Chemical agents and the immune response

Our plain-English summary of Chemical agents and the immune response, by M.I. Luster, G.J. Rosenthal (Environmental Health Perspectives, 1993).

The study

• Authors: M.I. Luster, G.J. Rosenthal
• Journal: Environmental Health Perspectives
• Published: 1993;100:219-26
• Type of article: Review
• Cited by: 71 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Our desire to understand the potential adverse human health effects of environmental chemical exposure has coincided with an increased understanding of the immune system and an appreciation of its complex regulatory network. This has spawned a broad interest in the area of immunotoxicology within the scientific community as well as certain concerns in the public sector regarding chemical-induced hypersensitivity and immunosuppression. The incidence of alleged human sensitization to chemicals has increased, in part, due to the fact that chemical companies are moving to larger and/or different markets. It has been estimated that 35 million Americans suffer from allergic disease, of which 2-5% are from occupational exposure. Although there is not yet a clear understanding of dose-response relationships or disease predisposition, there are many well-defined examples (isocyanates, anhydrides) of chemical sensitizers in humans and experimental animals. Evidence that chemicals suppress immune responses in humans is considerably less well established, although there is a public perception that chemicals generally cause immunosuppression. This perception has been fueled by highly publicized legal cases and scientific controversies within the academic and industrial communities. As a consequence of these public and scientific concerns, many of the regulatory agencies are developing immunotoxicity testing guidelines. At the present, however, there are limitations on adequate human methodology and data that allow the extrapolation of animal data to assess human risk. The potential for human immunosuppression remains of concern, however, because of a large database generated from animal studies that demonstrates immunosuppression as well as reports of immunosuppression in humans inadvertently (e.g., halogenated aromatic hydrocarbons) or occupationally (asbestos, benzene) exposed to xenobiotics.(ABSTRACT TRUNCATED AT 250 WORDS)

In plain English

This article was a review of immunotoxicology, the study of how chemicals can disturb the immune system. It also briefly described the authors' own laboratory work. It was not a study of asbestos-exposed people and reported no new asbestos data. The review covered immune suppression, autoimmunity, allergy, and immune effects in the skin and lung. It listed asbestos, with silica and beryllium, among particulates reported to inhibit immune function, and described reports of immune changes after asbestos exposure as among the more substantiated human reports. According to the review, asbestos-related impairment of cell-mediated immunity in humans showed up as reduced delayed hypersensitivity responses, fewer circulating T cells and reduced T-cell proliferation. By contrast, patients with asbestosis showed hyperactive T-cell responses. The authors' own work found that pentamidine reduced the release of the immune signalling molecules interleukin 1 and tumor necrosis factor from lung immune cells. The authors concluded that a number of chemical agents can harm the immune system. They also stated that evidence of chemical immune suppression in humans is considerably less well established, and that human testing methods and the extrapolation of animal data are limited.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Narrative review of immunotoxicology, with brief description of the authors' own laboratory results (mainly on the drug pentamidine)
• Who was studied: No study population of its own; the review drew on animal studies, laboratory studies and reports in humans exposed to a range of chemicals and drugs
• Exposure: Many chemical agents and drugs. Asbestos (no fiber type specified) was discussed briefly as an inhaled particulate affecting lung and systemic immunity
• Main results:
  • The review described human reports of immune changes after exposure to asbestos, along with PCBs and silica, as more substantiated than unconfirmed reports for some other compounds
  • The review stated that asbestos impairs cell-mediated immunity in humans, shown by decreases in delayed hypersensitivity responses, in the numbers of circulating T cells, and in T-cell proliferation
  • The review stated that, in contrast, patients with asbestosis show hyperactive T-cell responses, often with increased serum immunoglobulins and secretory IgA
  • In the authors' own laboratory work, pentamidine at pharmacological doses inhibited the secretion, but not the transcription, of interleukin 1 and tumor necrosis factor by alveolar macrophages
• The authors' conclusion: The authors concluded that, from rodent studies and limited human observations, a number of environmental and chemical agents can adversely affect the immune system, causing immunosuppression, hypersensitivity or autoimmune disease. They also stated that evidence of chemical immune suppression in humans is considerably less well established.
• Limitations the authors state:
  • The authors stated that human methods and data for extrapolating animal results to human risk are limited
  • The authors stated that detecting subtle immune changes in exposed people is difficult: sensitive assays are lacking, well-defined recently exposed groups are hard to identify, and immune measures vary widely in the general population
  • The authors stated that the relevance of dose levels used in some animal studies, compared with likely human exposure, is of considerable concern

Topics

Medical terms in this study, explained in our Lexicon: Occupational Exposure, Dose-response relationship.

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