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Dr. Ali's Course on Allergy

The Oxygen Model of Allergy

Majid Ali, M.D.

An integrative model of clinical allergy is proposed that incorporates clinical and experimental observations in the following three areas: (1) Classical studies of IgE-mediated atopic response and, to a lesser degree, the other three types of Gell and Coombs' hypersensitivity responses; (2) An ecologic view of clinical allergy that includes sensitivity to environmental agents independent of the dose of the excitant; (3) An expanded, integrative perspective of hypersensitivity responses that focuses on oxidative-dysoxygenative dysfunction (ODD) that profoundly influences sensitivity reactions included in the first two categories. The proposed integrative model has a strong explanatory power for many hitherto poorly understood aspects of clinical allergy. For instance, none of the Gell and Coombs' or other recognized types of hypersensitivity reactions explain why certain antigen exposures evoke strong responses under one set of conditions but not under another in the same atopic individuals. Beyond that, the proposed model provides a scientifically sound basis for adding to specific antigen immunotherapy nutritional, antioxidant, detoxification, and oxygenative therapies to enhance clinical benefits.


In 1983, I recognized spontaneity of oxidation in nature as the primary drive in all oxidative phenomena in nature, and proposed it to be the primary mechanism for perpetuating oxidative molecular injury in biologic phenomena, including the human aging process.1 In a series of publications that followed, I explored the issues of: (1) the fundamental oxygen order of human biology2-5; (2) the impact of the molecular duality of oxygen on human health and disease6; (3) oxidative cell membrane injury7; (4) oxidative injury to intracellular matrix and mitochondria8; (5) oxidative phenomena in atopic disorders and multiple chemical sensitivity syndrome 9; (6) stunted allergen-specific IgG response to immunotherapy in patients with chronic fatigue syndrome10; (7) morphologic changes of oxidative coagulopathy (observed in freshly prepared peripheral blood smears with high-resolution [x15,000] phase-contrast microscopy) in ischemic coronary artery disease11; (8) the incidence and extent of oxidative coagulopathy in chronic fatigue syndrome, fibromyalgia,12 and environmental illness13; (9) clinical evidence of oxidative injury to the hormone-receptor-response element-gene activation cascades14; (10) oxidative regression to primordial cellular ecology15; and (11) oxidative-dysoxygenative basis of fibromyalgia.16 In this article, the classical studies of atopy and the core clinical concepts of environmental medicine are briefly reviewed to provide a framework for presenting the integrative oxidative-dysoxygenative model of clinical allergy.

The Classical Atopic Perspective

Modern concepts of allergy may be traced to Charles Robert Richet who described anaphylactic reaction in 1902.17 Four years later, Von Pirquet introduced the term allergy (derived from the Greek words allos [other] and ergia [energy]) for an altered state of immune responsiveness or "changed reactivity" of an individual.18 In 1911, Noon introduced specific antigen immunotherapy.19 In 1923, Coca and Cooke proposed the term atopy (derived from the Greek word atopos [meaning strange or uncommon]) for an abnormal state of hypersensitivity in an individual, rather than a hypersensitive response in a healthy individual, and believed that such sensitivity could not be transferred to animals or humans.20 Prausnitz and Kustner in 1921 laid the cornerstone for immunologic investigation of allergic phenomena by documenting the presence of a transferable skin-sensitizing factor in the serum of allergic individuals.21 In 1964, Gell and Coombs proposed their classification of four mechanisms of allergic reactions, Type-I reaction being the response mediated by the reaginic antibody.22 In the mid-1960s, Ishizaka established IgE as a new unique immunoglobulin on the basis of the following three principal criteria: its ability to bind the specific antigen, its unique antigenic determinants, and its correlation with biologic activity as demonstrated by the P-K technique.23 In 1966, Wide, et al.,24 described the radioallergosorbent (RAST) assay for semi-quantitative measurement of allergen-specific IgE antibodies, and ushered in the era of in vitro diagnosis of allergy. In 1980, my colleagues and I demonstrated local IgE production in plasma cells in the nasal mucosal of atopic persons25and in nasal polyps.26 The same year, my colleague, Madhava Ramanarayanan, and I described micro-ELISA assays for allergen-specific IgE and IgG antibodies and, to achieve a higher level of assay sensitivity and specificity, developed a methodology for accounting for a range of variability in the nonspecific binding among individual antigens.27,28 Employing that assay, Hurst and colleagues demonstrated the local production of allergen-specific IgE antibodies in the middle ear mucosa and firmly established such mucosa as the primary target of the atopic response.29

