March 31, 1987
820K87109
XYLENES
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or.
B), Lifetime HAs are not recommended. The chemical concentration values for
Group A or B carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
Because each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.
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This Health Advisory is based on information presented in the Office of
Drinking Water's Health Effects Criteria Document (CD) for Xylenes (U.S. EPA,
1985a). The HA and CD formats are similar for easy reference. Individuals
desiring further information on the toxicological data base or rationale for
risk characterization should consult the CD. The CD is available for review
at each EPA Regional Office of Drinking Water counterpart (e.g., Water Supply
Branch or Drinking Water Branch), or for a fee from th« National Technical
Information Service, U.S. Department of Commerce, 5285 Port Royal Rd.,
Springfield, VA 22161, PB # 86-117942/AS. The toll-free number is (800)
336-4700; in the Washington, D.C. area: (703) 487-4650.
II. GENERAL INFORMATION AND PROPERTIES
Xylene Ortho-
CAS No. 1330-20-7
Structural Formula CH3 CH3 CH3
CH3
Synonyms
0 Xylols; dimethylbenzene
Uses
0 As solvents for paints, inks and adhesives, and as components of
detergents and other industrial and household products.
Properties (Verschueren, 1983)
Xylene Ortho- Meta- Para-
Chemical Formula C8H10 C8H1° C8H10
Molecular Weight 106.16 106.16 106.16
Boiling Point 144.4°C 139.0°C 138.4°C
Melting Point -25°C -48«C -13°C
Density
Vapor Pressure, mm Hg, 20° C 5 6 6.5
Water Solubility, mg/1, 20° C 175 160
25« c — — 198
Log Octanol/Water Partition 3.12 3.20 3.15
Coefficienta
Taste Thresholdb 0.3-1.0 mg/L
6dolr~Threshold
Conversion Factor 1 ppm =4.3 mg/m3
a Leo et al. (1971)
b National Inst. for Water Supply (1977)
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Xylenes March 31, 1987
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Occurrence
0 Xylene occurs naturally as a component of petroleum oil.
0 Xylenes are produced in large amounts, 5 billion Ibs in 1982 (U.S. ITC,
1984). Xylenes are also produced indirectly in large volumes during
gasoline refining and other operations. Xylene content of gasoline
can be as high as several percent.
0 Releases of xylenes to the environment are largely to air due to their
volatile nature, with smaller amounts to water and soil. Releases of
xylenes to water are due to spills and leaks of gasoline and other
petroleum products and, to a lesser extent, from the disposal of waste
from paints, inks and other industrial products. Because of the wide-
spread use of petroleum products, releases of xylene occur nationwide.
0 Xylenes degrade rapidly in air with a half life of a few days. Xylenes
released to surface water rapidly volatilize to the air. Xylenes
released to the ground bind somewhat to soil and slowly migrate with
ground water. Xylenes are biodegraded readily in soils and surface
waters. In the absence of biodegradation, xylenes are expected to be
stable in ground water.
0 Xylenes occur at low levels in drinking water, food, and air. Xylene
occurs in both ground and surface public water supplies, with higher
levels occurring in surface water supplies. The EPA's Community
Water Supply Survey, found 3% of all ground water derived public
drinking water systems sampled had levels greater than 0.5 ug/L. The
highest level reported in ground water was 2.5 ug/L. The survey
reported that 6% of all surface water derived drinking water system
are contaminated at levels higher than 0.5 ug/L. Hone of the systems
were reported to contain levels higher than 5.2 ug/L. No information
on the occurrence of xylene in foods has been identified. Xylenes
are found in the air of urban and suburban areas at levels of approxi-
mately 2 ug/L. Because of the widely dispersed low levels of xylenes
reported in water, air is likely to be the major source of exposure.
III. PHARMACOKINETICS
Absorption
0 Xylenes are absorbed readily after inhalation. Data on absorption
after ingestion are not available. Sedivec and Flek (1976) exposed
human volunteers to 0.2 mg/L (200 mg/m3) o-, m- and p-xylene vapors
and also to their mixture at a ratio of 1:1:1 for an 8-hour period.
