Occupational exposure to ultrafine particles in police officers: no evidence for adverse respiratory effects.

BACKGROUND: Inhalation exposure to fine and ultrafine particles (UFPs) has been associated with respiratory diseases. However, little is known on the quality, threshold levels and concentration of these particles causing adverse health effects. METHODS: The impact of occupational exposure to submicrometer and UFPs was assessed in 30 healthy police shooting instructors by clinical investigation, self-assessment questionnaire, sputum and spirometry and compared to a control group. General laboratory chemistry parameters, circulating cytokines (interleukin [IL]-2, IL-4, IL-5, IL-6, IL-8, interferon-gamma [IFN-γ]), and granulocyte macrophage colony-stimulating factor (GM-CSF) in serum were measured. UFP exposure was recorded by Scanning Mobility Particle Sizer. RESULTS: Concentrations of submicrometer sized airborne particles (< 700 nm) measured between 3.34 × 105/cm3 and 7.58 × 105/cm3 at shooting sites, with highest concentrations found in the UFP range (< 100 nm). The size of the monodispersed particles ranged from 54.74 ± 16.25 nm to 98.19 ± 22.83 nm. Short term exposure (4 h) to high levels of UFPs caused an increase of IFN-γ in exposed subjects (p = 0.022). 24 h after exposure a significant decrease of IgG, albumin fibrinogen and factor VII was found. Neither directly after 4 h of high levels UFPs exposure nor 24 h after exposure subjective complaints or objective measurements indicating adverse respiratory effects in exposed subjects were found. CONCLUSIONS: No consistent indications for adverse respiratory or inflammatory effects directly following exposure and 24 h after exposure to high levels of UFPs in our study group were detected. However we showed the assessment of short-term exposure effects at a genuine occupational setting, which might is relevant when a risk assessment of high level occupational exposures to UFPs is considered.

Functional adrenergic receptor polymorphisms and idiopathic orthostatic intolerance.

OBJECTIVES: Idiopathic orthostatic intolerance (IOI) is a common disorder that is characterized by chronic orthostatic symptoms and substantial increases in heart rate and plasma norepinephrine concentrations that are disproportionately high while standing. Several features of the syndrome, including the tachycardia, tremulousness, and exaggerated norepinephrine have been considered potentially due to hypoactive or hyperactive states of adrenergic receptors of the sympathetic nervous system. The aim of this study was therefore to ascertain whether genotypes at eight polymorphic loci within five relevant adrenergic receptor genes (alpha2A, alpha2B, alpha2C, beta1 and beta2) influence the risk for IOI. METHODS: We studied 80 young men in military service (20 patients with IOI and 60 age-matched controls). All participants underwent a tilt table test including monitoring of blood pressure, heart rate and plasma catecholamines, in the supine position and during 30 min of standing. Genotyping at the eight loci (alpha2ALys251, alpha2BDel301-303, alpha2CDel322-325, beta1Gly49, beta1Arg389, beta2Arg16, beta2Glu27, beta2Ile164) was performed in all participants. Chi-square tests of independence were used to test for associations between IOI and genotype. In addition, an association of the polymorphisms with haemodynamic variables (heart rate, supine and upright blood pressure) was ascertained using one-way variance analysis. RESULTS: For the beta1Gly49 polymorphism we found a decrease in the risk of IOI among persons who were homozygous (odds ratio, 0.88; 95% confidence interval, 0.81-0.97). In addition, we found an association between beta1Gly49 and decreased heart rate in the upright position, regardless of IOI diagnosis. There were no associations with the other studied polymorphisms and IOI. CONCLUSIONS: Our current results suggest that the beta1Gly49 polymorphism is protective for IOI. This is likely one of several common genetic loci that may represent modifiers of IOI phenotypes.

Is inflammatory bowel disease an independent and disease specific risk factor for thromboembolism?

BACKGROUND: Patients with inflammatory bowel disease (IBD) are thought to be at increased risk of venous thromboembolism (TE). However, the extent of this risk is not known. Furthermore, it is not known if this risk is specific for IBD or if it is shared by other chronic inflammatory diseases or other chronic bowel diseases. AIMS: To compare the risk of TE in patients with IBD, rheumatoid arthritis, and coeliac disease with matched control subjects. PATIENTS AND METHODS: Study subjects answered a questionnaire assessing the history of TE, any cases of which had to be confirmed radiologically. A total of 618 patients with IBD, 243 with rheumatoid arthritis, 207 with coeliac disease, and 707 control subjects were consecutively included. All three patient groups were compared with control subjects matched to the respective group by age and sex. RESULTS: Thirty eight IBD patients (6.2%) had suffered TE. This was significantly higher compared with the matched control population with only 10 cases reported (1.6%) (p<0.001; odds ratio (OR) 3.6 (95% confidence interval (CI) 1.7-7.8)). Five patients with rheumatoid arthritis (2.1%) had suffered TE compared with six subjects (2.5%) in the control population matched to patients with rheumatoid arthritis (NS; OR 0.7 (95% CI 0.2-2.9)). TE had occurred in two patients with coeliac disease (1%) compared with four subjects (1.9%) in the control population matched to the coeliac disease group (NS; OR 0.4 (95% CI 0.1-2.5)). In 60% of TE cases in the IBD group, at least one IBD specific factor (active disease, stenosis, fistula, abscess) was present at the time TE occurred. CONCLUSIONS: IBD is a risk factor for TE. It seems that TE is a specific feature of IBD as neither rheumatoid arthritis, another chronic inflammatory disease, nor coeliac disease, another chronic bowel disease, had an increased risk of TE.

