Clinical environmental medicine

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Clinical environmental medicine (also: practical environmental medicine ) has the task of medical treatment of patients whose health complaints or conspicuous examination findings are attributed to environmental factors or stresses. Sometimes the causes of chronic diseases are found in the environment. The individual vulnerability (vulnerability) and susceptibility (sensitivity) of the patient are of particular importance. In addition to outpatient or inpatient diagnostics and therapy, clinical environmental medicine also includes research and teaching on prevention, diagnosis and therapy of diseases caused by environmental factors. Above all, differentiated diagnostics and therapy, i.e. the right to treatment, distinguish clinical environmental medicine from the area of ​​“environment and health” ( public health ), from toxicology , from occupational medicine and from hygiene .

The central subject is the diagnosis and therapy of diseases due to artificial (anthropogenic) as well as natural environmental pollution and their health-impairing effects, taking into account individual susceptibility and vulnerability. Due to the diversity of environmental medical influencing factors, this results in a wide variety of health effects, which can include almost all specialist areas.

Final diagnoses in clinical environmental medicine can therefore only be made after thorough, clarifying diagnostics with the assistance of other medical disciplines and confirmed there by additional clinical tests or targeted laboratory analyzes.

Environmental factors - previous disease models in contrast to those of clinical environmental medicine

In the context of clinical-curative environmental medicine, the term environmental factor refers to all external physical, biological and chemical stressors that affect our body. The range of these potentially pathogenic environmental factors thus ranges from toxic or immunogenic (allergenic) substances of natural, biological or synthetic origin to microbial pathogens and their toxins or metabolic products, physical fields and radiation as well as noise, air pollution and water pollution.

The environmental medical assessment of the effect of environmental factors on body functions is not only oriented towards toxicology. Rather, in addition to a toxicological and toxicological-cumulative (adding) consideration, the immune response to the environmental factors, i.e. H. especially the possibility of allergic sensitizations should be considered. In addition, the diverse possibilities of influencing environmental factors in biochemical and neurohormonal function chains must be taken into account both biologically and physicochemically. In the case of multiple exposure to various environmental factors, which are more the rule than the exception, there are also potentiation effects that have not yet been clearly assessed and that can go far beyond the additive summation effects.

Examples are the long-term effects of lipophilic (fat-soluble) toxins in the low dose range or the effects of endocrine disruptors (substances with a hormone-like effect) as well as heavy metals. The purely toxicological perspective that has been practiced over decades should be abandoned, because z. B. in the area of ​​the environmental factor "heavy metals", the displacement of endogenous "functional metals" does not necessarily have to be dose-related, especially in the case of chronic exposure. In addition, the complex redistribution and storage mechanisms from the transport medium blood into deeper body compartments, which are only partially accessible by means of mobilization methods, prevent linear measurement of environmental pollutants

In contrast to the acute, classical internal clinical pictures with functional organ diseases that are often diagnostically clearly distinguishable and traceable in linear causality, the focus in environmental medical diseases is often monocausally inexplicable systemic diseases on the basis of systemic inflammatory reactions, which elude the aforementioned categorizations due to their complexity. This also applies to chronic diseases such as B. the complex disturbances of the biological control circuits of the NEIS (neuro-endocrino-immune system).

Taking into account the individual susceptibility and the individual, genetically determined, measurable detoxification possibilities today, no blanket, conclusive toxicological assessment in the sense of a linear dose-effect principle can take place. Only an approximate assessment can be made on the basis of a probable causal exposure and impact assessment. Another factor that complicates the diagnosis lies in the sometimes long time span (latency) between exposure and manifestation of an environmental medical disease, especially in the case of long-term exposure (dose times time) that is subliminal in the toxicological sense. Clinical-curative environmental medicine is able to obtain evidence of environmental pollution through detailed anamnesis, patient guidance, elimination and provocation tests. Subsequent targeted analysis as well as avoidance measures (exposure stop) and the resulting relief or even recovery then underpin the diagnosis made.

Examination methods in clinical environmental medicine - specific perception of environmentally associated diseases. The diagnosis of environmental medical diseases is based on a detailed anamnesis. This includes the entire professional and private living environment, the family disposition as well as the consumption and eating habits of the patients from an environmental medical point of view.

All modern and classic medical examination techniques are used as part of diagnostics. In addition to modern laboratory diagnostic toxicological, immunological, endocrinological and metabolic physiological examination methods (see biomonitoring, effect monitoring), genetic analyzes, mobilization tests and imaging processes as well as nutritional and building biology examinations are also available. The laboratory analysis used in clinical environmental medicine includes environmental monitoring, biomonitoring, effect monitoring, disposition diagnostics and other special test procedures.