The amount absorbed or retained was 63.6% * 4.2% for all isomers.
Distribution
0 Using whole-body autoradiography to detect radiolabeled xylene and
metabolites, Bergman (1978) reported distribution of the compound in
many tissues and organs of exposed mice. 14C-m-Xylene was administered
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Xylenes March 31, 1987
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to mice by inhalation for 10 minutes. Whole mice were frozen and
sectioned before exposure to X-ray film. In mice sacrificed immediately
after xylene exposure, radiolabel was detected in the lungs, liver
and kidneys. Rapid distribution to the brain and adipose tissue also
was evident. Two hours after exposure, radiolabel in the lungs was
restricted to the bronchi. In addition to the previously noted
organs, radiolabel was detected in the intestine after two hours.
The last traces of xylene were detected in the adipose tissue of mice
sacrificed four hours after exposure.
0 In rats exposed to 14c-p-xylene for 1-8 hours by inhalation at 208
mg/m3 (48 ppm), radiolabel was detected (in decreasing concentration)
in the kidneys, subcutaneous fat, sciatic nerve, blood, liver, lungs,
spleen, muscles, cerebrum and cerebellum (Carlson, 1981). Distribution
to all tissues was rapid, allowing near maximal levels in tissues
(except in kidneys and subcutaneous fat) within one hour.
Metabolism
0 Metabolism of xylenes varies somewhat according to the isomer but, in
general, proceeds by oxidation of methyl groups and ring hydroxylation.
The resulting metabolites include methyl hippuric acid (95%) and
xylenols (1-2%) (Harper et al. 1975).
Excretion
Elimination of xylenes is primarily through urinary excretion of
metabolites, representing nearly 95% of the absorbed dose, and the
remaining 5% by pulmonary exhalation of unchanged solvent (Sedivec
and Flek, 1976; Astrand et al., 1978).
IV. HEALTH EFFECTS
Humans
0 Tho lowest oral lethal dose (LDLo) for humans has been reported as
50 mgAg (NIOSH, 1978).
0 Xylenes produce central nervous system disturbances as reflected in
changes in numerative ability, short-term memory and electroencephalo-
graphic patterns.
8 Gamberale et al. (1978) observed no adverse health effects in fifteen
male subjects at rest following 70 minutes of inhalational exposure
to xylene at 435 and 1300 mg/m3. However, in another experiment,
eight male subjects were exposed to xylene at 1300 mg/m3 with 30
minutes of exercise on a bicycle ergometer which was continued during
behavior tests. The authors concluded that there was evidence of
reduction in the performance level on three of the four tests. The
tests conducted were: simple addition and choice reaction time,
short-term memory and critical Hicker fusion frequency.
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Savolainen et al. (1980) observed adverse effects on the psycho-
physiological functions in eight male students following inhalational
exposure to m-xylene at 391 mg/m3 for five consecutive days and one
day after the weekend. Body balance, reach on time and manual coordi-
nation were impaired. However, tolerance against the observed effects
developed during one working week.
Animals
Short-term exposure
In rats, oral LD50 values range from 4,300 to 5,000 mg/kg(NIOSH, 1978),
whereas inhalation IG^QB (four hours) are 20,600 to 29,000 mg/m3
(Carpenter et al., 1975; Harper et al., 1975).
Long-term Exposure
8 Carpenter et al. (1975) exposed rats to mixed xylenes at 770, 2000 or
3500 mg/m3 for six hours/day, five days/week for 13 weeks duration.
No effects on body weight gain, hematology, blood chemistry, kidney,
or liver weights or tissue histology were reported at two lower dose
levels. At the highest dose level, one rat treated at 3500 mg/m3 for
seven weeks showed slight renal tubular regeneration and, at 13 weeks,
the response was noted in rats in a non-dose-related manner.
0 Jenkins et al. (1970) reported the results of repeated (30 exposures)
or continuous inhalation exposure (90 days) to o-xylene by rats,
guinea pigs, monkeys and dogs. The exposure levels were 337 or
3,358 mg/m3 in rats and monkeys. One of the dogs exhibited tremors
of varying severity throughout exposure. No significant effects were
observed with respect to body weight, hematology, and histopathological
examination at the lower dose of 337 mg/m3 xylene.
