PB-203 464
GUIDES FOR SHORT-TERM EXPOSURES OF THE PUBLIC
TO AIR POLLUTANTS. II. GUIDE FOR HYDROGEN
CHLORIDE
National Academy of Sciences-National
Research Council
Washington , D . C .
August 1971
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Guides for Short-Term Exposures of the Public to Air Pollutants
II. Guide for Hydrogen Chloride
by
The Committee on Toxicology
of the
National Academy of Sciences-National Research Council
Washington, D. C.
August 1971
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BIBLIOGRAPHIC DATA 1- Report No. 2.
SHEET APTD-0764
4. Title and Subtitle . '
Guides for ShortyTerm Exposures of the Public to Air
Pollutants II. Guide for Hydrogen Chloride
'. Author(s)
'. Performing Organization Name and Address
The Committee on Toxicology
National Academy of Sciences
National Research Council
2101 Constitution Avenue
Washington, D. C. 20418
12. Sponsoring Organization Name and Address
Environmental Protection Agency
Air Pollution Control Office
Research Triangle Park, North Carolina 27711
3. Recipient's Accession No.
5. Report Date
AuBUSt 1971
6.
8. Performing Organization Re-«.
No.
10. Project/Task/Work Unit
No.
11. Contract/Grant No.
CPA 70-57
13. Type of Report i: 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. 20418 in fulfillment of CPA
16. Abstracts I 70-5 /
Upon recognition of the fact that occasional peak additions of pollutants
to the ambient exposures of the public do occur, work was begun on the
preparation of these guides. Primary consideration was given to
literature dealing with single or intermittent brief exposures to hydro-
gen chloride or hydrochloric acid. The guides present threshold levels of
exposure and the corresponding responses or effects on: Animals; Man;
Vegetation; and Materials. The guide also presents; Short Term Public
Limits (STPL's) and Public Emergency Limits (PEL.'s). Analytical methods
for the measurement of hydrogen chloride are also included.
17. Key Words and Document Analysis. 17a. Descriptors
Air pollution
Exposure
Hydrogen chloride
Sensitivity
Toxicology
17b. Identifiers/Open-Ended Terms
Air pollution effects
Air pollution effects
Air pollution effects
Air pollution effects
I7e. COSATI Field/Group 13B
(Animals)
(Humans)
(Plants)
(Materials)
Short-term Public Limits (STPL's)
Public Emergency Limits (PEL's)
18. Availability Statement Un llmi te d
19..Security Class (This
Report)
UN'CLASSIFIF.D
20. Security Class (This
Page
"UNCLASSIFIED
21. No. of Pa.:es
16
22. P:ice
FORM NTIS-33 110-70)
USCOMM-OC «:.'.: ;• = ••
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Committee on Toxicology
Herbert E. Stokinger, Chairman Verald K. Rowe
Arthur B. DuBoie, Vice-Chairman C. Boyd Shaffer
Bertram D. Dinman Frank G. Standaert
Seymour L,. Friess James H. Sterner
Harold M. Peck Richard D. Stewart
Subcommittee on Hydrogen Chloride
Verald K. Rowe, Chairman
Kenneth Back
David Fas sett
Ralph C. Wands, Director
Advisory Center on Toxicology
National Academy of Sciences-National Research Council
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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 an-"! t.^ohnlcal
staff and contractors. It is not for
public distribution or atti'ibution
to the National Academy of Sciences
without prior written approval.
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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:
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.
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INTRODUCTION
The Air Pollution Control Office of the Environmental Protection
Agency has focused its initial concerns on long-term exposures of the
public to air pollutants. In addition to the long-term levels there are
occasional circumstances wherein the public may be exposed briefly to
relatively high concentrations. For example, batch process techniques in
industries may result in pulses of effluent. The testing and launching of
rockets releases exhaust products. Rapidly changing meteorological
conditions may result in short periods of locally high concentration of
stack effluents. Accidental releases of chemicals sometimes occur in
industrial areas or during transport, and may lead to exposure of the
public.
Recognizing that these occasional peak additions to the ambient
exposures of the public do occur, the Air Pollution Control Office has
requested the assistance of the Committee on Toxicology of the National
Academy of Sciences-National Research Council in providing Guides for
Short-Term Exposure Limits for Air Pollutants.
In preparing these guides, the Committee utilized the criteria
described in the National Academy of Sciences-National Research Council
document entitled "Basis for Establishing Short-Term Inhalation Exposure
Limits of the Public to Atmospheric Pollutants"(30). Primary considera-
tion was given to literature dealing with single or intermittent brief
exposures to the contaminant in question, in this case hydrogen chloride
or hydrochloric acid.
