PB-203 465
GUIDES FOR SHORT-TERM EXPOSURE OF THE PUBLIC TO
AIR POLLUTANTS. III. GUIDE FOR GASEOUS HYDROGEN
FLUORIDE
National Academy of Sciences-
National Research Council
Washington, D. C.
August 1971
NATIONAL rECHNiCAL INFORMATION SERVICE
Diftribute* ... 'to foster, serve
and promote the nation's
economic development
and technological
advancement.'
U.S. DEPARTMENT OF COMMERCE
This document has been approved for public release and sale.
-------
Guides for Short-Term Exposures of the Public to Air Pollutants
III. Guide for Gaseous Hydrogen Fluoride
by
The Committee on Toxicology
of the
National Academy of Sciences - National Research Council
Washington, D. C.
August 1971
-------
BIBLIOGRAPHIC DATA
SHEET
1. Repon Nol
APTD-0765
3.Jlecipient's Accession No.
4. Title and Subtitle
Guides for Short-Term Exposures of the Public to Air
Pollutants III. Guide for Gaseous Hydrogen Fluoride
5. Report Date
August 1971
7. Author(s)
8. Performing Organization Kept.
No.
9.Petformina Organization Name and Address
The Committee on Toxicology
National Academy of Sciences
National Research Council
2101 Constitution Avenue
Washington, D. C. 20418
10. Project/Task/Work Unit No.
11. Contract /Gram No.
CPA 70-57
12. Sponsoring Organization Name and Address
Environmental Protection Agency
Air Pollution Cpntrol Office
Research Triangle Park, North Carolina 27711
13. Type of Report & Period
Covered
14.
15. Supplementary Notes DISCLAIMER - This report was furnished to the Office of
Air Programs by National Academy of Sciences, National Research Council
2101 Constitution Avenue, Washington, D. C. 20A18 in fulfillment of
16. Abstracts [Contract 70-57
A report is presented which reviews experimental data and histories of
exposure to hydrogen fluoride of humans and experimental animals.
Specifically reviewed are: clinical and pathological effects of UF;
toxicity studies; and instances of apparent HF injury. A discussion is
presented of susceptibility of species to HF poisoning. Short-term
Public Limits (STPL's) and Public Emergency Limits (PEL's) are also
presented.
17. Key Words and Document Analysis. 17a. Descriptors
Air pollution
Exposure
Hydrogen Fluoride
Sensitivity
17b. Identifiers/Open-Ended Terms
Air pollution effects (Humans)
Air pollution effects -(animals)
Short-term Public Limits (STPL's)
Public Emergency Limits (PEL's)
17e. COSATI Field/Group 13B
18. Availability Statement Unlimited
19.. Security Class (This
Report)
UNCLASSIFlEf
20. Security Class (T
Page
- UNCLASSIFIED
ft-
his
21. No. of Pages
16
22. Price
FORM NT1S-30 (10-70)
USCOMM-DC 40329-P7I
-------
Committee on Toxicology
Herbert E. Stokinger, Chairman Verald K. Rowe
Arthur B. DuBois, Vice-Chairman C. Boyd Shaffer
Bertram D. Dinman Frank G. Stahdaert
Seymour L. Friess James H. Sterner
Harold M. Peck Richard D. Stewart
Subcommittee on Hydrogen Fluoride
Arthur B. DuBois, Chairman
M. L. Keplinger
Charles F. Reinhardt
David L. Stoddard
Ralph C. Wands, Director
Advisory Center on Toxicology
National Academy of Sciences-National Research Council
-------
Prepared under Contract No. CPA 70-57 between the
National Academy of Sciences, Advisory Center on
Toxicology and the Air Pollution Control Office of the
Environmental Protection Agency.
Contract Monitor:
Dr. Vaun A.. Newill, Director
Division of Health Effects Research
Air Pollution Control Office
Environmental Protection Agency
Durham, North Carolina
The information contained in this
letter is intended only as guidance
for your professional and technical
staff and contractors. It is not for
publi.c distribution or attribution
to the National Academy of Scienc&s
without prior written approval.
-------
NOTICE
The study reported herein was undertaken under the aegis of the
National Research Council with the express approval of the Governing
Board of the National Research Council. Such approval indicated that
the Board considered that the problem is of national significance; that
elucidation and/or solution of the problem required scientific or
technical competence and that the resources of the National Research
Council were particularly suitable to the conduct of the project. The
institutional responsibilities of the National Research Council were then
discharged in the following manner:
s
The members of the committee were selected for their individual
scholarly competence and judgment with due consideration for the
balance and breadth of disciplines. Responsibility for all aspects of this
report rests with the committee, to whom we express our sincere
appreciation.