0 Ultrastructural hepatic effects have been reported in rats following
subchronic oral exposure (200 mg/kg diet for up to 6 months) (Bowers
et al., 1982). Two types of intracellular vesicles in rats treated
with o-xylene were observed. One type appeared to be an extension of
the endoplasmic reticulum and the second vesicle type was associated
with the hepatocyte plasmalemma.
0 Tatrai et al. (1981) reported hepatomegally and ultrastructurally
evident proliferation of the smooth endoplasmic reticulum following
chronic inhalation exposure of 4750 mg/m3, eight hours/day, seven
days/week for one year in rats.
Reproductive Effects
0 No information was found in the available literature on the repro-
ductive effects of xylene.
Developmental Effects
e Twenty CFY rats, 240 to 280 g, were exposed to 1,000 mg/m3 of mixed
xylenes 24 hours/day during days 9 to 14 of pregnancy, and although
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there were increased incidences of fused sternebrae and extra ribs in
the offspring, the authors interpreted these as signs of embryotoxicity
rather than teratogenicity (Hudak and Ungvary, 1978). No signs of
maternal toxicity were noted. In-another study, Charles River rats
aged 12 weeks were exposed to 0, 100 or 400 ppm of xylenes (0, 434 or
1,730 mg/m3) during days 6 to 15 of pregnancy (25 rats per group); the
authors reported no signs of teratogenicity whether on the per-fetus
or the per-litter basis (Litton Bionetics, 1978).
Mutagenicity
0 Xylene was not mutagenic in the Ames test with or without activation
or in other short-term in vitro assays (Litton Bionetics, 1978).
Carcinogenicity
0 A long-term carcinogenicity bioassay in rats and mice has been
conducted by the NTP; however, the final report is not yet released
by the NTP (1986).
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA -
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Step 1: Determination of the Total Absorbed Dose (TAD)
Total absorbed dose = <1300 mg/m^)^^^) (p. 64) = 1U9 mg/kg/day
where :
1,300 mg/m3 = NOAEL based on absence of reduction in the performance
level on tests in humans.
1 m3 = assumed amount of air inhaled during one hour by a human
0.64 = 64% absorption factor in humans (Sedivek and Flek, 1976).
70 kg = assumed body weight of an adult.
Step 2: Determination of a One-day HA
One-day HA = <11-9 ngAg/day) (10 kg) . n.9 mg/L = 12 mg/L (12,000 ug/L)
(10) (1 L/day)
where:
11.9 mgAg/day = TAD.
10 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from a human study.
10 kg = assumed body weight of a child.
1 L/day • assumed daily water consumption of a child.
Ten-day Health Advisory
Insufficient data using oral exposure to calculate a Ten-day Health
Advisory are available currently. The Longer-term HA for the 10 kg child
(7800 ug/L) is recommended for a ten-day exposure.
Longer-term Health Advisory
The study by Carpenter et al. (1975) is the most appropriate basis for
calculating a Longer-term HA. A group of male rats were exposed by inhalation to
mixed xylenes at 770, 2000, or 3500 mg/m3 for six hours/day on five days/week
for up to thirteen weeks. No effects on body weight, hematology, blood
chemistry, kidney or liver weight, or tissue histology were observed at 770
or 2000 mg/m3 exposure levels of xylene. Based on the 2000 mg/m3 exposure
level as a NOAEL, a Longer-term HA may be derived for a 10 kg child as follows:
Step 1: Determination of the Total Absorbed Dose (TAD)
TAD - (2,000 mg/m3) (6 hours/day) (1 m3/hour) (5/7) (0.64) = ?8
(70 kg)
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where:
2,000 mg/m3 = NOAEL based on the absence of various toxicological
parameters in rats.
6 hr/day « duration of exposure.
i m3/hr = assumed respiratory volume for a rat.
5/7 = Conversion of 5 day/week dosing regimen to daily dosing
regimen.