Environmental monitoring

As part of environmental monitoring , external, potentially pathogenic (disease-causing) loads from professional, private and leisure areas are examined. These include, for example, exposure to chemicals (such as herbicides, wood preservatives, solvents, pesticides), molds and their toxins, heavy metals, dental materials, toner dust, etc., but also physical exposure (radiation, magnetic fields, noise, climate, etc.) and psychosocial factors.

Biomonitoring

Under biomonitoring refers to the measurement of harmful substances and / or their metabolites (metabolic products) in the organism. In human biomonitoring, one examines tissue samples, blood, urine, saliva, stool, breath, breast milk, hair, teeth or sperm. It must be noted that the environmental factor to be examined within the body is always subject to complex physicochemical active and passive redistribution mechanisms due to hydrophilic or lipophilic properties. The current measured value represents a snapshot and must be interpreted accordingly. In addition, such a measured value must always be interpreted in connection with the anamnestically determined exposure and the clinical picture. In addition, clinical-curative environmental medicine makes an explicit distinction between toxic, inflammatory-immunological, endocrine and neurofunctional reactions or combinations of these types of reaction to environmental factors. For the following genetic reasons, these can lead to very different individual disease courses for individual patients with apparently the same exposure to environmental factors. Here, individual vulnerability and susceptibility, multifactorial stress, long-term stress even in the low dose range, accumulation and deposition of toxins and stressful metabolic products as well as reactive metabolic damage and the suppression of micronutrients play a decisive role.

Effect monitoring

In effect monitoring, biochemical changes are recorded as indications of the effect of an environmental factor in the organism. If they are detectable, they can objectify the pathogenesis of environmental health disorders. In toxicology, they allow an individual risk assessment for exposure to a pollutant. Enzymes, metabolites (metabolic products), proteins as well as hemoglobin and DNA adducts serve as markers of biochemical effects (effect markers). Examples of this are lead anemia due to the inhibition of heme biosynthesis or the inhibition of acetylcholinesterase by alkyl phosphates. Polyaromatized hydrocarbons (benzpyrene) induce DNA adducts. However, the sensitivity of the toxic effect markers known to date is often too low for the issues of chronic multiple exposure, which are mostly given in clinical environmental medicine. The better knowledge about biochemical and immunological pathomechanisms in environmental medical diseases has led to the fact that today numerous biomarkers can indicate the exposure to environmental pollutants, which is also an effect monitoring. Environmental pollution can, for example, lead to disturbances in the balance between radical formation and radical breakdown, which is why increased free radicals or oxidatively or nitrosatively modified molecules serve as indicators of the damaging effect on the cellular level ("oxidative or nitrosative stress"). Immune system parameters are also today considered to be an effect marker for increased environmental pollution or an expression of an individually increased inflammatory response to various environmental factors. With the cytokines (especially TNF-α, IL-6 or interferon-gamma-induced protein 10), blood markers are available that indicate systemic inflammation. The disadvantage of the immunological effect markers in particular is that they are not monocausally specific for certain environmental or pollutants, but rather indicate the reaction of the individual organism to the sum of the loads.

Disposition diagnostics

The range of known mechanisms in the development of environment-associated diseases is large. In the context of clinical environmental medicine, they range from exogenously disease-causing environmental factors (e.g. chemicals, pesticides, heavy metals) to the pathogenesis of genetically associated diseases due to an innate deficient breakdown of foreign substances. Clinical environmental medicine uses genetic diagnostics to find explanations for the genetic susceptibility of diseases associated with the genetic environment as well as approaches for an optimized therapy taking into account the genetic differences in the metabolism of numerous drugs and pollutants. Genes of the human genome and its gene products are in constant interaction with the environment and especially with ubiquitous foreign substances. Diseases associated with the genetic environment are often characterized by the fact that the pathogenetic relevance only becomes apparent during or even after exposure to a foreign substance. Genetically determined differences also mean that exposure to a foreign substance does not have the same disease-causing significance for everyone. With the help of molecular genetic methods it is possible to estimate the individual susceptibility and also tolerance to numerous foreign substances.

The variety of known mechanisms in the context of clinical environmental medicine ranges from genetically determined HLA disposition to insufficient or missing detoxification performance of corresponding enzyme groups (CYPs, NAT2, GSTs, SOD etc.) as well as neuroendocrine dysfunctions (COMT, MAOA, MTHFR) to excessive toxification (poisoning) of biological or chemical environmental factors as a result of increased enzyme activities. So e.g. For example, the clinical significance with regard to exposure to exogenous substances as well as their toxicological effects and excretion largely depend on the interaction of the so-called phase I and phase II enzymes involved in the metabolism of xenobiotics.

