Fluoridi U Amb Canada

NATIONAL AMBIENT AIR QUALITY OBJECTIVES FOR
HYDROGEN FLUORIDE (HF)
SCIENCE ASSESSMENT DOCUMENT
A Report by the CEPA/FPAC Working Group on

Air Quality Objectives and Guidelines
ACKNOWLEDGEMENTS
This report is published under section 8 of the Canadian Environmental Protection Act (CEPA).
Any inquiries concerning this publication or requests for copies should be directed to either of
the following officials:
Director
Science Assessment and
Policy Integration Division
Atmospheric Environment Service
Environment Canada
4905 Dufferin Street
Toronto, Ontario M3H 5T4
Director
Bureau of Chemical Hazards
Environmental Health Centre
Health Canada
Tunney's Pasture
Ottawa, Ontario K1A 0L2
This report has been prepared by the following people:

M. Bourgeau, Health Canada, Environmental Health Directorate
D. Clapin, Health Canada, Environmental Health Directorate
K. Foster, Alberta Environmental Protection, Environmental Assessment Division
R. Jones, Ontario Ministry of Environment and Energy, Phytotoxicology Section
M. Prior, Alberta Ministry of Health, Environmental Health Services Branch
M. Shepherd, Environment Canada, Atmospheric Environment Service
P. Walsh, Quebec Environment
Final technical editing and desktop publishing by Astroff Corkum Ross Associates Inc.
July 1996
ISBN 0-662-25641-7
Catalogue En42-17/6-1997E
TABLE OF CONTENTS
FIGURES AND TABLES ............................................................................................................iii
PREFACE .................................................................................................................................. v
1 INTRODUCTION...................................................................................................................1
2 RECOMMENDED REFERENCE LEVELS FOR HYDROGEN FLUORIDE ...........................3

2.1 Rationale for the Reference Levels for Gaseous Hydrogen Fluoride (HF).....................4
2.2 Summary of Animal Effects, and the Rationale for Limiting Fluoride Accumulation
in Forage .......................................................................................................................6
2.3 Summary of Human Health Effects ...............................................................................7
3 BACKGROUND ....................................................................................................................9
3.1 Physical and Chemical Characteristics of Hydrogen Fluoride........................................9
3.2 Sources .........................................................................................................................9
3.3 Monitoring Methodologies............................................................................................10
3.4 Environmental Levels in Canada .................................................................................14
3.5 Ambient Air Objectives and Standards in Other Jurisdictions ......................................14
4 EFFECTS ON VEGETATION .............................................................................................19
4.1 Effects of Fluorides on Vegetation...............................................................................19
4.2 Fluoride Accumulation in Vegetation ...........................................................................21
4.3 Canadian Case Studies ...............................................................................................24
4.3.1 Phosphorus Reduction Long Harbour, Newfoundland ......................................24
4.3.2 Phosphorus Fertilizer Production Port Maitland, Ontario...................................26
4.3.3 Aluminum Reduction Cornwall Island, Ontario ..................................................26
4.3.4 Aluminum Reduction Arvida, Quebec................................................................27
4.3.5 Aluminum Manufacturing Kitimat, British Columbia ...........................................28
4.3.6 Aluminum Engine Casting Windsor, Ontario .....................................................28
4.3.7 Uranium Processing Port Hope, Ontario ...........................................................28
4.3.8 Tile Manufacturing Niagara, Ontario..................................................................29
4.3.9 Brick Manufacturing Southern Ontario ..............................................................29
4.3.10 ........................................................... Fibreglass Manufacturing Guelph, Ontario 29
4.3.11 ........................................................................ Oil Refining Mississauga, Ontario 30
4.4 Interactive Effects of HF with Other Gaseous Pollutants .............................................30
Science Assessment Document for HF i CEPA/FPAC WGAQOG July 1996

5 EFFECTS ON LIVESTOCK AND WILDLIFE ......................................................................33
5.1 Pharmacokinetics ........................................................................................................33
5.2 Pharmacodynamics .....................................................................................................34
5.2.1 Acute Toxicity ....................................................................................................34
5.2.2 Chronic Toxicity .................................................................................................35
5.2.3 Developmental Toxicity, Reproductive Effects and Carcinogenesis..................35
5.2.4 Fluorides............................................................................................................35
5.3 Conclusion ...................................................................................................................37
6 EFFECTS ON EXPERIMENTAL ANIMALS ........................................................................39
6.1 Acute Toxicity ..............................................................................................................39
6.2 Short-term Toxicity.......................................................................................................41
6.3 Long-term Toxicity and Carcinogenicity Studies ..........................................................43
6.4 Reproductive Toxicity, Teratology and Genotoxicity Studies .......................................45
6.5 Conclusion ...................................................................................................................45
7 EFFECTS ON HUMAN HEALTH ........................................................................................47
7.1 Pharmacokinetics ........................................................................................................47
7.1.1 Absorption .........................................................................................................47
7.1.2 Distribution ........................................................................................................48
7.1.3 Excretion ...........................................................................................................50
7.1.4 Monitoring Exposure to Gaseous Fluoride by Pharmacokinetic Parameters .....52
7.2 Pharmacodynamics .....................................................................................................53
7.3 Effects in Humans .......................................................................................................56
7.3.1 Acute and Short-term Health Effects.................................................................56
7.3.2 Chronic Health Effects.......................................................................................58
7.4 Summary of Health Effects of Inorganic Fluorides as Reported by CEPA...................68
7.5 Human Exposure Assessment.....................................................................................70
7.6 Summary and Conclusion............................................................................................72
8 REFERENCES ...................................................................................................................75
8.1 Comprehensive Surveys..............................................................................................75
8.2 Literature Cited ............................................................................................................75
Appendix HF Reference Dose Database ................................................................................97
Science Assessment Document for HF ii CEPA/FPAC WGAQOG July 1996

FIGURES
Fig. 1 Regression analysis of HF-exposure data......................................................................5
Fig. 2 Average monthly ambient HF concentration.................................................................16
Fig. 3 HF fluoridation rate monthly averages for Ontario, 1991–92........................................17
TABLES
Table 1 Reference levels for HF in ambient air, and maximum level of accumulated fluoride
in vegetation .................................................................................................................3
Table 2 Estimates of HF air emissions ....................................................................................10
Table 3 Capacity of Canadian aluminum producers, 1992......................................................11
Table 4 Locations of coal-burning electricity generating utilities in Canada ............................12
Table 5 Ambient HF concentration ranges at selected Canadian sites, 1980–91 ...................15
Table 6 Ambient air quality standards and objectives for gaseous fluorides (µg m-3),
and fluoride levels in vegetation (µg g-1 DW), in other jurisdictions ............................18
Table 7 Susceptibility of animals to fluoride by ingestion ........................................................37
Table 8 Estimates of NOAEL and LOAEL for mice and rats ...................................................37
Table 9 Estimated upper bound of daily intake of gaseous fluorides ......................................71
Science Assessment Document for HF iii CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF iv CEPA/FPAC WGAQOG July 1996
PREFACE
The Canadian Environmental Protection Act responses by the population, the
(CEPA), passed into law in 1988, replaces ecosystems, and organisms in the
and builds upon the Clean Air Act and the environments are considered. However,
Environmental Contaminants Act. The given the range of these sensitivities, the
opening statement of the Act declares that resulting objectives may not protect
"the protection of the environment is everyone. A document outlining the process
essential to the well-being of Canada." followed in reviewing and interpreting
CEPA allows the federal government to scientific information leading to the
assess substances and control their impact recommendation of objectives is published
through national environmental quality separately.1
objectives, guidelines, codes of practice,
The levels recommended as a result of this
and/or regulations.
process accommodate two tiers, defined as
Provincial governments have the primary follows:
responsibility in many areas of air pollution
• The Reference Level is a level above
control, with federal actions integrated with
which there are demonstrated effects on
those of the provinces. The CEPA
human health and/or the environment. It
Federal/Provincial Working Group on Air
provides a scientific basis for establishing
Quality Objectives and Guidelines, consisting
goals for air quality management.
of representatives of federal, provincial and
territorial departments of environment and • The Air Quality Objective represents the
health, reviews and recommends ambient air air quality management goal for the
quality objectives. protection of the general public and the
environment in Canada. It is a level based
Canada's National Ambient Air Quality
upon consideration of scientific, social,
Objectives prescribe targets for air quality,
economic and technological factors.
measured at the relevant receptor (persons,
plants, animals, materials). Development of The process of establishing air quality
objectives follows a process which integrates objectives is a dynamic and continuous one.
the review of physical and chemical This document recommends Reference
properties and sources; environmental, Level(s) for hydrogen fluoride.
animal and human health effects; The air quality objectives are established to
environmental and human exposure provide the current state of knowledge about
assessment within a framework of risk an air-quality parameter, a uniform scale for
assessment. These targets may incorporate assessing the quality of air in all parts of
some element of cost-benefit-risk, reflecting Canada, and guidance to governments for
a philosophy of environmental health making risk-management decisions such as
protection and long-term risk reduction while planning control strategies and setting local
recognizing technological and economic standards.
limits. The broad range of potential
1
CEPA/FPAC, Working Group on Air Quality Objectives and Guidelines (1996) Protocol for the Development of National Ambient Air
Quality Objectives
Science Assessment Document for HF v CEPA/FPAC WGAQOG July 1996
It is recognized that not all locations in exceeded. The expectation is that strategies
Canada will meet these air quality objectives be put into place to reduce ambient air
immediately, or at all times, and that priority concentrations to below these targets as
given to meet these values may be based soon as practicable. The principles of
on factors such as available control continuous improvement and non-
technology, costs, benefits, and the degree degradation of environmental quality are
to which the recommended levels are advocated.
Science Assessment Document for HF vi CEPA/FPAC WGAQOG July 1996

1 INTRODUCTION
This document reviews the scientific which plants are exposed to HF, the
literature regarding the effects of gaseous concentration of HF in the air, and intervals
fluorides on vegetation, animals and between HF exposures, affect the extent of
humans. The available data have been accumulation and damage. For the
compiled, and studies that provide protection of vegetation from HF damage,
information which can be used to derive a reference levels for each of 1-, 7-, 30- and
reference level for gaseous HF have been 90-day periods are proposed in this
extracted and evaluated. This evaluation document.
provides the basis for the proposal of a
The second environmental effect is the effect
reference level for each of four time periods.
of fluorides accumulated in vegetation on
Each reference level represents an ambient-
herbivores (livestock and wildlife). Fluorides
air HF concentration above which an effect is
of all forms, both within the leaf and adhering
likely to occur. Information on gaseous HF
to the exterior plant surface, contribute to
effects on humans and animals is also
fluoride toxicity. Additionally, some plants
provided in this document to assist in
may accumulate levels of fluoride which are
assessing the impact of HF in situations of
harmful to herbivores, but which are not toxic
extreme exposure.
to the plants. Therefore, there is no means
While sufficient data is available to support the by which the proposed HF reference levels
derivation of a reference level for each of the can be used to estimate fluoride levels in
four periods, the number of species tested forage plants, or that can be considered
under conditions expected to occur in Canada adequate for the protection of herbivores.
is limited. Additionally, there is an indication Consequently, for the protection of wildlife
that some plants of economic (grapevine, and livestock, a reference level for total
peach) or natural (wild grape) importance in fluoride content in plants is presented.
Canada may be affected at the proposed
Although not used in the derivation of the
levels; however, direct evidence is lacking.
reference levels, data regarding the effects
Further research will determine if these levels
of fluorides on animal and human health are
require revision. It is recommended that
included in this document. This material
monitoring of ambient HF levels be conducted
provides information on multi-pathway
in those areas in which potentially sensitive
exposure routes as well as information about
species grow or are cultivated (e.g., vineyards,
acute HF exposures.
peach orchards), and which are located near
sources of airborne fluorides. Derivation of an This document represents an expert
Air Quality Objective for HF should await the synthesis of the available scientific literature.
completion of these additional studies and A listing of comprehensive scientific reviews
monitoring efforts. that provide additional details in support of
this synthesis is given in References.
Fluorides have two different environmental
effects. Fluorides accumulate and cause Unless explicitly stated otherwise, all units
damage in vegetation; this is the primary in this document are given as micrograms of
environmental effect. The period during hydrogen fluoride per cubic metre (µg HF m-3)
Science Assessment Document for HF 1 CEPA/FPAC WGAQOG July 1996

for ambient concentration levels, or as micro-
grams of fluoride per gram dry weight
(µg F g-1 DW) for fluoride accumulation in
forage.

2 RECOMMENDED REFERENCE
LEVELS FOR HYDROGEN FLUORIDE
The recommended reference levels for of HF in ambient air, and fluoride
hydrogen fluoride (HF) in ambient air are accumulation in forage, above which an
presented in table 1. Also presented is the effect on vegetation, and on animals which
recommended reference level for maximum feed on this vegetation, may be expected
fluoride accumulation in forage. These from airborne fluorides.
concentrations represent the concentrations
Table 1 Reference levels for HF in ambient air, and maximum level of accumulated
fluoride in vegetation
Averaging time
Level 24 hours 7 days 30 days 90 days Receptor
Reference level 1.1 0.5 0.4 0.4 Vegetation
(µg HF m-3)
Vegetation fluoride level 30 Livestock and wildlife
(µg F - g-1 DW)
Hydrogen fluoride is the most prevalent expected to be exposed to HF well below the
gaseous fluoride. There is no phytotoxic effects level. Human studies revealed a
information available for the covalently NOAEL (No Observable Adverse Effect
bonded gaseous fluorides, SF6 or CF4. Level) of 0.9 mg m-3 HF for skin and eye
These covalently bonded gases do not irritation and a NOAEL of 2.1 mg m-3 for
dissociate to form the fluoride ion (as does irritation of the respiratory tract. The odour
HF) and subsequent phytotoxic impacts are threshold ranged from 0.02 to 0.22 mg m-3.
expected to be negligible.
HF gas is a potent acute toxicant when
The gaseous HF concentration in ambient air animals are exposed to large quantities
varies from 0.01 to 1.65 µg m-3 in Canada acutely via the respiratory route. The
and the U.S.A. Levels are higher adjacent to chemical properties of the compound
facilities which emit HF. Ambient levels range account for its pharmacodynamic properties:
from 100 to 10,000 times less than the it dissociates when mixed with water to form
estimated effect level derived from human a strong acid resulting in burns, and it binds
studies. Children, people with impaired to calcium resulting in sequestration of
kidney function, industrially exposed calcium and alteration of bone calcium
workers, and persons living in the vicinity of (chronic exposure). From the weak chronic
a point source of fluoride emissions may be study data, it appears as though a continual
at somewhat greater risk than the general exposure to mammals should not exceed
population, though all such groups are 7 mg m-3.

2.1 RATIONALE FOR THE type of curve (quadratic, polynomial) is not
REFERENCE LEVELS FOR obvious, and in fact, none of the curves (up
to a third-order polynomial) adequately
GASEOUS HYDROGEN
described the data, and none gave an
FLUORIDE (HF) equation from which reference levels
Based on the literature review presented in considered protective could be calculated.
the remainder of this document, it is
Although the data set likely does not meet
concluded that vegetation is more sensitive
the requirements for statistical treatment
than human health to the toxic effects of
(random, normal distribution), statistical
fluorides. Therefore, the reference levels are
methods may be used as tools to help derive
based on the results from investigations into
the reference levels. The results of such
the effects of HF on plants. Experimental
analyses must be evaluated in the context of
data from 13 investigations into the effects of
what is known about the effects of HF on
HF on plants, representing 32 separate
plants, and the reference levels calculated
effects results, have been judged acceptable
using such methods should be examined
for use (see appendix). This data set
very carefully to determine if they represent
includes 18 points from studies using plants
an acceptable level of protection expected
of horticultural importance, 10 from studies
from the reference levels. The question to be
using agricultural species, and 4 from studies
answered is: Do the reference levels
of effects on forest (conifer) species. There
calculated using mathematical or statistical
is insufficient data within each of these
methods adequately describe a relationship
classes to derive separate reference levels
between the duration of HF exposure and
for each class.
the dose (or concentration) above which an
Coulter et al. (1985) found that injury in effect of HF on plants may be expected?
Gladiolus had a closer relationship to the HF
Regression analysis, including a calculation
dose than to HF concentration, duration of
of confidence intervals, was chosen as the
exposure, or frequency of exposure. For this
best tool to assist in the derivation of the
reason, each selected HF treatment was
reference levels. The results of this analysis
converted to a dose (concentration multiplied
are presented in fig. 1; it is based on data
by the duration of exposure), which has the
selected from the scientific literature shown
units µg days m-3. This normalization assists
in the appendix. It is important to note that
in the comparison of studies.
some of the data points presented in fig. 1
Since the data were selected on the basis of should carry greater weight than others,
expert judgement, and because many of the based on experimental and statistical rigour
studies did not present a measure of included in the study. However, since
variability or analysis of normality associated variability associated with each of the points
with the data, the data set of 32 points does is not given, it is not possible to give greater
not satisfy many assumptions required for weight to some of the points. Given this
analysis by most statistical methods. Curve- deficiency, the lines and the reference levels
fitting techniques may be useful in making derived from them must be evaluated
sense of the data; however, choice of the carefully.

The reference levels were calculated from Steel and Torrie (1980) for calculating
the lower confidence level for 1-, 7-, 30- and confidence intervals. The levels are
90-day periods using equations presented by presented in table 1.
Fig. 1 Regression analysis of HF-exposure data selected from the scientific

literature shown in the appendix. The upper and lower 95% confidence
levels are indicated by hatched lines. The lower 95% confidence level was
used to calculate the reference levels for 1, 7, 30 and 90 days.
Evaluation of these levels must include an greenhouses for 24 hours. Treatment with
examination of the points which fall below 2.10 µg m-3 for 1 day per week for 7 weeks
the lower limit, since they represent caused burning on Gladiolus leaf tips
instances where plants may be damaged by (McCune et al., 1966). While Gladiolus is
HF at doses and concentrations below the generally believed to be the most sensitive
recommended reference levels. Seven data species in terms of response to HF
points lie below this line (fig. 1); these points exposure, several of the data points well
were extracted from six studies. An above the 95% confidence level were
assessment of each of these studies is extracted from Gladiolus studies. The small
required to determine if the reference levels amount of leaf damage observed in these
derived from this line are protective. studies is judged to be insufficient cause to
Leaf injury in Gladiolus following HF modify the reference levels calculated from
the line representing the 95% confidence
exposure represents two of the seven points.
interval.
Adams et al. (1956) reported that a small
amount of leaf injury (0.7% of the leaf length The third point below the 95% confidence
was necrotic) was observed at 0.85 µg m-3 levels was extracted from MacLean et al.
when treated in small fumigation (1982). Leaf necrosis was observed

following treatment of Jerusalem cherry with was conducted under as close to natural
0.90 µg m-3 for 24 hours in the dark, followed conditions as are technically possible at this
by a light period without HF. Damage only time. While peanut does not represent a crop
occurred following transfer to the light. Dark of importance in Canada, yield reductions in
exposure for a duration approximating a this species under these conditions raise the
Canadian summer night (ca. 6 to 8 hours) possibility that other cultivated crops,
was not investigated. This type of exposure particularly related legumes, may be similarly
is artificial, and while it does add to the affected.
understanding of HF responses in plants, it is
Solberg et al. (1955) reported that a
not appropriate to lower the calculated
concentration of 0.51 µg m-3 for 24 hours
reference levels based on this study.
injured one in five ponderosa pine trees
First injury on grape leaves was observed at (see appendix). While this study may
0.17 µg m-3 after 99 continuous days of indicate a level of HF below the proposed
fumigation, and at 83 days following reference levels that could cause damage,
continuous treatment with 0.27 µg m-3 Solberg et al. (1955) reported only nominal
(Murray, 1984). This is the time to first HF concentrations; actual treatment
observable injury on the leaves, and fruit concentrations were not measured or
yield and quality were not affected. These reported. Without this information, the
effects are not sufficient to modify the validity of the data cannot be evaluated, and
interpretation of the data represented by the this study was not used in the derivation of
95% line. the reference level as presented in fig. 1.
Peach tree growth was reduced by about Thus, while the regression analysis
25%, with a minor amount of leaf necrosis, at presented in this section does not satisfy
0.34 µg m-3 for 110 days; this point falls just statistical requirements, the analysis was
below the 95% confidence level (Hill and used as a tool to assist in the evaluation of
Pack, 1983). This is a substantial effect, and currently available scientific data. Based on
since peaches are grown in Canada, it must this evaluation, the recommended reference
be seriously considered. However, the point levels are judged to represent an acceptable
is very close to the 95% line; adjusting the level of protection.
line downward to include this study would
cause the reference levels to be lowered by
a very small amount. The effect represented 2.2 SUMMARY OF ANIMAL
by this point (Hill and Pack, 1983), and it's EFFECTS, AND THE
proximity to the line used to derive the
RATIONALE FOR LIMITING
reference level, makes it apparent that
further work on the effects of HF on peach FLUORIDE ACCUMULATION IN
trees is required. FORAGE
Peanut yield was reduced when treated with Minimal data is available from which to
0.26 µg m-3 HF for 105 days in the field in assess the effects of gaseous HF on
open-top chambers (Murray and Wilson, livestock, wildlife or experimental animals
1990). This study used levels of HF which (Rousseaux, 1995). Due to scarcity of data
are likely to occur in the environment, and collected for a few exposure periods, some

of which are gleaned from older studies of (0.4 µg m-3 for 30 days) is at the low end of
varying analytical precision or accuracy, it is this range. A study by Davison and
not appropriate to recommend exposure Blakemore (1976) on forage exposed to
guidelines to protect animal health. HF is a 0.54 µg m-3 fluorides for 30 days resulted in
potent, acute toxicant when animals are a fluoride concentration of 33 µg g-1 dry
exposed to large quantities acutely via the weight in washed forage. The recommended
respiratory route. Since HF rapidly becomes air quality objectives for HF will not likely
a fluoride salt, the majority of the toxicity result in the accumulation of fluorides in
issues can be considered under the forage from HF in amounts which would
evaluation of the toxicity of fluorides. induce fluorosis in livestock and wildlife. It is
Generally, HF toxicity can be attributed to important to note that the measurement of
the corrosive action of hydrofluoric acid, forage fluoride content should be performed
sequestering of free calcium to form calcium on unwashed forage samples to ensure that
fluoride, and the alteration of the the contribution of particulate forms of
hydroxyapatite crystal in osseous materials. fluoride, as well as any other fluoride
The recommended reference levels for HF adhering to the exterior surfaces of the plant,
are approximately two orders of magnitude are included in the analysis, since they are
less than those observed to have adverse metabolically active and can contribute to
effects on animals. fluorosis in animals.
Fluoride uptake by livestock and wildlife via A reference level of 30 µg F- g-1 dry weight
the accumulation of fluoride in forage may be forage is recommended for the protection of
of concern near sources of fluoride wildlife and livestock from fluorosis
emissions. The accumulation of fluoride by originating from fluoride accumulation in
vegetation is dependent upon the amount of forage (table 1).
ambient fluoride (gaseous or particulate), the
pattern of exposure, the plant species and
the environment before, during and following 2.3 SUMMARY OF HUMAN HEALTH
exposure. It is not possible to calculate EFFECTS
previous ambient-air HF levels from
Inhaled fluorides are rapidly absorbed in the
vegetation fluoride content, although
upper respiratory tract; close to 100% of
vegetation fluoride monitoring can be used to
inhaled HF is absorbed. The fate or effects
assist in the diagnosis of animal injury and in
of absorbed fluorides are essentially
the identification of fluoride sources.
independent of the fluoride source or the
Concentrations of 20 to 40 µg F- g-1 dry
route of exposure. About 50% of absorbed
weight forage have been observed to cause
fluoride is retained in the body.
adverse effects in livestock (Suttie, 1969;
Approximately 99% of the fluoride in the
Joseph-Enriquez et al., 1990). Various
body is found in the skeleton, the remainder
experiments demonstrated that different
is distributed in soft tissue.
types of forage could accumulate up to
-1
40 µg g dry weight fluoride when they were Studies in humans revealed a NOAEL
exposed to 0.33 to 1.3 µg m-3 fluorides for (No Observable Adverse Effect Level) of
-3
30 days (National Research Council, 1971). 0.9 mg m airborne HF for skin and eye
The reference level recommended in table 1 irritation and a NOAEL of 2.1 mg m-3 for

irritation of respiratory tract. The odour workers being exposed to multiple air
threshold ranged from 0.02 to 0.22 mg m-3. pollutants, it is impossible to establish a
Clinical studies and most epidemiological NOAEL for gaseous fluorides. In humans, no
studies on the inhalation of fluorides were effects of chronic exposure to airborne HF
not adequately designed to derive a NOAEL on kidneys, brain, thyroid, haematopoietic
for systemic effects, or to identify clear effect system, or sensitivity were convincingly
level. Often the individual exposure of established at exposure levels to be
fluorides by the ambient air is not monitored. realistically feasible in ambient air or causing
In workplace studies, people are exposed to skeletal alterations or effects on the
many other potentially toxic compounds in respiratory tract. No specific epidemiologic
addition to gaseous and particulate fluorides data on carcinogenic effects of airborne
in the ambient air. Cross-sectional studies fluoride were available.
were too small in number. Only a few chronic
The ambient air concentration of gaseous
epidemiological studies provide some
fluoride varies from 0.01 to 1.65 µg m-3 in
quantitative information on the exposure
Canada and the U.S.A.. The exposure levels
level indicative for toxic effects on skeleton
in most parts of Canada are below 5 µg m-3.
(fluorosis and osteosclerosis) and the
Ambient exposures range from 100 to
respiratory tract. However, a distinct NOAEL
10,000 less than the estimated effect level
for airborne fluoride including HF could not
derived from human studies. Children,
be established. From the indicative estimates
people with impaired kidney function,
it can be concluded that levels below 1.78 to
industrially exposed workers, and persons
2.5 mg m-3 airborne HF for an exposure time
living in the vicinity of a point source of
of 8 hours are generally considered not to
fluoride emissions may be at somewhat
cause skeletal alterations. Pulmonary effects
greater risk than the general population,
are reported to appear in children above
though all such groups are expected to be
200 µg F m-3 for gaseous fluoride (and
well below the effects level.
300 µg F m-3 for particulate fluoride). For

3 BACKGROUND
Fluorine (F2) is a halogen that exists as a gas fog of aqueous hydrofluoric acid. Wet
under standard conditions. It is a light yellow- deposition is the primary removal mechanism
green, pungent, acrid gas. Fluorine is too of HF from the atmosphere.
reactive to be found in the environment in its
elemental state and exists as inorganic
fluoride (F-, free ionic, matrix-bound, and 3.2 SOURCES
ionically and covalently bonded in inorganic The major natural source of gaseous fluoride
compounds) or organic fluoride (covalently (primarily as HF) emissions are volcanoes.
bound in organic compounds). Fluorides Other sources of inorganic fluorides to the
exist in the atmosphere as gases and environment are mineral weathering and
particulates. Gaseous fluorides at ambient from marine aerosols. Global releases of HF
temperatures and pressures are hydrogen from volcanic sources are estimated to be 6
fluoride (HF), sulphur hexafluoride (SF6) and to 6,000 ktonnes, 10% of which are injected
carbon tetrafluoride (CF4). Polymeric into the stratosphere. Much of the volcanic
fluorides are H3F3, H4F4, silicon fluoride HF is removed by precipitation. The primary
(SiF4), and hydrofluorisilic acid (H2SiF6). anthropogenic emission sources in Canada
Common particulate fluorides are aluminum are aluminum smelting operations (~75%),
fluoride (AlF3), cryolite (Na3AlF6), fluoropatite coal-burning facilities (~10%), and chemical
(CaF2•3Ca3P2O8), calcium fluoride (CaF2) production (~6%). Table 2 summarizes
and sodium fluoride (NaF). estimated HF emissions in Canada.
Atmospheric fluorides affect the growth, Canadian consumption of HF is ~70 ktonnes.
development and productivity of vegetation. HF is manufactured from calcium fluoride
The effects of gaseous fluorides are more and used in the production of synthetic
phytotoxic than those of particulate fluorides cryolite, aluminum trifluoride, motor gasoline
because they are more readily absorbed by alkylates, chlorofluorocarbons, uranium
vegetation. tetrafluoride and uranium hexafluoride.
Canadian aluminum production utilizes the
synthetic cryolite produced in Canada.
3.1 PHYSICAL AND CHEMICAL
There are 11 primary aluminum producers in
CHARACTERISTICS OF
Canada: one in Kitimat, British Columbia,
HYDROGEN FLUORIDE and 10 in Quebec (table 3). All of the
HF is the most reactive form in which fluorine aluminum in Canada is produced by the Hall-
exists in the environment. It is a colourless, Heroult process (Environment Canada,
pungent, acrid gas at room temperature. It is 1976, 1994): the electrolytic dissociation of
highly soluble in many organic solvents and alumina (Al2O3) dissolved in a molten cryolite
water, where it forms hydrofluoric acid. (Na3AlF6) bath. Electrolysis occurs in a
carbon crucible (acting as the cathode)
Approximately 75% of the atmospheric
within a steel shell. Carbon anodes are
gaseous fluoride exists as HF. Combined
suspended above the cell and the aluminum
with water, HF vapour forms an aerosol or
metal forms at the cathode in the bottom of

the crucible. Oxygen gas is released at the vapours and particulate silicon fluoride.
anode, burning the carbon anode. The These gases are scrubbed prior to discharge
electrolysis cell operates continuously, and into the atmosphere. The control efficiency
fresh alumina and cryolite are added to the for volatile fluoride emissions varies from
cell as required. Hoods over the cell collect 75% to 99%.
the volatilized fluoride, hydrofluoric acid
Table 2 Estimates of HF air emissions

