Air Manganese Research Articles

Autonomic Function in Manganese Alloy Workers

The observation of orthostatic hypotension in an index case of manganese toxicity lead to this prospective attempt to evaluate cardiovascular autonomic function and cognitive and emotional neurotoxicity in eight manganese alloy welders and machinists. The subjects consisted of a convenience sample consisting of an index case of manganese dementia, his four co-workers in a “frog shop” for gouging, welding, and grinding repair of high manganese railway track and a convenience sample of three mild steel welders with lesser manganese exposure also referred because of cognitive or autonomic symptoms. Frog shop air manganese samples 9.6–10 years before and 1.2–3.4 years after the diagnosis of the index case exceeded 1.0 mg/m3in 29% and 0.2 mg/m3in 62%. Twenty-four-hour electrocardiographic (Holter) monitoring was used to determine the temporal variability of the heartrate (RR′ interval) and the rates of change at low frequency (0.04–0.15 Hz) and high frequency (0.15–0.40 Hz). MMPI and MCMI personality assessment and short-term memory, figure copy, controlled oral word association, and symbol digit tests were used. The five frog shop workers had abnormal sympathovagal balance with decreased high frequency variability (increased ln LF/ln HF). Seven of the eight workers had symptoms of autonomic dysfunction and significantly decreased heart rate variability (rMSSD) but these did not distinguish the relative exposure. Mood or affect was disturbed in all with associated changes in short-term memory and attention in four of the subjects. There were no significant correlations with serum or urine manganese. Power spectrum analysis of 24-h ambulatory ECG indicating a decrease in parasympathetic high frequency activation of heart rate variability may provide a sensitive index of central autonomic dysfunction reflecting increased exposure to manganese, although the contribution of exposures to solvents and other metals cannot be excluded. Neurotoxicity due to the gouging, welding, and grinding of mild steel and high manganese alloys (11–25%) merits air manganese and neuropsychologic surveillance including autonomic function by Holter monitoring of cardiovagal activation.

Thermal and chemical events in the decomposition course of manganese compounds

Thermogravimetry and differential thermal analysis, infrared spectroscopy (solid phase and gas phase), and X-ray diffraction were used to characterize the pathways of the decomposition of the hydrated acetate, oxalate and nitrate of manganese in air. The non-isothermal activation energy ( ΔE, kJ mol −1) was determined for the thermal processes monitored throughout the decomposition course. The results showed that Mn( CH 3 COO) 2·4 H 2 O dehydrates in three steps up to 130 °C, and then decomposes to a mixture of manganese oxides Mn 3O 4 (major) and Mn 2O 3 (minor) through the intermediates Mn(OH)CH 3COO and/or MnOCH 3COO and MnCO 3. MnC 2 O 4·2 H 2 O dehydrates in one step at 150 °C, and then decomposes via MnCO 3 into Mn 3O 4 (hausmannite structure) at 350 °C. Mn( NO 3) 2·4 H 2 O undergoes stepwise dehydration up to 175 °C, and decomposes above 200 °C via an unstable oxynitrate intermediate yielding MnO 2; this decomposes at about 550 °C to the α-Mn 2O 3 phase.

Manganese induced parkinsonism: an outbreak due to an unrepaired ventilation control system in a ferromanganese smelter.

Several cases of parkinsonism were found in a ferromanganese smelter after the ventilation system had broken down and had not been repaired for eight months in 1985. To determine the aetiology and prevalence of parkinsonism, 132 workers were submitted to thorough medical examination and estimated air concentrations of carbon monoxide and manganese at different worksites. Only six of eight workers performing electrode fixation or welding during 1985 developed parkinsonism. They were exposed for 30 minutes each day, seven days a week, to high concentrations of air manganese (greater than 28.8 mg/m3). There was a consistent trend between the index of exposure to manganese and signs and symptoms exhibited by extrapyramidal systems. After repair of the ventilation system, the air concentration of manganese during electrode fixation and welding decreased to less than 4.4 mg/m3; furthermore, no new cases of parkinsonism have been observed. Workers with parkinsonism recovered partially after removal from original worksites and treatment with levodopa. It is concluded that the outbreak resulted from exposure to high concentrations of manganese fumes through the breakdown of the ventilation system.

Origins of manganese in air particulates in California.

The proportions of manganese to other metals in samples of airborne fine particles taken at some sites in California have increased greatly since the beginning of 1985. Here, data are presented which indicate that the addition of manganese to leaded gasoline is largely responsible for this increase. Concentrations of manganese, silicon, titanium, iron, lead and other elements in airborne particles were measured using energy-dispersive X-ray fluorescence analysis. Coefficients of correlation among levels of manganese, iron and lead measured at twenty sites in California were calculated. Levels of manganese and iron are generally highly correlated because of the presence of large amounts of these elements in the earth’s crust. Levels of airborne manganese and lead at sites In Southern California are often highly correlated, suggesting a vehicular source of manganese. Observed manganese concentrations are apportioned into two major sources: the earth’s crust and motor vehicles. The apportionment indicates that vehicular emissions of manganese may account for a significant part of the total at urban sites in Southern California. At most other sites, the contribution from vehicles is found to be far smaller than that from the earth’s crust.

Determination of manganese in air and biological material.

Determination of manganese in air and biological material.