The Ecologic Perspective

During the next two decades, a wide gulf developed between IgE researchers and clinical ecologists who focused on clinically verifiable patterns of hypersensitivity reactions that could not be explained on the basis of IgE-mediated or other immunologic sensitivity mechanisms. The discipline of clinical ecology was defined as the study of the effects of the environment upon the individual by the pioneers of the field, including Randolph,30 Rea,31 and Waickman.32 Chemical sensitivity was defined as an adverse response of an individual to environmental chemicals at levels that are generally considered safe.33 Thus, chemical sensitivity is independent of the dose of excitant. The core concept of chemical sensitivity holds that clinical expression of an adverse reaction is determined by the following: (1) the body tissue or organ involved; (2) the chemical nature of the excitant trigger; (3) the biochemical individuality of the person (the individual susceptibility of the person to a given excitant); (4) the length of the exposure; (5) and the existence of concurrent but unrelated stressors as well as synergism among them (the concept of total load).33 Four general principles that govern the cause-and-effect relationships in clinical ecology are: (1) total load; (2) adaptation (first described by Selye34 and including masking or acute toxicologic tolerance); (3) bipolarity consisting of an initial stimulatory phase followed by a depressive phase; and (4) biochemical individuality.

In my view, clinical ecology was an important advance beyond the classical atopy because it could explain a broad spectrum of clinical manifestations not accounted for by the latter. The IgE researchers continued to focus on issues of single-allergen sensitivity and consequences of specific immunotherapy in such disorders. The ecologists, while recognizing the theoretical merit of such work, found those findings to be of very limited clinical value since allergic persons invariably suffer from multiple sensitivities. After decades of doubt and denial,35,36 the existence of multiple chemical sensitivity syndrome was finally acknowledged and its relevance to the management of the classical allergy understood.37

During the early 1980s, many clinical observations led me to investigate the role of altered states of the bowel ecosystem on the clinical manifestations of hypersensitivity reactions.2,3 For example, a marked improvement in symptoms of atopic dermatitis was observed in many patients with empirical therapies that putatively "restored the bowel health." Relief of constipation was associated with relief of sinusitis headache in others. Symptoms of allergic rhinitis often subsided with antifungal therapies.12 Such observations led the author to introduce the concept of altered states of bowel ecology as the basis for heightened hypersensitivity states.

The Oxidative-dysoxygenative Perspective

Notwithstanding the great advances in both classical allergy and clinical ecology, certain fundamental aspects of clinical hypersensitivity reactions remained unexplained. For instance, eczema lesions flare more in some weeks than in others in the same person. Lifestyle stressors exaggerate bronchospasm more on some days than on others in the same asthma sufferer. Symptoms of Crohn's colitis and ulcerative colitis remit and relapse for no apparent reason in most instances. Food sensitivity reactions vary over a broad range in the same individual. Allergic rhinitis becomes more intense on some days when pollen count is low and abates on days when pollen counts are high. The phenomenon of "spreading sensitivity reactions" (long vigorously denied by IgE researchers) is increasingly recognized in chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivity syndrome. The molecular basis of the above cannot be understood on the basis of the known immunologic responses. Such considerations led me38 and others39 to look beyond those responses and focus on issues of redox homeostasis. Recently, I put forth an oxidative-dysoxygenative model as the molecular basis for fibromyalgia.16 Extended studies of freshly prepared peripheral blood smears with high-resolution phase-contrast microscopy in collaboration with my colleague, Omar Ali, led to the description and characterization of oxidative coagulopathy (figures 1-4).4 The oxidative nature of oxidative coagulopathy was established by its reversal by antioxidants in the early stages.

