As illness among employees became apparent,
the project was halted. A more thorough investigation into the chemical history
of the collection was initiated. At the same time, ASM requested that industrial
hygienists from the University of Arizona Department of Risk Management and Safety
assist in identifying chemicals emitted from the deteriorating negatives and any
hazards the chemicals presented.
No data in available regarding the initial photo processing, on-site storage,
or climate control in the field for the negatives. No records exist documenting
methods of care in storage or transportation in the field. Manufacturers of some
negatives are unidentified. References to the manufacturers "Defender,"
"AGFA," and "Kodak" are embossed on the borders of other sheet
films.
Correspondence directly with the Kodak laboratories in Rochester provided no
helpful information regarding the hazards posed by degrading chemical constituents
of early sheet films. However, according to Shaw in Overexposure (1983:289), deteriorating nitrates negatives can decompose to nitrogen oxide gases
and a powdered film base that also can be irritating to skin, eyes, and the respiratory
system. More specifically, cellulose nitrate, the first flexible base used in the
photographic process, deteriorates to gaseous nitrogen oxides that in turn deteriorate
to nitric acid. The chemicals involved in this deterioration include:
Nitric Oxide (NO)
Nitrogen Dioxide (NO2)
Nitrous Oxide (N2O)
Nitric Acid (HNO3)
The nitrogen oxide gases are primarily deep lung irritants, although irritation
of the eye and other mucous membranes may accompany exposure. Repeatedly inhaled,
low concentrations can result in chronic headaches, blurred vision, loss of appetite
and other symptoms of systemic damage. Acute exposure to nitrogen oxide gases facilitates
such symptoms as fever, nausea, dypsnea, and vomiting. Chronic exposures generally
result in bronchial irritation and possible development of an emphysema-like condition1.
Nitric Oxide
Presently no data from animal or human studies suggest that nitric oxide (NO)
is a health hazard at concentrations encountered in ambient air. It is potentially
toxic because it oxidizes to NO2 (Mueller & Hitchcock,
1969:672), although this reaction is slow at concentrations below 50 ppm.
Nitrogen Dioxide
Nitric oxide oxidizes in the air to form nitrogen dioxide (NO2)
in a light-catalyzed reaction. Nitrogen dioxide is highly toxic by inhalation (Shaw,
1983:3.141). It has the ability to penetrate to the deep lung, affecting the terminal
bronchioles and alveoli. Cellular damage in these areas leads to release of fluid
in the lung (pulmonary edema). Increased exposure may result in decreased area in
the lung for gaseous exchange, suggestive of emphysema. In addition, chronic nitrogen
dioxide exposure may lead to increased incidence of lung infection due to damage
to the mucous-producing and ciliated cells of the airways. Animal studies have shown
that concentrations approaching those found in ambient air can cause pathological
changes in the lungs which are suggestive of the start of a disease process (Mueller
& Hitchcock, 1969:673).
Swelling of ciliated cells of the lung and loss of cilia has been demonstrated
in a rare chronically exposed to nitrogen dioxide at levels of 17ppm (Stephens,
1972). Accumulation of cellular debris is seen also. These impairments in lung cells
result in decreased compliance and increased breathing rate typical with exposure
to a deep lung irritant. Regeneration of cilia occurs to some extent after termination
of exposure to such levels of nitrogen dioxide.
However, rabbits demonstrated alteration in lung collagen after exposure to only
0.25 ppm NO2, but at 6 hours per day for 6 days. Effects
were still evident in animals sacrificed 7 days after exposure (Buell et al. 1966).
In addition, membrane damage associated with altered lung compliance was seen in
beagles exposed to 3-7 ppm NO2 for a period of 1 hour
(Dowell, 1971), and 5 rats exposed to 0.5 or 1 ppm NO2 for 6 consecutive hours demonstrated morphologic change in lung mast cells (Thomas
et al. 1967:33). This evidence seems to indicate that the development of respiratory
dysfunction is as influenced by the length as by the level of exposure.
Considering nitrogen dioxide a potential low-level contributor to injuries at
ASM, measurements were taken to quantify how much of this contaminant was present
in the work environment.
Two general air-sampling methods were utilized. One was a direct-reading Bendix/Gastec
colorimetric indicating tube for nitrogen dioxide; the other employed personal air
sampling pumps affixed to fritted bubblers (NIOSH Method PCAM 108) to collect air
samples over a period of time to obtain time-weighted average concentrations of
this particular contaminant.
Continuous monitoring for nitrogen dioxide was performed by Steve Holland, Department
of Risk Management and Safety, University of Arizona, at the museum worktable and
under the plastic sheeting where negatives were stored. NO2 concentrations in the room were not detectable (<0.3 parts per million [ppm})
by the standard NIOSH methods, but the concentration of nitrogen dioxide under the
plastic sheeting measured approximately 2ppm of nitrogen dioxide (vs. OSHA standard
of 5 ppm, and TLV2 of 3 ppm). Employees were exposed to this level upon entering the room where they
continued to work for periods of 2-6 hours at a time.
Nitrous oxide
Nitrous oxide may be a gaseous nitrogen oxide present in the decomposition of
aged film products, also. Chronic exposure to this agent, a common anesthetic, has
been linked to various nervous system disorders only at very high levels.
Nitric acid
Gaseous nitrogen dioxide may combine with water (e.g. perspiration, high humidity)
to form nitric acid. Nitric Acid is an oxidizing agent and is very corrosive. Response
to contact with this reactive compound is typical of exposure to a primary irritant
and involves disturbance of the mucous membranes of the eye, nose, and throat. The
fumes given off by nitric acid solutions are highly toxic by inhalation. Repeated
exposure may cause chronic bronchitis and emphysema (Shaw, 1983:3.042). The corrosiveness
of this chemical may also lead to browning of the teeth and skin ulcerations.
Silver salts
Silver salts were also considered as a possible skin irritant, due to their likely
presence in the emulsion of negatives. These salts are quite soluble and have been
associated with dermatitis in industrial workers. The symptoms reported by museum
workers included significant skin irritation on the neck, face and hands. Air samples
collected on 37mm Millipore HA filters and analyzed by atomic absorption spectrophotometry
indicated non-detectable levels of silver salts (<2.0 g/M3),
although these compounds may have had an effect through skin contact, without becoming
airborne. |