Source sector Air releases (tonnes year-1) Relative Contributions
Biogenic
Volcanic emissions 0.06–6 × 106 100
Anthropogenic
Primary aluminum producers 4,063.4 75
Coal-burning utilities 543.1 10
Chemical producers 305.3 6
Steel producers 238.9 4
Phosphate fertilizer producers 107.6 2
Magnesium producers 100 2
Other 51.3 1
Total 5,409.6 100
Source: Environment Canada, 1994
HF is also emitted from coal-burning utilities a local source on surrounding areas or to

(table 4). The primary coal types used in provide information on a specific area of
Canada are bituminous and sub-bituminous. concern as identified by total ambient
A small amount of lignite coal is also burned. fluoride
The HF emission factors for bituminous and
lignite coals are 0.12 kg HF Mg-1 coal and
0.01 kg HF Mg-1 coal, respectively (Emmel
et al., 1989).
3.3 MONITORING
METHODOLOGIES
HF is not monitored by Environment Canada
or the provinces on a continuous basis.
Measurements are made on a site specific
basis, typically to characterize the impact of

monitoring. The two most prevalent methods term record of total ambient fluoride levels.
used in Canada for monitoring total ambient Currently, passive techniques are used to
fluorides are the passive and the dual-tape assess general dispersion conditions around
sampler methods. a source, and to locate a potential area of
concern which may then be examined using
Passive techniques do not differentiate
an HF-specific methodology.
between gaseous and particulate forms of
ambient fluorides, but provide information on
overall fluoridation rates. This cannot be
directly related to vegetation impact or to the
accumulation of fluoride in forage. Passive
methods provide an inexact quantification of
HF since fluoride collection depends upon
local meteorological conditions, which control
the flux of fluoride to and from the collecting
surface, and retention of HF on the sampler
surface. Error rates of up to 50% have been
reported (Ontario Ministry of the
Environment, 1979). Passive techniques are
inexpensive and robust, and do serve to
provide a long-
Table 3 Capacity of Canadian aluminum producers, 1992

Producers Plants Capacity (tonnes)
Alcan Smelters and Chemicals Ltd. Kitimat, B.C. 272,000
Isle-Malign, Alma, Que. 73,000
Beauharnois, Que. 48,000
Grande-Baie, Que. 180,000
Arvida, Jonquière, Que. 232,000
Laterrière, Que. 204,000
Shawinigan, Que. 84,000
Aluminerie de Bécancour Inc. Bécancour, Que. 360,000
Canadian Reynolds Metals Company Baie-Comeau, Que. 400,000
Ltd.
Aluminerie Lauralco Inc. Deschambault, Que. 215,000
Aluminerie Alouette Inc. Sept-Îles, Que. 215,000
Total 2,283,000
Source: Natural Resources Canada, 1995

In order to determine whether or not a region Environment, 1979; Bumbaco and Shelton,
may be exceeding the recommended air 1978, 1982). The "plates" or "candles" are
quality reference levels for HF or ambient HF exposed to the atmosphere for a given time
objectives, one of the HF-specific period (of the order of a month) sheltered by
methodologies must be used (discussed at a petri dish or louvred case. Analysis
the end of this section). involves solution extraction of the filter paper
followed by analysis for total fluorides using
The passive "fluoride plate" or "fluoride
a fluoride ion-specific electrode. Resultant
candle" methods for monitoring ambient
fluoride concentrations are expressed as
fluorides have been used as a qualitative
fluoridation rates in units of µg F- cm-2 per 30
index of gaseous fluoride levels (Korruri,
days. Identification and quantification of the
1984). These methods use a circular or
fluoride on the filter paper may also be made
cylindrical filter paper impregnated with an
using a mass spectrometer.
alkaline solution (Ontario Ministry of the
Table 4 Locations of coal-burning electricity generating utilities in Canada

Name Lat. (N) Long. (W) Name Lat. (N) Long. (W)
Glace Bay, N.S. 46.2 59.95 Richard L. Hearn, Ont. 43.7 79.33
Lingan, N.S. 46.2 60.03 Thunder Bay, Ont. 48.4 89.22
Maccan, N.S. 45.7 64.25 Brandon, Man. 49.8 99.88
Point Tupper, N.S. 45.6 61.37 Selkirk, Man. 50.2 96.87
Trenton, N.S. 45.6 63.63 Amy Street, Winnipeg, Man. 49.9 97.15
Chatham, N.B. 47.0 65.47 Boundary Dam, Sask. 49.1 102.98
Dalhousie #2, N.B. 48.1 66.40 Estevan, Sask. 49.1 102.98
Grand Lake #2, N.B. 46.1 66.02 Poplar River, Sask. 49.1 105.52
Atikokan, Ont. 48.8 91.62 Battle River, Alta. 52.6 112.07
J. Clarke Keith, Ont. 42.3 83.10 H. R. Milner, Alta. 53.9 118.50
Lakeview, Ont. 43.6 79.55 Sheerness, Alta. 51.5 111.67
Lambton, Ont. 42.8 82.43 Keephills, Alta. 53.5 114.55
Nanticoke, Ont. 43.6 79.55 Sundance, Alta. 53.5 114.55
Wabamun, Alta. 53.6 114.48
Source: Statistics Canada, 1990
Adams (1961) was able to derive an papers, direct measurements of gaseous HF

equation which related data obtained from were made (continuous air withdrawal,
limed papers to atmospheric HF levels. In fluoride adsorption onto a glass substrate,
this work, HF was added to air entering a followed by titration to measure fluoride)
growth chamber and, therefore, the only which allowed the development of a
fluoride present was HF. In addition to limed correlation between atmospheric HF and
Science Assessment Document for HF 3-12 CEPA/FPAC WGAQOG July 1996

fluorides trapped on the papers. This is a Double paper-tape samplers (dual-tape
very simple situation compared with field samplers) have been developed for
measurement of ambient fluoride levels in monitoring ambient gaseous and particulate
air. It was concluded that direct conversion fluorides (ASTM, 1991). Individual air
from limed paper data to atmospheric HF samples may be collected automatically over
concentrations in the field is not possible time periods of minutes to three hours.
(Adams, 1961), and that the limed papers
The paper tapes are removed from the
are only useful to delineate areas of fluoride
sampler and treated so as to dissolve the
contamination, to determine relative
fluoride, and the solubilized fluoride is
intensities of fluoride pollution among sites,
analyzed by potentiometric or photometric
and to monitor changes in pollution intensity
methods. This monitoring method provides
due to reductions in emissions or addition of
the means of automatically separating and
new emission sources to an area. Sidhu
collecting atmospheric particulate and acidic
(1979) monitored atmospheric fluoride levels
gaseous-fluoride samples. Interferents with
in the vicinity of a phosphorous reduction
the methodology are particulate-metal salts
plant using both sodium formate papers
and acid aerosols or gases which may
(which are also effective fluoride traps) and
neutralize or acidify the alkali-treated tapes.
sequential samplers. The use of these
Contamination of the acidic gaseous-fluoride
different techniques at the same site allowed
fraction by small particulate fluorides (<1 µm)
the derivation of an equation that could be
is usual. For a one-hour sample, the
used to calculate total atmospheric fluoride
precision expressed as the relative standard
concentrations (µg F- m-3) from limed-paper
deviation is 5% in the range of 1 to 3 µg F
data (µg F- dm-2 week-1). However, since the
m-3. Fluoride recovery is usually 95% for
proportion of HF in the total atmospheric
known amounts of fluoride in the range of 2
fluoride load was not known, Sidhu (1979)
to 20 µg m-3.
did not determine the amount HF in the
atmosphere at the monitoring sites. Adams One review of double-tape sampling
(1961) also acknowledged this shortcoming, methods has estimated detection limits of
and pointed out that limed-paper monitoring 0.07 µg HF m-3 for a 2-hour sample (Zankel
is susceptible to variation due to changes in et al. 1987). However, operationally, large
the environment, particularly to temperature variations in the measured ambient HF
and wind velocity, both of which will affect concentrations monitored by dual-tape
the amount of fluoride trapped by the samplers may occur due to variations in air-
papers. Error rates of up to 50% have been sample flow rates (Bisson et al., 1995). Thus,
reported (Ontario Ministry of the the accuracy of the method is questionable.
Environment, 1979; ASTM, 1991) since the The precision of measurement of the trapped
flux of fluoride to and from the collecting HF is high; Bisson et al. (1995) have stated
surface (and its retention of it) depends that sample repeatability is satisfactory and
greatly upon local meteorological conditions. the percentage error small, with detection
-3
However, passive methods are useful in limits of 0.3 µg F m on the filter, and
defining a potential area of environmental quantification limits of 1.1 µg F m-3.
impact from HF. Nevertheless, until the sampling airflow
problems are solved, precise analytical

measurement of trapped fluoride is not emissions may warrant a study of ambient
useful. HF levels elsewhere in Canada. No
information is available on indoor
Commercial instruments, which use a liquid
concentrations.
scrubber and fluoride ion specific electrodes,
are available for continuous monitoring. The data in table 5 illustrate the variation in
The measurement principle is to continuously HF concentration ranges across Canada.
sample ambient air, removing solid particles More intensive and continuous monitoring
in a cyclone separator, and scrubbing the air has been performed by the B.C. Ministry of
sample in an aerosol gas scrubber, followed Environment, Lands and Parks in association
by analysis of the condensed aerosol gas with Alcan in Kitimat, B.C., using a
with the ion-selective electrode. Operational continuous methodology, and by the Ontario
detection limits are approximately Ministry of Environment and Energy in
0.1 to 0.2 µg F m-3. There are no known southern Ontario using fluoride candles.
interferents with the methodology. Fig. 2 shows the variation in the monthly HF
concentration averages from January 1992
Real-time analysis of HF may also be
to July 1994 at each of four sites near
performed with an atmospheric pressure
Kitimat. During that period, the average
chemical ionization tandem mass
monthly concentration exceeded the
spectrometer (De Brou et al., 1991). The ion
recommended 30-day reference level of 0.4
chemistry is dominated by dissociative
µg m-3 twice at the Minnette site in 1992; for
attachment reactions:
five consecutive months (Jan. to May 1993)
R- + HX è X- + HR at the Alcan Dock and once at the Workshop
where R refers to OH, SO2 or CO3 and X site (July 1993).
refers to F- or Cl-. The X- ion may arise from HF monitoring by the Ontario Ministry of
a variety of F- or Cl- containing species, Environment and Energy is performed to
therefore this method is only a good identifier establish relative amounts of gaseous
of HF in the absence of other fluorinated fluorides present over an extended
species. Established spectra are used to period of time, primarily to assess
identify HF in a complex matrix which vegetation effects (Ontario Ministry of
includes other fluorinated species. The Environment and Energy, 1991, 1992). This
standard monitoring period is 30 minutes, passive monitoring technique provides data
with instantaneous measurements acquired in units of µg per 100 cm2 per 30 days. This
every five seconds. Real-time detection limits information cannot accurately be translated
are in the range of 0.2 to 0.5 µg m-3. -3
to µg m (as discussed in previous section),
3.4 ENVIRONMENTAL LEVELS IN therefore the data presented in fig. 3 should
be viewed from the perspective of providing
CANADA
information on relative changes in ambient
Mean atmospheric levels in Canada range HF concentrations. There is no obvious
from 0.01 to 1.0 µg F- m-3 (Environment seasonal pattern over the two years. In 1991
Canada, 1994). Current areas of concern in and 1992, the highest annual arithmetic
Canada are in the provinces of British means and monthly values were recorded
Columbia, Ontario and Quebec. However,
future industrial installations with HF
in Hamilton. This station is immediately potential hazards to public health and the
adjacent to a brick manufacturer. environment from HF considering a range of
events that included worst-case accidental
releases (Environmental Protection Agency,
3.5 AMBIENT AIR OBJECTIVES 1993). Analysis of public exposure to routine
AND STANDARDS IN OTHER emissions were not included due to the focus
on worst-case releases.
JURISDICTIONS
Various agencies around the world have air Additionally, other jurisdictions have
quality objectives and guidelines for gaseous established a limit on vegetation fluoride
fluorides (table 6). The United States has not accumulation. These limits are also
set a federal standard for gaseous fluorides summarized in table 6. Since they are based
(as HF); however, the U.S., as required by on the same information as reviewed in this
the U.S. Clean Air Act 1990, identified document, it is not surprising that the limits
are essentially the same.
Table 5 Ambient HF concentration ranges at selected Canadian sites, 1980–91

Source and location Year(s) Dist. Statistic Concentration Reference
(km) range (µg m-3)
1. Lead and zinc mining 1990–91 <5 mean levels 0.43–0.59 EC†, 1993
and phosphate fertilizer
operation, Trail, B.C.
2. Lead and zinc smelter 1984–85 0.6–10.5 range 0.13–0.60 White et al.,
and fertilizer operation, 1986
Trail, B.C.
3. Hydrofluoric acid plant, 1987–90 near growing 0.076–2.36 Gizyn, 1991
Amherstburg, Ont. season
4. Steel plant, 1991 near mean 0.17–0.24 EC, 1993
Hamilton, Ont.
5. Residential area, 1981 mean 0.03 McGrath,
Toronto, Ont. 1983
6. Brick manufacturing 1980–81 0.8 mean 0.07–0.73 McGrath,
plant, Brampton, Ont. 1983
7. New York Aluminum 1987–91 1.6–4 mean 0.43–0.85 EC, 1994
smelter, Cornwall
Island, Ont.
8. Aluminum smelters, 8 mean 0.1–0.71 EC, 1993
Quebec
9. Lead smelter, 1988–90 near yearly avg. 0.027–0.06 Murphy,
Belledune, N.B. 1991
10. Phosphorous reduction 1980 1.4 average 2.45 EC, 1994
plant, Long Harbour, 8 0.4
Nfld. 18.7 0.06
11. Background, Alert, remote mean 0.00568 Barrie and
N.W.T. Hoff, 1985

Source: Environment Canada, 1994
† EC = Environment Canada

Fig. 2 Average monthly ambient HF concentration from January 1992 through July 1994
at four sites near Kitimat, B.C..

Fig. 3 HF fluoridation rate monthly averages for Ontario, 1991–92, for: (a) urban areas
and (b) rural areas.
(a)
(b)

Table 6 Ambient air quality standards and objectives for gaseous fluorides (µg m-3), and
fluoride levels in vegetation (µg g-1 DW), in other jurisdictions
Vegetation
Jurisdiction 90 days 30 days 7 days 24 hours 12 hours Other
content
Canada (proposed 0.4 0.4 0.5 1.1 — — 30
Reference Levels)
Manitoba — — — 0.40 D† — — —
— — — 0.85 A — — —
Newfoundland — 0.45 — 0.90 — — —
Ontario (Apr. 15 to — 0.34 — 0.86 — — —
Oct. 15)
British Columbia — 0.35 0.55 0.85 — — —
Montreal Urban — 0.34 — 0.86 — 1.85 —
Community (8 hours)
2.00
(1 hour)
Kentucky — 0.82 1.64 2.86 3.68 — gr. season -
40
2-mo. - 60
1-mo. - 80
Maryland — — — 1.20 — 0.4 (72 —
hours)
New York — 0.80 1.65 2.85 3.70 — —
South Carolina — 0.80 1.60 2.90 3.70 — —
Tennessee — 1.20 1.60 2.90 3.70 — —
Washington — 0.84 1.70 2.90 3.70 0.5 (Mar. to —
Oct.)
Australia
New South Wales — 0.84 1.7 2.9 3.7 — —
Victoria 0.59 — 2.0 2.9 — — —
Japan — — 0.5 1.0 — — —
Netherlands — 0.8 — 2.8 — 0.4 —
(growing
season)
New Zealand — 0.5 1.0 — — 70 (1 hour)
Norway — 0.4 — 1.0 — — —
Sources: (Streeton, 1990; International Union of Air Pollution Associations, 1992
† D = desirable; A = acceptable

4 EFFECTS ON VEGETATION
A considerable amount of research has been fluoride injury, the exact mechanisms by
conducted on the effects of fluoride on which fluorides injure higher plants are not
higher plants, with a number of extensive well known. Much of this work has involved
review articles written. This section is based the study of various enzymes, systems or
primarily on a review of the following organelles in vitro by exposing whole plants
references: Drury et al. (1980), Environment or plant parts to sodium fluoride solutions.
Canada (1994), Linzon (1971), McLaughlin Fluorides have been found to inhibit or
(1991), Miller (1993), National Research stimulate enzymes involved in glycolysis,
Council (1971), Thomas and Alther (1966), respiration, photosynthesis, metabolite
Treshow and Pack (1970), Weinstein (1970, transport across membranes and other
1977) and Zwiazek (1994). processes. Depending on many factors,
fluorides may inhibit or stimulate respiration,
which is one of the earliest symptoms of
4.1 EFFECTS OF FLUORIDES ON fluoride toxicity. Respiration inhibition is
VEGETATION possibly linked to the inhibition of respiratory
enzymes, while stimulations may be linked to
Injury to plants results from absorption of
fluoride acting as an uncoupler of
fluoride by the plant. Gaseous fluorides are
phosphorylation. In vitro, fluorides may affect
readily absorbed, whereas particulate
membranes by inhibiting ATPase, disrupting
fluorides collect on external surfaces and
the membrane pH gradient, and blocking
cause little or no injury unless dissolved by
chloride antiport movement. In vivo
precipitation or dew and absorbed.
experiments involving HF fumigation of white
Absorption of atmospheric fluorides by plants
pine seedlings show that changes in
can result in high concentrations of fluoride
membrane permeability, greater electrolyte
in leaves, but only slightly elevated amounts
leakage, plasma membrane lipid composition
have been found in stems and roots. Injured
and increased plasma membrane ATPase
portions of leaves usually contain more
activity occur during the early stages of
fluoride than uninjured portions. The lowest
fluoride injury. No changes in mesophyll cell
concentrations of fluoride are found in the
structure were observed before the
fruit and seeds of plants. The length of plant
appearance of visible injury.
exposure to atmospheric fluoride is important
because the effect of fluoride is cumulative. The mechanisms by which some plants are
However, inactivation of fluoride within the more tolerant to fluoride than other plants
plant, growth dilution, physiological condition are also not well understood. Tolerant plants
of the plant, plant nutrient status, fumigation may be able to deactivate fluoride better
dynamics, stomatal activity and loss from the than sensitive plants. Possible mechanisms
plant make direct comparison between of fluoride deactivation in plants include
concentrations of fluoride in the air and plant shifts to fluoride insensitive metabolic
impossible. pathways, removal from sites of enzyme
inhibition via reactions with organic
While a considerable amount of work has
compounds, reaction with cationic sites,
been carried out on non-visible or metabolic

sequestration in vacuoles, and translocation tissue by a darker zonate line. All forms of
to the leaf surface. In addition to injury are not present in all injured plants.
physiological effects, fluorides can cause
Fluoride injury to plants may be acute or
mutagenic effects such as chromosomal
chronic. Acute fluoride injury is caused by
aberrations, bridges, fragments and
short-term exposures to high concentrations
multipolar mitosis.
of atmospheric fluorides. Inactivation and
A number of factors influence the action of translocation of fluoride cannot keep pace
fluorides on vegetation and the uptake and with absorption, resulting in leaf lesions. The
accumulation of fluoride by plants. These amount of accumulated fluoride could be
factors include temperature, relative less than that required to cause chronic
humidity, wind speed, soil moisture, plant injury because sudden absorption of high
nutrition, stage of growth and plant species. concentrations of fluoride disrupts plant
Injury symptoms similar to those caused by metabolism quickly. Chronic fluoride injury is
atmospheric fluorides may also be due to caused by variable exposure periods at
other agents, such as insects, disease, different concentrations of atmospheric
nutritional disorder, and adverse weather. fluoride. Plants absorb fluoride slowly and
the unidirectional distal movement of the
Gaseous fluorides enter the leaves of plants
fluoride eventually results in the
primarily through the stomata. Injury rarely
accumulation of concentrations sufficient to
occurs at the absorption site, as the fluorides
cause injury or cell death. The concentration
dissolve within the aqueous phase of the
of fluoride in the leaf tips and margins or
substomal cavity and move as ions through
injured areas is higher than in the rest of the
the apoplastic space of the mesophyll cell
leaf. Lesions continue to enlarge as the
walls with the transpirational stream to the
plants are subjected to low concentrations of
leaf tips and margins, where fluoride
atmospheric fluorides. With continued
accumulates. When the accumulated fluoride
exposure, the necrotic areas spread inward
concentration exceeds a certain threshold
from the margins of leaves of dicotyledonous
level, which varies with plant species and
plants and downward from the leaf tips of
with varieties of the same species, leaf injury
conifers and monocotyledonous plants. The
occurs. Fluoride injury symptoms vary
necrotic areas may extend across large veins
considerably, depending on whether the
and even cross the midrib in deciduous
vegetation is narrow-leaved or broad-leaved,
leaves. (This is a pattern seldom seen in
relative susceptibility to fluoride, the
sulphur dioxide-caused lesions.) Premature
concentration in the air, and duration of
defoliation follows leaf injury on some plants,
exposure. The injury may take the form of
and while others retain their leaves, the
chlorosis (yellowing of the leaves due to
leaves often have desiccated margins that
chlorophyll reduction) or necrosis (killing of
break away. Exposure of coniferous tree
leaf cells). In general, plants injured by
foliage to atmospheric fluoride results in
chronic atmospheric fluoride usually display
chlorotic needle tips followed by reddening
leaf chlorosis. Necrosis generally occurs at
(likely needle necrosis). Needle elongation is
the leaf tips and margins, and these necrotic
retarded and the needles may be shed
areas may be separated from healthy leaf
prematurely. Corn leaves, if not actually
injured with collapse of leaf areas, show a

general mottled appearance. In Gladiolus, tip display no foliar injury. The relative sensitivity
burn gradually extends down the leaf and of different plant species and varieties to
kills all tissue, including veins. As the fluoride fluoride is generally based on visible foliar
concentration increases and duration injury symptoms and their relationship to
decreases, marginal injury predominates, fluoride dose, fluoride concentration in the
expanding across the leaf, occasionally leaf, or threshold dose for visible foliar injury.
leaving an isolated green tip. In rare However, it has recently been shown
instances, flower bracts might develop (McLaughlin, 1991) that for nine tree species
marginal burn in a severe fumigation, with there was very little agreement between the
the petals sometimes displaying injury. Some fluoride sensitivity ratings based on foliar
investigators have observed a black tip injury and sensitivity ratings based on the
condition in cherries, while others have noted reduction of annual xylem growth during a
a soft spot along the suture line of peaches 20-year period of high fluoride emissions
following HF exposure. Fruit drop and poor around an aluminum smelter. Oak and
fruit set have been observed in orchards maple, which were classed as tolerant based
subjected to heavy fumigations. on foliar injury, were sensitive to intermediate
based on xylem growth.
Accurate prediction of fluoride accumulation,
4.2 FLUORIDE ACCUMULATION IN and knowledge of plant responses to
VEGETATION accumulated fluoride, would allow the
In Ontario, maple foliage ranges from >0.5 establishment of guidelines which would limit
to 10 µg F g-1 DW. Plants exhibit a broad fluoride uptake and minimize
range in their sensitivity to injury from fluoride-induced damage. In its most simple
atmospheric fluorides. Sensitivity varies not form, uptake can be expressed as
only among species but among varieties of Fv = kCt + b [1]
the same species. Sensitive plant species
include varieties of apricot, barley, blueberry, where Fv is plant fluoride content
sweet corn, Douglas fir, Gladiolus, grape, (µg F g-1 DW), k is the accumulation
Manitoba maple (box elder), peach, pine, constant for the species, C is the ambient
plum, St. John's wort, tulip, and western concentration of HF (µg m-3), t is the duration
larch. Sensitive varieties of Gladiolus and of exposure (days), and b is the y-intercept
strains of eastern white pine may display leaf (theoretically, b is the amount of fluoride
injury with accumulations of less than present in the tissue as a result of
-1
30 µg g DW in the injured leaves. Plants of accumulation from natural sources). Gritsan
intermediate resistance, such as apple and (1992) developed predictive equations based
raspberry, may not display injury until they on the format of equation [1] for field-grown
have accumulated 100 µg g-1 DW. Plants wheat and barley, and for seedlings of wheat
strongly resistant to fluorides, such as wheat and barley grown in growth chambers.
and alfalfa, may not display leaf injury until Accumulation constants for barley were
accumulated concentrations exceed two-fold greater than for wheat in both
200 µg g-1 DW. Bitternut hickory can environments. Accumulation of fluoride has
accumulate up to 1,000 µg g-1 DW and been examined in grapevine (Doley, 1982),
where it was found that both b and k varied

with the total dose provided to the plants. In a very simplistic sense, foliar fluoride may
MacLean and Schneider (1973) compared be considered to be compartmentalized into
fluoride accumulations in continuously interior and exterior compartments. Fluoride
fumigated forage (a mixture of timothy grass which remains in the interior compartment
and red clover) to fluoride accumulations in may be physiologically active, while that on
plants intermittently fumigated with HF. the exterior is not. Under natural conditions,
Plants exposed continuously to HF rainfall may wash the leaves of exterior
accumulated more fluoride than those fluorides. De Temmerman (cited in van der
exposed intermittently to the same total HF Eerden, 1991) accounted for the effect of
dose. Investigations of fluoride accumulation rainfall and the decline in fluorides as a
by orchard grass and alfalfa led McCune and function of time with the equation
Hitchcock (1971) to derive predictive
Fv = 128F30.13 F20.59 F10.45 e-0.0043N [3]
equations based on the format of equation
[1]. However, while these regressions were where F1, F2 and F3 are the average
highly significant, they only accounted for ambient fluoride levels in the preceding
54% (orchard grass) and 70% (alfalfa) of the 1st, 2nd and 3rd weeks prior to grass
variability. Further investigation revealed that sampling, respectively, and N is the rainfall
the time between the end of the exposure (mm) in the preceding two weeks. Variation
period and sampling was an important in the amount of foliar fluoride with the
parameter in determining fluoride levels. In season was observed by van der Eerden
alfalfa, fluoride concentrations declined with (1991), who incorporated a "seasons index"
an apparent half-life of about eight days. To into his predictive model.
account for this, the regression equation As illustrated by these equations, the
Fv = 4.21C 0.82
t 0.70
e -0.032D
[2] accumulation of fluoride by plants is
dependent upon the amount of fluoride, the
was derived, where D is the number of days
pattern of fluoride exposure, the plant
between the end of fumigation and the time
species, and the environment before, during
that the samples were harvested for
and following exposure. These models
analysis, and e is the base of the natural
generate valid predictions only under the
logarithm. Similar analysis of the
conditions from which the data originate (van
post-fumigation period length only slightly
der Eerden, 1991; MacLean et al., 1989).
improved the regression fit for orchard grass,
The reverse of this situation (i.e., the use of
and this improvement was not statistically
vegetation fluoride content as a quantitative
significant.
measurement of ambient HF levels) is also
Some plants are able to reduce leaf internal invalid (MacLean et al., 1969), although
fluoride levels by exporting fluoride to the vegetation fluoride monitoring can be used
exterior leaf surface. This ability varies by as a qualitative tool to assist in the diagnosis
species, with cotton and tomato being of injury and in the identification of fluoride
relatively efficient at exuding fluorides sources. Chemical analysis is a valuable tool
(Jacobson et al., 1966). Davison (1982) in diagnosing fluoride injury. Plants in
reviewed the literature on the loss of fluoride polluted areas continually accumulate
from leaves, and noted that losses may be of fluoride, and thus repeated analysis can
the same magnitude as accumulation rates. indicate the relative intensity of injury. Also,