From our microscopic observations we inferred that oxidosis of blood (oxidative coagulopathy) is the primary mechanism that links redox disruptions of the bowel ecosystem with clinicopathologic consequences of oxidosis in all microecologic cellular and macroecologic tissue-organ ecosystems of the body.13,40 Thus, changes of oxidative coagulopathy were deemed morphologic evidence of systemic dysregulation of the redox homeostasis. The role of such dysregulation in the pathogensis and clinical symptomatology of allergic diathesis, to our knowledge, had not been explored. It seemed self-evident to us that all mediator responses of hypersensitivity reactions would be greatly amplified by oxidative coagulopathy and its cellular consequences. The clinical manifestations of hypersensitivity states in such an oxidative-dysoxygenative context were seen as surface phenomena profoundly influenced by the foundational changes in redox homeostasis in the trio of the bowel, blood, and liver ecosystems.

Though the role of systemic oxidosis in clinical allergy, as reflected by microscopic changes in oxidative coagulopathy, had not been investigated, it is noteworthy that the role of local factors involved in redox homeostasis in nasal and bronchial allergy has drawn considerable attention. The nasal and bronchial mucosa excretes nitric oxide (NO), a ubiquitous and potent modulator of redox homeostasis.41-43 Among its many biologic roles NO also modulates ciliary motion.44 Of direct relevance to the present discussion is the observed increased NO excretion in allergic rhinitis.45,46 Topical use of an NO synthase inhibitor (N-nitro-L-arginine-methyl-ester [L-NAME]) in limited studies did not increase nasal cavity volume.47,48 However, such findings do not in any way diminish the importance of the fundamental redox phenomena that underlie clinical symptomatology. Another line of evidence pointing to the importance of redox dysregulation in clinical allergy is increased immediate bronchial sensitivity to inhaled ozone.49 In allergic asthma, the late phase responses to allergens are also enhanced by ozone exposure.50 In normal subjects, ozone increases mast cell tryptase and the number of polymorphonuclear cells in the nasal lavage fluid. It seems safe to predict that future studies will uncover the oxidative-dysoxygenative underpinnings in all cellular and mediator allergic responses. Specifically, such responses include switch from proinflammatory and proallergic Th2 subtype T helper cells to allergy-inhibiting Th1 subtype, and biochemical pathways mediated by cytokines (such as IL-4, IL-5, and GM-CSF) as well as monocyte chemotactic proteins (such as MCP-1, MCP-2, and MCP-3) and have been recently reviewed.51,52

Integrative Therapies for Allergic Disorders

My colleagues and I tested the theoretical validity of the proposed oxidative-dysoxygenative model of clinical allergy by conducting clinical outcome studies with integrative management plans that focus on all the relevant oxidative and dysoxygenative factors. Highly atopic patients with indolent disorders responded well only when broad-based redox-restorative therapies were vigorously administered. Specifically, such outcome studies included patients with chronic fatigue syndrome,12,38 fibromyalgia,53 asthma,54 Crohn's disease,55 and young atopic women with oligomenorrhea and amenorrhea14 The clinical picture in patients in those studies was dominated by allergic symptoms and the presence of IgE antibodies with specificity for a host of mold and other inhalant allergy was established with previously described micro-ELISA assay.27 Data obtained with such trials provide significant support for the theoretical precepts for the proposed ODD hypothesis. Evidently, all such evidence must be considered indirect. However, it is noteworthy in this context that the number of biologic variables in such syndromes is very large. It seems highly unlikely that studies can ever be designed in such a way that direct evidence for one-cause one-effect relationships between intracellular oxidative-dysoxygenative phenomena and clinical symptomatology can be established.

Immunotherapy for IgE-Mediated Disorders

The precise diagnosis and the optimal management of IgE-mediated responses must be considered as the centerpiece of all integrative allergy management plans. The details of methodologies used at the Institute have been previously described.56,57 The immunologic consequences of specific antigen immunotherapy were assessed by measuring allergen-specific IgG antibodies.28

