Measurement and reduction of occupational exposure to inhaled anaesthetics.

The occupational exposure of hospital staff to inhaled anaesthetics was investigated using a personal sampling device that provides a measure of the average concentrations breathed by a person over a period of time, as distinct from the spot sampling in the general environment. The anaesthetist''s average exposure to nitrous oxide and halothane during complete operating sessions was twice that expected from simple dilution of the escaping gases by the operating room ventilation. The sampling technique was also used to evaluate the effect of (1) redirection of the waste gas outflow; (2) active scavenging connected to the piped vacuum system. Short-period studies under controlled conditions in the operating theatres and anaesthesia induction rooms showed that the anaesthetist''s exposure could be reduced two- or fourfold by redirecting the outflow and another four- to sixfold by active scavenging. Exposures during complete operating sessions were reduced two- to seven-fold by scavenging.     

The mutagenicity of electrocautery smoke.

Careful analysis of electrocautery smoke produced during breast surgery has found organic compounds that are unidentifiable with current analytical techniques. The purpose of this study was to determine the potential mutagenicity of the smoke produced by the electrocautery knife during reduction mammaplasty. Multiple air samples were collected in the operating room during two reduction mammaplasty procedures. Airborne smoke particles were tested for mutagenic potential in both tester strains of Salmonella typhimurium (TA98 and TA100) using the standard Salmonella microsomal test (Ames test). All testing was performed by the Hazard Evaluations and Technical Assistance Branch of the National Institute of Occupational Safety and Health. The smoke produced with the electrocautery knife during reduction mammaplasty was found to be mutagenic to the TA98 strain. The Ames test, an established technique for evaluating the mutagenicity of a substance, was convincingly positive for the smoke collected during the breast surgery. Whether the smoke represents a serious health risk to operating room personnel is not known. Development of techniques to limit electrocautery smoke exposure in the operating room appears to be needed, and surgeons should attempt to minimize their exposure.     

A Review of the Epidemiology of Trichloroethylene and Kidney Cancer

The occupational epidemiological studies of trichloroethylene (TCE) exposure and kidney cancer are reviewed. Seven occupational cohort studies, conducted in the U.S., Finland, and Sweden involving over 130,000 workers, do not report statistically increased risks of kidney cancer among TCE-exposed workers. These studies were based on well-defined cohorts and exposure assessments involving urine biomonitoring or some type of job exposure matrix. In contrast, two German studies reported eight- to eleven-fold increased risks for renal cancer among TCE-exposed workers. However, numerous methodological and analytical shortcomings severely limit any interpretation of the German studies. We conclude that the more reliable epidemiologic data do not support a causal relationship between kidney cancer and TCE exposure.     

Exposure to anesthetic gases and Parkinson’s disease: a case report

Background

The administration of anesthetics determines depression of the central nervous system and general anesthesia by inhalation may cause an environmental pollution of the operating rooms. It may therefore conceive a possible occupational etiology of Parkinson's Disease (PD).

Case presentation

In a Caucasian male aged 59 years, PD was diagnosed by brain scans with a presynaptic radioactive tracer of the dopaminergic system. Family history was negative for Parkinson’s disease or essential tremor. He was a smoker, a moderate consumer of coffee and alcohol, and never exposed to pesticides/metals. For 30 years (since the age of 29 until today), he worked as an anesthesiologist in private clinics in the Veneto (Northern Italy), exposed to anesthetic gases. The time elapsed from first exposure to onset of disease is 22 years, fulfilling the requirement of the induction/latency period. A literature search demonstrated unacceptable levels of anesthetic gases in public hospitals of the Veneto region from 1990 to 1999. This exposure was presumably high also in private hospitals of the region until at least 2007, when an overexposure to sevoflurane was repeatedly measured in this patient. The association between occupational exposure to anesthetic gases and risk of Parkinson’s disease was supported by a case-control study (reporting a two-fold increase in the risk of PD associated with a clinical history of general anesthesia) and a cohort study comparing mortality from PD between US anesthesiologists and internists (showing a statistically significant excess (p=0.01) in anesthesiologists compared to internists). Numerous recent mechanistic studies (in vitro essays and in vivo short-term studies) strengthened the association between exposure to anesthetic gases (nitrous oxide, halothane, isoflurane, levoflurane) and PD.