the fluoride emission source can usually be Kentucky (table 6). A maximum of 20 to
determined since the fluoride concentration 30 µg F g-1 DW is suggested for forage
in plants increases with proximity to the fluoride content in section 5 of this
source. document. The ambient guidelines proposed
for HF will probably not result in the
When considering fluoride content of plants
accumulation of fluorides in amounts which
to be used as forage, all forms of fluoride
would induce fluorosis. However, near
must be taken into account since all fluorides
sources of fluoride emission where plants
are metabolically active (to differing degrees)
are exposed to multiple forms of fluoride,
within a herbivore. To account for both
monitoring of fluoride content in unwashed
gaseous and particulate loadings onto
forage samples is necessary to ensure that
forage (grass), Blakemore (cited in van der
animals are not exposed to harmful dietary
Eerden, 1991) derived the regression
fluoride levels.
Fv = -31.1 + 0.67FG1 + 281FAg + 223FAp [4]
Soil normally contains between 20 and 500
where FG1 is the fluoride content of the grass ppm fluoride. In Ontario, the typical range for
one week prior to sampling, and FAg and FAp fluoride in medium to fine textured soils is
are the average atmospheric gaseous and between 20 and 160 ppm. Atmospheric
particulate fluoride concentrations during the fluoride emissions that are not removed by
preceding week, respectively. Consideration other receptors eventually settle on soil and
of both particulate and gaseous fluorides is increase its fluoride content. The application
necessary in areas close to facilities which of fertilizer can also increase soil fluoride
emit fluorides, since both forms are likely to content. In alkaline soils, most of the fluoride
be present in and on the plant. is immobilized on clay particles with little root
Analysis of washed tissues will provide an uptake occurring in plants. More fluoride is
indication of the internal fluoride content of soluble in acidic or saline soils, where
the tissue. The analysis of unwashed tissue sodium replaces calcium as the dominant
samples will result in a determination of total cation, and greater root uptake takes place.
fluoride content, which includes internal and The lesions on leaves caused by uptake of
external fluorides. When analyzing for soluble fluorides from soils are quite similar
fluoride levels in forage, determination of to those caused by absorption of
total fluoride is the only meaningful, practical atmospheric fluorides, but in some species
analysis. For the protection of livestock and there tends to be a greater degree of injury
wildlife, limits on forage fluoride content have to the interior than to the margins of leaves.
been proposed or established. A limit of Analyses show that plant roots can contain
55 µg F g-1 DW has been suggested by very high fluoride concentrations (1,000 to
-1
van der Eerden (1991). Kentucky standards 6,000 µg g DW) when fluoride enters from
include limits of 80, 60 and 40 µg F- g-1 DW the soil, whereas the concentration is very
in forage for average 1-month, 2-month low (about 10 µg g-1 DW) in roots when
and growing season fluoride levels, fluoride enters via the leaves.
respectively. These limits were proposed by There has been little research conducted on
Suttie (1969), and were accepted by Mitchell the effects of accumulated fluorides on
et al. (1981) and adopted by the State of insects. Jia-xi and Yong-mei (1988) found a

threshold level of about 30 µg F- g-1 DW in concentrations near two aluminum smelters
mulberry leaves for an effect of fluoride on within the Saguenay–Lac Saint-Jean region
feeding silkworms (increased mortality, of Quebec before 1978 and after the 1984
decreased weight gain in larvae). Insects completion of a depollution program showed
(pollinators, predators, foliage feeders, and that the area of influence (defined as total
cambial region feeders) collected from an fluoride levels >50 µg L-1 melted snow) was
area near a fluoride emission source were approximately 3,000 km2 and 100 km2,
found to have elevated fluoride levels respectively (Ouellet, 1987). It was further
relative to those collected from control areas surmised that the greater portion of this
at least 50 miles distant from the source reduction was attributable to reductions in
(Dewey, 1973). Pollinating and foliage particulate fluorides rather than to gaseous
feeding insects accumulated the most HF. It was estimated that in 1975, HF
fluoride. The effects of the accumulated represented 50% of the volatilized fluoride
fluoride on insect physiology, reproduction, emissions from the aluminum smelters, and
and behaviour were not investigated. approximately 80% in 1984. It is not
expected that the impact from HF emissions
would extend beyond approximately 30 km
4.3 CANADIAN CASE STUDIES from a given major source.
Common industrial sources of fluoride
emissions in Canada include the production
4.3.1 Phosphorus Reduction
of super-phosphate fertilizers, uranium
hexafluoride, hydrofluoric acid, Long Harbour, Newfoundland
chlorofluorocarbons, fibreglass, appliances, A number of major studies on the various
ceramic tiles, bricks, aluminum smelting and effects of fluoride emissions on vegetation
casting, steel manufacturing, and have been conducted in the vicinity of a
petrochemical refineries. Listed below are a phosphorus reduction plant at Long Harbour,
number of examples documenting the impact Newfoundland (Linzon, 1978a; Roberts and
of fluoride emissions on vegetation in the Thompson, 1980; Sidhu 1979, 1982a,
vicinity of some these industrial sources. 1982b; Sidhu and Staniforth, 1986;
Staniforth and Sidhu, 1984; Thompson et al.,
The range of impact from a given source is
1979). The facility first became operational in
usually estimated from observed fluoride ion
1968 and fluoride injury to trees was first
concentrations in vegetation and surface
observed in 1970. Fluoride emissions were
materials such as leaf litter or snow. For the
both gaseous and particulate, with the
Long Harbour, Newfoundland, phosphorous
impact of the particulate being restricted to
reduction plant (no longer in operation) over
the immediate vicinity of the plant. HF and
a 20-week period, no vegetation damage
SiF4 are the main fluorides emitted. The
was observed beyond 13 km from the source
investigation of the fluoride impact was
(Sidhu, 1979). Extrapolating from leaf litter,
conducted to a distance of 20 km downwind
rain and snow water fluoride measurements,
of the facility in 1973, 1974 and 1975
the range of impact did not extend beyond
(Thompson et al., 1979). Injury to balsam fir,
30–35 km from the source (Sidhu, 1982a,
black spruce and white spruce ranged from
1982b). Comparison of snow fluoride
complete defoliation to trace tip burn.

Marginal fluoride injury was observed on dominant balsam fir and black spruce trees
white birch and alder. Fluoride levels in within 5 km north of the phosphorus
conifer foliage ranged from 281 µg g-1 DW in manufacturing plant had been killed (Linzon,
the severely injured zone to 44 µg g-1 DW in 1978a). Chemical analyses of samples
the lightly injured zone to 7 µg g-1 DW in collected from balsam firs showed fluoride
controls. Soil fluoride concentrations ranged foliage levels over 100 times higher at a
from 908 ppm to 58 ppm to 10 ppm in the distance of 2 km from the source than at
respective zones. Fluoride deposition to the 20 km. Considerable amounts of fluoride
soil was five times greater from precipitation could be washed off the affected foliage,
than from leaf litter (Sidhu, 1982a, 1982b). suggesting that both particulate and gaseous
In black spruce needles, fluoride levels of fluorides were present in the area’s fluoride
100 to 200 µg g-1 DW covered 12 km2, 50 to emissions.
100 µg g-1 DW covered 31 km2, 20 to
Fluoride levels in the lichens Cladina
50 µg g-1 DW covered 23 km2, and 10 to
raniferina and Cladina stellaris correlated
20 µg g-1 DW covered 88 km2. The extent of
inversely with distance from the phosphorus
observed fluoride injury covered 80 km2; no
reduction plant at Long Harbour, following
visible injury was observed with foliage levels
the direction of the prevailing NE winds
up to 20 µg g-1 DW.
(Roberts and Thompson, 1980). Fluoride
In 1976, foliage of balsam fir, black spruce, concentrations in the lichens ranged from
larch and white birch displayed severe 2,830 µg g-1 DW in the severely damaged
symptoms of fluoride injury up to a distance area to 15.5 µg g-1 DW in the lightly
of 8 km from the source. Moderate damaged area to 6.4 µg g-1 DW in controls.
symptoms were observed between 8 and 9 Trace damage occurred at concentrations of
km, light symptoms from 9 to 12 km, and no 25 µg g-1 DW. Symptoms consisted of
symptoms beyond 12 km (Sidhu, 1979). discolouration and loss of structure. The
At the end of the 1976 growing season, fluoride concentration in lichens was twice
maximum fluoride concentrations in the that of the soil humus and half that of
foliage of these tree species in the zone bryophytes at the sample locations.
between 0 and 12 km from the plant were
The effects of fluoride emissions on the
265, 96, 411, and 357 µg g-1 DW,
flowering and fruit production of blueberries
respectively. Beyond 12 km, the fluoride
and raspberries, and on the foliage, cones
concentrations in the foliage of the same
and seeds of balsam fir, black spruce and
tree species were less than 20 µg g-1 DW.
larch were studied at six sites downwind from
Air monitoring, using sodium-formate plates,
the Long Harbour plant in the summer of
gave a calculated maximum fluoride level of
1982 (Sidhu and Staniforth, 1986; Staniforth
about 5 µg m-3 (6.1 ppb) at a distance of
and Sidhu, 1984). Fluoride levels, using
0.7 km from the source. Beyond 12 km, the
sodium-formate plates, ranged from
calculated level was 0.20 µg m-3 (0.24 ppb)
11.38 µg F m-3 at 1.4 km to 0.08 µg F m-3
or less.
at 18 km. The highest levels occurred in July
During another investigation of forest during the flowering of the blueberries and
damage at Long Harbour in the summer of raspberries. Flower mortalities were 89% for
1977, it was observed that over 80% of the blueberries and 78% for raspberries at the

highest fluoride site with a 21- and 10-fold surveys around the facility from 1969 until
reduction in seed production respectively, as 1985, one year after it ceased manufacturing
well as a significant decrease in size, operations in July 1984 (McLaughlin, 1981,
quantity and dry weight. Fluoride levels in the 1986). Forage was collected biweekly during
foliage ranged from 403 and 216 µg g-1 DW the growing season from 1975 to 1980 as
to 8 and 9 µg g-1 DW for raspberry and part of a control order that would result in
blueberry, respectively. Fluoride injury was the temporary shutdown of the facility if the
observed on the raspberry foliage. At the average fluoride content of the foliage
same six locations, chlorosis, necrosis, exceeded 80 ppm (80 µg g-1 DW, unwashed
needle damage and defoliation to balsam fir, material) for any one-month period,
black spruce and larch occurred when the 60 µg g-1 DW for any two-month period, or
fluoride concentration of the foliage 35 µg g-1 DW over the growing season. After
exceeded 20 µg g-1 DW. Injury occurred 1980, collections were made on a one-month
where airborne fluoride levels exceeded basis. In 1984, at a location 2,300 m east of
0.85 µg F m-3. Reduction in seed size, the plant fluoride levels ranged from
germination rate, number of seeds per cone, 17 ppm µg g-1 DW in April to 40 µg g-1 DW
number of cones per tree, number of fertile in August and back down to 11 µg g-1 DW
trees, and size reduction, distortion, or in October. Similar levels and seasonal
mortality of cones occurred under the same pattern had been observed at the same
fluoride gradient as for the blueberry and location in 1979 and 1980. During the
raspberry. Seed production on the windward same period, 4,600 m east of the plant,
side of the trees was significantly less than fluoride levels in foliage ranged from 2 to
on the leeward side. Reproduction failure 5 µg g-1 DW and there was no seasonal
and past mortality of fluoride damaged pattern. In 1985, fluoride levels in foliage
conifers have resulted in their being replaced dropped to 7 to 14 µg g-1 DW at the first
by the more tolerant hardwoods, birch and location and <1 to 2 µg g-1 DW at the second
alder. It is important to note that the location, with no seasonal trend observed.
calculation of airborne fluoride levels (in µg F The pattern of fluoride levels in forage near
m-3) from the sodium-formate plate data is the gypsum setting ponds over a seven year
specific for only this study, and represents period, as old ponds were capped and new
total fluoride levels, rather than gaseous HF ponds brought on line, showed that these
levels. ponds were a significant localized source of
fluoride emissions.
Fluoride levels (unwashed) and injury
4.3.2 Phosphorus Fertilizer Production
evaluations of maple foliage (red, silver,
Port Maitland, Ontario
sugar and Manitoba) were determined at
Inorganic fluoride emissions from a 30 locations within 6 km of the plant in
phosphorous fertilizer facility in Port September of each year. The highest
Maitland, Ontario, was associated with fluoride level in 1984 was 67 µg g-1 DW, 500
damage to conifers and deciduous trees m east of the plant and 26 µg g-1 DW, 600 m
facing the prevailing winds (Hall et al., 1968). south of the plant. Both stations had levels of
The Ontario Ministry of the Environment 400 µg g-1 DW in 1982 and 1983, and
conducted extensive terrestrial assessment 840 µg g-1 DW and 1,270 µg g-1 DW,

respectively, in 1979. There was a steady remarkable recovery in the radial growth
increase in the fluoride levels of maple following the abatement measures
foliage throughout the growing season. (McLaughlin and Emerson, 1984), and little
In 1979, 500 m east of the facility, fluoride or no fluoride injury has occurred on the new
levels were 50 µg g-1 DW in June, growth of needles (Linzon, 1986). The levels
255 µg g-1 DW in July and 840 µg g-1 DW in of fluoride in maple foliage and injury to
September. Injury on maple foliage in 1983 sensitive species has remained relatively
was observed up to 3.2 km NE of the facility. constant since 1978 (Emerson, 1994b). In
In 1984, it was limited to two sites within 1993, the highest level of fluoride in
500 m, and there was no injury in 1985. unwashed maple foliage was 155 µg g-1 DW
Wild grape, a fluoride-sensitive species, was at the site 1.6 km NE of the facility, and
used to delineate the zone of fluoride injury fluoride levels decreased rapidly with
around the operation. In 1983, the injury increasing distance.
zone extended 5 km NE of the plant and
A dendroecological study was conducted on
covered an area of 23.6 km2. This zone
nine tree species found on Cornwall Island in
remained unchanged (24.2 km2) in 1984 and
order to determine sensitivity ranking based
decreased to 1.4 km2 in 1985.
on annual tree ring-growth reduction and to
determine if reduction in growth occurred in
the absence of foliar injury (McLaughlin,
4.3.3 Aluminum Reduction
1991). The study looked at growth over three
Cornwall Island, Ontario
periods: pre-operation of the aluminum
Studies were started in 1969 on Cornwall smelter, 20 years of high, uncontrolled
Island, Ontario, to document the effects of fluoride emissions and 12 years of reduced
fluorides emitted from an aluminum reduction fluoride emissions. All species except green
plant located immediately to the south, in ash showed significant growth reductions
Massena, New York (Linzon, 1971). At a during the period of high emissions. There
sampling station about 1.6 km NE of the was no growth reduction during the period of
plant, eastern white pine needles had reduced emissions. During the period of high
accumulated 135 µg g-1 DW fluoride. The emissions, there was a deterioration in the
pines displayed an orange-red terminal relationship between climate and growth,
necrosis on their needles, showing severe and a consistent relationship between
injury; many were dead. Trembling aspen reduced growth and fluoride levels in
trees had 495 µg g-1 DW fluoride in injured vegetation and air. Based on growth
foliage and displayed reddish-brown reduction, the ranking of the nine species
marginal lesions. At a control location about from most sensitive to least sensitive was:
6.4 km NE of the source, eastern white pine trembling aspen, sugar maple, eastern white
and trembling aspen foliage displayed no pine, red oak, American beech, basswood,
-1
injury and contained less than 20 µg g DW. shagbark hickory, black cherry, and ash.
Since 1959, the aluminum company had Based on growth reduction, trembling aspen,
emitted 139 kg F hr-1 until abatement red oak and sugar maple were more
measures in 1972 reduced the emissions to sensitive than the literature rankings based
about 34 kg F hr-1. The eastern white pines on foliar injury, while black cherry was more
on Cornwall Island demonstrated a tolerant. The study concluded that foliar

injury is an unreliable indicator of the total 4.3.5 Aluminum Manufacturing
effect of fluoride on forest trees. Kitimat, British Columbia
A study of the effects of atmospheric
fluorides on tree growth in the vicinity of an
4.3.4 Aluminum Reduction aluminum manufacturer at Kitimat, British
Arvida, Quebec Columbia, was started in 1973 (Bunce, 1984,
Studies were conducted on the effects of HF 1985). A grid pattern containing 64
on epiphytic lichens and mosses near an permanent sample plots was established,
aluminum reduction facility at Arvida, increment cores were taken from the trees to
Quebec (Leblanc et al., 1971, 1972). Lichen measure tree growth, and foliage was
and moss-bearing bark discs were cut from collected for chemical analysis of fluoride
trees in an unpolluted area, fixed to trees at content. The forest area surrounding the
various sites near the aluminum facility, and smelter was segregated into an inner zone
left for periods of 4 and 12 months. At a (high effect), an outer zone (low effect), and
distance of 1 km from the source, the lichens a surrounding zone (no effect). Hemlock
accumulated 990 µg g-1 DW fluoride in 4 forests were severely damaged in the inner
months compared to 70 µg g-1 DW in a zone to a distance of about 8 km from the
control area located 40 km from the source. smelter. The growth rate of the forests from
During the same period, mosses 1954 to 1973 was reduced by 28% in the
accumulated 570 µg g-1 DW fluoride in inner zone and by 19% in the outer zone
compared to 20 µg g-1 DW in the control compared to growth rates before the smelter
area. Both species accumulated fluorides began operation in 1954. Fluoride in hemlock
even at a distance of 15 km from the foliage in 1974 measured 271 µg g-1 DW in
aluminum plant (190 µg g-1 DW in lichens the inner zone, and 163 µg g-1 DW in the
after 4 months, and 78 µg g-1 DW in mosses outer zone. Abatement measures were taken
after 12 months). They also calculated an at the smelter in 1974, and from 1974 to
index of atmospheric purity (IAP) which was 1979, the rate of fluoride emission was
based on the number of epiphytes, reduced by 64% of pre-1974 emissions (from
frequency of coverage and the resistance 5,500 kg day-1 to 2,000 kg day-1). The tree
factor of each epiphyte found on Populus growth reduction of 2,800 m3 per year
balsamifera at 42 sites covering an area of declined to 620 m3 during 1974–79. The
250 km2 within 15 km of the facility. While a fluoride content of hemlock foliage in the
total of 54 epiphytes, 9 bryophytes and 45 inner zone decreased to 87 µg g-1 DW in
lichens were recorded within the study area, 1979, and to 29 µg g-1 DW in the outer zone.
none was found within one kilometre of the The basal area decrease in forest growth
facility. IAP values ranged from 0, indicating remained high in the inner zone for the
no epiphytes found, near the plant to 103 period 1974–79, but a small positive
away from the facility. The IAP values increase in forest growth occurred in the
increased with increasing distance from the outer zone.
facility, suggesting that fluoride emissions
from the facility were affecting both the
density and frequency of epiphytes on
Populus balsamifera.

4.3.6 Aluminum Engine Casting since 1974. The levels ranged from a
Windsor, Ontario maximum of 46 µg g-1 DW in Manitoba
Fluoride accumulation in silver maple foliage maple 300 m west of the facility, to 4 µg g-1
and grass was found around a large DW 750 m west of the facility, with a
aluminum engine casting plant in Windsor, consistent gradient of decreasing fluoride
Ontario (Gizyn, 1994). Fluoride injury was levels with increasing distance. Levels varied
limited to trace amounts on wild grape within significantly from year to year depending on
400 m of the plant. Fluoride levels in uranium production. At the site 300 m east of
unwashed grass ranged from 183 µg g-1 DW the facility, fluoride levels in maple foliage
100 m east of the plant, to 2 µg g-1 DW 1 km (µg g-1 DW) ranged from a low of 20 in 1984
west of the plant. Fluoride levels in and 1986 to 1,075 in 1980 and 1,330 in
unwashed silver maple foliage ranged from 1977.
188 to 20 µg g-1 DW. The pattern of elevated
fluoride levels in grass and maple was
correlated with the prevailing wind patterns. 4.3.8 Tile Manufacturing
Niagara, Ontario
Soft suture disorder of peaches was reported
4.3.7 Uranium Processing from three orchards within one-half mile of a
Port Hope, Ontario facility manufacturing field drainage tile in the
Since 1974, the Ontario Ministry of Niagara Peninsula of Ontario (Drowly et al.,
Environment and Energy has conducted 1963). Early maturing varieties of peaches
annual assessment surveys to monitor the were the most susceptible to soft suture
impact of emissions from a uranium disorder. In two of the orchards, severe leaf
processing plant on the local terrestrial drop occurred in June, with characteristic
ecosystem (McLaughlin, 1988). The facility in fluoride injury on the leaves. Monthly
Port Hope, Ontario, produces uranium collections were made of peach leaves
hexafluoride and uranium dioxide; fluoride during the summers of 1960 and 1961.
and uranium are emitted into the atmosphere Fluoride levels in unwashed peach leaves
during production. In 1986, trace to light from the affected orchards averaged 40 to
injury (<1% to 10% injury to individual 50 µg g-1 DW compared to 27 µg g-1 DW
leaves) was observed on Manitoba and silver from control orchards. There was no
maple (moderately sensitive to fluoride) significant difference between the washed
within distances of 300 to 750 m. In 1987, and unwashed leaves, suggesting that
the same zone was rated at moderate (11– the emissions were mainly gaseous. The
35%) to severe (>35%) injury. Trace injury application of lime sprays to the peach trees
was observed up to 1,100 m downwind of reduced the incidence of soft suture.
the facility. In 1987, fluoride injury was also
observed on the fluoride sensitive plants
tulip, hosta, canna lilies, Gladiolus, wild 4.3.9 Brick Manufacturing
grape and St. John's wort to a distance of Southern Ontario
1.5 km NE of the facility. Fluoride levels in Investigations of fluoride injury to and the
unwashed maple foliage from 12 sites accumulation of fluoride in vegetation have
around the facility were the second lowest been carried out around a number of

brickworks in southern Ontario since the prominent in addition to fluoride marginal
early 1970s (Emerson, 1977, 1984, 1994a). necrosis. By 1972, when fluoride emissions
The zones of influence are generally had been eliminated, fluoride injury
localized around these operations, with injury symptoms had been totally replaced by
on sensitive species such as wild grape, boron injury. At the sampling station closest
eastern white pine and Manitoba maple to the facility, seasonal average fluoride
being moderate (11–35% injury on some concentrations (µg g-1 DW) in washed silver
leaves) up to 300 m downwind and light (2– maple foliage went from 613 in 1969 and
10% injury on some leaves) up to 500 m 1,600 in 1970 to 21 in 1973 and 26 in 1974.
downwind. Fluoride levels in unwashed Manitoba maple and buckthorn at other
maple foliage within 300 m of the brickworks locations showed a similar pattern. In 1969,
range from 100 to 360 µg g-1 DW, between fluoride accumulation in foliage, as defined
300 and 700 m downwind were 25 to 90 µg by a seasonal average fluoride concentration
g-1 DW, and drop off to 5 to 15 µg g-1 DW at of greater than 50 µg g-1 DW, extended
1 km from the brickworks. The levels of 2,000 m downwind of the facility. This
fluoride in washed foliage is marginally lower distance was reduced to 250 m in 1972 and
or no different than unwashed foliage, less than 30 m by 1974. There was no
indicating that the majority of the fluoride significant difference between the washed
emissions from these brickworks are and unwashed fluoride content in the leaves
gaseous in nature. of all three species, indicating the emissions
were primarily gaseous.
4.3.10 Fibreglass Manufacturing

Guelph, Ontario 4.3.11 Oil Refining
Fluoride and boron injury to natural Mississauga, Ontario
vegetation and in Gladiolus biomonitoring The sudden appearance of injury on Scot's
plots were studied around a fibreglass pines up to 5 km from an Ontario oil refinery
manufacturing facility in Guelph, Ontario, was investigated (Linzon, 1978b). The
from 1969 to 1976 (Temple et al., 1978). maximum amount of fluoride found in
Fluoride and boron were used as a severely injured Scot's pine needles was
component of the flux in the four glass- 16.3 µg g-1 DW, while the lowest amount of
melting furnaces. Fluoride emissions went fluoride found in the needles of control Scot's
from being uncontrolled in 1969 through a pines was 1.3 µg g-1 DW. In addition, eastern
series of control measures to total white pine, spruce, larch, plum, and
elimination of fluoride from the Manitoba maple displayed both marginal
manufacturing process in 1972. In 1969, necrosis and bifacial lesions in the central
severe fluoride injury on Manitoba maple, portions of the leaves. A histopathological
silver maple and buckthorn leaves was study was conducted on the injured Scot's
observed 150 m from the facility, with light pine needles (Linzon and Tung, 1976).
injury extending for another 150 m. In 1971, Cellular damage included collapsed
with the reduction of fluoride but not boron mesophyll cells, hypertrophied transfusion
emissions, the extent of injury remained the parenchyma cells in the stele, a compressed
same, but boron injury became more phloem and collapse of the endodermal ring

of cells surrounding the stele. The relative to SO2 treatment alone. HF (0.27 µg
combination of symptomatology, resistance, m-3) reduced peanut yield, while SO2 (279 µg
and sensitivity of different species, the m-3) reduced the number of pods and kernels
chemical analysis results, and the per plant without significantly reducing total
histopathological findings confirmed that the yield. The interactive effect on plant
injuries had been caused by an acute HF productivity of the two fumigants was less
fumigation. than additive. Navy bean yield increased at
141 µg SO2 m-3; this stimulatory effect was
removed by treatment with 0.25 µg HF m-3.
4.4 INTERACTIVE EFFECTS OF HF Overall, Murray and Wilson (1990)
WITH OTHER GASEOUS concluded that the effects of HF and SO2 are
often antagonistic since HF reduced the
POLLUTANTS
effects induced by SO2 exposure; however,
Marcross corn that was fumigated the actual responses are species-specific.
continuously with 0.56 µg m-3 and 191 µg m-3
SO2 for 12 days developed injury symptoms In wheat and barley, as in the experiments
that were greater than the sum of the effects outlined above, the responses to joint
of the two contaminants acting independently treatment with HF (0.38 µg m-3) and SO2
(Mandl et al., 1975). Similar results were (130 or 267 µg m-3) were complex, but
obtained by Murray and Wilson (1988a), who mostly antagonistic (Murray and Wilson,
reported that HF (up to 1.05 µg m-3) and SO2 1988c). The effects of SO2 alone were often
(up to 271 µg m-3) synergistically increased counteracted by treatment with HF.
visible leaf injury in some species of Fumigation of Marcross corn with HF
Eucalyptus. In a second series of experiments, (1.5 µg m-3) and NO2 (2,280 µg m-3), with a
HF (0.38 µg m-3) and SO2 (267 µg m-3) applied total dose of 2,280 µg HF days m-3 (which
through the growing season were antagonistic approximates a 24-day treatment period)
on leaf area, having less of an effect than resulted in less leaf damage than exposure
either compound alone (Murray and Wilson, to the same HF dose alone (Amundson et
1988b). However, the effects of these al., 1982). This was attributed to the
compounds on stem weight and above-ground increased leaf resistance induced by NO2,
plant weight were synergistic. Applied which likely resulted in reduced HF uptake
together, HF (1 or 3 µg m-3) and SO2 (260 or through the stomates.
780 µg m-3) both delayed the development of
Co-exposure to HF (1.0 µg m-3 for 4 hours
common blight on red kidney bean and
every second day over 8 days) and O3
resulted in smaller disease lesions (Laurence
(0.06 µl L-1 for 4 hours every second day
and Reynolds, 1986).
over 8 days, alternating with the HF
Simultaneous fumigation of soybean plants treatment) resulted in protection of 21-day-
-3 -3
with 0.26 µg HF m and 277 µg SO2 m old corn plants from HF damage (chlorophyll
did not reduce bean yield to the extent of loss and membrane leakage), relative to
SO2 fumigation alone (Murray and Wilson, ozone treatment alone (MacLean, 1990).
1990). The same treatments applied to Fluoride accumulation was enhanced in both
maize resulted in lower cob dry weights, the HF alone and HF + O3 treatments;
although kernel yield was not affected

however, HF alone had no effect on at this time to derive reference levels for HF
chlorophyll levels or membrane integrity. in the presence of other gases. As shown by
the experiments discussed above, these
The complexity of responses of plants to
gases may act antagonistically, additively, or
simultaneous or intermittent fumigations by
synergistically even within the same plant,
HF and other pollutants makes it impossible
depending upon the endpoint measured.

