PO BOX 165, TUSCOLA, ILLINOIS
JULY 25, 1983
Report on Study 420-1171
This is a follow up to our telephone discussion of today on the above report
which we have received recently. A copy of the report without the very extensive
Appendix Section is enclosed for your perusal. Dr. McCunney, Boston office, has a complete copy of the report.
The report indicated that after 4 weeks exposure of the rats to CAB-O-SILŪ
N70-TS hydrophobic fumed silica at a level of 30 mg/m3 there is damage to the lung tissue of the rats. After 6 and 12 week recovery periods, there does appear to be some healing of the tissue. Toxigenics personnel indicated no evidence of silicosis in the tissue, however, the exposure of the animal
to the hydrophobic silica will eventually result in some loss of lung capacity through the resultant scarring in areas affected
by the silica.
I would be interested in your comments on the study and the text of the warning
notice with which we will advise our existing and future customers of these new test results.
I will send you a copy of the latter tomorrow. I would appreciate a reply
on this matter by the end of the week if possible.
Also, for your information, I have enclosed copies of translations of two inhalation
studies carried out on the competitive hydrophobic fumed silicas, Degussa R972 and Wacker-Chemie H20, by a Dr. Klosterkotter. At this time, we are planning quite a lot of development work in the Pilot Plant in
1984 on treated fumed silica, one of which will be a match for Degussa R972. Obviously,
I want to make sure that we take whatever steps necessary to properly protect our people during these experiments. I look forward to your comments with interest.
Many thanks for your help in these matters.
NOTES ON MCCUNNEY/GREG
VISIT TO TUSCOLA JAN 11 84
Dr. Robert McCunney Medical Director of Health – Cabot
Reports to R. Champie
BSc Chem Eng –
– Univ of Minnesota
Occupational Health/Medicine – Harvard Univ
Aug 1983 joined Cabot 50% time
50% Goddard Memorial
Hospital, Staughton, Mass
Runs program on Occupational Health
Set up programs for ~100 companies
Dr. Douglas Grey
reports to Don Rivin
BSc Science/Administration –
2 years ROTC commission
– Chem Corp/Health Physics
5 years Aerojet General in late 60’s – Industrial Hygiene
1967-72 Industrial Hygiene/Toxicology
– University Cincinnati
MSc Industrial Hygiene – theses solvent evaporation
Environmental Health – thesis
“Characteristics of Cascade Impacter Collecter”
1972-74 Northwestern University
Trained MDs in Environmental Health
– Los Alamos – Aerosol Research
Olin Corp – New Haven
– Mgr Indust Hygiene
Had 5 hygienists working for him
1983 – Univ of New Haven
McCunney initial comments on Klosterkotter studies on
R972 & H20.
Feels no toxic effects rats died from dust overloading lung system i.e. physical effect (obstruction). Reduces lung efficiency – animal becomes more open to lung infections.
Effect of dust particles on lung tissue – inflammation →
macrophages → fibrosis →air sacs become hardened – lose efficiency.
HC Question. If lung gets more
and more hardened scarred tissue – does lung capacity increase again in time as new tissue formed – McCunney not sure
General Comments on Tour
– D side/Pilot Plant/
1BC baggine area – clean
– protection procedures sound good
Gave health safety – MSDS sheets NTOTS, COS, COGIIG – both
ACTION Next meeting, tentative
Wed 8 Feb, HC confirm
Review article on Oregon study
Locate other industrial studies on animals showing death from obstructive means
Conduct a medical survey for X stalline (sic) silica
feels this is worst case situation
Review of hydrophobic silica studies – Dugussa
refs – Barbara Davis
NB/ Don Rivin wants Grey to become involved with things such as SASSI
Study No. 420-1171
Interim Pathology Report
Histopathology _ VC-II and T-IV groups
As detailed in the attached individual animal reports, the primary effect of
the test article was limited to the lung. All of the T-IV rats regardless of
sex had a moderate to very severe chronic alveolar/interstitial consolidative lesion usually diffuse in distribution. Elements of this lesion suggested an active process; namely the occurrence of alveolar
foam cells, a protein rich alveolar transudate, and an interstitial edema with prominent interstitial macrophages.