Conclusion

In view of the limited evidence of human studies and the sufficient evidence of experimental studies, the high exposure to anesthetic gases could have induced PD in the subject under study.

     

Unusual Non-Occupational Exposure to Metals

Exposure to metals at workplaces is well known and in many cases occupational studies led to an adoption of limit values. For airborne concentrations of substances as metals refer to the “Maximaleo Arbeitsplatz-Konzentration” (MAK) in Germany or the “Threshold Limit Value” (TLV) in USA. Biological monitoring consists of an assessment of overall exposure to chemicals at the workplace and in the environment. The “Biologischer Arbeitsstoff Toleranzwert” (BAT) in Germany and the “Biological Exposure Index” in the USA serve as reference values. Besides these occupational limit values, reference values exist in Germany for the background exposure of the non occupationally exposed general population. In some cases the reference values are exceeded without any occupational exposure. Several cases of unusual environmental exposure to cobalt, mercury and manganese are reported. In such cases, it is often difficult to evaluate the measured concentration. In Germany, therefore, the “Human-Biomonitoring-Werte” (HBMValues) have been adopted in order to evaluate such high background exposures. The HBM-concept is presented. Environmental exposure to metals is usual within some limits. Reference values are helpful for an assessment. Unusual exposure occurs and the physician should be alert to symptoms of poisoning.     

Sub-chronic inhalation of high concentrations of manganese sulfate induces lower airway pathology in rhesus monkeys

Background

Neurotoxicity and pulmonary dysfunction are well-recognized problems associated with prolonged human exposure to high concentrations of airborne manganese. Surprisingly, histological characterization of pulmonary responses induced by manganese remains incomplete. The primary objective of this study was to characterize histologic changes in the monkey respiratory tract following manganese inhalation.

Methods

Subchronic (6 hr/day, 5 days/week) inhalation exposure of young male rhesus monkeys to manganese sulfate was performed. One cohort of monkeys (n = 4–6 animals/exposure concentration) was exposed to air or manganese sulfate at 0.06, 0.3, or 1.5 mg Mn/m³ for 65 exposure days. Another eight monkeys were exposed to manganese sulfate at 1.5 mg Mn/m³ for 65 exposure days and held for 45 or 90 days before evaluation. A second cohort (n = 4 monkeys per time point) was exposed to manganese sulfate at 1.5 mg Mn/m³ and evaluated after 15 or 33 exposure days. Evaluations included measurement of lung manganese concentrations and evaluation of respiratory histologic changes. Tissue manganese concentrations were compared for the exposure and control groups by tests for homogeneity of variance, analysis of variance, followed by Dunnett''s multiple comparison. Histopathological findings were evaluated using a Pearson''s Chi-Square test.

Results

Animals exposed to manganese sulfate at ≥0.3 mg Mn/m³ for 65 days had increased lung manganese concentrations. Exposure to manganese sulfate at 1.5 mg Mn/m³ for ≥15 exposure days resulted in increased lung manganese concentrations, mild subacute bronchiolitis, alveolar duct inflammation, and proliferation of bronchus-associated lymphoid tissue. Bronchiolitis and alveolar duct inflammatory changes were absent 45 days post-exposure, suggesting that these lesions are reversible upon cessation of subchronic high-dose manganese exposure.

Conclusion

High-dose subchronic manganese sulfate inhalation is associated with increased lung manganese concentrations and small airway inflammatory changes in the absence of observable clinical signs. Subchronic exposure to manganese sulfate at exposure concentrations (≤0.3 mg Mn/m³) similar to the current 8-hr occupational threshold limit value established for inhaled manganese was not associated with pulmonary pathology.     