5 EFFECTS ON LIVESTOCK AND WILDLIFE
Review of the literature revealed a dearth of 5.1 PHARMACOKINETICS
information concerning the effects of
HF has the potential to cause significant
hydrogen fluoride on livestock and wildlife
injury due to the unique toxicity of the
which are exposed to hydrogen fluoride
dissociated fluoride ion (Bertolini, 1992).
mainly by the respiratory route. Some dermal
Upon contact with water, HF gas rapidly
exposure may occur when hydrogen fluoride
forms hydrofluoric acid. This acid readily
mixes with water to form hydrofluoric acid.
gives up the reactive fluorine atom which,
Indirect exposure may occur through
with cations, forms a fluoride salt. Calcium is
ingestion of fluoride deposited on vegetation.
rapidly altered to form calcium difluoride, an
Generally, it was found that mammals are almost insoluble fluoride salt. These two
less sensitive to the effects of hydrogen chemical reactions account for the toxicity of
fluoride than are plants. The difference in HF:
sensitivity is approximately 1,000 times,
• acidic burns caused by hydrofluoric acid;
depending on the duration and manner of
exposure. For this reason, it is suggested • sequestration of calcium as calcium
that the adverse effect on plants be used to fluoride resulting in hypocalcemia;
derive the reference level. • alteration of the calcium containing
Airborne fluorine compounds will eventually hydroxyapatite crystal in bone, resulting in
be deposited on and incorporated into, or fluorosis.
contaminate the surface of, plant tissues No pharmacokinetic studies of HF were
eaten by animals. Indirect exposure to found for livestock and wildlife. However, the
airborne fluorine compounds is generally kinetics of sodium fluoride (NaF) were
more significant than direct exposure; that is, studied in a group of three adult ewes which
ingestion is more pivotal than inhalation in had been given NaF intravenously at three
fluorosis. Therefore, consideration of an dose levels (0.15, 0.375, and 0.75 mg kg-1
ambient air guideline to protect livestock and body weight). Data were analyzed using both
wildlife from the adverse effects of fluorine or compartmental and non-compartmental
HF must take into account the inhaled approaches. A three-compartment open
portion of the total dose of fluoride, the model was selected to describe the data.
portion ingested in food and water and the Comparison of the different parameters
portion absorbed through the skin. indicated the absence of change with dose
This review approaches evaluation of the level, suggesting that fluoride behaved
effects of HF in terms of its pharmacokinetic linearly at the doses under study. The
effects (the effect of the body on the half-life of the elimination was 2.57 ± 1.28
chemical) and its pharmacodynamic effects hours, the steady-state volume of distribution
(the effect of the chemical on the body). was 0.26 ± 0.5 l kg-1, and the body clearance
There were insufficient data available to was 0.105 ± 0.26 l kg-1 h-1.
create a table showing effects following a Dermal absorption has not been described in
24-hour exposure to livestock and wildlife. animals, but probably occurs in whole-body

exposure studies. As hydrofluoric acid, 5.2.1 Acute Toxicity
dermal absorption is rapid and can be fatal in The acute toxicity of HF in livestock and
humans (Bertolini, 1992) and possibly wildlife has been poorly described. In a
animals. As a concentrated acid, hydrofluoric toxicologic pathological study mainly based
acid causes burns. However, burns may take on rodent exposure, dogs and rabbits were
several hours to develop at concentrations of exposed to concentrations of 6% to 50% of
20 to 50%. During this time, a large dose of the LC50 (median lethal concentration)
fluoride ions has been absorbed. These concentrations for rats (Rosenholz et al.
patients may die of hypocalcemia, a critical 1963). Rat LC50 concentrations had been
situation caused by sequestration of calcium established following exposure periods of
by fluoride. This cationic imbalance can 5, 15, 30, and 60 minutes to be
cause death by heart failure in a manner 4,074 mg HF m-3 (4,970 ppm),
similar to the disease “milk fever” 2,205 mg HF m-3 (2,690 ppm),
(hypocalcemia) seen in periparturient cows in 1,672 mg HF m-3 (2,040 ppm), and
veterinary medicine. 1,074 mg HF m-3 (1,310 ppm), respectively.
No studies on tissue distribution of fluoride The methodology did not describe the
were found that dealt with HF; however, the method of exposure in enough detail to
fluoride atom would be distributed primarily in determine whether whole-body or nose-only
tissues high in calcium. Because of its exposure had occurred. The eye irritation
affinity to calcium, fluoride concentrations would indicate that probably whole-body
are highest in bones and teeth following exposure had occurred.
chronic administration (Schupe et al., 1992). Clinically, animals exposed to near-lethal
Acute administration results in it binding to concentrations showed signs of conjunctival
blood calcium, hence the use of sodium and nasal irritation. Extensive nasal
fluoride as an anticoagulant. secretions, lacrimation, pawing at the nose
No elimination studies could be found; and sneezing were noted. Non-lethal
however, most fluoride is eliminated by the exposures also revealed clinical
kidneys (Bartik and Piskac, 1981). abnormalities. Rabbits (n=5) exposed to
50% of the rat (n=20) LC50 showed
respiratory distress lasting a few hours
5.2 PHARMACODYNAMICS following exposure, lacrimation, nasal
discharge, pawing at the nose, and
In the real-world situation, acute poisoning
reddened conjunctivae. Pawing at the nose
by fluorine, or HF, is rarely encountered in
continued for several hours following
domestic animals. Acute poisoning by
exposure. The animals appeared depressed
fluorides and hexafluoroplumbic salts, used
and weak for at least 24 hours and appeared
as pesticides, is more common (Bartik and
sluggish for an additional day. Signs of nasal
Piskac, 1981). There are a few reports of
and conjunctival irritation usually were not
accidental or intentional exposure to HF. For
seen after about four days (Rosenholz et al.,
the purposes of this review, they will be
1963).
classified by their temporal nature.
Dogs (n=2) were exposed to approximately
25% of the rat LC50 concentrations and

showed blinking, periodic sneezing, haematological parameters, and state that
coughing, and signs of general discomfort elevated mean corpuscular volume (MCV)
during the exposure. After removal from the values correlated with levels of sodium
chamber, the dogs rubbed their noses and fluoride. They also claim that decreased total
bodies on grass, suggesting some skin erythrocytes (RBC), haemoglobin (Hb),
irritation (also indicating probable whole-body packed cell volume (PCV), and mean
exposure). No skin lesions were noted. corpuscular haemoglobin (MCH) levels were
Although the cough disappeared within two associated with the elevated MCV values.
days, it reappeared upon exercise. All Evaluation of the data showed that the MCV
coughing ceased after a week to ten days. values were elevated in comparison to
Haematological data did not show any control animals, when mathematically
changes compared with pre-exposure data compared. However, there were no groups
and normal ranges for dogs (Rosenholz that fell out of the normal range for each
et al., 1963). parameter, indicating that the mathematical
differences were not biologically significant.
The pathologic portion of the Rosenholz et
Serum fluoride levels of the camels that
al. (1963) study was confined to the rats
received the greatest exposure (1.56 mg m-3;
exposed to HF. It should be noted that the
1.90 ppm) were seen to be ten times that of
clinical signs seen in the rabbits and dogs
the control group (0.09 mg m-3; 0.11 ppm).
occurred at doses 1,000,000 times the
The assay methodology is not detailed, nor
proposed ambient air quality reference level
are the exact criteria for the definition of
for HF.
fluorosis in the camels. For these reasons,
this paper should not be considered in the
5.2.2 Chronic Toxicity reference level derivation for ambient HF
concentrations.
Chronic HF toxicity has not been well
characterized owing to the nature of the
reactive molecule , which does not remain in
5.2.3 Developmental Toxicity,
the body as HF very long. For all intents and
Reproductive Effects and
purposes, chronic HF toxicity should be
Carcinogenesis
considered as chronic fluoride toxicity.
Chronic fluoride toxicity has been well No studies were found that dealt with the
reviewed elsewhere and will not be for the developmental, teratological, reproductive or
core of this review (Agency for Toxic carcinogenic effects of HF in livestock and
Substances and Disease Registry, 1993; wildlife.
U.S. National Academy of Sciences, 1974).
A case report of HF toxicosis in camels is 5.2.4 Fluorides
foound in Karram and Ibrahim (1992). These
Fluoride salts are present in most animal
workers evaluated the hemograms from 114
foods and occur naturally in many water
camels at various distances from a
supplies (Schupe et al., 1992). Fluoride salts
super-phosphate factory in Egypt. The
enter the mammalian body mainly through
authors took and analyzed blood sera and
ingestion, and may be passed on to the fetus
whole blood to determine fluoride levels and
(Schupe et al., 1992). Usually only small

quantities enter via the respiratory tract as changes in the skeletal system (Machoy
dusts (Ontario Ministry of Labour, 1983). et al., 1991).
Absorption of fluoride salts through the skin
is insignificant (Cass, 1961). The U.S.
Environmental Protection Agency (cited in
World Health Organization, 1984) lists the
most common sources of excessive fluoride
salts for livestock as follows:
• forage crops, usually the major source of

an animal's diet, which have been
contaminated by HF and fluoride salt
emissions, or wind-blown or rain-splashed
soil with a high fluoride salt content;
• water with a high fluoride content;
• feed supplements and mineral mixtures

that have not been properly defluorinated;
• forage crops grown in soils with a high

fluoride salt content.
The first of these sources is of primary
interest in the present context. The most
frequent causes of excessive fluoride salt
concentration in vegetation are industrial
emissions of HF and other fluoride salts.
Volcanic eruptions releasing HF can also
result in high concentrations of fluoride salts
in plants (Kessabi et al., 1984). The earliest
report of this phenomenon is from Icelandic
literature following volcanic eruptions about a
1,000 years ago (Roholm, 1937), but similar
effects were reported following the eruptions
of Mount Hekla in 1963. Eruptions in the
Lonquimay volcanic complex in the Andes
were the cause of bovine fluorosis in the
southern part of Chile (Araya et al., 1990).
The fluoride content of the ash was 75 to
100 µg g-1 and fluoride contaminated forage
was the main route of cattle intoxication.
Wildlife, such as deer, are also at risk of
contamination by fluoride-containing
industrial emissions, often detected by

One of the more aggressive forms of sulphate has been reported to alleviate
intoxication is the inhalation and ingestion of dose-related fluorosis (Kessabi et al., 1986).
dust containing fluoride, since this causes an Fluoride crosses the bovine placenta, which
abrasive local action on the respiratory and acts as a partial barrier (Schupe and Bagley,
digestive systems in addition to the usual 1992). Pharmacokinetics of fluoride (see
systemic effects (Bartik and Piskac, 1981). section 7.1) have been determined in sheep
(Joseph-Enriquez et al., 1990). The effects
Injury caused by fluoride salts (fluorosis) in
of fluorosis have been described in cattle
livestock develops progressively when total
(Schupe et al., 1992) and camels (Karram
fluoride dietary concentrations exceed 20 to
and Ibrahim, 1992).
30 µg g-1 (U.S. National Academy of
Sciences, 1974). Here the fluorine atom Animals differ in their susceptibility to
binds to calcium, rendering the calcium ingestion, as shown in table 7. Ingestion
atoms unavailable for their normal bodily would represent the indirect route of
functions. Diagnosis of fluorosis is based on exposure to airborne fluorine compounds.
clinical observations, especially of dental and Based on the previous review, the lowest
skeletal lesions, lameness, biopsy of tail level of fluoride in forage or feed which
bones, determination of fluoride in the total appears to lead to adverse effects is
diet, effects on appetite, decreased milk 40 µg g-1 DW in the most sensitive species.
production or body growth and, where The atmospheric concentration of HF which
applicable, post mortem examination. The would lead to such levels appear to be 0.33
simultaneous administration of aluminium to 1.3 µg m-3 fluorides for 30 days.
Laying or 400
breeding hens
Table 7 Susceptibility of animals to
fluoride by ingestion Turkeys 400
Animal Fluoride feed levels Source: World Health Organization, 1984
affecting performance
(µg g-1)
5.3 CONCLUSION
Beef or dairy 40
heifers In addition to the dearth of information on
effects at different exposure levels, time of
Mature beef or 50
exposure does not support the development
dairy heifers
of a 24-hour exposure reference level for the
Finishing cattle 100
protection of livestock and wildlife. From the
Feeder lambs 150 weak chronic study data, it appears as
Breeding ewes 60 though a continual exposure on mammals
Horses 60 should not exceed 7 mg m-3. This
concentration is more than three orders of
Growing dogs 100
magnitude greater than that recommended
Finishing pigs 150 for the HF reference level based on the
Breeding sows 150 effects of HF on plants.
Growing or boiler 300 Airborne fluorine compounds will eventually
chickens be deposited on and incorporated into, or

contaminate the surface of, plant tissues accounts for its pharmacodynamic
eaten by animals. Indirect exposure to properties: it mixes with water to form a
airborne fluorine compounds is generally strong acid resulting in burns, and it binds to
more significant than direct exposure; that is, calcium resulting in sequestration of calcium
ingestion is more pivotal than inhalation in and alteration of bone calcium (chronic
fluorosis. Therefore, consideration of an exposure). As HF rapidly becomes a fluoride
ambient air guideline to protect livestock and salt, the majority of the toxicity issues can be
wildlife from the adverse effects of fluorine or considered under the evaluation of the
HF must take into account the inhaled toxicity of fluorides. No chronic exposure
portion of the total dose of fluoride, the studies were available for HF.
portion ingested in food and water, and the
It is concluded that while plants are more
portion absorbed through the skin.
likely to be affected at lower concentrations
HF gas is a potent, acute toxicant when of HF than livestock and wildlife, protection
animals are exposed to large quantities of farm and wild animals from fluorosis can
directlyly via the respiratory route. The be achieved by implementing a maximum
chemical properties of the compound level of fluorides in feed and forage.

6 EFFECTS ON EXPERIMENTAL ANIMALS
There are a number of reports on the effects the rabbits and guinea pigs exposed.
of hydrogen fluoride on experimental Damage to liver, kidneys and lungs was
animals, usually rodents. observed in animals exposed to 245 mg m-3.
Dipasquale and Davis (1971) reported the
lethal concentration for 50% of the exposed
6.1 ACUTE TOXICITY population (LC50) for a five-minute exposure
This section includes results from studies to HF for rat and mouse to be 14,400 and
where animals were exposed to HF for 24 5,000 mg F- m-3, respectively.
hours or less. HF and other gaseous The 60-minute LC50 values for rats and mice
fluorides such as tetrafluoride induce were reported to be 1,100 and 270 mg F- m-
3
respiratory tract damage. If this damage is , respectively (Wohlschlagel et al., 1976).
not in itself lethal, systemic intoxication may When rats were exposed through inhalation
follow (World Health Organization, 1984). to HF for 5, 15, 30, or 60 minutes, the
Five guinea pigs and five rabbits died in 0.5 LC50s were 4,060, 2,200, 1,670 and
and 1.5 hours, respectively, after exposure 1,070 mg HF m-3, respectively. The LC50
to 540 mg m-3 HF (660 ppm). When five for guinea pigs with an exposure time of
guinea pigs and five rabbits were exposed to 15 minutes was 3,540 mg HF m-3. Irritation
205 mg m-3 HF (250 ppm), they died within of the mucous membranes of the eyes and
1.0 and 3.0 hours. All animals showed nose, weakness, and a decrease in body
severe signs of irritation from the start of the weight was observed in the HF-exposed
experiment, with increasingly laboured animals (World Health Organization, 1984).
breathing. Autopsy showed ulceration of the Acute inflammation and focal necrosis of the
upper respiratory tract and of the cornea of nasal mucosa, irritation of the skin, necrosis
the eyes. The lungs were hyperaemic and of the renal tubular epithelium, congestion of
edematous. At 40 mg m-3 (50 ppm), five the liver and vacuolisation of its cells and
guinea pigs died in two hours, whereas the myeloid hyperplasia of the bone marrow
five rabbits displayed severe signs of were found histologically (World Health
physical distress after three hours of Organization, 1984).
-3
exposure. At a concentration of 25 mg m The HF LC50 value is three to five times
(30 ppm), guinea pigs died after a day, while higher than the fluorine LC50 value in rats. In
rabbits were in such poor condition that they general, the gradient of susceptibility in
were sacrificed. Continuous exposure at 8 laboratory rodents is mice>rats>guinea pigs
mg m-3 (10 ppm) for 5 days was not fatal to (Rosenholtz et al., 1963; Agency for Toxic
either species. In addition to laboured Substances and Disease Registry, 1993).
breathing, the guinea pigs showed only slight
Sub-lethal inhalation exposure of rats and
irritation of the eyes (Ronzani, 1909, cited in
mice to fluorine or HF affects the respiratory
Heitman, 1976).
system (mild congestion, disperse), liver
Machle et al. (1934) reported that exposure (coagulation necrosis and cloudy swelling),
to 1,000 to 1,500 mg HF m-3 for five minutes kidney (coagulation and necrosis) and
caused death in a significant proportion of mucous membranes (irritation of eyes and

nose) (Keplinger and Suissa, 1968). In this and rats were 374 mg m-3 and 792 mg HF m-
3
study, rats, mice and guinea pigs, rabbits , respectively (Vernot et al., 1977). McEwen
and dogs were exposed to fluorine for 5 and Vernot (1971) reported that, following a
minutes at 820 mg m-3 (1,000 ppm), 15 5-minute exposure to HF, most of the
minutes at 57 mg m-3 (70 ppm), 30 minutes exposed animals experienced pulmonary
at 45 mg m-3 (55 ppm), or 60 minutes at 37 edema of varying severity, and pulmonary
mg m-3 (45 ppm). This non-linear effect haemorrhage was a common finding in
illustrates the difficulty in extrapolating to animals that died during or shortly after
24-hour ambient concentrations. These exposure to HF at levels above the LC50
sublethal concentrations did not result in any value.
significant differences in haematological
Inhalation of HF constitutes the most
parameters. Gross evaluation of the animals
common route of exposure; however, there
sacrificed serially after exposure showed that
are data to suggest that absorption does not
the lungs had the greatest change of any
only occur at the level of the alveolar
organ (the nasal passages were bypassed).
epithelium. In a study of the regional
Lesions seen included congestion,
disposition and absorption of inhaled HF
petechiation, and diffuse consolidation.
(36 to 176 mg F m-3) in male Long-Evans
These lesions decreased in severity with
rats, it was seen that virtually all inhaled HF
time after exposure. The interpretation of
was deposited in the upper respiratory tract.
these lesions was not given by the authors,
Less than 0.1% was found to pass into the
although their appearance is typical of
lungs thus leaving 99.7% absorbed in the
diffuse bronchiolar and alveolar damage.
upper respiratory tract. The authors
Histopathology revealed that coagulation
concluded that although the upper
necrosis was present in the lower airways
respiratory tract serves to protect the lower
and the alveoli, consistent with hydrofluoric
respiratory tract in rats, most of the
acid damage. The explanation for the
absorption into the blood stream results from
hepatic coagulation necrosis is more difficult
absorption at the lower site (Morris and
since the zonal nature of the lesion was not
Smith, 1982).
given. If hydrofluoric acid had been
swallowed in substantial quantities, then In another experiment (Stavert et al., 1991),
absorption of the compound into the portal biologically significant damage to the middle
tree could have resulted in zonal coagulation and lower airways occurred when male
necrosis. The anticipated distribution of this Fischer-344 rats were forced to breathe
necrosis would be periportal in nature. approximately 1,066 mg m-3 (1,300 ppm) of
HF vapour for five minutes. These animals
The acute toxicity of five-minute exposure to
were intubated with endotrachial tubes, thus
HF was studied also by Higgins et al. (1972)
bypassing the nasal cavity. It is clear from
in rats and mouse in an observational period
the above experiments that the nasal cavity
of seven days. The five-minute LC50 was
protects the lower airways from the corrosive
14,900 mg m-3 HF (18,200 ppm) and for mice
-3
effects of gaseous HF, and acts as the major
5,120 mg m HF (6,247 ppm). The same
site of absorption of this compound.
LC50s for mice and rats were also reported
by McEwen and Vernot (1971). For a 60- The pathology seen in the rats acutely
minute exposure, the LC50 values for mice exposed to HF can be attributed to the

corrosive nature of the compound, once it findings. All surviving animals had lost up to
comes into contact with the water associated 23% of their original weight and had severe
with the exposed epithelium and forms anemia. After five HF-exposed guinea pigs
hydrofluoric acid. In the upper respiratory had been immunized, they showed a marked
tract severe epithelial necrosis, decrease in the production of specific
fibrinopurulent exudate and submucosal antibodies, and their resistance to bacterial
inflammation indicate that a full thickness infection in the lungs was reduced. While
epithelial burn had occurred in the nasal exposed to HF, the animals were less
cavity of rats treated with 1,066 mg m-3 resistant than controls to the effects of
(1,300 ppm) HF for 30 minutes (Stavert et inoculation with diplococous and tuberculous
al., 1991). bacilli; the opposite was true for anthrax
(Ronzani, 1909, cited in Heitman, 1976).
Mild suppurative tracheitis was present in the
Nevertheless, these results seem to indicate
proximal trachea of these treated animals
an immunotoxic effect of airborne HF.
(Stavert et al., 1991). This less severe lesion
Further studies by Ronzani (1909, cited in
decreases in severity the more distal it is
Heitman, 1976) using HF concentrations of
from the nose. This may indicate a decrease
6, 4, and 2.5 mg m-3 (7.5, 5, and 3 ppm)
in the concentration of HF as it is removed
established 2.5 mg m-3 (3 ppm) as the
from the air space higher up the airway.
NOAEL (No Observable Adverse Effect
The lungs also showed mild irritation,
Level), because in a 30-day study with
characterized by infiltration of neutrophils in
16 rabbits, 20 guinea pigs and 3 pigeons,
the alveoli. There was no description of
exposure to HF did not cause any pathologic
necrosis of alveolar epithelium, known for its
changes.
exquisite sensitivity to insult.
Machle and Kitzmiller (1935) reported that no
externally obvious adverse effects were
6.2 SHORT-TERM TOXICITY noted in rabbits, guinea pigs and Rhesus
The only gaseous fluoride exposure studies monkeys exposed to 15.2 mg HF m-3 for a
that have been reported are for HF, and of total of 309 hours (six to seven hours per
those few reports the exposure durations day over about 10 weeks, observed for up to
were one day to one year. eight more months post-exposure). Two
guinea pigs became sick and died after
Fifteen rabbits, 21 guinea pigs and four 134 and 160 hours of exposure. Both of
-3
pigeons were exposed to HF at 8 mg m these animals showed liver and lung damage
(10 ppm) for two 3-hour periods per day (one had pulmonary haemorrhage), and one
for 31 days. During this period, two rabbits, had kidney damage. The surviving animals
seven guinea pigs and one pigeon died. were normal in behaviour and appearance,
At autopsy, opacity of the cornea with but had decreased growth rates. Some had
ulcerations, lesions of the nasal mucous decreased erythrocyte counts. At necropsy,
membranes, emphysematous lungs, these rabbits and guinea pigs exhibited
bronchopneumonitis, and interstitial varying degrees of lung, liver and kidney
pneumonitis were found. The autopsy of one damage. The Rhesus monkeys revealed
of the rabbits surviving the exposure periods kidney damage only. The authors indicate
showed similar, but less severe, pathologic that the lower limit of toxic HF concentrations

in air lies between 30 and 2.5 mg m-3 based cortical degeneration and necrosis were
on older studies (Ronzani, 1909, cited in noted in 27 of 30 animals. At the 7 mg HF m-
3
Heitman, 1976; Flury and Zernik, 1931). level, localized haemorrhagic areas in
the lungs were observed only in one dog.
Stokinger (1949) performed a toxicity study
A progressive increase of fluoride in the
in which 29 rats, 20 mice, 20 guinea pigs,
animal bones was detected at the
18 rabbits and 4 dogs were exposed to
25 mg HF m-3 exposure level, from 25 to
gaseous HF at concentrations of 25 and
95 hours. The fluoride concentration in the
7 mg m-3 for six hours per day, six days per
rats’ teeth increased 300%. A somewhat
week for five weeks. A second group of
smaller increase was found in the femur. In
animals (15 rats, 20 mice, 10 guinea pigs,
maxillary and mandibular bone of the dogs,
10 rabbits and 5 dogs) were exposed to
increases of fluoride concentrations ranged
7 mg HF m-3 for the same period.
from 200 to 300%. The fluoride
Subcutaneous haemorrhages, particularly
concentration of animal bones exposed to 7
around the eyes and on the feet, were
mg HF m-3 for 166 hours was somewhat
observed in rats and, to a lesser degree, in
lower than that of in the high exposure level.
mice. In dogs, an inflammation of the scrotal
According to Heitman (1976) for this study at
epithelium was seen after three days’
almost equal HF concentrations times
exposure. These effects were observed
exposure time (HF dose), the fluoride
mainly at the 25 mg HF m-3 exposure level,
deposition in bone and teeth was
although haemorrhagia to lesser extent was
approximately the same. In this study of
also noticed on the feet of rats exposed to
Stokinger (1949) a distinct NOAEL (No
7 mg HF m-3. Death occurred only at
Observable Adverse Effect Level) could not
25 mg HF m-3 in all rats and mice. Deaths
be established, as some slight haemorrhagic
occurred in rats throughout the entire
changes in the lung were still observed at the
exposure period, while all mice died by
lowest level tested (7 mg HF m-3). Stokinger
17 hours of exposure. At the 25 mg HF m-3
et al. (1950) reported the effects of airborne
concentration, rats showed pronounced
HF on 29 rats exposed 6 hours per day, 5
weight loss; rabbits showed a slight loss,
days per week at an average concentration
dogs showed none while guinea pigs, after a
of 8 mg HF m-3 for total of 124 hours
consistent gain, lost weight following the third
(approximately 4 weeks). In this study no
week of exposure. No species showed any
-3 adverse effects due to exposure to HF were
significant effects on weight at the 7 mg m
observed, indicating that the NOAEL could
level. No effects were noted on blood-
be 8 mg HF m-3 at that exposure regime for 4
calcium alkaline phosphatase or serum
weeks. However, no higher exposure level
proteins in dogs and rabbits. There was a
were tested in this study.
significant increase in blood fibrogen level in
dogs and rabbits exposed to 25 mg HF m-3, Changes in the lipoid, cholesterol and total
while the prothrombin level remained normal. lipid content in the lungs and liver have been
At autopsy, 27 out of 44 animals exposed to studied in 4 series of experiments on
-3
25 mg HF m showed haemorrhages and 337 white rats, exposed to HF, H2S and SO2
edema of the lungs. Degenerative testicular for 4 hours daily during 4 months. Isolated
changes and ulcerations of the scrotum and combined effects of theses gases
were found in four dogs. In rats, renal induced phasic changes of varying degree,

depending on the gas concentration. The (and decreased under the effect of H2S).
lipid content in the lungs was reduced under A NOAEL in this study is not indicated
the effect of gas in low concentrations, and (Aitbaev, 1984).
in the liver it increased under the effect of HF
Inhaled HF (10 mg m-3 for 14 days) increases
plasma cholesterol levels very significantly in
normal guinea pigs and in guinea pigs with
chronic latent vitamin C deficiency. Ascorbic
acid deficiency significantly increased
plasma cholesterol levels in exposed animals
and controls. But ascorbic acid deficiency
produced an increase in cholesterol less
important than HF inhalation. These results
showed that vitamin C deficiency and HF
inhalation both produce an increase of
cholesterol level, but they do not interact.
The mechanism of cholesterol increase has
been investigated. In HF inhalation, the
activity of cholesterol 7 alpha-hydroxylating
system containing cytochrome P450 does not
decrease in the liver microsomes (Dousset
et al., 1984).
Two experiments studied the effect of HF
inhalation on lipid metabolism in guinea pigs
(Phillibert et al., 1991). In the first
experiment, control was established before
guinea pigs were exposed to 7 mg HF m-3 for
96 hours, following which the effects were
measured on their plasma cholesterol, non-
esterified fatty acids and cyclic AMP.
Exposed guinea pigs showed no weight
change, but their plasma fluoride
concentration increased significantly, from
8.5 to 203.2 µmol L-1 . Mean plasma
cholesterol and free fatty acids also
increased significantly. As well, plasma
cAMP had increased, which could be the
cause of changes in lipid parameters.
However, experiments with theophylline
showed that the increase in plasma
cholesterol was mediated by the increase of
plasma.