0.64 - absorption efficiency in humans.
70 kg = assumed body weight of an adult.
Step 2: Determination of the Longer-term HAs
For a 10 kg child:
Longer-term HA = (78 mg/kg/day) (10 kg) = 7>8 /L (7 800 ug/D
(100) (1 L/day)
where:
78 mg/kg/day » TAD.
10 kg = assumed body weight of a child.
100 - uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
For a 70 kg adult:
Longer-term HA - (78 mg/kg/day) (70 kg) „ 27.3 mg/L (27,300 ug/L)
(100) (2 L/day)
where:
78 mgAg/day * TAD.
70 kg • assumed body weight of an adult.
100 » uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
2 L/day = assumed daily water consumption of an adult.
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Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classifed as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
Compound-specific, chronic ingestion data for xylenes do not exist at
this time. In the absence of appropriate ingestion studies, the Lifetime
Health Advisory for xylenes will be derived from the inhalation studies of
Jenkins et al. (1970) instead of the Bowers et al. (1982) study, even
though the route and duration of exposure used in the Jenkins study are not
ideal for development of a Lifetime HA.
The study by Bowers et al. (1982) was designed primarily to investigate
the first hepatocyte changes following long-term exposure to low levels of
o-xylene or other methylbenzenes administered to aged male rats, weighing 800
to 900 g, in the diet at 200 mgAg food for up to six months prior to electron
microscopic examination of their livers, but not other tissues. Certain
major weaknesses of this study rule out its consideration in the development
of a Lifetime HA. These weaknesses are: (1) the use of aged animals weighing
800 to 900 g in the experiment; (2) the stability of o-xylene was not monitored
(i.e., any loss due to evaporation not mentioned); (3) the use of a single
exposure level; (4) the lack of histological examination of tissues other
than liver of animals on test diet; and (5) ultrastructural changes in the
hepatocytes of rats ingesting o-xylene was not stated specifically for o-xylene.
The inhalation study by Jenkins et al. (1970) was selected as the basis
for the Lifetime HA. In sthis study, o-xylene was administered by inhalation
to rats, guinea pigs, monkeys and dogs for 30 repeated exposures at 3,358
mg/m3, eight hours/day, five days/week or 90 days continuous exposure at
337 mg/m3. At 3,358 mg/m3, two rats died on the third day of exposure and
another rat and one monkey died on day seven; one of the dogs exhibited
tremors of varying severity throughout the exposure. Besides the above
mentioned observations, no significant effects were observed with respect to
body weight, hematology, and histopathological examination at,either dose.
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Using 337 mg/m3 as a NOAEL, the Lifetime HA for a 70 kg adult is calcu-
lated as follows:
Step 1: Determination of the Total Absorbed Dose (TAD):
TAD = 037 mg/m3) (20 m^day) (0.64) = 6U62 mg/kg/day
70 kg
where:
337 mg/m3 • NOAEL based on the absence of toxicological effects in rats.
20 m3/day = assumed respiratory volume per day of a rat.
0.64 = assumed absorption factor for xylenes (64%).
70 kg = assumed body weight of an adult.
Step 2: Determination of the Reference Dose (RfD)
RfD = 61.62 mg/kg/day _, o.06162 mg/kg/day
(1,000)
where:
61.62 mg/kg/day = TAD.
1,000 - uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study
of less-than-lifetime duration.^ _^
Step 3: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL - <0.06162 mgAg/day) (70 kg) = 2.16 mg/L (2,200 ug/L)
(2 L/day)
where:
0.06162 mgAg/day - RfD.
70 kg * assumed body weight of an adult.
2 L/day » assumed daily water consumption of an adult.
Step 4: Determination of Lifetime HA:
Lifetime HA - 2 mg/L x 0.20 - 0.4 mg/L (400 ug/L)
where:
2 mg/L - DWEL.
0.20 » assumed relative source contribution of water.
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It should be noted that an estimated concentration for detection by
taste and odor in surface water was 0.3 to 1.0 mg/L (National Inst. for Water
Supply, 1977) and that the HA may exceed these thresholds for some individuals.