Classification of worker exposures

The classification of jobs or workers by exposure is an important undertaking in any occupational epidemiological study. Hitherto, the exposure classification designs have been strongly motivated by a desire to generate a sufficient number of exposure classes for the determination of a potential exposure-response relationship. Thus, the partitioning of exposures has been more or less arbitrary. The misclassification problems created by the selection of an arbitrary number of exposure assignment classes have not been addressed. In any quantitative exposure classification scheme, specific job titles may be indistinguishable in existing employment records; therefore, between worker variability must be addressed when characterizing worker exposures. Also, industrial hygiene exposure measurements frequently used to characterize worker exposures are often treated as valid representations of exposures; but they are neither random nor systematic evaluations of worker exposures. As a result they do not represent sampling from the proper exposure stratification of workers. These observations suggest that the selection of exposure groups should be based on a more rigorous examination of the data and its limitations. Considering the probability of any given worker being placed into the proper class as the probability of finding the mean exposure for that worker within the class boundary, the general equations to quantify the misclassification rates for any classification design as well as the exposure class limits and their width for any acceptable misclassification rate are developed. If between worker variability could not be calculated from the available exposure measurements, then it might be estimated from the proper data compiled from the literature. By considering an acceptable level of exposure misclassification, it is possible to calculate the allowable number of exposure classes and the proper partitioning ratio for these classes. Thus, the trade-off between misclassification and number of exposure classes might be a satisfactory solution to this difficulty encountered in occupational epidemiology.     

Cytogenetic analysis of buccal cells from shoe-workers and pathology and anatomy laboratory workers exposed to n-hexane, toluene, methyl ethyl ketone and formaldehyde.

People employed in the shoe manufacture and repair industry are at an increased risk for cancer, the strongest evidence being for nasal cancer and leukaemia. A possible causal role for formaldehyde is likely for cancer of the buccal cavity and nasopharynx. Exfoliated buccal cells are good source of tissue for monitoring human exposure to inhaled and ingested occupational and environmental genotoxicants. To assess the cytogenetic damage related to occupational exposure to airborne chemicals during shoe-making and the processes in pathology and anatomy laboratories, the micronuclei (MN) count per 3000 cells was measured in buccal smears from shoe-workers (group I, n = 22) exposed to mainly n-hexane, toluene and methyl ethyl ketone (MEK) and from anatomy and pathology staff (group II, n = 28) exposed to formaldehyde (FA). Eighteen male university staff were used as controls. The mean time-weighted average (TWA) concentrations of n-hexane, toluene and MEK in 10 small shoe workshops were 58.07 p.p.m., 26.62 p.p.m. and 11.39 p.p.m., respectively. The measured air concentrations of FA in the breathing zone of the anatomy and pathology laboratory workers were between 2 and 4 p.p.m. Levels of 2,5-hexadione (2,5-HD) and hippuric acid (HA), metabolic markers of n-hexane and toluene exposure, respectively, were significantly higher in the urine of workers in group I than in control subjects (p < 0.001 and p < 0.01, respectively). The mean (+/- SD) MN (0/00) [corrected] frequencies in buccal mucosa cells from workers in group I, group II and controls were 0.62 +/- 0.45%, 0.71 +/- 0.56% and 0.33 +/- 0.30%, respectively (p < 0.05 and p < 0.05 compared with controls for group I and group II, respectively). The effects of smoking, age and duration of exposure on the frequency of micronucleated buccal cells from workers in all three groups studied were also evaluated. Overall, the results suggest that occupational exposure to organic solvents, mainly n-hexane, toluene, MEK and FA, may cause cytogenetic damage in buccal cells and that use of exfoliated buccal cells seems to be appropriate to measure exposure to organic solvents.     

Psycho-sensorimotor performance in divers exposed to six and seven atmospheres absolute of compressed air.

In the present study, we investigated the psycho-sensorimotor abilities of divers exposed to 6 ATA (50 m of sea water; corresponding to legal limit for occupational diving in North America, United Kingdom, and Northern Europe), or 7 ATA (60 m; the legal limit in France and Southern Europe) of compressed air (1 ATA = 100,000 Pa), using psychometric tests of manual dexterity, visual choice reaction time, and number ordination. The results of the present study showed that abilities in these tests were not significantly altered by pressure exposure to 6 ATA of compressed air. However, data obtained at 7 ATA showed slight but significant decreases in performance. Nevertheless, a few subjects presented large decreases in performance ranging from -20% to -25% of control. Finally, our results supported the ergonomic point of view that the laws limiting occupational diving to 6 ATA (50 m) are better adapted to reality and the requirements of underwater activity.     

