Proposal on limits for chemical exposure in saturation divers' working atmosphere: the case of benzene.

Saturation diving is performed under extreme environmental conditions. The divers are confined to a limited space for several weeks under high environmental pressure and elevated oxygen partial pressure. At present, divers are protected against chemical exposure by standard exposure limits only adjusted for the increased exposure length, i.e. from 8 to 24 hours a day and from 5 to 7 days a week. The objective of the present study was to indicate a procedure for derivation of occupational exposure limits for saturation diving, termed hyperbaric exposure limits (HEL). Using benzene as an example, a procedure is described that includes identification of the latest key documents, extensive literature search with defined exclusion criteria for the literature retrieved. Hematotoxicity and leukemia were defined as the critical effects, and exposure limits based upon concentration and cumulative exposure data and corresponding risks of leukemia were calculated. Possible interactions of high pressure, elevated pO2, and continuous exposure have been assessed, and incorporated in a final suggestion of a HEL for benzene. The procedure should be applicable for other relevant chemicals in the divers' breathing atmosphere. It is emphasized that the lack of interactions from pressure and oxygen indicated for benzene may be completely different for other chemicals.

Simulated diving after heat stress potentiates the induction of heat shock protein 70 and elevates glutathione in human endothelial cells.

Heat stress prior to diving has been shown to confer protection against endothelial damage due to decompression sickness. Several lines of evidence indicate a relation between such protection and the heat shock protein (HSP)70 and HSP90 and the major cellular red-ox determinant, glutathione (GSH). The present study has used human endothelial cells as a model system to investigate how heat stress and simulated diving affect these central cellular defense molecules. The results demonstrated for the first time that a simulated dive at 2.6 MPa (26 bar) had a potentiating effect on the heat-induced expression of HSP70, increasing the HSP70 concentration on average 54 times above control level. In contrast, a simulated dive had no significant potentiating effect on the HSP90 level, which might be due to the higher baseline level of HSP90. Both 2 and 24-h dive had similar effects on the HSP70 and HSP90, suggesting that the observed effects were independent of duration of the dive. The rapid HSP response following a 2-h dive with a decompression time of 5 min might suggest that the effects were due to compression or pressure per se rather than decompression and may involve posttranslational processing of HSP. The exposure order seemed to be critical for the HSP70 response supporting the suggestion that the potentiating effect of dive was not due to de novo synthesis of HSP70. Neither heat shock nor a simulated dive had any significant effect on the intracellular GSH level while a heat shock and a subsequent dive increased the total GSH level approximately 62%. Neither of these conditions seemed to have any effect on the GSH red-ox status.

Anti-C5a monoclonal antibodies and pulmonary polymorphonuclear leukocyte infiltration--endothelial dysfunction by venous gas embolism.

Venous gas embolism (VGE) impairs endothelial function although there is no apparent mechanical damage to the endothelial layer. We investigated whether a monoclonal antibody against the complement anaphylatoxine C5a would affect endothelial dysfunction and pulmonary polymorphonuclear leukocyte infiltration caused by low-grade VGE. Six rabbits were pre-treated with the anti-C5a monoclonal antibody whereas a sham monoclonal antibody was administrated to six other animals 30 min before VGE. Six untreated rabbits subjected to an identical protocol except antibody treatment were used for control. The monoclonal anti-C5a antibody reduced PMN infiltration compared to the control group ( P<0.03). There were no major signs of apoptosis in endothelial cells inside the pulmonary artery in any of the examined animals. There was reduced PMN infiltration and improved endothelium-dependent relaxation in the sham-antibody group, these effects were however not significant. In conclusion, anti-C5a protects the endothelium against injury caused by small amounts of gas bubbles.

Small amounts of venous gas embolism cause delayed impairment of endothelial function and increase polymorphonuclear neutrophil infiltration.

Gas bubbles from decompression and gas embolization lead to endothelial dysfunction and mechanical injury in the pig, rabbit and lamb. In the study presented here, 0.01 ml air/min/kg was infused through a catheter into the jugular vein in 12 rabbits for 60 min. The endothelial response was measured using tension measurements in the blood vessel wall, and morphological changes where quantified using light microscopy and image processing. Percent lung water content was calculated and used to estimate the severity of pulmonary oedema. The infusion led to a significant decrease in the acetylcholine-mediated endothelial-dependent vasodilatation in the pulmonary artery 6 h after the infusion (6-h group, n = 6). A decrease in substance-P-mediated endothelial-dependent vasodilatation was also detected. No changes where seen in a group of rabbits examined 1 h after infusion (l-h group, n=6). The impaired endothelial-dependent vasodilatation caused by the bubbles is probably biochemical in origin, since no visible changes were seen in the endothelial layer. A significant increase in polymorphonuclear neutrophils was observed in the 6-h group compared to the l-h group. This study demonstrates that small numbers of bubbles, corresponding to "silent bubbles", lead to an impairment of the endothelial-dependent vasoactive response.