Adjunctive Nutrient, Herbal, and Oxygenative Therapies

The clinical outcome in allergy treatment is markedly enhanced if issues of lifestyle, stress and the ecologic integrity of the bowel, blood, and liver ecosystems are addressed. This becomes a critical issue when allergy symptomatology is a major part of diverse chronic immune disorders such as fibromyalgia, Crohn's colitis, multiple sclerosis, and multiple chemical sensitivity syndrome. The details of integrative management protocols in use at the Institute and clinical outcome data obtained with those plans have been previously described.10-15 Figure 5 shows the schema of an ecologic model in use at the Institute to assist clinicians for establishing therapeutic priorities as well as for patient education. Extensive clinical experience has led me to the conclusion that the bowel, blood, and liver ecosystems form the foundation of human redox, enzymatic, and detoxification defenses. My colleagues and I prescribe nutrient, herbal, and oxygenative protocols for restoring the various ecosystems of the body for individual patients in light of the total clinical context, rather than blinded and controlled trials of individual therapeutic agents. The latter approach, we have pointed out earlier, negates the very essence of the integrative approach to clinical problems. In this section, some salient aspects of antioxidant, herbal, and oxygenative protocols are included for the general interest of the reader (Tables 1-4). Table 1 shows our recommendations for atopic but generally healthy persons as well as those with chronic immunologic disorders, such as chronic fatigue syndrome, fibromyalgia, and chemical sensitivity syndrome. In selected cases, individualized parenteral nutrient support is very beneficial. Intramuscular protocols A and B may be given on alternate weeks for four to six weeks in selected cases (Tables 3 &4).

Table 1. General Guidelines for Nutrient and Redox-Restorative Supplements for Atopic Patients With and Without Indolent Immune Disorders


Atopic Individuals Without Chronic Indolent Immune Dysfunction

Atopic Individuals With Chronic Indolent

Immune Dysfunction



C, 1,000 to 2,000 mg;

E, 200 to 400 IU;

A, 5,000 to 7,500 IU;

D, 100 to 250 IU;

B-complex, 25-50 mg;

B12, 1,000 mcg weekly for four weeks.


C, 3,000 to 5,000 mg;

E, 400 to 800 IU;

A, 10,000 to 15,000 IU;

D, 100 to 250 IU;

B-complex, 30-50 mg;

B12, 1,000 to 5,000 mcg weekly for four to six weeks .


Magnesium, 1,000 to 1,500 mg;

Calcium, 750 to 1,000 mg;

Potassium, 200 to 400 mg;

Chromium, 100-300 mcg;

Selenium, 100-300 mcg;

Molybdenum, 100-300 mcg.

Magnesium, 1,500 to 2,500 mg;

Calcium, 1,000 to 1,500 mg;

Potassium, 400 to 600 mg;

Chromium, 400-600 mcg;

Selenium, 400-600 mcg;

Molybdenum, 400-600 mcg.

Redox-Restorative Substances

Glutathione, 200-300 mg;

N-acetylcysteine, 200-300 mg; Methylsulfonylmethane, 200 to 500 mg; Lipoic acid, 100 to 200 mg; Taurine, 500 to 1,000 mg; Coenzyme Q10, 30 to 50 mg;

Pycnogenol, 50 to 100 mg.

Glutathione, 600-800 mg;

N-acetylcysteine, 600-800 mg; Methylsulfonylmethane, 1,000 to 1,500 mg; Lipoic acid, 300 to 500 mg; Taurine, 1,500 to 2,000 mg; Coenzyme Q10, 100 to 150 mg;

Pycnogenol, 100 to 150 mg.


Table 2. Composition of Adjunctive Nutrient and Herbal Protocols for the Bowel


One billion spores of Lactobacillus acidophilus, Lactobacillus bulgaricus, Bifidobacterium in a base of complex vegetable fiber, magnesium sulfate, vitamin B complex, l-histidine, l-arginine, pantethine, aloe vera.


Alfalfa, 500 mg; pau d'arco,100 mg; allium, 100 mg; licorice root extract, 200 mg.


Calcium caprylate, 50 mg; magnesium caprylate,50 mg; grapefruit seed extract, 25 mg; aloe vera, 1 mg; spirulina, 10 mg.


Grapefruit seed extract, 50 mg; allium, 50 mg; pau d'arco, 500 mg.


Par-quing, 150 mg; pau d'arco 150 mg; beet root fiber, 200 mg; guar gum, 100 mg.


Echinacea, 200 mg; goldenseal root, 150 mg; astragalus root, 150 mg; burdock root 150 mg.


Table 3. Composition of Intramuscular Protocol A




Magnesium sulfate.

