In Vitro Responsiveness of Lymphocytes to Phytohemmagglutinin

Abstract

Peripheral blood lymphocytes from 20 human subjects exposed to 784 microgram/m3 ozone for 4 hours, and from 11 subjects exposed to clean air for the same length of time were studied for in vitro responsiveness to phytohemagglutinin (PHA). Thymus-derived (T) lymphocyte response to PHA (normal response is proliferation of lymphocytes) was significantly suppressed (P less than .01) in samples obtained immediately after subjects' exposure to ozone. Recovery of response occurred 2 weeks postexposure. Responses were unchanged in subjects exposed to clean air. Existing studies suggest that ozone exposure may generate free radicals or other reactive molecules or both, that could be responsible for immediate changes in metabolic events leading to blockage or inhibition of deoxyribonucleic acid (DNA) synthesis in T lymphocytes as shown in this study. It is possible that some prerequisite to active cell metabolism such as ribonucleic acid (RNA) may be impaired by ozone exposure. The significance of the suppression of T-cell response noted in this study is that: (1) if continuous exposures to ozone are shown to induce an immunosuppressed state for a significant time period, an important factor in carcinogenesis might be elucidated; (2) immunosuppression may cause a progression of an already present tumor; (3) immunosuppression may enable endogenous latent infections such as tuberculosis to reactivate; and (4) immunosuppression may explain in part the relationship between chronic oxidant air pollution and influenza-like illnesses in population.

Ozone Exposure Impairs Antigen-Specific Immunity but Activates IL-7-Induced Proliferation of CD4−CD8−Thymocytes in Balb/cMice

“…It is generally accepted that O 3 exposure markedly decreases thymus weight index and thymocyte proliferation in response to mitogens (Peterson et al, 1978;Fujimaki et al, 1984;Dziedzic & White, 1986;Feng et al, 2001). However, no report was found so far concerning the effect of O 3 exposure on the composition or development of thymocytes in an animal exposure model.…”

Chemical nature and immunotoxicological properties of arachidonic acid degradation products formed by exposure to ozone.

“…After exposure, solutions were removed from the exposure chambers and used in cell bioassays or analyzed for hydroperoxides and/or carbonyl compounds. In studies designed to examine the reactivity of 03-exposed AA with GSH, solutions of 03-exposed AA (900 p1) were incubated (60 min, 370C) with GSH (100 pl in PBS with pH adjusted to 7.4; final GSH concentrations of 1-100 mM) or 10 mM GSH with GSH peroxidase (5 U/ml). In some experiments, we incubated solutions (60 min, 370C) with catalase (120 U/ml) and SOD (107 U/ml) and/or ethanol (1 mM) to scavenge H202, 02-, and hydroxyl radical, respectively, before adding the solutions to bioassays.…”

Acute, Subchronic, and Chronic Exposure to a Simulated Urban Profile of Ozone: Effects on Extrapulmonary Natural Killer Cell Activity and Lymphocyte Mitogenic Responses

“…0, also affects lymphocyte function in both the lung (Burleson et al, 1989) and mediastinal lymph nodes (Dziedzic and White, 1986). In addition to these effects on pulmonary immune responses, 0, has been shown to sup ress the response of human peripheral blood leukocytes (PBL) to T-cel P mitogens following both in vivo and in vitro exposure (Peterson et al, 1978b(Peterson et al, , 1981; Orlando et al, 1988; Becker et al, 1989) and to suppress phagocytic and bactericidal activity of polymorphonuclear leukocytes (Peterson et al, 1978a) and B-cell rosette formation (Savino et al, 1978) in PBL from 0,-exposed volunteers. In mice the response of spleen cells to T-cell mitogens was also suppressed (Aranyi et al, 1983) following 0, exposure, as were the antibody and delayed-type hypersensitivity responses to sheep red blood cells (Fujimaki et al, 1984(Fujimaki et al, , 1987.…”