Environmental illness: fatigue and cholinesterase activity in patients reporting hypersensitivity to electricity.

The lack of a pathophysiological marker hinders studies on environmental illnesses of unknown origin. Hence, research focused on the identification of such a marker is a priority. This study investigated the nature and a possible etiology of fatigue in hypersensitivity to electricity (the most commonly reported environmental illness in Sweden). The aim was to test the hypothesis that perceived fatigue was due to alterations in cholinesterase activity. The study group consisted of 14 people who reported a hypersensitivity to electricity, including disabling fatigue. We assessed cholinesterase activity three times: twice based on current symptoms reported by the subjects (severe fatigue attributed to electromagnetic fields and absence of this symptom) and once at a randomly selected time. No significant reduction in acetylcholinesterase was identified in any subject. Examined on a group level, no significant reduction in activity was identified at the time of severe fatigue, and no correlation between reported degree of fatigue and cholinesterase activity was observed. Fatigue attributed to electromagnetic fields was nonphysical and showed a significant correlation to difficulties in concentrating. The results do not support the hypothesis that a change in cholinesterase activity mediates fatigue in people reporting hypersensitivity to electricity.

DNA adducts in human nasal mucosa and white blood cells from smokers and non-smokers.

The goal of the present study was to measure the levels of DNA adducts in human nasal mucosa cells and in total white blood cells in relation to smoking. DNA was isolated from samples of 20 healthy volunteers (six smokers and 14 non-smokers). The levels of DNA adducts were measured by 32P-postlabelling assay. In smokers the mean DNA adduct levels were 3.3 and 17.0 adducts/10(8) nucleotides in total white blood cells and nasal mucosa cells respectively. The corresponding values in non-smokers were 2.0 and 6.8 adducts/10(8) nucleotides. The mean adduct level was significantly higher in nasal mucosa cells than in total white blood cells both in smokers and non-smokers. The mean adduct levels in smokers' nasal mucosa cells were significantly higher than those in non-smokers. Thus the nasal mucosa cells constituted a sensitive tissue for the determination of cigarette smoking induced DNA adducts. Combining the sensitivity of the 32P-postlabelling assay with the specificity of the nasal mucosa to the airborne chemical exposures, the DNA adduct analysis from human nasal mucosa cells represents a method of choice in the assessment of exposure to airborne carcinogens.

DNA adduct formation in the human nasal mucosa as a biomarker of exposure to environmental mutagens and carcinogens.

Human exposure to chemical compounds, often termed xenobiotics, has been linked to a number of enhanced incidences of various neoplasias. A majority of these enter the human body through inhalation. Most xenobiotics are metabolized in the body to more hydrophilic metabolites before excretion in the urine and bile. During this process, promutagens and procarcinogens could be activated and could interact with proteins as well as DNA to form adducts. DNA adducts formed by chemical carcinogens can, therefore, be used as biomarkers of exposure and other host factors. This study that DNA adduct analysis can be performed on cells from human nasal mucosa. Using the nasal lavage procedure performed on 20 healthy volunteers, 5 x 10(5) to 5 x 10(6) cells were obtained from which 5 to 40 micrograms DNA was isolated. DNA adducts were analyzed by the 32-P-postlabeling assay. The DNA adduct levels ranged between 1.4 and 6 adducts/10(8) nucleotides. In addition to its simplicity, the nasal lavage procedure is an inexpensive, noninvasive procedure that requires no anesthetics or special equipment. Moreover, the cells obtained are the first to come in contact with air pollutants. DNA adduct analysis from human nose mucosa cells could therefore be used to develop a technique suitable for the assessment of exposure to chemical carcinogens through inhalation.