The second experiment consisted of three months of HF exposure an increase in both
groups with 14 guinea pigs per group: a total lactate dehydrogenase (LDH) and
control group, a group treated with orally creatinine-kinase (CK) and in the myocardial
administered simvastatin (a drug inhibiting LDH and CK-MB isoenzymes was detected.
the activity of beta-hydroxy beta- methyl (Bourbon et al., 1979). From these results, it
glutamyl CoA {HMG-CoA-reductase}, which is indicated that a long-term exposure to 125
regulates the biosynthesis of cholesterol), to 203 µg HF m-3 will cause cardiotoxic
and a group exposed to 7 mg m-3 for 96 effects, and thus a NOAEL cannot be
hours. These studies provide no information established.
to establish NOAEL. It was demonstrated
In another long-term inhalation study, 50
that inhaled HF modifies the biosynthesis
guinea pigs were subjected to an
regulation of cholesterol by an effect on the
atmosphere containing 150 µg HF m-3 for 18
HMG-CoA reductase activity.
months in order to evaluate the histological
and biochemical effects on kidney
functioning. Unexposed guinea pigs were
6.3 LONG-TERM TOXICITY AND used as a control group. In this study there
CARCINOGENICITY STUDIES were also interim kills at six and 12 months.
There are very few long-term toxicity studies The only effect observed in the HF-exposed
of gaseous HF. The studies involve guinea pigs was a transient increase of
exposures for periods greater than one year. calciurea and phosphaturea. The authors
concluded that inhaled HF did not cause any
In one study, guinea pigs and rabbits were
alteration of kidney function in either the
exposed to as little as 24.5 mg HF m-3 for six
biological or histological parameters of the
hours daily for a total of 41 hours; they were
kidney and its function (Rioufol et al., 1982).
autopsied 18 hours post exposure. There
This study did not provide a real NOAEL.
were no deaths among the animals left alive
and observed for one year (Machle and No animal bioassays have been reported on
Kitzmiller, 1935; Machle et al., 1934). the potential carcinogenicity of inhaled
fluorides (Thiessen, 1988).
In a long-term inhalation study, 50 guinea
pigs were exposed to an atmosphere varying Because of the nature of the compound,
from 125 to 203 µg HF m-3 for 18 months in chronic low-level exposure to HF can be
order to study the effects on the metabolism treated as being equivalent to fluoride salts.
of myoardial cells and biochemical serum Table 8 lists reported NOAELs and LOAELs
parameters indicative for cardiac cell (Lowest Observable Adverse Effect Levels)
damage. An unexposed group of guinea pigs for mice and rats. More detailed information
served as control. In the study there were about fluoride salts can be found in Agency
also interim kills at six and 12 months. After for Toxic Substances and Disease Registry
six months of exposure to HF a significant (1993), National Research Council (1971)
increase in the oxygen consumption of and Drury et al. (1980). Longer-term effects
myocardial cells, whereas a strong significant of HF have been investigated in rats, mice,
decrease in oxygen consumption was guinea pigs, rabbits and dogs. All species
observed after 12 and 18 months of were exposed to 7 or 24 mg m-3 HF for six
exposure. In addition, after 12 and 18 hours per day, six days per week for 30 days

(Stokinger, 1949). Marked species pig, rabbit or dog exposed at this
differences were noted. All rats and mice concentration died. No animal of any species
exposed to 24 mg m-3 died, but no guinea died following exposure to 7 mg m-3.
Table 8 Estimates of NOAEL and LOAEL for mice and rats

NOAEL (mg F2 m-3) LOAEL (mg F2 m-3)
Mice Rats Mice Rats
Mean + SD* 106 + 67 75 + 31 153 + 75 146 + 65
Range 23 - 263 42 - 132 45 - 303 71 - 263
Source: Agency for Toxic Substances and Disease Registry, 1993
* Standard deviation
No Observable Adverse Effect Levels and other biological endpoints (Alexeeff

(NOAELs) and Lowest Observable Adverse et al., 1993).
Effect Levels (LOAELs) for rats and mice
have been estimated (Agency for Toxic
Substances and Disease Registry, 1993), 6.4 REPRODUCTIVE TOXICITY,
and are presented in table 8. These data TERATOLOGY AND
refer to lethality. The NOAELs quoted are for
GENOTOXICITY STUDIES
the following endpoints:
With the exception of a study in Drosophila,
• rat, rabbit and dog haematology no specific genotoxicity experiments with
(24 mg m-3 for 6 hours per day, airborne HF or other fluorides are reported.
6 days per week),
Several authors have suggested the
• renal disease in rats (7 mg m-3 for 6 hours potential mutagenicity of either HF or sodium
per day, 6 days per week), fluoride (NaF) to lower (bacteria, yeasts) and
• neurological effects (0.03 mg m-3 for higher plants (Drosophila) or mammals
5 months undisclosed exposure), and (Caspary et al., 1987; Cole et al., 1986;
Gerdes, 1971; Gerdes et al., 1971; Mitchell
• testicular degeneration (7 mg m for
-3
and Gerdes, 1973; Mohamed, 1977;
6 hours per day, 6 days per week for
Mohamed and Kenner, 1969; Tsutsui et al.,
30 days).
1984 a, 1984b, 1984c; Voroshilin et al.,
The equivalent information is not available 1973, 1975). On the other hand, Leonard et
for livestock or other animals. The latter al. (1977) found no increase in chromosome
raises the issue of robustness of the aberrations in the leucocytes of cattle with
reported concentrations because of changes chronic fluoride poisoning, nor did Voroshilin
in chemical methods. et al. (1973) or Obe and Slasic-Erben (1973)
The use of lethality data from experimental in human leucocytes treated in vitro with 18
animals may overestimate the practical and 54 mg L-1 NaF. Temple and Weinstein
threshold of the effects of fluorine and HF (1978) were unable to demonstrate
since the slopes are steeper than for irritation mutagenicity of HF in tomato plants. Martin

et al. (1979) found no evidence for increased chromosome aberration in mice following
exposure to NaF administered orally, nor did
they find NaF to be mutagenic in a bacterial
(Salmonella) mutagenesis assay and it did
not induce gene inversion in Sacheromyces
cerevisiae. A review by the International
Agency for Research on Cancer (1982)
found that NaF is not mutagenic in
Salmonella or Drosophila, and both the US
EPA (Federal Register, 1985) and the Safe
Drinking Water Committee (1977) concluded
that the mutagenicity of fluoride in humans
has not been demonstrated (Thiessen,
1988). Little or no effect was noted on
chromosomes when mouse oocytes were
exposed in vitro to a fluoride concentration of
200 mg L-1 in media for up to 14 hours.
Sheep and cow oocytes were unaffected by
a concentration of 100 mg L-1 in media for 24
hours (Jagiello and Lin, 1974). Mohamed
and Chandler (1977) reported that the
number of cells from bone marrow or
spermatocytes with chromosomal
abnormalities increased in mice with a
fluoride dose in drinking-water of 1 mg L-1 or
more. Owing to various inconsistencies and
lack of proper double-blind procedures, the
results of Mohamed and Chandler (1977)
have been questioned (Victoria Committee,
1980; World Health Organization, 1984).
6.5 CONCLUSION
With the paucity of data in experimental
animals, it becomes difficult to establish air
quality objectives . Furthermore, the
chemical analytical procedures used in the
older references (i.e., pre-1950s) may not be
as precise or accurate as today's methods.
At best, the conclusions can only address
acute exposure to HF. Human sensory levels
may be more sensitive than animal studies in
establishing tolerable levels for brief human

exposures (Rosenholz et al., 1963). For 1968; Wohlschlagel et al., 1976) to the
example, it appears that humans (Largent, irritant effects of fluorine or HF, perhaps by
1961; Machle et al., 1934) might be more an order of magnitude.
sensitive than rats (Keplinger and Suissa,

7 EFFECTS ON HUMAN HEALTH
Acute exposure to gaseous fluoride is rare in 20 (Heitman, 1976). To account for any
a non-occupational setting. Hydrogen uncertainty in the figures for hydrogen
fluoride and fluorine are extremely toxic, fluoride and other airborne fluorides, the
posing immediate danger to health and life. environmental limits are expressed in mg m-
3
Both gases can cause severe respiratory instead of in ppm. Especially at high
damage or skin burns on contact. Skin burns exposure levels, the best way to express the
and respiratory damage caused by hydrogen concentration for review of toxicological
fluoride are the only toxic effects of hydrogen studies is in mg m-3 if possible (if given).
fluoride that are not attributable solely to the When units for airborne hydrogen fluoride
action of the fluoride ion. Systemic fluoride are converted from ppm to mg m-3 in this
poisoning usually occurs from hydrogen report, it is assumed that airborne hydrogen
fluoride absorbed via the lungs or the skin fluoride exists as a monomer. If it is clear
(Thiessen, 1988). that the data refer to hydrogen fluoride, a
conversion factor can be applied, and these
Following exposure to gaseous fluorides and
calculated figures are indicated in
hydrogen fluoride by either inhalation or
parentheses. If total gaseous fluoride is
dermal contact, systemic effects are based
indicated, it is not possible to express the
on the fluoride absorbed and in circulation in
units other than as given, unless the
the body. Under these circumstances,
molecular weight or a conversion factor is
systemic toxicity parallels the toxicity of
provided by the authors.
ingested fluoride. Where possible, this
discussion is limited to aspects of the toxicity
of gaseous hydrogen fluoride. A more
complete overview of fluoride toxicity can be 7.1 PHARMACOKINETICS
found in several extensive reviews (World
Health Organization, 1984; Thiessen, 1988;
7.1.1 Absorption
Government of Canada, 1993).
Inhaled fluorides consist primarily of
A comparison of the properties of hydrogen hydrogen fluoride and particulate fluorides,
fluoride with those of other hydrogen halides both of which can be deposited in the
indicates deviations from expected values respiratory tract (World Health Organization,
because of polymerization of the hydrogen 1984). Hydrogen fluoride, which is highly
fluoride molecule. The degree of soluble, is rapidly taken up in the upper
polymerization varies depending on the respiratory tract (World Health Organization,
partial pressure of the hydrogen fluoride and 1984) and quickly absorbed into the system,
the temperature. At airborne concentrations either directly from the respiratory tract or
of hydrogen fluoride at or near the following translocation to the gastrointestinal
recommended limits in the workplace, the tract via nasal mucus (Morris and Smith,
partial pressure will be low enough that the 1982). Close to 100% of inhaled hydrogen
polymerization of hydrogen fluoride is fluoride is absorbed (Machle and Largent,
negligible. In this situation, it is probable that 1943; Thiessen, 1988). Absorption of inhaled
the molecular weight of hydrogen fluoride is fluorides is dependent on several factors,

including the chemical nature of the fluoride processes (Collings et al., 1952; Charkes et
and of other substances that may have been al., 1978; World Health Organization, 1984;
co-ingested or co-inhaled. Fluoride from Thiessen, 1988). Approximately 35–48% of
inhaled dust is absorbed as rapidly as from systemically absorbed fluoride from any
inhaled hydrogen fluoride, but the total source is retained in the human body (Hodge
fluoride is less than from gaseous fluorides and Smith, 1965; World Health Organization,
(Collings et al., 1952). Hydrogen fluoride is 1984; Thiessen, 1988). At low fluoride
readily absorbed through the skin of uptake levels (non-occupational, <4.0–5.0
individuals accidentally exposed in the mg/day), there may be very little cumulative
workplace, leading to hydrofluoric acid burns storage of fluoride (McClure et al., 1945).
(Burke et al., 1973; Tepperman, 1980; World Studies with radioactively labelled fluoride
Health Organization, 1984). suggested that the body retains about 60%
of intravenously injected fluoride (Charkes et
Absorption of any fluoride appears to be a
al., 1978; World Health Organization, 1984).
passive process (Drury et al., 1980). Fluoride
The half-life for uptake by bone tissue is very
from any source is thought to be transported
short, about 13 minutes; both blood and
across biological membranes primarily as
extracellular fluid levels decrease rapidly.
molecular hydrogen fluoride (Whitford et al.,
Approximately 99% of fluoride in the body is
1976; Guttknecht and Walter, 1981; Whitford
found in the skeleton. The remaining portion
and Pashley, 1984). At physiological pH (in
is distributed between the blood and soft
blood, intracellular fluid or mucus), fluoride
tissues (World Health Organization, 1984;
from any source exists primarily as the
Thiessen, 1988).
fluoride ion (F ), although a small amount of
molecular hydrogen fluoride exists in Fluoride in human serum exists in both ionic
equilibrium with the ion. The fate and effects and nonionic forms (Taves, 1968a, 1968b;
of absorbed inorganic fluorides are World Health Organization, 1984). At least
essentially independent of the fluoride half of the fluoride in the human body
source (Thiessen, 1988). consists of organic fluoride (perfluorinated
fatty acid derivatives containing 6–8 carbon
atoms) and non-ionizable fluoride from F- or
7.1.2 Distribution hydrogen fluoride (Ophaug and Singer,
Once absorbed by the human body after 1977; Morris and Smith, 1983; World Health
inhalation, fluoride is transported through the Organization, 1984; Thiessen, 1988). Guy
body via the bloodstream and is then et al. (1976) indicated that human serum
retained in the tissues, predominantly the contains much smaller quantities of
skeleton, or excreted, mainly in the urine uncharacterized organic fluorocarbons. The
(World Health Organization, 1984). About amount of non-ionic fluoride is related to the
75% of the fluoride in blood is present in the total fluoride intake or uptake (Ophaug and
plasma; the rest is found mainly in or on the Singer, 1977; Morris and Smith, 1983; World
red blood cells (Carlson et al., 1960a, 1960b; Health Organization, 1984; Thiessen, 1988).
Hosking and Chamberlain, 1977; World However, if the fluoride intake or uptake is
Health Organization, 1984; Thiessen, 1988). high, the ionic form may predominate (World
Both the uptake of fluoride in calcified Health Organization, 1984). For the general
tissues and urinary excretion are fast population at a steady-state exposure to

fluoride, the plasma concentration of The precise mechanism of fluoride
inorganic (ionic) fluoride is directly related to incorporation into bone is not completely
the inorganic fluoride concentration of clear (Drury et al., 1980; Rioufol et al., 1983;
drinking water (World Health Organization, World Health Organization, 1984). The
1984). On the basis of the general general conclusion is that absorbed fluoride
pharmacological behaviour of fluorides, this is incorporated into hard tissues primarily by
relationship also holds for the uptake of an exchange process and by incorporation
gaseous fluorides. into the apatite during bone mineralization
(Thiessen, 1988). It has been suggested that
In a group of rural Chinese, organic fluoride
fluoride in extracellular fluid enters the
was found to contribute about 17% to serum
apatite crystal by a three-stage ion exchange
fluoride (Belisle, 1981). The half-life of
process. Hydroxyapatite of bone mineral
fluoride in plasma ranged from two to nine
exists as extremely small crystals surrounded
hours, depending on the dose level (Guy
by a hydration shell. Fluoride first enters the
et al., 1976; Ekstrand et al., 1978; Singer
hydration shell, in which the ions are in
and Ophaug, 1979; World Health
equilibrium with those of the surrounding
Organization, 1984). For the same intake,
tissue fluids and those of the apatite crystal
plasma fluoride/ ion concentration increases
surface. The second-stage reaction consists
significantly with age (Carlson et al., 1960a;
of an exchange between fluoride from the
Singer and Ophaug, 1979; World Health
hydration shell and the hydroxyl group at the
Organization, 1984). This might be explained
crystal surface. Once it has entered the
by a faster uptake by younger bone tissue,
surface of the crystal, fluoride is more firmly
which is less saturated with fluoride
bound. In the third stage, some of the
(Weatherell, 1966; World Health
fluoride may migrate deeper into the crystal
Organization, 1984). In addition, because of
as a result of recrystallization (World Health
the accumulation of fluoride in the skeleton,
Organization, 1984).
increased amounts may be released by the
bone remodelling process into the plasma of The amount of fluoride present in bone
older individuals (World Health Organization, depends on a number of factors, including
1984). fluoride intake, age, sex, bone type and the
topography of the bone. About half of
The study of the distribution of fluoride from
absorbed fluoride is deposited in the
inhaled gaseous fluorides, including
skeleton, where it has a long half-life. The
hydrogen fluoride, is complicated by fluoride
concentration of fluoride in bone increases
taken up orally by drinking water or food and
with age (Jackson and Weidmann, 1958;
by absorption through skin. Animal studies
Smith et al., 1982; World Health
with labelled gaseous fluorides would be the
Organization, 1984). Fluoride can be
ideal source of information on the
released from bone, as is evidenced by its
pharmacokinetics of gaseous fluorides
appearance in the urine in increasing
(see section 6.1).
amounts after exposure has ceased or
decreased (Largent et al., 1952; Grandjean
7.1.2.1 Bone
et al., 1983; World Health Organization,
Fluoride ions are taken up by bone through 1984). Hodge and Smith (1970) suggested,
replacement of hydroxyl ions in bone apatite. on the basis of published data, that such

removal of fluoride takes place in two phases Organization, 1984). The average
— a rapid process taking weeks and concentration of fluoride in dentine is 2–3
probably involving ion exchange in the times that in enamel and is affected by
hydration shell, and a slower phase with an growth and mineralization. As with bone and
average half-life of about eight years owing enamel, dentin fluoride concentrations are
to osteoclastic resorption of bone. Human higher in the surface regions than in the
data suggest that 2–8% of absorbed fluoride interior (U.S. National Academy of Sciences,
is excreted during 18 days following the 1971; World Health Organization, 1984).
initial retention (Spencer et al., 1975, 1981).
Because of a slower remodelling process, 7.1.2.3 Soft Tissues
fluoride is released more slowly from
The concentrations of fluoride in human soft
compact bone such as iliac crest than from
tissues reported by different authors vary
trabecular bone (Baud et al., 1978; World
greatly (World Health Organization, 1984). In
Health Organization, 1984).
general, however, only very small amounts
of fluoride are found in the normal soft
7.1.2.2 Teeth tissues. The highest levels are seen in the
The factors controlling the incorporation of kidneys (Hodge and Smith, 1965; U.S.
fluoride into dental structure have been Environmental Protection Agency, 1980;
reviewed by Weidmann and Weatherell Heifetz and Horowitz, 1986; Thiessen, 1988).
(1970), who concluded that the situation is Fluoride has a relatively short biological half-
essentially the same as that pertaining to life in these organs, and the soft tissue
bone (World Health Organization, 1984). fluoride concentration is therefore practically
Cementum is more similar to bone than are in equilibrium with that in the plasma. Unlike
enamel and dentine, but its fluoride fluoride in bone, the concentration does not
concentration has been found to be higher increase with age or duration of exposure
than that of bone (Singer and Armstrong, (Underwood, 1971; Drury et al., 1980;
1962). However, unlike bone, which can Thiessen, 1980; World Health Organization,
continue to take up fluoride throughout an 1984).
individual's lifetime, teeth incorporate fluoride
only during the period of calcification, which 7.1.2.4 Transplacental Transfer
is up to about age 12 in humans (Drury et al.,
Fluoride crosses the placenta. A study by
1980). Once formed, enamel and dentin
Armstrong et al. (1970) measured fluoride
differ from bone in that they do not undergo
from maternal uterine vessels and the
continuous remodelling. Fluoride
umbilical vein and artery at caesarean
concentrations in these tissues also vary with
section in human patients. The authors did
site, age and surface attrition, and they
not find any significant gradient between
increase with systemic and topical exposure
maternal and foetal blood levels, indicating
to fluoride (Weatherell et al., 1977;
that there is no placental barrier for fluoride.
Schamschula et al., 1982; World Health
At higher fluoride levels, a partial barrier may
Organization, 1984). In adults, fluoride
exist (Gedalia, 1970). The fluoride content of
concentrations measured in the surface layer
the foetal skeleton and teeth increases with
of enamel range from 900 to 2,700 mg kg-1
the age of the foetus and with the fluoride
(Berndt and Stearns, 1979; World Health

concentration in the mother (Gedalia, 1970; placenta, but it rarely seems to be excreted
World Health Organization, 1984). in milk to any extent (World Health
7.1.3 Excretion 7.1.3.1 Urine

The principal route of fluoride excretion is via Approximately half of absorbed fluoride is
the urine. Some excretion takes place excreted in urine (Drury et al., 1980; World
through sweat and faeces, and fluoride also Health Organization, 1984). Urinary excretion
appears in saliva. Fluoride crosses the is the major route of fluoride clearance from
the blood and from the body. Fluoride
clearance is less than that of creatinine
(approximately 0.15 L kg-1 body weight per
hour; Ekstrand et al., 1977b). Fluoride
appears rapidly in the urine after absorption.
Intravenously injected fluoride is excreted
even more rapidly (Ekstrand et al., 1977b:
Charkes et al., 1978; World Health
Organization, 1984). Renal fluoride ion
excretion involves glomerular filtration
followed by pH-dependent tubular
reabsorption. Reabsorption occurs by non-
ionic diffusion of hydrogen fluoride (Whitford
et al., 1976) and therefore is greater in acidic
urine than in alkaline urine (i.e., fluoride
removal from the body is greater in alkalosis
than in acidosis) (Reynolds et al., 1978;
Whitford et al., 1979). Several factors may
influence the urinary excretion of fluoride,
such as total current exposure, previous
exposure, age, urinary flow, urine pH and
kidney status (Whitford et al., 1976; Ekstrand
et al., 1978, 1982; Schiffl and Binswanger,
Urinary excretion of fluoride is decreased in
cases of renal failure or dysfunction, and
retention (i.e., bone deposition) of fluoride
increases accordingly (Gerster et al., 1983;
Kono et al., 1984a, 1984b). People with
renal dysfunction are therefore at a higher
risk for adverse health effects due to
fluoride. Some of the fluoride excreted
originates from fluoride released during bone

remodelling. Thus, excretion rates may average individual exposures were between
increase slightly with age, but no sex 1.2 and 3.9 mg m-3, six hours per day. No
difference in fluoride excretion has been
found (Toth and Sugar, 1976; Van de Putte
et al., 1977; World Health Organization,
1984). Younger persons who are actively
forming bone minerals excrete less fluoride
(i.e., a lower proportion of the absorbed
dose) than do adults. In situations in which
humans attain extremely high plasma levels
of fluoride, acute kidney dysfunction may
ensue, with decreased clearance of fluoride
(World Health Organization, 1984).
7.1.3.2 Faeces
Some fluoride is also excreted in the faeces.
Fluoride in the faeces is primarily ingested
fluoride that was not absorbed, and fluoride
excreted into the gastrointestinal tract does
not appear to be a major source of faecal
fluoride (Machle and Largent, 1943). This
implies that the concentration of fluoride in
the faeces will be low after dermal or
inhalation exposure to fluoride. The
proportion of the ingested fluoride that is
eliminated in the faeces varies depending on
circumstances (U.S. Environmental
Protection Agency, 1980; Maheswari et al.,
1981; Spencer et al., 1981; World Health
Organization, 1984). In persons not
occupationally exposed to fluoride and not
using fluoridated water, the faecal
elimination of fluoride is usually less than 0.2
mg/day (U.S. National Academy of Sciences,
1971). That some fluoride can be excreted
into the gastrointestinal tract is suggested by
the findings of Largent (1961), who found
that the faecal fluoride content of human
volunteers increased (2.5- to 6.7-fold,
highest amount was 0.70 mg/day) during a
period
(2–4 weeks) of hydrogen fluoride inhalation
-3
, or 0.9–8.1 ppm). The

coincident increase in oral fluoride (food or between 2 and 8 µg L-1, less than those in
water) was noted that might have accounted most milk substitutes (Thiessen, 1988).
for the observations.
7.1.3.3 Other Excreta 7.1.4 Monitoring Exposure to Gaseous

Fluoride by Pharmacokinetic Para-
Usually, only a few percent of the fluoride
taken up is excreted in perspiration. meters
However, under conditions of excessive Kono et al. (1987) measured urinary fluoride
sweating, as much as 50% of the total concentrations pre-shift and post-shift in 142
fluoride excreted may be lost via this route. workers exposed to hydrogen fluoride in their
These conditions can occur in cases of very workplace at a level of 3 ppm (2.5 mg m-3)
active persons or in people in hot climates and in 80 unexposed workers (ages 18–59).
and whose water intake is therefore very They reported a linear relationship between
high (Crosby and Shepherd, 1957; World the mean urinary fluoride concentrations and
Health Organization, 1984; Thiessen, 1988). the hydrogen fluoride concentration in the
After five young men ingested 4.0–5.0 mg of air. The mean urinary fluoride value was
fluoride per day, the fluoride concentration in 4 mg kg-1 for exposed workers.
their sweat was 0.3–1.8 mg L-1 ; two weeks Pre- and post-shift serum and urine samples
after cessation of the exposure, the of 142 hydrogen fluoride workers were
concentration was 0.2–0.3 mg L-1 (McClure compared with those of 270 unexposed
et al., 1945). workers (Kono et al., 1992). The pre-
Less than 1% of absorbed fluoride is exposure levels of serum and urinary fluoride
reported to appear in saliva (Carlson et al., in hydrogen fluoride workers were found to
1960a; Ericsson, 1969; World Health be higher than the control values, suggesting
Organization, 1984). Salivary fluoride that fluoride excretion from the body did not
concentrations are proportional to plasma return to control levels in the inter-shift period
fluoride concentrations and were found to be (12 hours). The post-shift serum and urinary
about 65% of plasma levels (Ekstrand et al., fluoride concentrations of hydrogen fluoride
1977a; World Health Organization, 1984; workers were significantly higher than the
Thiessen, 1988). In fact, saliva does not pre-shift concentrations. A good correlation
represent pure excretion, because most of was obtained between serum fluoride and
the fluoride will be recycled in the body. urinary fluoride concentrations. There was a
However, the fluoride content of the saliva is linear relationship between mean serum
of major importance for maintenance of fluoride concentration and hydrogen fluoride
fluoride levels in the oral cavity (World Health concentration in the workplace. A mean
Organization, 1984). serum fluoride concentration of 82.3 µg L-1
was estimated to correspond to an
The concentration of fluoride in human milk
atmospheric hydrogen fluoride concentration
is quite similar to that in plasma (Ekstrand
of 3 ppm (2.5 mg m-3). This is the maximum
et al., 1981), and significant exposure to
allowable environmental concentration
fluoride through human milk is therefore very
recommended by the Japanese Association
unlikely (World Health Organization, 1984).
of Industrial Health (1964) and by the
Observed fluoride levels in human milk are