500 mg/ml

1.5 ml

Calcium glycerrhate/lactate

10 mg/ml

1.5 ml

Vitamin B12

10,000 mcg/ml

0.5 ml

Vit.B complex


1 ml

Pantothenic acid

250 mg/ml

0.5 ml


100 mg/ml

0.5 ml


5 mg/ml

0/6 ml


25 mcg/ml

0.5 ml


40 mcg/ml

0.4 ml



0.5 ml

* Multivitamin protocol includes the following: thiamine, 25 mg; riboflavin, 5 mg; niacin, 50 mg; niacinamide, 50 mg; pantothenic acid, 12.5 mg; pyridoxine, 7.5 mg; ascorbic acid, 500 mg; vitamin A, 5,000 IU; vitamin D, 500 IU; vitamin E, 2.5 IU.


Table 4. Composition of Intramuscular Protocol B




Magnesium sulf.

500 mg/ml

3 ml

Calcium gly/lac

10 mg/ml

4 ml

Vitamin B12

10,000 mcg/ml

0.5 ml



The proposed integrative model of clinical allergy evolved in three phases of the author's experimental and clinical work. In the first phase, the focus was on classical immunology in general, and on in vitro methodologies for the diagnosis of IgE-mediated disorders in particular. In the second phase, the focus shifted to ecologic issues concerning the allergic individual. In the third phase, emphasis was on issues of oxidosis and dysoxygenosis that greatly amplify IgE-mediated responses. Furthermore, allergic symptomatology was seen within the broader context of oxidative-dysoxygenative injury to the bowel, blood, and liver ecosystems. A case is made for adding adjunctive nutrient, herbal, and redox-restorative therapies to the specific antigen immunotherapy for improving clinical outcome. Such adjunctive therapies were found to be especially beneficial in cases in which allergic symptomatology is associated with microscopic evidence of oxidative coagulopathy and clinical features of persistent fatigue, myalgia, abdominal symptoms, and cognitive dysfunctions.



Legends to Figures

Figure 1 shows the schema of the Pyramid of Trios of Human Ecosystems that is used as a model for establishing clinical priorities for atopic patients with indolent chronic immune disorders such as chronic fatigue syndrome, fibromyalgia, chemical sensitivity syndrome.

Figure 2 shows a high-resolution (x15,000) phase-contrast photomicrograph of the freshly prepared peripheral blood smear of a healthy subject used as a control

Figures 3 shows high-resolution morphology of loose (soft) microclot in the peripheral blood smears of highly atopic 8-year-old girl with diffuse eczema.

Figure 4 shows zones of congealed plasma (small arrows) and two microclots (larger arrows) in a 34-year-old atopic woman with fibromyalgia.

Figure 5 illustrates the morphologic features of three microplaques formed when microclots in the circulating blood are compacted into microplaques with layered appearance.

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1. Ali M. Spontaneity of oxidation in nature and Aging. Monograph, Teaneck, New Jersey, 1983.

2. Ali M. The agony and death of a cell. Syllabus of the Instruction Course of the American Academy of Environmental Medicine, Denver, Colorado, 1985.

3. Ali M. Spontaneity of oxidation and chronic disease. In: Syllabus of the Instruction Course of the American Academy of Environmental Medicine, Denver, Colorado, 1992.

4. Ali M. Ascorbic acid reverses abnormal erythrocyte morphology in chronic fatigue syndrome. Am J Clin Pathol. 1990;94:515.

5. Ali M. Ascorbic acid prevents platelet aggregations by norepinephrine, collagen, ADP and ristocetin. Am J Clin Pathol. 1991;95:281.

6. Ali M. Spontaneity of oxidation in nature is the root cause of all illness. In: RDA: Rats, Drugs and Assumptions. pp. 199-304. Life Span, Denville, New Jersey, 1995.

7. Ali M. Molecular basis of cell membrane injury. In: Syllabus of the Instruction Course of the American Academy of Environmental Medicine. Denver, Colorado, 1990.

8. Ali M, Ali O. AA Oxidopathy: the core pathogenetic mechanism of ischemic heart disease. J Integrative Medicine 1997;1:1-112.

9. Ali M. Molecular basis of cell membrane injury. In: Syllabus of the Instruction Course of the American Academy of Environmental Medicine. Denver, Colorado, 1990.