Effects of inhaled carbon monoxide on acute lung injury in mice

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are major causes of morbidity and mortality in the intensive care unit, but despite continuing research few effective therapies have been identified. In recent years, inhaled carbon monoxide (CO) has been reported to have cytoprotective effects in several animal models of tissue injury. We therefore evaluated the effects of inhaled CO in three different in vivo mouse models of ALI. Anesthetized C57BL/6 mice were ventilated with oxygen in the presence or absence of CO (500 parts per million) for 1 h before lung injury was induced by lipopolysaccharide (LPS) or oleic acid (OA) administration. Ventilation was then continued with the same gases for a further 2-3 h, with hemodynamic and respiratory parameters monitored throughout. Intratracheal LPS administration induced lung injury with alveolar inflammation (increased lavage fluid neutrophils, total protein, and cytokines). In contrast, intravenous LPS induced a predominantly vascular lung injury, with increased plasma TNF and increased neutrophil activation (surface Mac-1 upregulation and L-selectin shedding) and sequestration within the pulmonary vasculature. Intravenous OA produced deteriorations in lung function, reflected by changes in respiratory mechanics and blood gases and lavage fluid neutrophil accumulation. However, addition of CO to the inspired gas did not produce significant changes in the measured physiological or immunological parameters in the mouse models used in this study. Thus the results do not support the hypothesis that use of inhaled CO is beneficial in the treatment of ALI and ARDS.     

Sister-chromatid exchanges in operating room personnel.

Sister-chromatid exchange (SCE) analysis was carried out in 67 operating room personnel (anaesthetists M.D.; anaesthesia nurses and anaesthesia unit technicians) exposed to waste anaesthetic gases such as halothane, nitrous oxide and isoflurane and in 50 healthy unexposed controls. The SCE frequencies were increased significantly in operating room personnel as compared to controls. A significant increase in SCEs was found in non-smoking operating room personnel as compared to non-smoking controls. This study supports the existence of an association between occupational exposure to mutagens and an increase in SCEs in lymphocytes.     

Lack of Complete Exposure Pathways for Metals in Natural and FGD Gypsum

Use of wallboard made from synthetic gypsum generated via flue-gas desulfurization (FGD) by coal-fired power plants (FGD gypsum) raised questions concerning the potential for exposure to residual trace metals. Because gypsum is widely used (e.g., in wallboard), any issue with metals could have far-reaching implications. A conceptual site model evaluated potential human health exposure pathways for metals in gypsum, through consideration of data for 21 metals including samples of natural (mined) gypsum, and of FGD gypsum. Because there are no screening values for gypsum, comparisons were made to background soil concentrations and to risk-based concentrations for metals in soil termed preliminary remedial action goals (PRGs), which assume more frequent and prolonged contact with particulate soil than would be likely for gypsum, and thus provide a health protective means for evaluation of exposure. Additional screenings evaluated occupational exposure and agricultural use of gypsum. Maximum metal concentrations in natural and FGD gypsum samples were either consistent with background concentrations or much lower than PRGs for residential or agricultural soil, or workplace air, and thus exposure pathways for these media were considered incomplete. Separate analyses of mercury volatilization were conducted, and this pathway was also found to be incomplete.     

Altered surfactant protein A gene expression and protein metabolism associated with repeat exposure to inhaled endotoxin

Chronically inhaled endotoxin, which is ubiquitous in many occupational and domestic environments, can adversely affect the respiratory system resulting in an inflammatory response and decreased lung function. Surfactant-associated protein A (SP-A) is part of the lung innate immune system and may attenuate the inflammatory response in various types of lung injury. Using a murine model to mimic occupational exposures to endotoxin, we hypothesized that SP-A gene expression and protein would be elevated in response to repeat exposure to inhaled grain dust and to purified lipopolysaccharide (LPS). Our results demonstrate that repeat exposure to inhaled endotoxin, either in the form of grain dust or purified LPS, results in increased whole lung SP-A gene expression and type II alveolar epithelial cell hyperplasia, whereas SP-A protein levels in lung lavage fluid are decreased. Furthermore, these alterations in SP-A gene activity and protein metabolism are dependent on an intact endotoxin signaling system.     

