Antibodies to morphine in workers exposed to opiates at a narcotics manufacturing facility and evidence for similar antibodies in heroin abusers

Biagini, Raymond E.; Klincewicz, Stephen L.; Henningsen, Gerry M.; MacKenzie, Barbara A.; Gallagher, J.S.; Bernstein, David I.; Bernstein, I. Leonard

doi:10.1016/0024-3205(90)90604-p

Cited by 39 publications

(14 citation statements)

References 33 publications

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“…As with isocyanate-induced asthma, specific antibodies against plicatic acid and against morphine have been found, respectively, in symptomatic and asymptomatic workers exposed to red cedar or to morphine [44,55].…”

Section: Immunological Mechanismmentioning

confidence: 99%

Mechanisms and pathology of occupational asthma

Mapp

Saetta²,

Maestrelli³

et al. 1994

Eur Respir J

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M Me ec ch ha an ni is sm ms s a an nd d p pa at th ho ol lo og gy y o of f o oc cc cu up pa at ti io on na al l a as st th hm ma a More than one mechanism may be operative in occupational asthma. Among the mechanisms proposed, immunological mechanisms and airway inflammation play an important role. There is evidence to confirm that T-lymphocyte activation and local accumulation in the bronchial wall of activated eosinophils occurs in asthma of diverse aetiology, i.e. immunoglobulin E (IgE)-mediated, occupational and intrinsic.Neurogenic pathways should be further investigated as a potential mechanism of modulation and amplification of airway inflammation in occupational asthma.

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Section: Immunological Mechanismmentioning

confidence: 99%

Mechanisms and pathology of occupational asthma

Mapp

Saetta²,

Maestrelli³

et al. 1994

Eur Respir J

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show abstract

“…These antibodies are also present in some subjects with no history of asthma and a negative inhalation challenge. As in isocyanateinduced asthma (32), specific antibodies against plicatic acid and against morphine have been found, respectively, in symptomatic and asymptomatic workers exposed to red cedar or to morphine (33,36). Under certain circumstances (exposure to high-molecular-weight compounds and to certain low-molecular-weight compounds), the presence of specific IgE or IgG is useful in the diagnosis of occupational asthma, whereas in others, their presence is a biological marker of exposure and must be associated with pulmonary function tests to detect the clinical onset of the disease.…”

Section: Antibody-mediated Hypersensitivitymentioning

confidence: 97%

Human Leukocyte Antigen Associations in Occupational Asthma Induced by Isocyanates

Mapp

Balboni

Baricordi

et al. 1997

Am J Respir Crit Care Med

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Exposure to diisocyanates is recognized as a leading cause of occupational asthma. Occupational asthma induced by isocyanates shares many characteristics with immunoglobulin E (IgE)-mediated asthma: in both, the responsible agent is known, and the clinical presentation, response to inhalation challenge in the laboratory, and response to antiasthma drugs are similar. Although asthma mediated by an IgE mechanism occurs in atopic subjects, occupational asthma induced by isocyanates occurs mostly in nonatopic asthmatics, and an IgE-mediated mechanism has not been consistently demonstrated. However, activated T lymphocytes, methacromatic cells, and eosinophils are increased in the bronchial mucosa of allergic and nonallergic asthmatics and subjects with occupational asthma induced by isocyanates, suggesting similar, probably immunologically mediated mechanisms for both nonoccupational and occupational asthma. Occupational asthma occurs in up to 5-10% of the exposed subjects. Evaluation of major histocompatibility complex (MHC) class II genes in exposed subjects who develop toluene diisocyanate (TDI) asthma has shown a negative association with HLA-DQB1*0501 and a positive association with HLA-DQB1*0503 alleles. In addition, a high proportion of TDI asthmatics express the HLA-DQB1*0503-associated aspartic acid at residue 57, suggesting that HLA-DQ may have a key role in conferring susceptibility. Thus, asthma induced by the low-molecular-weight agent TDI may result from an immunologic reaction due to the interaction of genetic susceptibility with exposure in the workplace.

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“…We assayed OPA-specific IgE and IgG antibodies in triplicate by indirect enzyme-linked immunosorbent assay detection of the immunocomplexes with a labeled immunoglobulin as previously described [Biagini et al 1990;Biagini et al 1996;Crowther 2001]. We assayed specific IgE and IgG at 1:10 and 1:100 dilutions of test sera.…”

Section: Ortho-phthalaldehyde-specific Antibody Testingmentioning

confidence: 99%

“…We performed competitive inhibition assays [Biagini et al 1990;Christopoulos and Diamandis 1996] for all sera exhibiting positive binding to OPA-HSA antigen with an optical density of at least 0.2. We mixed aliquots of test sera, diluted 1:5, with equal volumes of blocking buffer (antibody control), 1, 10, 100, or 1000 micrograms per milliliter of OPA-HSA conjugate, and also 1, 10, 100, 1000 micrograms per milliliter of mock-conjugated HSA, and incubated them overnight on a rotary shaker at room temperature.…”

mentioning

confidence: 99%

Evaluation of ortho-phthalaldehyde in eight healthcare facilities.

2015

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Antibodies to morphine in workers exposed to opiates at a narcotics manufacturing facility and evidence for similar antibodies in heroin abusers

Cited by 39 publications

References 33 publications

Mechanisms and pathology of occupational asthma

Mechanisms and pathology of occupational asthma

Human Leukocyte Antigen Associations in Occupational Asthma Induced by Isocyanates

Evaluation of ortho-phthalaldehyde in eight healthcare facilities.

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