Although the reports of our study committees are not submitted
for approval to the Academy membership nor to the Council, each report
is reviewed by a second group of scientists according to procedures
established and monitored by the Academy's Report Review Committee.
Such reviews are intended to determine, inter alia, whether the major
questions and relevant points of view have been addressed and whether
the reported findings, conclusions and recommendations arose from the
available data and information. Distribution of the report is permitted
only after satisfactory completion of this review process.
-------
INTRODUCTION
This is one of a series of documents prepared by the Committee on
Toxicology of the National Academy of Sciences-National Research Council,
with the support of the Advisory Center on Toxicology, at the request of
the Air Pollution Control Office of the Environmental Protection Agency.
A subcommittee was appointed to prepare the document which was then
endorsed by the Committee.
In preparing this document the subcommittee was guided by the
principles set forth in the first document of this series: "Basis for
Establishing Short-Term Inhalation Exposure Limits of the Public to
Atmospheric Pollutants," (1) and the National Academy of Sciences-National
Research Council report, "Fluorides, " (2) now in preparation by the
Committee on Biologic Effects of Atmospheric Pollutants of the Division
of Medical Sciences. The latter document treats the effects of HF on
vegetation and animals, and methods for the analysis for airborne concen-
trations. Therefore, this report gives only minimal attention to the effects
of HF on vegetation and animals and no attention to analytical procedures.
Most of the authoritative work on hydrogen fluoride gas dates from
the mid-1940's, although there are a few significant contributions from
earlier periods. In most of the documents published prior to the late
1960's, mathematical units expressing concentrations vary. For ease of
comparison, all units expressing atmospheric concentration have been
converted to mg/m^, considering HF as a monomolecular compound
where 1 ppm = 0.8184 mg/m . In those few instances where parts by
volume are more appropriate, either ppm or ppb has been used.
Some atmospheric standards for HF already exist. For instance,
occupational levels recommended by the American Conference of Govern-
mental Industrial Hygienists set the threshold limit value (TLV) for an
eight-hour work day at 2 mg/m^ . By application of the ACGIH Permissible
Excursion (Time-weighted) rule, a maximum atmospheric concentration
for HF of 4. 0 mg/m^ is permitted, provided it is compensated by an
equivalent excursion below the limit during the workday. The state of
Pennsylvania has adopted an atmospheric limit for HF of 2 mg/m3 for
15 minutes (3) and the National Academy of Sciences-National Research
Council Committee on Toxicology recommended emergency exposure
limits for HF of 16 mg/m^ for ten minutes, 8 mg/m^ for 30 minutes, and
approximately 7 mg/m^ for 60 minutes applicable only to military and
space operations (4).
Experimental data and histories of exposures are reviewed in this
report and recommendations for short-term exposure limits of the public
are made.
-------
Physical-Chemical Properties
At atmospheric pressure, below 19° C, hydrogen fluoride is a
corrosive, fuming, nearly colorless liquid. Above 19° C it is gaseous.
HF has a monomolecular weight of 20.01, but at 1 atmosphere
pressure and at a temperature below 100° C it exists as an associated
molecule up to H^F^, with an average molecular weight of 50 to 55.
Some authors (5) have considered the possibility that toxicity may be
related to molecular species, but this concept has not been thoroughly
explored.
Hydrogen fluoride gas has a density of 0. 921 g/1 at 0° C and
1 atmosphere of pressure and is very soluble in water. When anhydrous
liquid HF is vaporized into the atmosphere it is an almost colorless gas
cloud that forms a fog upon combination with moisture in air. This fog
is an aerosol of hydrofluoric acid, which is corrosive to almost all
inorganic and organic materials.
Sources of HF
Active volcanoes are the only known natural source of gaseous HF.
Gaseous effluents from fumaroles and volcanoes contribute background
levels of HF throughout the world. This gas has been detected at locations
far removed from man-made sources (6).
Many industrial processes contribute gaseous HF to the atmosphere.
The gas is an effluent of processes such as aluminum reduction, phosphate
fertilizer manufacturing, petroleum refining, manufacture of fluorocarbon
compounds; the making of brick, pottery, glass, and ceramics; ferro-
enamel production, metal fluxing agents used in foundries and metal-
fabricating plants, welding processes, and the burning of coal. Coal may
contain 40 to 295 ppm of fluoride depending on its source, some of which
is released as HF on burning.
