Chemistry Reference
In-Depth Information
Soluble compounds of beryllium (such as the sulfate
and the fl uoride) exert the acute and subacute effects,
whereas insoluble alloys and intermetallics (the oxides
and the ores) usually produce health effects after long-
term exposure or longer deposition within the system.
The chief site of vulnerability from beryllium is the
lung; however, nonpulmonary locations of granulo-
matous lesions may exist in many other organs such as
the liver, spleen, abdominal lymphatic nodes, kidney,
bone marrow, or skin.
to soluble beryllium salts, but it was also recorded
after exposure to metallic dust, beryllium oxide, and
hydroxide (Eisenbud
et al
., 1948). The pathogenesis of
infl ammatory changes is probably connected with the
acidity of beryllium salts, and the clinical parameters—
progression of infl ammatory process, its intensity, and
the duration of illness, depend on the dose-response
relationship (Van Ordstrand
et al
., 1943). In high-
level exposure, the clinical symptoms of pneumoni-
tis appear within 72 hours after exposure, whereas
radiological abnormalities occur within several weeks
(Maier and Newman, 1998). Recovery lasts for several
weeks or months; however, some fatal cases were also
noted. The treatment consists in the cessation of expo-
sure, bed rest, systemic glucocorticoids, and oxygen
therapy. Although in practice the severe cases of acute
beryllium disorder are rare, the milder forms should be
considered in the differential diagnosis of respiratory
diseases with infectious etiology (Mroz
et al
., 2001).
7.1 Local Effects
7.1.1 Skin Contact
7.1.1.1 Humans
Occupational exposure to soluble beryllium salts
may cause skin reaction such as edematous, erythema-
tous, and papulovesicular dermatitis, mainly on the
exposed surfaces. Those changes usually disappear
after cessation of exposure. Beryllium may also cause
conjunctivitis in occupationally exposed workers,
as well as act on mucous membranes of oral cavities
producing gingivitis in persons with dental implants
made from alloys including beryllium (Haberman
et al
., 1993). Granulomatous necrotic changes and
ulcerations caused by skin penetration by insoluble
beryllium salts were also observed. Skin changes like
papular and granulomatic rash were found to accom-
pany chronic beryllium disease in workers exposed to
oxide beryllium dust.
The pathological changes mentioned previously
are based on delayed allergic hypersensitivity, which
was proved
in vitro
in lymphocyte-blast transforma-
tion test (Hanifi n
et al
., 1970) and migration inhibiting
test of macrophages (Henderson
et al
.,1972) and also
in vivo
using skin patch testing with beryllium sulfate
(Curtis, 1951).
7.1.2.2 Animals
Acute chemical pneumonia after inhalation exposure
to beryllium compounds was induced experimentally
in different kinds of animals (Stokinger
et al
., 1950). The
observed pathological changes were similar to those
in humans. In animals exposed to beryllium sulfate at
a concentration of 13 mg/m
3
for 1 hour, proliferative
changes were noted after 3 weeks, mostly concerning
the lung macrophages (mice), type II alveolar epithelial
cells (rats), and interstitial cells and epithelium (mice
and rats). Hyperplasia of type II alveolar epithelial
cells was accompanied with the thickening of intersti-
tium infi ltrated with macrophages and neutrophils. The
presence of alveolar macrophages with ragged cellular
membranes was a visible feature. In another experi-
ment, interstitial pneumonia without granulomas was
noted in rats exposed to 4.05
g/m
3
beryllium as beryl-
lium sulfate (mass median diameter, 1.9
µ
µ
m) for 1 hour
(Sendelbach
et al
., 1989).
Hall
et al
. (1950) observed that insoluble beryllium
compounds also provoked acute pneumonia. High-fi red
(1150-1450°C) BeO did not induce lung damage in most
of experimental animals, besides mild phagocytic cell
response typical for exposure to every kind of inhaled
molecules, in comparison with low-fi red (400°C) BeO,
which almost at 10 times lower concentrations caused
death in rats and lung damage in dogs.
Metallic beryllium can also produce lung injury,
however, at higher concentrations than the beryllium
salts do. It has been noted that 50-minute exposure
to metallic beryllium dust at the dose of 0.8 mg/m
3
(MMAD, 1.4
7.1.1.2 Animals
Skin allergy and beryllium skin granulomas (Dutra,
1951), similar to those observed in humans, were
induced experimentally in pigs and guinea pigs (Ale-
kseeva, 1965).
7.1.2 Inhalation
7.1.2.1 Humans
Acute toxicity of beryllium at concentrations usu-
ally >25
g/m
3
is manifested by skin, eye, nose, and
throat irritation, followed by upper and lower airway
infl ammation, pulmonary edema, and (>100
µ
g/m
3
)
chemical pneumonitis (Maier
et al
., 1998). Acute beryl-
lium disease occurs mainly in the case of exposure
µ
m) (initial lung burden of approxi-
mately 0.625 mg) resulted in necrotic hemorrhagic
pneumonia and interstitial fi brosis as a consequence
µ