The detection tests for immunological sensitizations represent a further important pillar for recording individual dispositions. In addition to the lymphocyte transformation test (LTT) for recording type IV sensitizations, cellular methods are used to detect allergic immediate type reactions and cytokine-based stimulation tests are used to detect immunotoxicological sensitivities.

Therapy in clinical environmental medicine

In addition to the endogenous individual predispositions of the patient, the therapeutic options for environmental medical diseases result from the exogenous causal factors diagnosed in each case, insofar as these can be determined. In general, avoiding exposure and eliminating or reducing the four most important stressors (physical, chemical, biological and psycho-social) is the primary therapeutic measure. This is followed by the renovation of the living and working environment, the individual elimination of deficiencies in micronutrients, metabolic activation and modulation as well as nutritional advice, active detoxification therapies, through alloplastic materials (dentures / endoprostheses, etc.) and possible immunological and toxicological secondary reactions are taken into account.

Diseases of clinical environmental medicine

The chronic consequences of long-term exposure to environmental pollutants in the above The environmental medical sense is often presented as multifactorial syndromes. Examples are diseases such as CFS (Chronic fatigue syndrome = Chronic fatigue syndrome ) and MCS (Multiple chemical sensitivity = multiple chemical intolerance ). Some neuroinflammatory diseases and other chronic diseases that are symptomatically treated in conventional medicine can in part be causally justified with environmental medical explanatory models and then be treated sustainably. Examples include depressive disorders after long-term exposure to neurotoxic solvents or indications of intolerance to dental metals in patients with connective tissue diseases, fibromyalgia or autoimmune diseases.

Somato-psychic differential diagnosis: Clinical-curative environmental medicine borders pathologies that can be proven by environmental medicine from psychosomatic clinical pictures such as B. the somatization disorder. Many latently or chronically suffering from environmental medical diseases are stigmatized by the non-acceptance of their complaints by unskilled specialists and a health system that largely does not cover environmental medical diseases. On the other hand, those affected are often psychosomatized or even psychiatricized. Severe, long-lasting, primarily somatic symptoms can still trigger the formation of secondary mental illnesses (such as cancer). The resulting comorbidities make the diagnostic clarification of the underlying causalities in the sense of the primary trigger more difficult.

Environmental clinical medicine guidelines

The actions of clinical environmental medicine are based on the guidelines published by the German Professional Association of Environmental Medicine (dbu).

Basic, advanced and advanced training in clinical environmental medicine

A certified further training was carried out annually until 2004 by the German Professional Association of Environmental Medicine (dbu) and the European Academy for Environmental Medicine (EUROPAEM). The change to the training regulations initiated by the German Medical Association in 2004 has transformed the certified education in environmental medicine into an optional advanced training course. There is currently no training in clinical environmental medicine due to a lack of capacity at German universities. The lessons offered are limited to the area of ​​environment and health. Further training in clinical environmental medicine is carried out according to a modulated curriculum of the German Medical Association (BÄK) by the German Professional Association of Environmental Medicine (dbu) and the European Academy for Environmental Medicine (EUROPAEM). A curricular environmental dental training is offered by the German Society for Environmental Dentistry (DEGUZ).