Occupational exposure to electric and magnetic fields during work tasks at 110 kV substations in the Tampere region

The occupational exposure to electric and magnetic fields during various work tasks at seven 110 kV substations in Finland's Tampere region was studied. The aim was to investigate if the action values (10 kV/m for the E‐field and 500 µT for the B‐field) of the EU Directive 2004/40/EC were exceeded. Electric and magnetic fields were measured during the following work tasks: (1) walking or operating devices on the ground; (2) working from a service platform; (3) working around the power transformer on the ground or using a ladder; and (4) changing a bulb from a man hoist. In work task 2 “working from a service platform” the measured electric field (maximum value 16.6 kV/m) exceeded 10 kV/m in three cases. In the future it is important to study if the limit value (10 mA/m²) of Directive 2004/40/EC is exceeded at 110 kV substations. The occupational 500 µT action value of the magnetic flux density field (B‐field) was not exceeded in any working situation. Bioelectromagnetics 31:252–254, 2010. © 2009 Wiley‐Liss, Inc.     

Paternal radiation exposure and leukaemia in offspring: the Ontario case-control study.

OBJECTIVES--To test the hypothesis that there is an association between childhood leukaemia and the occupational exposure of fathers to ionising radiation before a child''s conception. DESIGN--Case-control study with eight matched controls per case. SETTING--Regions of Ontario, Canada, with an operating nuclear facility. SUBJECTS--Cases were children (age 0-14) who died from or were diagnosed as having leukaemia from 1950 to 1988 and were born to mothers living in the vicinity of an operating nuclear facility. Controls were identified from birth certificates, matched by date of birth and residence at birth. There were 112 cases and 890 controls. MAIN OUTCOME MEASURES--Paternal radiation exposure was determined by a record linkage to the Canadian National Dose Registry. RESULTS--Six fathers of cases and 53 fathers of controls had had a total whole body dose > 0.0 mSv before the child''s conception, resulting in an odds ratio of 0.87 (95% confidence interval 0.32 to 2.34). There was no evidence of an increased leukaemia risk in relation to any exposure period (lifetime or six months or three months before conception) or exposure type (total whole body dose, external whole body dose, or tritium dose), except for radon exposure to uranium miners, which had a large odds ratio that was not significantly different from the null value. CONCLUSIONS--The findings of this study in Ontario did not support the hypothesis that childhood leukaemia is associated with the occupational exposure of fathers to ionising radiation before the child''s conception.     

Presynaptic Dopaminergic Function in the Nucleus Accumbens Following Chronic Opiate Treatment and Precipitated Withdrawal

Naloxone treatment at three days following implantation of pellets containing morphine base increased uptake of tritiated dopamine by the nucleus accumbens but did not alter efflux of tritiated dopamine by the nucleus accumbens or tritiated norepinephrine by the hippocampus. At six days following placement of pellets containing morphine base, withdrawal score was increased after treatment with either saline or naloxone, indicating that animals were undergoing spontaneous opiate withdrawal. Fractional efflux of tritiated dopamine was decreased at this time point following intermittent stimulation with 317 and 1000 M 4-aminopyridine, for striatal slices obtained from animals pretreated with either saline or naloxone. For the nucleus accumbens at six days after placement of morphine pellets, similar decreases in the efflux of tritiated dopamine were only observed in slices obtained from naloxone treated animals. Fractional dopamine efflux was also diminished after in vitro exposure to rising concentrations of 4-aminopyridine, amphetamine, or cocaine for tissue obtained from the nucleus accumbens, but not for slices from the striatum at six days following morphine pellet implantation. In conclusion, deficits in dopamine efflux by the nucleus accumbens occur at a time when animals are undergoing spontaneous opiate withdrawal at six days following morphine pellet implantation, but do not occur at an earlier time point when withdrawal is precipitated by naloxone treatment. These deficits are apparent for brain slices obtained from the striatum or nucleus accumbens after exposure to rising concentrations of different in vitro treatments, with tissue obtained from the nucleus accumbens being more sensitive than the striatum to dopamine efflux produced by a wider range of treatments.     