10. Ali M, Bajwa Z, Ali O. Impaired allergen-specific IgG response in chronic fatigue syndrome. Am J Clin Pathol 1994;101:394.

11. Ali M. Oxidative coagulopathy. In: Syllabus of the Capital University of Integrative Medicine, Washington, D.C., 1997.

12. Ali M. Hypothesis: Chronic fatigue is a state of accelerated oxidative molecular injury. J Advancement in Medicine. 1993;6:83-96.

13. Ali M. The basic equation of life. The Butterfly and Life Span Nutrition. The Institute of Preventive Medicine Press, Denville, New Jersey, 1992, pp 225-236.

14. Ali, M. Oxidative menstrual dysfunction (OMD-I). J Integrative Medicine 1998;3:125-139

15. Ali M. Oxidative regression to primordial cellular ecology (ORPEC): Evidence for the hypothesis and its clinical significance. J Integrative Medicine 1998;2:4-55.

16. Ali M, Ali O. Fibromyalgia: An oxidative-dysoxygenative disorder (ODD). J Integrative Medicine 1999;3:17-37.

17. Richet, C. and Porter, P. De l'action anaphylaique de certains venins. C R Soc Biol (Paris) 1902; 54:170.

18. Von Pirquet, C. Allegie, Muench Med Wochenschr 1906; 53:1457. In Gell, PGH, and Coombs, RRA, eds. Clinical aspects of immunology. Philadelphia: F. A. Davis Co., 1963:40.

19. Noon, L. Prophylactic inoculation against hayfever. Lancet 1911: 1:1572.

20. Coca AF, Cooke RA. On the classification of the phenomena of hypersensitiveness. J. Immunol 1923; 8:163.

21. Prausnitz, C. and Kustner, H. Studien uber die Uberempfindlichkeit. Zentralbl Bakteriol (Orig A) 1921: 86:160.

22. Coombs, RRA, and Gell, PGH. Classification of allergic reactions responsible for clinical hypersensitivity and disease. In: Gell, PGH and Coombs, RRA,eds. Clinical aspects of immunology, Oxford: Blackwell Scientific Publications, 1963:575-596.

23. Ishizaka, K, Ishizaka, T, and Hornbrook, MM. Physicochemical properties of reaginic antibody. V. Correlation of reaginic activity with E globulin antibody. J. Immunol 1966; 97:840.

24. Wide, L, Bennich, H, and Johansson, SGO: Diagnosis of allergy by an in-vitro test for allergen antibodies. Lancet 1967; 2:1105.

25. Ali M, Fayemi AO, Nalebuff DJ; Localization of IgE in adenoids and tonsils: An immunoperoxidase study. Arch otolaryngol. 105:695-697,1979.

26. Ali M, Mesa-Tejada R, Fayemi AO, Nalebuff DJ, Connell JT: Localization of IgE in tissues by an immunoperoxidase technique. Arch Pathol Lab Med. 103:274-275, 1979.

27. Ali M and Ramanarayanan MP: A computerized micro-ELISA assay for allergen-specific IgE antibodies. Am J Clin Pathol 1984;81:591.

28. Ali M, Ramanarayanan MP, Nalebuff DJ, et al: Serum concentrations of allergen-specific IgG antibodies in inhalant allergy: Effect of specific immunotherapy. Am J Clin Pathol. 1983;80:290.

29. Hurst D, Weekley M, Ramanarayanan M. Evidence of possible localized specific immunoglobulin E production in middle ear fluid as demonstrated by ELISA testing. Otolaryngol Head Neck Surg. 1999;121:224-30.

30. Randolph TG. Human Ecology and Susceptibility to the Chemical Environment, 1962. Springfield, Illinois. Charles C. Thomas.

31. Rea William J. Chemical Sensitivity: Tools of Diagnosis and Methods of Treatment (Volume 4). Lewsi Publishing, Dallas, Texas, 1997.

32. Waickman FJ. Vojdani A. Putting chemical and environmental sensitivities in perspective.Otolaryngologic Clinics of North America, Vol 31, No. 1 Feb, 1998.

33. Rea WJ. Clinical ecology: A role in diagnosing environmental illness. Annual New England Occupational Medicine Association Conference, Harvard School of Public Health. 1987.

