocyte populations is, however, limited. It is of some interest, therefore, that two recent articles from different teams of investigators have shed new light on the role of polarized T-lymphocyte responses in the development of allergic contact dermatitis and occupational asthma in humans. The implications for understanding of chemical allergy in humans are explored in this Commentary.
    Journal of Immunotoxicology 09/2013; · 1.57 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The ability to be sensitized to experimental contact allergens declines significantly with increasing age, from as early as age 40 years. In contrast, the rate of contact allergy to chemical allergens (haptens) in cosmetic products significantly increases with age. This has been explained previously on the basis of greater cumulative exposure in the older age groups. However, outbreaks of contact allergy to preservatives in cosmetic products recorded soon after their introduction to the market have also shown a significantly higher rate among older adult age groups. This association with increasing age cannot be readily explained by exposure history or pattern, and is not compatible with a sensitizing/stimulatory reaction that degrades with age as the sole immune response. From this, the existence of a second, tolerizing/regulatory arm to the immune response to cutaneous haptens that possibly becomes less effective with age at a higher rate than the sensitizing/stimulatory arm can be inferred. This reinforces the view that current clinical and experimental observations of allergic contact dermatitis are best explained by an immune system with the functional ability to produce both sensitizing/stimulatory and tolerizing/regulatory responses.
    Contact Dermatitis 09/2013; 69(3):129-37. · 2.93 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: One explanation for the large increase in the prevalence of atopic disease during the last 50 years in developed countries is the 'hygiene hypothesis'. This proposes that a reduced exposure to pathogenic microorganisms at a key period(s) during development result in the maintenance or acquisition of an atopic phenotype. Alternatively, or additionally, we have postulated that increased exposures to chemicals generally, and to irritant/haptenic chemicals in particular, during critical windows of pregnancy/ early life development have also contributed to changes in the prevalence of atopic disease. Having previously reviewed the potential roles of oral and cutaneous exposures to chemicals on the subsequent diagnosis of atopic disease, we here consider possible evidence of a role for exposure to airborne chemicals as a contributory factor in acquired susceptibility to atopic allergy. After controlling for known confounders five specific maternal occupations during pregnancy have been implicated as being associated with subsequent atopic disease in offspring. Each of these occupations is characterised by high and persistent exposure to airborne chemicals. High level exposure to volatile organic compounds in the domestic environment either during maternal pregnancy or in early life, is also associated with development of childhood atopic disease. Similarly, sustained exposure to airborne chlorinated chemicals from swimming pools during childhood has been associated with the development of atopic allergy. A possible immunological basis for these associations is that exposure to certain airborne chemicals, even at low levels, can result in the delivery of 'danger' signals that, in turn, bias the immune response toward the selective induction or maintenance of preferential Th2-type immune responses consistent with the acquisition of allergic sensitisation. This article is protected by copyright. All rights reserved.
    British Journal of Dermatology 08/2013; · 3.76 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background. Dimethylfumarate (DMF) was the cause of a major outbreak of allergic contact dermatitis as a consequence of its use as an antifungal agent in leather products, particularly in furniture, with what became known as 'toxic sofa dermatitis'. Objectives. To determine whether the frequency and severity of reactions to DMF arose as a function of its intrinsic potency and/or the nature and extent of exposure. Methods. The intrinsic potency of DMF was measured with the standard local lymph node assay (LLNA), with determination of an EC3 value, which is the threshold in the LLNA and serves as an indicator of relative skin-sensitizing potency in humans. Results. The EC3 value for DMF was 0.35% when tested in dimethylformamide as a vehicle, indicating that DMF is a strong, but not an extreme, skin sensitizer in this mouse model. Conclusions. DMF appears to have a sensitizing potency in the mouse that is very similar to that of formaldehyde, which is also a strong human skin sensitizer. However, the frequency and intensity of allergic contact dermatitis reactions to DMF suggest that it was the prolonged, repeated and occlusive exposure to this chemical over large skin areas, combined with the strong sensitizing potency, that generated the 'perfect storm' conditions that caused the DMF epidemic.
    Contact Dermatitis 04/2013; · 2.93 Impact Factor
  • David A Basketter, Ian Kimber
    Contact Dermatitis 04/2013; 68(4):244-5. · 2.93 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The skin immune system's propensity to produce allergic contact dermatitis (ACD) to harmless chemicals, whilst otherwise being an efficient defence system, represents a dermatological paradox. We postulate that a major role in signaling in ACD is played by Toll-like receptor (TLR) 2 and TLR4 that arises from their activation by extracellular DAMPs (danger associated molecular patterns). Ligand activation of TLR4/2 results in the expression of interleukins (IL) IL-1β, IL-6, IL-12, IL-18 and IL-23, tumour necrosis factor-α (TNF-α) and interferon-α (IFN-α). These cytokines promote acquisition of sensitisation, and facilitate elicitation of contact allergy, via multiple mechanisms, including the recruitment of CD4+ T helper (Th) cells, Th1 and Th17 cells. As Th1 cells secrete large amounts of Danger Associated Molecular Pattern molecules (DAMPs), a DAMP immune circuit (positive feedback loop) is created. This is an important driver of skin sensitisation and skin inflammation. Pathogenic extracellular bacteria, but not commensal bacteria, produce PAMPs (Pathogen-Associated Molecular Pattern molecules), that stimulate the expression of Th1 and Th17-promoting cytokines via TLR 2 and 4. This also induces an immune circuit. The ability of the skin immune system to activate host defence mechanisms and to distinguish between pathogenic bacteria and commensals provides an explanation why skin sensitisation and ACD develops; processes that rely on the same biological pathways. These pathways may also shed light on pathogenesis of chronic pustular inflammatory dermatoses (e.g. acne vulgaris). The existence of safety signals from commensal bacteria that prevent initiation of these pathways may represent opportunities for novel therapeutic approaches to the treatment of inflammatory skin diseases.
    British Journal of Dermatology 02/2013; · 3.76 Impact Factor