Individual evidence

  1. ^ A. Beyer, D. Eis (ed.): Practical Environmental Medicine , loose-leaf collection, Springer-Verlag, Berlin, Heidelberg, New York April 1994, 1st edition, ISBN 3-540-57698-3 .
  2. ↑ German Medical Association: Structured curricular training in environmental medicine. Texts and materials from the German Medical Association for advanced training and further education. 2006, p. 5 (PDF) .
  3. ^ A b B. Weiss, K. Reuhl: Delayed neurotoxicity ": A silent toxicity. In: LW Chang (Ed.): Principles of Neurotoxicology. Marcel Dekker, New York 1994, ISBN 0-8247-8836-2 , pp. 765-784.
  4. a b S. Böse-O'Reilly, S. Kammerer (Ed.): Guide to Environmental Medicine. Urban & Fischer, Munich 2000, ISBN 3-437-41020-2 .
  5. a b c d e f g h i j F. Bartram, A. Bauer, V. v. Baehr, CH. Bückendorf, HP. Donate, V. Engelhardt, W. Huber, M. Klehmet, K. Müller, P. Ohnsorge, C. Mai, JM. Träder: Action-oriented environmental medical practice guidelines. Long version. German Professional Association of Environmental Medicine eV Practice Guidelines in Environmental Medicine. German Occupational Association of Environmental Medicine (eds.) Berlin 2011 (PDF) .
  6. ^ A b Y. W. Chen, CY Yang, CF Huang et al .: Heavy metals, islet function and diabetes development. In: Islets. 1 (3), 2009, pp. 169-176. doi: 10.4161 / isl.1.3.9262
  7. JG Koppe, A. Bartonova, G. Bolte et al: Exposure to multiple environmental agents and their effect. In: Acta Pediatrica Supplements. 95 (453) Oct 2006, pp. 106-101, doi : 10.1080 / 08035320600886646
  8. M. Caba, E. Meza, SM Waliszewski, C. Martínez-Valenzuela: Inverse correlation among organochlorine pesticide levels to total lipid serum contents: a preliminary study in Veracruz, México. In: Environmental Monitoring and Assessment. 187 (7), 2015, p. 467. doi: 10.1007 / s10661-015-4694-0 .
  9. a b J. Y. Min, KB Min: Association between total blood mercury and exhaled nitric oxide in US adults. In: Nitric Oxide. 29, 2013, pp. 53-58. doi: 10.1016 / j.niox.2012.12.005 .
  10. a b D. Echeverria, JS Woods, NJ Heyer et al .: The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans. 22. In: Neurotoxicology Teratology. 28 (1), 2006, pp. 39-48, doi: 10.1016 / j.ntt.2005.10.006 .
  11. a b H. J. Seidel: Clinical environmental medicine. Shaker Verlag, Aachen 2005, ISBN 3-8322-4254-6 .
  12. a b W. Dott, HF Merk, J. Neuser, R. Osieka (ed.): Textbook of environmental medicine. Wissenschaftliche Verlagsgesellschaft, Stuttgart 2002, ISBN 3-8047-1816-7 .
  13. a b c d E. Schnakenberg: Possibilities of molecular genetic diagnostics in environmental medicine - an overview. In: Environment Medicine Society. 20, 2007, p. 265. Umwelt-medizin-gesellschaft.de ( Memento from April 26, 2009 in the Internet Archive )
  14. F. Bartram: Immune-induced inflammatory processes through chronic exposure to chemicals. In: Environment-Medicine-Society. 18 (3), 2005, pp. 202-208 ( Umwelt-medizin-gesellschaft.de ( Memento from April 26, 2009 in the Internet Archive )).
  15. ^ V. von Baehr: On the current state of laboratory medicine. In: Environment Medicine Society. 2 (2), 2007, pp. 99-105 ( Umwelt-medizin-gesellschaft.de ( Memento from April 26, 2009 in the Internet Archive )).
  16. H. Marquardt, SG Schäfer (Ed.): Textbook of Toxicology. 2nd Edition. Wissenschaftliche Verlagsgesellschaft, 2003, ISBN 3-8047-1777-2 .
  17. Patricia Ruiz, Ally Perlina, Moiz Mumtaz, Bruce A. Fowler: A Systems Biology Approach Reveals Converging Molecular Mechanisms that Link Different POPs to Common Metabolic Diseases. In: Environmental Health Perspectives . 124, 2016, doi: 10.1289 / ehp.1510308 .
  18. M. Tsuji: Useful biomarkers for assessing the adverse health effects of PCBs in allergic children: pediatric molecular epidemiology. In: Environmental Health Preventive Medicine. 20 (1), 2015, pp. 3–11. doi: 10.1007 / s12199-014-0419-1
  19. B. Hennig, P. Meerarani, R. Slim et al .: Proinflammatory properties of coplanar PCBs: in vitro and in vivo evidence. In: Toxicology Applied Pharmacology. 181 (3) 2002, pp. 174-183, doi: 10.1006 / taap.2002.9408 .
  20. C. Fenga, S. Gangemi, S. Catania, A. De Luca, C. Costa: IL-17 and IL-22 serum levels in greenhouse workers exposed to pesticides. In: Inflammation Research. 63 (11), 2014, pp. 895-897. doi: 10.1007 / s00011-014-0769-6
  21. ^ E. Valentine-Thon, K. Müller, G. Guzzi, S. Kreisel, P. Ohnsorge, M. Sandkamp: LTT-MELISA is clinically relevant for detecting and monitoring metal sensitivity. In: Neuroendocrinology Letters. 27 Suppl 1, 2006, pp. 17-24. ( Archived copy ( Memento of the original from May 5, 2017 in the Internet Archive ) Info: The archive link was automatically inserted and not yet checked. Please check the original and archive link according to the instructions and then remove this note. ) @1@ 2Template: Webachiv / IABot / www.nel.edu
  22. ^ HU Hill: Multiple Chemical Sensitivity (MCS). 3. Edition. Shaker, 2010, ISBN 978-3-8322-9046-7 .
  23. ^ R. Straub: The Origin of Chronic Inflammatory Systemic Diseases and their Sequelae. 1st edition. Academic Press, 2015, ISBN 978-0-12-803321-0 .