Evaluation of Carcinogenic Potential
0 The carcinogenic potential of xylene will be assessed when the report
of the NTP animal bioassay for carcinogenicity (1986) is available
for review.
0 IARC has not evaluated the xylenes for their carcinogenic potential.
0 Applying the criteria proposed in EPA's guidelines for assessment of
carcinogenic risk (U.S. EPA, 1986), the xylenes may be classified in
Group D: Not classified. This category is for agents with inadequate
animal evidence of carcinogenicity.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 NAS (1980) calculated SNARLs (Suggested-no-adverse-response-levels)
for xylenes in drinking water. The NAS-SNARL value was 21 mg/L
xylene for a 1-day exposure and 11.2 mg/L for a 7-day exposure (for
a 70 kg adult).
0 U.S. EPA (1981) also provided draft HAs for a 1-day, 10-day, and
longer-term exposure to xylenes in drinking water. These HAs for a
10 kg child were 12.0 mg/L, 1.2 mg/L, and 0.62 mg/L of xylene,
respectively.
0 ACGIH (1981) has recommended a TWA of 100 ppm.
VII. ANALYTICAL METHODS
0 Analysis of xylene(s) is by a purge-and-trap gas chromatographic pro-
cedure used for the determination of volatile aromatic and unsaturated
organic compounds in water (U.S. EPA, 1985b). This method calls for
the bubbling of an inert gas through the sample and trapping benzene
on an adsorbent material. The adsorbant material is heated to drive
off xylene(s) onto a gas chromatographic column. The gas chromatograph
is temperature programmed to separate the method analytes which are
then detected by the photoionization detector. This method is
applicable to the measurement of xylene(s) over a concentration range
of 0.02 to 1500 ug/L. Confirmatory analysis for xylene(s) is by mass
spectrometry (U.S. EPA, 1985c). The detection limit for confirmation
by mass spectrometry is 0.2 ug/L.
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Xylenes March 31, 1987
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VIII. TREATMENT TECHNOLOGIES
0 Treatment technologies which will remove xylene from water include
granulated activated carbon (GAG) and aeration. Limited data suggest
that conventional treatment may be partially effective in xylene
removal.
0 Dobbs and Cohen (1980) developed adsorption isotherms for several
organic compounds including p-xylene. It was reported that Filtrasorb*
300 carbon exhibited adsorptive capacities of 130 mg, 85 mg, 54 mg
and 35 mg p-xylene/g carbon when the initial xylene concentrations
were 10, 1.0, 0.1 and 0.01 mg/L, respectively. These values along
with Freundlich constants of K = 85 and 1/n • 0.19 indicate that
p-xylene and its closely related isomers, o-xylene and m-xylene, should
be amenable to carbon adsorption. Powdered activated carbon (PAC)
added at the well field to xylene-contaminated water containing 0.03
to 0.5 ug/L removed 60 to >99% of the xylene (U.S. EPA, 1985d). The
higher the xylene load the less efficient the adsorption. GAC was
slightly less effective when used o" water containing 0.05 ug/L in
xylene. In 16 samples tested the average removal efficiency was 50%
(McCarty et al., 1979a). When the m-xylene (0.046 ug/L) and p-xylene
(0.012 ug/L) were measured separately only 20% and 17% removals were
experienced using adsorption on GAC. Each of these studies, however,
were conducted on wastewater containing a number of organic contaminants
and therefore are not completely representative of what might be
expected with potable water treatment.
8 Xylene is amenable to aeration on the basis of its Henry's Law Constant
of 255 atoms at 20°C (U.S. EPA, 1985d). Although only 19% of the
xylene in wastewater could be removed by aeration, the process was
much more successful in the treatment of potable well water contaminated
by a gasoline spill (McCarty et al., 1979b). At air-to-water ratios
of 17 to 1 or greater, 80 to 100% removal of all three xylene isomers
was accomplished. At low air to water ratios (8:1), poor removal per-
formance was experienced. Average influent concentrations for the
o, m and p isomers were 10, 2.9 and 6.9 ug/L, respectively.