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Hydrogen Chloride
Hydrogen chloride (HC1) is a colorless hygroscopic gas with a
molecular weight of 36. 5 and a boiling point of -84. 9° C. Because of its
high solubility in water (82. 3g/100 cc cold water), hydrogen chloride
readily forms aqueous hydrochloric acid. Under normal atmospheric
conditions HC1 will exist as an aqueous acid aerosol; conditions of
unusually low relative humidity may allow for the existence of anhydrous
hydrogen chloride. The toxic effects of high concentrations of this
anhydrous form may be more severe than those of the aqueous form
because of the dehydrating action of the gas on exposed tissues (1).
At 25° C and 760mm Hg 1. 49 mg HCl/m3 of air is equivalent to
1 ppm.
Effects on Animals
At sufficiently high concentrations, HC1 acts as a primary irritant,
especially to the eyes and the moist mucous membranes of the respira-
tory tract. Effects of various concentrations of HC1 on rabbits, cats, and
guinea pigs were reported by Flury and Zernick (2) in 1931 (Table I).
Machle Łt_aJU (3) generated hydrogen chloride gas by mixing
aqueous HC1 with concentrated sulfuric acid and exposed rabbits, guinea
pigs, and one monkey to various concentrations for various time intervals.
Their observations are summarized in Table II.
Cralley (4) examined the effects of hydrogen chloride on mucociliary
activity of sections of excised rabbit trachea. The hydrogen chloride was
generated by mixing sodium chloride and sulfuric acid. The excised
tracheal tissue was maintained in a constant temperature-humidity
chamber and observed microscopically. Ciliary activity in the excised
tissue ceased, without recovery, upon exposure to hydrogen chloride
at 90 mg/m3 (60 ppm) for five minutes or 45 mg/m3 (30 ppm) for ten
minutes. Concentrations of 45 mg/m^ (30 ppm) to 600 mg/m^ (400 ppm)
for time intervals of 3. 2 minutes to 0. 5 minutes respectively caused
reversible ciliary inhibition.
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Table I
Species
Effects of HC1 Reported by Flury (2)
Concentration Time
Effects
Cats, Rabbits
Rabbits, guinea pigs
Rabbits, guinea pigs
Rabbits, guinea pigs
100-140 ppm
300
1350
3400
up to 6 hr
6 hr
75 min
90 min
Runny nose and
salivation. No
sequelae
Catarrh and
cloudy cornea
Strong respira-
tory irritation
and distress.
Corneal opacity.
Fatalities 2-6
days post-exposure
Table II
Hydrogen Chloride Toxicity by Machle (3)
Rabbits,
Rabbits,
Rabbits,
Rabbits,
Rabbits,
and one
guinea pigs 4300 ppm
guinea pigs 700 ppm
guinea pigs 3700 ppm
guinea pigs 70 ppm
guinea pigs 30 ppm
monkey
30 min
6 hr
5 min
5 days, 6 hr
each
6 hr/day
5 days/wk
4 weeks
100% fatal
100% fatal
No deaths
No effects
No effects
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Effects on Man
Hydrogen chloride and hydrochloric acid act as contact irritants.
Severity depends on the intensity of exposure and on the tissue involved.
The epithelium and mucous membranes of the respiratory tract and the
conjunct!vae of the eyes are the most sensitive sites of action because
the irritants are readily absorbed by these moist tissues (5,6).
Inhalation of 1500 mg/m3 (1000 ppm) is dangerous within one hour
(1,5). Although concentrations between 75 and 150 mg/m3 .(50 and 100
ppm) have been reported to be tolerable for periods up to one hour (1),
Heyroth (7) states that normal work is impossible at concentrations in
this range.
Acute Response to HC1
Depending on the severity of exposure, the physiological responses
to the inhalation of irritating levels of HC1 are: coughing, pain, inflamma-
tion, edema, and desquamation in the upper respiratory tract, i. e. , the
nasal passages and larynx. If concentrations are high enough, acute irri-
tation may bring about constriction of the larynx and bronchi, closure of
the glottis and breath holding.
Fatal inhalation ot HC1 would be expected only when the victim is
unable to escape from the contaminated atmosphere.
Response to Repeated HC1 Exposure
ten Bruggen Gate (8) has reported an increased incidence of dental
erosion in workers employed in industries that use large quantities of
various acids including HC1. Although he does not report the levels of acid
mist in the work environment, he states that increased ventilation and
other control methods reduced the incidence of erosion below that observed
in poorly controlled work areas.
Bleeding of the nose and gums, and ulceration of the mucous
membranes, have also been attributed to repeated occupational exposure
to high levels of HC1 mist (9,10).
