Assessment of physical, environmental, and cardiac strain in 43 operators (wearing protective equipment) conducting clean-up of heavy oil products

Background. The aim of the study was to organise an assessment of the physical strains and environmental exposure to hydrocarbon derivatives in persons involved in shoreline clean-up of heavy oil products, in order to investigate the dangers of oil spill clean-up. Material and methods. Forty-three healthy volunteers wearing protective equipment cleaning up an artificial shoreline underwent cardiac strain measurements, as well as a study of thermal stress (approximate WBGT index, water loss, measurement of internal body temperature before and after physical activity). A subjective assessment of perceived exertion was correlated to articular strain indicators recorded for the weight of loads lifted, movement frequency, and the range of movement. Environmental exposure was determined by using portable hydrocarbon detectors. Results. For adult subjects in good physical condition, in neutral temperatures, oil spill clean-up is considered non-arduous. However, in sedentary, stressed subjects exposed to difficult climatic conditions, cleanup can be considered hard to extremely hard. In terms of environmental exposure, slight traces of toluene appeared once out of a total of 18 analysed samples. Conclusions. The sample studied was subject to physical articular strains and presented variable cardiac strain; environmental exposure was, on the other hand, slight when involving cleaning up heavy petroleum products. The subjects liable to carry out this activity are more tolerant to the efforts required when they are healthy, fit, young adults, in the non-arduous thermal conditions recorded in this study

HDAC Inhibitors Act with 5-aza-2′-Deoxycytidine to Inhibit Cell Proliferation by Suppressing Removal of Incorporated Abases in Lung Cancer Cells

5-aza-2′-deoxycytidine (5-aza-CdR) is used extensively as a demethylating agent and acts in concert with histone deacetylase inhibitors (HDACI) to induce apoptosis or inhibition of cell proliferation in human cancer cells. Whether the action of 5-aza-CdR in this synergistic effect results from demethylation by this agent is not yet clear. In this study we found that inhibition of cell proliferation was not observed when cells with knockdown of DNA methyltransferase 1 (DNMT1), or double knock down of DNMT1-DNMT3A or DNMT1-DNMT3B were treated with HDACI, implying that the demethylating function of 5-aza-CdR may be not involved in this synergistic effect. Further study showed that there was a causal relationship between 5-aza-CdR induced DNA damage and the amount of [3H]-5-aza-CdR incorporated in DNA. However, incorporated [3H]-5-aza-CdR gradually decreased when cells were incubated in [3H]-5-aza-CdR free medium, indicating that 5-aza-CdR, which is an abnormal base, may be excluded by the cell repair system. It was of interest that HDACI significantly postponed the removal of the incorporated [3H]-5-aza-CdR from DNA. Moreover, HDAC inhibitor showed selective synergy with nucleoside analog-induced DNA damage to inhibit cell proliferation, but showed no such effect with other DNA damage stresses such as γ-ray and UV, etoposide or cisplatin. This study demonstrates that HDACI synergistically inhibits cell proliferation with nucleoside analogs by suppressing removal of incorporated harmful nucleotide analogs from DNA