American Conference of Governmental effects on inorganic phosphate and
Industrial Hygienists (1967). potassium concentrations in serum
(Boink, 1993).
In a similar study, Kono et al. (1993)
recorded hair, urine, and serum fluoride The literature on the influence of fluoride on
concentrations pre- and post-shift in workers enzyme systems is extensive. Both activating
exposed to hydrogen fluoride in the and inhibiting effects on enzymes have been
workplace. This study confirmed the linear described. Fluoride (as F- or as
relationship between serum and urinary undissociated hydrogen fluoride) may exert a
fluoride concentrations and the hydrogen direct action on the enzyme itself. More
fluoride concentration in the workplace. The frequently, however, the effect is indirect,
results support the speculation that fluoride involving complexation with a metal (e.g.,
is excreted in the hair after long-term Ca2+ or Mg2+) associated with the enzyme
exposure to hydrogen fluoride. The studies (Edwards et al., 1984; World Health
of Kono et al. (1987, 1992, 1993) suggest Organization, 1984; Anonymous, 1985;
that actual exposure to hydrogen fluoride Thiessen, 1988).
can be monitored by determining the serum,
Reviews of the literature (Hodge and Smith,
urinary and hair fluoride concentrations.
1965; Taves, 1970; Wiseman, 1970; Drury
Ehrnebo and Ekstrand (1986) monitored et al., 1980; Swedish Fluoride Commission,
individual plasma and urine fluoride 1981) suggest that low concentrations (about
concentrations pre- and post-shift in workers 10 µmol/L, i.e., 0.18 mg L-1) of fluoride in
at an aluminum plant in Sweden. They serum (but still much higher than normal) will
concluded that when fluoride exposure and stabilize and activate several soluble and
body burden are to be studied on an membrane-bound enzyme systems,
individual basis, the area under the plasma including adenyl cyclase (World Health
concentration–time curve and the amount of Organization, 1984). Alkaline phosphatase
fluoride excreted give better quantitative activity may be increased by fluoride (Farley
information than urinary fluoride et al., 1983), but changes in serum activity
concentration measurements. levels of this enzyme, and in serum calcium
and phosphate, have been found to be
minimal in potroom workers with skeletal
7.2 PHARMACODYNAMICS fluorosis (Boillat et al., 1979).
Fluoride toxicity involves at least four At higher serum fluoride concentrations
categories of major functional derangements (at least 0.3 mg L-1), fluoride will inhibit many
(Hodge, 1969; Gosselin et al., 1984; enzymes (World Health Organization, 1984).
Thiessen, 1988): (1) inhibition of enzymes Pyrophosphatase, for instance, is inhibited
controlling glycolysis or other vital pathways; by about 50% at 0.4 mg L-1, a level that is
(2) hypocalcaemia, resulting from binding higher than that found in the plasma of an
or precipitation of calcium by fluoride; individual with a skeletal fluoride content of
-1
(3) cardiovascular collapse caused by 6,000 mg kg and exposure to fluoride levels
hypotension and circulatory shock; and of 19 mg L-1 in drinking water (Ericsson et al.,
(4) damage to specific organs, primarily the 1973). In rats, fluoride ion has been shown
brain and the kidneys. Fluoride also has to be a potent inhibitor of liver cytosolic

pyrophosphatase (Baykov et al., 1992), the compounds could be part of a common
equilibrium inhibition constant for this mechanism for the skeletal and dental
enzyme being an order of magnitude lower effects of fluoride. Studies on rats have
than that for enolase. Baykov et al. (1992) shown that the proteoglycans undergo
suggested that fluoride-induced inhibition of molecular changes, particularly in terms of
pyrophosphatase may lead to an increase decreased size, during the development of
in cellular pyrophosphatase, which in turn dental fluorosis (Smalley and Embery, 1980).
inhibits fatty acid oxidation, protein and In rabbits, glycosaminoglycans show major
nucleic acid synthesis and bone formation changes, with the novel appearance of
and growth. dermatan sulphate, an
iduroglycosaminoglycan in fluorotic bone
Among the results of enzyme inhibition by
(Jha and Susheela, 1982a, 1982b). The
fluoride are hyperkalaemia and metabolic
serum of patients with endemic fluorosis
acidosis (Gosselin et al., 1984; World Health
(both skeletal and dental) contains
Organization, 1984). In acute fluoride
decreased concentrations of sialic acid and
poisoning, inhibition of metalloenzymes
increased levels of glycosaminoglycans
involved in essential processes can cause
compared with controls. Parallel results have
vital functions such as the initiation and
been reported for rabbits dosed with sodium
transmission of nerve impulses to cease.
fluoride at 10 mg kg-1 body weight daily for
Fluoride has been shown to affect the
eight months (Jha et al., 1983).
metabolism of glucose, lipids, cholesterol
and collagen in mammals, as well as the The strong affinity of fluoride for calcium
formation of bones and teeth, and many of results in hypocalcaemia. Fluoride
these metabolic effects are probably due to intoxication following dermal exposure to
the effects of fluoride on the enzymes hydrogen fluoride solutions or ingestion of
involved (Watanabe et al., 1975; Aitbaev, fluoride salts is characterized by severe
1984; Dousset et al., 1984; Drozdz et al., hypocalcaemia. Total calcium concentrations
1981, 1984; Den Besten, 1986; Thiessen as low as 1 mmol/L (normal 2.2–2.6 mmol/L)
et al., 1988; Boink, 1993). In these cases, have been found in the plasma of patients
serum fluoride levels, when reported, were at intoxicated with fluoride, whereas total
least 50 µg L-1 (Thiessen et al., 1988). protein, which binds approximately half of
Studies in humans have shown minimal the calcium present in plasma, was normal
increases in urinary cyclic adenosine (Boink, 1993). This fluoride-induced
monophosphate excretion and unchanged hypocalcaemia was accompanied by a rise in
plasma levels following an oral intake of plasma parathyroid hormone, indicating that
about 7 mg fluoride, which resulted in peak the normal physiological response to
plasma fluoride levels of about 0.3 mg L-1 hypocalcaemia of the parathyroid gland is
(Mornstad and Van Dijken, 1982). not affected by fluoride in humans or in
animals (Simpson et al., 1980; Kono et al.,
In the mineralization of bones and teeth, the
1982; Boink, 1993). It has been postulated
proteoglycans and their constituent
that fluorapatite is responsible for the
glycosaminoglycans form an integral part of
hypocalcaemia (Simpson et al., 1980; Boink,
the organic matrix of these tissues. Fluoride-
1993). If the formation of fluorapatite is
induced changes in the formation of these
involved in the aetiology of hypocalcaemia,

its structural formula [3Ca3(PO4)2 CaF2] and in experimental fluoride intoxication in
suggests that the inorganic phosphate dogs, rats and pigs, hyperkalaemia has been
concentration in plasma will decrease during observed (Baltazar et al., 1980; Boink,
fluoride intoxication (Boink, 1993). This is 1993). Hyperkalaemia can result in
indeed the case (Handler, 1945; Boink, ventricular fibrillation of the heart associated
1993). Changes in serum inorganic with
phosphate concentrations are the result of a
combination of (1) phosphate release from
cells, (2) calcium mobilization from bone
matrix, compensating for hypocalcaemia,
during which process phosphate ions are
released, (3) formation of fluorapatite, during
which process phosphate ions are bound,
and (4) impaired renal tubular phosphate
metabolism (Boink, 1993). After
intraperitoneal administration of sublethal
doses of fluoride in rats, increased urinary
phosphate excretion is observed (Kessabi
et al., 1980).
Hypocalcaemia in cases of acute fluoride
poisoning will often result in severe
involuntary muscle contractions (tetany)
(Gosselin et al., 1984). Many of the other
effects of fluoride, including cardiac
arrhythmias and other effects often
associated with acute systemic fluoride
poisoning, are thought to be caused by
hypocalcaemia (Abkurah et al., 1972;
Tepperman, 1980; Kono et al., 1982;
Gosselin et al., 1984; Heifetz and Horowitz,
1986; Thiessen, 1988).
Fluoride-induced potassium leakage from
erythrocytes has an absolute requirement for
the presence of extracellular calcium (Lepke
and Passow, 1968). McIvor and Cummings
(1987) suggested that fluoride causes
potassium leakage from erythrocytes by
inhibiting Na+,K+-ATPase, which in turn leads
to a rise in intracellular sodium concentration
and subsequent Na+–Ca2+ exchange. In two
fatal cases of fluoride intoxication of humans
(Baltazar et al., 1980; McIvor et al., 1983)

peaking of the T-waves in the 7.3 EFFECTS IN HUMANS
electrocardiogram (Baltazar et al., 1980).
A number of case reports on acute or chronic
Hypokalaemia has also been reported in one
poisoning by inhalation or exposure of skin
human case study (Abkurah et al., 1972).
to airborne hydrogen fluoride have been
Cardiovascular collapse is one of the two published, some of which have already been
most common immediate causes of death in reviewed by Heitman (1976), the World
cases of acute fluoride poisoning (Gosselin Health Organization (1984) and Thiessen
et al., 1984). The hypotension and circulatory (1988). Very little information from clinical
shock that are involved result from a studies is available on other gaseous
combination of factors such as fluid and fluorides. Most of the clinical cases of
electrolyte losses (due to vomiting and poisoning by hydrogen fluoride or other
diarrhoea or intragastric bleeding) and fluorides do not provide accurate quantitative
central vasomotor depression. Brain damage data; at best, they provide some indication of
from acute fluoride poisoning can cause the exposure levels leading to symptoms of
such symptoms as convulsions, lethargy, toxicity.
stupor and coma. Respiratory failure (the
Most case studies of acute or chronic
other leading cause of death in fluoride
intoxication by inhalation of hydrogen
poisoning) is thought to be of central nervous
fluoride or skin exposure concern accidents
system origin (Gosselin et al., 1984). Renal
in the work environment, whereas acute
injury, including transient diabetes insipidus,
intoxication with liquid hydrogen fluoride or
may also result from acute fluoride
fluoride salts was associated with suicidal or
poisoning, although it is probably not a major
accidental ingestion of fluoride-containing
concern in cases of chronic fluoride
products used in the home (World Health
exposure. Note that renal failure does not
appear to be a cause of death in fluoride
poisonings (Gosselin et al., 1984). More Gaseous fluoride compounds attack tissues
severe nephrotoxicity, also including much more vigorously than fluoride salts.
diabetes insipidus, may occur from exposure The toxicity of some gaseous inorganic
to fluorine-containing anaesthetic agents fluoride compounds decreases in the
such as methoxyflurane or enflurane (World following order: F2O, F2, HF, BF3 and H2SiF6
Health Organization, 1984; Thiessen, 1988). (World Health Organization, 1984).
Because of the chemical similarities between The odour threshold for hydrogen fluoride is
the halogens iodine and fluorine, there has reported to range from 0.02 to 0.22 mg m-3
been much interest in the possible effects of (0.02–0.27 ppm) (Sadilova, 1967; Lindberg,
fluoride on the thyroid (e.g., formation of 1968).
goitre) (Day and Powell-Jackson, 1972;
World Health Organization, 1984). Other
investigations have failed to reveal any
evidence that fluoride is responsible for any
disorder of the thyroid (Demole, 1970; Royal
College of Physicians, 1976; Sonneborn and
Mandelkow, 1981).

7.3.1 Acute and Short-term Health 50 mg m-3 (61 ppm), the same effects were
Effects noticed with the exception of the skin
In general, practically all the organs and irritation, but tickling and discomfort in the
systems are affected in acute fluoride larger air passages were noticeable with
poisoning after oral exposure to hydrogen each inspiration. At 26 mg m-3 (32 ppm), eye
fluoride or fluorides. The manifestations and nose irritation was mild and could be
include vomiting (sometimes blood-stained), tolerated for several minutes. There was no
diffuse abdominal pain of spasmodic type, coughing or sneezing. The taste of hydrogen
diarrhoea, cyanosis, severe weakness, fluoride was reported at all three
dyspnoea, muscle spasm, pareses and concentrations.
paralyses, cardiovascular disorders, Largent (1952) listed the increasing intensity
convulsions and coma (Hodge and Smith, of acute effects of increasing concentrations
1965; World Health Organization, 1984; of gaseous fluorides on the basis of
Thiessen, 1988). Although much has been controlled exposures of volunteers as
reported on acute poisoning by hydrogen follows: 2.1 mg m-3 (3 ppm) caused no local
fluoride and other fluorides, the exact cause immediate effects; 7 mg m-3 (10 ppm)
of death is not yet known (Boink, 1993). caused discomfort in many subjects; 21 mg
Massive impairment of the functioning of vital m-3 (30 ppm) revealed complaints in all
organs results in cell damage and necrosis. subjects and made them object to staying in
Terminally, there is a characteristic shock- the test environment; brief exposure to 42
like syndrome (World Health Organization, mg m-3 (60 ppm) caused definite irritation of
1984). the conjunctiva and nasal passages and
Gaseous fluorides can trigger a local tickling and discomfort of the pharynx and
reaction, causing considerable damage to trachea; and 84 mg m-3 (120 ppm), the
the skin, eyes and respiratory tract (World highest concentration tolerated (less than
Health Organization, 1984). Hydrogen one minute by two male subjects), resulted in
fluoride vapour was reported to also cause the previously mentioned effects and
skin burn (Browne, 1974; Largent, 1961). At smarting of the skin. Thus, the NOAEL in this
a concentration averaging 2.1–4.7 mg m-3 experiment for local effects was 2.1 mg F- m-
3
(2.6–5.7 ppm), hydrogen fluoride was .
reported to cause very slight irritation of the Elkins (1959) reported complaints of
face and eyes; frequent cutaneous erythema nosebleeds in workers engaged in the
was noticed; in one case, flaking of the hydrogen fluoride etching process and in one
epithelium, resembling sunburn, was seen. plant where welders were exposed to
-3
Machle et al. (1934) reported the effects of fluoride at 0.4–0.7 mg m .
airborne hydrogen fluoride on two human In an experimental inhalation study with
subjects. The highest concentration that the hydrogen fluoride, five human volunteers
subjects were able to tolerate for more than were exposed six hours per day, five days
one minute was 100 mg m-3. At this level, per week, for 10–50 days, at average
there was smarting of the exposed skin in concentrations of 1.42–4.74 ppm hydrogen
less than one minute, and conjunctival and fluoride (1.16–3.89 mg m-3). Slight irritation of
respiratory irritation was marked. At the nose was noticed in all subjects at

concentrations averaging 2.59–4.74 ppm exposed to airborne hydrogen fluoride were
hydrogen fluoride (2.12–3.89 mg m-3), examined for symptoms of intoxication, and
ranging from 1.8–7.9 ppm (1.5–6.5 mg m-3). their emergency room and hospital records
No signs or symptoms of liver toxicity or were studied. Most persons present at the
respiratory tract irritation were reported at emergency room were female (56%) or
these average concentrations (Largent, black (60%), and their mean age was 33.9
1961). The NOAEL for skin and eye irritation years. The most frequently reported
in this study was 0.9 mg m-3 (1.1 ppm). A symptoms were eye irritation (41.5%),
NOAEL for systemic effects could not be burning throat (21%), headache (20.6%) and
established. shortness of breath (19.4%). Physical
examination results were normal for 49% of
Pulmonary exposure to gaseous hydrogen
the cases. Decreased pulmonary function
fluoride may occur independently of or
was demonstrated by a pulmonary function
simultaneously with skin exposure.
test (42.3% < 80% of the predicted value for
Continued inhalation of hydrogen fluoride
forced expiratory volume in the first second
results in coughing, choking and chills,
[FEV1]). Hypoxaemia (<80 mm Hg in 17.4%)
lasting 1–2 hours after exposure. In the next
and hypocalcaemia (<8.5 mg dL-1 in 16.3%)
one or two days, fever, coughing, chest
were also noted. Ninety-four individuals were
tightness, rales and cyanosis may develop,
hospitalized, with an average stay of
indicating delayed pulmonary oedema
approximately two days, and more than 83%
(Dreisbach, 1971). The signs and symptoms
of all cases were discharged with a primary
progress for a day or two and then regress
diagnosis of "hydrogen fluoride exposure."
slowly over a period of a few weeks. At
There were no fatalities. The ambient air
higher exposures to gaseous hydrogen
concentration of hydrogen fluoride was not
fluoride, the delicate tissues of the lung may
monitored (Vernon et al., 1991; Wing et al.,
be intensely and even fatally irritated.
1991). Neither an effect level nor a NOAEL
A report by Gaugl and Wooldridge (1983) could be established.
suggested that pulmonary damage due to
Serum fluoride concentrations of 3–
inhibition of surfactant synthesis may result
15.5 mg L-1 have been associated with fatal
from systemic fluoride poisoning, even if the
cases of fluoride poisoning, from oral
fluoride was not inhaled. Death from acute
ingestion of fluorides, skin burns and
fluoride poisoning, whether from hydrogen
inhalation of hydrogen fluoride (Greendyke
fluoride inhalation or burns from ingestion of
and Hodge, 1964; Hodge and Smith, 1965;
fluoride salts, is usually from cardiac or
Yolken et al., 1976; Tepperman, 1980;
respiratory failure and generally occurs within
Gosselin et al., 1984). One case was
24 hours (Heifetz and Horowitz, 1986;
reported in which the serum fluoride level at
Thiessen, 1988).
autopsy was only 67 µg L-1 (Burke et al.,
As a result of an accident with the 1973), although one victim of oral fluoride
convection section of a hydrogen fluoride (NA2SiF6) poisoning survived despite a
alkylating heater of an oil refinery, an serum fluoride concentration of 14 mg L-1 six
estimated 24,000 kg of caustic hydrogen hours after ingestion (Yolken et al., 1976).
fluoride were released from a storage tanker.
In total, 939 persons who were potentially

The major route of clearance of excess about 3% of the predicted normal values,
fluoride from the body following poisoning is with no significant difference between the
the urinary system, and urinary fluoride chemical workers and the control group. The
levels as high as 87 mg L-1 (3.5 hours after residual volume expressed as 5% of total
the poisoning accidents) have been reported lung volume was 30.8% in the chemical
(Burke et al., 1973; Yolken et al., 1976). workers and 26.8% in the box plant workers,
Fluoride concentration also increased in soft with both values within normal limits (35%,
tissues following fatal intoxication. Levels of upper limit). This difference could be
10.6 mg kg-1, 4.6–11.6 mg kg-1, 4.4– explained by the difference in average age
11.2 mg kg-1 and 12.4–15.6 mg kg-1 have of the two groups. If a correction were made
been reported in heart, kidney, liver and lung for age and smoking, no effect of work-
tissue, respectively, following fatal intake of related exposure would be established. The
sodium fluoride (Hodge and Smith, 1965). urinary fluoride concentration before the shift
in the exposed group ranged from 0.33 to
0.48 mg L-1, compared with 0.95–26.6 mg L-1
7.3.2 Chronic Health Effects after the shift. For the control group, these
The clinical and epidemiological studies ranges were 0.50–1.88 and 0.50–2.38 mg L-
1
described in this section have been , respectively.
organized according to the predominant type In a plant for the electrolytic extraction of
of effect investigated or observed in each aluminum, which began operating in 1973,
study. 207 workers were medically examined in
view of some complaints of respiratory
7.3.2.1 Effects on the Respiratory System symptoms, which they associated with
Leidel et al. (1967) studied the effects of occupational exposure. The exposures
chemical irritations on exposed workers measured at different working places ranged
(305) in a chemical plant where hydrogen between 0.27 (0.32 ppm) and 4.1 mg m-3
fluoride was only one of the primary (5.0 ppm) for hydrogen fluoride, between
chemicals produced. The control group 0.02 and 1.6 mg m-3 for particulate fluorides
consisted of 88 workers in a box plant. and between 0.08 and 4.0 mg m-3 for sulphur
Twenty-eight samples of airborne hydrogen dioxide. The exposure levels were
fluoride were taken, with sampling periods occasionally higher than the threshold limit
-3
ranging from 10 to 30 minutes. The values in Yugoslavia (1.7 mg m [2.1 ppm]
concentration of hydrogen fluoride ranged for hydrogen fluoride; 1 mg m-3 for fluoride
from 0.07 to 10.0 ppm (0.06–8.2 mg m-3), expressed as F; and 10 mg m-3 for sulphur
with a mean of 1.03 ppm (0.85 mg m-3). The dioxide). The results of the study showed
samples for particulate fluoride were all that only 4.9% of workers had symptoms
under 0.5 mg m-3 (0.1–0.49 mg m-3). The defined as chronic bronchitis (87% of
mean age of the chemical plant workers was workers were <40 years of age). On the
44 years, 14 years older than that of the box other hand, a rather large number (10.2%)
plant workers. The observed values for complained of paroxysmal wheezing with
forced vital capacity (FVC), one-second dyspnoea. Out of 21 subjects with such
forced expiratory volume (FEV1) and complaints, 19 claimed that the broncho-
FEV1/FVC for the total group were within constrictive symptoms appeared after they

had started to work in the potrooms. Only A study was carried out on 1,242 aluminum
two of them had similar symptoms earlier. smelter workers to assess the impact on the
Pulmonary function tests revealed a slight lungs of exposure to multiple pulmonary
decrease in the mean values (compared with irritants, including gaseous and particulate
the predicted values) of FVC and FEV1 and fluoride and sulphur dioxide. A pulmonary
a higher decrease in the mean values of risk index was generated for each worker
mean expiratory flow, particularly in those which accounted for the nature, intensity,
workers who complained of paroxysmal duration and multiplicity of exposure. History
wheezing with dyspnoea. Owing to the and symptoms of pulmonary disease,
technological process used in the plant, it is spirometry and chest X-rays were performed
most likely that the respiratory effect is due on all 1,242 individuals, whereas single-
to the action of hydrogen fluoride (and breath diffusing capacity was tested in 460.
particulate fluoride). However, the The results were then compared in those at
mechanism of increased respiratory low, moderate and high pulmonary risk.
susceptibility remains to be clarified (Saric Highly significant differences were observed
et al., 1979). The design of the study did not between those with abnormal FEV1s and
permit an exact identification of the toxic FEFs and a high pulmonary risk index.
cause or the establishment of a NOAEL. Twenty-nine percent of all the workers and
10% of the 460 in whom the diffusing
A group of 74 workers in a hydrogen fluoride
capacities were tested were also found to
plant who had been exposed to hydrogen
be abnormal (Carnow and Conibear, 1978).
fluoride (periodically severely) for an average
No exposure levels were indicated, and no
of 2.7 years was studied. On a few
association could be drawn between the
occasions, there had been cases of upper
results and exposure to hydrogen fluoride
respiratory tract irritation. Repeated chest
alone (only an abstract was available).
X-rays over a five-year period did not reveal
any visible evidence of lung changes and did Ernst et al. (1986) explored the relationship
not differ from those of unexposed workers. between respiratory symptoms and lung
Periodic clinical examinations did not reveal function and exposure to ambient air
any incidence of pulmonary infection in the pollution consisting of particulate and
exposed workers (Evans, 1940). gaseous fluorides. The subjects were 253
North American Indian children 11–17 years
Johnson et al. (1973) conducted a study of
of age living on the Akwasasne reserve,
an aluminum reduction facility for the primary
which is adjacent to an aluminum smelter.
purpose of collecting and analysing airborne
Among boys, closing volume was increased
dust, coal tar, pitch volatiles, fluorides,
in those raised closest to the smelter
carbon monoxide and sulphur dioxide.
compared with those having lived most of
Although obstructive airway changes had
their lives farthest from this source of air
developed in some workers, the investigators
pollution. The ambient hydrogen fluoride
concluded that it was not justified to link the
concentration in the air was not reported. In
changes to a particular exposure because of
both sexes, there was a significant linear
the many contaminants involved in the
relationship between increasing CV/VC%
potroom area.
and the amount of fluoride contained in a
spot urine sample. The authors concluded

that exposure to fluoride air pollution in the exposure values were 1.77 (0.49–4.5) mg m-
3
community may be associated with for total dust and 0.31 (0.1–0.5) mg m-3 for
abnormalities in small airways. The total (gaseous and particulate) fluorides. The
implication of these abnormalities for future "worst-case" estimates showed mean values
respiratory health is unknown. No fluoride for gaseous fluorides of up to 3.13 mg m-3
concentrations in urine were included in this during work with gas skirt exchanges. The
report. aluminum potroom workers had obstructive
lung function impairment with a significant
Children living in the vicinity of a phosphate
decrease in expiratory flow and an increase
processing facility and exposed to fluoride
in residual volumes. Diffusing capacity was
concentrations ranging from about 100 to
found to be lower than in the controls. No
500 µg m-3 exhibited an impairment of
bronchial hyperreactivity was found in the
respiratory function. It is noted, however, that
aluminum potroom workers. The exposure to
it is unknown whether the concentrations
inhaled alumina and particulate and gaseous
were gaseous or total fluoride, and no other
fluorides in the plant was low, 15–20% of the
pollutants were recorded (Gezondheidsraad,
Swedish exposure limits (10 mg m-3 for
1981). In another study, no effects on
alumina and 2 mg m-3 for fluorides). The
respiratory function were observed at
finding of only modest lung function
gaseous fluoride concentrations up to
alterations with no bronchial hyperreactivity
16 µg m-3 (Biersteker and Boleij, 1986).
in the aluminum potroom workers is not
The effects on the respiratory tract as consistent with the results of other
observed in health assessments with regard investigators. This discrepancy can probably
to exposure were discussed by Wibowo and be explained by the fact that the exposure to
Zielhuis (1986). Occupational exposure to inhaled contaminants in the investigated
inorganic fluoride at concentrations of aluminum plant was low (Larsson et al.,
500 µg m-3 (200 µg/m3 gaseous fluorides) 1989).
was concluded to cause an increase in the
Golusinski et al. (1973) examined the
incidence of irritations of the upper
mucosa in 130 aluminum plant workers
respiratory tract. However, these results may
exposed to hydrogen fluoride. Monitoring of
have been influenced by other air pollutants.
hydrogen fluoride concentrations in the
In another study, exposures to considerably
atmosphere of electrolytic halls showed that
higher levels of gaseous hydrogen fluoride
the concentration of hydrogen fluoride often
(1,700 µg m-3, or 2,074 ppb) were reported
considerably exceeded 0.5 mg m-3 (0.6 ppm,
not to cause any appreciable effect on the
the Polish threshold limit value). In 30% of
respiratory tract (Wibowo and Zielhuis,
these workers, chronic inflammatory
1986).
changes, either hypertrophic or atrophic
Lung function and bronchial reactivity were rhinitis, were observed in the nasal mucosa.
measured in 38 aluminum potroom workers Biopsy specimens of septal mucosa were
with no airway symptoms and in 20 healthy examined histologically. In the patients with
referents (office workers). All participants hypertrophic rhinitis, numerous inflammatory
were non-smokers. The magnitude of infiltrates, consisting of mononuclear cells,
exposure to airborne dust (alumina) and were observed. The blood vessels were
fluorides was determined. The mean dilated, and extravasations of erythrocytes