In recent years there has been a change in aluminum-reduction
processes, using a synthetic cryolite manufactured using HF, rather
than naturally occurring cryolite. This process, as well as the production
of HF itself, also contributes to atmospheric levels of the gas.
Most of the modern industrial plants whose operations can release
HF to the atmosphere have scrubbers that are reported to be about 95%
-------
efficient, whereas less modern plants are estimated to have control
efficiencies as low as 80%.
Within the past decade another potential source of atmospheric
HF has appeared: this is liquid-fueled rockets employing propellant
oxidizers consisting of mixtures of liquid fluorine and liquid oxygen. In
the event of accidental release of these liquid oxidizers to the atmosphere,
which would almost certainly be attended by fire, the resultant products
would include HF. HF also is a product of normal combustion of the fuel
in these rocket engines.
Increased use of HF for a variety of applications similarly increases
the need to transport the material from place of manufacture to place of
use. Temporary storage facilities at both locations and transfer from
storage containers to other containers are operational requirements. In
each instance there is danger of accidental spills that could result in
exposure of occupational personnel and the public.
Clinical and Pathological effects of HF
The primary effect of acute exposure to gaseous HF in concentra-
tions above a few mg/mr is irritation of the skin, eyes, and respiratory
passages. In addition, localized tissue damage may occur as a result of
the corrosive nature of this compound at concentrations above the
recommended limits.
There are several published accounts of the clinical effects in man
of acute poisoning with gaseous HF. Local irritation of the mucous
membranes of the eyes, nose, throat,and bronchi is reported by
Sollmann (7) and Williams (8). In addition, there may be difficulty in
breathing. An individual exposed to more than 10 mg/m^ will almost
immediately experience a biting or burning sensation in the nose, followed
by a nasal discharge and, occasionally, a nosebleed; burning of the eyes
and lacrimation also occur. Exposure to higher concentrations may lead
to pulmonary edema and respiratory distress with an onset that may be
delayed 12 to 24 hours. This may be accompanied by gastroenteritis,
with nausea, vomiting, abdominal burning, diarrhea, and collapse.
Exposure to lethal concentrations produces muscular weakness and
tremors, clonic convulsions, a drop in blood pressure, and moderate
cyanosis; and death may result from sudden respiratory or cardiac
arrest.
There are but a few reports of pathological findings available from
fatal HF poisonings. According to one report (9) the heart was dilated,
the bronchial tree was acutely inflamed with a partially ulcerated mucosa,
and the lungs were edematous,congested, and severely hemorrhagic.
-------
Additional pathological studies have been done on experimental
animals exposed to either lethal or nonlethal concentrations of HF (10,11,
12). Pulmonary changes, mainly hemorrhage, edema, and congestion,
are consistently seen in acute HF poisoning. The severity of the change
is more or lees proportional to the duration and concentration of exposure
to HF. Lesions can be found in the kidney, liver, and nasal passages.
Also, bone marrow obtained seven days after exposure shows an increased
cellularity, but with a disproportionate increase in myeloid cells.
Toxicity Studies
Several groups of workers have studied the effects of HF gas on
experimental animals. Machle and co-workers (10) conducted time-
concentration studies on rabbits and guinea pigs at concentrations ranging
from 24 to 8000 mg/m^ for periods of five minutes to 41 hours. They
found that exposure for five minutes or longer to concentrations greater
than 1500 mg/m^ may be lethal to rabbits and guinea pigs. Exposure to
1000 mg/m^ for 30 minutes caused changes in the lungs, but no deaths,
in either species of animals. Concentrations below 100 mg/m^ for five
hours produced lung damage, but no deaths, in rabbits or guinea pigs.
The primary tissue damage was manifested by hemorrhage, edema, or
congestion. At concentrations of HF above 2000 mg/m^ areas of the
cornea were eroded, there was necrosis of turbinates, necrosis of
heart muscles, alveolar and interstitial hemorrhage, edema, emphysema,
and, in those that survived several days following exposure, broncho-
pneumonia. Also, in the animals exposed at the higher concentrations, the
liver showed necrosis of the parenchyma and destruction of cytoplasm;
the spleen was edematous and congested and the kidneys showed some
degenerative changes in renal tubules and glomeruli.