Thresholds of Effects
Although Leonardos _et al^ (11) reported the odor threshold for HC1
to be 15 mg/m (10 ppm), lower values have been reported by a number of
others. Patty (13) states that "most people can detect 1. 5-7 mg/m3
(1-5 ppm); 7-15 mg/m3 (5-10 ppm) is disagreeable. " Elkins (14) reports
all concentrations above 15 mg/m3 (10 ppm) to be irritating, although he
mentions that workers develop some apparent tolerance.
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Melekhina (12), using a. test panel of 16 volunteers between the ages
of 17-36, reports an odor threshold for HC1 of 0. 39 mg/m3 (0. 26 ppm).
In contrast to the method employed by Leonardos _e_t aL (11), who con-
sidered the "odor threshold" to be the minimum concentration detectable
by all the test panel members, Melekhina considered the "threshold" to
be the minimum concentration detected by the most sensitive volunteer.
Effects on Vegetation
Hydrogen chloride has been reported to be of only minor concern as
a phytotoxic air pollutants. Heck et_al. (15), in a review of the literature,
indicate that field observations of HC1 injury to plants in the United States
have been few.
In comparison to some of the other phytotoxic air pollutants, HC1
has a relatively low order of hazard to plants. The threshold of injury for
HC1 is apparently 7-15 mg/m3 (5-10 ppm) if continued for a few hours.
Levels of 0. 06 mg/m3 ( 0. 03 ppm) ozone for four hours, 0. 07 mg/m3
(0. 1 ppm) hydrogen fluoride for two hours, and 0.06 mg/m3 (0.05 ppm)
ethylene for six hours are the injury thresholds for certain other phytotoxic
air pollutants (18).
Viburnum and larch seedlings were killed in less than two days by
exposure to HC1 at 7-30 mg/m3 (5-20 ppm). Local lesions were observed
on fir, beech, and oak after exposure for one hour to 1500 mg/m3
(1000 ppm) HC1. Exposure of maple, birch, and pear trees for 1 hr/day
for 80 days to 3000 mg/m3 (2000 ppm) produced necrosis along the leaf
margins (15).
Shriner and Lacasse (in 15) exposed 28-day-old tomato plants to HC1
for two hours at 7 mg/m3 (5 ppm) and observed leaf necrosis within 72
hours of the exposure.
Damage to maple, cherry, redbud, rose, and begonia foliage, due
to HC1 and Cl2 emissions from a glass-manufacturing plant, has been
reported by Hindawi (16). Stack emissions from the plant averaged
490 mg/m3 (329 ppm) HC1 and 2.1 mg/m3 (0. 73 ppm) C12. No air samples
were taken at the site(s) of vegetation injury. High chloride levels were
found in both injured and uninjured plants, so that no correlation between
chloride levels and degree of injury could be made. The author concludes
that chemical analysis of plant tissue is unsuitable for diagnosing chloride
injury resulting from air pollution. In this regard Bohne (17) discusses
some of the difficulties of determining the effects of HC1 emissions on
plants, e.g. , (a) normal chlorine content of leaves differs greatly among
species and within populations of the same species; (b) the high solubility
of chlorine compounds allows for the "washout" of the chloride by precipi-
tation or removal via the sap flow.
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Guide Values for Short-Term Limits
Short-term public exposures are those occurring at predictable
times and arising from single or, occasionally, repeated events. Where
exposure can be predicted there is no justification for submitting the
public to any appreciable risk (30).
Experimental data as well as data collected from occupational situa-
tions indicate that the chief effect of HC1 upon those exposed is primary
irritation, mostly of the moist mucous membranes of the upper respiratory
tract.
It has been reported in the United States that the odor threshold for
HC1 is between 1. 5 and 15 mg/m3 (1-10 ppm), and that concentrations
greater than 8-15 mg/m^ (5-10 ppm) are disagreeable or irritating. Pre-
vention of odor becomes a significant factor for longer exposures.
It is desirable to keep the short-term public limits below the level
of irritation that may lead to singificant discomfort.
Short-Term Public Limits (STPL's)
10 min 6 mg/m3 (4 ppm)
30 min 3 mg/m^ (2 ppm)
60 min 3 mg/m3 (2 ppm)
1 hr daily 3 mg/m3 (2 ppm)
5 hr/day, 3-4 days/mo 1 mg/m^ (0. 7 ppm)
These levels are time-weighted averages not considered to present
any health hazard. It should be recognized that excursions above these
levels are likely to produce objectionable odors and/or irritation.
