Lymphocyte subpopulations in workers exposed occupationally to styrene

Mutti, A.; Buzio, C.; Perazzoli, F.; Bergamaschi, E.; Bocchi, M.C.; Selis, L.; Mineo, F.; Franchini, I.

La Medicina del Lavoro 83(2): 167-177

1992


ISSN/ISBN: 0025-7818
PMID: 1630405
Accession: 040613740

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Abstract
In a group of 32 workers occupationally exposed to styrene, the distribution of lymphocyte subsets was investigated by automated flow cytometry. The group under study consisted of 22 male and 10 female workers aged 39.7, D.S. = 10 years and employed for 6.8 years in factories manufacturing glass fibre-reinforced plastics. A control group (12 males and 7 females) recruited according to the same selection criteria was simultaneously examined. Environmental and biological monitoring was used to characterize styrene exposure. In styrene-exposed workers, phenotypic analysis of peripheral blood revealed a reduced proportion of T helper lymphocytes and a relative increase in the T suppressor subset, leading to a significant inversion of the helper/suppressor ratio (0.92) among heavily exposed workers (greater than 50 ppm, 8h-TWA) as compared to less exposed workers and controls (1.37 and 1.43 respectively). The proportion of natural killer (NK) T lymphocytes was significantly increased among styrene workers. The proportion of B lymphocytes was unchanged as compared to the control group. Dose-response relationships were clearly apparent for the observed increases in the prevalence of abnormalities: none of control subjects showed more than 2 (out of 8) abnormal values as compared to 20 and 40% of styrene workers belonging respectively to the low and high exposure group (p less than 0.007). Only a minority of controls exhibited abnormally high levels of both NK and suppressor T lymphocytes (0-5%), the corresponding figures for styrene workers being 7-10% (low exposure) and 45% (high exposure). As a whole, the findings support the hypothesis of the immunotoxicity of styrene, which could be due either to direct effects on lymphocytes or to indirect mechanisms possibly mediated by neuroendocrine changes.