Publication Stats

9k Citations
1,061.48 Total Impact Points

Institutions

  • 2013
    • The Kings College
      Brooklyn, New York, United States
  • 2008–2013
    • The University of Manchester
      • Faculty of Life Sciences
      Manchester, ENG, United Kingdom
    • University of Surrey
      Guilford, England, United Kingdom
  • 2012
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
    • BASF SE
      Ludwigshafen, Rheinland-Pfalz, Germany
    • Universität Konstanz
      Constance, Baden-Württemberg, Germany
  • 1994–2012
    • Liverpool John Moores University
      • School of Pharmacy and Biomolecular Sciences
      Liverpool, ENG, United Kingdom
  • 2007–2011
    • King's College London
      • St John's Institute of Dermatology
      London, ENG, United Kingdom
    • Státní Zdravotní Ústav
      Praha, Praha, Czech Republic
    • Lhasa Limited
      Leeds, England, United Kingdom
  • 2009
    • European Commission - Joint Research Centre
      • Institute for Health and Consumer Protection
      Brussels, BRU, Belgium
  • 2007–2009
    • University of Liverpool
      • Centre for Drug Safety Science
      Liverpool, ENG, United Kingdom
  • 1998–2008
    • Procter & Gamble
      Cincinnati, Ohio, United States
  • 1988–2008
    • Unilever
      Londinium, England, United Kingdom
  • 2006
    • Health and Safety Executive
      Liverpool, England, United Kingdom
  • 2002–2006
    • Syngenta
      Bâle, Basel-City, Switzerland
  • 2004
    • L'Oréal
      Lutetia Parisorum, Île-de-France, France
    • Aichi Medical University
      • Department of Dermatology
      Japan
  • 2003–2004
    • Imperial College London
      • Division of Molecular Biosciences
      Londinium, England, United Kingdom
  • 2002–2004
    • IT University of Copenhagen
      København, Capital Region, Denmark
  • 1997–2004
    • University of Strasbourg
      Strasburg, Alsace, France
  • 2000
    • AstraZeneca
      Tukholma, Stockholm, Sweden
  • 1999
    • Universitätsklinikum Erlangen
      • Department of Dermatology
      Erlangen, Bavaria, Germany
  • 1995
    • University of Pennsylvania
      • Department of Dermatology
      Philadelphia, PA, United States
  • 1993–1995
    • European Centre for Ecotoxicology and Toxicology of Chemicals
      Bruxelles, Brussels Capital Region, Belgium
  • 1989–1994
    • The Lister Hospital
      Londinium, England, United Kingdom