In another study (5), designed to bracket maximal and minimal
effects, five species of animals inhaled HF concentrations of 25 mg/m^
or 7 mg/m^ for 166 hours in repeated, daily six-hour exposures for
approximately 30 days. Exposure to the higher concentration was lethal
to 100% of the rats and mice, but not lethal to guinea pigs, rabbits, and
dogs. Among the surviving animals, the rabbits showed a slight loss in
weight, the dogs were apparently unaffected, and the guinea pigs began
to lose weight after the third week of exposure. Exposure to the low
concentration did not interfere with normal weight gains in any of the
animals except the rabbits. Three species, the dog, rabbit, and rat,
were examined for pathological changes following exposure to both con-
centrations of HF. At the 25 mg/m3 level there was moderate hemorrhage
and edema of the lungs in all three species, ulceration of the scrotum in
dogs and renal cortical degeneration and necrosis in the rat. At the
7 mg/m^ level, localized hemorrhages were found in the lungs of one dog
-------
out of five examined, and no changes were observed in the rat or rabbit.
Rosenholtz and co-workers (11) studied rats, rabbits, guinea pigs,
and dogs to make possible a better estimate of the LC5Q (the concentra-
tion calculated to be lethal to 50% of a group of experimental animals)
from single exposures to high concentrations of HF for short periods of
time. The JLC's were as follows:
Species Exposure Time
(minutes) (mg/m3)
Rat 5 4060
Rat 15 2200
Guinea Pig 15 3540
Rat 30 1670
Rat 60 1070
Signs of toxicity in the animals included irritation of the conjunctiva,
nasal tissues, and respiratory system. The survivors ceased to show
these signs about one week after the exposure. Pathological lesions were
observed in the kidney and liver, the severity of which was directly
related to the dosage received. The external nares and nasal vestibules
were black and, at dosages causing considerable mortality, those areas
showed zones of mucosal and submucosal necrosis. The skin of animals
exposed to high (lethal) concentrations showed superficial subcutaneous
and deep dermal zones of acute inflammation. The hair of these animals
could be pulled out with ease and the skin ruptured under minimal tension.
The rat was found to be the most susceptible species of those tested,
which confirmed the findings of Stokinger (5). Additional evaluations were
made at nonlethal concentrations of HF that approximated 50%, 25%, 12. 5%,
and 6% of the rat LC$Q.
Exposure of animals to nonlethal concentrations produced similar
clinical signs that decreased in intensity and duration with decreasing
dosage. At 6% of the rat LC50 level (250 mg/m3 in rats for 15 minutes
and 80 mg/m in rats for 60 minutes), clinical signs decreased to mild
irritation of the eyes and nose. These signs disappeared shortly after
withdrawal from the chamber. Few pathological changes were seen at
sub-lethal concentrations, although the skin was not examined histo-
pathologically. Two rabbits, one exposed at 1020 mg/m^ for 15 minutes,
and one at 700 mg/m^ for 15 minutes, showed pulmonary changes ranging
from intense intra-alveolar septal congestion to frank hemorrhage with a
discrete lobular distribution.
In connection with the animal studies reported by Machle (10), some
observations were made on two humans. After one minute at 100 mg/m ,
there was smarting of the skin, conjunctival and respiratory irritation,
and recognition of the flat sour taste of HF. Exposure at 50 mg/m3 was
-------
exceedingly uncomfortable, as shown by irritation of mucous membranes,
but there was no smarting of the skin. At 26 mg/m^ irritation decreased
and the ability to taste gas was delayed, but the atmosphere was uncomfort-
able throughout the three-minute period of exposure.
Instances of Apparent HF Injury
Even though there are numerous industrial processes that can cause
HF injury to workers and closely associated nonworkers, there are few
records of such injuries. However, there are several well-documented
reports of injuries resulting from accidental exposures to ruptured
containers of anhydrous HF (9).
Although gaseous HF undoubtedly played some role in these accidents,
the major effect is associated with the liquid state. The information does,
however, emphasize the extreme hazard of HF and the clinical develop-
ments encountered. In three separate events, a total of eight men were
splashed with liquid HF. In one event, involving four men, one died of
pulmonary edema approximately two hours after the accident. The other
three survived, but suffered severe chemical burns. In the other two
events, all four men died; two of them in two hours, one in four hours,
and one ten hours after the accident. Consciousness remains until death,
which is usually sudden, from respiratory distress and cardiac arrest.