Long-term monitoring of sister chromatid exchanges and micronucleus frequencies in pharmacy personnel occupationally exposed to cytostatic drugs.

OBJECTIVES: Many antineoplastic drugs were found to have carcinogenic, mutagenic and teratogenic potential. The aim of this study was to carry out cytogenetic and internal dose monitoring of hospital pharmacy personnel regularly involved in the preparation of cytostatic agents, in order to test possible cytostatics-induced genotoxic effects due to occupational exposure under routine working conditions, and in cases of accidental contamination. METHODS: Platinum in whole blood and anthracyclines in plasma were measured to assess internal exposure to cytostatics. The level of cytogenetic damage was determined in peripheral blood lymphocytes with the micronucleus test and the sister chromatid exchange assay. Five series of monitoring were performed over a period of 2 years. RESULTS: No significant differences in the mean frequencies of sister chromatid exchanges (SCE) and micronuclei (MN) were found between occupationally exposed probands and controls (9.9 +/- 1.4 vs 10.1 +/- 1.2 SCEs/cell and 21.2 +/- 7.2 vs 23.3 +/- 7.5 MN/2000 binucleated (BN) cells, n = 16). Significant elevations of SCE or MN were detected in seven out of 12 cases of accidental contamination at the workplace, whereas no increase in platinum in blood and anthracyclines in plasma was observed in these probands. Two cases of non-reported contamination were identified by measurement of epirubicin in plasma. Smoking was found to increase the SCE significantly. No correlation between individual SCE scores and MN scores was observed. CONCLUSIONS: Our findings support a transient increase in SCE or MN after relevant exposure to cytostatic drugs in cases of accidental contamination. The lack of significant differences in SCE and MN between hospital pharmacy personnel and unexposed controls, points to high standards of safety at the corresponding workplaces.

[Pseudostenocardia due to exposure to "electrosmog"]. / Pseudostenokardie bei Belastung durch "Elektrosmog".

HISTORY AND REASON FOR ADMISSION: A 44-year-old man had anginal-like complaints. He was convinced that cardiac problems had been caused by electromagnetic fields. INVESTIGATIONS: Apart from hypertension and hyperlipidaemia there were no other significant findings. ECG, ergometry Holter-ECG were normal. EXPERIMENT: We tried to verify with a double-blind provocation test if the patient's complaints had been caused by electromagnetic fields. The patient was exposed to an electric instrument without being aware whether it was switched on or off. He was questioned about his perception of the presence of an electric current. CONCLUSION: The results of the test showed that there was no causal relation between the patient's angina-like-symptoms and electromagnetic fields. The phenomenon of electrosensitivity was probably caused by psychological mechanisms.

Olestra increases faecal excretion of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Two patients with chloracne had concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) of 144,000 and 26,000 pg/g blood lipids. Olestra, a non-digestible, lipophilic dietary fat substitute accelerated the patients' intestinal excretion of TCDD by eight to ten fold. This is sufficient to reduce the normally observed elimination half life of TCDD from about 7 years to 1-2 years.

Pulmonary function and symptoms of welders.

OBJECTIVE: As the findings on changes in pulmonary function of welders have been inconsistent, this study aimed to analyze respiratory symptoms and pulmonary function among welders and controls with particular emphasis on small airways dysfunction. METHODS: Cross-sectional analysis, using spirometry and a standardized questionnaire, was used to evaluate 521 participants, 166 of whom (64 welders and 102 controls) were evaluated for pulmonary symptoms, occupational inhalative exposures, leisure time activities, and anamnestic data. RESULTS: The welders reported more pulmonary symptoms than the controls. They exhibited a decreased mean expiratory flow (MEF) at 25% and 50% of vital capacity (MEF25, MEF50) while the other parameters tested (forced vital capacity, forced expiratory volume in 1 s) were unchanged compared with the controls. Multivariate regression analysis revealed that smoking explained the observed variance; only in MEF25 the duration of welding exposure had a significant influence on this parameter. CONCLUSIONS: The significantly reduced flow values among the welders compared with the controls indicates the presence of small airways disease. Differences in smoking habits accounted for more than double the differences in MEF25 than did chronic welding fume exposure, confirming the role of the former as the main risk factor leading to the decline in lung function. Longitudinal studies are needed to evaluate the long-term effects of chronic welding fume exposure, in particular with a view to identifying especially susceptible workers.

Acquired dyschromatopsia in combined exposure to solvents and alcohol.

HYPOTHESIS: Does occupational exposure to solvents in combination with alcohol intake give rise to acquired color vision defects? METHOD: A total of 138 individuals exposed to solvents (toluene, xylene, trichloroethylene, tetrachloroethylene) were examined using Lanthony's D-15 test and compared with 100 nonexposed controls. The extent of color vision loss was quantitatively assessed based on Bowman's color confusion index (CCI). A cumulative exposure index was calculated from the hours of exposure per day and the years of exposure. In 30 persons who were exposed to trichloroethylene and tetrachloroethylene, urinary trichloroacetic acid was assessed as a parameter of exposure. Alcohol intake was calculated as based on interviews of patients in grams of ethyl alcohol per week. RESULTS: Individuals who consumed more than 250 g alcohol/week and were simultaneously exposed to solvents showed a significantly elevated CCI (P = 0.0044). No significant correlation emerged between trichloroacetic acid excretion in the urine or the cumulative exposure index and the CCI. CONCLUSION: The combination of alcohol intake and occupational exposure to solvents discloses the risk of acquired subclinical color vision defects.