0 Air stripping is an effective, simple and relatively inexpensive
process for removing xylene and other organics from water. However,
use of this process then transfers the contaminant directly to the
air stream. When considering use of air stripping as a treatment
process, it is suggested that careful consideration be given to the
overall environmental occurrence, fate, route of exposure, and various
hazards associated with the chemical.
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Xylenes March 31, 1987
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IX. REFERENCES
ACGIH. 1981. American Conference of Governmental Industrial Hygienists.
TLVs - Threshold limit values for chemical substances in workroom air
adopted by ACGIH for 1981. Cincinnati, OH.
Astrand, I., J. Engstrom and P. Ovrum. 1978. Exposure to xylene and ethyl-
benzene. I. Uptake, distribution and elimination in man. Scand. J.
Work Environ. Health. 4(3):185-194.
Bergman, K. 1978. Application of whole-body autoradiography to distribution
studies of organic solvents. Int. Symp. Control Air Pollut. Work Environ.
(Part 2):128-139.
Bowers, D.E., Jr., M.S. Cannon and D.H. Jones. 1982. Ultrastructural changes
in livers of young and aging rats exposed to methylated benzenes. Am. J.
Vet. Res. 43(4):679-683.
Carlson, A. 1981. Distribution and elimination of carbon C14-labeled
xylene in rats. Scand. J. Work Environ. Health. 7:51-55.
Carpenter, C.P., E.R. Kinkead, D.L. Geary, Jr., L.J. Sullivan and J.M. King.
1975. Petroleum hydrocarbon toxicity studies: V. Animal and human
response to vapors of mixed xylenes". Toxicol. Appl. Pharmacol.
33:543-558.
Dobbs, R.A., and J.M. Cohen. 1980. Carbon adsorption isotherms for toxic
organics. EPA 600/8-80-023. MERL, EPA. Cincinnati, Ohio.
Gamberale, F., G. Annwall and M. Hultegren. 1978. Exposure to xylene and
ethylbenzene. III. Effects on central nervous functions. Scand. J.
Work Environ. Health. 4:204-211.
Harper, C., R.T. Drew and J.R. Fouts. 1975. Benzene and p-xylene: A com-
parison of inhalation toxicities and in vitro hydroxylations. In;
D.J. Jollow, J.J. Kocsis, R. Snyder and H. Vainio, eds. Biologically
reactive intermediates. London, England: Plenum Press, pp. 302-311.
Hudak, A., and G. Ungvary. 1978. Embryotoxic effects of benzene and its
methyl derivatives: toluene, xylene. Toxicology. 11:55-63.
Jenkins, L.J., R.A. Jones and J. Siegel. 1970. Long-term inhalation screening
studies of benzene, toluene, o-xylene and cumene on experimental animals.
Toxicol. Appl. Pharmacol. 16:818-823.
Leo, A., C. Hansch and D. Elkins. 1971. Partition coefficients and their
uses. Chera. Rev. 71:583.
Litton Bionetics, Inc. 1978. Mutagenicity evaluation of xylene: Final
report. LBI Project No. 20847. Submitted to American Petroleum Institute,
Washington, D.C. 150 pp.
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Xylenes March 31, 1987
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McCarty, P.L., D. Argo and M. Reinhard. 1979a. Operational experiences
with activated carbon adsorbers at Water Factory 21. J. AWWA.
11:683-689.
McCarty, P.L., K.H. Sutherland, J. Graydon and M. Reinhard. 1979b. Volatile
organic contaminants removal by air stripping. Presented at the Seminar
on Controlling Organics in Drinking Water, American Water Works Annual
Conference, San Francisco, CA.
Middleton, F.M., A.A. Rosen and R.H. Burttschell. 1958. Taste and odor
research tools for water utilities. J. Am. Water Works Assoc. 50:21-28.
NAS. 1980. National Academy of Sciences. Drinking Water and Health, Volume 3.
National Academy Press. Washington, D.C. p. 181.
National Institute for Water Supply. 1977. Compilation of odor threshold
values in air and water.
NIOSH. 1978. Registry of toxic effects of chemical substances. U.S.
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