Characteristically, the respiratory tree is inflamed and the lungs
moderately to severely congested.
There are other reported cases of severe poisonings and deaths
among workers in superphosphate factories, fertilizer factories, among
welders, garage workers, waterworks employees, and enamel-factory
workers (11). In most of these cases the clinical picture in part resembles
HF poisoning, but other fluoride-containing particulates and gases such
as SiF4» phosgene (from the high temperature decomposition of halogenated
hydrocarbons) and a variety of fluoride dusts, also were present.
Species Susceptibility to HF Poisoning
Plants are more susceptible to damage from gaseous HF than are
animals, although among plant species there is a wide variation in
tolerance. Some plants, gladiolus for example, may be severely damaged
by airborne concentrations as low as 3 ng/mr (leading to accumulations
of 20 ppm in plant tissues), whereas camellia can tolerate tissue accumula-
tion to as much as 1500 ppm. There is a complex and poorly understood
relationship between airborne concentrations and levels that accumulate in
plants. Grasses and forage crops vary throughout a wide range in
accumulation and tolerance. HF is absorbed systemically through the
-------
stems and leaves of plants. The absorbed fluorides migrate to the margins
of the leaves where early evidence of damage appears as yellowing or
browning of tissues.
Cattle, sheep, and goats that feed on fluoride-contaminated forage
may sicken and die from chronic fluoride poisoning, fluorosis, a not
uncommon occurrence in areas where effluents containing fluorides affect
grazing lands. Animals with a total dietary intake of fluoride greater than
300 ppm per day are likely to develop fluorosis. A generally accepted
guide (14) for fluoride concentration in animal forage is based on an annual
average of no more than 40 ppm of fluoride by dry weight.
Inhaled HF, even in heavily contaminated areas, contributes so
small a fraction of the total intake by grazing animals that it cannot be
considered an important factor in either chronic or acute systemic
poisoning.
Atmospheric Concentrations of HF
National surveillance programs conducted since the mid-19601 a
reveal atmospheric levels of fluoride ranging from 0. 5 to 1. 89 ug/m^
in urban areas and 0. 05 to 0.16 (ig/m^ in nonurban areas (15).
Huffstutler (16), reporting on fluoride concentrations within a 7-1/2 mile
radius in an area of Florida where a number of fertilizer plants are
operated, found a four-hour sample peak of 100 jj.g fluoride/m^ one year,
and a maximum four-hour sample average of 2. 7 ug fluoride/m^ in
another year. Similarly, he reports a 24-hour sample peak of 68 |ig
fluoride/m^, and a maximum 24-hour sample average of 4. 3 (jig fluoride/m3.
These studies have been carried out over a period of seven years and the
1969 data show a marked decrease both in peak levels and in sample
period averages as a result of improved scrubbing procedures.
As with other gaseous contaminants, the greatest hazard is down-
wind from the effluent stacks. Workers in the immediate environment
of operations involving HF may not be as readily or as heavily exposed
as nonworkers some several hundred yards downwind. Beyond two or
three miles downwind, mixing and dilution with air reduces HF below
detectable or background levels.
Guides for Short-Term and Emergency Exposures of the Public to HF
The basis for setting limits for short-term exposure of the public
and for emergency exposure of the public to air pollutants is detailed in
the first document of this series, "Basis for Establishing Guides for
Short-Term Exposures of the Public to Air Pollutants" (1)
-------
Experimental data and occupational experience indicate that man
is susceptible to irritation and possible injury from gaseous HF. At
10 mg/m3 the mucosa are irritated; at 26 mg/m3 for three minutes he
is uncomfortable and able to taste the gas; at 50 mg/m3 the severity of
the irritation increases; and at 100 mg/m3 a stinging sensation of the
skin is added and other irritations are so severe as to make exposure
for more than one minute intolerable. Since the primary irritant action
of HF is on the mucosa, particularly the respiratory mucosa, it is
important to recognize the more sensitive segments of the population,
e.g. , the asthmatics and bronchitics, as the limiting factors.
The following recommendations are time-weighted averages, which
are considered not to present any health hazard. It should be recognized,
however, that excursions above these averages are likely to produce
objectionable odors and, possibly, minimal irritation.