Public Emergency Limits (PEL1 s)
Emergency exposure limits for the public situations in which
pollutants escape in an uncontrolled manner at unpredicted times and
places as the result of accidents such as damage to transportation equip-
ment or fire in a chemical storage facility. Although, under optimum
conditions, the STPL's require that there be no adverse health effects,
the PEL's recognize the possibility of some temporary discomfort,
provided, of course, that the effect is reversible and that no serious
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sequelae result from it. For this reason the following PEL's are
recommended. It is felt that the impact maybe no more than strong
odor or, at the most, slight irritation of the mucous membranes.
10 min 10 mg/m3 (7 ppm)
30 min 5 mg/m3 (3 ppm)
60 min 5 mg/m3 (3 ppm)
The preceding limits are proposed as tentative values, with the
recommendation that appropriate research (perhaps such as that
described in reference 22) be done in order to determine the effects of
HC1 inhalation on those persons having preexisting pulmonary disease.
Effects on Materials
Although it is generally accepted that hydrochloric acid is corro-
sive to most metals (21), there is little information in the literature
dealing with the corrosive effects of HC1 at such levels as might be found
in the general environment over the time periods considered in this
document. Long-term effects of HC1 on materials have been studied by
Barton and Bartonova (19), and Hama and Curley (20).
Analytical Methods
HC1 can be collected by passing contaminated air through either
water or alkaline solution. While several methods are available for
analysis of HC1 or the chloride ion, no single method is free from inter-
ference by other contaminants that might be present in the air.
In the absence of other acids in the air, HC1 levels can be deter-
mined by collecting it in a known quantity of alkali solution and titrating
the excess alkali (23). However, serious errors can occur at low levels
of HC1 if there are also relatively high concentrations of carbon dioxide
*>*
Most experimental studies examining the effects of HC1 inhalation have
been done on healthy animals and observations on humans have involved
normal workers. Carefully controlled experimental work on human
volunteers having preexisting pulmonary disease is necessary to determine
if such persons are actually more susceptible to the effects of HC1.
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in the atmosphere. By collecting the HC1 in a 1:1 mixture of glycerol and
water, those errors can be avoided. A small amount of silicone antifoamer
will prevent foaming of the solution during sampling (24).
Elkins (25) describes two methods for the analysis of HC1 in air:
1) The HC1 is collected in 0. 005 N NaOH, acidified with acetic acid and
titrated with 0. 01N AgNO3, using chromate indicator (10%
2) the HC1 is collected in 0. 005 N NaOH and acidified with 2 N
(without shaking) 1 ml of 0.1 N AgNC>3 is added, and after 30 minutes the
transmission of light through the solution is measured on a photometer -
sensitivity to 1 ppm (1. 5 mg/m^) is reported for this method. Jacobs (26)
describes several methods of analysis for HC1 and chlorides, one of
which (Volhard Method) is based on the reaction of thiocyanate with
excess ferric ions to form a pink or red color that can be measured
spectrophotometrically or organoleptically. A modification of this method
involves the reaction of mercury thiocyanate. In this case the chloride
ion releases thiocyanate, which reacts with ferric ions, forming the red
complex, hexacyanatoferrate (27, 29).
A direct method for measuring chloride ions in solution utilizes a
chloride ion electrode. As in the case of glass pH electrodes, the chloride
ion electrode measures electrical potential across a layer of water-
immiscible ion exchanger held in place by an inert porous membrane.
The chloride ion electrode can be used for either individual determina-
tions or continuous monitoring. A sensitivity down to 0. 35 ppm (10-5ji)
is reported (28).
The potential interference from other contaminants in any air
sample may make it necessary to employ more than one method of
analysis for the determination of HC1. The determination of HC1 in the
presence of chlorine is described in detail in reference 31.
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References
1. Henderson, Y. and Haggard, H. W. Noxious Gases. 2nd ed. , New
York. Reinhold. 1943.(p. 126-127).
2. Flury, F. and Zernick, F. Schadliche Gttse. Berlin. Verlag von
Julius Springer. 1931. (p. 126).
3. Machle, W. , Kitzmiller, K. V. , Scott, E. W. and Treon, J. F.
The effect of the inhalation of hydrogen chloride. J. Ind. Hyg.
Toxicol. 24:222-228, 1942.
4. Cralley, L. V. The effect of irritant gases upon the rate of ciliary
activity. J. Ind. Hyg. Toxicol. 24:193-198, 1942.
5. Elkins, H. B. The Chemistry jjf Industrial Toxicology, New York,
Wiley. 1959. (p. 8-9).