Generally lesions present in the VC-II rats and the tissues other than the
lung of the T-IV rats were typical of spontaneous and expected lesions of this species and strain at this age. These lesions were not compound related.
V. Becker DVM 5-11-83
A Subsidiary of Whittaker Corporation
PPG INDUSTRIES, INC./ONE
GATEWAY CENTER/PITTSBURGH, PENNSYLVANIA
October 10, 1980
Mr. L.J. Faenza
125 High Street
Realizing that you are on jury duty and probably will not see this letter for
some time, I will be patient for your reply.
In your letter to me of September 25 you stated your opposition to the 2mg/m3
TWA for BAA silica dust given in the second draft Silica Standard. This was brought
up during our meeting on October 7 and it was agreed that we would substitute in the third draft any value you suggested and
were able to justify on the basis of feasibility. I would recommend that the
justification be as complete as possible so that those reading the standard or investigating its basis would be convinced
of the practical impossibility of going lower than your recommended TWA.
I would like to add to this my plea for some documentation from Cabot regarding
human safety given a history of exposure to given levels of BAA silica dust. This
need not be more than a memo report which could be filed. Such information would
serve to negate the NIOSH results and support your recommended TWA.
Let me know if you want any further discussion of this.
ASTM E-34 T.G. 16
CABOT CORPORATION 125 High
Street, Boston, MA 02110
October 22, 1980
Mr. Donald D. Dunnom
Supervisor, Health and Safety Services
PPG Industries, INC
1 Gateway Center
Pittsburgh, PA 15222
Since I am fortunate enough to have an extremely and efficient secretary, I’m
getting my mail at home so that I can handle the various affairs of state while on jury duty.
So—I’m able to respond to your letter of October 10th.
Unfortunately, Don, we don’t have much in terms of data relative to human
safety which I could submit to substantiate our opinion for a higher TTLV for Cab-o-Sil.
We do have a 20 year X-ray history file which shows no pulmonary disease manifested in workers exposed to fairly high
concentrations of dust over this period of time. However, because of various
legal problems, we have always hesitated to quote from this data. The only other
documentation we have is this study which Catherine Aranyl did, but these findings, as you know, are not that conclusive. Besides, they don’t do much to prove anything on humans, per se. I’ll have to give this more thought.
In any event, it seems to me that it ought to be fairly obvious to anyone,
including NIOSH, that it is damn near impossible to maintain dust levels of our material, or any material of similar particle
dimension for that matter. At 2 mg/m3 under anything but a virtually sterile atmosphere.
Anyway, I’ll get back to you on this with something.
Louis J Faenza
p.s. Have you heard anything further
from Schleyer on the proposal for the “Silica Association”?
Box 188, Tuscola, ILlinois
from: hector cochrane
sugject: cab-o-silŪ n70-ts fumed silica
As I mentioned in my letter of July 25, in light of the new data given in Toxigenics
Study 420-1171 we need to change the warning statements on our packaging and literature concerning the inhalation of cab-o-silŪ n70-ts hydrophobic fumed
silica. Drafts of the new statements are included with this letter.
I would appreciate your comments on them with any suggested changes as soon
cab-o-silŪ n70-ts fumed silica
contains treated silica
avoid breathing dust
use only with exhaust ventilation
or niosh approved respirator.
Continued inhalation of
cab-o-silŪ n70-ts hydrophobic fumed silica dust may cause pulmonary inflammation. This product should only be used with adequate exhaust ventilation or NIOSH approved
health safety literature
Histological examination of rats exposed to cab-o-silŪ n70-ts hydrophobic
fumed silica at 0.06 mg/l air for six hours followed by an exposure level of 0.031 mg/l air for various times up to 4 weeks
was associated with a chronic-active pulmonary inflammatory process. Twelve weeks
after the four weeks of exposure, the pulmonary inflammation was more localized, however, histologic markers of chronicity
were evident; namely interstitial fibrosis and interstitial collagen proliferation.
Granulomatous responses were not seen.