Chemistry Reference
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level compared with the permissive levels in occupa-
tional exposure used earlier still exceeds the average
exposure from ambient air by a factor of more than 10 4
and is approximately 2.5 times the average exposure
from the diet. The study by Roels et al . (1992) reported
a lowest observable adverse effect level (LOAEL) of
0.150 mg/m 3 and suggested an 8-hour TWA of 0.09 mg/
m 3 for total dust as a protective level to prevent the
onset of neurotoxic effects. The LOAEL for total dust
derived by Lucchini et al . (1999) was 0.10 mg/m 3 based
on neurobehavioral changes. A LOAEL calculated by
Mergler et al . (1994) was 0.035 mg/m 3 for the respirable
fraction, based on neurotoxicity in alloy workers in a
ferromanganese and silicomanganese alloy plant.
As far as occupational exposure to manganese from
the combustion of MMT is concerned, in a study per-
formed by Sierra et al . (1995) in Montreal, Canada, it
was shown that 10% of the manganese exposure of the
garage mechanics was due to MMT.
Occupational exposure to maneb and mancozeb can
occur by inhalation or dermal routes during formula-
tion and spray application of these pesticides (HSDB,
1999).
4.3 Working Environment
In the workplace, exposure to manganese occurs
mostly by inhalation of manganese fumes or man-
ganese-containing dusts. This is a concern mainly in
the ferromanganese, iron, and steel, dry cell battery,
and welding industries (WHO, 1986). Exposure also
occurs during manganese mining and ore process-
ing. In mining operations, manganese concentrations
of 250 mg/m 3 or even higher have sometimes been
found (Ansola et al ., 1944, Rodier, 1955). High-speed
drilling machines used to be the main cause of a large
amount of manganese dioxide dust emitted in the
working environment. In dry cell battery plants and
ferromanganese plants, the concentrations of man-
ganese in air are lower. Values up to 5.8 mg/m 3 , but
occasionally also higher, have been reported (Emara
et al ., 1971; Šaric et al ., 1977; Suzuki et al ., 1973). More
recently in the United States in steel manufacturing
facilities. a mean of 0.066 mg/m 3 median of 0.051 mg/
m 3 as respirable dust, and 0.18 mg/m 3 in total dust
have been reported (Gibbs et al ., 1999). Among mine-
workers, average exposure intensity across all jobs
as Mn in total dust was 0.21 mg/m 3 in South African
mineworkers (Myers et al ., 2003a). In another study
on miners in the Middle East, average concentrations
were much higher, between 62 and 114 mg/m 3 of Mn
in total dust, because of less effective control meas-
ures (Mashardi Abar Boojar and Goodarzi, 2002). For
the ferroalloy industry, average inhalable manganese
exposures, measured using IOM personal inhalable
samplers, were 0.254 mg/m 3 , and respirable exposures
were 0.028 mg/m 3 in Norway (Ellingsen et al ., 2000).
Average exposure levels as Mn measured in total dust
with the traditional CFFC samplers were 0.054 mg/m 3
among Italian ferroalloy workers (Lucchini et al ., 1999).
Among welders, manganese concentrations can vary
from 0.1 mg/m 3 (Kucera et al ., 2001) to 1.5 mg/m 3 (Lu
et al ., 2005) and 4 mg/m 3 (Korczynski, 2000), with peak
exposure levels more frequently reached in the ship-
building industry.
An important point is that in ferromanganese plants,
but also in dry cell battery plants, the size distribu-
tion of manganese aerosols is such that small particles
prevail absolutely compared with mine operations,
where only a smaller proportion of respirable particles
(<5
5 TOXICOKINETICS
5.1 Absorption
5.1.1 Inhalation
There are no quantitative animal data on absorp-
tion rates for inhaled manganese. Because manganese
dioxide and other inhaled manganese compounds are
practically insoluble in water, only manganese in par-
ticles small enough to reach the alveolar lining will be
absorbed into the blood (WHO, 1981).
Particles that are deposited in the upper airways
may be moved by mucociliary transport to the throat,
where they are swallowed and enter the stomach. This
process has been found to account for clearance of a
signifi cant fraction of manganese-containing particles
initially deposited in the lung (Drown et al ., 1986; Mena
et al ., 1969; Newland et al ., 1987). Mena et al . found in
17 humans exposed to a nebulized solution of manga-
nese chloride and in 4 subjects exposed to manganese
oxide in a similar fashion that 40-70% of the deposited
amount was recovered in feces. Both compounds were
labeled with 54 Mn. In a study performed by Tjälve et al .
(1996), the uptake of manganese in brain regions of
weanling male Sprague-Dawley rats after intrana-
sal administration of 4
m) are usually encountered. There is also some
evidence that aerosols formed by condensation may
be more harmful than those formed by disintegration
(WHO, 1981). This is most probably caused by the dif-
ferences in the particle size distribution.
Assuming a level of 1 mg/m 3 TWA (NIOSH, 2005)
as recommended limit exposure (REL), maximum
exposure would be 10 mg manganese/day. This low
µ
g/kg 54 Mn was investigated.
Whole-body autoradiography of the rats at different
time points revealed that the olfactory bulb contained
the most measured manganese at 1, 3, and 7 days after
µ
 
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