6. Haggard, H. W. Action of irritant gases upon the respiratory tract.
J. Ind. Hyg. 5:390-398, 1923-4.
7. Heyroth, F. F. "Halogens". IN F. A. Patty, ed. Industrial Hygiene
and Toxicology. Vol. II. 2nd ed. , New York. Interscience. 1963.
(p. 831-857).
8. ten Bruggen Gate, H. J. Dental erosion in industry. Brit. J. Ind.
Med. 25:249-266, 1968.
9. Heyroth, F. F. op. cit.
10. Schwartz, L. , Tulipan, L. and Birmingham, D. J. Occupational
Diseases of the Skin. 3rd. ed. Philadelphia. Lea and Febiger. 1957.
11. Leonardos, G., Kendall, D. and Barnard, N. J. Odor threshold
determination of 53 odorant chemicals. Presented at the 61st
Annual Meeting of the Air Pollution Control Association, St. Paul,
Minn., June 23-27, 1968.
12. Melekhina, V. P. The problem of combined action of three mineral
acids. IN: Levine, B.S. U.S. S. R. Literature on Air Pollution and
Related Occupational Diseases. 16:76-81 [n.d.]
13. Heyroth, F. F. op. cit.
14. Elkins, H.B. op. cit.
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15. Heck, W. W. , Daines, R. H. , and Hindawi, I. J. Other phytotoxic
pollutants. IN: J. S. Jacobson and A. C. Hill (eds.), Recognition
of Air Pollution Injury to Vegetation; A Pictorial Atlas. TR-7
Agricultural Committee Informative Report No. 1. Air Pollution
Association. Pittsburgh, 1970.
16. Hindawi, I. J. Injury by sulfur dioxide, hydrogen fluoride and
chlorine as observed and reflected on vegetation in the field.
Air Pollution Control Assoc. , J. 18:307-312 May 1968.
17. Bohne, H. Problems of determining the effect of gaseous chlorine
emissions upon plants. Staub. 29:41-42, Sept. 1969.
18. Hindawi, I. J. Air Pollution Injury to Vegetation. National Air
Pollution Control Administration Publ. No. AP-71. 1970.
19. Barton, K. and Bartonova, S. Mechanism of Fe", Zn~ and Cu~
corrosion in humid atmospheres containing HC1 vapors. Collection
Czechoslovak Chemical Communications, 32:2431-38 1967.
20. Hama, G. M. and Curley, L. C. Corrosion of combustion equipment
by chlorinated hydrocarbon vapors. Air Engineering, p. 38-42
April 1965.
21. Hydrochloric Acid, Aqueous and Hydrogen Chloride, Anhydrous.
Manufacturing Chemists Association Chemical Safety Data Sheet
SD-39. 1970.
22. von Nieding, G. , Wagner, M. , Kreckeler, H. , Smidt, U. , and
Muysers,K. Absorption of NG"2 on low concentrations in the
respiratory tract and its acute effects on lung function and circu-
lation. Presented at the Second International Clean Air Congress,
December 6-11, 1970, Washington, D. C.
23. Heyroth, F. F. op. cit. p. 850.
24. Miller, F. , Scherberger, R. , Brockmyre, H. and Fassett, D. W.
Determination of acetic acid in air. Am. Ind. Hyg. Assoc. Quart.
17:221-224, 1956.
25. Elkins, H. B. op. cit. pp. 343-345.
26. Jacobs, M. B. The Analytical Chemistry of Industrial Poisons,Hazards,
and Solvents. 22nd ed. N. Y. Interscience Publs. 1949. (pp. 378-382).
27. Thompson, R. J. (Acting Chief, Laboratory Services Section,
Division of Air Quality and Emission Data, APCO, Cincinnati,
Ohio. ) Personal communication.
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28. Orion Research Laboratories. Cambridge, Mass. Data Sheet:
Model 92-17 (Liquid Ion Exchange). Chloride Ion Activity
Electrode. 1967.
29. Iwasaki, I., Utsumi, S. , Hagion, K., and Ozawa, T. A new
spectrophotometric method for the determination of email amounts
of chloride using the mercuric thiocyanate method. Bull. Chem.
Soc. Japan 29:860-864 Nov 1956.
30. National Academy of Sciences-National Research Council,
Committee on Toxicology. Basis for establishing guides for
short-term exposure of the public to a;r pollutants. May 1971.
31. Atmospheric Emissions From Hydrochloric Acid Manufacturing
Process. Cooperative Study Project Manufacturing Chemists
Association, Inc. and Public Health Service. National Air
Pollution Control Administration. Durham, No»-'.h Carolina.
NAPCA Publication No. AP-54, September 1^9. (pp. 34-42)
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