Cognitive symptoms and welding fume exposure.

BACKGROUND: Prevalence of moderate to severe cognitive symptoms is markedly higher in UK professional divers who have also worked as a welder (28%) than in either divers who have not welded (18%) or offshore workers who have worked neither as a diver nor as a welder (6%). OBJECTIVES: To determine whether cognitive symptoms are related to welding fume exposure or diving. METHODS: Three age-matched groups of male workers were studied using postal questionnaire: professional divers who had worked as a welder (PDW, n = 361), professional welders who had not dived (NDW, n = 352), and offshore oil field workers who had neither dived nor welded (NDNW, n =503). Health-related quality of life was assessed by the Short Form 12 questionnaire (SF12). Cognitive symptomatology was assessed using the Cognitive Failures Questionnaire (CFQ). A single variable for welding fume exposure (mg m(-3) days) was calculated, incorporating welding experience in different environments and using different welding techniques and respiratory protective equipment. The level of fume exposure during hyperbaric welding operations was measured during such work as ambient PM(10) (particles of 10 µm or less). Diving exposure was assessed as the number of dives performed plus the number of days spent working during saturation diving. RESULTS: Questionnaires were returned by 153 PDW, 108 NDW, and 252 NDNW. SF12 scores were the same in all groups and fell within normative values. Mean (95% CI) CFQ scores were higher in PDW [40.3 (37.7-42.9)] than in both NDW [34.6 (31.6-37.7)] and NDNW [32.1 (30.4-33.9)], but the scores in no groups fell outside the normative range. The mean PM(10) exposure during hyperbaric welding operations was 2.58 mg m(-3). The geometric mean mg m(-3) days (95% CI) for welding fume exposure in NDW [33 128 (24 625-44 567) n = 85] was higher than for that in PDW [10 904 (8103-14 673) n = 112]. For PDW the geometric mean (95% CI) diving exposure was 1491 [(1192-1866) n = 94] dives and days in saturation. In the general linear model regression analyses adjusted for age, alcohol consumption, and somatization, there was no signification association of CFQ score with either welding fume exposure (F = 0.072, P = 0.79, n = 152) or diving exposure (F = 0.042, P = 0.84, n = 74). CONCLUSIONS: In conclusion, cognitive sympomatology was not related to retrospectively assessed measures of welding fume exposure or diving experience. In addition, the levels of cognitive symptomatology, even in PDW, did not exceed normative values.

Regulation of T-lymphocyte CCL3 and CCL4 production by retinal pigment epithelial cells.

PURPOSE: Retinal pigment epithelial (RPE) cells have an important role in the immune suppression associated with the immune privilege of the eye. Some aspects of this remain unclear and this study aimed to determine how RPE cells could influence the production of chemokines by T lymphocytes. METHODS: T lymphocytes, separated from peripheral blood of normal volunteers, and RPE cells, cultured from donor eyes, were cultured separately and together, either in contact or in transwells. Supernatants were analyzed for CCL3, CCL4, and soluble CD54 (sCD54) by ELISA. Blocking agents were used to determine which soluble mediators were involved. RESULTS: Coculture of RPE cells with activated lymphocytes resulted in a reduction in CCL3 and CCL4 production by lymphocytes, primarily by soluble mediators. Soluble CD54 was markedly increased on coculture of lymphocytes with RPE cells. Soluble CD54 reduced CCL3 and CCL4 production by RPE cells, and inhibition of CCL3 and CCL4 on coculture with RPE cells was reduced by anti-CD54. Blocking prostaglandin E2 (PGE2) abrogated the inhibition of CCL4, but not CCL3, by RPE cells. Blocking TGFß and nitric oxide production had no effect. CONCLUSIONS: RPE cells are able to down-regulate high levels of CCL3 and CCL4 production by T lymphocytes by using the soluble mediators sCD54 and PGE2. Reducing this production of CCL3 and CCL4 will dampen down the cascade effect and recruitment of more inflammatory cells, protecting the retina from an excessive immune response.