Production of a uniform cellular injury by raster scanning of cells for the study of laser bioeffects

Efforts to understand laser bioeffects in cells and tissues have been hindered by a nonuniform cellular response of the specimen, resulting in graded biochemical effects. In addition, the small beam diameters of commonly used lasers limit the number of cells expressing a response to numbers inadequate for the study of biochemical effects. For a limited emission power, expansion of the beam diameter reduces the irradiance, thus requiring longer exposure durations to produce a cellular response. Cultured human retinal epithelial cells were exposed as a single spot ("tophat" exposure) from a carbon dioxide (CO₂) laser operating at 10.6 µm or scanned with a raster system and compared with thermal injury produced with heated saline for short periods (1–9 s) at relatively high temperature (55–70°C). Cell viability and induction of the 70 kDa heat shock protein were evaluated as indicators of the cellular response. Initial attempts to use a tophat (uniform energy distribution) exposure resulted in a nonuniform cellular response (and nonuniform energy distribution) due to diffraction effects from the 2-mm selection aperture. However, raster scanning for appropriate times with the CO₂ laser yielded uniform cell viability and heat shock protein synthesis that were comparable to dipping cells in heated saline. Because scanning results in a homogeneous exposure of cells, the described scanning technique may be applied to studies of cellular responses to other lasers to evaluate photochemical and photomechanical effects. carbon dioxide laser     

Occupational cancer: experience in Ontario.

This paper reviews the experience of the Workmen''s Compensation Board of Ontario in identifying cases of cancer that could be attributed to occupational hazards. Worker''s claims for compensation are allowed if there is reasonable medical evidence that their cancer was caused by exposure to risk factors associated with their occupation. Details of the types of cancer associated with specific carcinogens or fields of employment are discussed. About 50% of the cases were related to exposure in particular industrial operations that functioned for relatively brief periods. The number of deaths from cancer identified as being caused by occupational factors is compared with the total for cancer from all causes in Ontario during the period 1971 through 1975. Although all workers eligible for compensation may not have been identified, the data suggest that less than 1% of cancer is presently caused by occupational factors.     

Lack of behavioral effects in the rhesus monkey: high peak microwave pulses at 1.3 GHz

The current safety standards for radiofrequency and microwave exposure do not limit the peak power of microwave pulses for general or occupational exposures. While some biological effects, primarily the auditory effect, depend on pulsed microwaves, hazards associated with very high peak-power microwave pulses in the absence of whole-body heating are unknown. Five rhesus monkeys, Macaca mulatta, were exposed to peak-power densities of 131.8 W/cm2 (RMS) while performing a time-related behavioral task. The task was composed of a multiple schedule of reinforcement consisting of three distinct behavioral components: inter-response time, time discrimination, and fixed interval. Trained monkeys performed the multiple schedule during exposure to 1.3-GHz pulses at low pulse-repetition rates (2-32 Hz). No significant change was observed in any behavior during irradiation as compared to sham-irradiation sessions. Generalization of these findings to experimental results with higher peak-power densities, other pulse rates, different carrier frequencies, or other behaviors is limited.     

Remote effects of occupational and non-occupational exposure to electromagnetic fields of power-line frequency. Epidemiological studies

A retrospective cohort study of mortality in the personnel of power-supply plants in the European regions of Russia was carried out. The exposure of the personnel to electromagnetic fields of power-line frequency (PF) was taken into account. Statistically non-significant raise of mortality from leukemia was found, compared to low mortality rates due to all other causes including cancer of any type. Standardized mortality ratio (SMR) was equal to 2.03 (95% CI = 0.23-7.31). In the retrospective case-control study the haemoblastosis development risk under occupational PF EMF exposure was evaluated. The data of 571 "cases" and 1208 "controls" interview showed that odd ratio (OR) was 1.64 (95% CI = 0.8-3.1). In another retrospective case-control study the risk of the haemoblastosis development in children due to parents PF EMF occupational exposure was evaluated. The data of 208 "cases" and 319 "controls" interview showed that the odd ratio (OR) was 1.69 (95% CI = 0.7-3.3). A retrospective cohort study of mortality in a settlement situated near a high-voltage (500 kV) substation, which took into account PF EMF levels in residential areas, revealed low mortality rates, except leukemia mortality (SMR 1.3; 95% CI = 0.2-7.0). The obtained data do not allow excluding a possibility of PF EMF leukogenic effect.