were noted. The connective tissue stroma was reported over the two-year period,
showed evidence of oedema and regardless of the exposure level. Although
hyperactivity of the sero-mucous glands. In the authors recognized that recall bias and
the atrophic mucosa, fibrosis and behavioural sensitization possibly led to an
hyalinization of connective tissue stroma overestimation of the effect, they concluded
were seen associated with moderate that it was difficult to dismiss the
inflammatory infiltrates and evidence of interpretation that hydrogen fluoride
hypoactivity of the glands. exposure indeed caused health problems in
the community that continued for at least two
Burr et al. (1990) studied the health situation
years after the accident. No hydrogen
of workers in a glass company as related to
fluoride or other gaseous fluoride
exposure to noise and a number of air
concentrations in ambient air were reported.
pollutants, such as organic solvents and
hydrogen fluoride. The exposure to hydrogen A case report describes the symptoms of a
fluoride ranged from 0.34 to 3.0 mg m-3 57-year-old worker who had been working
(0.41–3.66 ppm). As well as the 171 workers' for 10 years, eight hours a day, in the
complaints of occupational pneumoconiosis, alkylation unit of an oil company, where
hearing loss and cumulative disorders were volatile fluorides were possibly released to
also diagnosed. The authors concluded that the atmosphere during loading and
the workers were potentially exposed to unloading and where tar residues that
cumulative trauma, acid mists and noise. No liberated fluoride fumes on exposure to air
specific associations between hydrogen were frequently produced. The worker was
fluoride exposure and toxic symptoms could possibly exposed to variable and unknown
be concluded, owing to multiple exposures. concentrations of hydrogen fluoride, either
from ambient air or from fumes. Episodes of
Following an accident at an oil refinery in
obvious acute poisoning were not
Texas City, Texas, which released about
uncommon, when immediate contact with the
40,000 pounds of hydrogen fluoride (Vernon
fumes caused symptoms and signs of
et al., 1991; Wing et al., 1991), a population-
intense eye irritation, tearing, blurred vision
based epidemiological study was conducted
and marked dyspnoea with severe
to evaluate the impact of the accident on the
respiratory tract pain and coughing. If he
health of the surrounding community (Dayal
could not get quickly away, the worker
et al., 1992). Exposure assessment was
developed nausea, epigastric pain, vomiting
done using a multipronged approach through
and sudden weakness. Such apparent acute
a door-to-door survey of 10,811 individuals.
episodes occurred approximately 10–15
A symptom survey resulting in 1,994
times a year. The noxious and irritating
completed interviews was conducted with a
odour of hydrogen fluoride was stated to
stratified random sample selection. The
have been identified. Within 1–2 years after
results showed a strong relationship (p < 10-
4 starting this work, the worker began having
) between the exposure (not given in the
rectal incontinence with diarrhoea. He
publication) and symptoms reported
developed severe headaches, increasing
following the accident and two years later,
weakness upon exertion and pain in the
most notably breathing and eye symptoms.
lower back. Leg and back pain became so
However, substantial improvement in health
severe that medical consultation was

necessary after eight years. The symptoms degree osteosclerosis, the findings were
progressed, and intellectual dysfunction was more pronounced. The outer boundaries of
also diagnosed. Finally, osteoarthritis of the the bones had become more irregular,
spine was diagnosed, abnormalities in the insertions of the tendons had started to
bladder were detected and lung function was calcify and the cortical substance of the long
decreased considerably (Waldbott and Lee, bone was widened, restricting the medullary
1978). No accurate exposure levels were canal. In third-degree osteosclerosis, the
measured. bone had become radiographically opaque
and the insertions of tendons, ligaments and
7.3.2.2 Effects on Bones and Teeth interosseous membranes were calcified. The
Roentgenological examinations of the lumbar first evidence of changes was found in the
spine of hydrogen fluoride workers showing pelvis and lumbar spine. As the process
high urinary fluoride concentrations (4.31– advanced, the changes spread to the rest of
26.6 mg L-1) did not show any skeletal the spinal column and the ribs, with
fluorosis. In a follow-up study of four workers extremities affected last. The degree of
two years later, one worker showed a slight radiological changes increased with the
first-degree osteosclerosis, which was not duration of employment. No exposure data
associated with disability. This worker had were given.
been employed for 11 years in a hydrogen A case of intoxication by long-term exposure
fluoride plant (Leidel et al., 1967). (15 years) to airborne hydrogen fluoride of a
Peperkorn and Kahling (1944) performed 40-year-old worker in a hydrogen fluoride
clinical and radiological examinations of 47 plant was reported by Peperkorn and Kahling
workers exposed to airborne hydrogen (1944). After seven years of employment,
fluoride, hydrofluoric acid and cryolite. No the worker began to have "rheumatic pains,"
quantitative exposure data were given. which, over the years, increased until he
Nearly all of the workers complained of mild became totally disabled. He complained of
to moderate back pain and stiffness, with stiffness in all joints, except hands and feet.
pain in the cervical spine in some cases. He had difficulty breathing when walking or
Some complained of pain in the thighs and climbing. He was prematurely aged,
knees. The majority of the men reported emaciated and pale, had a stiff posture and
shortness of breath on exertion. There was walked with small steps. Chest expansion
little evidence of cough, expectoration or was limited, as were movements of the
asthmatic conditions. Except for a few cases spine, hips and shoulders. Red and white
of skin burns, physical and chemical clinical blood cell counts, sedimentation, blood
findings were normal. Seventy-two percent of calcium and urinalysis were all reported
the workers showed osteosclerotic changes normal. No urinary fluoride levels were
varying from first degree to third degree. obtained. X-rays of the skeletal system
Characteristics of first-degree osteosclerosis showed third-degree osteosclerosis
included increased bone density and (Heitman, 1976). Exposure levels of airborne
thickened and misshapen structure of the hydrogen fluoride were not determined.
trabeculae, with the marginal contours of the A clinical study was carried out on a group of
bones exhibiting slight blurring. In second- workers exposed intermittently to hydrogen

fluoride and, to a lesser degree, calcium workers in spot samples ranged from 0.89 to
fluoride dust in a hydrofluoric acid 49.3 mg L-1 (with a mean of 10.8 mg L-1).
manufacturing plant, during an observation
In a clinical study workers at a phosphoric
period of five years. The exposure took place
acid producing plant, hydrogen fluoride and
during repair, and concentrations ranged
silicon tetrafluoride were released, but the
from 11 to 21 mg F- m-3 (13–26 ppm). The
airborne fluoride concentration was
mean urinary fluoride excretion of exposed
maintained below 3 ppm and averaged
workers was 3.65 mg L-1 (ranging from 4 to
2.4 ppm gaseous fluoride. Medical and
24 mg L-1). No significant effects on chest
radiological examinations revealed no
X-ray, haemoglobin or red and white blood
abnormalities. No consistent urinary fluoride
cell counts were detected. Roentgenological
excretion above 5 mg L-1 was observed
examinations of the pelvis and spine of 10
(Rye, 1961).
men working with the greatest potential
exposure did not show skeletal fluorosis after Derryberry et al. (1963) reported the
five years of intermittent exposure (Machle prevalence of osteosclerosis in 74 workers in
and Evans, 1940). a fertilizer manufacturing plant in relation to
fluoride exposure. Fluorides in the form of
Dale and McCauley (1948) provided data on
dust and gases in varying combinations and
the medical and dental conditions of workers
concentrations were produced throughout
engaged in the production of hydrofluoric
the process. A weighted airborne exposure
acid for 2–33 years. Eleven unexposed
was calculated for the period of employment
office and warehouse workers served as
of each worker. The individual exposure to
controls. No workplace airborne hydrogen
fluoride was 0.50–8.32 mg m-3, with 1.78–
fluoride levels were determined, but it was
7.73 mg m-3 being associated with increased
reported that window glass in a building
bone density observed in workers. The
housing the hydrofluoric acid retorts
difference in averages between the
corroded in a few months' time and had to be
increased bone density group (average
replaced periodically. Some workers in close
fluoride exposure 3.38 mg m-3) and the
proximity to the retorts experienced transitory
remainder of the exposed group, which
hyperaemia of the exposed skin. The skin of
showed significantly less bone density
the faces and hands appeared dehydrated, -3
(average fluoride exposure 2.62 mg m ),
roughened and irritated in the majority of the
was evaluated by the National Institute for
workers. Dental examinations showed fewer
Occupational Safety and Health (1977).
caries and fillings in the exposed group. In
Within the group of workers with increased
the trabecular pattern of the osseous
bone density, 60.9% of the urine samples
structure of the upper and lower jaws,
contained fluoride at concentrations of
changes were seen in 24 of the 40 workers,
4.0 mg L-1 or greater, compared with 47.5%
and questionable changes in eight. The bone
of the samples submitted by the group of
changes were characterized by an increase
workers without increased bone density.
in the number and thickness of trabeculae
This difference was significant (ranging from
and a corresponding decrease in the
p < 0.02 to p < 0.08). The average fluoride
intratrabecular and canalicular species. The
concentrations in urine for the increased
urinary fluoride excretion of 34 exposed
bone density group and the group without an

increase were 5.12 and 4.53 mg L-1, long-term exposure to fluoride at levels
respectively. These results demonstrate an above the threshold limit value is skeletal
association between increased fluoride alterations, or osteosclerosis. Following this
concentrations in the urine and an increase effect, exostosis and calcinoses of the
in suspected cases of osteosclerosis. ligaments occur.
Kaltreider et al. (1972) reported the results of In Germany, fluorosis with skeletal
roentgenographic examinations and urinary alterations rarely occurs. In a study in which
fluoride studies of potroom workers in two urine samples of individuals exposed to 2.4
aluminum plants. In one plant, 76 of 79 ppm airborne fluoride for eight hours were
potroom workers X-rayed revealed increased measured, it was concluded that the fluoride
bone density. Forty-six (58.2%) were concentration in urine increased in the first
classified as having slight fluorosis, showing two hours from 0.5 to 4 mg L-1 and in the
only accentuation of trabeculation and slight next 10 hours to 8 mg L-1; it then decreased
blurring of the bone structure; four (5.1%) in the next 12 hours to the initial
had moderate diffuse structureless bone concentration (Rye, 1961; Massmann 1981).
appearance; and 26 (32.9%) were classified Based on these observations, Massmann
as having marked fluorosis. Limited motion (1981) proposed a limit for fluoride of 7.0 mg
of the dorsolumbar spine was found in 22 L-1 in a 24-hour urine sample.
(20.6%) of the entire group of 107 potroom
In a study of 1,242 employees in an
workers and in none of the control group.
aluminum smelter using the Soderburg
The average fluoride exposure (eight-hour
process, Carnow and Conibear (1981)
working day) for the potroom workers ranged
reported that clinical musculoskeletal effects
from 2.4 to 6.0 mg m-3. The average urinary
can occur before skeletal fluorosis becomes
fluoride concentration in spot samples
apparent radiologically. Questionnaire
ranged from 8.7 to 9.6 mg L-1. The average
responses suggested an increased incidence
urinary fluoride excretion for the controls was
of musculoskeletal diseases with increasing
0.7 mg L-1. The investigation in the second
total fluoride exposure during employment.
potroom plant revealed no useful information
On the other hand, X-rays of the chest and
on possible toxic effects caused by exposure
lumbar spine failed to indicate any
to airborne fluorides.
differences related to the exposure index.
Massmann (1981) reviewed occupational As recognized by the authors of this paper,
epidemiological studies on fluorine and its this group of workers was heterogeneous,
inorganic fluorides. In Germany, the chemical exposures were mixed and
threshold limit values were reported to be ergonomic problems might have occurred.
0.1 ppm for fluorine, 3 ppm for hydrogen Unfortunately, the fluoride levels and the
fluoride (2.5 mg m-3) and 2.5 mg m-3 for lengths of exposure were not reported, thus
fluoride. Exceedances of these threshold making a dose–response relationship
limit values may lead to toxic effects and impossible to determine. The employees of
disease, such as fluorosis. Fluorosis is the same smelter were examined four years
characterized by stiffness and immobility of later by Chan-Yeung et al. (1983). The
the spine and "rheumatic" pains in the back exposure levels were determined, and two
and extremities. The most sensitive effect of control groups were examined. The fluoride

exposure level in the potroom was about 7.3.2.3 Effects on Kidneys
0.5 mg m-3 for the subgroup with the highest There are no clear indications from clinical
exposure. The authors were not able to case studies or epidemiological studies that
confirm the finding of Carnow and Conibear airborne hydrogen fluoride or other fluorides
(1981) that clinical musculoskeletal effects cause nephrotoxicity. Therefore, a NOAEL
could occur before skeletal fluorosis relating to potential nephrotoxicity for
becomes apparent radiologically. airborne hydrogen fluoride or other fluorides
It has been suggested that no discernible cannot be established. The information on
radiological or clinical signs of osteosclerosis potential nephrotoxicity comes from studies
will appear if the air concentrations of on humans exposed orally or parenterally to
inorganic fluoride in the workplace remain hydrogen fluoride, other fluorides or fluorine
below 2.5 mg m-3 and the urinary fluoride compounds.
concentration of workers does not exceed In cryolite workers, Roholm (1937) found
4 mg L-1 pre-shift (collected at least 48 hours only insignificant haematuria and no
after previous occupational exposure) and albuminuria. A possible relationship between
8 mg L-1 post-shift over long periods of time albuminuria and fluoride exposure was
(Dinman et al., 1976a; Hodge and Smith, suggested by Derryberry et al. (1963), but
1977). U.S. recommendations for the Kaltreider et al. (1972) were unable to show
threshold limit value for air fluoride have any chronic effects on the kidney. No renal
been established on the basis of these data disorder has been related to fluoride in areas
(National Institute for Occupational Safety of endemic fluorosis (Jolly et al., 1969) or to
and Health, 1977). However, some countries cases of industrial fluoride exposure (Dinman
recommend lower values. The former Soviet et al., 1976b; Smith and Hodge, 1979). No
Union recommended 1.0 mg m-3 as the cases of renal signs or symptoms are
threshold limit value for air fluoride mentioned in connection with prolonged
concentrations expressed as hydrogen intake of fluoride in the treatment of
fluoride (Gabovich and Ovrutskiy, 1969; osteoporosis and osteospongiosis (Causse
International Labour Organization, 1980; et al., 1980; Schamschula, 1981; Dixon,
U.S. Environmental Protection Agency, 1983), although a thorough examination of
1980). The correlation between fluoride kidney function may not have been carried
levels in the ambient air, fluoride levels in the out. No indications of increased frequency of
urine and the development of skeletal kidney diseases or disturbed kidney
changes needs further documentation functions have been recognized in areas
(World Health Organization, 1984). with fluoride concentrations in water of 8 mg
-1 -1
In a few individual cases of human exposure L (Leone et al., 1954, 1955), 2.0–5.6 mg L
to a high concentration of airborne hydrogen (McClure, 1946; Geever et al., 1958) and 1.0
fluoride, mottling of the teeth was described mg L-1 (Summens and Keitzer, 1975).
(Heitman, 1976; World Health Organization, Although there are no reports of fluoride-
1984). No other cases of dental fluorosis induced chronic renal disorders in healthy
after exposure to airborne fluorides have individuals, several studies have dealt with
been reported. The exposure levels at which the possible influence of fluoride on people
these effects occur have not been provided. with manifest kidney diseases. In patients

with kidney failure, fluoride excretion is these data are difficult to apply to the case of
decreased, and the ionic plasma fluoride exposure to airborne hydrogen fluoride or
concentration is higher than normal (Juncos other fluorides and the possibility of induction
and Donadio, 1972; Berman and Taves, of nephrotoxicity.
1973; Hanhijaervi, 1974). The capacity of the
An important finding of the previous studies
skeleton to store fluoride may provide a
is that people already suffering from
sufficient safety margin (Hodge and Smith,
insufficient kidney function might be at risk
1954; Hodge and Taves, 1970). On the other
from the toxic effects of fluorides owing to a
hand, it also seems plausible that an
decreased elimination of fluoride.
increased plasma fluoride concentration may
result from fluoride liberation from the bone
7.3.2.4 Carcinogenicity
resorption process involved in certain kidney
diseases. Patients with diabetes insipidus No specific epidemiological evidence is
may absorb excess amounts of fluoride available on the potential carcinogenicity to
because of the large quantities of fluids humans of hydrogen fluoride or other inhaled
ingested (World Health Organization, 1984; fluorides. Increased rates of cancer have
Thiessen, 1988). been reported for workers in several
occupations involving possible fluoride
In the case of fluoride-containing anaesthetic
exposure, including aluminum production,
agents, nephrotoxic effects were discovered
fluorspar mining and stainless steel pickling
as a side-effect related to the metabolites of
(de Villiers and Windish, 1964; Ahlborg et al.,
methoxyflurane or enflurane (Hagood et al.,
1981; World Health Organization, 1984;
Grandjean et al., 1985). However, all these
Kidney damage is related to the high serum
situations involved mixed exposures to
levels of fluoride and may show up days
several chemicals (e.g., radon in fluorspar
after anaesthesia.
mining, polycyclic aromatic hydrocarbons in
Although peak fluoride levels associated with aluminum production, and metal compounds
acute nephrotoxic effects have frequently and irritating acids in the stainless steel
been higher than 50 µg L-1, the total dose pickling house), and fluoride could not be
may be of more importance (Marier, 1982). specifically implicated as the cause of the
Changes in kidney function have been cancers (de Villiers and Windish, 1964; Drury
reported at lower fluoride levels (Jarnberg et et al., 1980; Ahlborg et al., 1981; World
al., 1979). At serum fluoride levels averaging Health Organization, 1984; Grandjean et al.,
about 6 µmol/L after enflurane anaesthesia, 1985). A correlation has also been
no nephrotoxic effects were seen, but blood demonstrated between cancer rates and
and urine levels of phosphorus changed industrial pollution from steel mills, which
considerably (Duchassing et al., 1982). It is emit fluoride among other things; again, no
not yet clear whether this circulating fluoride specific pollutant could be identified as the
is directly related to the nephrotoxicity or major cause of the increased cancer rates
whether fluoride is only indicative of (Drury et al., 1980; Thiessen, 1988).
metabolites of enflurane and methoxyflurane
The possible carcinogenic potential of
that formed during the biotransformation and
fluoride in drinking water has been
that caused the nephrotoxicity. Therefore,
investigated by comparing rates of cancer in

areas with artificially and naturally fluoridated 7.3.2.5 Reproductive Effects and
water. The International Agency for Teratogenicity
Research on Cancer (1982) concluded that Few reports are available concerning
when "proper account was taken of the industrial fluoride exposure of women. The
differences among population units, in one available epidemiological study of
demographic composition, and in some female workers in a superphosphate plant
cases also in their degree of industrialization found a higher incidence of gynaecological
and other social factors, none of the studies problems (e.g., menstrual irregularities,
provided any evidence that an increased vaginal and uterine inflammation, toxicosis
level of fluoride in water was associated with during pregnancy, untimely discharge of
an increase in cancer mortality." The U.S. amniotic fluid) in production workers than in
National Academy of Sciences (1977) and the control group of office workers and
the U.S. Environmental Protection Agency housewives (Hodge and Smith, 1977; Smith
(1985) also agreed that the available and Hodge, 1979). The production workers
information does not suggest that fluoride in were exposed to dust concentrations of 5–57
drinking water has increased the rate of mg m-3 and fluoride concentrations of 0.8–
cancer mortality. The U.S. Environmental 2.8 mg m-3 but specific information is not
Protection Agency (1985) stated that "there available on the possible correlation of
is not enough information to conclude that gynaecological problems with fluoride
fluoride presents a cancer risk to humans," concentrations in the workplace air or in the
but it has not officially classified fluoride or urine of the workers. No difference between
hydrogen fluoride with respect to groups was found in the numbers of
carcinogenicity (Thiessen, 1988). pregnancies, miscarriages or births.
No reports of increased incidence of either
spontaneous abortions or births of abnormal
fetuses have come from communities in the
United States with natural fluoride levels of
4 mg L-1 or more in drinking water (Hodge
and Smith, 1977; Smith and Hodge, 1979).
The U.S. Environmental Protection Agency
(1985) concluded that there is inadequate
evidence to support an association between
fluoride in U.S. drinking water and either
reproductive or teratogenic effects
(Thiessen, 1988).
7.3.2.6 Other Health Effects

Other effects of chronic fluoride exposure in
humans have been reported occasionally,
including thyroid injury, anaemia,
hypersensitivity and dermatological reactions

(Spira, 1944; Hodge, 1960; Waldbott, 1961, There is evidence that fluoride is genotoxic,
1973, 1980, 1981; McLaren, 1976; Waldbott based on the outcome of in vitro and in vivo
and Lee, 1978). None of these effects has studies. Sodium fluoride induced recessive
been convincingly established, particularly lethal mutations in Drosophila melanogaster
for fluoride concentrations likely to be and cytogenetic damage after intraperitoneal
encountered by the general public (Princi, injections in rodents. Generally, however, in
1960; Kaltreider et al., 1972; U.S. National studies in which fluoride was administered to
Academy of Sciences, 1977; Smith and laboratory animals by routes of exposure
Hodge, 1979; World Health Organization, similar to those by which humans are
1984; U.S. Environmental Protection normally exposed (i.e., orally), fluoride had
Agency, 1985). The U.S. Environmental no effect upon the frequency of
Protection Agency (1986) established an oral chromosomal aberrations, micronuclei, sister
Reference Dose for fluoride of 0.06 mg kg-1 chromatid exchange, DNA strand breaks or
body weight per day for children, an intake sperm morphology. The mechanism by
that corresponds to a fluoride level of 1 mg L- which sodium fluoride induces genetic
1
(1 ppm) in water. Neither dental nor skeletal alterations is not known; however, it is not
fluorosis occurs at this level. An inhalation likely due to an interaction between the
reference dose is not available (Thiessen, fluoride ion and DNA. Rather, it may be a
1988). secondary effect of the actions of fluoride
that results from its inhibition of enzymes
involved in DNA synthesis and/or repair.
7.4 SUMMARY OF HEALTH (Government of Canada, 1993)
EFFECTS OF INORGANIC Because there are inconclusive data on the
FLUORIDES AS REPORTED BY carcinogenic effects of inorganic fluoride and
CEPA because inorganic fluoride is not directly
genotoxic to DNA, the CEPA assessment
Inorganic fluorides, including gaseous
(Government of Canada, 1993) based its
fluorides, were assessed as part of the
toxicological evaluation on the NOAEL for
requirements of the Canadian Environmental
the most sensitive phenomenon in long-term
Protection Act (CEPA) (Government of
studies in both laboratory animals and
Canada, 1993). Carcinogenic effects of
humans. Based on the available data, it is
inorganic fluorides were reviewed in a large
evident that, following long-term exposure,
number of ecological studies, in studies with
skeletal effects in humans occur at dose
laboratory animals and in epidemiological
levels of exposure lower than those
studies. The CEPA report concluded that the
associated with other adverse health effects,
available data are inadequate to assess
which is likely a consequence of the
carcinogenicity in humans. This conclusion
accumulation of inorganic fluoride almost
supports earlier conclusions by the
exclusively in bone. Therefore, effects on the
International Agency for Research on Cancer
skeleton are considered to be the most
(1982), the World Health Organization
relevant in assessing the toxicological effects
(1984) and the U.S. Environmental
of long-term exposure to inorganic fluorides.
Protection Agency (Thiessen, 1988).
The lowest reported NOAEL for effects of
fluoride on the skeleton in Sprague-Dawley

rats was 1.8 mg kg-1 body weight per day the limitations of the protocol and
(and for Fischer-344 rats, 2.7 mg kg-1 body characteristics of the patients in these
weight per day). However, rats are generally studies. Moreover, these clinical studies
considered to be less sensitive than humans were undertaken to assess the considered
or larger animals to the toxicological effects beneficial effects. There are also limitations
of fluorides, owing to differences in in the experimental design of epidemiological
toxicokinetics and skeletal development. investigations. In addition, owing to the lack
Dogs and pigs are considered more of data on individual exposures in
appropriate models for the examination of epidemiological studies, it is difficult to derive
the potential effects of various agents on the meaningful conclusions concerning the
skeleton in humans. However, only short- exposure–response relationship for possible
term experiments with fluorides in dogs and skeletal effects associated with exposure to
pigs have been performed. Administration of fluoride.
fluoride at 0.32 and 2 mg kg-1 body weight
Estimating an effects threshold for the
per day to dogs and pigs, respectively, did
development of skeletal fluorosis (or related
not cause overtly pathological effects on the
changes) in humans exposed to inorganic
bone or on the general health of the animals.
fluoride is further complicated by differences
Owing to the availability of data, although in the radiological diagnosis of early-stage
limited, on exposure–response relationships skeletal fluorosis among health care
in humans and the interspecies variations in professionals, as well as by the multiplicity of
response to fluoride, the results of factors that may influence the amount of
epidemiological studies on the effects of fluoride deposited in bones. (Government of
fluoride in humans were taken into account Canada, 1994)
in the derivation of an effect level for
Nevertheless, considering the limitations of
inorganic fluoride. Case reports or
human studies and complicating factors
descriptive ecological studies of skeletal
involved, when the results are evaluated
fluorosis or osteosclerosis were not
collectively, the available data indicate that
adequately documented. There is also
potentially adverse effects associated with
limited quantitative information on exposure
skeletal fluorosis are likely to be observed at
to inorganic fluoride and the development of
fluoride intakes greater than approximately
skeletal effects in occupationally exposed -1
200 µg kg body weight per day. Although
workers (Government of Canada, 1993).
the relative risk of hip, wrist or spinal fracture
Inconsistent results of inherently limited
was increased in some groups of women
cross-sectional studies of small populations
residing in an elevated fluoride community
exposed to often unspecified concentrations
(72 µg kg-1 body weight per day) compared
of fluoride in the vicinity of industrial sources
with control communities, the estimated
contribute little to an assessment of an
intake of fluoride by these women was likely
exposure–response relationship for skeletal
underestimated, and the calcium intake was
effects associated with exposure to fluoride.
only 25% from normal. It is concluded,
Information obtained from clinical studies, in
therefore, on the basis of available data, that
which sodium fluoride was administered to
skeletal fluorosis is likely to be observed at
patients for the treatment of osteoporosis,
intakes greater than approximately
was considered to be inadequate, owing to

200 µg kg-1 body weight per day. Moreover, relatively low and are not expected to pose
predicted concentrations of fluoride in bone a significant problem with respect to human
resulting from a daily fluoride intake of exposure in the general population.
200 µg kg-1 body weight per day or higher
are within the range of those reported to be
associated with effects on the skeleton
(Government of Canada, 1993).
Based on the limited available data, adverse
effects upon haematopoietic, hepatic or renal
function are not expected to occur at this
fluoride intake level of 200 µg kg-1 body
weight per day, but at fluoride levels of about
387 µg kg-1 body weight per day or higher.
There are insufficient quantitative data
available from studies in humans from which
to conclude unequivocally that exposure to
this level of inorganic fluoride would have
adverse effects upon human reproduction
and development or on the central nervous
and immune systems (Government of
Canada, 1993).
The CEPA report concluded that, based
on available information, the estimated
average daily intakes of inorganic fluoride,
which range from approximately 0.5 to
160 µg fluoride by various age groups
in the general population (or up to
167 µg fluoride/kg bw/day by those in
the vicinity of point sources of inorganic
fluorides) are less than the level
(200 µg fluoride/kg bw/day) at which
adverse effects upon the skeleton (most
sensitive end-point on the basis of available
data in humans) are
anticipated.(Government of Canada, 1993)
7.5 HUMAN EXPOSURE

ASSESSMENT
Fluorides exist in both gaseous and
particulate forms. In Canada, ambient
concentrations of gaseous fluorides are

The levels of fluoride in ambient air in most recorded (Environment Canada, 1988,
parts of Canada are generally low or 1989).
undetectable (i.e., <0.05 µg m-3), although
No information on the concentration of
available data are limited. the average
fluoride in the indoor air of homes within
(monthly) mean concentration of fluoride in
Canada has been identified (Government of
an unspecified number of samples of
Canada, 1993). It may be assumed that
ambient air collected from as residential area
some gaseous fluorides enter the indoor air
in Toronto, Ontario (January 1981 – July
environment in conjunction with the
1981), was 0.03 µg m-3 (detection limit not
infiltration of outdoor air.
specified) (McGrath, 1983). This is similar to
the mean fluoride concentration of <0.05 µg
m-3 (detection limit 0.05 µg m-3) reported for
4,411 samples of ambient air collected in
1968 from 29 rural and 147 non-industrial
urban locations throughout the United
States; fluoride was not detected in any of
the rural samples (n=724), whereas the
concentration of fluoride in urban air
(n=3687) ranged from <0.05 to 1.65 µg m-3,
(Government of Canada, 1993).
For additional information on environmental
levels of hydrogen fluoride in Canada, refer
to section 3.4.
Higher ambient concentrations of gaseous
fluorides may be observed in the immediate
vicinity of industrial sources. Monitoring data
indicate that ambient air concentrations
measured in the vicinity of fluoride-emitting
industries can be up to an order of
magnitude greater than concentrations in
ambient air sampled at other locations.
Industrial sources found to release gaseous
fluorides include aluminum smelters, steel
plants and phosphorus plants. These
sources have been monitored in 11 locations
across Canada and are listed in table 5.
Monitoring data for gaseous fluorides in air
surrounding industries clearly show
concentrations much higher than in rural and
urban areas. Mean concentrations are
approximately 1.0 µg m-3. Concentrations as
high as 23.08 µg m-3 have also been