Short-Term Public Limits (STPL's)
The limits for short-term exposure of the public to air pollutants
are established in view of the possibility of repeated events in the same
locality. These events, such as intentional release of HF to the atmosphere,
are assumed to be controllable with respect to concentration and duration
of release so that the limit is not exceeded. No adverse health effects,
however transient, are anticipated at the limits set forth below:
STPL's
10-30 and 60 min 3 mg/m3 (4 ppm) (frequency
limit 1 hr daily)
5 hr/day, 3-4 days/mo 1 mg/m3 (1 ppm)
Public Emergency Limits (PEL's)
Public emergency limits represent values necessary to cope with
an accidental, unpredictable, or uncontrollable event. The PEL assumes
that some temporary discomfort may accrue to the public but that any
effect resulting from the exposure is reversible and without residual
damage.
PEL's
10 min 8 mg/m3 (10 ppm)
30 min and 4 mg/m3 ( 5 ppm)
60 min
-------
Research Needs
The data from industrial experience and laboratory experimenta-
tion are insufficient to permit a relaxation in efforts to determine the
toxic hazards of atmospheric hydrogen fluoride. It is hoped that this
guide will serve as a stimulus for occupational health authorities and
researchers to investigate further the effects of HF on the health and
welfare of the public and on the environment so that greater confidence
can be placed in the recommended limits.
-------
REFERENCES
1. National Academy of Sciences-National Research Council Report to
the Air Pollution Control Office, Environmental Protection
Agency, Basis for Establishing Short-Term Inhalation Exposure
Limits of the Public to Atmospheric Pollutants. 1 971.
2. National Academy of Sciences-National Research Council Report.
Fluorides. In press.
3. Pennsylvania Department of Health, Division of Occupational Health.
Short-Term Limits for Exposure to Airborne Contaminants. A
Documentation. 1967-1969.
4. National Academy of Sciences-National Research Council, Basis for
Establishing Emergency Inhalation Exposure Limits Applicable
to Military and Space Chemicals. 1964.
5. Stokinger, Herbert E. "Toxicity following inhalation of fluorine and
hydrogen fluoride. " IN Pharmacology and Toxicology of Uranium
Compounds, edited by Carl Voegtlin and Harold C. Hodge.
New York, McGraw-Hill. 1949. p. 1021-1057.
6. MacDonald, H. E. Fluoride as air pollutant. Fluoride Qtly. Repts.
(Internatl Soc. for Fluoride Res. ) 2:4-12 Jan 1969.
7. Sollmann, To raid. A Manual of Pharmacology and its Applications
to Therapeutics and Toxicology. 8th ed. Philadelphia, Saunders.
1957. p. 1104.
8. Williams, Charles R. "Atmospheric contamination from the casting
of magnesium. " J. Ind. Hyg. Toxicol. 24:277-280 Nov 1942.
9. Eagers, R. Y. Toxic Properties of Inorganic Fluorire Compounds.
New York, Elsevier. 1969. 152 p.
10. Machle, Willard, Frederick Thamann, Karl Kitzmiller, and Jacob
Cholak. "The effects of the inhalation of hydrogen fluoride. I.
The response following exposure to high concentrations. "
J. Ind. Hyg. 16:129-145 March 1934.
11. Rosenholtz, Mitchell J. , Theophilus R. Carson, Maurice H. Weeks,
Frank Wilinski, Duane F. Ford, and Fred W. Oberst.
"A Toxicopathologic study in animals after brief single exposures
to hydrogen fluoride. " Am. Ind. Hyg. Assoc. J. 24:253-261 May-
June 1963.
-------
12. Keplinger, M. L. Report of toxic effects of fluorine following
short-term inhalation. NASA contract NCR 10-007-012. Rept.
No. NASA-CR-100415. Dec 31, 1968. 273 p.
13. Krechniak, J. Fluoride hazards among welders. Fluoride Qtly.
Rcpts. (Internatl. Soc. for Fluoride Res.) 2:13-24 Jan. 1969.
14. Suttie, J. W. "Air quality standards for the protection of farm
animals from fluorides." Air Pollution Control Assoc., J.
19:239-242 April 1969.
15. U.S. Department of Health, Education, and Welfare. Public Health
Service. Robert A. Taft Sanitary Engineering Center, Cincinnati,
Ohio. Air pollution measurements of the National Air Sampling
Network Analysis of suspended particulate samples collected
1953-1957. Public Health Service Publication No. 637. 1958.
16. Huffstutler, K. K. "Fluoride concentrations in various receptors
near phosphate industries." Paper presented at the 63rd Annual
Meeting of the Air Pollution Control Association, St. Louis,
Mo. , June 14-18, 1970.
------- |