34 Selye H. The general adaptation syndrome and the diseases of adaptation. J Allergy. 1946;17:23-31.

35. Kahn E. Letz G. Clinical ecology: Environmental medicine or unsubstantiated theory? Ann Int Med. 1989;111:104-6.

36. Sparks PJ, Daniell W. Black DW, et al. Multiple chemical sensitivity syndrome: A clinical perspective. J Occupational Medicine. 1994;36:718-737.

37. Cullen MR. The worker with multiple chemical sensitivities: An overview. State Art Rev Occup Med. 1987; 2:655-661.

38. Ali M. Experience with intravenous nutrient therapy for allergic patients with chronic fatigue. Am Acad Otolaryngic Allergy Abstracts, Summer 1992; p23.

39. Bradford R. Henry A. Oxidology. 1997. Bradford Research Institute. San Diego.

40. Ali M. Seven Principles of Integrative Medicine. Aging Healthfully Magazine. Vol 1, No. 1, Spring 1999. Aging Healthfully Press, Denville, New Jersey.

41. Lundberg JO, Farkas-Szallasi T. Weitzberg E, et al. High nitric oxide production in human paranasal sinus. Nat Med 1995;1:370-3

42. Lundberg JO, Rinder J, Weitzberg E, et al. Nasally exhaled nitric oxide in humans originate mainly in the paranasal sinuses. Acta Physiol Scand 1994;152:431-2

43. Zapol WM, Hurford WE. Inhaled nitric oxide in adult respitory distress syndrome and other lung diseases. Adv Pharmacol 1994;31:513-30.

44. Furukawa K. Harrison DG, Saleh D, et al. Expression of nitric oxide synthase in the human nasal mucosa. Am J Respir Crit Care Med 1996;153:847-50

45. Garrelds IM, van Amsterdam JG, de Graff-in't Veld C, et al. Nitric oxide metabolites in nasal lavage fluid of patients with house dite mite allergy. Thorax 1995;50:275-9.

46. Martin U, Bryden K, Devoy M, Howath P. Increased levels of exhaled nitric oxide during nasal and oral breathing in subjects with seasonal rhinitis. J Allergy Clin Immunol 1996;l97:768-72.

47. Dear JW, Ghali S, Foreman JC. Attenuation of human nasal airway responses to bradykinin and histimine by inhibitors of nitric oxide synthase. Br J Pharmacol 1996;118:1177-82.

48. Rinder J, Lundberg JON, Anggard A, et al. Effects of topical nasal decongestants, L-arginine and nitric oxide synthase inhibition on nasal cavity volume in man. Am J Rhinol 1996;10:399-408.

49. Molfino N, Wright S, Katz I, et al.Effect of low concentrations of ozone on inhaled allergen responses in asthmatic subjects. Lancet 1991;338:199-203

50. Peden D, Seltzer R, Devlin R. Ozone exposure has both a priming effect in allergen-induced responses and an intrisic inflammatory action in the nasal airways of perennially allergic asthmatics. Am J Respir Crit Care Med 1995;151:1336-45.

51. Holgate ST. The epidemic of allergy and asthma. Nature. 1999:402:B2-4 (Suppl).

52. Cookson W. The alliance of genes and environment in asthma and allergy. Nature. 1999; 402: B5-11 (Suppl).

53. Ali M. Intravenous Nutrient Protocols in Molecular Medicine. Monograph. The Institute of Preventive Medicine, Bloomfield, New Jersey, 1987.

54. Ali M, Juco J, Fayemi A, et al. Efficacy of ecologic-integrative management protocols for reversal of fibromyalgia, J Integrative Medicine 1999;1:48-63

55. Ali M, Ali O, Alfred et al. Efficacy of an integrative program including intravenous and intramuscular nutrient therapies for arrested growth. J Integrative Medicine 1998;2:56-69.

56. Al M. In-Vitro Allergy: Diagnosis and Management. In: Textbook Otolaryngology and Head Neck Surg, 1989, pp 320-346. Elsevier, New York.

57. Ali M. Experience with intravenous nutrient therapy for allergic patients with chronic fatigue. Am Acad Otolaryngic Allergy Abstracts, Summer 1992; p23.



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