The estimated upper bound of daily intake of Canada, 1992; Government of Canada,
gaseous fluorides from ambient air by five 1993; Government of Canada, Supporting
age groups of Canadians in several locations Documentation, 1993; Environment Canada,
across the country are shown in table 9 1994).
(McGrath, 1983; Health and Welfare
Table 9 Estimated upper bound of daily intake of gaseous fluorides

Age and daily intake (µg/kg body weight per day)
Mean
Location conc. in air 0–6 7 months 5–11 12–19 20+ yearse
monthsa
b
(µg m-3) – 4 years yearsc yearsd
Ambient airf 0.03g 0.01 0.01 0.01 0.01 0.01

Cornwall, Ont. 0.79 0.23 0.30 0.35 0.29 0.26
Cornwall, Ont. 0.85 0.24 0.33 0.38 0.31 0.28
Cornwall, Ont. 0.43 0.12 0.17 0.19 0.16 0.14
Toronto, Ont. 0.07 0.02 0.03 0.03 0.03 0.02
Brampton, Ont. 0.73 0.20 0.28 0.32 0.27 0.24
Long Harbour, Nfld. 0.15 0.04 0.06 0.07 0.06 0.05
Long Harbour, Nfld. 0.14 0.04 0.05 0.06 0.05 0.05
Trail, B.C. 0.59 0.17 0.23 0.26 0.22 0.19
Arvida, Que. 0.67 0.19 0.26 0.30 0.25 0.22
Grande Baie, Que. 0.10 0.03 0.04 0.04 0.04 0.03
Laterrière, Que. 0.14 0.04 0.05 0.06 0.05 0.05
Beauharnois, Que. 0.10 0.03 0.04 0.04 0.04 0.03
a 3
Assumed to weigh 7 kg and breathe 2 m air per day (Health and Welfare Canada, 1992).
b 3
c 3
d 3
e 3
f
See table 3, "Ambient Air," in Government of Canada (1993).
g -3
Based on a mean concentration of inorganic (gaseous and particulate) fluoride in ambient air of 0.03 µg m , reported for
Toronto, Ontario (McGrath, 1983), and assuming the concentration in indoor air is identical to that in outdoor (ambient) air.
7.6 SUMMARY AND CONCLUSION essentially independent of the fluoride

source or the route of exposure. About 50%
Inhaled fluorides are rapidly absorbed in the
of absorbed fluoride is retained in the body.
upper respiratory tract; close to 100% of
Approximately 99% of the fluoride in the
inhaled hydrogen fluoride is absorbed. The
body is found in the skeleton; the remainder
fate and effects of absorbed fluorides are
is distributed in soft tissues. The half-life for

uptake by bone tissue is very short (about Clinical studies and most epidemiological
13 minutes). A portion of circulating fluoride studies on the inhalation of fluorides are not
(50%) is inorganic fluoride, and the adequately designed to allow a NOAEL for
remainder consists of organic fluorides. The systemic effects to be derived or a clear
inorganic fluoride content increases with the effect level to be identified. In many cases,
fluoride exposure level. The other half of individual exposures to fluorides in ambient
absorbed fluoride is rapidly eliminated from air were not monitored. In workplace studies,
the body. The majority is excreted by urine, people are exposed to many other potentially
and only a few percent is excreted in faeces toxic compounds in addition to gaseous and
and sweat. Urinary excretion of fluoride is particulate fluorides in the ambient air,
decreased in cases of renal dysfunction. In making it impossible to establish an
pregnant women, fluoride crosses the indicative NOAEL for gaseous fluorides. Only
placenta. Measurement of fluoride in serum, a few chronic epidemiological studies
urine or bone can under certain conditions provide some quantitative information on
serve to monitor exposure to gaseous exposure levels indicative of toxic effects on
fluorides. the skeleton (fluorosis and osteosclerosis)
and the respiratory tract. In humans, no
The pharmacodynamics of fluoride are
effects of chronic exposure to airborne
characterized by fluoride's effects on many
hydrogen fluoride on kidneys, brain, thyroid
enzyme systems and their complexing effect
or the haematopoietic system have been
on metal ions. At high exposure levels, these
convincingly established at exposure levels
properties result in several effects such as
considered to be representative of those
cardiovascular collapse, hypocalcaemia,
normally encountered in ambient air or
hyperkalaemia and skeletal alterations.
causing skeletal alterations or effects on the
Concentrations of gaseous fluorides in air respiratory tract. No specific epidemiological
that may pose a concern to human health data on the carcinogenic effects of airborne
have been reviewed in the CEPA fluoride are available. A definitive NOAEL for
Assessment Report for Inorganic Fluorides airborne fluoride, including hydrogen
(Government of Canada, 1993), as well as a fluoride, cannot be established from the
contract report on the health effects of available studies.
gaseous fluorides prepared for Health
For intake of fluorides by other exposure
Canada (Speijers, 1995). Health effects in
routes, it has been concluded by several
experimental studies are generally observed
review bodies that there is insufficient
at dose concentrations more than 100 times
evidence concerning any carcinogenic
mean concentrations found in ambient air.
properties of inorganic fluorides. In addition,
Studies in humans have revealed a NOAEL there is inadequate evidence to support an
of 0.9 mg m-3 of airborne hydrogen fluoride association between exposure to fluorides by
for skin and eye irritation and a NOAEL of different exposure routes and reproductive or
2.1 mg m-3 as fluoride for irritation of the teratogenic effects. As it is known from oral
respiratory tract. The odour threshold for studies that, at least for skeletal alterations,
hydrogen fluoride ranges from 0.02 to rats are less sensitive than humans, it is
0.22 mg m-3. prudent to rely mainly on the toxicological
data in humans for a toxicological evaluation.

Both for laboratory animals and for humans, most sensitive effect, are reported to appear
it can be concluded that adequate in children, the most sensitive receptor, at
toxicological studies with gaseous fluorides gaseous fluoride concentrations above 200
(including hydrogen fluoride) are very limited. µg m-3 (and 300 µg m-3 for particulate
fluoride). This concentration can be
From studies in occupationally exposed
considered a LOAEL for children (Turner et
adults, it can be concluded that, in general,
al., 1993).
exposure to airborne hydrogen fluoride levels
below 1.78–2.5 mg m-3 for an eight-hour The ambient air concentration of gaseous
work day will not cause skeletal alterations. fluoride ranges from <0.05 to 1.65 µg m-3 in
The occupational exposure limit for fluoride Canada and the United States. In most parts
of 2.0 mg m-3 per eight-hour shift of Canada, the exposure levels are below
corresponds to a fluoride intake of 286 µg 0.05 µm m-3. Ambient exposures range from
kg-1 body weight per day for a 70-kg adult 100 to 10,000 times less than the estimated
exposed to an equivalent concentration in effect level derived from human studies.
ambient air for 24 hours. This, then, is a Children, people with impaired kidney
NOAEL for skeletal effects. This can be function, industrially exposed workers and
compared with the CEPA report's conclusion persons living in the vicinity of a point source
(Government of Canada, 1993) that of fluoride emissions may be at somewhat
potentially adverse effects associated with greater risk than the general population,
skeletal fluorosis are likely to be observed at although all such groups are expected to be
fluoride intakes above about 200 µg kg-1 exposed to concentrations well below the
body weight per day. Pulmonary effects, the effect level.

Science Assessment Document for HF 7-81 CEPA/FPAC WGAQOG July 1996
8 REFERENCES
8.1 COMPREHENSIVE SURVEYS 8.2 LITERATURE CITED

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Thiessen, K.M. (1988) Summary Review of C.G. Aman (1981) Laryngeal cancer and
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APPENDIX HF REFERENCE DOSE DATABASE

Appendix HF Reference Dose Database
Study Conc.
Author(s) Year Journal Vol. pg Species Cultivar Life Stage Age
No. (µg m-3)
1 Adams, D.F., C.G. Shaw, and W.D. 1956 Phytopathology 46 587-591 Gladiolus Ethyl Cave Cole 4th true leaf 0.85
Yerkes Jr.
1 Adams, D.F., C.G. Shaw, and W.D. 1956 Phytopathology 46 587-591 Gladiolus Ethyl Cave Cole 4th true leaf 1.46
Yerkes Jr.
1 Adams, D.F., C.G. Shaw, and W.D. 1956 Phytopathology 46 587-591 Ponderosa Pine needles 50% 5 yr 1.46
Yerkes Jr. (Pinus ponderosa ) exposed
2 Solberg, R.A., D.F. Adams, and H.A. 1955 Proceedings of the Third National 164-176 Ponderosa Pine 4ft tall 0.61
Ferchau Air Pollution Symposium (Pinus ponderosa )
2 Solberg, R.A., D.F. Adams, and H.A. 1955 Proceedings of the Third National 164-175 Ponderosa Pine 4ft tall 0.20
Ferchau Air Pollution Symposium (Pinus ponderosa )
3 MacLean, D.C., R.E. Schneider, 1977 J. Amer. Soc. Hort. Sci. 102(3) 297-299 Green bean Tendergreen life span 0.60
and D.C. McCune (Phaseolus vulgaris
L.)
3 MacLean, D.C., R.E. Schneider, and 1977 J. Amer. Soc. Hort. Sci. 102(3) 297-299 Tomato Fireball life span 0.60
D.C. McCune (Lycopersicon
esculentum )
4 Zwiazek, J.J. 1994 Ontario Ministry of Environment White pine (Pinus seedlings 9 wks 0.61
and Energy, Research Technology strobus L.)
Branch, PIBS 2807, ISBN 0-7778-
0383-6
0383-6
0383-6
5 MacLean, D.C., and R.E. Schneider 1981 Environmental Pollution (Series A) 24 39-44 Wheat (Triticum Olaf anthesis 0.90
aestivum L.)
5 MacLean, D.C., and R.E. Schneider 1981 Environmental Pollution (Series A) 24 39-44 Wheat (Triticum Olaf boot stage 0.90
aestivum L.)
6 MacLean, D.C., R.E. Schneider, 1982 Environmental Pollution (Series A) 29 27-34 Jerusalem cherry 3 months 0.90
and L.H. Weinstein (Solanum pseudo-
capsicum L.)
7 Madkour, D., and L.H. Weinstein 1987 Environmental Toxicology and 6 627-634 Soybean (Glycine Hodgson veg. growth 0.70
Chemistry max L.)
7 Madkour, D., and L.H. Weinstein 1987 Environmental Toxicology and 6 627-633 Soybean (Glycine Hodgson veg. growth 3.50
Chemistry max L.)
8 Coulter, C.T., M.R. Pack, and C.W. 1985 Atmospheric Environment 19 (6) 1001- Gladiolus Snow Velvet 2 to 3 leaf stage 31 days old 2.90
Sulzbach 1007
8 Coulter, C.T., M.R. Pack, and C.W. 1985 Atmospheric Environment 19 (6) 1001- Gladiolus T210 2 to 3 leaf stage 31 days old 2.90
Sulzbach 1007
8 Coulter, C.T., M.R. Pack, and C.W. 1985 Atmospheric Environment 19 (6) 1001- Gladiolus T210 2 to 3 leaf stage 31 days old 2.90
Sulzbach 1007
8 Coulter, C.T., M.R. Pack, and C.W. 1985 Atmospheric Environment 19 (6) 1001- Gladiolus T210 2 to 3 leaf stage 31 days 2.90
Sulzbach 1007 old
Sulzbach 1007 old
Note: Scientific Data Used to Derive the Reference Levels is Indicated in Bold Face Type

Study Duration Dose Significant

Dose Protocol Endpoint Measured Effect Variability Comments
No. (days) Period (p<=.05)
1 1.00 0.85 1 standard leaf necrosis, inj. Yes - - Conc. in paper expressed as ppb (v/v?). Converted to µg m-3
chamber index=0.7 by x 1.22. Leaf injury index = % of leaf length injured.
2 6.60 4.03 7 standard time to first injury Yes - 20% Conc. in paper expressed as ppb (v/v?). Converted to µg m -3 by
chamber x 1.22. Duration is average time to first injury on 5 plants.
Treatment concentrations not measured. Dose includes periods
between exposures.
2 19.80 4.03 30 standard time to first injury Yes - 56% Conc. in paper expressed as ppb (v/v?). Converted to µg m -3 by
chamber x 1.22. Duration is average time to first injury on 5 plants.
Treatment concentrations not measured. Dose includes periods
between exposures.
3 43.00 25.80 30 standard 25% (F.W.) Yes 0.01 -
open-top marketable yield loss
3 93.00 55.80 90 standard growth, fruiting, fruit No - -

open-top production
4 2.00 1.22 1 standard increased plasma Yes - - Conc. in paper expressed as ppb (v/v?). Converted to µg m-3
chamber membrane leakage by x 1.22.
4 5.00 12.20 7 standard first injury Yes - - Conc. in paper expressed as ppb (v/v?). Converted to µg m-3
chamber by x 1.22.
4 20.00 12.20 30 standard first injury Yes - - Conc. in paper expressed as ppb (v/v?). Converted to µg m-3
chamber by x 1.22.
5 4.00 3.60 7 standard yield loss Yes 0.05 -

open-top
5 4.00 3.60 7 standard yield loss Yes 0.05 -

open-top
6 1.00 0.90 1 standard leaf necrosis Yes - - Injury occured when exposed in the dark and then brought
chamber into light. Lowest dose presented which caused an effect.
7 9.00 6.30 7 standard reduced C No 0.05 - Non-sensitive endpoint.

open-top translocation
7 9.00 31.50 7 standard reduced C Yes 0.05 - Non-sensitive endpoint.
open-top translocation
8 16 of 32 days 31.67 30 standard Overall average of - - Approx. 2 µg m -3/48hr with 48hr no exposure for 32 days. No
chamber 5.6% leaf area necrosis control (non-fumigated) for comparison and detection of a
significant effect.
8 16 of 32 days 45.83 30 standard Overall average of - - Approx. 2 µg m -3/48hr with 48hr no exposure for 32 days. No
(average) chamber 11.1% leaf area control (non-fumigated) for comparison and detection of a
necrosis. significant effect.
8 16 of 32 days 45.63 30 standard Average of 10.8% leaf - - Alternating 48 hr fumig. w/ 48 hr. non-fumig., total of 8
(average) chamber area necrosis. fumigations during the 32 day period. No control (non-fumig.),
therefore, there's no way of knowing if the effect observed is
statistically significant.
8 16 of 32 days 45.63 30 standard 16.7% leaf area Yes 0.05 - Alternating 96 hr fumig. w/ 96 hr non-fumig., total of 5
(average) chamber necrosis. fumig. in 32 days. Sign. greater effect than in 24 and 48 hr
fumigations in preceeding 2 lines. Therefore, this effect
would be significantly greater than a control, even though a
control is absent.
8 16 of 32 days 45.83 30 standard 15.4% leaf area Yes 0.05 - 96 hr fumig., 192 hr non-fumig., 192 hr fumig., 192 hr non-
(average) chamber necrosis. fumig., 96 hr fumig., Sign. greater effect than in intermittent
24 and 48 hr fumig. above. Therefore, this effect would be
significantly greater than a control, even though a control is
absent.

Study Conc.
No. (µg m-3)
Sulzbach 1007 old
9 McCune, D.C., T.L. Lauver, and K.S. 1991 Canadian Journal Forest Research 21 756-761 White spruce (Picea early summer 2 yr 2.63
Hansen glauca Moench.)
9 McCune, D.C., T.L. Lauver, K.S. 1991 Canadian Journal Forest Research 21 756-761 White spruce (Picea early summer 2 yr 5.14
Hansen glauca Moench.)
9 McCune, D.C., T.L. Lauver, and K.S. 1991 Canadian Journal Forest Research 21 756-761 Black spruce (Picea early summer 2 yr 2.29
Hansen mariana Mill.)
10 Murray, F. 1983 J. Amer. Soc. Hort. Sci. 108(4) 526-529 Grapevine (Vitis Shiraz early fruit to mature 0.17
sinifer L.) harvest
sinifer L.) harvest
sinifer L.) harvest
11 Murray, F. 1984 Environmental Pollution (Series A) 36 337-349 Grapevine (Vitis Shiraz growing season mature 0.27
sinifer L.)
sinifer L.)
sinifer L.)
sinifer L.)
12 Hitchcock, A.E., P.W Zimmerman, 1962 Contributions from Boyce 21 303-344 Gladious numerous varieties - - 0.16
and R.R. Coe Thompson Institute
13 Pack, M.R. 1972 Journal of the Air Pollution Control 22(9) 714-717 Strawberry Marshall growing season 0.55
Association
Association
Association
14 Mandl, R.H., L.H. Weinstein, and 1975 Environmental Pollution 9 133-143 Barley (Hordeum Dickinson seedling 10 days 0.72
M. Keveny vulgare L.)
14 Mandl, R.H., L.H. Weinstein, and 1975 Environmental Pollution 9 133-143 Corn (Zea mays L.) Marcross seedling 10 days 0.63
M. Keveny
15 Murray, F., and S. Wilson 1988c Environmental Pollution 55 239-249 Barley (Hordeum Clipper life span 0.38
vulgare L.)
15 Murray, F., and S. Wilson 1988c Environmental Pollution 55 239-249 Wheat (Triticum Halberd life span 0.38
aestivum L.)
16 Pack, M.R. 1971 Journal of the Air Pollution Controll 21(3) 133-137 Green bean Tendergreen life span 2.10
Assoc. (Phaseolus vulgaris
L.)
17 McCune, D.C., A.E. Hitchcock, and 1966 Contrib. Boyce Thompson Inst. 23(8) 295-299 Gladiolus Snow Princess 3 leaf stage 4 - 8 wks 2.10
L.H. Weinstein
18 Mohamed, A.H., J.D. Smith, and 1966 Can. J. Genet. Cytol. 8 575-583 Tomato 309-7-1-2 pre-flowering 3.00
H.G. Applegate (Lycopersicon
esculentum Mill.)
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Alfalfa (Medicago Ranger 2.50
Animals, and Humans" ed. J.L. sativa L.)
Schupe, H.B Peterson, N.C. Leone
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Barley (Hordeum Bonneville 0.34
Animals, and Humans" ed. J.L. vulgare L.)


8 16 of 32 days 45.83 30 standard 17.5% leaf area Yes 0.05 - 192 hr fumigation, 384 hr non-fumig., 192 hr fumig. Sign.
(average) chamber necrosis. greater effect than in intermittent 24 and 48 hr fumig. above.
Therefore, this effect would be significantly greater than a
control event though a control is absent.
9 2.08 5.48 7 standard apical necrosis - - No control for comparison.

open-top
9 2.08 10.71 7 standard 16% of trees with - - No control for comparison.

open-top apical necrosis
9 3.25 7.44 7 standard 30% of trees with - - No control for comparison.

open-top apical necrosis
10 64.00 10.88 90 standard no necrosis No - -

open-top
10 64.00 17.92 90 standard no yield effect No - -
open-top
10 64.00 17.92 90 standard foliar necrosis on 5% - - Marginal response (5% necrosis). No statistical comparison to
open-top of the leaves control. No effect on fruit yield or quality.

open-top
open-top
11 99.00 16.83 90 standard days to first injury Yes - - Well controlled experiment.
open-top
11 83.00 22.41 90 standard days to first injury Yes - - Well controlled experiment.
open-top
12 9.00 1.44 7 early 2.5-6.0 cm tip burn - - Poor statistical treatment of the data. Experiments inadequately
chamber controlled.
13 112.00 61.60 90 standard fruit wt. No 0.05 - No significant effect at this dose.
chamber
13 112.00 61.60 90 standard fruit development Yes 0.05 - Difficult to accurately calculate dose from the information
chamber given.
13 112.00 224.00 90 standard fruit wt. Yes 0.05 - Difficult to accurately calculate dose from the information
chamber given.
14 27.00 19.44 30 standard 6.7% leaf necrosis Yes - SD = 5.3%
chamber
14 27.00 17.01 30 standard necrotic lesions on Yes 0.001 -

chamber leaves increased
15 90.00 34.20 90 standard no. of grains/ear Yes 0.05 - Reduced no. of grains/ear offset by increased grain wt. and
open-top decreased by 6.25% number of tillers.
15 90.00 34.20 90 standard yield components No - - Wheat is not a sensitive species.

open-top
16 90.00 189.00 90 standard less vigorous F1 Yes - - This is not a sensitive endpoint. Statistical treatment of the data
chamber progeny is weak.
17 7 of 49 days 14.70 90 standard 40 mm leaf tip burn Yes - -

chamber
18 4.00 12.00 7 standard chromosomal Yes - - Treatments >4 days had effects as well. No leaf damage
chamber abnormalities (mitosis observed.
and meiosis)
19 26.00 65.00 30 greenhouse chlorosis, growth No - -

fumigation
19 107.00 36.38 90 greenhouse chlorosis, growth, No - -

fumigation yield

Study Conc.
No. (µg m-3)
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Sugar beets 0.43
Animals, and Humans" ed. J.L.
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Bean (Phaseolus Lima 0.64
Animals, and Humans" ed. J.L. sp.)
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Bean (Phaseolus Lima 0.40
Animals, and Humans" ed. J.L. sp.)
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Celery 0.89
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Celery 0.66
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on 105-115 Corn (Zea mays L.) 0.41
Vegetation, Animals, and Humans"
ed. J.L. Schupe, H.B Peterson, N.C.
Leone
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on 105-115 Corn (Zea mays L.) 0.47
Leone
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on 105-115 Gladiolus 0.66
Leone
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Gladiolus 1.38
Leone
Leone
Leone
Leone
ed. J.L. Shupe, H.B Peterson, N.C.
Leone
Leone
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Onion (Alium ) growing season 1.12


19 167.00 71.81 90 greenhouse plant weight, size, root No - -
fumigation sugar content

fumigation yield

fumigation yield

fumigation yield

fumigation yield
19 65.00 26.65 90 greenhouse 59% of leaves with Yes - -

fumigation chlorsis
19 45.00 21.15 90 greenhouse 37% of leaves with Yes - -

fumigation chlorsis
19 65.00 42.90 90 greenhouse 98% necrosis, 27% Yes - -

fumigation yield loss
19 72.00 99.36 90 greenhouse 73% necrosis, 76% Yes - - Treatment dose far too high relative to known sensitivity of
fumigation yield loss gladiolus to HF.

19 91.00 43.68 90 greenhouse 60% necrosis Yes - -

fumigation




19 128.00 143.36 90 greenhouse necrosis, growth, yield No - -

fumigation

Study Conc.
No. (µg m-3)
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on 105-115 Peach (Prunus ) 0.34
Leone
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on 105-115 Peach (Prunus sp.) 0.41
Leone
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Potato (Solanum growing season 0.44
Animals, and Humans" ed. J.L. tuberosum )
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Prune (Prunus sp.) 0.89
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Spinach 0.42
19 Hill, A.C., and M.R. Pack 1983 in "Fluorides, Effects on Vegetation, 105-115 Wheat (Triticum 0.38
Animals, and Humans" ed. J.L. aestivum L.)
20 Murray F., and S. Wilson 1988b Environmental and Experimental 28 343-349 Eucalyptus 18 months 0.38
Botany (Eucalyptus
tereticornis )
21 Murray F., and S. Wilson 1990 Journal of Experimental Botany 30 215-223 Soybean (Glycine Dragon 50 days old 0.27
max L.)
21 Murray F., and S. Wilson 1990 Journal of Experimental Botany 30 215-223 Maize (Zea mays QK 958 54 days old 0.26
L.)
21 Murray F., and S. Wilson 1990 Journal of Experimental Botany 30 215-223 Peanut (Arachis Virginia Bunch 53 days 0.27
hypogaea L.) old
21 Murray F., and S. Wilson 1990 Journal of Experimental Botany 30 215-223 Navy bean Gallaroy 26 days old 0.25
(Phaseolus vulgaris
L.)


fumigation growth
19 73.00 29.93 90 greenhouse severe chlorosis, 1% Yes - -

fumigation necrosis

fumigation
19 51.00 45.39 90 greenhouse necrosis Yes - - No description of results, and no quantitative description of
fumigation necrosis.

fumigation

fumigation
20 90.00 34.20 90 open-top, specific leaf area (cm2 Yes 0.01 Eucalyptus is not a Canadian species, nor are there close
field g-1) relatives. Therefore this data isn't used in the Ref. Level
calculation.
21 91.00 24.57 90 open-top, Yield No - No sign. effect on yield or yield components.
field
21 70.00 18.20 90 open-top, Yield No - Sign. reduction in no. of immature kernels; no effect on yield or
field any yield component.
21 105.00 28.35 90 open-top, Yield Yes 0.001
field
21 49.00 12.25 90 open-top, Yield No - Sign. reduction in avg. bean wt., compensated for by sign.
field increase in number of pods and beans per plant. No net effect on
yield.

Fluoridi U Amb Canada

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NATIONAL AMBIENT AIR QUALITY OBJECTIVES FOR

HYDROGEN FLUORIDE (HF)

SCIENCE ASSESSMENT DOCUMENT

A Report by the CEPA/FPAC Working Group on

This report has been prepared by the following people:

FIGURES AND TABLES ............................................................................................................iii

2 RECOMMENDED REFERENCE LEVELS FOR HYDROGEN FLUORIDE ...........................3

Science Assessment Document for HF i CEPA/FPAC WGAQOG July 1996

Appendix HF Reference Dose Database ................................................................................97

Science Assessment Document for HF ii CEPA/FPAC WGAQOG July 1996

Fig. 1 Regression analysis of HF-exposure data......................................................................5

Fig. 2 Average monthly ambient HF concentration.................................................................16

Fig. 3 HF fluoridation rate monthly averages for Ontario, 1991–92........................................17

Table 2 Estimates of HF air emissions ....................................................................................10

Table 3 Capacity of Canadian aluminum producers, 1992......................................................11

Table 4 Locations of coal-burning electricity generating utilities in Canada ............................12

Table 5 Ambient HF concentration ranges at selected Canadian sites, 1980–91 ...................15

Table 7 Susceptibility of animals to fluoride by ingestion ........................................................37

Table 9 Estimated upper bound of daily intake of gaseous fluorides ......................................71

Science Assessment Document for HF iii CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF vi CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 1 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 2 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 4 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 4 CEPA/FPAC WGAQOG July 1996

Fig. 1 Regression analysis of HF-exposure data selected from the scientific

Science Assessment Document for HF 5 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 6 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 7 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 8 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 9 CEPA/FPAC WGAQOG July 1996

Table 2 Estimates of HF air emissions

HF is also emitted from coal-burning utilities a local source on surrounding areas or to

Science Assessment Document for HF 10 CEPA/FPAC WGAQOG July 1996

Table 3 Capacity of Canadian aluminum producers, 1992

Science Assessment Document for HF 11 CEPA/FPAC WGAQOG July 1996

Table 4 Locations of coal-burning electricity generating utilities in Canada

Adams (1961) was able to derive an papers, direct measurements of gaseous HF

Science Assessment Document for HF 3-12 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 13 CEPA/FPAC WGAQOG July 1996

Table 5 Ambient HF concentration ranges at selected Canadian sites, 1980–91

Science Assessment Document for HF 15 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 16 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 17 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 18 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 19 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 20 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 21 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 22 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 23 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 24 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 25 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 26 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 27 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 28 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 29 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 30 CEPA/FPAC WGAQOG July 1996

4.3.10 Fibreglass Manufacturing

Science Assessment Document for HF 31 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 32 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 33 CEPA/FPAC WGAQOG July 1996

Science Assessment Document for HF 35 CEPA/FPAC WGAQOG July 1996